Oral Health in America: A Report of the Surgeon General Department of Health and Human Services U.S. PUBLIC HEALTH SERVICE Pt IN O Xy NAT SzLAy « National Institute of Dental and Craniofacial Research Oyen Suggested Citation U.S. Department of Health and Human Servi ces. Oral Health in America: A Report of the Surgeon General. Rockville, MD: U.S. Department of Health-and Human Services, National Institute of Dental and Craniofacial Research, National Institutes of Health, 2000. eee Message from Donna E. Shalala Secretary of Health and Human Services The intent of this first-ever Surgeon General's Report on Oral Health is to alert Americans to the full meaning of oral health and its importance to general health and well-being. Great progress has been made in reducing the extent and severity of common oral diseases. Successful prevention measures adopted by communities, individuals, and oral health professionals have resulted in marked improvements in the nation’s oral and dental health. The terms oral health and general health should not be interpreted as separate entities. Oral health is integral to general health, this report provides important reminders that oral health means more than healthy teeth and that you cannot be healthy without oral health. Further, the report outlines existing safe and effective disease prevention measures that everyone can adopt to improve oral health and prevent disease. However, not everyone is experiencing the same degree of improvement. This Surgeon General's report addresses the inequities and disparities that affect those least able to muster the resources to achieve optimal oral health. For whatever the reason, ignoring oral health problems can lead to needless pain and suffering, causing devastating complications to an individual's well- being, with financial and social costs that significantly diminish quality of life and burden American society. For a third decade, the nation has developed a plan for the prevention of disease and the pro- motion of health, including oral health, embodied in the U.S. Department of Health and Human Services document, Healthy People 2010. This Surgeon General's Report on Oral Health empha- sizes the importance of achieving the Healthy People goals to increase quality of life and eliminate disparities. As a nation, we hope to address the determinants of health—individual and environ- mental factors—in order to improve access to quality care, and to support policies and programs that make a difference for our health. We hope to prevent oral diseases and disorders, cancer, birth defects, AIDS and other devastating infections, mental illness and suicide, and the chronic diseases of aging. We trust that this Surgeon General's report will ensure that health promotion and disease pre- vention programs are enhanced for all Americans. This report proposes solutions that entail part- nerships—government agencies and officials, private industry, foundations, consumer groups, health professionals, educators, and researchers—to coordinate and facilitate actions based on a National Oral Health Plan. Together, we can effect the changes we need to maintain and improve oral health for all Americans. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL iii Foreword The growth of biomedical research since World War II has wrought extraordinary advances in the health and well-being of the American people. The story is particularly remarkable in the case of oral health, where we have gone from a nation plagued by the pains of toothache and tooth loss to a nation where most people can smile about their oral health. The impetus for change—to take on the challenge of addressing oral diseases as well as the many other health problems that shorten lives and diminish well-being—led to the postwar growth of the National Institutes of Health. In 1948 the National Institute of Dental Research—now the National Institute of Dental and Craniofacial Research—joined the National Cancer Institute and the National Heart, Lung, and Blood Institute as the third of the National Institutes of Health. The Institute’s research initially focused on dental caries and studies demonstrating the effec- tiveness of fluoride in preventing dental caries, research that ushered in a new era of health promo- tion and disease prevention. The discovery of fluoride was soon complemented by research that showed that both dental caries and periodontal diseases were bacterial infections that could be pre- vented by a combination of individual, community, and professional actions. These and other appli- cations of research discoveries have resulted in continuing improvements in the oral, dental, and craniofacial health of Americans. Today, armed with the high-powered tools, automated equipment, and imaging techniques of genetics and molecular and cell biology, scientists have set their sights on resolving the full array of craniofacial diseases and disorders, from common birth defects such as cleft lip and palate to the debilitating chronic oral-facial pain conditions and oral cancers that occur later in life. The National Institute of Dental and Craniofacial Research has served as the lead agency for the development of this Surgeon General's Report on Oral Health. As part of the National Institutes of Health, the Institute has had ready access to ongoing federal research and the good fortune to work collaboratively with many other agencies and individuals, both within and outside government. The establishment of a Federal Coordinating Committee provided a formal mechanism for the exchange of ideas and information from other departments, including the U.S. Department of Agriculture, Department of Education, Department of Justice, Department of Defense, Department of Veterans Affairs, and Department of Energy. Active participation in the preparation and review of the report came from hundreds of individuals who graciously gave of their expertise and time. It has been a pleasure to have had this opportunity to prepare the report, and we thank Surgeon General David Satcher for inviting us to participate. Despite the advances in oral health that have been made over the last half century, there is still much work to be done. This past year we have seen the release of Healthy People 2010, which emphasizes the broad aims of improving quality of life and eliminating health disparities. The recently released U.S. General Accounting Office report on the oral health of low-income popula- tions further highlights the oral health problems of disadvantaged populations and the effects on their well-being that result from lack of access to care. Agencies and voluntary and professional organizations have already begun to lay the groundwork for research and service programs that directly and comprehensively address health disparities. The National Institutes of Health has joined these efforts and is completing an agencywide action plan for research to reduce health dis- parities. Getting a healthy start in life is critical in these efforts, and toward that end, a Surgeon ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL v Foreword General's Conference on Children and Oral Health, The Face of a Child, is scheduled for June 2000. Many other departmental and agency activities are under way. The report concludes with a framework for action to enable further progress in oral health. It emphasizes the importance of building partnerships to facilitate collaborations to enhance educa- tion, service, and research and eliminate barriers to care. By working together, we can truly make a difference in our nation’s health—a difference that will benefit the health and well-being of all our citizens. Ruth L. Kirschstein MD Harold C. Slavkin DDS Acting Director Director National Institutes of Health National Institute of Dental and Craniofacial Research vi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Pretace from the Surgeon General U.S. Public Health Service As we begin the twenty-first century, we can be proud of the strides we have made in improving the oral health of the American people. At the turn of the last century, most Americans could expect to lose their teeth by middle age. That situation began to change with the discovery of the properties of fluoride, and the observation that people who lived in communities with naturally fluoridated drinking water had far less dental caries (tooth decay) than people in comparable com- munities without fluoride in their water supply. Community water fluoridation remains one of the great achievements of public health in the twentieth century—an inexpensive means of improving oral health that benefits all residents of a community, young and old, rich and poor alike. We are fortunate that additional disease prevention and health promotion measures exist for dental caries and for many other oral diseases and disorders—measures that can be used by individuals, health care providers, and communities. Yet as we take stock of how far we have come in enhancing oral health, this report makes it abundantly clear that there are profound and consequential disparities in the oral health of our citi- sens. Indeed, what amounts to a “silent epidemic” of dental and oral diseases is affecting some pop- ulation groups. This burden of disease restricts activities in school, work, and home, and often sig- nificantly diminishes the quality of life. Those who suffer the worst oral health are found among the poor of all ages, with poor children and poor older Americans particularly vulnerable. Members of racial and ethnic minority groups also experience a disproportionate level of oral health prob- lems. Individuals who are medically compromised or who have disabilities are at greater risk for oral diseases, and, in turn, oral diseases further jeopardize their health. The reasons for disparities in oral health are complex. In many instances, socioeconomic fac- tors are the explanation. In other cases, disparities are exacerbated by the lack of community pro- grams such as fluoridated water supplies. People may lack transportation to a clinic and flexibility in getting time off from work to attend to health needs. Physical disability or other illness may also limit access to services. Lack of resources to pay for care, either out-of-pocket or through private or public dental insurance, is clearly another barrier. Fewer people have dental insurance than have medical insurance, and it is often lost when individuals retire. Public dental insurance programs are often inadequate. Another major barrier to seeking and obtaining professional oral health care relates to a lack of public understanding and awareness of the importance of oral health. We know that the mouth reflects general health and well-being. This report reiterates that gen- eral health risk factors common to many diseases, such as tobacco use and poor dietary practices, also affect oral and craniofacial health. The evidence for an association between tobacco use and oral diseases has been clearly delineated in every Surgeon General's report on tobacco since 1964, and the oral effects of nutrition and diet are presented in the Surgeon General's report on nutrition (1988). Recently, research findings have pointed to possible associations between chronic oral infections and diabetes, heart and lung diseases, stroke, and low-birth-weight, premature births. This report assesses these emerging associations and explores factors that may underlie these oral- systemic disease connections. To improve quality of life and eliminate health disparities demands the understanding, compas- sion, and will of the American people. There are opportunities for all health professions, individu- als, and communities to work together to improve health. But more needs to be done if we are to make further improvements in America’s oral health. We hope that this Surgeon General's report ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL vii Preface will inform the American people about the opportunities to improve oral health and provide a plat- form from which the science base for craniofacial research can be expanded. The report should also serve to strengthen the translation of proven health promotion and disease prevention approaches into policy development, health care practice, and personal lifestyle behaviors. A framework for action that integrates oral health into overall health is critical if we are to see further gains. David Satcher MD, PhD Surgeon General viii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments This report was prepared by the Department of Health and Human Services under the direction of the National Institutes of Health, National Institute of Dental and Craniofacial Research. Ruth L. Kirschstein MD Acting Director, National Institutes of Health, DHHS, Bethesda, MD Harold C. Slavkin DDS Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD David Satcher MD, PhD Assistant Secretary for Health and Surgeon General, Office of Public Health and Science, Office of the Secretary, Washington, DC Nicole Lurie MD, MSPH Principal Deputy Assistant Secretary for Health, Office of Public Health and Science, Office of the Secretary, Washington, DC Beverly L. Malone PhD, RN, FAAN Deputy Assistant Secretary for Health, Office of Public Health and Science, Office of the Secretary, Washington, DC Arthur Lawrence PhD Assistant Surgeon General, USPHS, Deputy Assistant Secretary for Health (Operations), Office of Public Health and Science, Office of the Secretary, Washington, DC Kenneth Moritsugu MD, MPH Deputy Surgeon General, USPHS, Office of the Surgeon General, Office of the Secretary, Washington, DC Allan S. Noonan MD, MPH Captain, USPHS, Office of the Surgeon General, Office of the Secretary, Washington, DC “Indicates Coordinating Author ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL PROJECT TEAM Caswell A. Evans DDS, MPH Project Director and Executive Editor Assistant Director, Los Angeles County Department of Health Services, Los Angeles, CA Dushanka V. Kleinman DDS, MScD Co-Executive Editor Assistant Surgeon General, USPHS Deputy Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD William R. Maas DDS, MPH, MS Assistant Surgeon General, Chief Dental Officer, USPHS Director, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Joan S. Wilentz MA Science Writer and Editor, Bethesda, MD Roseanne Price ELS Editor, Silver Spring, MD Marla Fogelman Editor, Silver Spring, MD CONTRIBUTORS Margo Adesanya DDS Staff Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Alfredo Aguirre DDS, MS Director and Associate Professor, Advanced Oral and Maxillofacial Pathology, State University of New York at Buffalo School of Dental Medicine, Buffalo, NY *Ronald Andersen PhD, MA Wasserman Professor of Health Services and Professor of Sociology, University of California Los Angeles School of Public Health, Los Angeles, CA Acknowledgments Jay R. Anderson DMD, MHSA Chief Dental Officer, Division of Community and Migrant Health, Bureau of Primary Health Care, Health Resources and Services Administration, DHHS, Rockville, MD Kenneth J. Anusavice PhD, DMD Associate Dean for Research, Chair. Department of Dental Biomaterials, University of Florida College of Dentistry, Gainesville, FL *Kathryn A. Atchison DDS, MPH Professor and Associate Dean for Research, University of California Los Angeles School of Dentistry, Los Angeles, CA James Bader DDS, MPH Professor, University of North Carolina School of Dentistry, Chapel Hill, NC Charles Bertolami DDS, D.Med.Sc. Dean, University of California San Francisco School of Dentistry, San Francisco, CA Aljernon Bolden DMD, MPH Director, Community Health Programs and Co- Director, Division of Dental Public Health, Boston University Goldman School of Dental Medicine, Boston, MA L. Jackson Brown DDS, PhD Associate Executive Director, American Dental Association, Chicago, IL Janet A. Brunelle MS Statistician (retired), National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD . Brian A. Burt BDS, MPH, PhD Professor of Dental Public Health, Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI Nita Chainani-Wu DMD, MPH University of California San Francisco School of Dentistry, San Francisco, CA David W. Chen MD, MPH Commander, USPHS, Deputy Director, Division of Associated, Dental, and Public Health Professions, Bureau of Health Professions, Health Resources and Services Administration, DHHS, Rockville, MD Joseph Ciardi PhD Consultant, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Betty DeBerry-Summer DDS, MPH Captain, USPHS, Chief Dental Officer, Bureau of Primary Health Care, Health Resources and Services Administration, DHHS, Bethesda, MD Teresa A. Dolan DDS, MPH Professor and Associate Dean, University of Florida College of Dentistry, Gainesville, FL *Chester W. Douglass DMD, PhD Professor and Chair, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA M. Ann Drum DDS, MPH Captain, USPHS, Acting Director, Division of Research, Education and Training, Maternal and Child Health Bureau, Health Resources and Services Administration, DHHS, Rockville, MD Thomas F. Drury PhD Senior Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Burton L. Edelstein DDS, MPH _ Director, Children’s Dental Health Project, American Academy of Pediatrics, Washington, DC Frederick C. Eichmiller DDS Director, Paffenbarger Research Center, American Dental Association Health Foundation, National Institute of Standards and Technology, Gaithersburg, MD Mary P. Faine MS, RD, CD Associate Professor and Director of Nutrition Education, University of Washington School of Dentistry, Seattle, WA Denise J. Fedele DMD, MS Chief Professional Development and Research in Dental Care Clinical Research, Veterans Administration Medical Health Care System, Department of Veterans Affairs, Perrypoint, MD Christopher H. Fox DMD, DMSc Director of Professional Relations, Europe, Colgate- Palmolive Co., New Jersey Philip C. Fox DDS Director, Research and Development Affiliation, Amarillo Biosciences, Inc., Amarillo, TX Lawrence J. Furman DDS, MPH Captain, USPHS, Head, Department of Health Services, U.S. Merchant Marine Academy, Kings Point, NY Isabel Garcia DDS, MPH Captain, USPHS, Special Assistant for Science Transfer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD *Robert J. Genco DDS, PhD Distinguished Professor and Chair, Department of Oral Biology, State University of New York at Buffalo School of Dental Medicine, Buffalo, NY Gretchen Gibson DDS, MPH Director, Special Care Dental Clinics, Veterans Administration North Texas Healthcare Systems, Department of Veterans Affairs, Dallas, TX x ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Sharon M. Gordon DDS, MPH Director, Office of Education, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Catherine Hayes DMD, DMSc Assistant Professor, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA Alice M. Horowitz PhD Senior Scientist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Herschel Horowitz DDS, MPH Consultant, Dental Research and Public Health, Bethesda, MD jeffrey Hyman DDS, PhD Epidemiologist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Amid I. Ismail BDS, MPH, DrPH Professor, University of Michigan School of Dentistry, Ann Arbor, MI : * Marjorie Jeffcoat DMD Rosen Professor and Chair, Department of Periodontics, University of Alabama School of Dentistry, Birmingham, AL Candace Jones RDH, MPH Captain, USPHS, Director, Dental Diseases Prevention Program, Indian Health Service, DHHS, Rockville, MD David Jones DDS, MPH Captain, USPHS (retired), Rockville, MD Judith A. Jones DDS, MPH Senior Research Associate, Veterans Administration Center for Health Quality, Outcomes and Economic Research, Department of Veterans Affairs and, Associate Professor, Boston University Goldman School of Dental Medicine, Bedford, MA Kaumudi J. Joshipura BDS, DSc Assistant Professor, Harvard School of Dental Medicine, Boston, MA Linda M. Kaste DDS, PhD Associate Professor and Division Director, Division of Dental Public Health and Oral Epidemiology, Medical University of South Carolina College of Dental Medicine, Charleston, $C William Kohn DDS, MS Captain, USPHS, Associate Director for Science, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Marv Sue Lancaster RN, MA Health Education Specialist, Centers for Disease Control and Prevention, DHHS, Atlanta, GA ORAL HEALTH IN AMERICA: Acknowledgments Linda LeResche ScD Research Professor, University of Washington School of Dentistry, Seattle, WA James Lipton DDS, PhD Captain, USPHS, Assistant Director for Training and Career Development, National Institute of Dental and Craniofacial Research, DHHS, Bethesda, MD Reginald Louie DDS, MPH Captain, USPHS, Regional Dental Consultant, Health Resources and Services Administration, DHHS, San Francisco, CA *Irwin D. Mandel DDS Professor Emeritus, Columbia University School of Dental and Oral Surgery, New York, NY Stephen E. Marcus PhD ° Epidemiologist, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD Frank Martin DDS, MPH Captain, USPHS, Assistant Chief, Dental Services Branch (retired), Indian Health Service, DHHS, Rockville, MD Wendy E..Mouradian MD Director, Children’s Hospital and Regional Medical Center, Departments of Pediatrics, Pediatric Dentistry, Medical History and Ethics, University of Washington, Seattle, WA *Linda Niessen DMD, MPH, MPP Professor, Baylor University College of Dentistry and Vice President, DENTSPLY International, York, PA Ruth E. Nowjack-Raymer RDH, MPH Public Health Researcher, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Steven Offenbacher DDS, PhD, MMSc Professor and Director, Center for Oral and Systemic Diseases, University of North Carolina, Chapel Hill, NC H. Whitney Payne, Jr. DDS, MPH Captain, USPHS, Chief of Dental Services, Federal Correctional Institution, Federal Bureau of Prisons, Department of Justice, Seogoville, TX Edward Peters DMD Instructor in Oral Health and Epidemiology, Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA Douglas E. Peterson DMD, PhD Professor and Head, Department of Oral Diagnosis, University of Connecticut School of Dental Medicine, Farmington, CT Maryann Redford DDS, MPH Health Scientist Administrator, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD A REPORT OF THE SURGEON GENERAL xi Acknowledgments *Susan Reisine PhD Professor, University of Connecticut School of Dental Medicine, Hartford, CT John Rossetti DDS, MPH Captain, USPHS, Chief Dental Officer, Health Resources and Services Administration, DHHS, Rockville, MD *R. Gary Rozier DDS, MPH Professor, Department of Health Policy Administration, University of North Carolina School of Public Health, Chapel Hill, NC Susan Runner DDS, MA Captain, USPHS, Branch Chief Dental Devices, Center for Devices and Radiological Health, Food and Drug Administration, Rockville, MD John S. Rutkauskas DDS, MS Executive Director, American Association of Pediatric Dentistry, Chicago, IL Margaret Scarlett DMD Captain, USPHS, Office of the Secretary, Office of Public Health and Science, DHHS, Washington, DC Don Schneider DDS, MPH Captain, USPHS, Chief Dental Officer, Health Care Financing Administration, Center for Medicaid and State Operations, DHHS, Baltimore, MD Stephen T. Schultz DDS, MS, MPH Lieutenant Commander. U.S. Navy, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Robert H. Selwitz DDS, MPH Captain, USPHS, Senior Dental Epidemiologist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Gerald Shklar DDS, MS Charles A. Brackett Professor of Oral Pathology, Harvard School of Dental Medicine, Boston, MA Charles Shuler DMD, PhD Director, Center for Craniofacial Molecular Biology, George and Mary Lou Boone Professor of Craniofacial Molecular Biology, University of Southern California School of Dentistry, Los Angeles, CA Gary Slade BDSc, DDPH, PhD Assistant Professor, University of North Carolina School of Dentistry, Chapel Hill, NC Ronald P Strauss DMD, PhD Professor, School of Dentistry and School of Medicine, University of North Carolina, Chapel Hill, NC Lawrence Tabak DDS, PhD Senior Associate Dean for Research, University of Rochester School of Medicine and Dentistry, Rochester, NY George W. Taylor DMD, DrPH Assistant Professor of Dentistry, University of Michigan School of Dentistry, Ann Arbor. MI Amardeep Singh Thind MD, PhD Assistant Professor, University of California Los Angeles School of Public Health, Los Angeles, CA Scott L. Tomar DMD, DrPH Epidemiologis/Dental Officer, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Benedict I. Truman MD, MPH Senior Scientist and Epidemiology Program Officer, Centers for Disease Control and Prevention, DHHS, Atlanta, GA William Wathen DMD Associate Dean, Center for Professional Development, Baylor College of Dentistry, Dallas, TX *Jane A. Weintraub DDS, MPH Lee Hysan Professor and Chair, Division of Oral Epidemiology and Dental Public Health, University of California San Francisco School of Dentistry, San Francisco, CA *B. Alex White DDS, DrPH Assistant Program Director, Economic, Social, and Health Services Research, Kaiser Permanente Center for Health Research, Portland, OR Deborah Winn PhD Senior Investigator, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Athanasios I. Zavras DMD, MS, DMSc Assistant Professor, Department of Health Policy and Epidemiology, Harvard School of Dental Medicine, Boston, MA SENIOR REVIEWERS Clifton Dummett Sr. DDS Distinguished Professor Emeritus, University of Southern California School of Dentistry, Los Angeles, CA Helen C. Rodriguez-Trias MD, FAAP Past-President, American Public Health Association, Brookdale, CA John Stamm DDS, DDPH, MScD Dean, University of North Carolina School of Dentistry, Chapel Hill, NC REVIEWERS Michael C. Alfano DMD, PhD Dean, New York University College of Dentistry, New York, NY Myron Allukian Jr. DDS, MPH Director, Oral Health, Boston Public Health Commission, Boston, MA xii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Alexia Antczak-Bouckoms DMD, ScD, MPH, MS Assistant Professor of Medicine, Tufts University School of Medicine, Medford, MA Howard L. Bailit DMD, PhD Health Policy and Primary Care Research Center, University of Connecticut Health Center, Farmington, CT David Barmes BDSc, DDSc, MPH Special Expert for International Health, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Bruce J. Baum DMD, PhD Chief of Gene Therapy and Therapeutic Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD stephen C. Bayne MS, PhD Professor, University of North Carolina School of Dentistry, Chapel Hill, NC James D. Beck PhD Kenan Professor, University of North Carolina School of Dentistry, Chapel Hill, NC tugenio Beltran DMD, MPH, MS, BrPH Senior Research Fellow, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Adanta, GA Henning Birkedal-Hansen DDS, PhD Scientific Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Karina Boehm MPH Chief, Health Promotion Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD William H. Bowen BDS, PhD Welscher Professor of Dentistry, School of Dentistry, University of Rochester Medical Center, Rochester, NY Norman $. Braveman PhD Associate Director for Clinical, Behavioral and Health Promotion Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS. Bethesda, MD Bruce B. Brehm DMD, MPH Lieutenant Colonel, U.S. Army, Tri-Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda, MD Patricia S. Bryant PhD Director, Behavioral and Health Promotion Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Maria Teresa Canto MS, DDS, MPH Public Health Research Specialist, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Acknowledgments Eli Capilouto DMD, MPH, ScD Dean, School of Public Health, University of Alabama at Birmingham, Birmingham, AL Victoria A. Cargill MD, MSCE Medical Officer, Office of AIDS Research, National Institutes of Health, DHHS, Bethesda, MD D. Walter Cohen DDS Chancellor Emeritus, Medical College of Pennsylvania, Hahneman University, Philadelphia, PA Lois K. Cohen PhD Director, Office of International Health, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Robert J. Collins DMD, MPH Deputy Executive Director, International and . American Associations for Dental Research, Alexandria, VA Stephen B. Corbin DDS, MPH Director of Health and Research Initiatives, Special Olympics, Inc., Washington, DC James G. Corrigan PhD Evaluation Officer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD James J. Crall DDS, ScD Chairman, Department of Pediatric Dentistry, University of Connecticut School of Dental Medicine, Farmington, CT Ananda P Dasanayake BDS, MPH, PhD Associate Professor, Department of Oral Biology University of Alabama School of Dentistry, Birmingham, AL Dominick P DePaola DDS, PhD President and CEO, The Forsyth Institute, Boston, MA Richard D’Eustachio DDS Private Practice, Cherry Hill, NJ Ray Dionne DDS, PhD Captain, USPHS, Clinical Director, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Marylin Dodd RN, PhD Professor, University of California San Francisco School of Nursing, San Francisco, CA Scott Dubowsky DMD, FAGD Private Practice, Bayonne, NJ Robert Dumbaugh DDS, MPH Dental Executive Director, Palm Beach County Health Department, Palm Beach, FL Joel Epstein DMD, MSD Research Associate Professor, Department of Oral Medicine, University of Washington School of Dentistry, Seattle, WA ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xiii Acknowledgments Ronald Ettinger BDS, MDS, DDSc Professor, Department of Prosthodontics and Dows Institute for Dental Research, University of lowa, Iowa City, IA Raymond Fonseca DMD Dean, University of Pennsylvania School of Dental Medicine, Philadelphia, PA Allan J. Formicola DDS Dean, School of Dental and Oral Surgery, Columbia University, New York, NY Jane L. Forrest Ed.D., RDH Assistant Dean, Dental Hygiene Research and Instructional Technology, Director, National Center for Dental Hygiene Research, University of Southern California School of Dentistry, Los Angeles, CA Robert T. Frame DMD, MS, CHE Assistant Under Secretary for Health for Dentistry, Department of Veterans Affairs, Washington, DC Raul |. Garcia DMD Professor and Chair, Department of Health Policy, Boston University Goldman School of Dental Medicine, Boston, MA Jay Alan Gershen DDS, PhD Executive Vice Chancellor, University of Colorado Health Sciences Center, Denver, CO Michael Glick DMD Professor of Oral Medicine, Director, Programs for Medically Complex Patients, University of Pennsylvania School of Dental Medicine, Philadelphia, PA Barbara F Gooch DMD, MPH Dental Officer, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Adanta, GA John Greene DMD, MPH Dean Emeritus, University of California San Francisco School of Dentistry, San Rafael, CA Deborah Greenspan BDS, DSc, ScD (he), FDSRCS Ed (hon) Professor of Clinical Oral Medicine, University of California San Francisco School of Dentistry, San Francisco, CA John S. Greenspan BSc, BDS, PhD, FRCPath Professor and Chair, Department of Stomatology, University of California San Francisco School of Dentistry, San Francisco, CA Robert O. Greer DDS, ScD Professor of Pathology and Medicine, University of Colorado Health Sciences Center, Schools of Medicine and Dentistry, Denver, CO David Grembowski PhD Professor of Health Services and Dental Public Health Sciences, University of Washington, Seattle, WA Ellen R. Gritz PhD Professor and Chair, Department of Behavioral Science, M.D. Anderson Cancer Center, University of Texas, Houston, TX Kenneth A. Gruber PhD Chief, Chronic Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Kevin Hardwick DDS, MPH Captain, USPHS, International Health Officer, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Hazel J. Harper DDS, MPH. Private Practice, Washington, DC John Hauth MD Professor, Interim Chairman and Director, Center for Research in Women’s Health, University of Alabama at Birmingham, Birmingham, AL Maxine Hayes MD, MPH Assistant Secretary, Community and Family Health, Washington State Department of Health, Olympia, WA Marc W. Heft DMD, PhD Professor and Director of the Claude Pepper Center, University of Florida College of Dentistry, Gainesville, FL Joseph Henry DDS, PhD, ScD Dean Emeritus, Howard University College of Dentistry and Professor, Harvard School of Dental Medicine, Boston, MA Mark C. Herzberg DDS, PhD Professor, University of Minnesota School of Dentistry, Minneapolis, MN Alan R. Hinman MD, MPH Senior Consultant for Public Health Programs, Taskforce for Child Survival and Development, Decatur, GA Cynthia Hodge DMD, MPH Private Practice, Nashville, TN Dorthe Holst DDS, MPH Professor, Department of Community Denustry, University of Oslo, Oslo, Norway John P. Howe III MD President, University of Texas Health Science Center at San Antonio, San Antonio, TX David Johnsen DDS, MS Dean and Professor of Pediatric Dentistry, University of Iowa College of Dentistry, lowa City, IA Ralph Katz DMD, PhD Professor, Department of Behavioral Science and Community Health, University of Connecticut School of Dental Medicine, Farmington, CT H. Asuman Kiyak MA, PhD Director, Institute on Aging and Professor, University of Washington School of Dentistry, Seattle, WA xiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Kenneth S. Kornman DDS, PhD Chief Scientific Officer, Interleukin Genetics, Inc., San Antonio, TX Elent Kousvelari DDS, DSc Health Scientist Administrator, National Institute of Dental and Craniofacial Research, National Institutes of Health. DHHS, Bethesda, MD javanth ¥. Kumar DDS, MPH ssistant Director, Bureau of Dental Health, New York State Department of Health, Albany, NY Ravmond Kuthy DDS, MPH Professor and Chair, Preventive and Community Dentistry, University of lowa College of Dentistry, lowa City, TA Ira Lamster DDS, MMSc Professor and Vice Dean, Columbia University School of Dental and Oral Surgery, New York, NY Philip R. Lee MA, MD Professor Emeritus of Social Medicine and Senior Advisor, Institute for Health Policy Studies, University of California San Francisco School of Medicine, San Francisco, CA Racquel Z, LeGeros BS, MS, PhD Professor, Department of Dental Materials Science and Director, Research Center for Minority Oral Health, New York University College of Dentistry, New York, NY David Locker BDS, PhD Professor, Faculty of Dentistry, University of Toronto, loronto, Canada Stiuurt Lockwood DDS, MPH Dental Officer/Epidemiologist, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Harold Loe DDS Director Emeritus, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Florida and Norway G.M. Nana Lopez DDS, MPH Dental Program Manager, City of Austin, Austin, TX Mark D. Macek DDS, PhD, MPH Assistant Professor, Department of Oral Health Care and Delivery, University of Maryland School of Dentistry, Baltimore, MD Dolores M. Malvitz DrPH Chief. Surveillance Investigations and Research Branch, Division of Oral Health, Centers for Disease Conwol and Prevention, DHHS, Atlanta, GA Dennis F Mangan PhD Chief. Infectious Disease and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Acknowledgments Kathleen Mangskau RDH, MPA Director, North Dakota Oral Health Program, North Dakota Department of Health, Bismarck, ND Georgetta Manning-Cox DDS, MPH Chairman, Community Dentistry and Associate Professor, Howard University College of Dentistry, Washington, DC Don Marianos DDS, MPH Consultant in Public Health, Pinetop, AZ Gary C. Martin DDS, MPH Lieutenant Colonel, U.S. Air Force, Tri-Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda, MD . Ricardo J. Martinez MD, MPH Director, Division of Extramural Research, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Richard Mascola DDS Private Practice, Jericho, NY Carolyn Beth Mazzella RN Assistant Surgeon General, USPHS, Office of the PHS Chief Nurse, Health Resources and Services Administration, DHHS, Rockville, MD Kim McFarland DDS, MS Dental Health Director, State of Nebraska, Nebraska Department of Health, Lincoln, NE J. Michael McGinnis MD Senior Vice President and Director, Health Group, The Robert Wood Johnson Foundation, Princeton, NJ Robert Mecklenburg DDS, MPH Coordinator, Tobacco and Oral Health Initiatives for the Tobacco Control Research Branch, National Cancer Institute, DHHS, Bethesda, MD Roseann Mulligan DDS, MS Professor and Chairman, Department of Dental Medicine and Public Health, University of Southern California School of Dentistry, Los Angeles, CA Juan M. Navia PhD Professor Emeritus, University of Alabama at Birmingham, Birmingham, AL Edward O’Neil PhD, MPA Professor, Dental Public Health and Hygiene, Director, Center for Health Professions, University of California, San Francisco, San Francisco, CA Roy C. Page DDS, PhD Professor, Departments of Periodontics and Pathology, Schools of Dentistry and Medicine, University of Washington, Seattle, WA No-Hee Park DMD, PhD Dean, School of Dentistry, University of California Los Angeles, Los Angeles, CA ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xv Acknowledgments Steven Perlman DDS, MScD Associate Professor of Pediatric Dentistry, Boston University Goldman School of Dental Medicine, Boston, MA Poul Erik Petersen DDS, Dr Odont Sci, BA, MSc Professor, University of Copenhagen, School of Dentistry, Copenhagen N, Denmark Kathy Phipps RDH, DrPH Associate Professor, Oregon Health Sciences University, Newport, OR Scott Presson DDS, MPH Captain, USPHS, Chief, Program Services Branch, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Francisco Ramos-Gomez DDS, MS, MPH Associate Professor, Department of Growth and Development, University of California San Francisco, San Francisco, CA E. Diane Rekow DDS, PhD Professor and Chair, Department of Orthodontics, University of Medicine and Dentistry of New Jersey, Newark, NJ Michael Rethman DDS, MS Colonel, U.S. Army, Chief of Periodontics, Tripler Dental Clinic, Honolulu, HI S. Timothy Rose DDS, MS Private Practice, Appleton, WI Bruce Rothwell DMD, MSD Associate Professor and Chairman, University of Washington, Restorative/Hospital Dentistry, Seattle, WA Shirley B. Russell PhD Professor and Chairperson, Department of Microbiology, Associate Dean for Research, Meharry Medical College, Nashville, TN Ann L Sandberg PhD Chief, Neoplastic Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Charles Sanders DDS Dean, Howard University College of Dentistry, Washington, DC Michéle J. Saunders DMD, MS, MPH Endowed Professor of Clinical Dentistry, University of Texas Health Science Center, San Antonio, TX Crispian Scully MD, PhD, MDS Dean, Director of Studies and Research, International Centers for Excellence in Dentistry and Eastman Dental Institute for Oral Health Care Sciences, University College of London, London, England Leslie W. Seldin DDS, PC Private Practice, New York, NY Aubrey Sheiham BDS, PhD, DHC Professor, Department of Epidemiology and Public Health, University College London Medical School, London, England Cynthia Sherwood DDS Private Practice, Independence, KS Mark D. Siegal DDS, MPH Chief, Bureau of Oral Health Services, Ohio Department of Health, Columbus, OH Sol Silverman Jr. MA, DDS Professor of Oral Medicine, University of California San Francisco School of Dentistry, San Francisco, CA Susan FE Silverton MD, PhD Assistant Professor and Enid Neidle Scholar, University of Pennsylvania-School of Dental Medicine, Philadelphia, PA Jeanne Sinkford DDS, MS, PhD Associate Executive Director, American Dental Education Association, Washington, DC Judy A. Small PhD Chief, Craniofacial Anomalies and Injuries Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS, Bethesda, MD Christian Stohler DMD, Dr.Med.Dent William R. Mann Professor and Chair, Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, M1 George Stookey PhD Executive Associate Dean, Indiana University School of Dentistry, Indianapolis, IN Michael Till DDS, PhD Dean, University of Minnesota School of Dentistry, Minneapolis, MN Richard Valachovic DMD, MPH Executive Director, American Dental Education Association, Washington, DC Clemencia M. Vargas DDS, MPH, PhD Assistant Professor, University of Maryland School of Dentistry, Baltimore, MD Rueben Warren DDS, MPH, DrPH Associate Administrator for Urban Affairs, The Agency for Toxic Substances and Disease Registry, DHHS, Atlanta, GA Reginald Wells PhD Deputy Commissioner, Administration for Children and Families, Administration on Developmental Disabilities, DHHS, Washington, DC Terrie Wetle PhD Deputy Director, National Institute on Aging, National Institutes of Health, DHHS, Bethesda, MD David A. Whiston DDS Private Practice, Falls Church, VA xvi ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL yrdell Wilson DDS, MPH Bureau Chief, State of Connecticut Department of Public Health, Avon, CT Kenneth M. Yamada MD, PhD Branch Chief, Craniofacial Development Biology and Regeneration, National Institute of Dental and Craniofacial Research, National Institutes of Health, DHHS. Bethesda, MD EDITORIAL AND PRODUCTION ASSISTANTS The Editorial Staff of the KEVRIC Company, Inc., silver Spring, MD PROJECT ASSISTANTS Anne Breitenbach \taurice Champagne MA stephanie A. Dopson MSW, MPH Katherine E. Krizek Marco P. Maertens tdith McAllister JD Georgia A. Mcintyre catherine McNish RDH, MHS FEDERAL COORDINATING COMMITTEE Lois Albarelli Aying Services Program Specialist, Administration on Aging, DHHS, Washington, DC ( hervl Austein-Casnoff MPH Director, Public Health Policy, Office of the Assistant Sceretary for Planning and Evaluation, DHHS, Washington, DC William F Benson Acting Principal Deputy Assistant Secretary for Aging (retired), Administration on Aging, DHHS, Washington, DC Mohandas Bhat BDS, MDS, DrPH Senior Science Advisor, Office of International Health Programs, U.S. Department of Energy, Germantown, MD Donna Blum MS, RD Nutritionist, Department of Agriculture, Alexandria, VA tne Bothwell DDS, MPH, PhD Captain, USPHS, Assistant Chief, Dental Services Branch (retired), Indian Health Service, DHHS, Rockville, MD ©. Richard Buchanan DMD Deputy Director for Dentistry, Department of Veterans Affairs, Washington, DC ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Acknowledgments Claude Earl Fox MD, MPH Administrator, Health Resources and Services Administration, DHHS, Rockville, MD Patricia A. Grady PhD, RN, FAAN Director, National Institute of Nursing Research, National Institutes of Health, DHHS, Bethesda, MD Elizabeth Jacobson PhD Deputy Director for Science, Center for Devices and Radiological Health, Food and Drug Administration, DHHS, Rockville, MD Wanda K. Jones Dr. PH. Deputy Assistant Secretary for Health, Office of Women’s Health, DHHS, Washington, DC Lireka P Joseph Dr. PH. Captain, USPHS, Director, Office of Health and Industry Programs, Center for Devices and Radiological Health, Food and Drug Administration, DHHS, Rockville, MD Douglas B. Kamerow MD, MPH Assistant Surgeon General, USPHS, Director, Center for Practice and Technology Assessment, Agency for Healthcare Research and Quality, DHHS, Rockville, MD Mireille B. Kanda MD, MPH Director of Health and Disability Services, Head Start Bureau, Agency for Children, Youth, and Families, DHHS, Washington, DC Rod F Kirk DDS Captain, USPHS, Chief, Dental Program, Federal Bureau of Prisons, Department of Justice, Washington, DC Kenneth W. Kizer MD, MPH Under Secretary for Health (retired), Department of Veterans Affairs, Washington, DC William Kohn DDS Captain, USPHS, Associate Director for Science, Division of Oral Health, Centers for Disease Control and Prevention, DHHS, Atlanta, GA Thomas M. Leiendecker DDS, MPH Commander, U.S. Navy, Assistant Professor, Tri-Service Center for Oral Health Studies, Uniformed Services University of the Health Sciences, Department of Defense, Bethesda, MD Lawrence McKinley DDS Captain, U.S. Navy, Senior Consultant for Dentistry, Tricare Management Activity, Department of Defense, Falls Church, VA Edward Sondik PhD Director, National Center for Health Statistics, Centers for Disease Control and Prevention, DHHS, Hyattsville, MD xvii Acknowledgments Sue Swenson Ron J. Vogel Commissioner, Administration on Developmental Acting Deputy Administrator of the Food and Disabilities, Administration for Children and Families, Nutrition Programs, Food and Nutrition Service, DHHS, Washington, DC Department of Agriculture, Alexandria, VA Jeanette Takamura Assistant Secretary for Aging, Administration on Aging, DHHS, Washington, DC xviii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL a Contents Executive Summary 1 THE CHALLENGE, +4 THE CHARGE, 4 THE SCIENCE BASE FOR THE REPORT, 5 ORGANIZATION OF THE REPORT, 5 Part One: What Is Oral Health? 5 Part Two: What Is the Status of Oral Health in America? 6 Part Three: What Is the Relationship Between Oral Health and General Health and Well-being? 6 Part Four: How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 7 Part Five: What Are the Needs and Opportunities to Enhance Oral Health? 9 MAJOR FINDINGS, 10 A FRAMEWORK FOR ACTION, 11 CONCLUSION, 13 REFERENCES, 13 PROJECT TEAM, 13 PART ONE WHAT IS ORAL HEALTH? 15 Chapter 1 The Meaning of Oral Health 17 THE CHALLENGE, 19 THE CHARGE, 19 THE SCIENCE BASE FOR THE REPORT, 19 ORGANIZATION OF THE REPORT, 20 What Is Oral Health? 20 What Is the Status of Oral Health in America? 20 What Is the Relationship Between Oral Health and General Health and Well-being? 20 How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? 21 What Are the Needs and Opportunities to Enhance Oral Health? 21 A Call to Action, 21 Chapter 2 The Craniofacial Complex 23 CONTACT AND COMMUNICATION, 23 Taste and Smell, 23 Touch, Temperature, and Pain, 24 Speech, 25 THE ORAL CAVITY, 25 The Oral Mucosa, 25 The Teeth, 26 The Salivary Glands, 26 The Immune System, 27 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xix Contents CRANIOFACIAL ORIGINS, 28 Early Development, 29 Genetic Controls, 30 THE AGING OF CRANIOFACIAL TISSUES, 31 The Teeth, 31 The Jaws, 31 / The Oral Mucosa, 32 Sensory and Motor Functioning, 32 The Salivary Glands, 32 FINDINGS, 32 REFERENCES, 33 PART TWO WHAT IS THE STATUS OF ORAL HEALTH IN AMERICA? 35 Chapter 3 Diseases and Disorders 7 37 DENTAL AND PERIODONTAL INFECTIONS, 37 Dental Caries, 37 Periodontal Diseases, 39 SELECTED MUCOSAL INFECTIONS AND CONDITIONS, 42 Oral Candidiasis, +2 Herpes Simplex Virus Infections, 43 Oral Human Papillomavirus Infections, 43 Recurrent Aphthous Ulcers, 43 ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS, 44 Heightening the Risk, 44 Prevention and Management, 47 DEVELOPMENTAL DISORDERS, 47 Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis, 47 Cranial Bone and Dental Anomalies, 48 Craniofacial Defects Secondary to Other Developmental Disorders, 49 Craniofacial Manifestations of Single-Gene Defects, 49 INJURY, 50 Sports, 50 Falls, 50 Motor Vehicle Collisions, 50 Violence, 51 SELECTED CHRONIC AND DISABLING CONDITIONS, 51 Sjogren's Syndrome, 51 Acute and Chronic Oral-Facial Pain, 52 Temporomandibular Disorders, 52 A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS, 53 FINDINGS, 53 REFERENCES, 53 xx ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents Chapter + The Magnitude of the Problem 61 WHO HAS WHAT DISEASES AND CONDITIONS? 63 Dental Caries, Periodontal Diseases, and Tooth Loss, 63 Oral and Pharyngeal Cancers and Precancerous Lesions, 67 Selected Mucosal Infections and Diseases, 70 Developmental Disorders, 71 Injury, 72 Chronic and Disabling Conditions, 73 WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES, 74 Racial and Ethnic Minorities, 74 Women’s Health, 77 Individuals with Disabilities, 78 i, UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? 79 Dental Care Utilization, 80 Variation by Sex, Race/Ethnicity, Income, and Insurance, 81 Variation by Oral Health Status, 82 Reasons for Nonutilization, 83 Unmet Needs, 83 Outcomes of Appropriate Levels of Access and Utilization: An Example, 83 ORAL HEALTH STATUS IN CHANGING TIMES, 87 FINDINGS, 89 REFERENCES, 89 PART THREE WHAT 1S THE RELATIONSHIP BETWEEN ORAL HEALTH AND GENERAL HEALTH AND WELL-BEING? 95 Chapter 5 Linkages with General Health 97 THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE, 97 Physical Signs and Symptoms of Disease and Risk Factors, 97 Oral Manifestations of HIV Infection and of Osteoporosis, 101 Oral-fluid-based Diagnostics: The Example of Saliva, 103 Conclusion, 104 THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION, 104 Oral Infections and Bacteremia, 104 Oral Infections as a Result of Therapy, 105 Infective Endocarditis, 107 Oral Infections and Respiratory Disease, 108 Oral Transmission of Infections, 108 Conclusion, 109 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxi Contents CRANIOFACIAL ORIGINS, 28 Early Development, 29 Genetic Controls, 30 THE AGING OF CRANIOFACIAL TISSUES, 31 The Teeth, 31 The Jaws, 31 The Oral Mucosa, 32 Sensory and Motor Functioning, 32 The Salivary Glands, 32 FINDINGS, 32 REFERENCES, 33 PART TWO WHAT IS THE STATUS OF ORAL HEALTH IN AMERICA? 35 Chapter 3 Diseases and Disorders 37 DENTAL AND PERIODONTAL INFECTIONS, 37 Dental Caries, 37 Periodontal Diseases, 39 SELECTED MUCOSAL INFECTIONS AND CONDITIONS, 42 Oral Candidiasis, +2 Herpes Simplex Virus Infections, 43 Oral Human Papillomavirus Infections, 43 Recurrent Aphthous Ulcers, 43 ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS, 44 Heightening the Risk, 44 Prevention and Management, 47 DEVELOPMENTAL DISORDERS, 47 Craniofacial Anomalies Caused by Altered , Branchial Arch Morphogenesis, 47 Cranial Bone and Dental Anomalies, 48 Craniofacial Defects Secondary to Other Developmental Disorders, 49 Craniofacial Manifestations of Single-Gene Defects, 49 INJURY, 50 Sports, 50 Falls, 50 Motor Vehicle Collisions, 50 Violence, 31 SELECTED CHRONIC AND DISABLING CONDITIONS, 51 Sjogren's Syndrome, 51 Acute and Chronic Oral-Facial Pain, 52 Temporomandibular Disorders, 52 A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS, 53 FINDINGS, 53 REFERENCES, 53 xX ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents Chapter 4 The Magnitude of the Problem 61 WHO HAS WHAT DISEASES AND CONDITIONS? 63 Dental Caries, Periodontal Diseases, and Tooth Loss, 63 Oral and Pharyngeal Cancers and Precancerous Lesions, 67 Selected Mucosal Infections and Diseases, 70 Developmental Disorders, 71 Injury, 72 . Chronic and Disabling Conditions, 73 WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES, 74 Racial and Ethnic Minorities, 74 Women's Health, 77 Individuals with Disabilities, 78 UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE ~ KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? 79 Dental Care Utilization, 80 Variation by Sex, Race/Ethnicity, Income, and Insurance, 81 Variation by Oral Health Status, 82 Reasons for Nonutilization, 83 Unmet Needs, 83 Outcomes of Appropriate Levels of Access and Utilization: An Example, 83 ORAL HEALTH STATUS IN CHANGING TIMES, 87 FINDINGS, 89 REFERENCES, 89 PART THREE WHAT 1S THE RELATIONSHIP BETWEEN ORAL HEALTH AND GENERAL HEALTH AND WELL-BEING? 95 Chapter 5 Linkages with General Health 97 THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE, 97 Physical Signs and Symptoms of Disease and Risk Factors, 97 Oral Manifestations of HIV Infection and of Osteoporosis, 101 Oral-fluid-based Diagnostics: The Example of Saliva, 103 Conclusion, 104 THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION, 104 Oral Infections and Bacteremia, 104 Oral Infections as a Result of Therapy, 105 Infective Endocarditis, 107 Oral Infections and Respiratory Disease, 108 Oral Transmission of Infections, 108 Conclusion, 109 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxi Contents ASSOCIATIONS AMONG ORAL INFECTIONS AND DIABETES, HEART DISEASE/STROKE, AND ADVERSE PREGNANCY OUTCOMES, 109 The Periodontal Disease—Diabetes Connection, 109 The Oral Infection—Heart Disease and Stroke Connection, 115 Periodontal Disease and Adverse Pregnancy Outcomes, 120 Conclusion, 122 IMPLICATIONS OF THE LINKAGES, 122 FINDINGS, 123 REFERENCES, 123 Chapter 6 Effects on Well-being and Quality of Life 133 THE CULTURAL CONTEXT, 134 Cultural Models, 134 Combining Perspectives, 134 ORAL-HEALTH-RELATED QUALITY OF LIFE DIMENSIONS, 135 Functional Dimensions, 135 Psychosocial Dimensions, 137 Indirect Economic Costs, 142 RATINGS OF ORAL HEALTH, 144 Global Ratings, 144 Satisfaction Ratings, 144 ORAL-HEALTH-RELATED QUALITY OF LIFE MEASURES, 144 HEIGHTENED EXPECTATIONS, 146 FINDINGS, 146 REFERENCES, 147 PART FOUR HOW IS ORAL HEALTH PROMOTED AND MAINTAINED AND HOW ARE ORAL DISEASES PREVENTED? 153 Chapter 7 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease 155 WEIGHING THE EVIDENCE THAT INTERVENTIONS WORK, 155 PREVENTION AND CONTROL OF DENTAL CARIES, 158 Fluoride, 158 Fluoridation of Drinking Water, 160 School Water Fluoridation, 162 Dietary Fluoride Supplements, 162 Fluoride Mouthrinses, 165 Fluoride Varnishes, 165 Dental Sealants, 166 PREVENTION AND CONTROL OF PERIODONTAL DISEASES, 168 Community Programs to Prevent Gingivitis, 169 Prevention of Periodontitis, 169 Summary, 169 PREVENTION AND CONTROL OF ORAL AND PHARYNGEAL CANCERS, 169 Community-based Interventions, 170 Early Diagnosis of Oral and Pharyngeal Cancers, 171 Summary, 172 xxii ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Contents PREVENTION AND CONTROL OF CRANIOFACIAL BIRTH DEFECTS, 172 Summary, 173 PREVENTION AND CONTROL OF INTENTIONAL AND UNINTENTIONAL INJURY, 173 Craniofacial Injuries, 173 . Summary: Prevention of Craniofacial Injuries, 176 ORAL HEALTH PROMOTION AND DISEASE PREVENTION KNOWLEDGE AND PRACTICES, 176 Dental Caries Prevention, 177 Periodontal Disease Prevention, 178 Oral Cancer Prevention and Early Detection, 178 Summary, 179 BUILDING UPON SUCCESS, 179 FINDINGS, 181 REFERENCES, 181 Chapter 8 Personal and Provider Approaches to Oral Health 189 INDIVIDUAL RESPONSIBILITY: PERSONAL APPROACHES TO ORAL HEALTH, 189 "Daily Hygiene and Dental Caries Prevention, 189 Daily Hygiene and the Prevention of Periodontal Diseases, 190 Healthy Lifestyles, 190 Care Seeking, 190 PROVIDER-BASED CARE, 191 Risk Assessment, 192 Diagnostic Tests, 193 Oral Health Assessment, 193 Changing Approaches to Selected Diseases and Conditions, 196 Chronic Craniofacial Pain and Sensorimotor Conditions, 211 Temporomandibular Disorders, 211 Mucosal and Autoimmune Diseases, 212 FACTORS AFFECTING FUTURE HEALTH CARE PRACTICES, 212 Evidence-based Practice, 213 Clinical Practice Guidelines, 213 Science and Technology Contributions, 214 Broadening the Base for the Provision of Oral Health Care, 216 FINDINGS, 216 REFERENCES, 216 Chapter 9 Provision of Oral Health Care 223 COMPONENTS OF PROFESSIONAL CARE, 223 The Dental Component, 223 The Medical Component, 225 The Public Health Component, 225 Areas of Overlap, 227 EXPENDITURES FOR ORAL HEALTH CARE, 227 FINANCING AND REIMBURSEMENT, 229 Insurance, 229 The Changing Market, 231 Federal and State Programs, 233 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL xxiii Contents FACTORS AFFECTING THE CAPACITY TO MEET ORAL HEALTH NEEDS, 234 Numbers of Dental Personnel, 235 Sex and Racial/Ethnic Composition of Dental Personnel, 236 Student Indebtedness and Its Effects, 237 Personnel Needs for Faculty and Clinical Research, 238 Curriculum Needs, 238 Taking Care of Those Most in Need, 239 TWENTY-FIRST CENTURY CHALLENGES: WHAT LIES AHEAD? 239 FINDINGS, 240 REFERENCES, 241 PART FIVE WHAT ARE THE NEEDS AND OPPORTUNITIES TO ENHANCE ORAL HEALTH? 243 Chapter 10 Factors Affecting Oral Health over the Life Span 245 HEALTH IN THE CONTEXT OF SOCIETY, 245 Historical Models, 245 Contemporary Models, 246 CHANGING VULNERABILITIES THROUGHOUT LIFE, 249 Children, 249 Adolescents and Young Adults, 257 Midlife Adults, 258 Older Americans, 262 ACHIEVING ORAL HEALTH THROUGHOUT LIFE, 267 FINDINGS, 269 REFERENCES, 269 Chapter 11 Facing the Future 275 THE PAST AND PRESENT AS PROLOGUE, 275 The Pioneers, 275 Vital Statistics, 275 Health Improvement, 276 DIVERSITY OF DISEASES AND PATIENTS, 276 TRANSFORMING TREATMENTS, 276 TRANSFORMING HEALTH PROFESSIONAL EDUCATION, 276 TRANSFORMING HEALTH CARE, 277 ORAL HEALTH—NOT YET FOR ALL, 277 HOPE FROM SCIENCE AND TECHNOLOGY, 278 A FRAMEWORK FOR ORAL HEALTH, 280 REFERENCES, 281 Chapter 12 A Call to Action 283 MAJOR FINDINGS, 283 A FRAMEWORK FOR ACTION, 284 CONCLUSION, 287 Index 289 xxiv ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL a Executive Summary Publication of this first Surgeon General's Report on Oral Health marks a milestone in the history of oral health in America. The report elaborates on the meaning of oral health and explains why oral health is essential to general health and well-being. In the course of the past 50 years, great progress has been made in understanding the common oral diseases— dental caries (tooth decay) and periodontal (gum) diseases—resulting in marked improvements in the nation’s oral health. Most middle-aged and younger Americans expect to retain their natural teeth over their lifetime and do not expect to have any serious oral health problems. The major message of this Surgeon General's report is that oral health is essential to the general health and well-being of all Americans and can be achieved by all Americans. However, not all Americans are achieving the same degree of oral health. In spite of the safe and effective means of maintaining oral health that have benefited the majority of Americans over the past half century, many among us still experience needless pain and suffering, complications that devastate overall health and well-being, and financial and social costs that diminish the quality of life and burden American society. What amounts to “a silent epidemic” of oral diseases is affecting our most vulnerable citizens— poor children, the elderly, and many members of racial and ethnic minority groups (GAO 2000). (See box entitled “The Burden of Oral Diseases and Disorders.”) The word oral refers to the mouth. The mouth includes not only the teeth and the gums (gingiva) and their supporting tissues, but also the hard and soft palate, the mucosal lining of the mouth and throat, the tongue, the lips, the salivary glands, the chewing muscles, and the upper and lower jaws. Equally important are the branches of the nervous, immune, and vascular systems that animate, protect, and nourish the oral tissues, as well as provide con- nections to the brain and the rest of the body. The genetic patterning of development in utero further reveals the intimate relationship of the oral tissues to the developing brain and to the tissues of the face and head that surround the mouth, structures whose location is captured in the word craniofacial. A major theme of this report is that oral health means much more than healthy teeth. It means being free of chronic oral-facial pain conditions, oral and pharyngeal (throat) cancers, oral soft tissue lesions, birth defects such as cleft lip and palate, and scores of other diseases and disorders that affect the oral, dental, and craniofacial tissues, collectively known as the craniofacial complex. These are tissues whose functions we often take for granted, yet they represent the very essence of our humanity. They allow us to speak and smile; sigh and kiss; smell, taste, touch, chew, and swallow; cry out in pain; and convey a world of feelings and emotions through facial expressions. They also provide protection against microbial infections and environmental insults. The craniofacial tissues also provide a useful means to understanding organs and systems in less accessible parts of the body. The salivary glands are a model of other exocrine glands, and an analysis of saliva can provide telltale clues of overall health or disease. The jawbones and their joints function like other musculoskeletal parts. The nervous system apparatus underlying facial pain has its counterpart in nerves elsewhere in the body. A thorough oral examination can detect signs of nutritional defi- ciencies as well as a number of systemic diseases, including microbial infections, immune disorders, injuries, and some cancers. Indeed, the phrase the mouth is a mirror has been used to illustrate the wealth of information that can be derived from examining oral tissues. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 1 Executive Summary New research is pointing to associations between chronic oral infections and heart and lung diseases, stroke, and low-birth-weight, premature births. Associations between periodontal disease and dia- betes have long been noted. This report assesses these associations and explores mechanisms that might explain the oral-systemic disease connections. The broadened meaning of oral health parallels the broadened meaning of health. In 1948 the World Health Organization expanded the definition of health to mean “a complete state of physical, mental, and social well-being, and not just the absence of infirmity.” It follows that oral health must also include well-being. Just as we now understand that nature and nurture are inextricably linked, and mind and body are both expressions of our human biology, so, too, we must recognize that oral health and general health are inseparable. We ignore signs and symptoms of oral disease and dysfunction to our The Burden of Oral Diseases and Disorders Oral diseases are progressive and cumulative and become more com- plex over time. They can affect our ability to eat, the foods we choose, how we look, and the way we communicate. These diseases can affect economic productivity and compromise our ability to work at home, at school, or on the job. Health disparities exist across population groups at all ages. Over one third of the U.S. population (100 million people) has no access to community water fluoridation. Over 108 million chil- dren and adults lack dental insurance, which is over 2.5 times the num- ber who lack medical insurance. The following are highlights of oral. health data for children, adults, and the elderly. (Refer to the full report for details of these data and their sources.) Children e Cleft lip/palate, one of the most common birth defects, is esti- mated to affect 1 out of 600 live births for whites and 1 out of 1,850 live births for African Americans. @ Other birth defects such as hereditary ectodermal dysplasias, where all or most teeth are missing or misshapen, cause lifetime prob- lems that can be devastating to children and adults. e Dental caries (tooth decay) is the single most common chronic childhood disease—5 times more common than asthma and 7 times more common than hay fever. @ Over 50 percent of 5- to 9-year-old children have at least one cavity or filling, and that proportion increases to 78 percent among 17- year-olds. Nevertheless, these figures represent improvements in the oral health of children compared to a generation ago. e There are striking disparities in dental disease by income. Poor children suffer twice as much dental caries as their more affluent peers, and their disease is more likely to be untreated. These poor-nonpoor detriment. Consequently, a second theme of the report is that oral health is integral to general health. You cannot be healthy without oral health. Oral health and general health should not be interpreted as separate entities. Oral health is a critical component of health and must be included in the provision of health care and the design of community programs. The wider meanings of oral and health in no way diminish the relevance and importance of the two leading dental diseases, caries and the periodontal diseases. They remain common and widespread, affecting nearly everyone at some point in the life span. What has changed is what we can do about them. Researchers in the 1930s discovered that people living in communities with naturally fluoridated water supplies had less dental caries than people drinking unfluoridated water. But not until the end differences continue into adolescence. One out of four children in America is born into poverty, and children living below the poverty line (annual income of $17,000 for a family of four) have more severe and _ untreated decay. © Unintentional injuries, many of which include head, mouth, and neck injuries, are common in children. e@ Intentional injuries commonly affect the craniofacial tissues. @ Tobacco-related oral lesions are prevalent in adolescents who currently use smokeless (spit) tobacco. @ Professional care is necessary for maintaining oral health, yet 25 percent of poor children have not seen a dentist before entering kindergarten. @ Medical insurance is a strong predictor of access to dental care. Uninsured children: are 2.5 times less likely than insured children to receive dental care. Children from families without dental insurance are 3 times more likely to have dental needs than children with either pub- lic or private insurance. For each child without medical insurance, there are at least 2.6 children without dental insurance. e Medicaid has not been able to fill the gap in providing dental care to poor children. Fewer than one in five Medicaid-covered children received a single dental visit in a recent year-long study period. Although new programs such as the State Children’s Health Insurance Program (SCHIP) may increase the number of insured children, many will still be left without effective dental coverage. e@ The social impact of oral diseases in children is substantial. More than 51 million school hours are lost each year to dental-related illness. Poor children suffer nearly 12 times more restricted-activity days than children from higher-income families. Pain and suffering due to untreated diseases can lead to problems in eating, speaking, and attending to learning. 2 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL of World War II were the investigators able to design and implement the community clinical trials that confirmed their observations and launched a better approach to the problem of dental caries: prevention. Soon after, adjusting the fluoride content of commu- nity water supplies was pursued as an important pub- lic health measure to prevent dental caries. Although this measure has not been fully imple- mented, the results have been dramatic. Dental caries began to decline in the 1950s among children who grew up in fluoridated cities, and by the late 1970s, decline in decay was evident for many Americans. The application of science to improve diagnostic, treatment, and prevention strategies has saved bil- lions of dollars per year in the nation’s annual health bill. Even more significant, the result is that far fewer people are edentulous (toothless) today than a gen- eration ago. Adults @ Most adults show signs of periodontal or gingival diseases. Severe periodontal disease (measured as 6 millimeters of periodontal attachment loss) affects about 14 percent of adults aged 45 to 54, @ Clinical symptoms of viral infections, such as herpes labialis (cold sores), and oral ulcers (canker sores) are common in adulthood, affecting about 19 percent of adults 25 to 44 years of age. e Chronic disabling diseases such as temporomandibular disor- ders, Sjogren’s syndrome, diabetes, and osteoporosis affect millions of Americans and compromise oral health and functioning. @ Pain is a common symptom of craniofacial disorders and is accompanied by interference with vital functions such as eating, swal- lowing, and speech. Twenty-two percent of adults reported some form of oral-facial pain in the past 6 months. Pain is a major component of trigeminal neuralgia, facial shingles (post-herpetic neuralgia), tem- poromandibular disorders, fibromyalgia, and Belt’s palsy. @ Population growth as well as diagnostics that are enabling ear- lier detection of cancer means that more patients than ever before are undergoing cancer treatments. More than 400,000 of these patients will develop oral complications annually. @ Immunocompromised patients, such as those with HIV infec- tion and those undergoing organ transplantation, are at higher risk for oral problems such as candidiasis. e Employed adults lose more than 164 million hours of work each year due to dental disease or dental visits. @ For every adult 19 years or older without medical insurance, ‘there are three without dental insurance. @ A little less than two thirds of adults report having visited a dentist in the past 12 months. Those with incomes at or above the poverty level are twice as likely to report a dental visit in the past 12 months as those who are below the poverty level. Executive Summary The theme of prevention gained momentum as pioneering investigators and practitioners in the 1950s and 1960s showed that not only dental caries but also periodontal diseases are bacterial infections. The researchers demonstrated that the infections could be prevented by increasing host resistance to disease and reducing or eliminating the suspected microbial pathogens in the oral cavity. The applica- tions of research discoveries have resulted in contin- uing improvements in the oral health of Americans, new approaches to the prevention and treatment of dental diseases, and the growth of the science. The significant role that scientists, dentists, den- tal hygienists, and other health professionals have played in the prevention of oral disease and disabili- ty leads to a third theme of this report: safe and effec- tive disease prevention measures exist that every- one can adopt to improve oral health and prevent disease. These measures include daily oral hygiene Older Adults e Twenty-three percent of 65- to 74-year-olds have severe peri- odontal disease (measured as 6 millimeters of periodontal attachment loss). (Also, at all ages men are more likely than women to have more - severe disease, and at all ages people at the lowest socioeconomic lev- els have more severe periodontal disease.) @ About 30 percent of adults 65 years and older are edentulous, compared to 46 percent 20 years ago. These figures are higher for those living in poverty. e@ Oral and pharyngeal cancers are diagnosed in about 30,000 Americans annually; 8,000 die from these diseases each year. These cancers are primarily diagnosed in the elderly. Prognosis is poor. The 5- year survival rate for white patients is 56 percent; for blacks, it is only 34 percent. e Most older Americans take both prescription and over-the- counter drugs. In all probability, at least one of the medications used will have an oral side effect—usually dry mouth. The inhibition of sali- vary flow increases the risk for oral disease because saliva contains antimicrobial components as well as minerals that can help rebuild tooth enamel after attack by acid-producing, decay-causing bacteria. Individuals in long-term care facilities are prescribed an average of eight drugs. e At any given time, 5 percent of Americans aged 65 and older (currently some 1.65 million people) are living in a long-term care facil- ity where dental care is problematic. @ Many elderly individuals lose their dental insurance when they retire. The situation may be worse for older women, who generally have lower incomes and may never have had dental insurance. Medicaid funds dental care for the low-income and disabled elderly in some states, but reimbursements are low. Medicare is not designed to reim- burse for routine dental care. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 3 Executive Summary procedures and other lifestyle behaviors, community programs such as community water fluoridation and tobacco cessation programs, and provider-based interventions such as the placement of dental sealants and examinations for common oral and pha- ryngeal cancers. It is hoped that this Surgeon General's report will facilitate the maturing of the broad field of craniofacial research so that gains in the prevention of craniofacial diseases and disorders can be realized that are as impressive as those achieved for common dental diseases. At the same time, more needs to be done to ensure that messages of health promotion and dis- ease prevention are brought home to all Americans. In this regard, a fourth theme of the report is that general health risk factors, such as tobacco use and poor dietary practices, also affect oral and craniofa- cial health. The evidence for an association between tobacco use and oral diseases has been clearly delin- eated in almost every Surgeon General's report on tobacco since 1964, and the oral effects of nutrition and diet are presented in the Surgeon General's report on nutrition (1988). All the health professions can play a role in reducing the burden of disease in America by calling attention to these and other risk factors and suggesting appropriate actions. Clearly, promoting health and preventing dis- eases are concepts the American people have taken to heart. For the third decade the nation has developed a plan for the prevention of disease and the promo- tion of health, embodied in the U.S. Department of Health and Human Services (2000) document, Healthy People 2010. As a nation, we hope to elimi- nate disparities in health and prevent oral diseases, cancer, birth defects, AIDS and other devastating infections, mental illness and suicide, and the chron- ic diseases of aging. To live well into old age free of pain and infirmity, and with a high quality of life, is the American dream. Scientists today take that dream seriously in researching the intricacies of the craniofacial com- plex. They are using an ever-growing array of sophis- ticated analytic tools and imaging systems to study normal function and diagnose disease. They are com- pleting the mapping and sequencing of human, ani- mal, microbial, and plant genomes, the better to understand the complexities of human development, aging, and pathological processes. They are growing cell lines, synthesizing molecules, and using a new generation of biomaterials to revolutionize tissue repair and regeneration. More than ever before, they are working in multidisciplinary teams to bring new knowledge and expertise to the goal of understand- ing complex human diseases and disorders. THE CHALLENGE This Surgeon General's report has much to say about the inequities and disparities that affect those least able to muster the resources to achieve optimal oral health. The barriers to oral health include lack of access to care, whether because of limited income or lack of insurance, transportation, or the flexibility to take time off from work to attend to personal or fam- ily needs for care. Individuals with disabilities and those with complex health problems may face addi- tional barriers to care. Sometimes, too, the public, policymakers, and providers may consider oral health and the need for care to be less important than other health needs, pointing to the need to raise awareness and improve health literacy. Even more costly to the individual and to socie- ty are the expenses associated with oral health prob- lems that go beyond dental diseases. The nation’s yearly dental bill is expected to exceed $60 billion in 2000 (Health Care Financing Administration 2000). However, add to that expense the tens of billions of dollars in direct medical care and indirect costs of chronic craniofacial pain conditions such as tem- poromandibular disorders, trigeminal neuralgia, shingles, or burning mouth syndrome; the $100,000 minimum individual lifetime costs of treating cranio- facial birth defects such as cleft lip and palate; the costs of oral and pharyngeal cancers; the costs of autoimmune diseases; and the costs associated with the unintentional and intentional injuries that so often affect the head and face. Then add the social and psychological consequences and costs. Damage to the craniofacial complex, whether from disease, disorder, or injury, strikes at our very identity. We see ourselves, and others see us, in terms of the face we present to the world. Diminish that image in any way and we risk the loss of self-esteem and well-being. Many unanswered questions remain for scien- tists, practitioners, educators, policymakers, and the public. This report highlights the research challenges as well as pointing to emerging technologies that may facilitate finding solutions. Along with the quest for answers comes the challenge of applying what is already known in a society where there are social, political, economic, behavioral, and environmental barriers to health and well-being. THE CHARGE The realization that oral health can have a significant impact on the overall health and well-being of the nation’s population led the Office of the Surgeon General, with the approval of the Secretary of Health and Human Services, to commission this report. 4 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Recognizing the gains that have been made in disease prevention while acknowledging that there are popu- lations that suffer disproportionately from oral health problems, the Secretary asked that the report “define, describe, and evaluate the interaction between oral health and health and well-being [quality of life], through the life span in the context of changes in society.” Key elements to be addressed were the determinants of health and disease, with a primary focus on prevention and “producing health” rather than “restoring health”; a description of the burden of oral diseases and disorders in the nation; and the evidence for actions to improve oral health to be taken across the life span. The report also was to fea- ture an orientation to the future, highlighting lead- ing-edge technologies and research findings that can be brought to bear in improving the oral health of individuals and communities. THE SCIENCE BASE FOR THE REPORT This report is based on a review of the published scientific literature. Standards established to determine the quality of the evidence, based on the study design and its rigor, were used where appropriate. In addition, the strength of the recommendations, where they are made, is based on evidence of effectiveness for the population of interest. The scope of the review encompassed the international English literature. Recent systematic reviews of the literature are referenced, as are selected review articles. A few referenced articles are in press, and there are occasional references to recent abstracts and personal communications. The science base in oral health has been evolving over the past half century. Initial research in this area was primarily in the basic sciences, investigating mechanisms of normal development and pathology in relation to dental caries and periodontal diseases. Prevention research has included controlled clinical studies, with and without randomization, as well as community trials and demonstration research. More recent research has broadened the science base to include studies of the range of craniofacial diseases and disorders and is moving from basic science to translational, clinical, and health services research. The clinical literature includes the full range of studies, from randomized controlled studies to case studies. Most of the literature includes cross-section- al and cohort studies, with some case-control studies. General reviews of the literature have been used for Chapters 2 through 10. Chapter 4 includes both pub- lished and new analyses of national and state data- bases that have been carefully designed and for which Executive Summary quality assurance has been maintained by the Centers for Disease Control and Prevention. Studies of smaller populations are also included where rele- vant. In Chapter 5, tables present information on the association of oral infections and systemic condi- tions, and in Chapter 7, tables exhibit oral disease prevention and health promotion measures. The published literature related to the development of new technologies, their potential impact, and the need for further research are described in the course of addressing the requested futures orientation. The report was generated with the advice and support of a Federal Coordinating Committee composed of representatives of ageneies with oral health components and interests. The chapters were based on papers submitted by experts working under the guidance of a coordinating author for each chapter. Independent peer review was conducted for all sections of the report at various stages in the process, and the full manuscript was reviewed by a number of senior reviewers as well as the relevant federal agencies. All who contributed are listed in the Acknowledgments section of the full report. ORGANIZATION OF THE REPORT The report centers on five major questions, which have been used to structure the report into five parts. Part One: What Is Oral Health? The meaning of oral health is explored in Chapter 1, and the interdependence of oral health with general health and well-being is a recurrent theme through- out the volume. Chapter 2 provides an overview of the craniofa- cial complex in development and aging, how the tis- sues and organs function in essential life processes, and their role in determining our uniquely human abilities. Our craniofacial complex has evolved to have remarkable functions and abilities to adapt, enabling us to meet the challenges of an ever-chang- ing environment. An examination of the various tis- sues reveals elaborate designs that serve complex needs and functions, including the uniquely human function of speech. The rich distribution of nerves, muscles, and blood vessels in the region as well as extensive endocrine and immune system connec- tions are indicators of the vital role of the craniofacial complex in adaptation and survival over a long life span. In particular, the following findings are noted: e Genes controlling the basic patterning and segmental organization of human development, and specifically the craniofacial complex, are highly ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 5 Executive Summary conserved in nature. Mutated genes affecting human development have counterparts in many simpler organisms. e There is considerable reserve capacity or redundancy in the cells and tissues of the craniofacial complex, so that if they are properly cared for, the structures should function well over a lifetime. e The salivary glands and saliva subserve tast- ing and digestive functions and also participate in the mucosal immune system, a main line of defense against pathogens, irritants, and toxins. e Salivary components protect and maintain oral tissues through antimicrobial components, buffering agents, and a process by which dental enamel can be remineralized. Part Two: What Is the Status of Oral Health in America? Chapter 3 is a primer describing the major diseases and disorders that affect the craniofacial complex. The findings include: e Microbial infections, including those caused by bacteria, viruses, and fungi, are the primary cause of the most prevalent oral diseases. Examples include dental caries, periodontal diseases, herpes labialis, and candidiasis. e The etiology and pathogenesis of diseases and disorders affecting the craniofacial structures are multifactorial and complex, involving an inter- play among genetic, environmental, and behavioral factors. e Many inherited and congenital conditions * affect the craniofacial complex, often resulting in dis- figurement and impairments that may involve many body organs and systems and affect millions of chil- dren worldwide. e Tobacco use, excessive alcohol use, and inappropriate dietary practices contribute to many diseases and disorders. In particular, tobacco use is a risk factor for oral cavity and pharyngeal cancers, periodontal diseases, candidiasis, and dental caries, among other diseases. e Some chronic diseases, such as Sjogren's syn- drome, present with primary oral symptoms. e Oral-facial pain conditions are common and often have complex etiologies. Chapter 4 constitutes an oral health status report card for the United States, describing the magnitude of the problem. Where data permit, the chapter also describes the oral health of selected population groups, as well as their dental visit behavior. The findings include: e Over the past five decades, major improve- ments in oral health have been seen nationally for most Americans. e Despite improvements in oral health status, profound disparities remain in some population groups as classified by sex, income, age. and race/eth- nicity. For some diseases and conditions, the magni- tude of the differences in oral health status among population groups is striking. e Oral diseases and conditions affect people throughout their life span. Nearly every American has experienced the most common oral disease, den- tal caries. ro e Conditions that severely affect the face and facial expression, such as birth defects, craniofacial injuries, and neoplastic diseases, are more common in the very young and in the elderly. e Oral-facial pain can greatly reduce quality of life and restrict major functions. Pain is a common symptom for many of the conditions affecting oral- facial structures. e National and state data for many oral and craniofacial diseases and conditions and for popula- tion groups are limited or nonexistent. Available state data reveal variations within and among states in pat- terns of health and disease among population groups. e Research is needed to develop better meas- ures of disease and health, to explain the differences among population groups, and to develop interven- tions targeted at eliminating disparities. Part Three: What Is the Relationship Between Oral Health and General Health and Well-being? Chapters 5 and 6 address key issues in the reports charge—the relationship of oral health to general health and well-being. Chapter 5 explores the theme of the mouth as reflecting general health or disease status. Examples are given of how oral tissues may signal the presence of disease, disease progression, or exposure to risk factors, and how oral cells and fluids are increasingly being used as diagnostic tools. This is followed by a discussion of the mouth as a portal of entry for infections that can affect local tissues and may spread to other parts of the body. The final sec- tions review the literature regarding emerging associ- ations between oral diseases and diabetes, heart dis- ease and stroke, and adverse pregnancy outcomes. 6 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The findings include: e Many systemic diseases and conditions have oral manifestations. These manifestations may be the initial sign of clinical disease and as such serve to inform clinicians and individuals of the need for fur- ther assessment. e The oral cavity is a portal of entry as well as the site of disease for microbial infections that affect general health status. e The oral cavity and its functions can be adversely affected by many pharmaceuticals and other therapies commonly used in treating systemic conditions. The oral complications of these therapies can compromise patient compliance with treatment. e Individuals such as immunocompromised and hospitalized patients are at greater risk for gen- eral morbidity due to oral infections. e Individuals with diabetes are at greater risk for periodontal diseases. e Animal and population-based studies have demonstrated an association between periodontal diseases and diabetes, cardiovascular disease, stroke, and adverse pregnancy outcomes. Further research is needed to determine the extent to which these asso- ciations are causal or coincidental. Chapter 6 demonstrates the relationship between oral health and quality of life, presenting data on the consequences of poor oral health and altered appear- ance on speech, eating, and other functions, as well as on self-esteem, social interaction, education, career achievement, and emotional state. The chapter introduces anthropological and ethnographic litera- ture to underscore the cultural values and symbolism attached to facial appearance and teeth. An examina- tion of efforts to characterize the functional and social implications of oral and craniofacial diseases reveals the following findings: e Oral health is related to well-being and qual- ity of life as measured along functional, psychosocial, and economic dimensions. Diet, nutrition, sleep, psychological status, social interaction, school, and work are affected by impaired oral and craniofacial health. e Cultural values influence oral and craniofa- cial health and well-being and can play an important role in care utilization practices and in perpetuating acceptable oral health and facial norms. e Oral and craniofacial diseases and their treatment place a burden on society in the form of lost days and years of productive work. Acute dental conditions contribute to a range of problems for employed adults, including restricted activity, bed days, and work loss, and school loss for children. In addition, conditions such as oral and pharyngeal Executive Summary cancers contribute to premature death and can be measured by years of life lost. e Oral and craniofacial diseases and condi- tions contribute to compromised ability to bite, chew, and swallow foods; limitations in food selection; and poor nutrition. These conditions include tooth loss, diminished salivary functions, oral-facial pain condi- tions such as temporomandibular disorders, alter- ations in taste, and functional limitations of prosthet- ic replacements. e Oral-facial pain, as a symptom of untreated dental and oral problems and as a condition in and of itself, is a major source of diminished quality of life. It is associated with sleep deprivation, depression, and multiple adverse psychosocial outcomes. e Self-reported impacts of oral conditions on social function include limitations in verbal and non- verbal communication, social interaction, and inti- macy. Individuals with facial disfigurements due to craniofacial diseases and conditions and their treat- ments may experience loss of self-image and self- esteem, anxiety, depression, and social stigma, these in turn may limit educational, career, and marital opportunities and affect other social relations. e Reduced oral-health-related quality of life is associated with poor clinical status and reduced access to care. Part Four: How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? The ‘next three chapters review how individuals, health care practitioners, communities, and the nation as a whole contribute to oral health. Chapter 7 reviews the evidence for the efficacy and effective- ness of health promotion and disease prevention measures with a focus on community efforts in pre- venting oral disease. It continues with a discussion of the knowledge and practices of the public and health care providers and indicates opportunities for broad- based and targeted health promotion. The findings include: e Community water fluoridation, an effective, safe, and ideal public health measure, benefits indi- viduals of all ages and socioeconomic strata. Unfortunately, over one third of the U.S. population (100 million people) are without this critical public health measure. e Effective disease prevention measures exist for use by individuals, practitioners, and communities. Most of these focus on dental caries prevention, such as fluorides and dental sealants, where a combination of services is required to ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 7 Executive Summary achieve optimal disease prevention. Daily oral hygiene practices such as brushing and flossing can prevent gingivitis. e Community-based approaches for the pre- vention of other oral diseases and conditions, such as oral and pharyngeal cancers and oral-facial trauma, require intensified developmental efforts. e Community-based preventive programs are unavailable to substantial portions of the under- served population. e There is a gap between research findings and the oral disease prevention and health promotion practices and knowledge of the public and the health professions. e Disease prevention and health promotion approaches, such as tobacco control, appropriate use of fluorides for caries prevention, and folate supple- mentation for neural tube defect prevention, high- light opportunities for partnerships between commu- nity-based programs and practitioners, as well as col- laborations among health professionals. e Many community-based programs require a combined effort among social service, health care, and education services at the local or state level. Chapter 8 explores the role of the individual and the health care provider in promoting and maintain- ing oral health and well-being. For the individual, this means exercising appropriate self-care and adopting healthy behaviors. For the provider, it means incorporating the knowledge emerging from the science base in a timely manner for prevention and diagnosis, risk assessment and risk management, and treatment of oral diseases and disorders. The- chapter focuses largely on the oral health care provider. The management of oral and craniofacial health and disease necessitates collaborations among a team of care providers to achieve optimal oral and general health. The findings include: e Achieving and maintaining oral health require individual action, complemented by profes- sional care as well as community-based activities. e Individuals can take actions, for themselves and for persons under their care, to prevent disease and maintain health. Primary prevention of many oral, dental, and craniofacial diseases and conditions is possible with appropriate diet, nutrition, oral hygiene, and health-promoting behaviors, including the appropriate use of professional services. Individuals should use a fluoride dentifrice daily to help prevent dental caries and should brush and floss daily to prevent gingivitis. e All primary care providers can contribute to improved oral and craniofacial health. Inter- disciplinary care is needed to manage the oral health-general health interface. Dentists, as primary care providers, are uniquely positioned to play an expanded role in the detection, early recognition, and management of a wide range of complex oral and general diseases and conditions. e Nonsurgical interventions are available to reverse disease progression and to manage oral dis- eases as infections. e New knowledge and the development of molecular and genetically based tests will facili- tate risk assessment and management and improve the ability of health care providers to customize treatment. e Health care providers can successfully deliv- er tobacco cessation and other health promotion pro- grams in their offices, contributing to both overall health and oral health. e Biocompatible rehabilitative materials and biologically engineered tissues are being developed and will greatly enhance the treatment options avail- able to providers and their patients. Chapter 9 describes the roles of dental practi- tioners and their teams, the medical community, and public health agencies at local, state, and national levels in administering care or reimbursing for the costs of care. These activities are viewed against the changing organization of U.S. health care and trends regarding the workforce in research, education, and practice. e Dental, medical, and public health delivery systems each provide services that affect oral and craniofacial health in the U.S. population. Clinical oral health care is predominantly provided by a pri- vate practice dental workforce. e Expenditures for dental services alone made up 4.7 percent of the nation’s health expenditures in 1998—$53.8 billion out of $1.1 trillion. These expenditures underestimate the true costs to the nation, however, because data are unavailable to determine the extent of expenditures and services provided for craniofacial health care by other health providers and institutions. e The public health infrastructure for oral health is insufficient to address the needs of disad- vantaged groups, and the integration of oral and gen- eral health programs is lacking. e Expansion of community-based disease prevention and lowering of barriers to personal oral health care are needed to meet the needs of the population. e Insurance coverage for dental care is increasing but still lags behind medical insurance. 8 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL For every child under 18 years old without medical insurance, there are at least two children without dental insurance; for every adult 18 years or older without medical insurance, there are three without dental insurance. e Eligibility for Medicaid does not ensure enrollment, and enrollment does not ensure that individuals obtain needed care. Barriers include patient and caregiver understanding of the value and importance of oral health to general health, low reimbursement rates, and administrative burdens for both patient and provider. e A narrow definition of “medically necessary dental care” currently limits oral health services for many insured persons, particularly the elderly. e The dentist-to-population ratio is declining, creating concern as to the capability of the dental workforce to meet the emerging demands of society and provide required services efficiently. e Anestimated 25 million individuals reside in areas lacking adequate dental care services, as defined by Health Professional Shortage Area (HPSA) criteria. e Educational debt has increased, affecting both career choices and practice location. e Disparities exist in the oral health profession workforce and career paths. The number of under- represented minorities in the oral health professions is disproportionate to their distribution in the popu- lation at large. e Current and projected demand for dental school faculty positions and research scientists is not being met. A crisis in the number of faculty and researchers threatens the quality of dental educa- tion; oral, dental, and craniofacial research; and, ulti- mately, the health of the public. e Reliable and valid measures of oral health outcomes do not exist and need to be developed, val- idated, and incorporated into practice and programs. Part Five: What Are the Needs and Opportunities to Enhance Oral Health? Chapter 10 looks at determinants of oral health in the context of society and across various life stages. Although theorists have proposed a variety of models of health determinants, there is general consensus that individual biology, the physical and socioeconomic environment, personal behaviors and lifestyle, and the organization of health care are key factors whose interplay determines the level of oral health achieved by an individual. The chapter provides examples of these factors with an emphasis ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Executive Summary on barriers and ways to raise the level of oral health for children and older Americans. The findings include: e The major factors that determine oral and general health and well-being are individual biology and genetics; the environment, including its physical and socioeconomic aspects; personal behaviors and lifestyle; access to care; and the organization of health care. These factors interact over the life span and determine the health of individuals, population groups, and communities—from neighborhoods to nations. e The burden of oral diseases and conditions is disproportionately borne by individuals with low socioeconomic status at each life stage and by those who are vulnerable because of poor general health. e Access to care makes a difference. A complex set of factors underlies access to care and includes the need to have an informed public and policymakers, integrated and culturally competent programs, and resources to pay and reimburse for the care. Among other factors, the availability of insurance increases access to care. e Preventive interventions, such as protective head and mouth gear and dental sealants, exist but are not uniformly used or reinforced. e Nursing homes and other long-term care institutions have limited capacity to deliver needed oral health services to their residents, most of whom are at increased risk for oral diseases. e Anticipatory guidance and risk assessment and management facilitate care for children and for the elderly. e Federal and state assistance programs for selected oral health services exist; however, the scope of services is severely limited, and their reimburse- ment level for oral health services is low compared to the usual fee for care. Chapter 11 spells out in greater detail the prom- ise of the life sciences in improving oral health in the coming years in the context of changes in American—and global—society. The critical role of genetics and molecular biology is emphasized. Chapter 12, the final chapter, iterates the themes of the report and groups the findings from the earlier chapters into eight major categories. These findings, as well as a suggested framework for action to guide the next steps in enhancing the oral health of the nation, are presented below. Executive Summary MAJOR FINDINGS Oral diseases and disorders in and of themselves affect health and well-being throughout life. The burden of oral problems is extensive and may be par- ticularly severe in vulnerable populations. It includes the common dental diseases and other oral infections such as cold sores and candidiasis that can occur at any stage of life, as well as birth defects in infancy and the chronic facial pain conditions and oral can- cers seen in later years. Many of these conditions and their treatments may undermine self-image and self- esteem, discourage normal social interaction, cause other health problems, and lead to chronic stress and depression as well as incur great financial cost. They may also interfere with vital functions such as breath- ing, food selection, eating, swallowing, and speaking and with activities of daily living such as work, school, and family interactions. Safe and effective measures exist to prevent the most common dental diseases—dental caries and periodontal diseases. Community water fluoridation is safe and effective in preventing dental caries in both children and adults. Water fluoridation benefits all residents served by community water supplies regardless of their social or economic status. Professional and individual measures, including the use of fluoride mouthrinses, gels, dentifrices, and dietary supplements and the application of dental sealants, are additional means of preventing dental caries. Gingivitis can be prevented by good personal oral hygiene practices, including brushing and flossing. Lifestyle behaviors that affect general health such as tobacco use, excessive alcohol use, and poor dietary choices affect oral and craniofacial health as well. These individual behaviors are asso- ciated with increased risk for craniofacial birth defects, oral and pharyngeal cancers, periodontal dis- ease, dental caries, and candidiasis, among other oral health problems. Opportunities exist to expand the oral disease prevention and health promotion knowl- edge and practices of the public through community programs and in health care settings. All health care providers can play a role in promoting healthy lifestyles by incorporating tobacco cessation pro- grams, nutritional counseling, and other health pro- motion efforts into their practices. There are profound and consequential oral health disparities within the U.S. population. Disparities for various oral conditions may relate to income, age, sex, race or ethnicity, or medical status. Although common dental diseases are preventable, not all members of society are informed about or able to avail themselves of appropriate oral-health- promoting measures. Similarly, not all health providers may be aware of the services needed to improve oral health. In addition, oral health care is not fully integrated into many care programs. Social, economic, and cultural factors and changing pop- ulation demographics affect how health services are delivered and used, and how people care for themselves. Reducing disparities requires wide- ranging approaches that target populations at high- est risk for specific oral diseases and involves improving access to existing care. One approach includes making dental insurance more available to Americans. Public coverage for dental care is minimal for adults, and programs for children have not reached the many eligible beneficiaries. More information is needed to improve America’s oral health and eliminate health dispari- ties. We do not have adequate data on health, dis- ease, and health practices and care use for the U.S. population as a whole and its diverse segments, including racial and ethnic minorities, rural popula- tions, individuals with disabilities, the homeless, immigrants, migrant workers, the very young, and the frail elderly. Nor are there sufficient data that explore health issues in relation to sex or sexual ori- entation. Data on state and local populations, essen- tial for program planning and evaluation, are rare or unavailable and reflect the limited capacity of the U.S. health infrastructure for oral health. Health serv- ices research, which could provide much needed information on the cost, cost-effectiveness, and out- . comes of treatment, is also sorely lacking. Finally, measurement of disease and health outcomes is need- ed. Although progress has been made in measuring oral-health-related quality of life, more needs to be done, and measures of oral health per se do not exist. The mouth reflects general health and well- being. The mouth is a readily accessible and visible part of the body and provides health care providers and individuals with a window on their general health status. As the gateway of the body, the mouth senses and responds to the external world and at the same time reflects what is happening deep inside the body. The mouth may show signs of nutritional defi- ciencies and serve as an early warning system for dis- eases such as HIV infection and other immune sys- tem problems. The mouth can also show signs of general infection and stress. As the number of sub- stances that can be reliably measured in saliva increases, it may well become the diagnostic fluid of choice, enabling the diagnosis of specific disease as well as the measurement of the concentration of a variety of drugs, hormones, and other molecules of interest. Cells and fluids in the mouth may also be 10 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL used for genetic analysis to help uncover risks for disease and predict outcomes of medical treatments. Oral diseases and conditions are associated with other health problems. Oral infections can be the source of systemic infections in people with weakened immune systems, and oral signs and symp- toms often are part of a general health condition. Associations between chronic oral infections and other health problems, including diabetes, heart dis- ease, and adverse pregnancy outcomes, have also been reported. Ongoing research may uncover mech- anisms that strengthen the current findings and explain these relationships. Scientific research is key to further reduction in the burden of diseases and disorders that affect the face, mouth, and teeth. The science base for dental — diseases is broad and provides a strong foundation for further improvements in prevention; for other craniofacial and oral health conditions the base has not yet reached the same level of maturity. Scientific research has led to a variety of approaches to improve oral health through prevention, early diagnosis, and treatment. We are well positioned to take these pre- vention measures further by investigating how to develop more targeted and effective interventions and devising ways to enhance their appropriate adop- tion by the public and the health professions. The application of powerful new tools and techniques is important. Their employment in research in genetics and genomics, neuroscience, and cancer has allowed rapid progress in these fields. An intensified effort to understand the relationships between oral infections and their management, and other illnesses and con- ditions is warranted, along with the development of oral-based diagnostics. These developments hold great promise for the health of the American people. A FRAMEWORK FOR ACTION All Americans can benefit from the development of a National Oral Health Plan to improve quality of life and eliminate health disparities by facilitating collab- orations among individuals, health care providers, communities, and policymakers at all levels of socie- tv and by taking advantage of existing initiatives. Everyone has a role in improving and promoting oral health. Together we can work to broaden public understanding of the importance of oral health and its relevance to general health and well-being, and to ensure that existing and future preventive, diagnos- tic, and treatment measures for oral diseases and dis- orders are made available to all Americans. The fol- lowing are the principal components of the plan: Executive Summary Change perceptions regarding oral health and dis- ease so that oral health becomes an accepted com- ponent of general health. e Change public perceptions. Many people con- sider oral signs and symptoms to be less important than indications of general illness. As a result, they may avoid or postpone needed care, thus exacerbat- ing the problem. If we are to increase the nation’s capacity to improve oral health and reduce health disparities, we need to enhance the public's under- standing of the meaning of oral health and the rela- tionship of the mouth to the rest of the body. These messages should take into account the multiple lan- guages and cultural traditions that characterize America’s diversity. e Change policymakers’ perceptions. Informed policymakers at the local, state, and federal levels are critical in ensuring the inclusion of oral health serv- ices in health promotion and disease prevention pro- grams, care delivery systems, and reimbursement schedules. Raising awareness of oral health among legislators and public officials at all levels of govern- ment is essential to creating effective public policy to improve America’s oral health. Every conceivable avenue should be used to inform policymakers— informally through their organizations and affilia- tions and formally through their governmental offices—if rational oral health policy is to be formu- lated and effective programs implemented. e Change health providers’ perceptions. Too little time is devoted to oral health and disease topics in the education of nondental health professionals. Yet all care providers can and should contribute to enhancing oral health. This can be accomplished in several ways, such as including an oral examination as part of a general medical examination, advising patients in matters of tobacco cessation and diet, and referring patients to oral health practitioners for care prior to medical or surgical treatments that can dam- age oral tissues, such as cancer chemotherapy or radiation to the head and neck. Health care providers should be ready, willing, and able to work in collabo- ration to provide optimal health care for their patients. Having informed health care professionals will ensure that the public using the health care sys- tem will benefit from interdisciplinary services and comprehensive care. To prepare providers for such a role will involve, among other factors, curriculum changes and multidisciplinary training. Accelerate the building of the science and evidence base and apply science effectively to improve oral health. Basic behavioral and biomedical research, clinical trials, and population-based research have ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 11 Executive Summary been at the heart of scientific advances over the past decades. The nation’s continued investment in research is critical for the provision of new knowl- edge about oral and general health and disease for years to come and needs to be accelerated if further improvements are to be made. Equally important is the effective transfer of research findings to the pub- lic and health professions. However, the next steps are more complicated. The challenge is to understand complex diseases caused by the interaction of multi- ple genes with environmental and behavioral vari- ables—a description that applies to most oral dis- eases and disorders—and translate research findings into health care practice and healthy lifestyles. This report highlights many areas of research opportunities and needs in each chapter. At present, there is an overall need for behavioral and clinical research, clinical trials, health services research, and community-based demonstration research. Also, development of risk assessment procedures for indi- viduals and communities and of diagnostic markers to indicate whether an individual is more or less sus- ceptible to a given disease can provide the basis for formulating risk profiles and tailoring treatment and program options accordingly. Vital to progress in this area is a better under- standing of the etiology and distribution of disease. But as this report makes clear, epidemiologic and sur- veillance databases for oral health and disease, health services, utilization of care, and expenditures are limited or lacking at the national, state, and local levels. Such data are essential in conducting health services research, generating research hypotheses, planning and evaluating programs, and identifying emerging public health problems. Future data collec- tion must address differences among the subpopula- tions making up racial and ethnic groups. More attention must also be paid to demographic variables such as age, sex, sexual orientation, and socioeco- nomic factors in determining health status. Clearly, the more detailed information that is available, the better can program planners establish priorities and targeted interventions. Progress in elucidating the relationships between chronic oral inflammatory infections, such as peri- odontitis, and diabetes and glycemic control as well as other systemic conditions will require a similar intensified commitment to research. Rapid progress can also occur with efforts in the area of the natural repair and regeneration of oral tissues and organs. Improvements in oral health depend on multidisci- plinary and interdisciplinary approaches to biomed- ical and behavioral research, including partnerships among researchers in the life and physical sciences, and on the ability of practitioners and the public to apply research findings effectively. Build an effective health infrastructure that meets the oral health needs of all Americans and inte- grates oral health effectively into overall health. The public health capacity for addressing oral health is dilute and not integrated with other public health programs. Although the Healthy People 2010 objec- tives provide a blueprint for outcome measures, a national public health plan for oral health does not exist. Furthermore, local, state, and federal resources are limited in the personnel, equipment, and facilities available to support oral health programs. There is also a lack of available trained public health practi- tioners knowledgeable about oral health. As a result, existing disease prevention programs are not being implemented in many communities, creating gaps in prevention and care that affect the nation’s neediest populations. Indeed, cutbacks in many state budgets have reduced staffing of state and territorial dental programs and curtailed oral health promotion and disease prevention efforts. An enhanced public health infrastructure would facilitate the develop- ment of strengthened partnerships with private prac- titioners, other public programs, and voluntary groups. There is a lack of racial and ethnic diversity in the oral health workforce. Efforts to recruit members of minority groups to positions in health education, research, and practice in numbers that at least match their representation in the general population not only would enrich the talent pool, but also might result in a more equitable geographic distribution of care providers. The effect of that change could well enhance access and utilization of oral health care by racial and ethnic minorities. A closer look at trends in the workforce disclos- es a worrisome shortfall in the numbers of men and women choosing careers in oral health education and research. Government and private sector leaders are aware of the problem and are discussing ways to increase and diversify the talent pool, including eas- ing the financial burden of professional education, but additional incentives may be necessary. Remove known barriers between people and oral health services. This report presents data on access, utilization, financing, and reimbursement of oral health care; provides additional data on the extent of the barriers; and points to the need for public-private partnerships in seeking solutions. The data indicate that lack of dental insurance, private or public, is one of several impediments to obtaining oral health care 12 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and accounts in part for the generally poorer oral health of those who live at or near the poverty line, lack health insurance, or lose their insurance upon retirement. The level of reimbursement for services also has been reported to be a problem and a disin- centive to the participation of providers in certain public programs. Professional organizations and gov- ernment agencies are cognizant of these problems and are exploring solutions that merit evaluation. particular concern has been expressed about the nations children, and initiatives such as the State Children’s Health Insurance Program, while not man- dating coverage for oral health services, are a positive step. In addition, individuals whose health is physi- cally, mentally, and emotionally compromised need comprehensive integrated care. Use public-private partnerships to improve the oral health of those who still suffer disproportionately from oral diseases. The collective and complementa- ry talents of public health agencies, private industry, social services organizations, educators, health care providers, researchers, the media, community lead- ers, voluntary health organizations and consumer groups, and concerned citizens are vital if America is not just to reduce, but to eliminate, health disparities. This report highlights variations in oral and general health within and across all population groups. Increased public-private partnerships are needed to educate the public, to educate health professionals, to conduct research, and to provide health care serv- ices and programs. These partnerships can build and strengthen cross-disciplinary, culturally competent, community-based, and community-wide efforts and demonstration programs to expand initiatives for health promotion and disease prevention. Examples of such efforts include programs to prevent tobacco use, promote better dietary choices, and encourage the use of protective gear to prevent sports injuries. In this way, partnerships uniting sports organiza- tions. schools, the faith community, and other groups and leaders, working in concert with the health com- munity, can contribute to improved oral and general health. CONCLUSION The past half century has seen the meaning of oral health evolve from a narrow focus on teeth and gin- giva to the recognition that the mouth is the center of Executive Summary vital tissues and functions that are critical to total health and well-being across the life span. The mouth as a mirror of health or disease, as a sentinel or early warning system, as an accessible model for the study of other tissues and organs, and as a potential source of pathology affecting other systems and organs has been described in earlier chapters and provides the impetus for extensive future research. Past discover- ies have enabled Americans today to enjoy far better oral health than their forebears a century ago. But the evidence that not all Americans have achieved the same level of oral health and well-being stands as a major challenge, one that demands the best efforts of public and private agencies and individuals. REFERENCES Health Care Financing Administration (HCFA). National Health Expenditures projections: 1998- 2008. Office of the Actuary. http://www.hefa.gov/ stats/NHE-Proj/. 2000 Apr 25. U.S. Department of Health and Human Services (USDHHS). Healthy People 2010 (Conference Edition, in two volumes). Washington; 2000 Jan. U.S. General Accounting Office (GAO). Oral health in low-income populations. GAO/HEHS-00-72. 2000 Apr. PROJECT TEAM Caswell A. Evans DDS, MPH Project Director and Executive Editor Assistant Director, Los Angeles County Department of Health Services Dushanka V. Kleinman DDS, MScD Co-Executive Editor Deputy Director, National Institute of Dental and Craniofacial Research, National Institutes of Health William R. Maas DDS, MPH, MS Chief Dental Officer, U.S. Public Health Service Director, Division of Oral Health, Centers for Disease Control and Prevention Harold C. Slavkin DDS Director, National Institute of Dental and Craniofacial Research, National Institutes of Health Joan S. Wilentz MA Science Writer and Editor Roseanne Price ELS Editor Marla Fogelman Editor July 2000 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 13 2 What Is Oral Health? The two chapters that follow explore the answer to this question, an answer that continues to evolve throughout the report. Oral health means more than healthy teeth and the absence of disease. It involves the ability of individuals to carry out essential functions such as eating and speaking as well as to contribute fully to society. Chapter 1, the introduction, explains how the meaning of oral health has developed in tandem with progress in understanding the two chief dental diseases—dental caries and periodontal diseases—which historically have been the major preoccupation of patients, providers, and research investigators alike. There is a marvelous success story here regarding the role of fluoride in preventing dental caries and the research that proved that dental caries and periodontal diseases are infections and can be prevented. These investigations were complemented by studies of the tissues of the mouth and adjacent areas—the craniofacial complex. Chapter 2 describes the tissues and organs of the craniofacial complex, providing a primer and guide to their essential features that emphasizes the ways they contribute to the richness of human experience, and at the same time protect and nurture the human body. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 15 8 re Sis L The Meaning of Oral Health The intent of this first-ever Surgeon General's report on oral health is to alert Americans to the full mean- ing of oral health and its importance in relation to general health and well-being. Great progress has been made in reducing the extent and severity of common oral diseases, and recent history has seen marked improvements in the nation’s oral and dental health, thanks to successful prevention measures adopted by communities, individuals, and oral health professionals. However, not everyone is experiencing the same degree of improvement. What amounts to a “a silent epidemic” of dental and oral diseases is affecting some population groups—a burden of dis- ease that restricts activities in school, work, and home, and often significantly diminishes the quality of life. ‘ The word oral, both in its Latin root and in com- mon usage, refers to the mouth. The mouth includes not only the teeth and the gums (gingiva) and their supporting connective tissues, ligaments, and bone, but also the hard and soft palate, the soft mucosal tis- sue lining of the mouth and throat, the tongue, the lips, the salivary glands, the chewing muscles, and the upper and lower jaws, which are connected to the skull by the temporomandibular joints. Equally important are the branches of the nervous, immune, and vascular systems that animate, protect, and nour- ish the oral tissues, as well as provide the connec- tions to the brain and the rest of the body. The genet- ic patterning of development in utero further reveals the intimate relationship of the oral tissues to the developing brain and to the tissues of the face and head that surround the mouth, structures whose location is captured in the word craniofacial. A major theme of this report is that oral health means much more than healthy teeth. It means being free of chronic oral-facial pain conditions, oral and pharyngeal (throat) cancers, oral soft tissue lesions, birth defects such as cleft lip and palate, and scores of other diseases and disorders that affect the oral, dental, and craniofacial tissues, collectively known as the craniofacial complex. These are tissues whose functions we often take for granted, yet they represent the very essence of our humanity. They allow us to speak and smile; sigh and kiss; smell, taste, touch, chew, and swallow; cry out in pain; and convey a world of feelings and emotions through facial expressions. They also provide protection against microbial infections and environmental insults. The craniofacial tissues also provide a useful means to understanding organs and systems in less accessible parts of the body. The salivary glands are a model of other exocrine glands, and an analysis of saliva can provide telltale clues of overall health or disease. The jawbones are examples of other skeletal parts. The nervous system apparatus underlying facial pain has its counterpart in nerves elsewhere in the body. A thorough oral examination can detect signs of nutritional deficiencies as well as a number of sys- temic diseases, including microbial infections, immune disorders, injuries, and some cancers. Indeed, the phrase the mouth is a mirror has been used to illustrate the wealth of information that can be derived from examining oral tissues. New research is pointing to associations between chronic oral infections and heart and lung diseases, stroke, and low-birth-weight, premature births. Associations between periodontal disease and diabetes have long been noted. This report assesses these associations and explores mechanisms that might explain these oral-systemic disease connections. In parallel with the broadened meaning of oral health, the meaning of health has evolved. The stan- dard definition of health, “freedom from disease, defect, or pain,” defines what health is not, rather ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 17 The Meaning of Oral Health than what it is. A more positive definition, one that the World Health Organization established in 1948, states that health is a complete state of physical, men- tal, and social well-being, and not just the absence of infirmity. The broadened meaning of oral health parallels the broadened meaning of health. In 1948 the World Health Organization expanded the definition of health to mean “a complete state of physical, mental, and social well-being, and not just the absence of infirmity.” It follows that oral health must also include well-being. Just as we now understand that nature and nurture are inextricably linked, and mind and body are both expressions of our human biology, $0, too, we must recognize that oral health and general health are inseparable. We ignore signs and symptoms of oral disease and dysfunction to our detriment. Consequently, a second theme of the report is that oral health is integral to general health. You cannot be healthy without oral health. Oral health and general health should not be interpreted as separate entities. Oral health is a critical component of health and must be included in the provision of health care and the design of community programs. The wider meanings of oral and health in no way diminish the relevance and importance of the two leading dental diseases, caries (tooth decay) and the periodontal diseases. They remain common and widespread, affecting nearly everyone at some point in the life span. What has changed is what we can do about them. At the start of the twentieth’ century, most Americans expected to be toothless by age 45, and most were. Expectations have changed, and most people now assume that they will maintain their teeth over their lifetime, and take active measures to do so. Researchers in the 1930s discovered that peo- ple living in communities with naturally fluoridated water supplies had less dental caries than people drinking unfluoridated water. But not until the end of World War II were the investigators able to design and implement the community clinical trials that confirmed their observations and launched a better approach to the problem of dental caries: prevention. Soon after, adjusting the fluoride content of commu- nity water supplies was pursued as an important pub- lic health measure to prevent dental caries. Although this measure has not been fully imple- mented, the results have been dramatic. Dental caries began to decline in the 1950s among children who grew up in fluoridated cities, and by the late 1970s, declines in decay were evident for many Americans. The application of oral science to improved diagnos- tic, treatment, and prevention strategies has saved billions of dollars per year in the nation’s annual health bill. Even more significant, the result is that far fewer people are edentulous (toothless) today than a generation ago. The theme of prevention gained momentum as pioneering investigators and practitioners in the 1950s and 1960s showed that not only dental caries ~ put also periodontal diseases are bacterial infections. The researchers demonstrated that the infections could be prevented by increasing host resistance to disease and reducing or eliminating the suspected microbial pathogens in the oral cavity. The applica- tions of research discoveries have resulted in contin- uing improvements in the oral health of Americans, new approaches to the prevention and treatment of dental diseases, and the growth of the science. The significant role that scientists, dentists, den- tal hygienists, and other health professionals have played in the prevention of oral disease and disabili- ty leads to a third theme of this report: safe and effec- tive disease prevention measures exist that every- one can adopt to improve oral health and prevent disease. These measures include daily oral hygiene procedures and other lifestyle behaviors, community programs such as community water fluoridation and tobacco cessation programs, and provider-based interventions such as the placement of dental sealants and examinations for common oral and pha- ryngeal cancers. It is hoped that this Surgeon General’s report will facilitate the maturing of the broad field of craniofacial research so that gains in the prevention of craniofacial diseases and disorders can be realized that are as impressive as those ‘achieved for common dental diseases. At the same time, more needs to be done to ensure that messages of health promotion and dis- ease prevention are brought home to all Americans. In this regard, a fourth theme of the report is that general health risk factors, such as tobacco use and poor dietary practices, also affect oral and craniofa- cial health. The evidence for an association between tobacco use and oral diseases has been clearly delin- eated in almost every Surgeon General's report on tobacco since 1964, and the oral effects of nutrition and diet are presented in the Surgeon General's report on nutrition (1988). All the health professions can play a role in reducing the burden of disease in America by calling attention to these and other risk factors and suggesting appropriate actions. Clearly, promoting health and preventing disease are concepts the American people have taken to heart. For the third decade the nation has developed a plan for the prevention of disease and the promo- 18 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL “ion of health, embodied in the U.S. Department of Health and Human Services (2000) document, Healthy People 2010. As a nation, we hope to elimi- nate disparities in health and prevent oral diseases, cancer, birth defects, AIDS and other devastating infections, mental illness and suicide, and the chron- ic diseases of aging. To live well into old age free of pain and infirmity, and with a high quality of life, is the American dream. Scientists today take that dream seriously in pur- suing the intricacies of the craniofacial complex. They are using an ever-growing array of sophisticat- ed analytic tools and imaging systems to study nor- mal function and diagnose disease. They are com- pleting the mapping and sequencing of human, ani- mal, microbial, and plant genomes, the better to understand the complexities of human development, aging, and pathological processes. They are growing cell lines, synthesizing molecules, and using a new generation of biomaterials to revolutionize tissue repair and regeneration. More than ever before, they are working in multidisciplinary teams to bring new knowledge and expertise to the goal of understand- ing complex human diseases and disorders. THE CHALLENGE This Surgeon General's report has much to say about the inequities and disparities that affect those least able to muster the resources to achieve optimal oral health. The barriers to oral health include lack of access to care, whether because of limited income or lack of insurance, transportation, or the flexibility to take time off from work to attend to personal or fam- ily needs for care. Individuals with disabilities and those with complex health problems may face addi- tional barriers to care. Sometimes, too, the public, policymakers, and providers may consider oral health and the need for care to be less important than other health needs, pointing to the need to raise awareness and improve health literacy. Even more costly to the individual and to socie- ty are the expenses associated with oral health prob- lems that go beyond dental diseases. The nation’s yearly dental bill is expected to exceed $60 billion in 2000 (Health Care Financing Administration 2000). However, add to that expense the tens of billions of dollars in direct medical care and indirect costs of chronic craniofacial pain conditions such as temporomandibular disorders, trigeminal neuralgia, shingles, or burning mouth syndrome; the $100,000 minimum individual lifetime costs of treating cranio- facial birth defects such as cleft lip and palate; the costs of oral and pharyngeal cancers; the costs of The Meaning of Oral Health autoimmune diseases: and the costs associated with the unintentional and intentional injuries that so often affect the head and face. Then add the social and psychological consequences and costs. Damage to the craniofacial complex, whether from disease, disorder, or injury, strikes at our very identity. We see ourselves, and others see us, in terms of the face we present to the world. Diminish that image in any way and we risk the loss of self-esteem and well-being. Many unanswered questions remain for scien- tists, practitioners, educators, policymakers, and the public. This report highlights the research challenges as well as pointing to emerging technologies that may facilitate finding solutions. Along with the quest for answers comes the challenge of applying what is already known in a society where there are social, political, economic, behavioral, and environmental barriers to health and well-being. THE CHARGE The realization that oral health can have a significant impact on the overall health and well-being of the nation’s population led the Office of the Surgeon General, with the approval of the Secretary of Health and Human Services, to commission this report. Recognizing the gains that have been made in disease prevention while acknowledging that there are popu- lations that suffer disproportionately from oral health problems, the Secretary asked that the report “define, describe, and evaluate the interaction between oral health and health and well-being [quality of life], through the life span in the context of changes in society.” Key elements to be addressed were the determinants of health and disease, with a primary focus on prevention and “producing health” rather than “restoring health”; a description of the burden of oral diseases and disorders in the nation; and the evidence for actions to improve oral health to be taken across the life span. The report also was to fea- ture an orientation to the future, highlighting lead- ing-edge technologies and research findings that can be brought to bear in improving the oral health of individuals and communities. THE SCIENCE BASE FOR THE REPORT This report is based on a review of the published scientific literature. Where appropriate, standards established to determine the quality of the evidence, based on the study design and its rigor, were used. In addition, the strength of the recommendations, where they are made, is based on evidence of effectiveness for the population of interest. The scope ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 19 The Meaning of Oral Health of the review encompassed the international English literature. Recent systematic reviews of the literature are referenced, as are selected review articles. A few referenced articles are in press, and there are occasional references to recent abstracts and personal communications. The science base in oral health has been evolving over the past half century. Initial research in this area was primarily in the basic sciences, investigating mechanisms of normal development and pathology in relation to dental caries and periodontal diseases. Prevention research has included controlled clinical studies, with and without randomization, as weil as community trials and demonstration research. More recent research has broadened the science base to include studies of the range of craniofacial diseases and disorders and is moving from basic science to translational, clinical, and health services research. The clinical literature in the oral health sciences includes the full range of studies, from randomized controlled studies to case studies. Most of the litera- ture includes cross-sectional and cohort studies, with some case-control studies. General reviews of the lit- erature have been used for Chapters 2 through 10. Chapter 4 includes both published and new analyses of national and state databases that have been care- fully designed and for which quality assurance has been maintained by the Centers for Disease Control and Prevention. Studies of smaller populations are also included where relevant. In Chapters 5 and 7, evidence tables are presented for the discussion of the association of oral infections and systemic condi- tions and for oral disease prevention and health pro- motion measures, respectively. Experts in the respec- tive fields contributed to the report, and independent expert peer review was conducted for all sections of the report. The published literature related to the development of new technologies, their potential impact, and the need for further research are described in the course of addressing the requested futures orientation. ORGANIZATION OF THE REPORT The report centers on five major questions, which have been used to structure the report into five parts. What Is Oral Health? The meaning of oral health is discussed in the open- ing pages of this chapter, and the interdependence of oral health with general health and well-being is, as noted, a recurrent theme throughout the volume. Chapter 2 provides an overview of the craniofacial complex in development and aging, how the tissues and organs function in essential life processes, and their role in determining our uniquely human abili- ties. The later chapters elaborate further on the meaning of oral health. Of particular importance is the discussion of oral health in relation to well-being and quality of life described in Chapter 6. What Is the Status of Oral Health in America? Chapter 3 is a primer describing the major diseases and disorders that affect the craniofacial complex. Chapter 4 constitutes an oral health status report card on the noninstitutionalized civilian population of the United States, describing the magnitude of the problem. It is based on the most recent national and state data available for a range of craniofacial dis- eases, disorders, and conditions. In general, the national data provide information categorized by sex, age, income (poor versus nonpoor), and broad racial and ethnic categories. In addition, the chapter includes a profile of the oral and general health of selected population groups. These include racial and ethnic groups such as African Americans, Hispanics, Asians, Native Hawaiians and Other Pacific Islanders, and American Indians/Alaska Natives. The health status of women and individuals with disabilities is highlighted. Although it is clearly desirable to describe the health status of additional populations, data are insufficient or lacking for groups defined by sexual orientation or rural residency or categorized - as homeless, migrant workers, or incarcerated. As an initial step toward understanding the burden of dis- ease in relation to the provision of care, available data on the number of dental visits are provided. What Is the Relationship Between Oral Health and General Health and Well-being? Chapters 5 and 6 address key issues in the charge— the relationship of oral health to general health and well-being. Chapter 5 explores the theme of the mouth as a mirror that in some measure can reflect general health or disease status. Examples are given of how oral tissues may signal the presence of dis- ease, disease progression, or risk factor exposure lev- els, and how oral cells and fluids are increasingly being used as diagnostic tools. This is followed by a discussion of the mouth as a portal of entry for infec- tions that can affect local tissues and may spread to other parts of the body. The next section reviews the 20 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL literature regarding emerging associations between oral diseases and disorders and diabetes, heart dis- ease and stroke, and adverse pregnancy outcomes. Chapter 6 demonstrates the relationship between oral health and quality of life, presenting data on the consequences of poor oral health and altered appear- ance on speech, eating, and other functions, as well as on self-esteem, social interaction, education, career achievement, and emotional state. Anthropological and ethnographic literature is introduced to underscore the cultural values and symbolism attached to facial appearance and teeth. How Is Oral Health Promoted and Maintained and How Are Oral Diseases Prevented? The next three chapters review how individuals, health care practitioners, communities, and the nation as a whole contribute to oral health. Chapter 7 reviews the evidence for the efficacy and effective- ness of oral health promotion and disease prevention measures with a focus on community efforts in pre- venting dental disease. It continues with a discussion of the need to expand efforts in such areas as oral cancer prevention. Chapter 8 explores the role of the individual and the health care provider in promoting and maintain- ing oral health and well-being. For the individual, this means exercising appropriate self-care and adopting healthy behaviors. For the provider, it means incorporating the knowledge emerging from the science base in a timely manner for prevention and diagnosis, risk assessment and risk management, and treatment of oral diseases and disorders. The chapter focuses largely on the oral health care provider. The management of oral and craniofacial health and disease necessitates collaborations among 4 team of care providers to achieve optimal oral and general health. Chapter 9 describes the roles of dental practi- tioners and their teams, the medical community, and public health agencies at local, state, and national levels in administering oral health care or reimburs- ing for the costs of care. These activities are viewed against the changing organization of U.S. health care The Meaning of Oral Health and trends regarding the workforce in research, edu- cation, and practice. What Are the Needs and Opportunities to Enhance Oral Health? Chapter 10 looks at determinants of oral health in the context of society and across various life stages. Although theorists have proposed a variety of models of health determinants, there is general consensus that individual biology, the physical and socio- economic environment, personal behaviors and lifestyle, and the organization of health care are key factors whose interplay determines the level of oral health achieved by an individual. The chapter provides examples of these factors and, in the latter half, illustrates their varying effects at different stages of the life span, with an emphasis on children and older Americans. Barriers and ways to raise the level of oral health that can be achieved at each life stage are presented. Chapter 11 spells out in greater detail the prom- ise of the life sciences in improving oral health in the coming years in the context of changes in American—and global—society. The critical role of genetics and molecular biology is emphasized. A Call to Action Chapter 12, the final chapter, summarizes the major findings of the report and suggests actions to guide the next steps in enhancing the oral health of the nation. The need for partnerships between public and private sectors in carrying out a proposed National Oral Health Plan is emphasized. To ensure progress, these partnerships need to include individ- ual patients and the general public and to reflect all population groups in the nation. All the health care disciplines need to be involved, along with industry, academia, and government, as well as health care organizations, health professional associations, health insurers, and patient groups. United by the evidence that oral health is essential to general health and well-being, the combined forces and collective wisdom of all interested parties and stakeholders can make optimal oral health a reality for all people. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 21 Dacre a it eae (HAP TL i ah i The Craniofacial Complex The first line a child draws on a face is usually the mouth. The mouth is the center of communication and contact. Along with the eyes, ears, and nose, it is positioned near the brain, ensuring close integration and coordination. We use the craniofacial complex— the oral, dental, and the other craniofacial tissues that house the organs of taste, vision, hearing, and smell—to experience and interact with the world around us. These sense organs have evolved to serve as superb information processors and aids to sur- vival. At the most elemental level, they enable us to sense our environment—from alerting us to preda- tors or poisons to recognizing family, friends, or prospective mates. Our ability to act on the nerve signals from these organs results from the abundant supply of paired cranial nerves that innervate the craniofacial tissues. No place in the body is as rich in both the number of sensory nerves and the ratio of motor nerves to mus- cle fibers as the face, and, within it, the mouth and teeth. The nerve circuits not only trigger protective reflexes to make us blink, gape, and start in surprise, but also enable us to perform countless functions we take for granted. We speak and taste and chew and swallow. We express our feelings through smiles and scowls, we grimace and cry out in pain; we murmur endearments and kiss our loved ones. Beyond the special senses of vision, hearing, taste, and smell, the craniofacial complex includes nerve endings sensitive to the bodys position in space and to touch, pressure, temperature, and pain. In sum, if the brain is the command-and-control cen- ter of the body, evolution has ensured that the staff reporting from the field and carrying out orders are stationed a strategic few inches away, in the craniofa- cial complex. , CONTACT AND COMMUNICATION Taste and Smell The developmental process by which vital nerve cen- ters came to be concentrated in the head, mouth, and teeth began early in evolution. Even paramecia have mouths, as do worms, bugs, and all more complex organisms. The mouth appears in the human embryo during the third week of development. By the thir- teenth or fourteenth week, the fetal mouth can open in response to stimulation of the lower lip. During the next 2 months, the fetus will practice protruding and then pursing the lips, eventually achieving the ability to suck vigorously at 29 weeks. In the mean- time, inspiratory gasps, tongue movements, lip curl- ing, and swallowing responses will have been estab- lished (Wilentz 1968). At birth, the taste buds are found on the roof of the mouth and in the throat, as well as on the tip, sides, and back of the tongue. Taste buds, such as those on the tip of the tongue, are particularly subject to wear and tear, and may be replaced every 2 weeks. The total number of buds diminishes over time, but there appears to be considerable reserve capacity, so there is normally little loss in the sense of taste as we age. It has been said that taste is 90 percent smell, and to some extent that is true. The taste cells that line the buds respond to only five known qualities: sweet, sour, salty, bitter, and glutamate. The experience of taste is a complex mixture of smell, temperature, taste, and texture. The day-old newborn responds to sweet stimuli. Suckling, the first oral function following the cry, is enhanced by the presence of lactose, the sugar in breast milk. Liquids sweetened with sugar or honey have been used widely after birth to stimulate appetite, and later to wean children from breast- ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 23 The Craniofacial Complex feeding. The ability to recognize a sweet taste clearly has survival value, enabling the recognition and selection of carbohydrates—a vital source of energy. The other taste modalities are also physiological- ly important. A sour taste, for example, can signal an unripe fruit. However, sour substances may be involved in more subtle biochemistry, such as main- taining the body’s ion balance. They also satisfy thirst and promote digestion by stimulating the secretion of saliva. A bitter taste is sufficiently unpleasant to evoke aversion, a useful response given that many bitter-tasting plant alkaloids are toxic. A salty taste indicates the presence of sodium, which is essential to maintaining the fluid balance between cells and the extracellular compartment. Humans probably began as herbivores before the advent of hunting and gathering and retained taste- discriminating ability as an evolutionary advantage. The combination of taste and smell remains impor- tant not only for the maintenance of an optimal diet (Young 1977), but also clearly for the pleasures of eating. , Unlike taste cells, olfactory cells can respond to many thousands of odorants, including ones that have been newly synthesized. Millions of olfactory receptors line a postage-stamp-sized area in the upper part of the nose, the olfactory epithelium. Although some smells may be judged universally as unpleasant or foul, others are subject to learning and cultural conditioning. For example, a ripe Roquefort cheese may delight some people, but repel others. The primary receptor cells of the olfactory sys- tem are neurons with fine hairs at one end that proj- ect into the olfactory epithelium to pick up the olfac- tory stimulus. The cells translate the stimulus to nerve impulses transmitted to the brain along the two olfactory nerves—one from each nostril. Olfactory neurons have the unusual ability to regen- erate (although recent studies suggest that neurons in other parts of the adult brain may also have this ability Johansson et al. 1999). Olfactory pathways are widely distributed in the brain, relaying to emo- tional and cognitive centers in the cortex. These con- nections undoubtedly account for the ability of odors to stir old memories as well as stimulate a range of feelings, from fear to sexual arousal. Touch, Temperature, and Pain The mouth also contains large numbers of nerve end- ings, similar to those found elsewhere in the body, that are sensitive to touch (mechanoreceptors), hot and cold temperatures (thermoreceptors), and pain (nociceptors). The dense concentration of these receptors in the facial skin, joints, muscle, and oral soft tissues, relayed to an image of the body mapped onto the sensory cortex of the brain, accounts for the finesse with which we can discriminate the qualities and precise location of these sensations. In particular, the periodontal ligament, which anchors the teeth in the jaws, is a tactilely sensitive tissue providing important feedback with regard to mastication (chewing) and dental occlusion (bite). As a test of this sensibility, a human hair placed between the tips of the fingers will rarely be sufficient to stimulate the nerve endings, but the same hair placed between the lips or incisors will instantly be felt. Pain and thermal sensitivity in the teeth are transmitted through nerve’ endings in the pulp. Because the pulp is in a narrow canal composed of connective tissue, blood vessels, and nerves and sur- rounded by hard tissue, any infection or inflamma- tion that would normally cause tissue to swell creates pressure on the pulpal nerves. That pressure, along with bacterial or immune system products that stim- ulate the nerve endings, produces the severe pain of pulpal infections. Neuroscientists have long studied oral-facial pain, not only because of its importance in oral dis- ease, but also because it provides an accessible model of pain elsewhere in the body. These investigations have greatly enriched our understanding of the basic mechanisms of pain perception and modulation. They have helped delineate the complex pathways and multiple transmitters that convey pain signals to the brain and spinal cord, as well as the mechanisms -and molecules that can modulate and inhibit noci- ceptive input. These studies have also exploited new brain-imaging techniques to confirm the wide distri- bution of pain pathways and relay centers in the cere- bral hemispheres and cerebellum. This research has generated new approaches to the control of acute and chronic pain. These approaches include the use of nonsteroidal, anti- inflammatory drugs and long-acting local anesthetics for acute oral and dental pain, and the use of more potent drugs, drug combinations, and other kinds of therapies to treat chronic pain. Researchers have emphasized the importance of adequate pain control in patients with chronic pain conditions. Otherwise, the constant barrage of signals can effect long-term changes in the brain that actually worsen the pain (producing hyperalgesia) and cause normally non- painful stimuli to be perceived as painful (a condition called allodynia). Unrelieved chronic pain may also suppress the immune system. Recently, investigators discovered a link between certain taste sensations, pain, and temperature. Their 24 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL findings indicate that capsaicin, the ingredient that makes hot peppers taste hot, binds to a receptor on the surface of nociceptors that also responds to nox- ;ous heat. The researchers have cloned the gene for the capsaicin receptor (called vanilloid receptor 1); they believe it is involved in several chronic pain con- ditions, especially those where inflammation plays a role, such as viral and diabetic neuropathy, rheuma- toid arthritis, and oral mucositis pain caused by can- cer chemotherapy or radiation (Caterina et al. 1997). There is evidence that the prevalence of a num- ber of pain conditions varies by gender and that men and women respond differently to different analgesic drugs. These findings have prompted studies aimed at determining whether there are sex differences in pain anatomy and neurochemistry and whether (and how) nociception is affected by sex hormones. Speech Human speech and language are the faculties that most distinguish us from other higher primates; they are also the links that bind people together in diverse social groups and cultures. Central to speech are laryngeal mechanisms involving the vocal cords. Equally critical are the res- piratory system, the pharynx, and the nasal and oral cavities. The tongue is the most important structure of the peripheral speech mechanisms, working in conjunction with the lips, teeth, and palate to pro- duce a rich repertoire of sounds. Abnormalities in oral structures, from missing or malformed teeth and malocclusion to cleft lip and palate, can seriously affect articulation. The movements of speech are orchestrated by brain centers that coordinate the muscles of mastication, facial expression, and jaw movements. Hearing impairments can also affect speech. To learn to speak, children must be able to hear others and monitor the feedback from their own voices. Congenital deafness and the serious hearing defects associated with some craniofacial syndromes (see Chapter 3) can severely compromise speech acquisition. THE ORAL CAVITY The mouth is the gateway to the body, performing dozens of functions that place high demands on its unique hard and soft tissues. The point of entry is the lips, which open into the oral cavity. The cheeks form the sides of the cavity, and the roof is formed by the palate, which separates the mouth from the nose above and the pharynx (throat) behind. The anterior The Craniofacial Complex palate is hard, formed by underlying bone, and serves as a shield against trauma to the face and head. The posterior palate is soft, composed of muscles and. connective tissue that blend into the walls of the pharynx. Hanging from the rear of the soft palate is the uvula, a mass of muscle and connective tissue. Under the tongue is the floor of the mouth, com- posed primarily of muscle and salivary glands. The paired tonsils and adenoids, important components of the immune system, lie at the sides of the palate and within the nasopharynx, respectively. The pharynx opens into channels leading either to the lungs for respiration or the esophagus for fur- ther digestion and passage to the stomach. This is a point of vulnerability: should food or some other obstruction lodge in the airway, it could lead to death by asphyxiation. Externally, the oral cavity is bounded by the maxilla (the upper jaw bone), attached to the crani- um, and the mandible (the lower jaw), attached to the temporal bone of the skull by the temporo- mandibular joint. The Oral Mucosa Except for the teeth, the oral tissues are covered by a mucous membrane called the oral mucosa, which varies in color from pink to brownish purple, depending on an individual’s skin color. Like skin, the oral mucosa acts as a major barrier against chem- ical irritants and mechanical forces; it can even with- stand temperatures that would be painful to the skin. In areas subject to chewing forces and food move- ments, the surface layer is relatively hard, composed of epithelial cells filled with insoluble keratin, the fibrous protein found in skin, nails, hair, and animal horn. Elsewhere—in the mucosal lining of the cheeks, for example—the surface layers are softer and more flexible, enabling the mobility we need to speak, chew, and make facial expressions. To aid in their barrier function, surface mucosal cells are square-shaped and closely juxtaposed, with special- ized organelles and cell products that promote cell- cell adherence. The cells can also secrete sticky mol- ecules to plug gaps between them and further impede penetration by damaging chemicals or microorgan- isms. Still another type of oral mucosa forms the peb- bly surface of the back and sides of the tongue. Lining the depths of these surface “papillae” are the taste buds. Interestingly, the epithelium that lines the gingi- val surface completely lacks a keratin layer, yet this “naked” epithelium lies next to one of the most dense concentrations of bacteria to be found in the body. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 25 The Craniofacial Complex Thus there is an opportunity for infectious agents or their byproducts to penetrate the naked epithelial barrier and initiate an inflammatory response, as hap- pens in gingival disease. Special cells in the basal layer of the oral mucosa generate replacements for surface cells as they wear out. The painful oral ulcers and oral mucositis that may develop in patients undergoing radiation or chemotherapy for head and neck cancer occur because these cancer-killing agents attack all cells undergoing rapid turnover, whether healthy or cancerous. The Teeth The most prominent features of the oral cavity are the teeth. The 20 primary, or deciduous, teeth erupt gen- erally between 6 months and 2 to 3 years of age and are succeeded by the permanent teeth beginning at about age 6. The primary teeth enable infants to eat solid foods, aid speech development, and serve as placeholders for the permanent dentition. Keeping primary teeth healthy is important, not only in spar- ing an infant pain and disease, but also in preserving the dimensions of the dental arches and lessening the risk of dental caries in the permanent teeth. A period of mixed primary and permanent dentition occurs from about ages 6 to 13. There are 28 to 32 perma- nent teeth, depending on whether the 4 wisdom teeth (third molars), which are last to erupt, are pres- ent. Teeth are anchored in the jaws by the periodon- tal ligament. This ligament connects the cervix (neck) of the tooth, at the junction between the crown and root, to the gingiva. Below that, the liga- ment connects the outer layer of the tooth root, the cementum, to the adjacent alveolar bone (the part of the jaw bone that supports the tooth roots). The evolutionary forces that shaped the human mouth designed an apparatus for optimal food intake. The front four upper and lower incisor teeth are chisel-shaped for biting, cutting, and tearing and exert forces of 30 to 50 pounds. The canines, or cuspids, are larger and stronger and have deeper roots than the incisors; their conical cusps are effective for ripping and tearing. The premolars, or bicuspids, and the molars are designed for heavy grinding and chewing, exerting forces as high as 200- plus pounds. The temporomandibular joint, the most complex synovial joint in the body, equips the human jaw with extraordinary mobility, enabling movements in three dimensions. Its range of motion is controlled by three sets of muscles of mastication—the masseter, temporalis, and pterygoid muscles (Oberg 1994). Chewing reduces food to small particles and mixes it with saliva to form a bolus for swallowing. The Salivary Glands Saliva is the mixed product of multiple salivary glands that lie under the mucosa. The three major glands are the paired parotid, submandibular, and sublingual glands. The parotids, near the ears, secrete a watery saliva into the mouth via ducts in the cheeks. The walnut-sized submandibular glands lie in the floor of the mouth and secrete a mucous fluid. The secretions of the almond-shaped sublingual glands, also in the floor of the mouth but near the front, usually join with those of the submandibular glands. Tiny minor salivary glands are scattered with- in the inner surfaces of the lips, cheeks, and soft and hard palates; these secrete a mucinous saliva directly onto the soft tissue surfaces. Saliva moistens food and provides mucinous pro- teins to lubricate the bolus for ease of swallowing. The combined movements of the tongue and cheeks move the bolus to the back of the mouth. Saliva also contains the enzyme amylase, which initiates the digestion of starch. By solubilizing food components and facilitating their interaction with the taste buds on the tongue and palate, saliva also contributes to taste enhancement. Tissue Protection The main function of saliva is not—as is commonly believed—to aid digestion, but to protect the integri- ty of the oral tissues. The moment a baby passes through the birth canal and takes its first breath, microbes begin to take up residence in its mouth. Later, as the teeth erupt, additional bacteria establish colonies on tooth surfaces (Mandel 1989). Nearly 500 species of microbes in all, most of which are not harmful, will colonize the oral cavity (Kroes et al. 1999). The microbes form a biofilm, in which their numbers greatly exceed the number of human inhab- itants on Earth. Millions of years before there were toothbrushes, dental floss, and water irrigators, evolutionary forces generated protective mechanisms to combat poten- tially harmful microbes. The physical flow of saliva helps to dislodge pathogens (viruses, bacteria, and yeast) from teeth and mucosal surfaces, just as tear- ing and blinking, sneezing, and coughing and expec- torating clear the eye, nose, and throat. Saliva can also cause microbes to clump together so that they can be swallowed before they become firmly attached. Saliva can destroy orally shed infected 26 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL white blood cells by virtue of its low salt content: the infected cells—of higher salt content—swell and burst when exposed to fluids of lower salinity (Baron etal. 1999). Salivary secretions, like tears and other exocrine gland secretions, are rich in antimicrobial compo- nents. Certain molecules in saliva, such as lysozyme, lactoferrin, peroxidase, and histatins, can directly kill or inhibit a variety of microbes; the histatins are par- ticularly potent antifungal agents (Xu et al. 1991). Several salivary proteins exhibit antiviral properties, including secretory leukocyte protease inhibitor (SLPI), recently discovered to have the ability to inhibit HIV from invading cells (Shugars and Wahl 1998). The ability of saliva to limit the growth of pathogens, in some instances even preventing them from establishing a niche in the biofilm community in the first place, is a major determinant of general as well as of oral health. When salivary flow is compro- mised, the gateway to the body can open wide to local as well as to systemic pathogens. Barrier and Buffering Properties Salivary components protect oral tissues in other ways as well. Mucins have unique properties that enable them to concentrate on mucosal surfaces and provide an effective barrier against drying and physi- cal and chemical irritants (Tabak 1995). They act as natural waterproofing, control the permeability of the tissue surfaces, and help limit penetration of potential irritants and toxins in foods and beverages, as well as toxic chemicals and potential carcinogens in tobacco and tobacco smoke and from other sources. This barrier function complements the bar- rier formed by the oral mucosa itself. The mucosa has a specific permeability coefficient that can change under various conditions of stress, nutritional status, and other challenges. Saliva contains several effective buffering sys- tems that can help maintain a normal pH when acidic foods and beverages are introduced, thereby protect- ing oral tissues against acidic attack. When swal- lowed, these buffers protect the esophagus, helping neutralize the reflux acids of conditions such as heartburn and hiatal hernia (Sarosiek et al. 1996). Wound Healing Saliva also contains molecules that nurture and pre- serve the oral tissues, even helping them to repair and regenerate (Mandel 1989, Tabak 1995, Zelles et al. 1995), Experimental studies have shown that wound healing is significantly enhanced by saliva, in ORAL HEALTH IN AMERICA: A The Craniofacial Complex part because of the presence of a potent molecule, epidermal growth factor (EGF) (Zelles et al. 1995). When swallowed, EGF can also protect the tissue surfaces of the esophagus (Sarosiek et al. 1996). Vascular endothelial growth factor (VEGF) has also been identified in saliva. VEGF stimulates blood ves- sels and may contribute to the remarkable healing capacity of oral tissues (Taichman et al. 1998, Zelles et al. 1995). Caries Protection Saliva also guards against dental caries (tooth decay), the disease that has been the greatest threat to teeth. Caries is caused by bacteria that generate acids that attack tooth mineral (see Chapter 3). The buffering systems in saliva, augmented by the neutralizing components urea and ammonium, counter the acid formation. The physical flow of saliva also helps flush out sugars and food particles that are the bacte- rial food source. Mineral salts in saliva—calcium and phosphate—can remineralize tooth enamel, effec- tively reversing the decay process. This regenerative function is greatly enhanced by the presence of fluo- ride in saliva. Finally, saliva forms a film on teeth made up of selectively adsorbed proteins that have a high affinity for tooth mineral. This acquired pellicle is insoluble and limits the diffusion of acids into the teeth and the dissolution of tooth mineral (Lamkin and Oppenheim 1993). The Immune System The salivary glands and the oral mucosa, along with the body's other mucosal linings and the lymphatic circulation, constitute a major component of the body's defense system—the mucosal immune system (Mestecky 1987). When the area of the oral mucosa is combined with the areas of the mucosal linings and passageways of the respiratory, gastrointestinal, uri- nary, and genital tracts, the total represents the largest surface area of the body—nearly +00 square meters, or 200 times larger than the total skin area. The great majority of infectious diseases affect, or are acquired through, mucosal surfaces. Immune cells that line the mucous membranes throughout the body secrete antibodies targeted to specific disease-causing microbes (Mandel and Ellison 1985). The mucosal immune system works in concert with the bloodborne immune system to detect and dispose of foreign substances and invading microbes. The two components of the immune system Con- sist of molecules and cells that provide both broad and specific defense mechanisms. In the broad group REPORT OF THE SURGEON GENERAL 27 The Craniofacial Complex are some circulating white blood cells (monocytes and granulocytes) associated with the inflammatory response. These cells migrate to a site of injury or infection and move into damaged tissues manifest- ing the four signs of inflammation: swelling, heat, redness, and pain. The cells promote an increase in blood flow to begin the healing process, and they recruit other cells able to engulf and dispose of the offending organism. The specific immune system is associated with two major classes of immune cells: T cells and B cells. T cells react to antigens (proteins associated with microbes or irritants) and can stimulate B cells to make antigen-specific antibodies. These are the Y- shaped molecules called immunoglobulins. T cells are the instruments of cell-mediated immunity; they are able to detect telltale surface markers on diseased or foreign cells that distinguish them from normal body cells. Some T cells can kill infected cells and cancer cells directly. T cells are also involved in the rejection of organ transplants. Certain T cells are memory cells, preserving the information from earlier encounters with specific pathogens. Thus they are able to initiate more rapid and effective responses in the event of a repeat encounter with the pathogen. Helper T cells assist in activating killer T and B cells. It is the loss of helper T cells that leads to the many infections that cause ill- ness and death in HIV disease. Still another group of T cells, suppressor T cells, moderates the activities of both B and T lymphocytes. Activated T cells generate and _ release cytokines—potent families of proteins, such as the interleukins, that can stimulate immune cells to divide, migrate, attack, and engulf invaders or partic- ipate in the inflammatory response. Other cytokines include varieties of tumor necrosis factor and adhesins (proteins that facilitate the binding of immune cells to each other or to blood vessel lin- ings). Feedback mechanisms provide a system of checks and balances to regulate cytokine production. The immune system interacts with the nervous and endocrine systems. For example, immune cytokines secreted into the brain can induce the fever associated with infection: the high temperature may help destroy the infectious agent. The brain's response to stress also has repercussions for the immune system. The hypothalamus-pituitary-adre- nal axis is a major pathway activated in response to stress, which results in the secretion of cortisol, the stress hormone, from the adrenal glands. Cortisol promotes the body's fight-or-flight mechanisms, but via feedback loops, cortisol acts to depress immune reactions. Much of what we know about the immune sys- tem has come from studies of serum factors, but research in the last two decades has generated much new information about mucosal immunity (McGhee and Kiyono 1999). The mucosal immune system can be divided into inductive and effector compartments. The nasal-associated lymphoreticular tissues (NALT) in the nasopharyngeal area (which includes the ton- sils) and the gut-associated lymphoreticular tissues (GALT) in gut tissue are inductive regions, where foreign invaders are encountered. If, for example, infectious bacteria are swallowed, they can stimulate immune cells in GALT to circulate T and B cells through the lymph system to various effector sites in the gastrointestinal and upper respiratory tracts and in the salivary and other exocrine glands. The B cells in the gland produce antibodies, designated S-IgA, to which is attached a secretory component (Mestecky and Russell 1997). These antibodies are the domi- nant type found in saliva, tears, breast milk, and colostrum and in the gastrointestinal and genitouri- nary. tracts. The uses of the mucosal immune system extend beyond its normal surveillance and defense func- tions. The tissues can be used as routes for delivery of oral (swallowed) or nasal (inhaled) vaccines, as sites for gene transfer to augment host defenses, and as a means of invoking oral tolerance—the suppres- sion of overactive or inappropriate immune respons- es that occur in chronic inflammatory and autoim- mune diseases (Baum and O’Connell 1995, Hajishengallis and Michalek 1999). CRANIOFACIAL ORIGINS The extraordinary successes of research in molecular genetics over the past decade, coupled with the National Institutes of Health’s project to map and sequence the human genome, have proved to be a boon in understanding craniofacial development. The use of automated gene-sequencing equipment, the Internet availability of genome databases, and the ability to transfer genes or create “knockout” ani- mals—in which a gene of interest has been eliminat- ed—have greatly facilitated progress. The events that govern the transformation of a fertilized human egg cell into a healthy newborn with all organs and sys- tems in place are being unfolded at the molecular level. Families of master and regulatory genes have been identified, and their role in controlling how the body's general shape and specialized tissues and organs are formed is coming to light. 23 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Early Development The Three Germ Cell Layers By the time the face and the mouth are ready to form, the human embryo is in the third week of develop- ment. The embryo has evolved from a sphere to an oval two-layered disk with a head-to-tail orientation. The outer layer is the epiblast and will become the ectodermal germ layer. A narrow groove, called the primitive streak, extends from the tail toward the center of the disk, where it ends in a spot surround- ing a small depression called the primitive pit. Epiblast cells migrate toward the streak and pit, detach from the surface, and slip downward to form the two additional germ cell layers, the mesoderm and, below that, the endoderm. The ectodermal layer gives rise to tissues that relate the body to the outside world: the nervous sys- tem: the sensory epithelium of the ears, nose, and eyes; skin, hair, nails, salivary glands, tonsils, and tooth enamel; and the pituitary, mammary, and sweat glands. At the head end, the mesodermal layer gives rise to a primitive connective tissue, called mes- enchyme, which will interact with the ectoderm to form parts of the head and mouth. The remaining mesoderm develops into the muscle, cartilage, bone, and subcutaneous skin tissue of the rest of the body. The mesoderm is also the origin of the vascular and urogenital systems (except for the bladder), the spleen, and the adrenal cortex. The innermost, endo- dermal layer provides the linings of the gut, the res- piratory system, bladder, liver, pancreas, thyroid and parathyroid glands, and parts of the middle ear. Neural Tube and Neural Crest Further migrations and descending movements of cells result in the formation of the notochord, a solid cord of cells along the midline that will become the backbone. The ectoderm above the notochord next thickens to form a neural plate. The sides of the plate curve up and inward to form a neural tube, beginning at the head, with fusion completed by the end of the fourth week. The tail end of the tube will form the spinal cord; the head end differentiates into the three parts of the primitive brain: the forebrain, midbrain, and hindbrain. What happens next is of central importance to the craniofacial complex: cells that were at the edges of the neural plate break away to form neural crest cells, which migrate to the forebrain area and to the nearby branchial arches, a series of swellings on either side of the embryo, adjacent to the hindbrain. The hindbrain becomes organized into eight rhom- The Craniofacial Complex bomeres, segments of future nerve tissue arranged in an orderly fashion so that the first two thombomeres innervate branchial arch 1, and so on. During the formation of the midbrain and hind- brain, cranial neural crest cells migrate into the developing facial areas and differentiate into neu- ronal and nonneuronal tissues. The neuronal tissues include the clusters of nerve cells (ganglia) that lie adjacent to the spinal cord, parts of the ganglia of four cranial nerves, and two of the meningeal layers of the brain. The nonneuronal tissues include major bones, cartilage, the dentin and cementum of teeth, and the various types of connective tissues of the craniofacial complex, as well as the muscles of the eye. The branchial arches give rise to the bones, car- tilage, nerves, muscles, and blood supply of succes- sive segments of the head and neck. The Face and Mouth The branchial arches play a key role in the formation of the facial structures. Toward the end of the fourth week of gestation, a primitive mouth appears. This “stomadeum” is flanked by a series of swellings, or prominences, derived from the first pair of branchial arches. A single frontonasal prominence forms the upper border of the stomadeum. On either side of this prominence are two thickened regions of ecto- derm—the nasal placodes. At the sides of the stom- adeum and below it are pairs of maxillary and mandibular prominences. In the course of the next 3 weeks, differential growth and movements of the various prominences and fusions of tissues that come together at the mid- line will sculpt the bridge, crest, sides, and tip of the nose, the upper and lower lips, and the upper and lower jaws (Bhaskar and Orban 1990, Sadler and Langman 1995). The external merger at the midline of a pair of prominences that helps to form the nose occurs inside the mouth as well, resulting in an intermaxil- lary segment that will contribute to the formation of the four upper incisors and parts of a small triangu- lar-shaped primary palate and the upper jaw. The bulk of the palate, the secondary palate, forms from shelflike outgrowths of the maxillary prominences. These growths appear in the sixth week, and in the following week fuse along the midline above the tongue. (The tongue appears at approximately 4 weeks, the front two-thirds forming from the first branchial arch, and the posterior third from parts of the second, third, and fourth branchial arches.) The palatal shelves also fuse with the primary palate along a triangular border called the incisive foramen. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL a The Craniofacial Complex This border is considered the line of division among clefting abnormalities. Lateral cleft lip, cleft upper jaw, and clefts between the primary and secondary palates are associated with defects anterior to the incisive foramen. Cleft palate and cleft uvula occur because of defects affecting closure of the palatal shelves posterior to the foramen (Bhaskar and Orban 1990, Sadler and Langman 1995). The Teeth Tooth development begins in the sixth week with the appearance of an epithelial band lining the upper and lower jaws. A part of the band develops into a dental lamina, which forms a series of projections into the jaw. These are the tooth buds and correspond to the sites of deciduous teeth. The epithelial tissue of the bud develops into an enamel organ that forms a cap over tissue that is differentiating in the jaw to become the dental papilla. The two structures—the enamel organ, derived from the epithelium, and the dental papilla, derived from neural crest mesenchyme— constitute the tooth germ. With further development, the tooth germ assumes a bell shape and separates from the oral epithelium. At the same time, the internal epithelial layer of the enamel organ undergoes a series of infoldings that will shape the future crown of the tooth. Mineralization of the tooth begins at the late bell stage. The first mineralized tissue to form is dentin, which provides the foundation for the deposition of enamel. The differentiation of the odontoblasts (the dentin-producing cells) depends on organizing influences from enamel organ cells. Thus the development of these two different hard tissues is a mutually dependent process. As dentin is laid down, the odontoblasts move toward the center of the papilla, trailing thin cellular processes, which become embedded in the mineral- ized matrix. When dentin formation is completed, dentin completely surrounds the pulp, protecting it from injury. The enamel layer of the tooth starts to form soon after the first dentin appears, synthesized by special enamel-forming cells, or ameloblasts, which develop from the enamel organ. The tooth root, and its outer layer of cementum, form only after the crown erupts. Genetic Controls Only in the last decade have scientists begun to understand how certain genes and gene families control embryonic development. Their findings have come from detailed studies of species ranging from fruit flies, nematodes, and zebrafish to frog, chick, mouse, and human embryos. In many cases, the simpler organism has been the source of discoveries of genes or developmental processes that are highly conserved in the course of evolution (Alberts et al. 1994). Research on the fruit fly, for example, has revealed that particular families of genes are respon- sible for the fundamental head to thorax to tail pat- terning of the fly’s body. Another set of genes deter- mines the back-to-front positioning of organs, and a third set subdivides this general body plan into a series of discrete segments. With further develop- ment, yet another family of genes confers a position- al memory on the cells within a segment. These “homeotic selector” genes ensure that cells in one part of a particular segment “know” that they are des- tined to be wings and not legs, or to be eyes and not antennae. In flies the homeotic genes are known as Hom genes. Their arrangement on the fly chromo- some is ordered with genes at one end of the chro- mosome specifying the developmental destiny of cells in the most anterior segments of the fly’s body and genes at the other end specifying the fate of cells in the most posterior segments. In the course of evolution, mammals have devel- oped four overlapping sets of positional memory gene clusters homologous to the fly's single Hom complex. The four mammalian Hox gene families are ordered in a similar anterior-posterior fashion along four different chromosomes. The mammalian genes appear to operate like the Hom genes: they code for DNA-binding proteins that control gene expression. The similarity from fly to human is particularly evi- dent when maps of the expression domains of Hom genes in anterior segments of the fly embryo are com- pared to maps of Hox gene expression as seen in the rhombomeres and branchial arches of mammals. Molecular genetic studies of flies and other non- mammalian species show some variation in how and when the basic body patterns and repeating segments are formed. Sometimes the head-to-tail pattern is laid down in the egg cell before fertilization—dictated by egg polarity genes. Although egg polarity genes do not operate in humans, mutations have been found in a human gene homologous to the fly egg polarity gene and account for serious syndromes in which there are defects in anterior organs, such as the pitu- itary gland and heart. None of these developmental controls work in isolation. Much remains to be understood about the genetic clock that determines when and where devel- opmental genes act, how they interact, and what 30 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL mechanisms are used to sustain as well as terminate their function. The systems that govern programmed cell death are also important: normal development depends as much on the elimination of cells as it does on the orderly movement, proliferation, and differen- tiation of cells. When it comes to processes that control the development of particular tissues or organs—bones, skin, or heart—developmental biologists observe that there is often an “organizer,” that is, a cell or set of cells that initiates the process. The organizer induces changes in the behavior of neighboring cells through cell-cell interactions, so that these cells develop into the specified type—bone or skin or heart muscle. The interaction with the neighboring cell is often in the form of a signaling molecule, such as a growth factor (e.g., transforming growth factor b, epidermal growth factor, fibroblast growth factor) that attaches to a receptor on the surface membrane of the recipient cell. This interaction is translated to the interior of the cell, where a chain of molecular interactions eventually reaches the cell nucleus to effect gene expression. One of the more startling dis- coveries of the past decade has been the finding that a series of mutations, each associated with a change in only one nucleotide of the gene for the fibroblast growth factor receptor—a so-called point muta- tion—accounts for a range of organ defects seen in at least a half dozen craniofacial syndromes. Interestingly, all these syndromes include craniosyn- ostosis, a premature closure of the bones that form the skull. THE AGING OF CRANIOFACIAL TISSUES Normal aging describes the developmental processes that begin at conception, continue in childhood, and merge gradually into maturation and senescence. The milestones of development such as the age when children teethe, begin to walk, talk, enter puberty, attain their full height, and so on, are under genetic and hormonal controls, subject to important envi- ronmental factors such as nutrition and exercise. Despite the complexity and interrelationships of the variables involved, a reasonably accurate picture of normal age-related changes in the craniofacial com- plex is emerging (Ship 1999). Barring major illness or injury, destructive behaviors, or severe or unusual environmental cir- cumstances, the cells, tissues, and fluids of the face and mouth are hardy survivors, eminently durable and functional over a long life span. For any given individual the combination of life experience and The Craniofacial Complex lifestyle (including medical and dental history) cre- ates a unique craniofacial portrait, one that inspired George Orwell to remark, “By the age of fifty, a man gets the face he deserves.” The Teeth One of the more dramatic discoveries in biomedical science in the twentieth century has been the realiza- tion that tooth loss is not an inevitable consequence of aging, but the result of disease or injury. Aging does produce a number of other dental changes, however. Teeth change in form and color with age. Wear and attrition alter the biting and chewing sur- faces, as do food choices and oral habits. The altered surface structure produces a different pattern of light reflection in older teeth, resulting in some yellowing and a general loss of translucency (Mjor 1986). Fully formed enamel is acellular, hence there is no meta- bolic activity or turnover as occurs in skin, for exam- ple. Dentin and cementum have limited cellular activity. In contrast, tooth pulp and periodontal liga- ment undergo relatively high levels of tissue turnover. Tooth surfaces can be eroded by chemical dissolution from fruit acids and from acids from sugars in foods such as soft drinks and candies. This destructive process can occur al any age, resulting in loss of translucency as well as some tissue loss from demineralization (Zero 1996). Countering the erosive forces are the natural components in saliva that help remineralize the enamel surface, a process that is enhanced when fluoride is present (see “Caries Protection” above). The cementum increases in thickness with age. Gingival recession caused by normal aging exposes the cementum to the oral environment (and is the origin of the expression “long in the tooth”). The exposed cementum can often be worn away mechan- ically, exposing the underlying dentin, which can then become hypersensitive. Dentin responds through a series of protective changes that work to close off the connections between dentin and nerves in the pulp, reducing transmission of painful stimuli. The Jaws The bones of the maxilla and mandible that support the teeth, called the alveolar processes, are, like bone elsewhere in the body, subject to cellular turnover in a coordinated process of bone resorption and ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 31 The Craniofacial Complex formation. Alveolar bone is well adapted to mechanical stresses, and changes continuously during facial growth, tooth eruption, tooth wear, and tooth loss. This lifelong adaptation makes orthodontic treatments to reposition teeth in adults possible. Because the primary function of alveolar bone is - to support the teeth, the loss of teeth will lead to bone atrophy, making prosthetic replacements diffi- cult. The rate of bone loss is affected by both local disease such as periodontal disease and systemic con- ditions such as osteoporosis (Bhaskar 1991). The Oral Mucosa The oral mucosa appears to age in much the same way as skin does. The oral epithelium thins and becomes less hydrated, increasing vulnerability to injury. The rate of cell division is slower, but the basic cell architecture and patterning of cell types through- out the oral cavity are maintained. It is not certain to what extent these changes are a natural consequence of aging; they may be due to altered protein synthe- sis or lowered responsiveness to regulatory mole- cules. They may also be an effect of diminished vas- cularity, which could limit cellular access to oxygen and nutrients (Mjor 1986). Overall immune system function deteriorates with age, and it is likely that mucosal immunity does as well. Such a decline could result in an increased tisk of transmission of infectious agents across the mucosa and probably contributes to delayed wound healing in oral tissues with aging. Sensory and Motor Functioning The high density of sensory nerve endings in the craniofacial tissues and their functional abilities are well-preserved in aging. There may be minor increas- es in threshold detection levels or in judgments of intensity, but, for the most part, sensory cells can turn over or have a built-in reserve capacity that allows for near-optimal functioning in aging. The exception is olfaction, which declines in both men and women with age. This decrement in smell may lead to some dissatisfaction with how foods taste and increased use of flavor enhancers to compensate. But for most people, the ability to enjoy food is not appreciably diminished as time goes by. Any dramat- ic change in sensory function—complaints of a con- tinued unpleasant taste or smell or the sudden com- plete loss of a sensory modality—should be taken seriously as a sign of possible oral or systemic disease or a side effect of medication and not dismissed as a natural by-product of aging, The distribution of motor fibers in the craniofa- cial tissues is also abundant and sufficiently fine- tuned to allow for a full range of movement of the tongue, jaws, and oral-facial muscles. There is some loss of muscle tone in aging, along with changes in tongue shape and function in articulating specific speech sounds. Subtle changes may also occur in preparing food for swallowing. As with sensory changes, these developments do not seriously inter- fere with motor function in healthy older adults. The Salivary Glands Studies of normative aging indicate that individuals vary in the quantity of “whole” saliva they produce. Whole saliva consists of the secretions of the various salivary glands plus other oral contents, such as cells shed from the mucosa. These individual patterns are consistent across the life span. In healthy adults, there is no diminution in the production of saliva from the major salivary glands in the course of aging. This constancy may seem surprising given the morphological changes documented in aging salivary glands. Both the parotid and the submandibular glands lose between 20 and 30 percent of their essen- tial tissue volume in the course of aging. The loss pri- marily affects the acinar components, the cells that secrete saliva. Increases in the number of ductal cells and in fat, vascular, and connective tissues compen- sate for this loss, however—evidence of the remark- able functional reserve capacity of the glands, which enables them to maintain a stable salivary output across the life span (Baum 1986), In contrast, studies of age-related changes in the chemistry of salivary secretions suggest that there are significant reductions in the concentration of mucins from the submandibular gland (Navazesh et al. 1992), which could result in reduced lubrication and contribute to a sensation of mouth dryness. There are also subtle changes in the protective ability of sali- vary secretory IgA antibody (Smith et al. 1987), FINDINGS Natural selection has served Homo sapiens well in evolving a craniofacial complex with remarkable functions and abilities to adapt, enabling the organ- ism to meet the challenges of an ever-changing envi- ronment. An examination of the various tissues reveals elaborate designs that have evolved to serve the basic needs and functions of a complex mammal as well as those that are uniqely human, such as 32 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL speech. The rich distribution of nerves, muscles, and blood vessels in the region as well as extensive endocrine and immune system connections is an indication of the vital role of the craniofacial complex in adaptation and survival over a long life span. In particular, e Genes controlling the basic patterning and segmental organization of human development, and specifically the craniofacial complex, are highly con- served in nature. Mutated genes affecting human development have counterparts in many simpler organisms. e There is considerable reserve capacity or redundancy in the cells and tissues of the craniofacial complex, so that if they are properly cared for, the structures should function well over a lifetime. e The salivary glands and saliva subserve tast- ing and digestive functions and also participate in the mucosal immune system, a main line of defense against pathogens, irritants, and toxins. e Salivary components protect and maintain oral tissues through antimicrobial components, buffering agents, and a process by which dental enamel can be remineralized. REFERENCES Alberts B, Bray D, Lewis J, Raff M, Roberts K, Watson JD. Cellular mechanisms of development. In: Molecular biology of the cell. 3rd ed. New York: Garland; 1994. p. 1036-137. . Baron S, Poast J, Cloyd MW. Why is HIV rarely trans- mitted by oral secretions? Saliva can disrupt orally shed, infected leukocytes. Arch Intern Med 1999 Feb 8;159(3):303-10. Bhaskar SN. Maxilla and mandible (alveolar process). In: Bhaskar SN, editor. Orban's oral histology and embryology. St. Louis (MO): Mosby Year Book; 1991. p. 239-59. Bhaskar SN, Orban BJ. Orban’s oral histology and embryology. 11th ed. St. Louis (MO): Mosby Year Book; 1990. Chapter 1, Development of the face and oral cavity. Baum BJ. Age changes in salivary glands and salivary secretions. In Holm-Pederson P Loe H, editors. Geriatric dentistry. Copenhagen: Munksgaard; 1986. p. 114-22. Baum BJ and O'Connell BC. The impact of gene thera- py on dentistry. J] Am Dent Assoc 1995:126:179-89. Caterina MJ, Schumacher MA, Tominaga M, Rosen TA, Levine JD, Julius D. The capsaicin receptor: a heat- activated ion channel in the pain pathway. Nature 1997;389:816-24. Hajishengallis G,-and Michalek SM. Current status of a mucosal vaccine against dental caries. Oral Microbiol Immunol 1999-;14:1-20. The Craniofacial Complex Johansson CB, Momma S, Clarke DL, Risling M, Lendahl U, Frisen J. Identification of a neural stem cell in the adult mammalian central nervous system. Cell 1999 Jan 8;96(1):25-34. Kroes I, Lepp PW, Relman DA. Bacterial diversity with- in the human subgingival crevice. Proc Natl Acad Sci USA 1999 Dec 7;96(25):14547-52. Lamkin MS, Oppenheim FG. Structural features of sali- vary function. Crit Rev Oral Biol Med 1993;4(3- 4):251-9. Mandel ID. The role of saliva in maintaining oral home- ostasis. J Am Dent Assoc 1989 Aug;119:298-304. Mandel ID, Ellison SA. The biological significance of the nonimmunoglobulin defense factors. In: Pruit K, Tenovuo J, editors. The lactoperoxidase system. New York: Marcel Dekker; 1985. p. 1-14. © McGhee JR, Kiyono H. The mucosal immune system. In: Paul WE, editor. Fundamental immunology. 4th ed. New York: Lippincott-Raven; 1999. p. 909-45. Mestecky J. The common mucosal immune system and current strategies for induction of immune respons- es in external secretions. J Clin Immunol 1987 Jul;7(4):265-76. Mestecky J, Russell MW. Mucosal immunoglobulins and their contribution to defense mechanisms: an overview. Biochem Soc Trans 1997 May;25(2):457- 62. Mjor IA. Age changes in the teeth. In: Holm-Pedersen P, Loe H, editors. Geriatric dentistry. Copenhagen: Munksgaard; 1986. p. 94-101. Navazesh M, Mulligan RA, Kipnis V, Denny PA, Denny PC. Comparison of whole saliva flow rates and mucin concentrations in healthy Caucasian young and aged adults. J Dent Res 1992 Jun;71(6):1275-8. Oberg S. Dissector for Netter’s atlas of human anatomy: discussions. Vol 2. Summit (NJ): Ciba-Geigy, 1994. Sadler TW, Langman J. Langman’s medical embryology. Baltimore: Williams & Wilkins; 1995. Sarosiek J, Scheurich CJ, Marcinkiewicz M, McCallum RW. Enhancement of salivary esophagoprotection: rationale for a physiological approach to gastroe- sophageal reflux disease. Gastroenterology 1996;110:675-81. Ship JA. The oral cavity. In: Hazzard WR et al., editors. Principles of geriatric medicine and gerontology. New York: McGraw-Hill; 1999. Shugars DC, Wahl SM. The role of the oral environment in HIV-1 transmission. J Am Dent Assoc 1998 Jul;129(7):851-8. Smith DJ, Taubman MA, Ebersole JL. Ontogeny and senescence of salivary immunity. J Dent Res 1987 Feb(2),66:451-6. Tabak L. In defense of the oral cavity: structure, biosyn- thesis, and functions of salivary mucins. Annu Rev Physiol 1995;57:547-64. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 33 The Craniofacial Complex Taichman NS, Cruchley AT, Fletcher LM, Hagi-Pavli EP. Paleolog EM, Abrams WR, Booth V, Edwards RM, Malamud D. Vascular endothelial growth factor in normal salivary glands and saliva: a possible role in the maintenance of mucosal homeostasis. Lab Invest 1998 Jul;78(7):869-75. Wilentz J. The senses of man. New York: Thomas Y. Crowell; 1968. Xu T, Levitz SM, Diamond RD, Oppenheim FG. Anticandidal activity of major human salivary his- tatins. Infect Immun 1991 Aug;59(8):2549-54. Young PT. Role of hedonic processes in development of sweet taste. In: Weiffenbach, JM, editor. Taste and development—the genesis of sweet preference. Bethesda (MD): National Institutes of Health, Public Health Service, U.S. Department of Health, Education and Welfare Report no. NIH 77-1068; 1977. p. 399-417. Zelles T, Purushotham KR, Macauley SP, Oxford GE, Humphreys-Beher MG. Saliva and growth factors: the fountain of youth resides in us all. J Dent Res 1995 Dec;74(12):1826-32. Zero DT. Etiology of dental erosion—extrinsic factors. Eur J Oral Sci 1996 Apr;104(2 Pt 2):162-77. 34 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL PF What Is the Status of Oral Health in America? To begin to answer this question, Chapter 3 guides the reader through a discussion of oral diseases and disorders in such categories as infections, inherited disorders, and neoplasms. Whether or not an individual succumbs to the disease or disorder in question depends on subtle interactions of genetic, environmental, and behavioral variables. Risk factors common to systemic diseases and disorders, such as tobacco use, excessive alcohol use, and inappropriate dietary practices, also contribute to many oral diseases and disorders. As more details on the causes of diseases unfold, specific strategies for disease prevention can be developed. Chapter 4 describes the magnitude of the problem facing the nation due to oral diseases and disorders. These conditions are prevalent and complex, and they affect individuals across the life span. Although major improvements have been seen nationally for most Americans, disparities exist in some population groups as classified by age, sex, income, and race/ethnicity. National and state-based epidemiologic data presented against the backdrop of demographic and socioeconomic variables provide some information on racial and ethnic minorities, but serious shortcomings exist. The paucity of data at national, state, and local levels extends to other populations, including indi- viduals with disabilities, those with alternate sexual orientation, migrant populations, and the homeless, and limits the capacity to fully document the magnitude of the problem and develop needed programs. The chapter provides a basis for understanding disparities in oral health by pre- senting available data on dental visits. More work is needed to understand the dimensions of oral health problems in the United States and the reasons for differences among populations. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 35 r Oh dai a A Diseases and Disorders As the gateway to the body, the mouth is challenged by a constant barrage of invaders—bacteria, viruses, parasites, fungi. Thus infectious diseases, notably dental caries and periodontal diseases, predominate among the ills that can compromise oral health. Injuries take their toll as well, with the face and head particularly vulnerable to sports injuries, motor vehi- cle crashes, violence, and abuse. Less common but very serious are oral and pharyngeal cancers, with a 5-year survival rate of hardly better than 50 percent (Kosary et al. 1995). Birth defects and developmental disorders frequently affect the craniofacial complex. These appear most commonly as isolated cases of cleft lip or palate, but clefting or other craniofacial defects can also be part of complex hereditary dis- eases or syndromes. Additionally, acute and chronic pain can affect the oral-facial region, particularly in and around the temporomandibular (jaw) joint, and accounts for a disproportionate amount of all types of pain that drive individuals to seek health care. Many systemic diseases such as diabetes, arthri- tis, osteoporosis, and AIDS, as well as therapies for systemic diseases, can directly or indirectly compro- mise oral tissues. The World Health Organization's International Classification of Diseases and Stomatology currently lists more than 120 specific diseases, distributed in 10 or more classes, that have manifestations in the oral cavity (WHO 1992). This chapter concentrates on six major oral dis- ease categories: dental and periodontal infections; mucosal disorders; oral and pharyngeal cancers, developmental disorders; injuries; and a sampling of chronic and disabling conditions, including Sjégren's syndrome and oral-facial pain. DENTAL AND PERIODONTAL INFECTIONS The most common oral diseases are dental caries and the periodontal diseases. Individuals are vulnerable to dental caries throughout life, with 85 percent of adults aged 18 and older affected. Periodontal dis- eases are most often seen in maturity, with the major- ity of adults experiencing some signs and symptoms by the mid-30s. Certain rare forms of periodontal dis- ease affect young people. The major oral health suc- cess story of the past half century is that both caries and periodontal diseases can be prevented by a com- bination of individual, professional, and community measures. Dental Caries The word caries derives from the Latin for rotten, and many cultures early on posited a tooth worm as the cause of this rottenness. By the twentieth century, caries came to describe the condition of having holes in the teeth—cavities. This description, although not incorrect, is misleading. In actuality, a cavity is a late manifestation of a bacterial infection. The bacteria colonizing the mouth are known as the oral flora. They form a complex community that adheres to tooth surfaces in a gelatinous mat, or biofilm, commonly called dental plaque. A cariogenic biofilm at a single tooth site may contain one-half- billion bacteria, of which species of mutans streptococci are critical components. These bacteria are able to ferment sugars and other carbohydrates to form lactic and other acids. Repeated cycles of acid generation can result in the microscopic dissolution of minerals in tooth enamel and the formation of an opaque white or brown spot under the enamel surface (Mandel 1979). Frequency of carbohydrate consumption (Gustafsson et al. 1954), physical ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 37 Diseases and Disorders characteristics of food (e.g., stickiness), and timing of food intake (Burt and Ismail 1986) also play a role. The essential role of bacteria in caries initiation was established in landmark experiments in the 1950s. Investigators observed that germ-free ani- mals fed high-sugar diets remained caries-free until the introduction of mutans streptococci (a particular group of bacterial strains having a number of com- mon characteristics, and which adhere tightly to the tooth). Later experiments demonstrated the trans- missibility of the bacteria from mother to litter and from caries-infected to uninfected cage-mates (Fitzgerald and Keyes 1960). Species of Lactobacillus, Actinomyces, and other acid-producing streptococci within the plaque may also contribute to the process (Bowden 1990). If the caries infection in enamel goes unchecked, the acid dissolution can advance to form a cavity that can extend through the dentin (the component of the tooth located under the enamel) to the pulp tissue, which is rich in nerves and blood vessels. The result- ing toothache can be severe and often is accompanied by sensitivity to temperature and sweets. Treatment requires endodontic (root canal) therapy. If untreat- ed, the pulp infection can lead to abscess, destruction of bone, and spread of the infection via the blood- stream. Dental caries can occur at any age after teeth erupt. Particularly damaging forms can begin early, when developing primary teeth are especially vulner- able. This type of dental caries is called early child- hood caries (ECC). Some 6 out of 10 children in the United States have one or more decayed or filled pri- mary teeth by age 5 (U.S. Department of Health and Human Services, National Center for Health Statistics 1997). ECC may occur in children who are given pacifying bottles of juice, milk, or formula to drink during the day or overnight. The sugar con- tents pool around the upper front teeth, mix with cariogenic bacteria, and give rise to rapidly progress- ing destruction (Ripa 1988). Other risk factors for ECC include arrested development of tooth enamel, chronic illness, altered salivary composition and vol- ume (resulting from the use of certain medications or malnourishment), mouth breathing, and blockage of saliva flow in a bottle-fed infant (Bowen 1998, Seow 1998). Although there have been continuing reductions in dental caries in permanent teeth among children and adolescents over the past few decades, caries prevalence in the primary dentition may have stabi- lized or increased slightly in some population groups (Petersson and Bratthall 1996, Rozier 1995). Reductions in caries in permanent teeth also have been proportionately greater on the smooth surfaces rather than on the pit-and-fissure surfaces character- istic of chewing surfaces. The gingival tissues tend to recede over time, exposing the tooth root to cario- genic bacteria that can cause root caries. An impor- tant risk factor for root caries in older people is the use of medications that inhibit salivary flow, leading to dry mouth (xerostomia). Saliva contains components that can directly attack cariogenic bacteria, and it is also rich in calci- um and phosphates that help to remineralize tooth enamel. Demineralization of enamel occurs when pH levels fall as a result of acid production by bacteria. It can be reversed at early stages’ if the local environ- ment can counteract acid production, restoring pH to neutral levels. Remineralization can occur through the replacement of lost mineral (calcium and phos- phates) from the stores in saliva. Fluoride in saliva and dental plaque and the buffering capacity of sali- va also contribute to this process. Indeed, it is now believed that fluoride exerts its chief caries-preven- tive effect by facilitating remineralization. Several studies have demonstrated that remineralization results in an increase in tooth hardness and mineral content, rendering the tooth surface more resistant to subsequent acid attack (Larsen 1987, Linton 1996, Retief 1983, Shannon 1978, Vissink et al. 1985, White 1988). Overt caries lesions develop when there is insuf- ficient time for remineralization between periods of acidogenesis, or when the saliva production is com- promised. Over 400 medications list dry mouth as a side effect, notably some antidepressants, antipsy- chotics, antihistamines, decongestants, antihyperten- sives, diuretics, and antiparkinsonian drugs (Sreebny et al. 1992). The effects of xerostomia may be partic- ularly severe in cancer patients receiving radiation to the head or neck because the rays can destroy sali- vary gland tissue rather than simply inhibiting sali- vary secretion. The professional application of dental sealants (plastic films coated onto the chewing surfaces of teeth) is an important caries-preventive measure that complements the use of fluorides. The films prevent decay from developing in the pits and fissures of teeth, channels that are often inaccessible to brushing and where fluoride may be less effective. The rate of caries progression through enamel is relatively slow (Berkey 1988, Ekanayake 1987, Shwartz et al. 1984) and may be slower in patients who have received regular fluoride treatment or who consume fluoridated water (Pitts 1983, Shwartz et al. 1984). Because a large percentage of enamel lesions remain unchanged over periods of 3 to 4 years, and 38 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL because progression rates through dentin are comparably slow (Craig et al. 1981, Emslie 1959, Kolehmainen and Rytomaa 1977), the application of infection control and monitoring procedures to assess caries risk status, lesion activity status, evidence of lesion arrest, and evidence of lesion remineralization over extended periods of time is recommended. Experts believe that the earlier mutans strepto- cocci are acquired in infancy, the higher the caries tisk. Most studies indicate that infants are infected before their first birthday, around the time the first incisors emerge. However, one study found the medi- an age of acquisition to be 26 months, coinciding with the emergence of the primary molars (Bowen 1998, Caufield et al. 1993, Seow 1998). DNA finger- printing has demonstrated that the source of trans- mission is usually the mother (Caufield et al. 1993). I is not clear why some individuals are more sus- ceptible and others more resistant to caries. Genetic differences in the structure and biochemistry of enamel proteins and crystals (Slavkin 1988), as well as variations in the quality and quantity of saliva and in immune defense mechanisms are among the fac- tors under study. Analysis of mutans streptococci genomes may also shed light, indicating which species are particularly virulent and which genes contribute to that virulence. Even the most protective genetic endowment and developmental milieu are unlikely to confer resistance to decay in the absence of positive person- al behaviors. These include sound dietary habits and good oral hygiene, including the use of fluorides, and seeking professional care. There are indications, however, that some destructive oral habits are on the rise, such as the use of smokeless (spit) tobacco products by teenage boys. Although the chief con- cern here lies in the long-term risk for oral cancers, spit tobacco that contains high levels of sugar is also associated with increased levels of decay of both crown and root surfaces (Tomar and Winn 1998). Periodontal Diseases Like dental caries, the periodontal diseases are infec- tions caused by bacteria in the biofilm (dental plaque) that forms on oral surfaces. The basic divi- sion in the periodontal diseases is between gingivitis, which affects the gums, and periodontitis, which may involve all of the soft tissue and bone supporting the teeth. Gingivitis and milder forms of periodontitis are common in adults. The percentage of individuals with moderate to severe periodontitis, in which the Diseases and Disorders destruction of supporting tissue can cause the tooth to loosen and fall out, increases with age. Gingivitis Gingivitis is an inflammation of the gums character- ized by a change in color from normal pink to red, with swelling, bleeding, and often sensitivity and ten- derness. These changes result from an accumulation of biofilm along the gingival margins and the immune system's inflammatory response to the release of destructive bacterial products. The early changes of gingivitis are reversible with thorough toothbrushing and flossing to reduce plaque. Without adequate oral hygiene, however, these early changes can become more severe, with infiltration of inflammatory cells and establishment of a chronic infection. Biofilm on tooth surfaces opposite the openings of the salivary glands often mineralizes to form calculus or tartar, which is covered by unmin- eralized biofilm—a combination that can exacerbate local inflammatory responses (Mandel 1995). A gin- gival infection may persist for months or years, yet never progress to periodontitis. Gingival inflammation does not appear until the biofilm changes from one composed largely of gram- positive streptococci (which can live with or without oxygen) to one containing gram-negative anaerobes (which cannot live in the presence of oxygen). Numerous attempts have been made to pinpoint which microorganisms in the supragingival (above the gum line) plaque are the culprits in gingivitis. Frequently mentioned organisms include Fusobacterium nucleatum, Veillonella parvula, and species of Campylobacter and Treponema. But as Ranney (1989) notes, “The complexity of the results defies any attempt to define a discrete group clearly and consistently associated with gingivitis.” Gingival inflammation may be influenced by steroid hormones, occurring as puberty gingivitis, pregnancy gingivitis, and gingivitis associated with birth control medication or steroid therapy. The pres- ence of steroid hormones in tissues adjacent to biofilm apparently encourages the growth of certain bacteria and triggers an exaggerated response [0 biofilm accumulation (Caton 1989). Again, thorough oral hygiene can control this response. Certain prescription drugs can also lead to gingi- val overgrowth and inflammation. These include the antiepileptic drug phenytoin (Dilantin); cyclosporin, used for immunosuppressive therapy in transplant patients, and various calcium channel blockers used in heart disease. Treatment often requires surgical removal of the excess tissue followed by appropriate personal and professional oral health care. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 39 Diseases and Disorders A form of gingivitis common 50 years ago but relatively rare today is acute necrotizing ulcerative gingivitis, also known as Vincent's infection or trench mouth. This aggressive infection is characterized by destruction of the gingiva between the teeth, sponta- neous bleeding, pain, and oral odor. People under extreme stress have an increased susceptibility. Spirochetes and other bacteria have been found in the connective tissue of those affected. An associa- tion between smoking and this type of gingivitis is well recognized and was demonstrated as early as 1946 (Pindborg 1947, 1949). This condition has been seen in some HIV-positive patients (Murray 1904). Treatment requires a combination of profes- sional periodontal treatment and antibacterial thera- py along with professional smoking cessation assis- tance as appropriate. Adult Periodontitis The most common form of adult periodontitis is described as general and moderately progressing, a second form is described as rapidly progressing and severe, and is often resistant to treatment. The mod- erately progressive adult form is characterized by a gradual loss of attachment of the periodontal liga- ment to the gingiva and bone along with loss of the supporting bone. It is most often accompanied by gingivitis (Genco 1990). It is not necessarily preced- ed by gingivitis, but the gingivitis-related biofilm often seeds the subgingival plaque. The destruction of periodontal ligament and bone results in the for- mation of a pocket between the tooth and adjacent tissues, which harbors subgingival plaque. The cal- culus formed in the pocket by inflammatory fluids and minerals in adjacent tissues is especially damag- ing (Mandel and Gaffar 1986). The severity of periodontal disease is determined through a series of measurements, including the extent of gingival inflammation and bleeding, the probing depth of the pocket to the point of resist- ance, the clinical attachment loss of the periodontal ligament measured from a fixed point on the tooth (usually the cemento-enamel junction), and the loss of adjacent alveolar bone as measured by x-ray (Genco 1996). Severity is determined by the rate of disease progression over time and the response of the tissues to treatment. Adult periodontitis often begins in adolescence but is usually not clinically significant until the mid- 30s. Prevalence and severity increase but do not accelerate with age (Beck 1996). One view proposes that destruction occurs at a specific site during a defined period, after which the disease goes into remission (Socransky et al. 1984). The current view is that the disease process may not be continuous but rather progresses in random bursts in which short periods of breakdown of periodontal ligament and bone alternate with periods of quiescence. These episodes occur randomly over ume and at random sites in the mouth. Part of the difficulty in determin- ing the pattern of progression reflects variation in the sensitivity of the instruments used to measure the loss of soft tissue and bone. The latest generation of probes finds evidence of both continuous and multi- ple-burst patterns of loss in different patients and at different times (Jeffcoat and Ready 1991). Most researchers agree that periodontitis results from a mixed infection but that a particular group of gram-negative bacteria are key to the process and markedly increase in the subgingival plaque. The bacteria most frequently cited are Porphyromonas gin- givalis, Prevotella intermedia, Bacteroides forsythus, Treponema denticola, and Actinobacillus actino- mycetemcomitans (Genco 1996). Their role in disease initiation and progression is determined in part by their “virulence factors.” These include the ability to colonize subgingival plaque, generate products that can directly injure tissues, and elicit an inflammatory or immune response. The potentially noxious bacte- rial products include hydrogen sulfide, polyamines, the fatty acids butyrate and propionate, lipopolysac- charide (also known as endotoxin), and a number of destructive enzymes. The interaction of this arsenal with the host response is at the core of periodontal pathology (Genco 1992, Socransky and Haffajee 1991, 1992). Sequencing of the genomes of several key periodontal pathogens is under way and should provide further insight into these pathogens as well as catalyze new treatment approaches. Delicate Balances. Neutrophils (a type of white blood cell) and antibodies are the major immune defenses against bacterial attack. Neutrophils move to the site of infection, where they engulf bacteria and elaborate antibacterial agents and enzymes to destroy bacteria. Although stimulation of the immune system to attack the offending bacteria is generally protective, immune hyperresponsiveness and hypersensitivity can be counterproductive, leading to the destruction of healthy tissue. Nevertheless, the neutrophil/anti- body axis is critical for full protection against peri- odontal diseases (Genco 1992). Also important is the release of certain potent molecules called cytokines and prostaglandins, especially prostaglandin E2 (PGE;) which can contribute to tissue destruction. Cytokines are proteins secreted by immune cells that help regulate immune responses and also affect bone, epithelial, 40 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and connective tissues. Most prominent in periodontal diseases are interleukin 1 (IL-1), tumor necrosis factor a (TNF-a), and interferon y (IEN-Yy). These cytokines mediate the processes of bone resorption and connective tissue destruction. Susceptibility and Resistance. PGE, may play a central role in the tissue destruction that occurs in peri- odontal diseases. Levels of PGE) in periodontal tissue are low or undetectable in health, increase in gingivi- tis, and rise significantly in periodontitis. Now there is increasing evidence that the level of PGE, pro- duced in response to bacterial challenge (especially by endotoxin) can be used as a measure of suscepti- bility (Offenbacher et al. 1993). Presumably, the level of PGE, production is sub- ject to genetic influence. Studies of identical and fra- ternal twins, either reared together or apart, provide evidence that genetic factors may indeed influence susceptibility or resistance to the common adult form of periodontitis (Michalowicz 1994). Recently, a commercial test for a genetic marker of susceptibility has been introduced. The marker is associated with increased production of a particular form of inter- leukin 18 (IL-18) when stimulated by periodonto- pathic bacteria (Kornman et al. 1997). Newman (1996) found that nonsmoking adults who are posi- tive for the marker are 6 to 19 times more likely to develop severe periodontitis. Susceptibility to adult periodontitis has also been explored in relation to a variety of behavioral and demographic variables as well as to the presence of other diseases. One of the strongest behavioral asso- ciations is with tobacco use. The risk of alveolar bone loss for heavy smokers is 7 times greater than for those who have not smoked (Grossi et al. 1995). Cigarette smoking also may impair the normal host response in neutralizing infection (Seymour 1991), resulting in the destruction of healthy periodontal tissues adjacent to the site of infection (Lamster 1992). Smokers also have decreased levels of salivary and serum immunoglobulins to Prevotella intermedia and Fusobacterium nucleatum (Bennet and Reade 1982, Haber 1994) and depressed numbers of helper T cells as well (Costabel et al. 1986). Finally, smok- ing alters the cells that engulf and dispose of bacte- ria—neutrophils and other phagocytes—affecting their ability to clear pathogens (Barbour et al. 1997). Epidemiologic studies have found that such additional factors as increasing age, infrequent dental visits, low education level, low income, co-morbidi- ties, and inclusion in certain racial or ethnic popula- tions are associated with increased prevalence of Diseases and Disorders periodontitis (Page 1995). It is important that epi- demiologic studies also take into consideration the fact that tobacco use, oral hygiene, professional pro- phylaxis, and routine dental care are correlated to socioeconomic status, as are race and ethnicity. Sex is another factor. Males tend to have higher levels of periodontal diseases, presumably because of a histo- ry of greater tobacco use and differences in personal care and frequency of dental visits. However, female hormones may play a protective role (as they do in protecting against osteoporosis) (Genco 1996). Certain systemic diseases heighten susceptibility. Epidemiological studies have confirmed that patients with diabetes mellitus, both type 1 and type 2, are more susceptible to periodontal diseases (Genco 1996), Measures such as the gingival index, pocket depth, and loss of attachment are more severe if the diabetic patients are smokers (Bridges et al. 1996). The likelihood of periodontal disease increases markedly when diabetes is poorly controlled. In con- trast, periodontal diseases respond well to therapy and can be managed successfully in patients with well-controlled diabetes. Such therapy can result in improvements in the diabetic condition itself (Mealey 1996) (see Chapter 5). There is some evidence that osteoporosis may be a risk factor for periodontal disease. More clinical attachment loss and edentulousness have been reported in osteoporotic than in nonosteoporotic women (Jeffcoat and Chestnut 1993). Two studies in 1996 showed that estrogen replacement therapy in postmenopausal women not only gives protection against osteoporosis, but also results in fewer teeth lost to periodontal disease (Grodstein et al. 1996, Jacobs et al. 1996). The less common rapidly progressive form of adult periodontitis typically affects people in their early 20s and 30s. It is characterized by severe ging)- yal inflammation and rapid loss of connective tissue and bone. Many patients have an inherent defect in neutrophil response to infection. Several systemic diseases have been associated with this form of peri- odontal disease, including type 1 diabetes, Down syndrome, Papillon-Lefevre syndrome, Chediak- Higashi syndrome, and HIV infection (Caton 1989). Specific bacteria associated with rapidly progressive disease include Porphyromonas gingivalis, Prevotella intermedia, Eikenella corrodens, and Wolinella recta (Scheutz et al. 1997). Most recently, mutations in the cathepsin C gene have been associated with the Papillon-Lefevre syndrome (Hart et al. 1999) and how the defect can result in periodontal disease (Toomers et al. 1999). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 41 Diseases and Disorders Refractory Periodontitis. Refractory periodontitis is not a specific form of disease, but refers to cases in which patients continue to exhibit progressive dis- ease at multiple sites despite aggressive mechanical therapy to remove biofilm and calculus, along with the use of antibiotics. Refractory sites exhibit elevat- ed levels of a number of different bacteria, with the dominant species different in different subjects. It is not known whether variations in pathogenicity of the bacteria, defects in the subject's defense systems, or combinations of these factors are responsible for the refractory nature of the disease (Haffajee et al. 1988). The adoption of new diagnostic technology to detect predominant bacterial species, followed by selective antibiotic treatment, may help resolve infection and disease in these patients. Early-onset Periodontitis The forms of periodontitis occurring in adolescents and young adults generally involve defects in neu- trophil function (Van Dyke et al. 1980). Localized juvenile periodontitis (LJP) mainly affects the first molar and incisor teeth of teenagers and young adults, with rapid destruction of bone but almost no telltale signs of inflammation and very little supragingival plaque or calculus. Actinobacillus actin- omycetemcomitans has been isolated at 90 to 100 per- cent of diseased sites in these patients, but is absent or appears in very low frequency in healthy or mini- mally diseased sites (Socransky and Haffajee 1992). It is possible that the bacteria are transmitted among family members through oral contacts such as kiss- - ing or sharing utensils, because the same bacterial strain appears in affected family members. However, evidence of a neutrophil defect argues for a genetic component. Another organism frequently associated with LJP is Capnocytophaga ochracea. Neither of these bacteria dominate in the generalized adult form of the disease, where Porphyromonas gingivalis is con- sidered of greatest significance (Schenkein and Van Dyke 1994). Prepubertal periodontitis is rare and can be either general or localized. The generalized form begins with the eruption of the primary teeth and proceeds to involve the permanent teeth. There is severe inflammation, rapid bone loss, tooth mobility, and tooth loss. The localized form of the disease is less aggressive, affecting only some primary teeth. The infection involves many of the organisms associ- ated with periodontitis, but the mix may differ some- what, with Actinobacillus actinomycetemcomitans, Prevotella intermedia, Eikenella corrodens, and several species of Capnocytophaga implicated (Caton 1989). Defects in neutrophil function noted in both forms of the disease (Schenkein and Van Dyke 1994) may explain why patients are highly susceptible to other infections as well (Suzuki 1988). SELECTED MUCOSAL INFECTIONS AND CONDITIONS Like the skin, the mucosal lining of the mouth serves to protect the body from injury. This lining is itself subject to a variety of infections and conditions, ranging from benign canker sores to often fatal cancers. Oral Candidiasis Chronic hyperplastic candidiasis is a red or white lesion that may be flat or slightly elevated and may adhere to soft or hard tissue surfaces, including den- tal appliances. It is caused by species of Candida, especially Candida albicans, the most common fungal pathogen isolated from the oral cavity. Normally, the fungi are present in relatively low numbers in up to 65 percent of healthy children and adults and cause no harm (McCullough et al. 1996). Problems arise when there is a change in oral homeostatis—the nor- mal balance of protective mechanisms and resident oral flora that maintain the health of the oral cavity— so that defense mechanisms are compromised (Scully et al. 1994). Under these circumstances the fungal organisms can overgrow to cause disease. A primary disruption in homeostasis occurs with the use of antibiotics and corticosteroids, which can markedly change the composition of the oral flora. Deficiencies in the immune and endocrine systems are also important. Indeed, the diagnosis of candidiasis in an otherwise seemingly healthy young adult may be the first sign of HIV infection. Other causes of candidia- sis include cancer chemotherapy or radiotherapy to the head and neck, xerostomia resulting from radia- tion to the head and neck, medications, chronic mucosal irritation, certain blood diseases, and other systemic conditions. Also, tobacco use has been iden- tified as a cofactor. Candidiasis often causes symptoms of burning and soreness as well as sensitivity to acidic and spicy foods. Patients may complain of a foul taste in the mouth. However, it can also be asymptomatic. Genomic analysis of the Candida albicans genome is helping investigators identify numerous genes that code for virulence factors, including enzymes that can facilitate adhesion to and penetration of mucous membranes. At the same time, researchers are explor- ing novel gene technologies to increase production of 42 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL a family of native salivary proteins, the histatins, that have known anticandidal and other antimicrobial effects. The most common form of oral candidiasis is denture stomatitis. It occurs when tissues are trau- matized by continued wearing of ill-fitting or inade- quately cleaned dental appliances and is described as chronic erythematous candidiasis. Another form, candidal angular cheilosis, occurs in the folds at the angles of the mouth and is closely associated with denture sore mouth (Tyldesley and Field 1995). Other common forms of Candida infection are pseudomembranous candidiasis (thrush), which may affect any of the mucosal surfaces, and acute erythe- matous candidiasis, a red and markedly painful vari- ant commonly seen in AIDS patients. In most cases, Candida infection can be con- trolled with antifungal medications used locally or systemically. Control is difficult, however, in patients with immune dysfunction, as in AIDS, or other chronic debilitating diseases. Often the organisms become resistant to standard therapy, and aggressive approaches are necessary (Tyldesley and Field 1995). The spread of oral candidiasis to the esophagus or lungs can be life-threatening and is one of the crite- ria used to define frank AIDS (Samaranayake and Holmstrup 1989). Herpes Simplex Virus Infections In any given year, about one-half-million Americans will experience their first encounter with the herpes simplex virus type 1 (HSV-1), the cause of cold sores. That first encounter usually occurs in the oral region and may be so mild as to go unnoticed. But in some people, particularly young children and young adults, infection may take the form of primary her- petic stomatitis, with symptoms of malaise, muscle aches, sore throat, and enlarged and tender lymph nodes, prior to the appearance of the familiar cold sore blisters. These blisters usually show up on the lips, but any of the mucosal surfaces can be affected. Bright-red ulcerated areas and marked gingivitis may also be seen (Tyldesley and Field 1995). Herpes viruses also cause genital infections, which are transmitted sexually. Both HSV-1 and HSV- 2 have been found in oral and genital infections, with HSV-1 predominating in oral areas and HSV-2 in gen- ital areas (Wheeler 1988). Herpes viruses have also been implicated as cofactors in the development of oral cancers. Crowded living conditions can result in greater contact with infected individuals, which aids in transmission of HSV (Whitley 1992). Diseases and Disorders Normally, the immune system mounts a success- ful attack on the viruses, with symptoms abating by the time neutralizing antibodies appear in the blood- stream, in about 10 days. However, herpes viruses are notorious for their ability to avoid immune detection by taking refuge in the nervous system, where they can remain latent for years. In oral herpes the virus commonly migrates to the nearby trigeminal gan- glion, the cluster of nerve cells whose fibers branch out to the face and mouth. In about 20 to 40 percent of people who are virus-positive, the virus may reac- tivate, with infectious virus particles moving to the oral cavity to cause recurrent disease (Scott et al. 1997). The usual site of a recurrent lesion is on or near the lips. Recurrences are rarely severe, and lesions heal in 7 to 10 days without scarring (Higgins et al. 1993). The recurrences may be provoked by a wide range of stimuli, including sunlight, mechanical trau- ma, and mild fevers such as occur with a cold. Emotional factors may play a role as well. Oral Human Papillomavirus Infections There are more than 100 recognized strains of oral human papillomavirus (HPV), a member of the papovavirus family, implicated in a variety of oral lesions (Regezi and Sciubba 1993). Most common are papillomas (warts) found on or around the lips and in the mouth. HPV is found in 80 percent of these oral squamous papillomas (de Villiers 1989). The virus has also been identified in 30 to 40 percent of oral squamous cell carcinomas (Chang et al. 1990) and has been implicated in cervical cancer as well. Whether a cancer or nonmalignant wart develops may depend on which virus is present or on which viral genes are activated. Oral warts are most often found in children, probably as a result of chewing warts on the hands. In adults, sexual transmission from the anogenital region can occur (Franchesi et al. 1996). In general, viral warts spontaneously regress after 1 or 2 years. The immune system normally keeps HPV infections under control, as evidenced by the increased prevalence of HPV-associated lesions in HIV-infected patients and others with immuno- deficiency. Recurrent Aphthous Ulcers Recurrent aphthous ulcers (RAL), also referred to as recurrent aphthous stomatitis, is the technical term for canker sores, the most common and generally ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 43 Diseases and Disorders mild oral mucosal disease. Between 5 and 25 percent of the general population is affected, with higher numbers in selected groups, such as health profes- sional students (Axéll et al. 1976, Embil et al. 1975, Ferguson et al. 1984, Kleinman et al. 1991, Ship 1972, Ship et al. 1967). The disease takes three clinical forms: RAU minor, RAU major, and herpetiform RAU. The minor form accounts for 70 to 87 percent of cases. The sores are small, discrete, shallow ulcers surrounded by a red halo appearing at the front of the mouth or the tongue. The ulcers, which usually last up to 2 weeks, are painful and may make eating or speaking diffi- cult. About half of RAU patients experience recur- rences every 1 to 3 months; as many as 30 percent report continuous recurrences (Bagan et al. 1991). RAU major accounts for 7 to 20 percent of cases and usually appears as 1 to 10 larger coalescent ulcers at a time, which can persist for weeks or months (Bagan et al. 1991). Herpetiform RAU has been reported as occurring in 7 to 10 percent of RAU cases. The ulcers appear in crops of 10 to 100 ata time, concentrating in the back of the mouth and lasting for 7 to 14 days (Bagan et al. 1991, Rennie et al. 1985). RAU can begin in childhood, but the peak peri- od for onset is the second decade (Lehner 1968). About 50 percent of close relatives of patients with RAU also have the condition (Ship 1965), and a high correlation of RAU has been noted in identical but not fraternal twins. Associations have been found between RAU and specific genetic markers (Scully and Porter 1989). , RAU has also been associated with hypersensi- tivities to some foods, food dyes, and food preserva- tives (Woo and Sonis 1996). Nutritional deficien- cies—especially in iron, folic acid, various B vita- mins, or combinations thereof—have also been reported, and improvements noted with suitable dietary supplements (Nolan et al. 1991). The two factors that have been found to have the strongest association with RAU are immunologic abnormality, possibly involving autoimmunity, and trauma (Lehner 1968, Ship 1996, Woo and Sonis 1996). Volunteers with and without a history of RAU were studied for their reaction to the trauma of a nee- dle prick to the inner cheek tissue. No ulcers devel- oped in non-RAU subjects, but nearly half of those prone to canker sores had a recurrence (Wray et al. 1981). RAU also can occur in a number of systemic dis- eases, including HIV infection, ulcerative colitis, Crohn's disease, and Behcet's disease (Ship 1996). In general, people who are immunocompromised are more susceptible to RAU, as are people with a variety of blood diseases. RAU itself does not give rise to other illnesses but is uncomfortable. Symptomatic treatment includes topical analgesics, antibacterial rinses, topi- cal corticosteroids, and a new prescription medica- tion that reduces pain and healing time (Khandwala et al. 1997, Ship 1996). ORAL AND PHARYNGEAL CANCERS AND PRECANCEROUS LESIONS In 2000, oral or pharyngeal cancer will be diagnosed in an estimated 30,200 Americans and will cause more than 7,800 deaths (Greenlee et al. 2000). Over 90 percent of these cancers are squamous cell carci- nomas—cancers of the epithelial cells. The most common oral sites are on the tongue, the lips, and the floor of the mouth. Oral cancer is the sixth most common cancer in U.S. males and takes a dispropor- tionate toll on minorities; it now ranks as the fourth most common cancer among African American men (Kosary et al. 1995). The prominent role of tobacco use, especially in combination with alcohol, in caus- ing these cancers is a major incentive to develop effective health promotion and disease prevention efforts. Heightening the Risk Oral cancer develops as a clone from a single geneti- cally altered cell (Solt 1981). It generally has a long ‘latency period and invariably develops from a pre- cancerous lesion on the oral mucosa, such as a white leukoplakia, or more commonly, a reddish erythro- plakia (Mashberg 1978, Shklar 1986). Both kinds of lesions are usually induced by tobacco use alone or in combination with heavy use of alcohol. The develop- ment of squamous cell carcinoma from initial ery- throplakia lesions has been well demonstrated exper- imentally. Silverman (1998) reported rates of malig- nant transformation for leukoplakias of between 0.13 and 17.5 percent. However, there is considerable debate as to the actual malignant potential of the leukoplakia lesion associated with the use of smoke- less (spit) tobacco. Meaningful data for determining a specific malignant transformation rate or relative risk of oral cancer due to smokeless tobacco use are difficult to obtain because of the confounding effects of other habits such as concurrent smoking and alco- hol consumption and because of the variations in smokeless (spit) products and how they are used. 44 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Another oral precancerous lesion that has received attention is submucous fibrosis. It is com- monly seen in India and Southeast Asia and is relat- cd to betel nut use (Canniff et al. 1986). Early epidemiologic studies identified behaviors such as smoking and environmental factors such as exposure to solar radiation and x-rays as causes of intraoral and lip cancers (Pindborg 1977). Researchers then sought experimentally to explain the mechanisms of initiation. In the 1980s and 1990s, investigators exploited the techniques of molecular biology and genetics to probe what was going on deep inside the cell. These studies revealed an abundance of systemic and local factors, including viral and fungal infections, that affect cell behavior. Some factors stimulate cell division and others inhibit it—even to the point of initiating a program of cell “suicide,” called apoptosis. How a given cell behaves at any given time in its life cycle is the net result of the signals it receives from neighboring cells and molecules, from circulating factors in the blood or immune system, and from its own internal controls. The following sections provide a brief description of these factors and how they may participate in enhancing the risk for the development of oral cancers. Tobacco and Alcohol Tobacco and alcohol are the major risk factors for oral cancers, and their effects have been studied for many years (Rothman and Keller 1972, Decker and Goldstein 1982). Tobacco contains substances that are frankly carcinogenic or act as initiators or pro- moters of carcinogenesis. Among these are N- nitrosonornicotine, 4-nitroquinoline-N-oxide, and benzpyrene. The most damaging carcinogens are found in the tars of tobacco smoke, but many forms of smokeless (spit) tobacco, including snuff, have been implicated in the development of mouth cancer (Advisory Committee to the Surgeon General 1986, International Agency for Research on Cancer 1985, Winn 1984). Other habits that have been related to oral cancer include chewing betel nut in the presence of tobacco, as is done primarily in Southeast Asia (Hirayama 1966, Mehta et al. 1981), and, more recently, using marijuana (Donald 1986). The role of alcohol in oral carcinogenesis has been demonstrated experimentally (Wight and Ogden 1998) and appears to be related to its damag- ing effect on the liver. Major metabolites of alcohol, such as acetaldehyde—a known carcinogen in ani- mals—may also be important. Alcohol is also thought to act as a solvent that facilitates the pene- Diseases and Disorders tration of tobacco carcinogens into oral tissues. That observation may partly explain why the combined use of tobacco and alcohol produces a greater risk for oral cancer than use of either substance alone. Indeed, tobacco and alcohol, working in tandem, are thought to account for 75 to 90 percent of all oral and pharyngeal cancers in the United States (Blot et al. 1988). Viruses The role of viruses in causing cancer in animals was established early in the century when Rous showed that a virus, later named the Rous sarcoma virus (RSV), caused tumors in chickens. The issue of whether viruses could cause cancer in humans remained unexplored until the mid-1970s, when Varmus and Bishop showed that RSV had a special gene, which they called src (for sarcoma), that could transform the cell it infected into a malignant cell (Bishop et al. 1978). It was an oncogene, OF cancer- causing gene. The researchers subsequently, and sur- prisingly, discovered that src was not native to the virus, but had been picked up by some ancestor virus from a chicken cell's own genome, where src had pre- sumably played a role in the chicken cell's normal growth and development. Somehow RSV was able to subvert svc when it infected a chicken cell to cause the cell to divide uncontrollably. Varmus and Bishop called the normal cellular src gene a proto-oncogene, meaning that it had the potential to be converted to an oncogene. Subsequent research led to the discov- ery of other viruses that could cause tumors in ani- mals and revealed the presence of proto-oncogenes in birds and mammals. These genes could also be con- verted to oncogenes, behaving exactly like those car- ried by cancer viruses. In 1982 an oncogene isolated from a human bladder cancer turned out to be virtu- ally identical to ras, the oncogene found in a rat sar- coma virus (Parada et al. 1982). Viruses that have been implicated in oral cancer include herpes simplex type 1 and human papillo- mavirus. Epstein-Barr virus, also a herpes virus, 1s now accepted as an oncogenic virus responsible for Burkitt's lymphoma, occurring primarily in Africa, and nasopharyngeal carcinoma, occurring primarily in China. HPV is a major etiologic agent in cervical cancer (Howley 1991), and has been found in associ- ation with oral cancer as well (Sugerman and Shillitoe 1997). HPV DNA sequences have been found in oral precancerous lesions as well as in squa- mous cell carcinomas (Adler-Storthz et al. 1986, Syrjanen et al. 1988), and experimental evidence has shown that HPV-16 can be an important cofactor in ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 45 Diseases and Disorders oral carcinogenesis (Park et al. 1991, 1995). Herpes simplex type 1 antibodies were demonstrated in patients with oral cancer, and herpes was found to induce dysplasia (abnormal cellular changes) in the lips of hamsters when combined with the application of tobacco tar condensate (Park et al. 1986). More recently, human herpes virus 8, a newly identified member of the herpes virus family, has been found in Kaposi’s sarcoma, an otherwise rare cancer occurring in patients with AIDS. These tumors often appear initially within the oral cavity (Epstein and Scully 1992). Other uncommon oral malignant tumors, such as Hodgkin's lymphoma and non-Hodgkin’s lymphoma, can also occur in the mouths of AIDS patients. In addition to viruses, infection with strains of the fungus Candida albicans has been linked to the development of oral cancers via the fungal produc- tion of nitrosamines, which are known carcinogens. Genetic Derangements Of the more than 50 known oncogenes, many have been reported to be present in oral cancer, and mul- tiple oncogenes have been reported in oral and pha- ryngeal cancer (Spandidos et al. 1985). Some of these are Bcl-1, c-erb-B2, c-myc, ins-2, and members of the ras family (Berenson et al. 1989, Bos 1989, Riviere et al. 1990, Somers et al. 1990, 1992). The genetic derangements that can give rise to oral cancer, including many mutations associated with the transformation of proto-oncogenes, have received notable attention (Sidransky 1995, Wong et al. 1996). In some instances a change in a single nucleotide base—a point mutation—in a gene encoding a proto-oncogene is enough to transform it into an oncogene. Cancerous changes may also involve alterations, deletions, and break points in chromosomes that affect the position of genes. Mutations that disarm the cells DNA repair mechanisms, as well as mutations in tumor suppres- sor genes, which inhibit abnormal cell growth, play a major role in cancer development. If an individual inherits or acquires a mutation in one or more tumor- suppressor genes, for example, the loss of this pro- tective mechanism reduces the number of other dele- terious changes needed for cancer to develop. Tumor suppressor genes suspected to be mutated _ in oral and pharyngeal cancers include those for Rb, pl6 (MTS1, CDKN2, or IN4a), and p53. Todd et al. (1995) recently reported a novel oral tumor suppres- sor gene, named “deleted in oral cancer-1 (doc-1).” of the group of tumor suppressor genes, that coding for p53 is considered of major importance, with muta- tions in the p53 gene detected in many types of can- cer (Greenblatt et al. 1994, Hollstein et al. 1991), including oral and pharyngeal cancer (Langdon and Partridge 1992, Somers et al. 1992). The p53 gene has been called the “guardian of the genome” (Lane 1992) because of its ability to recognize damage to a "cells DNA and stop the process of growth and divi- sion until the damage is repaired. If repair is not pos- sible, p53 can trigger apoptosis. Mutations in the p53 gene in oral cancer have been linked to smoking and alcohol use (Brennan et al. 1995). Loss of Immunosurveillance and Control The immune system can, aS first noted by Paul Ehrlich in 1909, seek and destroy initial clones of transformed cancer cells (Ehrlich 1957). Ehrlich called this process immunosurveillance, and it has been confirmed in experimental animals (Burnet 1970, Shklar et al. 1990) and in humans with induced immunosuppression (Penn 1975). One mechanism of immunosurveillance involves stimulating cytotoxic macrophages and lymphocytes to migrate to the tumor site and release tumor necro- sis factors a and ® (Shklar and Schwartz 1988). Another mechanism operative in oral cancer appears to be stimulation of Langerhans cells, a special group of immune cells, in the oral mucosa (Schwartz et al. 1985). Other immune cells implicated in tumor rejection are natural killer cells and lymphokine-acti- vated killer cells (Reif 1997). There is an increased incidence of cancer in patients with AIDS or other immunodeficient condi- tions or with induced immunosuppression prior to organ transplantation. In addition, there is evidence that smoking depresses the immune system (Chretien 1978), and this may be one of the ways in which smoking acts as a major risk factor in oral cancer. Growth Factors Immune cells are potent generators of growth factors and other molecules that can stimulate other cells to migrate and proliferate. This capacity is important in normal cell growth and turnover, in wound healing, and in coping with infection. Unfortunately, the release of growth factors can contribute to oral can- cer by stimulating keratinocyte (oral epithelial cell) proliferation (Aaronson 1991, Issing et al. 1993, Wong 1993). Increased levels of transforming growth factor a (TGF-a) and epidermal growth factor have been found in oral and pharyngeal cancers and there- fore could serve as markers for malignancy (Grandis and Tweardy 1993). Nicotine at high doses stimulates 46 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL the release of growth hormones, among other endocrine effects (Pomerleau and Pomerleau 1984, Seyler et al. 1984, 1986). Prevention and Management studies of experimental carcinogenesis are elucidat- ing the role of micronutrients in tumor development and progression. Alpha tocopherol (vitamin E) also has been studied as an antioxidant in nutritional approaches to the prevention or control of oral can- cer. Antioxidants can trap free radicals, the highly reactive molecules that build up in cells and can damage DNA. The control of oral cancer and precan- cerous lesions has been demonstrated experimental- ly using a variety of antioxidant micronutrients, such as retinoids, carotenoids, and glutathione, as well as alpha tocopherol. For example, it was found that alpha tocopherol inhibited tumor development and tumor angiogenesis (blood vessel formation) in ham- sters, as well as the expression of TGF-a, a potent angiogenesis stimulator (Shklar and Schwartz 1996). Animal research and tissue culture studies using ani- mal- and human-derived cancer cell lines have shown combinations of micronutrients to be more effective than single micronutrients and to work syn- ergistically. The nutrients not only were able to inhib- it experimental carcinogenesis, but also could com- pletely prevent tumor development and cause estab- lished squamous cell carcinomas to regress (Shklar and Schwartz 1993). The mechanisms of cancer con- trol by micronutrients are gradually becoming clari- fied and involve common pathways of activity at the molecular level (Shklar and Schwartz 1994). Clinical studies in humans have shown an inhibitory effect on oral leukoplakia (Benner et al. 1993, Blot et al. 1993, Garewal 1993, Garewal et al. 1990, Hong et al. 1986), suggesting a potential role for nutrients in the overall prevention and management of early oral cancer and precancerous leukoplakia. However, a recommenda- tion to employ such approaches clinically at this time is premature. DEVELOPMENTAL DISORDERS The importance of the face as the bearer of identity, character, intelligence, and beauty is universal. Craniofacial birth defects, which can include such manifestations as cleft lip or palate, eyes too closely or widely spaced, deformed ears, eyes mismatched in color, and facial asymmetries, can be devastating to the parents and child affected. Surgery, dental care, psychological counseling, and rehabilitation may Diseases and Disorders help to ameliorate the problems but often at great cost and over many years. Although each developmental craniofacial dis- ease or syndrome is relatively rare, the number of children affected worldwide is in the millions. In addition, craniofacial defects form a substantial com- ponent of many other developmental birth defects, largely because they occur very early in gestation, when many of the same genes that orchestrate the development of the brain, head, face, and mouth are also directing the development of the limbs and many vital internal organs, such as the heart, lungs, and liver. By about the third week after fertilization, the three germ layers of the embryo—the ectoderm, endoderm, and mesoderm—have formed, as well as the first of four sets of paired swellings—the branchial arches—that appear at the sides of the head end of the embryo. (See Chapter 2 for more details on this process.) Some craniofacial defects result from failure of the arches to complete their morphogenet- ic development. Other craniofacial defects are the result of the abnormal differentiation of cells derived from the ectoderm and endoderm or from ectomes- enchyme cells, which originate in a part of the ecto- derm (the neural crest), in interaction with future connective tissue (the mesenchyme). Craniofacial Anomalies Caused by Altered Branchial Arch Morphogenesis Cleft Lip/Palate and Cleft Palate The most common of all craniofacial anomalies—and among the most common of all birth defects—are clefts of the lip with or without cleft palate and cleft palate alone; these occur at a rate of 1 to 2 out of 1,000 births, resulting in over 8,000 affected new- borns every year. Cleft lip/palate and cleft palate are distinct conditions with different patterns of inheri- tance and embryological origins (Lidral et al. 1997, Murray et al. 1997). The male to female ratio of cleft lip/palate is 2:1; the ratio for cleft palate alone is just the reverse, 1:2. These anomalies result from the failure of the first branchial arches to complete fusion processes (Murray 1995, Robert et al. 1996). Clefting can occur independently or as part of a larger syndrome that may include mental retardation and defects of the heart and other organs. Not all cases of clefting are inherited: a number of teratogens (environmental agents that can cause birth defects) have been impli- cated, as well as defects in essential nutrients such as ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 47 Diseases and Disorders folic acid. Smoking by the mother during pregnancy also increases the risk. It is becoming increasingly evident that most diseases and disorders, not just craniofacial anomalies, result from interactions involving multiple genes and environmental factors. Infants with clefts have difficulty with vital oral functions such as feeding, breathing, speaking, and swallowing. They are also susceptible to repeated res- piratory infections. As these children grow, they must cope with the social consequences of a facial defor- mity, delayed and altered speech, frequent illness, and repeated surgeries that may persist through late adolescence. Current molecular epidemiology investigations have examined both syndromic and nonsyndromic (isolated) cleft lip/palate and cleft palate. Linkage studies have identified a number of candidate genes (Lewanda and Jabs 1994), including MSX1, RAR, an X-linked locus, and the genes for TGF-83 and TGF- a. The pattern of inheritance in cleft lip/palate and cleft palate suggests that between 2 and 20 genes may be involved, with one gene representing a major component in the development of the cleft. One of the common syndromic forms of cleft lip/palate, the Van der Woude syndrome, is caused by an autosomal dominant form of inheritance at a locus on chromo- some 1] (Sander et al. 1995). Future molecular genet- ic studies will be needed to provide the information necessary for prenatal diagnosis, calculation of risk, and potential gene therapy. The Treacher Collins Syndrome— Mandibulofacial Dysostosis Children with the Treacher Collins syndrome have downward-sloping eyelids; depressed cheekbones; a large fishlike mouth; deformed ears with conductive deafness; a small, receding chin and lower jaw; a highly arched or cleft palate; and severe dental mal- occlusion (Dixon 1996). These defects result from defective cranial neural crest cell differentiation, migration, and proliferation (see Chapter 2). Consequently, the first branchial arch structures are deficient, and all derivative craniofacial components are affected. The underdeveloped facial structures can con- tribute to airway blockage and repeated upper respi- ratory infections, either of which can be fatal. The faulty development of the ears leads to a conductive deafness. The severe facial deformities exacerbate the psychological difficulties these youngsters face. Investigators have identified the gene involved in an autosomal dominant form of the syndrome (Wise et al. 1997). The function of the gene is not yet known, but its identity will provide opportunities for prenatal diagnosis, gene therapy, and further under- standing of craniofacial development. The Pierre Robin Syndrome Deficient development of the first-branchial-arch- derived mandibular portion results in the lower jaw’s being set far back in relation to the forehead. As a result, the tongue is set back and may obstruct the posterior airway, compromising respiration (Elliott et al. 1995, Tomaski et al. 1995) and, in severe cases, leading to inadequate aeration and failure to thrive. The infant is also at risk for the development of cor pulmonale, an enlargement of the right ventricle of the heart that occurs secondarily to a chronic lung condition. Cleft palate may be another consequence. The DiGeorge/Velocardiofacial Syndrome The primary defect in the DiGeorge syndrome results from altered development of the fourth branchial arch and the third and fourth pharyngeal pouches (Goldmuntz and Emanuel 1997). Deficiencies affect- ing the thymus, parathyroid glands, and the great vessels that derive from these structures result. The facial features are subtle and include a squared-off nasal tip, small mouth, and widely spaced eyes. Similar facial features, along with heart defects, are seen in the velocardiofacial syndrome. Both syn- dromes are associated with deletions on the long arm of chromosome 22 (22ql1) (Gong et al. 1997, Gottlieb et al. 1997). Further characterization of this chromosomal deletion region will provide informa- tion on the specific gene(s) affected and its function in craniofacial development. The thymus defects severely compromise cellular immunity, depriving the body of thymus-derived T cells and paving the way for severe infectious disease. Inadequate or missing parathyroid glands cause severe hypocalcemia (low blood calcium levels) and seizures. The great vessel abnormalities alter cardiac output and lead to compromised circulation to heart tissues. Cranial Bone and Dental Anomalies Defects in the timing of developmental events can cause premature fusion of cranial bones. Impairments of tooth development can result from interruptions of the developmental sequence at sev- eral different stages. 48 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Craniosynostoses Some craniofacial anomalies are associated with so- called master genes that orchestrate a program by which the embryo assumes its basic shape. Craniosynostosis, which occurs in approximately 1 out of 3,000 births, is one such anomaly. It results in the premature fusion of the cranial sutures, a danger- ous condition that puts pressure on the developing brain. A number of diseases and syndromes, includ- ing Crouzon's, Apert’s, Boston-type craniosynostosis, Pfeiffer's, and Saethre-Chotzen, share this anomaly, but differ in other features, which can include struc- tural defects such as webbing of the hands and feet as well as mental retardation. Boston-type craniosynos- tosis has been linked to MSX2, one of the master genes. Several of the other syndromes involve point mutations at one or another locus in genes that code for fibroblast growth factor receptors (FGFR 1, 2, and 3) (Howard et al. 1997, Meyers et al. 1996). Collectively, these genes are associated with cell reg- ulation, either through mediating growth factor effects or by serving as transcription factors (Cohen 1997). Hereditary Hypodontia or Anodontia Conditions of underdeveloped teeth (hypodontia) or their complete absence (anodontia) have been corre- lated with specific genes, such as MSX1 and LEFI. The complete absence of teeth alters the bony devel- opment of the mandible and maxilla. Amelogenesis Imperfecta and Dentinogenesis Imperfecta Amelogenesis imperfecta and dentinogenesis imper- fecta are linked to defects in structural genes that code for proteins essential to the development of tooth enamel (amelogenesis imperfecta) or dentin (dentinogenesis imperfecta). The teeth are weak and extremely sensitive to temperature and pressure. The ordinary forces of chewing are painful and can lead to further wear and pain. The enamel matrix genes include tuftelin, ameloblastin, and amelogenin; researchers have begun to link mutations in these genes with amelo- genesis imperfecta. Similarly, genes labeled DSP and DPP have been characterized for dentin matrix and are associated with the inheritance of dentinogenesis imperfecta. Discases and Disorders Craniofacial Defects Secondary to Other Developmental Disorders A number of genetic diseases occur in which cranio- facial defects are secondary to a more generalized structural or biochemical defect. Osteogenesis Imperfecta Inherited mutations of collagen genes lead to a num- ber of “brittle bone” diseases characterized by defects in mineralized tissues that form from a collagen-rich matrix. Osteogenesis imperfecta presents a spectrum of deficiencies that includes fragile bones, clear or blue sclera, deafness, loose ligaments, and painful dentinogenesis imperfecta-like chartges in the teeth. Epidermolysis Bullosa—Recessive Dystrophic Type The gene defect in epidermolysis bullosa—recessive dystrophic type—manifests as blisters or bullae that appear shortly after birth on skin areas following minor trauma. Mutations in keratin genes that con- tribute to the epithelial cell cytoskeleton have been correlated with this condition. The oral manifestations include both mucosal bullae and altered teeth. Altered teeth with hypoplas- tic enamel develop and exhibit an increased suscepti- bility to caries. Oral bullae develop from even the slightest mucosal trauma. The condition is painful and dangerous because of the constant risk that the bullae will become infected. Craniofacial Manifestations of Single-Gene Defects In many craniofacial defects, mutations within a sin- gle gene manifest as complex syndromes with varied organ and limb defects as well as facial anomalies. Ectodermal Dysplasias The ectodermal dysplasias (EDs) are a family of hereditary diseases first observed by Charles Darwin over a century ago. They involve defects in two or more tissues derived from the ectoderm—skin, hair, teeth, nails, and sweat glands. The ectodermal struc- tures fail to differentiate properly owing to altered epithelial-mesenchymal signaling. A gene, EDA, at an X-linked locus has been linked to the syndrome, and ongoing research is aimed at determining the func- tion of the gene and the molecular mechanism of the syndromes (Kere et al. 1996, Zonana et al. 1994). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 49 Diseases and Disorders More recently, investigators have discovered genes linked to autosomal (i.e., non-sex-linked) forms of ED, displaying both dominant and recessive inheri- tance (Monreal et al. 1999). Oral manifestations of the ectodermal dysplasias are associated with the teeth. Alterations in tooth development can include hypodontia, anodontia, and conically shaped teeth. The Waardenburg Syndrome The Waardenburg syndrome has been subdivided into several types. All involve a variety of abnormali- ties in the position and appearance of the nose and eyes, with pigment changes that may cause one eye to differ in color from the other. Other signs include deafness, a mildly protruding jaw. cleft lip and palate, and skeletal deformities (Reynolds et al. 1995). The syndrome is inherited in an autosomal dominant manner with complete penetrance and variable expression. Specific genes associated with this syn- drome are members of the homeobox family that reg- ulate the transcription of other genes: Waardenburg type 1 with PAX3, Waardenburg type 2 with MITF, 3q14.1, and Waardenburg type 3 with PAX3, 2q35 (Asher et al. 1996). Cleidocranial Dysplasia The inheritance of a regulatory gene defect in clei- docranial dysplasia leads to features that include delayed tooth eruption, supernumerary teeth, altered or missing collarbones, short stature, and possible failure of cranial suture closure. The exact mecha- nism of the associated gene, CBFA1, located on chro- mosome 6, has not been determined but appears to be essential for bone development. INJURY The common perception is that injuries are random occurrences that are unpredictable and hence unpre- ventable. In actuality, experts in the field make the point that there are no basic scientific distinctions between injury and disease (Haddon and Baker 1981). Injuries have been categorized as “intention- al” and “unintentional.” People identified as being at risk for certain injuries, as well as the causes of those injuries, can be targeted for appropriate prevention strategies. Such an approach is broadly applicable to sports, falls, and motor vehicle injuries (unintention- al) as well as to injuries caused by abusive and vio- lent behaviors (intentional). Injuries are a major public health problem, out- ranking cancer and heart disease as a leading cause of death in some age groups of the population (Kraus and Robertson 1992). Cranial injuries in particular are a leading cause of mortality. Oral-facial injuries can bring disfigurement and dysfunction, greatly diminishing the quality of life and contributing to social and economic burdens (Reisine et al. 1989). The leading causes of oral and craniofacial injuries are sports, violence, falls, and motor vehicle collisions (Kraus and Robertson 1992). Oral cavity injuries may also be caused by foreign objects in food (Hyman et al. 1993). Sports Craniofacial sports injuries occur not only in contact sports, but also in individual activities such as bicy- cling, skating, and gymnastics, especially on trampo- lines. Each sport predisposes its participants to a Spe cific array of extrinsic risk factors (Pinkham and Kohn 1991). These include physical contact, projec- tiles such as balls and pucks, and the quality of the playing field and equipment. In contact sports the absence of protective equipment such as headguards and mouthguards is a major risk factor. In a recent survey of school-aged children in organized sports, football was the only sport in which the majority of participants used mouthguards and headgear (Nowjack-Raymer and Gift 1996). There are intrinsic risk factors as well, relating to characteristics of the individual participant. These include age, sex, injury history, body size, aerobic fit- ness and muscle strength, central motor control, and general mental ability (Taimela et al. 1990). Falls Falls are a major cause of trauma to teeth, primarily to incisors. Unlike bone fractures, fractures of the crowns of the teeth do not heal or repair, and affect- ed teeth often have an uncertain prognosis. Problems may develop later due to damage to the pulp. Motor Vehicle Collisions The effects of motor vehicle collisions may range from minor and reversible effects to long-term med- ical, surgical, and rehabilitative consequences. Post- traumatic headaches and chronic oral-facial pain can occur. Neuromuscular and glandular damage may cause short- or long-term problems with chewing, swallowing, and tearing or result in facial tics or paralysis. 50 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Violence The family is the single most frequent locus of vio- lence in Western society. Domestic violence includes child abuse, spousal and elder abuse, and abuse of the disabled. Child abuse is of particular concern to the oral health community because 65 percent of cases involve head and oral-facial trauma (Mathewson 1993, Needleman 1986) and dentists are required to report suspected cases of child abuse. In the young child, head injury is the most common cause of death. Psychological trauma from abuse can result in sleep disturbances, eating disorders, devel- opmental growth failure in young children, and nerv- ous habits such as lip and fingernail biting and thumb sucking. Effects may also include chronic underachievement in school and poor peer relation- ships (Mathewson 1993). In abusive families, physi- cal neglect is commonplace, with inadequate provi- sion of basic needs, including medical and oral health care (Mathewson 1993). SELECTED CHRONIC AND DISABLING CONDITIONS Oral, dental, or craniofacial signs and symptoms play a critical role in autoimmune disorders such as Sjogren's syndrome and in a number of chronic and disabling pain conditions. Sjogren’s Syndrome Sjogren's syndrome is one of several autoimmune dis- orders in which the body's own cells and tissues are mistakenly targeted for destruction by the immune system. Like other autoimmune conditions, Sjogren's syndrome is more prevalent among women. The ratio of females to males affected is 9:1, with symptoms usually developing in middle age. There are an esti- mated 1 to 2 million individuals in the United States with Sjogren's syndrome (Talal 1992). The disease occurs in two forms. Primary Sjogren's involves the salivary and lacrimal (tear) glands. In secondary Sjogren's the glandular involve- ment is accompanied by the development of a con- nective tissue or collagen disease, most often rheumatoid arthritis, lupus erythematosis, scleroder- ma, or biliary cirrhosis. The glandular involvement causes a marked reduction in fluid secretion, resulting in xerostomia and xerophthalmia (dry eyes). The constant oral dry- ness causes difficulty in speaking, chewing, and swal- lowing; the dry eyes often itch and feel gritty. There Diseases and Disorders is no cure for Sjogren's, and patients often carry eye- drops and water bottles or saliva substitutes in an attempt to provide symptomatic relief. Clinically, the reduction in salivary flow changes the bacterial flora, which, in addition to the reduction in salivary pro- tective components, increases the risk of caries and candidiasis (Daniels and Fox 1992). Recent studies have indicated that there is a reduction in masticato- ry function (Dusek et al. 1996) and an increased prevalence of periodontal disease (Najera et al. 1997). In advanced stages the salivary glands may swell because of obstruction and infection or lym- phatic infiltration. In both forms of the disease, other systems may eventually become affected. Nasal, laryngeal, and vaginal dryness may occur, as well as abnormalities in internal organs (Oxholm and Asmussen 1996). Diagnosis is difficult in the early stages, and women often report that it took many years and con- sultations with many specialists before they received the correct diagnosis. Diagnosis involves demonstra- tion of specific antibodies in the blood characteristic of an autoimmune disorder, a labial (minor) salivary gland biopsy, and a series of eye tests to measure flow rate and tissue characteristics. Confirmatory tests include an evaluation of salivary flow and chemistry. Patients with Sjogren's syndrome are at some risk of developing diseases such as non-Hodgkin's lym- phoma; clinical data indicate that such lymphomas develop in 5 percent of patients with Sjogren's syn- drome (Moutsopoulos et al. 1978). Histological examination shows that immune cells infiltrate the glands and cluster around the secretory elements, resulting in a breakdown of the normal structure of the gland. The mechanisms by which this occurs involve immune-cell-mediated inflammation and stimulation of the salivary gland cells themselves to produce tissue-destructive mole- cules such as cytokines. Another hypothesis is that a viral infection of the glands may trigger the immune response that leads to autoimmunity, whereas genet- ic or regulatory alterations might lead to abnormali- ties in apoptosis (Fox and Speight 1996). In addition to saliva substitutes and artificial tears, some medications, such as pilocarpine and cevimeline, are prescribed to increase salivary flow from the residual healthy gland tissue, again provid- ing symptomatic relief only. The problems that develop in the other organ systems are also treated symptomatically. At advanced stages, steroids are employed intermittently to alleviate problems. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 51 Diseases and Disorders Acute and Chronic Oral-Facial Pain Since the nineteenth century, when two dentists, Horace Wells and Frederick Morton, demonstrated the analgesic powers of nitrous oxide and ether, oral health investigators have been recognized leaders in the field of pain management worldwide. Their analyses of the cells, pathways, and molecules involved in the transmission and modulation of pain have given rise to a growing variety of medications, often combined with other approaches, that can con- trol acute and chronic pain. Pain researchers today stress that chronic pain can become a disease in itself, causing long-term detrimental changes in the nerv- ous system. These changes may affect resistance to other diseases as well as effectively destroy quality of life. Most people have experienced acute pain involv- ing teeth and the oral tissues at one time or another. Atypical Facial Pain Atypical facial pain is characterized by a continuous dull ache on one or both sides, most frequently in the region of the maxilla (the upper jaw). The pain tends to be episodic and is aggravated by fatigue, worry, or emotional upset. It is often accompanied by pain elsewhere in the body and depression. Once a dental cause can be ruled out, pain resolution depends on the successful use of antidepressants, psychotherapy, or both (Tyldesley and Field 1995). Tic Douloureux The oral-facial region is also subject to pain that can be paroxysmal or continuous along a distinct nerve distribution. The most frequently encountered of these oral facial neuralgias is tic douloureux, or trigeminal neuralgia, a disease of unknown etiology affecting one, two, or all three branches of the trigeminal nerve. The pain is highly intense and of a stabbing nature, and lasts for a few seconds. This transient attack may be repeated every few minutes or several hours. There may be no precipitating fac- tor, or it may occur in response to a gentle touch or a breeze wafting across the face—a condition experts call allodynia, the feeling of pain in response to a nor- mally nonpainful stimulus. On other occasions, there may be a specific trigger zone. Although spontaneous remission for weeks or months may occur, it is rarely permanent. Given the unknown, unpredictable nature of tic douloureux, it is not surprising that fear of pain comes to dominate these patients’ lives, as they avoid doing anything that might trigger an attack. Trigeminal neuralgia generally occurs in later life, but also occurs in younger individuals affected uv N by multiple sclerosis, where it is assumed to be asso- ciated with lesions (multiple sclerosis “plaques”) in the brain stem. Medical treatment depends largely on the use of a drug that has become a virtual specific, the antiepileptic drug carbamazepine. For those patients with no consequential adverse effects, it can control the disease. An alternative for chronic suffer- ers is the surgical removal of a small vein or artery that may be exerting pressure on the nerve root or the selective destruction of the nerve fibers them- selves using chemical or electrical methods. In many cases, these procedures can produce complete relief from pain (Tyldesley and Field, 1995). Temporomandibular Disorders Various etiological factors, including trauma, can give rise to pain and dysfunction in the temporo- mandibular joint and surrounding muscles, condi- tions collectively called temporomandibular disor- ders (TMDs). The pain may be localized or radiate to the teeth, head, ears, neck, and shoulders. Abnormal grating, clicking, or crackling sounds, known as crepitus, in the joint often accompany localized pain. Pain is also found in response to clinical palpation of the affected structures. TMDs are common, occur- ring in as many as 10 million Americans. Although surveys indicate that both sexes are affected, the majority of individuals seeking treatment are women of childbearing age, a phenomenon suggesting that hormonal influences should be investigated. ' Several factors can contribute to the onset or exacerbation of TMD symptoms. These factors include certain developmental anomalies; injury to the jaw from accidents or abuse; oral habits that greatly stress the joint and musculature, such as tooth grinding (bruxism); jaw manifestations of sys- temic diseases such as fibromyalgia and arthritic dis- eases; and some irreversible treatments for initial signs and symptoms. The multiplicity of factors that may cause or con- tribute to TMDs has unfortunately led to a multiplic- ity of treatments. Most of these treatments have not been tested in randomized controlled clinical trials. During the 1970s and 1980s, many individuals underwent surgery, which proved unsuccessful in many cases. Leading investigators have proposed standard- ized research diagnostic criteria to clarify the kinds of pathology that can give rise to TMDs and to classify the most common forms of TMDs. Such criteria could be used in designing clinical trials and could ultimately lead to better diagnostics, treatments, and prevention. The criteria use two dimensions or axes: ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL axis I delineates various forms of joint or muscle pathology; axis II explores pain-related disability and psychological status. The approach requires detailed clinical examinations and patient histories (Dworkin and LeResche 1992). A MIRROR, A MODEL, AND A BETTER UNDERSTANDING OF DISEASES AND DISORDERS Studying the diseases and disorders that affect cran- iofacial tissues can provide scientists with models of systemic pathology. Because some craniofacial tis- sues, such as bones, mucosa, muscles, joints, and nerve endings, have counterparts in other parts of the body and these tissues are often more accessible to research analysis than deeper-lying tissues, researchers studying craniofacial tissues can gain valuable insights into how cancer develops, the role of inflammation in infection and pain, the effects of diet and smoking, the consequences of depressed immunity, and the changes that can arise from a mutated gene. Other craniofacial tissues—teeth, gingiva, tongue, salivary glands, and the organs of taste and smell—are unique to the craniofacial complex. Study of the diseases affecting these tissues has revealed a wealth of information about their special nature as well as the molecules and mechanisms that normally operate for the protection, maintenance, and repair of all the oral, dental, and craniofacial tissues. When factors perturb these nurturing elements, the oral health scale can tip toward disease. When those fac- tors stem from systemic diseases or disorders, the mouth can sometimes mirror the body’s ill health. Similarly underscoring the connection between oral and general health are studies suggesting that poor dental health, mainly due to chronic dental infec- tions, may heighten the risk for both cardiovascular disease and stroke independently of factors such as social class and established cardiovascular risk fac- tors (Grau et al. 1997). The interplay between cran- iofacial and systemic health and disease has become a lively focus of interest and research, as discussed in Chapter 5. Current research on developmental disorders and diseases affecting the craniofacial complex is facilitating and complementing the intense effort of the Human Genome Project to map and sequence all 100,000 genes. This goal should be accomplished early in the twenty-first century and should begin to yield information on the genetic program that gov- erns morphogenesis, organ development, and disease etiology and pathogenesis, with the potential for Diseases and Disorders interventions that can correct errors in the program. The continued sequencing of the genomes of micro- bial pathogens involved in oral diseases also should lead to new diagnostic and preventive approaches. FINDINGS e Microbial infections, including those caused by bacteria, viruses, and fungi, are the primary cause of the most prevalent oral diseases. Examples include dental caries, periodontal diseases, herpes labialis, and candidiasis. e The etiology and pathogenesis of diseases and disorders affecting the craniofacial structures are multifactorial and complex, involving an interplay among genetic, environmental, and behavioral factors. e Many inherited and congenital conditions affect the craniofacial complex, often resulting in dis- figurement and impairments that may involve many body organs and systems and affect millions of chil- dren worldwide. e Tobacco use, excessive alcohol use, and inappro- priate dietary practices contribute to many diseases and disorders. In particular, tobacco use is a risk fac- tor for oral cavity and pharyngeal cancers, periodon- tal diseases, candidiasis, and dental caries, among other diseases. # Some chronic diseases, such as Sjogren's syn- drome, present with primary oral symptoms. e Oral-facial pain conditions are common and often have complex etiologies. REFERENCES Aaronson SA. 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Wray D, Graykowski EA, Notkins AL. Role of mucosal injury in iniuating recurrent aphthous stomatitis. Br Med J (Clin Res Ed) 1981 Dec 12:283(6306):1569- 70. Zonana J, Jones M, Clarke A, Gault J, Muller B, Thomas NS. Detection of de novo mutations and analysis of their origin in families with X linked hypohidrotic ectodermal dysplasia. J Med Genet 1994 Apr;31(4): 287-92. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 59 FOO The Magnitude of the Problem The range of oral, dental, and craniofacial diseases and conditions that take a toll on the U.S. population is extensive. This chapter provides highlights of dis- eases and conditions affecting the U.S. population using available national and state data to describe the burden of disease in the United States. To capture the dimensions and extent of these diseases and condi- tions, the data are presented where possible by demo- graphic measures such as race/ethnicity, sex, age, education, and economic status. Statistics and trends are presented for each of the six categories of oral dis- eases and disorders whose etiology and pathogenesis are described in Chapter 3: dental and periodontal infections, oral and pharyngeal cancers, mucosal infections and conditions, developmental disorders, intentional and unintentional injuries, and chronic and disabling conditions. Included are conditions as common as dental caries and periodontal diseases as well as relatively rare clefting syndromes. Also men- tioned are conditions that are more common in cer- tain demographic subpopulations—for example, Sjogren's syndrome and temporomandibular disor- ders, which are more common in women, and injuries, which are more common in men. (See Box 4.1 for a glossary of terms used in this chapter.) There is no single measure of oral health or the burden of oral diseases and conditions, just as there is no single measure of overall health or overall dis- ease. As a result, this chapter assembles clinical and epidemiologic measures for specific conditions affecting the craniofacial structures. Note too that the chapter presents an incomplete picture. State-specif- ic data on oral diseases are extremely limited. There is a paucity of national data on rare conditions as well as on the health of selected populations and their subgroups. Some characteristics and unique needs of these populations are highlighted, and a number of questions raised. More extensive analyses of the differences among racial/ethnic, sex, and income groups are warranted. The relationship of oral health to the use of dental services is described. However, the effects of health care visits and of spe- cific services rendered need further study. Most of the data in the figures and tables pre- sented in this chapter are derived from large, nation- ally representative surveys of the U.S. civilian, nonin- stitutionalized population. These include complex sample surveys, such as the National Health and Nutrition Examination Survey (NHANES), which use a sample of individuals selected with known probability to estimate the prevalence of particular characteristics and conditions in the nation as a whole. The multipurpose NHANES provides data on the frequency of the most common oral diseases and conditions. The most recent survey, NHANES Ill, was conducted by the National Center for Health Statistics (NCHS) of the Centers for Disease Control between 1988 and 1994. Trained interviewers gath- ered demographic, health, and related data from eli- gible households. Selected persons in these house- holds were invited to a mobile examination center, where they underwent multiple health assessments, including an oral examination by a trained dentist (NCHS 1996). Related surveys such as the National Health Interview Survey (NHIS) also use complex survey sampling and household interviews to obtain health information about the U.S. population (Kovar 1989), The NHIS conducted in 1989 included data on oral-facial pain conditions, several of these sur- veys have captured data on dental visits. The most extensive dental utilization survey that provides demographic and socioeconomic data and data on reasons for not visiting a dentist was conducted in 1989. Surveys conducted by the National Institute of Dental and Craniofacial Research of a probability sample of U.S. schoolchildren in 1979-80 and 1986- 87 (Snowden and Miller-Chisholm 1992) used ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 61 The Magnitude of the Problem BOX 4.1 Glossary Complex sample survey. A survey of individuals selected with known probability to estimate the prevalence and/or extent of particular characteristics and conditions. dfs. The count (number) of decayed (untreated) or filled primary tooth surfaces per person. dft. The count (number) of decayed (untreated) or filled primary teeth per person. DMES. The count (number) of decayed (untreated), missing (due to caries), or filled permanent tooth surfaces per person. DMFT. The count (number) of decayed, missing (due to caries),’ or filled permanent teeth per person. Epidemiology. The study of the distribution and determinants of disease frequency in human populations. Incidence. The number of cases of a disease, or condition, that occurs during a specified period of time. Inddence rate. The number of cases of a disease, or condition, that occurs during a specified period of time, per specified unit of population. Loss of periodontal attachment.’ The distance from the cementoenamel junction to the bottom of the gingival sulcus. Mortality rate. The number of deaths during a stated period of time divided by the total number of persons in the population. Prevalence. The number of existing cases of a disease, or condi- tion, at a designated point in time. Prevalence rate. The number of existing cases of a disease, or condition, at a designated point in time, per the number of per- sons in the population. Relative survival rate. Survival rates for persons with a partic- ular disease or condition corrected for the expected occurrence of death in persons in the age group. Survival rate. The number of persons surviving over a specified time period divided by the number of persons alive at the start of the time period. ‘In the Third National Health and Nutrition Examination Survey, the M (miss- ing) component of the DMFT (S) index reflects teeth (or tooth surfaces) miss- ing because of dental caries or periodontal disease. Teeth missing because of trauma, orthodontic treatment, or other non-disease-related reasons were not scored. 2 Periodontal disease status is assessed by measuring the distance from the gingival margin (FGM) to depth of the gingival sulcus, or pocket depth, and the distance from the gingival margin to the cementoenamel junction (FGM- CEJ).A third measure, loss of attachment, is determined by calculating the dif- ference between pocket depth and the FGM-CEJ distance. Loss of attachment is important because it serves as a measure of how much support from the tissues surrounding the tooth has been lost. ORAL HEALTH IN AMERICA: A REP similar oral examination procedures as in NHANES. Because school attendance is high in the United States, these surveys are considered representative of noninstitutionalized children throughout the United States and are used in this chapter. Record-based surveys are another approach to obtaining health data for the nation as a whole or for selected broad areas. Mortality statistics are obtained by determining the number of deaths in the United States and dividing that figure by the total U.S. pop- ulation as determined from U.S. Census data (Kovar 1989). Cancer statistics are derived from population- based cancer registries in selected large geographic areas of the United States usirig reports of cancer occurrences from hospitals, doctors, and laborato- ries. This data system, maintained by the National Cancer Institute, is called the Surveillance, Epidemiology, and End Results program (Ries et al. 1999), Birth certificate registries in geographic areas and surveys of health care facilities provide valuable snformation from record-based systems about other aspects of oral and craniofacial health such as birth defects (Schulman et al. 1993). The Centers for Disease Control and Prevention’s Behavioral Risk and State Surveillance System provides essential state data on edentulousness (Tomar 1997). In selected cases, survey findings other than from national prob- ability surveys are used. State-specific data are pro- vided for those conditions for which there are data from most states—that is, cancer mortality statistics and self-reports of edentulism. - Economic status is derived from annual income data. Unless otherwise stated, “poor” is defined in this chapter as an annual income below the U.S. poverty level. For both national and other surveys, the race and ethnicity terms used in this report are consistent with the terms used in the supporting documentation as referenced in the text and cited in the reference list. Available national data for most conditions are limited primarily to Hispanic, non- Hispanic black, and non-Hispanic white populations, due to the sampling design of the national surveys. The NHANES III oversampled Mexican Americans, so the data from that survey are available for this sub- population of Hispanics. ORT OF THE SURGEON GENERAL WHO HAS WHAT DISEASES AND CONDITIONS? Dental Caries, Periodontal Diseases, and Tooth Loss Dental Caries Dental caries is one of the most common childhood diseases. In this section, decayed refers to teeth with caries that have not been treated. The term filled refers to treated caries. Dental caries refers to both decayed and filled teeth. Among 5- to 17-year-olds, dental caries is more than 5 times as common as a reported history of asthma and 7 times as common as hay fever (Figure 4. 1). Prevalence increases with age. The majority (51.6 percent) of children aged 5 to 9 years had at least one carious lesion or filling in the coronal portion of either a primary or a permanent tooth. This proportion increased to 77.9 percent for 17-year-olds and 84.7 percent for adults 18 or older. Additionally, 49.7 percent of people 75 years or older had root caries affecting at least one tooth (NCHS 1996, NHANES Ill). Despite progress in reducing dental caries, indi- viduals in families living below the poverty level experience more dental decay than those who are economically better off. Furthermore, the caries seen in these individuals is more likely to be untreated than caries in those living above the poverty level (Figure 4.2); more than one third (36.8 percent) of poor children aged 2 to 9 have one or more untreat- ed decayed primary teeth, compared to 17.3 percent of nonpoor children. In addition to poverty level, the proportion of teeth affected by dental caries also varies by age and race/ethnicity. Poor Mexican American children aged | IGURE 4.1 Dental caries is one of the most common diseases among 5- to 17-year-olds Caries 58.6 Asthma Hay fever Chronic bronchitis T T T T T 1 0 10 20 30 40 50 60 70 Percentage of children and adolescents aged 5 to17 Note: Data include decayed or filled primary and/or decayed, filled, or missing permanent teeth. Asthma, chronic bronchitis, and hay fever based on report of household respondent about the sampled S- to 17-year-olds. Source: NCHS 1996. The Magnitude of the Problem > to 9 have the highest number of primary teeth affected by dental caries (a mean of 2.4 decayed or filled teeth) compared to poor non-Hispanic blacks (mean 1.5) and non-Hispanic whites (mean 1.9). Among the nonpoor, Mexican American 2- to 9-year- olds have the highest number of affected teeth (mean 1.8), followed by non-Hispanic blacks (1.3) and non- Hispanic whites (1.0). There are also differences by race/ethnicity and poverty level in the proportion of untreated decayed teeth for all age groups. Poor Mexican American chil- dren aged 2 to 9 have the highest proportion of untreated decayed teeth (70.5 percent), followed by poor non-Hispanic black children (67.4 percent) (Figure 4.3). Nonpoor children have lower propor- FIGURE 4.2 Ahigher percentage of poor people than nonpoor have at least one untreated decayed tooth 50 » 40 Wi Poor s 344 Bi Nonpoor s 30 wv Z £ 20 . g "9 2 10 3 5to 17 (primary 18+ (permanent and permanent teeth) teeth only) 209 (primary teeth only) . Age Source: NCHS 1996. | IGURE 4.3 Poor children aged 2 to 9 in each racial/ethnic group have a higher percentage of untreated decayed primary teeth than nonpoor children 80 < 70.5 z= 70 oz Bo 80 i 5S 50 Ze se” Z= 2s 30 Se Se 20 gs 37 10 & 0 — ae Non-Hispanic black Mexican American Non-Hispanic white @ Poorchildren Mf Nonpoor children Source: NCHS 1996. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 63 The Magnitude of the Problem tions of untreated decayed teeth, although the group with the lowest proportion (non-Hispanic whites) still has an average of 37.3 percent of decayed teeth untreated. Poor adolescents aged 12 to 17 in each racial/eth- nic group have a higher percentage of untreated decayed permanent teeth than the corresponding nonpoor adolescent group (Figure 4.4). Poor Mexican American (47.2 percent) and poor non- Hispanic black adolescents (43.6 percent) have more than twice the proportion of untreated decayed teeth than poor non-Hispanic white adolescents (20.7 per- cent). For nonpoor adolescents the proportion of untreated decayed permanent teeth is highest in non- Hispanic black adolescents (41.7 percent)—a pro- portion only slightly lower than for this group's poor counterparts (43.6 percent). The mean number of permanent teeth affected by dental caries (decayed or filled) for this age group is similar among Mexican Americans (2.7), non-Hispanic whites (2.5), and non-Hispanic blacks (2.3). As income level increases, the percentage of adolescents with decayed teeth decreases and the proportion of decayed teeth that have been filled increases (Vargas et al. 1998). Adult populations (aged 18 and older) show a similar pattern, with the proportion of untreated decayed teeth higher among the poor than the non- poor (Figure 4.5). Regardless of poverty level status, adult non-Hispanic blacks and Mexican Americans have higher proportions of untreated decayed teeth than their non-Hispanic white counterparts. FIGURE 4.4 Poor children aged 12 to 17 in each racial/ethnic group have a higher percentage of untreated decayed permanent teeth than nonpoor children 50 : > w me N Ww Ww om Oo Mm j l I | = in Percentage of decayed permanent teeth that are untreated per person = ou Pe | L L Non-Hispanic black Mexican American Non-Hispanic white BE Poor children Hi Nonpoor children Source: NCHS 1996. Improvements have been noted over the past 25 to 30 years with regard to dental caries. Among most age groups, the average number of teeth per person affected by dental caries has decreased, and the aver- age number of teeth per person that show no signs of infection, as well as the proportion of the population that is caries-free, has increased. Since 1971-74, major increases have been noted in the percentage of children and adolescents aged 5 to 17 who have never experienced dental caries in their permanent teeth. Younger adults have experi- enced a decline in dental caries during this time period, as measured by the average number of teeth without decay or fillings (Figure 4.6). These trends are not found among those 55 to 74 years of age. FIGURE 4.5 Poor adults aged 18 and older havea higher percentage of untreated decayed teeth than nonpoor adults 46.7 46.9 suas Li Ww Qo wm i Percentage of decayed teeth that are untreated per person —_ = ouM oOo MM \ | i L Non-Hispanic black Poor adults Mexican American Non-Hispanic white g@ Nonpoor adults Source: NCHS 1996. FIGURE 4.6 Since 1971-74, the average number of permanent teeth without decay or fillings has increased among 18- to 54-year-olds 20 19.6 18 16 15.7 14 oo 135 2 12.0 6 79 65 Age > 18-34 “tie 35-54 ae 55-64 —@ 65-74 Average number of sound permanent teeth per person > HD Co 1971-74 1988-94 Survey year Sources: NCHS 1975, 1996. 64 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The number of untreated decayed teeth per per- son across all age groups has also declined. Periodontal Diseases The presence of periodontal disease is measured clin- ically in several ways, one of which is by calculating the loss of periodontal attachment. Figure 4.7 shows that most adults 25 years and older have at least 2 mm or more loss of attachment. The disease is more serious as the amount of attachment loss and number of tooth sites affected increase. More severe disease can be defined as having 4 mm or more loss of attach- ment in at least one site. The percentage of adults with 6 mm or more loss of attachment at one or more sites increases at older age groups, with 19.0 percent of 55- to 64-year-olds and 23.4 percent of 65- to 74- The Magnitude of the Problem year-olds having this amount of loss or more. Figure 4.8 displays these data ina different format and shows that a small but increasing percentage of the popula- tion at each older age group has severe disease. At all ages, men are more likely than women to have at least one tooth site with a 6 mm or more loss of attachment (Figure 4.9). In addition to age and sex, the prevalence of periodontal loss of attachment also varies by racial/ethnic group (Figure 4.10). A higher percentage of non-Hispanic black persons at each age group have at least one tooth site with 6 mm or more of periodontal attachment loss as compared to other groups. Within each racial/ethnic group, the highest percentage affected is found among individu- als 70 years and older. At every age, a higher propor- tion of those at the lowest socioeconomic status FIGURE 4.7 The proportion of adults with at least one site 4mm or more, and 6 mm or more increases with age 100 : 89.8 86.4 80 60 40 Percentage of people 20 18-24 25-34 35-44 45-54 Age group 55-64 Sources: Adapted from NCHS 1996, Burt and Eklund 1999. with loss of periodontal attachment of 2 mm or more, 94.5 Loss of attachment “= 2mm or more 4 mmormore @ 6mm or more FIGURE 4.8 Although older adults have more periodontal attachment loss than younger adults, severe loss is seen among a small percentage of individuals at every age 100 90 Age 80 > 18-44 45-64 ” ~*~ 65+ 60 50 30 20 10 Cumulative percentage of people 11 3 5 Loss of periodontal attachment (mm) 7 9 Sources: Adapted from NCHS 1996, Burt and Eklund 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON FIGURE 4.9 Males are more likely than females to have at least one tooth site with 6 mm or more of periodontal loss of attachment : % 35.1 a 2 30 a. 5 25 2 20 5 15 5 10 5 0 75+ 25-34 35-44 45-54 55-64 65-74 Age group i Female @ Male Sources: Adapted from NCHS 1996, Burt and Eklund 1999. GENERAL 65 The Magnitude of the Problem (SES) level have at least one site with attachment loss of 6 mm or more, compared to those at higher SES levels (Figure 4.11) (Burt and Eklund 1999).' Gingivitis as measured by gingival bleeding, a sign of inflammation, is more evident among Mexican Americans (63.6 percent) than among non- Hispanic blacks (55.7 percent) and non-Hispanic whites (48.6 percent) (Albandar et al. 1999). Early-onset periodontitis, a severe, rapidly pro- gressive disease occurring in individuals under age FIGURE 4.10 Non-Hispanic blacks are more likely than other groups to have at least one tooth site with 6 mm or more of periodontal loss of attachment 50 45 40 35 30 25 Percentage of people 50-69 Age group 70+ Race/ethnicity Wi Non-Hispanic black Source: NCHS 1996. Mexican American Mf Non-Hispanic white 35, has been reported to be 4 times more common in males than in females (Lée and Brown 1991); among 13- to 17-year-olds, it has been found to be highest among African Americans (10.0 percent), as com- pared with Hispanics (5.0 percent) and whites (1.3 percent) (Albandar et al. 1997). Tooth Loss and Edentulism Although teeth are lost for a number of reasons, including trauma, orthodontic treatment, and removal of third molars (wisdom teeth), most teeth are lost because of periodontal disease or dental caries (Phipps and Stevens 1995, Neissen and Weyant 1989). By age 17, mote than 7.3 percent of US. children have lost at least one permanent tooth because of caries; by age 50, Americans have lost an average of 12.1 teeth, including the third molars. Men and women are nearly equally likely to be edentulous. Overall, a higher percentage of individu- als living below the poverty level are edentulous than are those living above (Figure 4.12). Individuals with incomes equal to or above twice the poverty level have a rate of edentulism of 6.9 percent. This rate is less than half the rate for those with incomes below twice the poverty level (14.3 percent). Although the overall rate of edentulism for adults 18 and older is approximately 10 percent (9.7 per- cent), the rate increases with age, so that about a third (33.1 percent) of those 65 and older are edentulous. Comparisons across race/ethnicity for the population 18 years and older indicate that the edentulous rate FIGURE 4.11 The percentage of adults w greater among persons of low socioeconomic status at all ages 40 ’ 35 s 30 ae = 25 ° 2 20 cs = 15 & 5 10 i 6 5 “9, ry. 0 = ni ae 18-24 25-34 35-44 45-54 Age group Socioeconomic status Low @ Middle © MM High Sources: Adapted from NCHS 1996, Burt and Eklund 1999. ith at least one tooth site with 6 mm or more of periodontal attachment loss is 37.8 36.2 75+ en Mn this section, income levels are defined as low (less than 185 to 350 percent of the poverty level), and high (350.1 percent 0 66 ORAL HEALTH IN AMERICA: A REPORT OF TH percent of the U.S. poverty level or below), middle (185.1 percent f the poverty level or higher). E SURGEON GENERAL for non-Hispanic whites is 10.9 percent, for non- Hispanic blacks, it is 8.0 percent, and for Mexican Americans, 2.4 percent. Non-Hispanic whites, both poor and nonpoor, have the highest rates of eden- tulism compared to non-Hispanic blacks and \exican Americans. Of the three population groups, Mexican Americans are the least likely to lose all of their teeth, and the proportion of Mexican Americans who are edentulous varies only slightly by economic status. A lower proportion of U.S. adults have lost all their natural teeth now than was the case two decades ago (Figure 4.13). The decline is most pro- nounced at older ages. Edentulism is one of a few conditions for which state-specific data exist. These data reveal a wide variation in the percentages of the population aged 65 and older who have no teeth, from a low of 13.9 percent in Hawaii to a high of 47.9 percent in West Virginia; this is more than a threefold difference (Table 4.1) (Tomar 1997). Reasons for these differ- ences are unknown at this time. Oral and Pharyngeal Cancers and Precancerous Lesions Oral and Pharyngeal Cancers Every year, about 1.2 million people develop cancer in the United States (based on 2000 estimates). Sites FIGURE 4.12 Complete tooth loss varies by race/ethnicity and poverty status: a higher percentage of poor and nonpoor non-Hispanic white adults (18 and older) have no teeth compared with non-Hispanic blacks and Mexican Americans 18.7 Percentage of people Non-Hispanic black Mexican American BH Poor adults Non-Hispanic white "1 Nonpoor adults The Magnitude of the Problem in the oral cavity and pharynx (throat) account for about 30,200 cases, or 2.4 percent of all cancers, and about 7,800 Americans die from these cancers each year (ACS 1999). The life of each person with these cancers is shortened by an average of 16.5 years. The median age at diagnosis of oral and pharyngeal can- cer is 64, and the rate of occurrence increases with age. More than 95 percent of oral cancers occur in individuals aged 35 and older (Ries et al. 1999). The overall 5-year survival rate for people with oral and pharyngeal cancers is 52 percent, which is worse than that for—among others—cancers of the prostate, corpus and uterus, breast, bladder, larynx, cervix, colon, and rectum in both blacks and whites (Ries et al. 1999). People with oral cancers detected at an early stage have a 5-year survival rate of 81.3 percent; however, only 35 percent of individuals with oral and pharyngeal cancers are diagnosed at an early stage. The 5-year survival rate drops to 21.6 percent FIGURE 4.13 The percentage of people without any teeth has declined among adults over the past 20 years 50 45.6 oe 40 s 2 3 33.3 Age ‘s -_ ra 28.6 65-74 £ Ht 55-64 = 20 20.1 435-54 & 18-34 1971-74 Survey years Sources: NCHS 1975, 1996. Source: NCHS 1996. TABLE 4.1 Five states with highest and lowest percentages of edentulous persons aged 65 and older States with Highest Percentage States with Lowest Percentage Percentage Percentage State Edentulous State Edentulous West Virginia 47.9 Hawaii 13.9 Kentucky 44.0 California 16.2 Louisiana 43.0 Oregon 16.5 Arkansas 39.2 Arizona 18.5 Maine 37.8 Wisconsin 19.4 Source: Tamar 1997. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 67 The Magnitude of the Problem among people diagnosed with advanced-stage can- cers (Ries et al. 1999). Compared to patients with other types of cancer, oral and pharyngeal cancer patients who survive have the highest rate of devel- opment of new cancers in the mouth or in other parts of the body (Winn and Blot 1985). Incidence rates for oral and pharyngeal cancers are higher for black individuals than for whites: 12.5 cases versus 10.0, respectively, per 100,000 people each year. In the United States, Asians and Pacific Islanders (7.9 per 100,000), American Indians and Alaska Natives (6.4 per 100,000), and Hispanics (5.8 per 100,000) have lower incidence rates than whites and blacks (Wingo et al. 1999). Figure 4.14 provides incidence rates for selected racial/ethnic groups by sex. Males have higher inci- dence rates than females; specifically, they are 2.6 times more likely to develop oral and pharyngeal cancers than women (Ries et al. 1999). The incidence rates of oral and pharyngeal cancers for black males are 39.6 percent higher than for FIGURE 4.14 Black White Asian and Pacific Islander American Indian and Alaska Native Hispanic? Males have higher incidence rates of oral and pharyngeal cancers than females 20.8 white males (20.8 versus 14.9, respectively, per 100,000 males per year). Rates for black and white females are the same (6.0 per 100,000 females per year) (Ries et al. 1999). Oral and pha- ryngeal cancers are the seventh most common cancer among white males and the fourth most frequently diagnosed cancer among black males (Figure 4.15) (Wingo et al. 1999). : Female @ Male Rate per 100,000 Note: Age adjusted to the 1970 U.S. standard, aData are unavailable for Hispanic females. Sources: Adapted from Wingo et al. 1999; SEER Program, 1990-96, Ries et al. 1999. 5 As for many other cancer sites, the overall 5-year survival rate for oral and pharyngeal can- cers is lower for blacks than for whites: 34 versus 56 percent FIGURE 4.15 and the fourth most common in black males Prostate gland [ior age ~ Lung & bronchus Fane Colon/rectum Urinary bladder Ea Lymphomas Fg Melanoma of skin Oral cavity & pharynx Leukemia 140 Kidney/renal Fl 12.6 Pancreas F% 9.8 4 - T 0 T T 1 White males Note: Age adjusted to the 1970 U.S. standard. Sources: Adapted from Wingo et al. 1999; SEER Program, 1990-96, Ries et al. 1999. t 50 100 150 200 250 Cancers of the oral cavity and pharynx are the seventh most common cancers in white males Prostate gland & Lung & bronchus eae 112.3 Colon/rectum 58.1 Oral cavity & pharynx a 20.8 Stomach iF 17.1 Urinary bladder q 15.6 Lymphomas a 15.4 Pancreas a 14.9 Kidney/renal y 145 Esophagus FT] 135 T T 1 T T 0 50 100 150 200 250 Black males Incidence rate per 100,000 R ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL (Ries et al. 1999) (Figure 4.16). However, only 19 percent of blacks with oral and pharyngeal cancers are diagnosed when the cancer is at the local, and more easily treatable, stage, compared to 38 percent for whites (Figure 4.17). At every stage of diagnosis, the survival rate for blacks is lower than for whites (Figure 4.18). The occurrence of cancers in specific sites with- in the oral cavity and pharynx varies by sex and race/ethnicity. A relatively rare subtype of pharyngeal cancer, nasopharyngeal cancer, occurs more often in American males and females of Chinese descent than among other racial/ethnic groups (Miller et al. 1996). Blacks are twice as likely as whites to develop cancers of the pharynx: 6.0 and 2.9 per 100,000 per year, respectively (Ries et al. 1999). Individuals with can- FIGURE 4.16 Five-year relative survival rates for selected cancers for whites and blacks Testis CEeoonae area ENSEENESER TEE rd 83 96 Thyroid Fai De aa we Wetad Mavanlaa easel a Prostate (Ggaaaialainnannnn UE EEREMNETS 84 93 Melanomas of skin [anal mapremreerercel 68 2 Breast (females) aa encores 7 | 7 Corpus & uterus, NOS ia &s Hodgkin's [aaa Urinary bladder i Cervix uteri Taam - Larynx eeeoeeieaneal Colon (oeeeneeeaiaieneaniae Kidney/renal (ina PETS Rectum Oral cavity & pharynx fia Non-Hodgkin's [i———aaan/an 41 Ovary (eae 47 Leukemias —iaadiaeieanll 33 Brain & NOS (ieee Multiple myeloma fala eee 3) Stomach Smee 2? Lung & bronchus fai Esophagus [jibe Liver & intrahepatic 6 Pancreas j i 5 10 2 30 4 50 60 70 80 90 100 Five-year relative survival rates @ White patients Note: NOS = not otherwise specified. Source: Kosary 1996. Black patients The Magnitude of the Problem cers of the pharynx generally have a worse survival rate than those with cancers in oral cavity sites: 5- year pharyngeal cancer survival rates range from 53.3 to 29.5 percent, depending on the subsite, whereas oral cavity cancer survival rates range from 94.3 to 48.3 percent. The incidence of lip cancer, a highly treatable cancer, is more common in. whites than among blacks (1.2 per 100,000 persons per year compared to 0.1). Overall, the incidence rate for oral cavity and pharyngeal cancers is decreasing, with an estimated annual percentage decrease of 0.5 percent per year between 1973 and 1996. There are wide variations in the incidence of site-specific cancers. The largest ’ FIGURE 4.17 Blacks are less likely to be diagnosed with a localized oral or pharyngeal cancer than whites 60 54 w Oo i White patients 33 Black patients 7 Oo tm o Percentage of people diagnosed 3 ay Oo Distant Unstaged Stage at diagnosis Source: Adapted from SEER Program, 1989-95, Ries et al. 1999. Localized Regional FIGURE 4.18 At every stage of diagnosis, the 5-year relative survival rates for blacks with oral and pharyngeal cancers are lower than for whites 90 WE White patients “3 Black patients Percentage of people surviving 5 years mm Ww WY & Wm an oma oo Oo oo lO Qo Localized Regional Distant Unstaged Stage at diagnosis Source: Adapted from SEER Program, 1989-95, Ries et al. 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 69 The Magnitude of the Problem annual declines in incidence were noted for lip can- cer (-3.4 percent per year between 1973 and 1996) (Ries et al. 1999). In contrast, the incidence of tongue cancer, the most common form of oral and pharyngeal cancer, may be increasing among young men (Day et al. 1994). Although overall mortality rates for oral and pha- ryngeal cancers declined by 1.6 percent per year between 1973 and 1996, the 5-year survival rate for individuals with oral and pharyngeal cancers has shown no improvement for the past 25 years (Ries et al. 1999). Mortality statistics by state allow for analysis of deaths due to oral cavity and pharyngeal cancers. Table 4.2 highlights the wide variation in mortality found in the country. The highest rate is in the District of Columbia—6.7 per 100,000 population, this is nearly 5 times the lowest rate, 1.4 in Utah. Again, reasons for this variation need to be studied (Ries et al. 1999). Tobacco-related Lesions — Tobacco use has been estimated to account for over 90 percent of cancers of the oral cavity and pharynx (Peto et al. 1995) and thus represents the greatest single preventable risk factor for oral cancer. Both smoking and spit (smokeless) tobacco (moist snuff and chewing tobacco) are associated with a number of other oral conditions, including oral mucosal lesions, that may progress to oral cancer (Silverman 1998). One type of tobacco-related lesion‘is seen in peo- ple who use spit tobacco. A national survey of U.S. schoolchildren in 1985-86 showed that 6.1 percent of males and 0.1 percent of females used spit tobacco. The survey also showed that 34.9 percent of current snuff users aged 12 to 17 and 19.6 percent of current adolescent chewing tobacco users had a spit tobacco lesion (Figure 4.19) (Tomar et al. 1997). The preva- TABLE 4.2 Five states with highest and lowest oral and pharyngeal cancer mortality rates States with Highest Rates States with Lowest Rates Mortality Rate per Mortality Rate per State 100,000 Population State 100,000 Population District of Columbia 67 Minnesota 2.0 Delaware 4.0 Wyoming 2.0 South Carolina 3.9 Colorado 2.0 Louisiana 35 North Dakota 18 Florida 34 Utah 14 Note: Ages adjusted to the 1970 standard population. Source: Ries et al. 1999. lence of tobacco-related lesions increased with increasing duration and frequency of spit tobacco use. In some American Indian tribes, both adolescent males and females commonly use spit tobacco and have an especially high frequency of spit tobacco lesions. On a Sioux reservation, 37.0 percent of stu- dents in grades 7 through 12 used spit tobacco. Spit tobacco lesions occurred in over one third of those tobacco-using adolescents (CDC 1988). In another study of Navajo adolescents, three fourths of male adolescents (75.4 percent) and one half of female adolescents (49.0 percent) used spit tobacco. Of Navajo adolescents who used spit tobacco, 25.5 per- cent had spit tobacco lesions—29.6 percent of males and 17.0 percent of females (Wolfe and Carlos 1987). Selected Mucosal Infections and Diseases Oral Herpes Simplex Virus Infections The prevalence of recurrent herpes lesions is estimat- ed to be between 15 and 40 percent (Scully 1989). The proportion of the U.S. population with herpes simplex virus type 1 (HSV-1) antibodies is 68.2 per- cent (as evidenced by positive antibody titer). The proportion reporting a history of herpes lesions in the past 12 months is 17.7 percent. The presence of anti- bodies and occurrence of herpes lesions vary by age (Figure 4.20). The frequency of recurrence also varies greatly, ranging from once to several times per year. Infection with the oral herpes simplex virus has been related to socioeconomic factors, with 75 to 90 percent of individuals from lower socioeconomic FIGURE 4.19 Tobacco-related oral lesions are more common in 12- to 17- year-olds who currently use spit tobacco 34.9 30- WH Current user 5. gy Former user 04 19.6 Percentage of people with lesion 5 Chewing tobacco user Snuff user Source: Adapted from Tomar et al. 1997. 70 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL populations developing antibodies by the end of the first decade of life (Whitley 1993a,b). In comparison, 30 to 40 percent of individuals from middle and upper socioeconomic groups evidence antibodies by the middle of the second decade of life. The prevalence of one or more herpes labialis lesions within the past 12 months is 8.4 percent for non-Hispanic blacks, 16.2 percent for Mexican Americans, and 19.7 percent for non-Hispanic whites (NHANES Ill). Recurrent Aphthous Ulcers Various epidemiologic studies of recurrent aphthous ulcers have indicated that the prevalence in the gen- The Magnitude of the Problem eral population can vary from 5 to 25 percent (Axéll et al. 1976, Embil et al. 1975, Ferguson et al. 1984, Ship 1972, Ship et al. 1967). In NHANES III, 17.2 percent of persons reported having a recurrent aphthous ulcer within the past 12 months, and occurrences were most common among young adults (18 to 24 years old) (Figure 4.21). In selected population groups, the prevalence of recurrent aphthous ulcers can be as high as 50 to 60 percent (Miller and Ship 1977, Ship et al. 1961, 1977). Other Mucosal Lesions Other mucosal conditions contribute to the burden of oral diseases. The following are among the most common: FIGURE 4.20 (cold sores/fever blisters} are common 4 Data not available for the 8- to 11-year-old age group. Source: NCHS 1996. Herpes simplex type 1 virus infection is widespread, and oral herpes lesions e Oral candidiasis (commonly called thrush) is a particular prob- lem for individuals with impaired immune function. A prevalence of "00 | 98.9 Age 9.4 percent has been reported in %0 me renal transplant patients (King et 2 80 5 we al. 1994); Samaranayake (1992) g 07 reports prevalences between 43 s 604 and 93 percent among HIV-infect- & 504 ed patients. It is estimated that 3.6 € 4 - percent of full denture wearers 5 0 4 have candidiasis. e Denture stomatitis, a condi- 0 - “ tion in which the mucosa under- 10 - = re » neath a denture becomes inflamed 0 om : a and sometimes painful, affects 25.6 Positive antibody to HSV-1? Had oral herpes lesion in past 12 months percent of people aged 18 and older who have two full dentures. FIGURE 4.21 Asubstantial percentage of the population, particularly among young adults, has experienced recurrent aphthous lesions (canker sores) in the past 12 months 30 25 20 8.4 Percentage who experienced lesion aA 18-24 25-44 Age group 8-11 12-17 Source: Adapted from NCHS 1996. Additionally, 32.2 percent of those with one full denture are affected, 26.7 percent of those with one or more partial den- tures, and 0.87 percent of those who do not have full or partial dentures. e Oral human papillomavirus infections, oral and genital papillomas (or condyloma acuminata, also called venereal warts), are especially common among HIV-positive patients. Human papilloma- viruses may be associated with some oral leukopla- kias with a high risk for malignant transformation (Palefsky et al. 1995). Developmental Disorders Numerous developmental disorders affect the oral, dental, and craniofacial complex. These include con- genitally missing teeth (all or specific tooth types); congenital problems involving tooth enamel, pulp, or dentin, and craniofacial birth defects or syndromes. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 71 The Magnitude of the Problem Cleft lip and palate are the most common congenital anomalies and may occur as isolated defects or as part of other syndromes. Other craniofacial defects and syndromes that have been the focus of recent genet- ics research include ectodermal dsyplasia, Treacher Collins syndrome, Apert’s syndrome, and Waarden- burg syndrome. Craniofacial defects and syndromes have many serious consequences including unusual facial features; severe functional problems, and the need for extensive surgical, medical, and rehabilita- tive interventions and prosthetic devices. Cleft Lip/Palate Oral clefts are one of the most common classes of congenital malformations in the United States, with prevalence rates in the general population of 1.2 per 1,000 births for cleft lip with or without cleft palate and 0.56 per 1,000 births for cleft palate alone (Schulman et al. 1993). These conditions affect facial appearance throughout life. The rate of oral clefts for whites is more than 3 times that for blacks (1.7 versus 0.5 per 1,000 live births) (Figure 4.22). Oral clefts are more common among North American Indians (3.7 per 1,000 births) (Lowry et al. 1989). Cleft palate occurs more fre- quently in females, whereas cleft lip or cleft lip/palate FIGURE 4.22 Cleft lip and cleft palate are among the most common congenital malformations, and prevalence varies by race Hydrocephalus Trisomy 21 Microcephalus a 3.7 1.07 Obstruction kidney/ureter Cleft lip & palate Paes Hip dislocation [ Pyloric stenosis T T T 0.0 05 1.0 15 20 25 3.0 35 40 Prevalence per 1,000 live births Bi Whites my Blacks tT T T Source: Schulman et al. 1993. _ ss is more common in males (Burman 1985, Fraser and Calnan 1961, Habib 1978, Owens et al. 1985). Malocclusions Malocclusions can occur due to congenital or acquired misalignments (crowding) of the teeth or jaws. In a national study of individuals between 8 and 50 years old, 25 percent were found to have no crowding of the incisors (front teeth), whereas 11 percent were found to have severe crowding (Brunelle et al. 1996). About 9 percent had a posteri- or crossbite, where there is poor contact of the back upper and lower chewing surfaces. This crossbite was most common in non-Hispanic whites. Severe over- jet—where the upper front teeth: project far for- ward—was found in approximately 8 percent of this population, with a similar percentage demonstrating a severe overbite—where the front top and bottom teeth greatly overlap when the mouth is closed. Less than 5 percent of non-Hispanic whites had an open bite, an inability to bring the upper and lower front teeth together. Injury Injuries to the head, face, and teeth are very com- mon. They can range in severity from the very mild to those that cause death. Although injuries have a major impact on oral health, data on the number and severity of head and face injuries in the United States are very limited.* Most of our knowledge about the number of injunes that occurs comes from more severe injuries that involve a visit to the emergency room. In 1993 and 1994, there were 20 million visits per year to emergency departments for craniofacial injuries. Less serious injuries can be treated on an outpatient basis. More than 5.9 million injuries in 1991 were treated by dentists in private offices (Gift and Bhat 1993). Overall, 25 percent of all persons aged 6 to 50 have had an injury that resulted in dam- age to one or more anterior teeth (Kaste et al. 1996a). An estimated 2.9 million emergency room visits for all age groups related to tooth or mouth injuries between 1997 and 1998. Twenty-five percent of these injuries were seen in children under the age of 4 (NCHS 1997b). The leading causes of head and face injuries that result in emergency room visits include falls, assaults, 2This section reports national data that should provide some estimation of the scope of craniofacial injuries in the population. However, the findings may not be directly comparable because they are from different sources at different times, and because those at risk for each type of injury are not quantified in most cases. 72 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL sports injuries, and motor vehicle collisions (De Wet 1981, Pinkham and Kohn 1991, Sane 1988). In the National Health Care Survey of emergency rooms, assaults and falls each accounted for 31 percent of sits related to head and face injury. Other studies have reported that up to 19 percent of head and face injuries are sports-related (McDonald 1994), and 5 percent of head and 19 percent of face injuries result from riding bicycles and tricycles (U.S. Consumer Product Safety Commission 1987). There are differences in rates of emergency room visits for head and face injuries among demographic groups. Males had higher rates than females, except among older adults. The rates of injury were higher for younger and older adults than for those in the middle years. Chronic and Disabling Conditions Oral-Facial Pain Oral-facial pain can greatly reduce quality of life. These types of pain may be due to tooth-related infections, mucosal sores, and irritations, and may include burning sensations, pain in the jaw joint area, and aching pain across the face or cheek. Over 39 million people, or 22 percent of adults 18 years of age and older in the civilian U.S. population, experi- enced at least one of five types of oral-facial pain dur- ing a recent 6-month period (Lipton et al. 1993). Based on the results of a national study of the preva- lence and distribution of oral-facial pain, it is esti- mated that during a 6-month period, 1 American adult in 8 (12.2 percent) suffers from toothache, | in 12 (8.4 percent) from painful oral sores, | in 19 63 percent) from jaw joint pain, and 1 in 71 (1.4 per- cent) from face or cheek pain (Lipton et al. 1993). The prevalence of toothache and pain due to oral sores decreases with age, whereas the prevalence of burning mouth pain increases with age. Women are twice as likely as men to report two specific types of oral-facial pain: jaw joint pain and face/cheek pain (Figure 4.23). Non-Hispanic blacks and Hispanics were slightly more likely to report toothache than non-Hispanic whites (Lipton et al. 1993). Adults liv- ing in poverty were more likely to report toothaches than adults living above the poverty level (Vargas et al. 2000). Temporomandibular Disorders Symptoms of temporomandibular disorders (TMDs) vary but may include severe pain in the jaw muscu- lature, severe pain or difficulty when opening the The Magnitude of the Problem mouth and chewing, headaches, and ear pain. Based upon assessments of pain in or around the jaw joint, these disorders are estimated to affect 10 million Americans (Lipton et al. 1993). Data from the few available population-based epidemiologic studies indicate that the prevalence of self-reported pain symptoms and clinical signs of TMD pain is between 5 and 15 percent, with peak prevalence in young and middle-aged adults (20 to 40 years of age) (Von Korff 1995). Although physical signs associated with TMDs have been shown to occur with nearly equal fre- quency among men and women, clinical studies have found that women in the third and fourth decades of life were much more likely than men of the same age to have sought care for reported facial pain in the tem- poromandibular region (Carlsson and LeResche 1995). Sjogren’s Syndrome Sjogren's syndrome, an autoimmune disorder that causes xerostomia (dry mouth), difficulty in swal- lowing, and xerophthalmia (dry eyes), is estimated to affect 1 to 2 million people in the United States (Talal 1992). The diagnosis is most often made in women in middle age. One estimate of the average annual incidence rate for Sjogren's syndrome, based on the Olmsted County, Minnesota, medical database, is about 3 to 5 cases per 100,000 population; this may be low, however (Pillemer et al. 1995). As with most other autoimmune conditions (e.g., rheumatoid arthritis, systemic lupus erythematosis), Sjogren's syndrome affects more women than men. The female-to-male ratio depends on the study, but may be as high as 9:1 (Fox 1996). FIGURE 4.23 Toothache is the most common source of oral-facial pain among adults 14 Prevalence per 1,000 persons 0.9 08 0.6 Toothache Oralsores Jaw joint Face/cheek Burning . mouth Pain category w female a Male Note: Data are for persons aged 18 and older locking back over the past 6 months. Sources: Adapted from NCHS 1989, Lipton et al.1993. | ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 73 The Magnitude of the Problem WHAT IS THE BURDEN OF DISEASE IN SELECTED POPULATIONS? CHALLENGES AND OPPORTUNITIES The national data provide a broad-brush picture of America’s oral health. For selected populations, how- ever, oral health and disease status has a different profile. By 2050 about 50 percent of the U.S. popula- tion is expected to be Asian, non-Hispanic black, Hispanic, and American Indian (Council of Economic Advisers 1998). Currently available data for these groups present a picture of disease that is generally poorer than that for non-Hispanic whites. These subgroups present a unique cluster of health, socioeconomic, and cultural issues. At the same time, data for the subgroups within each of these categories are lacking. In addition to racial/ethnic groups, other groups such as individuals with disabilities, the homeless, incarcerated individuals, and migrant workers have unique needs and challenges. Cutting across all subgroups are gender-specific health issues. For improvements to be made in America’s overall health, a better understanding of the full dimension of the problems faced by these populations and development of specific solutions are needed. This part of the chapter examines each subgroup in greater depth. Racial and Ethnic Minorities Although there have been gains in oral health status for the population as a whole, they have not been evenly distributed across subpopulations. Non- Hispanic blacks, Hispanics, and American Indians and Alaska Natives generally have the poorest oral health of any of the racial and ethnic groups in the U.S. population. Other health statistics, such as life expectancy and infant mortality, indicate that the general health of these groups is varied and also poor compared to other population groups (Council of Economic Advisers 1998). To address the elimination of these disparities in health—and also in housing, education, and other indicators of social and eco- nomic well-being—the administration has launched “The President's Initiative on Race: One America in the 21st Century.” Recommendations for improving the oral and general health status of racial and ethnic minorities are also a prominent feature of Healthy People 2010, the goal-setting health agenda devel- oped for the decade by the USDHHS (2000). African Americans Numerous studies over the decades have compared the health status of blacks and whites in American society, but relatively little systematic attention has been focused on the oral health of blacks. Although the overall oral health status of Americans has been improving, many oral diseases and conditions among blacks remain a serious problem—despite the fact that for almost three decades these disparities have been highlighted and recommendations made for addressing health issues including research, educa- tion, human resources, and delivery systems (National Dental Association 1972). These recom- mendations still represent opportunities for improve- ment in the oral health status of African Americans. Baseline data for the Healthy People 2010 objec- tives establish that, for children aged 2 to 4 years, 24.0 percent of non-Hispanic ‘blacks have experi- enced dental caries in their primary teeth, compared to 15.0 percent for their non-Hispanic white coun- terparts. For children aged 6 to 8, there were no dif- ferences among the races; but for 15-year-olds, a higher percentage of non-Hispanic blacks were affected than of whites. In addition the percentage of people of all ages who had untreated caries was sub- stantially higher for blacks than for whites—about twice as many. Higher levels of gingivitis and peri- odontal loss of attachment were also seen in non- Hispanic blacks as compared to non-Hispanic whites. A greater percentage of non-Hispanic blacks 18 years and older have missing teeth when compared to non-Hispanic whites. Relative to non-Hispanic whites, however, non-Hispanic blacks aged 18 and older are less likely to have lost all their teeth (eden- tulism) regardless of whether they are poor. - African American males have the highest inci- dence rate of oral cavity and pharyngeal cancers in the United States compared with women and other racial/ethnic groups (Wingo et al. 1999). The distri- bution of oral cancer cases reveals that blacks also have a higher proportion of pharyngeal cancer than oral cavity cancer compared to whites. Also, the 5- year relative survival rate (1989-95) for oral cancer was much lower among blacks than whites: 34 ver- sus 56 percent (American Cancer Society (ACS) 1999). This latter finding may be related to the fact that a high percentage of these cancers are diagnosed in later stages of disease in blacks as compared to whites (ACS 1999). On the other hand, for several conditions, African Americans have a lower disease burden than do whites. The incidence rate for cleft lip and cleft palate in African Americans is 0.54 per 1,000, about a third the rate for whites (1.70 per 1,000). Also the prevalence of having one or more herpes labialis lesion within the past 12 months is 50 percent less 74 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL than that for Mexican Americans and non-Hispanic whites. Hispanics Disparities in oral and general health status between Hispanic and non-Hispanic populations in the United States have been long recognized. Yet the health profile of Hispanics is incomplete due to insuf- ficient sampling of subgroups in national surveys, inconsistent or inadequate assessment of ethnicity, or ambiguities in reporting of ethnic identity (Hahn 1992). Recent efforts to improve data collection, identify subgroups, and provide more baseline data for Hispanics have addressed the situation somewhat, but much work remains to ensure accurate data for health planning and research (Delgado and Estrada 1993). Among preschool Hispanic children early child- hood caries is a particular concern. Two reports have documented early childhood caries among 12.9 per- cent of Hispanic children examined in San Antonio and 37 percent of predominantly Hispanic children in San Francisco (Garcia-Godoy et al. 1994, Ramos- Gomez 1999). Most recently, national survey data suggest that a higher proportion of Mexican American children ages 12 to 23 months may experi- ence dental caries than other race/ethnicity groups (Kaste et al. 1996b). Preliminary data from NHANES III indicate that young Mexican American children aged 2 to + are more likely to have experienced dental caries in their primary teeth, have on average more decayed and filled tooth surfaces, and have more untreated disease than either non-Hispanic white or non-Hispanic black children (Kaste et al. 1996b). Mexican American children aged 2 to 5 years—especially those from lower-income households—were more likely than their African American and non-Hispanic white counterparts to have one or more decayed primary teeth (Vargas et al. 1998). Dental caries continues to affect large numbers of school-age children and youth, as only 30 percent of Mexican Americans, 32 percent of non-Hispanic whites, and 41 percent of non-Hispanic blacks 12 to 17 years of age were free of caries in their permanent teeth (USDHHS 1996). However, most of the dental caries in the permanent teeth of non-Hispanic white children aged 12 to 17 had been treated or filled (87 percent), compared to 63 percent for Mexican Americans and 60 percent for non-Hispanic blacks. The only large-scale survey that permits compar- ison among Hispanic subgroups is the Hispanic Health and Nutrition Examination Survey (HHANES 1982-84). After controlling for age, sex, income, and The Magnitude of the Problem education, HHANES results show that Cuban American and Puerto Rican adults had about twice as many missing teeth as Mexican Americans. Puerto Ricans and Cuban Americans also had on average more filled teeth than Mexican Americans. Puerto Rican children and adults under 45 years old had more gingivitis than Cuban Americans and Mexican Americans; the highest prevalence of periodontal dis- ease was reported among Puerto Ricans compared to the two other Hispanic groups (Ismail and Szpunar 1990). A national survey found that employed Hispanic adults were twice as likely to have untreated dental caries as non-Hispanic whites. In this study, gingivi- tis and periodontal problems (attachment loss and pockets) were also among the more common prob- lems among the Hispanic adults studied (Watson and Brown 1995). Analysis of a more recent survey (NHANES Ii) that sampled Mexican Americans is particularly revealing. After adjusting for age, Sex, educational attainment, and annual family income, Mexican American adults are similar to their white non- Hispanic counterparts on most oral health indicators. However, among Mexican Americans, individuals in families with less than $20,000 annual income were 1.6 times less likely to have an intact dentition, 3.1 times more likely to have any untreated decay on the crowns of their teeth, and 4.2 times more likely to have severely decayed teeth (very large cavities or only the roots of teeth remaining) than non-Hispanic whites (Garcia and Drury 1999). Also, Mexican Americans were less likely to be edentulous regard- less of poverty status than either non-Hispanic whites or non-Hispanic blacks (Drury et al. 1999). These findings confirm the importance of con- trolling for sociodemographic factors in reporting on oral health status as well as the need to assess other factors related to health status. As a group, Hispanics have lower median incomes, higher poverty rates, more unemployment, and less education than non- Hispanic whites (Ramirez 1999). However, sociode- mographic factors are just one aspect of the questions raised when attempting to understand differences in oral health. The effect of financial barriers and nonfi- nancial factors such as language, culture, dietary pat- terns, and behaviors on access, care seeking, and health outcomes must also be examined. Variations in conditions such as diabetes also may contribute to differences in oral health. It is estimated that Hispanics will surpass African Americans as the country’s largest minority group by 3020 (U.S. Bureau of the Census 2000). Aggregate statistics obscure substantial variations within ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 75 The Magnitude of the Problem Hispanic subgroups. More than 20 different coun- tries of varied cultural, socioeconomic, and political backgrounds are currently included in this category of the U.S. population. Narrowing the gap in oral health between Hispanic and non-Hispanic groups will require improved data on health status, barriers to access, and disease factors underlying differences in oral health in these populations. Asians, Native Hawaiians, and Other Pacific Islanders National data for the oral health of Asian, Native Hawaiian, and other Pacific Islander (ANHPI) groups that can be generalized to the U.S. population are not available. Instead the profile of disease and health in this category is only available through studies of spe- cific states and locales. Among all ethnic groups in California in 1993 and 1994, Asian and Pacific Islander American (APIA) children in Head Start had the highest prevalence of early childhood caries—20 percent compared to 14 percent for all Head Start children (Pollick et al. 1997). These data are compa- rable to other survey findings of 16 to 20 percent and 29 percent early childhood caries among APIA chil- dren in Hawaii and California, respectively (Greer unpublished, Louie et al. 1990). A California study of 6- to 8-year-olds found dis- parities in the oral health status of APIA children in the state when compared to all children nationally. Among the California APIA children, 71 percent had untreated dental caries, with a significant portion of this group requiring urgent dental treatment. By comparison, NHANES III data indicate that in 1988- 94, 29 percent of children in the United States aged 6 to 8 years had untreated dental decay. There is variation in oral health status among subgroups of ANHPI children. In a recent survey in Hawaii, the prevalence of early childhood caries among APIA children was 16 percent, ranging from a low of 8 percent among Japanese children to a high of 25 percent among Filipino children. The preva- lence of untreated dental caries in 6- to 8-year-old APIA children was 39 percent, which ranged from a low of 16 percent among Japanese children to 40 per- cent among Native Hawaiians, 48 percent among Southeast Asians, and 62 percent among non-Native Hawaiian Pacific Islanders (Greer 1999). Oral cancer incidence and mortality rates for APIAs are lower than those for white non-Hispanics and African Americans. However, nasopharyngeal cancer incidence and mortality rates among Chinese and Vietnamese populations are many times higher than other groups (Miller et al. 1996), and therefore pose a unique health problem for these subgroups. Until recent years, vital statistics and other health-related data were virtually nonexistent for the APIA population. Data for this group generally appeared in the “other” category of national surveys, and thus were not helpful in determining specific population-based oral or general health needs. Little national focus has been given to defining and meas- uring the oral health problems and related health care needs of the APIA population. These needs are now highlighted in the 2010 Healthy People Oral Health Objectives. A few statewide oral health data exist for some APIA child populations, but no ethnic subgroupings can be assessed. Again, this category of the U.S. population is extremely heterogeneous. It is estimated that 76 percent is from one of five ethnic origins and that 74 percent in 1990 were foreign born. More than 63 percent live in four states: California, New York, Hawaii, and Texas. Con- sequently, determining the reasons for variations in oral health will require additional data. American Indian/Alaska Native Populations Data on the oral health of American Indians and Alaska Natives (AI/AN) are available through studies conducted by the Indian Health Service (IHS) (Niendorfs 1994). The AI/AN people constitute about 1 percent of the U.S. population, or an esti- mated 2.5 million people in 2000. Little is known or can be easily determined about the general or oral health status of the 1 million AVAN people not served by the IHS system. For this reason, with the exception of overall death rates obtained from census data, the statistics described in this section will be limited to the 1.5 million AV/AN served by the THS. By and large, this group represents AI/AN people liv- ing on or near reservations. Preliminary analyses of the IHS-wide Oral Health Status Survey of over 13,000 dental patients in 1999 revealed that some conditions have worsened and some improved since an earlier survey conducted in 1991 (IHS 1994, 2000). Across the IHS service pop- ulation there was a statistically significant increase in caries among adults over 55 as measured by the decayed, missing, and filled teeth index. The decayed and filled tooth rate increased from 7.5 to 8.8 teeth, with no change in the average number of missing teeth for this age group. Among AI/AN children across the IHS, there was a significant decline in caries in the permanent den- tition and a significant increase in caries in the pri- mary dentition. Among children aged 2 to 5 years, the increase in decayed and filled primary teeth sur- faces went from 8.6 to 11.4. In general, AIAN popu- lations have much greater rates of dental caries and 76 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL periodontal disease in all age groups than the gener- al U.S. population. AVAN children aged 2 to 4 years have 5 times the rate of dental decay compared to all children, and 6- to 8-year-old AV/AN children have about twice the rate of dental caries experience. Rates for untreated decay in these age groups are 2 to 3 times higher than in the same age groups in the gen- eral U.S. population. Periodontal disease in AV/AN adults is 2.5 times greater than in the general U.S. population. High prevalence rates of diabetes among AVAN populations are a significant contributing fac- tor to this periodontal disease (IHS 2000). Substantial unmet dental needs and quality of life issues have also been identified in THS surveys, which included studies of representative AVAN com- munities with regard to the effect of oral conditions on well-being and quality of life (Chen et al. 1997). (See Chapter 6 for a general discussion.) One third of schoolchildren report missing school because of den- tal pain. Twenty-five percent of schoolchildren avoid laughing or smiling, and 20 percent avoid meeting other people because of the way their teeth look. As a consequence of dental pain, almost a quarter of the adults are unable to chew hard foods, almost 20 per- cent report difficulty sleeping, and 15 percent limit their work and leisure activities. Three quarters of the elderly experience dental symptoms, and half perceive their dental health as poor or very poor and are unable to chew hard food. Almost half the adults avoid laughing, smiling, and conversation with oth- ers because of the way their teeth look. Again, the available data allow for obtaining a picture only of the AV/AN population residing on reservations where services, including dental servic- es, have been provided by the IHS or contracted to tribes or urban AI/AN organizations. In 1989, American Indians, residing in the current reservation states had a median household income of $19,897. Almost one third (31.6 percent) of AVANs lived below the poverty level. For some groups, diabetes and high rates of tobacco and alcohol use are preva- lent and contribute to poor oral health. Women’s Health Analysis of data from NHANES Ill indicates that women have benefited from the trend in general improvements in oral health that has been enjoyed by the U.S. population overall. Many, but not all, sta- tistical indicators show women to have improved their oral health status as compared to men (NHANES III, Redford 1993). Adult females are less likely than males at each age group to have severe periodontal disease as measured by periodontal loss The Magnitude of the Problem of attachment of 6 mm or more for any tooth. Both black and white females (6.0 and 6.0 per 100,000) have a substantially lower incidence rate of oral and pharyngeal cancers compared to black and white males, respectively (20.8 and 14.9 per 100,000). A higher prevalence of females than males have oral- facial pain, including pain from oral sores, jaw joints, face/cheek, and burning mouth syndrome. However, there are large areas for which information for either sex, even at the descriptive level, is only partial or nonexistent. Data gaps regarding craniofacial in- juries, soft tissue pathologies, and salivary gland dys- functions are notable examples. Most oral diseases and conditions are complex and represent the product of interactions between genetic, socioeconomic, behavioral, environmental, and general health influences (Chapters 3 and 5). Multiple factors may act synergistically to place sub- groups of women at higher levels of risk for oral dis- eases. For example, the comparative longevity of women, compromised physical status over time, and the combined effects of multiple chronic conditions often with multiple medications, can result in increased risk of oral disease (Redford 1993). Many women live in poverty, are not insured, and are the sole head of their household. For these women, obtaining needed oral health care may be difficult. In addition, gender-role expectations of women may also affect their interaction with dental care providers and could affect treatment recommendations as well (Redford 1993). During the past decade, women’s health has emerged as a significant issue in the nation’s health agenda. The scientific community is beginning to respond to this concern by studying and reporting the effects of sex and gender differences on health and disease management. Although most of the effort has focused upon women, comparisons with men’s health have begun to elucidate sex- and gender- specific differences. Research has demonstrated sex and gender dif- ferences in the response to kappa opioid analgesics for the control of postoperative pain (Gear et al. 1996), These findings have heightened conjecture about differences in the female and male nervous sys- tems in response to pain stimuli. There are studies in mice that suggest that there are sex-specific respons- es to pain and analgesics (Mogil et al. 1996, 1997). Taken together, these findings could help explain why women report certain painful conditions more than men; for example, temporomandibular joint disorders, trigeminal neuralgia, migraine headaches, and burning mouth syndrome (USDHHS 1999). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 77 The Magnitude of the Problem Recent research has also demonstrated sex and gender differences in taste perception. Women are more likely than men to be “supertasters” of a bitter compound known as 6-n-propylthyiouracil (PROP) (Bartoshuk et al. 1994). PROP supertasters experi- ence more intense tastes (particularly for bitter and sweet), a greater sensation of oral burning in response to alcohol, and more intense sensations from fats in food (Bartoshuk et al. 1994, 1996, Tepper and Nurse 1997). PROP supertasters also have more fungiform papillae on their tongues than medium PROP tasters or those who cannot taste PROP at all. The Agenda for Research on Women’s Health for the 21st Century noted that the ability to interpret oral health in the context of sex and gender was lim- ited by large gaps in knowledge. For example, perti- nent oral health data, even at the descriptive level, are partial or nonexistent for many conditions and dis- eases for either sex. In addition, limited knowledge of etiologic factors, natural history of diseases, behav- ioral and environmental differences—to name a few—decreases the utility of those data that are avail- able. For example, women are reported to be more inclined to self-care, to visit the dentist more often, and to be more likely to report symptoms such as pain. However, the effects of these behaviors on their oral health status cannot be determined fully. Figure 4.24 suggests content areas in the study of women’s oral health. Individuals with Disabilities No national studies have been conducted to deter- mine the prevalence of oral and craniofacial diseases among the various populations with disabilities. Several local and regional reports, however, provide some relevant data in this regard. For example, some smaller-scale studies show that the population with mental retardation or other developmental disabili- ties has significantly higher rates of poor oral hygiene FIGURE 4.24 : Content areas in the study of women’s health Oral Influences on Systemic Health Evidence for links between oral infection and diabetes Systemic influences on Oral Health Longevity Multiple chronic conditions Medication usage Cognitive impairments Physical confinement Compromised functional status Postmenopausal bone loss HIV Diabetes ~ Societal Influences on Women’s Health Caregiving Status as single head of household Poverty Gender role expectations Underinsurance Concern for aesthetics Access to care Craniofacial trauma Source: Adapted from Chesney and Ozer 1995 and reprinted in USDHHS 1999. Women and the Health Care System Treatment decision making Over/underutilization of professional services Health policy Diseases More Common in Women Than Men TMD, orai-facial pain, Sjogren's 7 syndrome, salivary gland dysfunction, burning mouth, alterations in taste, pregnancy-associated oral changes Oral Diseases Affecting the Most Women Caries Periadantal diseases Gender Influences on Health Risk Dental care utilization Self-care Eating disorders Unprotected sexual activity 78 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and needs for periodontal disease treatment than the general population, due, in part, to limitations in individual understanding of and physical ability to perform personal prevention practices or to obtain needed services. There is a wide range of caries rates among people with disabilities, but overall their rates are higher than those of people without disabilities. Much of the variation stems from where people reside (e.g., in large institutions where services are available versus in the community where services must be secured from community practitioners). Almost two thirds of community-based residential facilities report that inadequate access to dental care is a significant issue (Beck and Hunter 1985, White et al. 1995, Waldman et al. 1998, Dwyer, Northern Wisconsin Center for the Developmentally Disabled unpublished data, 1996). Parents consistently report dental care as one of the top needed services for their children with disabilities regardless of age (Haveman et al. 1997). Local studies of independent living cen- ters reported that 24 to 30 percent of adults with cerebral palsy, 14 percent with spinal cord injuries, 30 percent with head injuries, and 17 percent who were deaf had dental problems (Arnett 1994). Results from 1999 oral assessments of U.S. Special Olympics athletes (all ages), based on an extremely conserva- tive assessment protocol (without the use of x-rays, mirrors, or explorers), and carried out by the Special Olympics Special Smiles Program in 20 states, indi- cate that 12.9 percent of the athletes reported some form of oral pain, 39 percent demonstrated signs of gingival infection, and nearly 25 percent had untreat- ed decay (Special Olympics, Inc., unpublished data). Note that this is a population that tends to be from higher-income families. The oral health problems of individuals with dis- abilities are complex. These problems may be due to underlying congenital anomalies as well as to inabil- ity to receive the personal and professional health care needed to maintain oral health. There are more than 54 million individuals defined as disabled under the Americans with Disabilities Act, including almost a million children under age 6 and 4.5 million chil- dren between 6 and 16 years of age. A greater per- centage of males than females and of African Americans than Hispanics and whites have disabili- ties (Federal Interagency Forum 1997, Waldman et al. 1999). Children with disabilities have chronic physical, developmental, behavioral, and emotional limitations, including mental retardation, autism, attention deficit hyperactivity disorders, and cerebral palsy. Also, children from families with incomes below the poverty level are about one third more like- ly than children in nonpoor families to have an exist- The Magnitude of the Problem ing special health care need. Similarly, children from less educated households exhibit a higher likelihood of a special health care need. Children in single-par- ent families are about 40 percent more likely than children from two-parent households to have special health care needs (Newacheck et al. 1998). Deinstitutionalization has resulted in highlighting the problem these individuals have regarding access to dental care as they move from childhood to adult- hood, Availability of dental providers trained to serve special needs populations and limited third-party support for the delivery of complex services (see Chapter 9) further complicate the issues entailed in addressing the needs of this population. Given the wide variability among groups with disabilities, this review of oral health status and needs is quite limited. More in-depth assessment and analysis of the determinants of oral health status, access to care, and the role of oral health in the over- all quality of life and life expectancy of individuals with disabilities are needed (see Chapter 10). UTILIZATION OF PROFESSIONAL CARE: WHAT DO WE KNOW ABOUT THE RELATIONSHIP OF ORAL HEALTH AND USE OF DENTAL SERVICES? With few exceptions, maintenance of oral health through a lifetime requires timely receipt of advice for self-care, preventive therapies, early detection and treatment of problems, and restoration of function. Chapter 7 describes community-based and profes- sional interventions that have played a significant role in the improvement of oral health achieved over the past 50 years; their full promise has not, howev- er, been realized. Chapter 8 describes current and emerging strategies for personal and provider approaches to maintain and restore oral health, with tooth-conserving approaches being employed more and more frequently. As noted earlier, almost every- one experiences oral diseases and conditions over the course of a lifetime, and, unlike the common cold, most diseases do not resolve over time. Consequently, receipt of dental services complements self-care as a critical factor in achieving and main- taining good oral health. Although certain counseling and screening serv- ices provided by physicians are recommended (U.S. Preventive Services Task Force 1996), data to indi- cate how many persons receive such services or oral- health-related recommendations from their physi- cian are very limited. There are also no data on physi- cian-based services for oral and craniofacial condi- tions. The data that are available describe utilization ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 79 The Magnitude of the Problem of dental visits. Unfortunately, most of these data are cross-sectional, describing the experience of the pop- ulation in any given year, but providing little detail about how patterns of care over time contribute to oral health. Nevertheless, utilization of care is used as a surrogate measure of an individual's or a popula- tion's capacity to maintain or improve health status. An understanding of utilization of dental visits and differences in such visits among age, racial/ethnic, sex, and income groups is important in identifying opportunities for improvement in oral health that would follow from timely receipt of professional care. Characteristics of groups with different levels of dental care utilization suggest barriers to care as well as factors that predispose or enable access to dental care. Explanations for variation in utilization are alluded to in the following section, and are discussed in further detail in Chapter 10. More studies are needed to understand the dimensions of disease and the role of professional care and use of services. Also, for oral health in particular, the contributions of all health professions and the interdisciplinary nature of care need to be emphasized. Dental Care Utilization Visiting a health care provider at least once per year and the number of visits made within the past year are used as indicators of an individual's ability to access professional services. Dental care utilization statistics are traditionally based on an individual's reporting “at least one dental visit in the past year,” although there are variations with shorter recall intervals and different forms of the question. Depending on the question and survey method, annual dental care use estimates vary. The 1996 Medical Expenditures Panel Survey (MEPS) esti- mates that 43 percent of the U.S. population 2 years and older had at least one dental visit that year (MEPS 2000). Responding to a variation of a ques- tion that had been asked in many previous surveys, some 65.1 percent of the U.S. population 2 years and older reported in 1997 that they had visited a dentist in the preceding year (NCHS 1997b), up from 55.0 percent in 1983 (Bloom et al. 1992). The average number of visits per person remains at about two per year. Further research is needed to understand rea- sons for variations in estimates from different survey approaches, but differences among persons with dif- ferent characteristics are quite similar regardless of survey method. Data from the 1997 National Health Interview Survey, reprinted in Healthy People 2010, indicate that the highest percentage reporting at least one TABLE 4.3 Percentage of persons 25 years of age and older with a dental visit within the preceding year, by selected patient character- istics, selected years 1983" 19897 1990 1991 1993 Total” 53.9 589 62.3 582 608 Age 25 to 34 years 590 609 651 591 603 35 to 44 years 60.3 659 69.1 648 669 45 to 64 years 54.1 59.9 62.8 59.2 62.0 65 years and older 39.3 458 «3949.6 47.257 65 to 74 years 438 500 535 511 563 75 years and older 318 390 434 413 449 Sex‘ Male 517 56,20 588 55.5 58.2 Female 559 614. 656 608 63.4 Poverty status“? Below poverty 30.4 33.3 38.2 33.0 35.9 At or above poverty 558 62.1 654 61.9 643 Race and Hispanic origin‘ White, non-Hispanic 56.6 61.8 64.9 61.5 64.0 Black, non-Hispanic 39.1 43.3 49.1 443 473 Hispanic 421 489 538 43.1 462 Education‘ Less than 12 years 35.1 36.9 41.2 35.2 38.0 12 years 548 58.2 613 56.7 58.7 13 years or more 709 739 757 72.2 738 Education, race, and Hispanic origin’ Fewer than 12 years White, non-Hispanic 36.1 39.10 448 38.1 2 Black, non-Hispanic 317.0 3200379 33.0 33.4 Hispanic 338 6936.5 427 289 33.0 12 years White, non-Hispanic 566 598 628 588 604 Black, non-Hispanic 405 448 51.1 43.4 482 Hispanic? 487 565 599 495 54.6 13 years or more White, non-Hispanic 726 758 773 74.2 75.8 Black, non-Hispanic 544 57.2 644 617 613 Hispanic® 584 66.2 67.9 61.2 61.8 Data for 1983 and 1989 are not strictly comparable with data for later years. Data for 1983 and 1989 are based on responses to the question “About how long has it been since you last went to a dentist?” Starting in 1990, data are based on the question “During the past 12 months, how many visits did you make to a dentist?” Includes all other races not shown separately and unknown poverty status and educa- tion level. * Age adjusted. 4 Poverty status is based on family income and family size using Bureau of the Census poverty thresholds. © Persons of Hispanic origin may be of any race. Notes: Data are based on household interviews of a sample of the civilian noninstitu- tionalized population. Denominators exclude persons with unknown dental data. Estimates for 1983 and 1989 are based on data for all members of the sample house- hold. Beginning in 1990, estimates are based on one adult member per sample house- hold. Estimates for 1993 are based on responses during the {ast half of the year only. Source: Data from NCHS 1989. 80 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem dental visit was third-grade children (82 percent). Variation by Sex, Race/Ethnicity, Income, Those aged 25 years and older with less than a high and Insurance school education had the lowest rates (41 percent) for annual dental visits as compared to those with at east some college education (74 percent) (USDHHS Females had slig TABLE 4.4 Age-adjusted percentage distribution of persons 2 years and older by interval since last dental visit, by selected characteristics, 1989 Interval Since Last Dental Visit 1Yearto 2 Years to All LessThan LessThan LessThan 5 Years Intervals 1 Year 2Years 5Years orMore Never All ages 100.0 57.3 9.5 123 1.0 46 Sex Male 100.0 54.7 9.6 13.4 12.1 49 Female 100.0 59.9 9.4 11.2 10.1 44 Race White 100.0 59.5 91 116 105 44 Black 100.0 43.2 123 16.9 15.1 58 Other 100.0 51.6 9.7 14.0 10.8 6.7 Hispanic origin Non-Hispanic 100.0 58.5 9.4 12.0 108 4.1 Hispanic 100.0 46.0 10.5 14.6 BO 97 Mexican American 100.0 40.5 8.9 15.3 15.8 13.1 Other Hispanic 100.0 53.2 12.3 137 9.9 5.1 Place of residence MSA? 100.0 58.4 94, 19 10.1 45 Central city 100.0 54.9 10.1 12.9 10.9 = 5.1 Not central city 100.0 60.6 9.0 113 96 4.2 Not MSA? 100.0 53.6 97 13.6 14.1 511 Geographic region Northeast 100.0 60.7 10.4 107 90 35 Midwest 100.0 61.5 83 113 10.7 903.5 South 100.0 52.2 10.3 13.9 3.6 59 West 100.0 57.8 8.6 123 9.1 49 Education level Less than 9 years 100.0 30.6 9.9 18.4 30.6 5.9 9 to 11 years 100.0 39.0 10.7 20.3 23.5 13 12 years 100.0 54.6 10.6 15.0 144 05 13 years or mare 100.0 70.2 8.5 103 69 0.2 Family income Less than $10,000 100.0 42.2 10.9 16.3 20.1 7.0 $10,000 to $19,999 100.0 43.9 11.8 74 16.1 6.6 $20,000 to $34,999 100.0 58.2 10.5 3.2 104 46 $35,000 or more 100.0 72.5 78 8.5 55 29 Dental insurance coverage With private dental insurance 400.0 70.4 8.7 9.2 6.6 3.3 Without private dental insurance 100.0 50.8 10.7 15.4 142 60 4 MSA = metropolitan statistical area. Source: Bloom et al. 1992. Dental care utilization varies with sex and race/eth- nicity for individuals 25 and older (NCHS 1997a). htly higher rates of utilization (67 percent) than males (63 percent). Hispanic individuals had the low- est utilization (53 percent), and non-Hispanic whites had the high- est rates (68 percent). Table 4.3 provides an overview of utilization from 1983 through 1993. A higher percentage of females reported a dental visit than malés in each sur- vey year. Fewer non-Hispanic blacks and Hispanics reported a dental visit than non-Hispanic whites in each survey year. Income and education are also key vari- ables in utilization. In 1993, almost twice as many individuals 25 and older living at or above the poverty line had a dental visit than did those living below the poverty line in 1993 (64.3 versus 35.9 per- cent). Similarly, almost twice as many individuals with 13 years or more of education had a visit than did those with fewer than 12 years of education (73.8 versus 38.0 per- cent) in that same year. Data from the 1989 National Health Interview Survey showed that the overall age-adjusted num- ber of visits for blacks was 1.2 vis- its compared to 2.2 visits for whites (Bloom et al. 1992). Table 4.4 shows the percent- age distributions of the interval since their most recent dental visit for people aged 2 and older in selected demographic and socioe- conomic categories. Individuals who have never visited a dentist ranged from a high of 13.1 percent of Mexican Americans to 5.8 per- cent of blacks and 4.4 percent of whites. Eleven percent of the pop- ulation had not had a dental visit in 5 years or more. Individuals with fewer than 9 years of educa- tion represented the highest pro- portion, 30.6 percent, of those reporting no dental visit in 5 years ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 81 The Magnitude of the Problem or more, compared with 6.9 percent of those with 13 years or more of education. A larger proportion of individuals without private dental insurance had not had a dental visit in 5 years or more compared with those with private dental insurance (14.2 versus 6.6 percent). Hispanic individuals have the lowest rate of dental insurance coverage—29.0 percent, compared with 32.4 percent for non-Hispanic blacks and 41.8 percent for non-Hispanic whites (U.S. Bureau of the Census 1997). Professional care is necessary for several critical dental disease prevention measures, such as the application of dental sealants. Unfortunately, dental sealants are 3 times less likely to be found on the teeth of Mexican American and African American children than among white children aged 5 to 17 (Selwitz et al. 1996). Asian and Pacific Islander American children in California also demonstrated a low rate of sealant use (Pollick et al. 1997). Variation by Oral Health Status Utilization of dental care is associated with self- reported health status, as shown in Table 4.5. Of those who reported “excellent” or “very good” health, 61.4 percent had had a dental visit within the past year, compared with about 45.1 percent of those reporting “fair” or “poor” health. Functional limita- tions are also related to dental service utilization. Of those who reported no physical limitations in activi- ties, 58.5 percent reported a dental visit within the past year, compared to 46.6 percent of those who were unable to carry out their usual activities (Table 4.5) (Bloom et al. 1992). Whether a person had natural teeth was strongly associated with dental care utilization (Table 4.5). Dentate persons were more than 4 times more likely to report a dental visit within the past year than eden- tulous people: 65.5 versus 14.3 percent. Over half (55.2 percent) of those who were edentulous reported that they had not had a dental visit in 5 years or more. Recent analyses of data from NHANES III show that adults 18 and older who reported a dental visit in the past 12 months were nearly 9 times more like- ly to be dentate and 4.4 times more likely to have a complete dentition than adults who did not report visiting a dentist within the preceding 12 months. Dentate adults who reported a dental visit in the past 12 months were 3.1 times less likely to have untreat- ed coronal decay and 1.5 times less likely to have gingivitis than dentate adults who did not report a recent dental visit (T. Drury, NIDCR, personal com- munication, 1999). A study comparing individuals who had had a dental visit in the past 12 months with those who had not reported that dentate adults who had a recent visit were less likely to have untreated coronal and root caries, TABLE 4.5 pulpal pathology, and retained Age-adjusted percentage distribution of persons 2 years and older by interval since tooth roots. They also were more last dental visit, by selected health characteristics, 1989 likely to rate the general condition Interval Since Last Dental Visit of their teeth and gums as excel- lent or very good (Drury and 2 Years to Redford 2000). All LessThan 1Yearto LessThan 5 Years Examination of NHANES Ill intervals 1Year 2 Years 5Years orMore Never . . data by low socioeconomic status Assessed health status (SES) provides an additional per- Excellent or very good 100.0 61.4 9.3 11.2 9.0 43 spective. In a recent analysis, SES Good 100.0 51.9 10.1 13.9 12.6 5.8 was wien red by a com sosite Fair or poor 1000 45.1 10.0 166 0C(OCASD ; su y a compos) | . index based on educational attain- ee of activity i ment and the ratio of annual fami- nabie to carry on ste ly income to the poverty threshold. activity 100.0 46.6 98 5601665 Among all adults, people with Limited in amount or kind , of major activity 1000 © 523 9840s lower SES scores were nearly 9 Limited, but not in major times more likely to be edentulous activity 100.0 59.1 83 128 W7 42 than those with higher SES scores. Not limited in activity 100.0 58.5 9.5 12.0 10.1 46 Among the dentate, those with Dentition stat lower SES scores were 6 times entste “s 100.0 655 96 on 101 05 more likely to have coronal decay Edentulous 100.0 143 64 «'198~—S«55.D2-——s—«C and nearly 4 times less likely to have visited a dentist in the past 12 Source: Bloom et al. 1992. months (Drury et al. 1999). 82 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Reasons for Nonutilization Reasons for nonutilization of dental services are com- plex. Principal reasons cited by respondents of all ages (Bloom et al. 1992) are given in Table 4.6. Slightly less than half of those reporting no dental visit in the past year (46.8 percent) said that they per- ceived having no dental problem. This perception was the predominant response of individuals in all demographic categories, except for those 65 and older, who gave having no teeth as the predominant reason. Younger individuals were more likely than alder to cite “no dental problem.” Blacks were more likely to report “no problems” (58.5 percent) as a rea- son for no dental visit, compared to 44.3 percent of whites (Bloom et al. 1992). Having no teeth (14.3 percent) was the next most frequently reported reason for no dental visit. About half of the people 65 and older in the 1989 survey gave this as their reason for no dental visit— 39.2 percent of blacks compared to 51.2 percent of whites. The third most frequently cited reason was the cost of care, mentioned by 13.7 percent of respon- dents. Whites (14.3 percent) were more likely than blacks (11.4 percent) to cite cost. Other surveys have reported substantially higher percentages of individ- uals indicating cost as a barrier, particularly those in underserved or low-income areas (Bloom et al. 1992). The age group most sensitive to the cost of care was 18- to 34-year-olds, 19.1 percent of whom gave cost as the reason for no dental visit. Finally, a small proportion of respondents (4.3 percent) report- ed fear as a personal barrier to receipt of care. Unmet Needs Unmet health needs can be assessed in many ways. Because oral diseases are common and do not resolve over time in the absence of intervention, the lack of dental visits is used as an indicator of unmet health needs. In addition, the National Access to Care Survey documented the extent of dental care that individuals wanted but could not obtain (“wants”) in the total population and among various population subgroups (Mueller et al. 1998). About 8.5 percent of the U.S. population wanted, but did not obtain, den- tal care in 1994 (Table 4.7). In contrast, only 5.6 per- cent reported unmet medical or surgical care wants. Adult women aged 19 to 64 reported the greatest level of dental care wants; elderly people 65 and older had the lowest level. Blacks, people in fair or poor health or with one or more chronic conditions, and people living in the South reported higher levels of dental care wants than comparable groups. About The Magnitude of the Problem 16.4 percent of those in households whose family income was less than 150 percent of the poverty level reported dental care wants. More than 22 percent of the uninsured reported dental care wants. Insured children with special health care needs were 4 times more likely to report unmet need for dental care (23.9 percent versus 6.1 percent) if they were unin- sured than if they were insured, according to a recent analysis of data from the National Health Interview Survey (Newacheck et al. 2000). Outcomes of Appropriate Levels of Access and Utilization: An Example The effects on health of a system of care with assured access and positive expectations of care-seeking and utilization behavior have been demonstrated by the U.S. Department of Defense. There are currently over 1.4 million men and women on active duty in the U.S. military. The population is predominantly male (86 percent). The racial distribution is 68 percent white, 20 percent black, 7 percent Hispanic, 3 per- cent Asian, and 2 percent other groups. Slightly over 30 percent of active duty personnel are between the ages of 20 and 24, and 91 percent are younger than 40. In 1997, 59 percent were married. Seventy-six percent had a high school degree, and 19 percent were college graduates. Free dental care, one of the benefits provided to active duty military personnel, eliminates one of the significant barriers that has been identified as limiting access to care for many in the civilian population. In addition, military personnel are required to receive a dental examination annually, even if the individual perceives that he or she has “no problem.” Dental care is available to most military personne] at their duty station, eliminating the need to travel long distances. A comparison of the oral health and utilization of dental care of the military and civilian populations illustrates the impact of elimination of these barriers to care on oral health, even for persons from demographic groups that are traditionally underserved. In 1994 the Tri-Service Comprehensive Oral Health Survey examined and administered question- naires to 13,050 active duty military personnel using a complex, weighted survey design to examine the oral health status, dental treatment needs, dental uti- lization, and perceived need for care in this popula- tion (York et al. 1995). The study found that nearly all (99.2 percent) active duty military personnel had seen a dentist within the past 2 years. Eighty percent of active duty personnel received a dental examina- tion within the past year, 60 percent had a dental ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 83 The Magnitude of the Problem TABLE 4.6 Percentage of persons with no dental visit in past year by reason reported, by selected characteristics, 1989 All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth Important Reason Age All ages 100.0 43 37 17 46.8 143 23 87 2 to 17 years 100.0 13 15.0 15 56.8 0.2 19 119 18 to 34 years 100.0 5.9 19.1 24 52.4 0.7 3.2 9.5 35 to 64 years 100.0 58 12.8 15 43.3 17.8 2.2 84 65 years and older 100.0 2.2 4) 11 31.2 49.7 11 3.9 Sex Male All ages 100.0 40 13.0 15 49.1 A 2.6 93 2 to 17 years 100.0 1.2 149 13 56.2 *0.2 2.0 12.1 18 to 34 years 100.0 5.5 17.5 2.0 54.8 0.6 ° 34 97 35 to 64 years 100.0 5.4 V2 15 45.4 16.1 28 95 65 years and older 100.0 7 4.0 1.0 33.6 48.6 13 35 Female All ages 100.0 46 143 18 444 16.6 19 8.1 2 to 17 years 100.0 15 15.2 1.6 57.4 *0.2 18 11.6 18 to 34 years 100.0 6.5 21.0 29 49.5 0.8 3.0 93 35 to 64 years 100.0 6.2 144 15 411 19.5 1.6 73 65 years and older 100.0 25 42 1.2 225 50.6 0.9 41 Race White All ages 100.0 44 143 18 443 157 2.4 9.4 2 to 17 years 100.0 13 16.4 7 54.0 0.2 2.0 133 18 to 34 years 100.0 6.2 2077 2.6 49.6 07 3.4 40.6 35 to 64 years 100.0 5.8 13.0 1.6 413 19.0 24 9.1 65 years and older 100.0 24 37 11 30.5 51.2 1 3.9 Black All ages 100.0 40 14 1.0 58.5 8.8 1.5 5.1 2 to 17 years 100.0 13, 10.7 *07 68.3 *0.2 12 6.6 18 to 34 years 400.0 4.9 13.3 15 63.8 *07 25 46 35 to 64 years 100.0 6.0 W? 0.9 52.8 13.0 1.1 49 65 years and older 100.0 3.0 7.0 *10 36.6 39.2 *0.9 3.4 Other All ages 100.0 37 10.8 1.6 52.1 6.1 2.2 9.2 2 to 17 years 100.0 “7 11.4 *0.3 49.8 *0.0 *2.4 12.6 18 to 34 years 100.0 46 W7 *25 59.4 *0.3 *2.2 8.8 35 to 64 years 100.0 46 108 *19 51.0 8.2 *2.6 77 65 years and older 100.0 *28 *42 *07 314 449 *07 *5.9 Hispanic origin Non-Hispanic Ail ages 100.0 43 13.0 VW 45.7 15.6 2.2 9.1 2 to 17 years 100.0 13 14.4 13 56.2 0.2 19 12.8 18 to 34 years 100.0 6.0 18.9 25 51.6 07 3.2 10.1 35 to 64 years 100.0 58 12.0 15 425 18.8 2.2 87 65 years and older 100.0 2.1 40 11 30.9 50.4 11 3.9 Hispanic, total All ages 100.0 40 19.1 18 56.1 3.5 2.6 59 2 to 17 years 100.0 16 18.4 24 59.5 *0.1 2.2 73 18 to 34 years 100.0 5.2 20.1 15 57.9 *0.2 33 5.6 35 to 64 years 100.0 53 207 1.6 52.2 6.5 23 5.2 65 years and older 100.0 *46 8.2 14 40.7 319 *1.6 *3.4 84 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL The Magnitude of the Problem All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth important Reason Hispanic, Mexican American All ages 100.0 3.6 20.7 17 ‘56.2 2.4 23 53 2 to 17 years 100.0 *1.4 19.4 2.6 60.7 *0.1 2.2 55 18 to 34 years 100.0 47 21.0 *0.9 57.5 *0.1 28 48 35 to 64 years 100.0 5.2 243 14 50.1 45 17 6.4 65 years and older 100.0 *43 "1d *14 38.7 30.5 *18 *18 Hispanic, other All ages 100.0 47 16.3 2.0 55.9 53 3.1 7.0 2 to 17 years 100.0 *18 163 *19 56.9 *0.2 *2.0 113 18 to 34 years 100.0 6.2 18.5 24 58.7 *0.4 44 7.0 35 to 64 years 100.0 55 163 *18 54.9 8.9 3.1 38 65 years and older 100.0 *4.9 *57 14 428 33.2 14 **49 Place of residence MSA, total? All ages 100.0 44 13.4 18 46.6 12.8 24 9.0 2 to 17 years 100.0 13 14.1 14 55.7 0.3 2.0 12.1 18 to 34 years 100.0 57 18.5 2.6 51.6 0.5 33 9.6 35 to 64 years 100.0 6.1 12.6 16 43.1 16.0 2.4 87 65 years and older 100.0 23 42 1 31.4 47.6 12 40 MSA, central city? All ages 100.0 44 14.0 17 48.0 19 2.6 78 2 to 17 years 100.0 1.6 14.6 14 56.5 *0.2 2.0 10.0 18 to 34 years 100.0 53 179 25 54.2 0.4 3.6 8.4 35 to 64 years 100.0 6.4 14.1 13 43.9 148 25 73 65 years and older 100.0 25 47 13 31.5 46.3 VW 42 MSA, not central city’ All ages 100.0 43 13.0 18 45.5 13.5 23 9.9 2 to 17 years 100.0 12 137 14 55.1 *0.4 2.0 137 18 to 34 years 100.0 6.0 19.0 2.6 49.5 0.6 31 10.6 35 to 64 years 100.0 5.8 11.6, 17 42.6 16.8 24 9.6 65 years and older 100.0 2.1 3.9 1.0 313 48.5 0.8 40 Not MSA? ; All ages 100.0 4) 14.4 14 477 18.8 17 8.0 2 to 17 years 100.0 13 18.0 1.6 60.0 *0.1 15 11.2 18 to 34 years 100.0 6.9 21.1 17 55.4 42 27 9.1 35 to 64 years 100.0 49 3.1 12 43.8 23.1 1.6 77 65 years and older 100.0 2.0 39 1.0 30.7 55.2 0.9 35 Family income? Less than $10,000 All ages 100.0 3.8 19.7 17 42.8 22.5 14 6.4 2 to 17 years 100.0 *11 19.4 2.6 60.0 *0.3 19 9.6 18 to 34 years 100.0 57 28.8 2.4 517 *0.9 19 72 35 to 64 years 100.0 6.3 25.2 “41 35.5 25.1 14 54 65 years and older 100.0 2.0 6.6 *0.9 27.4 57.4 *07 3.9 $10,000 to $19,999 : All ages 100.0 40 18.8 15 47.0 17.4 17 6.5 2 to 17 years 100.0 14 219 14 58.8 “0.1 13 79 18 to 34 years 100.0 6.1 278 18 53.2 05 24 7.9 35 to 64 years 100.0 47 19.2 15 43.6 21.7 1.6 57 65 years and older 100.0 3.0 3.4 1.2 31.4 51.9 13 43 $20,000 to $34,999 All ages 100.0 48 13.7 17 513 W5 23 11.1 2 to 17 years 100.0 1.6 144 0.9 59.7 *0.1 17 13.8 18 to 34 years 100.0 6.4 18.1 28 547 0.8 33 123 35 to 64 years 100.0 6.4 12.5 14 46.2 18.5 2.0 10.2 65 years and older 100.0 18 2.4 3 38.5 477 "15 47 (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 85 The Magnitude of the Problem TABLE 4.6 continued All with No Visits Access No Dental Not Other in Past Year Fear Cost Problem Problem No Teeth Important Reason $35,000 or more All ages 100.0 59 68 2.6 523 8.1 41 14.1 2 to 17 years 100.0 11 5.8 2.0 56.8 *0.6 31 20.2 18 to 34 years 100.0 70 9.2 3.6 55.4 *0.6 54 13.4 35 to 64 years 100.0 78 6.0 23 49.7 13.2 4.0 129 65 years and older 100.0 *28 3.8 *1.6 379 41.6 *2.0 44 Dental insurance coverage With dental insurance All ages 100.0 6.2 72 25 53.2 10.1 34 15.2 2 to 17 years 100.0 12 78 1.2 61.4 *0.3 24 18.8 18 to 34 years 100.0 8.5 9.5 4) 55.5 0.8 51 16.3 35 to 64 years 100.0 8.0 6.0 22 48.8 17.4 31 137 65 years and older 100.0 25 *1.6 1 39.3 447 *1.0 57 Without dental insurance , All ages 100.0 4.0 18.5 15 487 17.2 2.0 7.0 2 to 17 years 100.0 16 20.5 17 60.1 *0.2 19 99 18 to 34 years 100.0 55 26.7 19 56.3 07 27 76 35 to 64 years 400.0 54 18.9 13 45.1 19.9 21 6.8 65 years and older 100.0 23 4.9 1.2 31.9 52.5 12 3.9 Insurance status unknown All ages 100.0 1.6 39 0.7 23.8 93 0.8 2.9 2 to 17 years 100.0 *0.6 47 *1.0 25.7 *0.1 *0.6 3.6 18 to 34 years 100.0 23 5.1 *0.9 28.2 *0.3 11 35 35 to 64 years 100.0 15 3.4 *03 20.8 9.2 *07 2.0 65 years and older 100.0 “14 *1.6 *0.6 198 36.8 *0.6 2.6 Limitation of activity Unable to carry on usual activity All ages 100.0 4.4 15.4 17 33.2 31.9 11 6.2 2 to 17 years 100.0 *6.0 *27.6 *0.0 36.6 *0.0 *15 *20.1 18 to 34 years 100.0 74 253 *1.9 471 *19 *19 6.1 35 to 64 years 100.0 54 18.3 *12 34.5 28.9 *11 6.6 65 years and older 100.0 17 6.6 2.4 26.0 49.9 *07 46 Limited in amount or kind of major activity All ages 100.0 4.4 15.2 19 34.5 29.7 7 75 2 to 17 years 100.0 17 18.9 *25 58.0 *9.3 *2.0 9.1 18 to 34 years 100.0 6.9 30.2 *3.9 443 *0.8 *18 10.4 35 to 64 years 100.0 6.1 17.6 VW 31.2 27.1 2.2 93 65 years and older 100.0 2.4 51 *1.2 26.3 54.3 1 3.9 Limited, but not in major activity All ages 100.0 44 12.4 0.9 343 35.8 15 63 2 to 17 years 100.0 17 28.0 *22 53.0 *0.0 7 *10.8 18 to 34 years 100.0 8.0 29.2 19 50.5 *14 *17 10.3 35 to 64 years 100.0 6.3 17.5 *0.8 35.3 24.0 *2.0 8.0 65 years and older 100.0 2.6 3.9 *0.6 28.2 544 *12 3.9 Not limited in activity All ages 100.0 43 13.5 17 49.6 10.4 2.4 9.2 2 to 17 years 100.0 13 14.7 14 56.9 0.2 19 19 18 to 34 years 100.0 58 18.2 24 52.9 0.6 33 96 35 to 64 years 100.0 5.8 3 15 46.1 15.1 24 8.6 65 years and older 100.0 2.1 34 0.9 34.3 473 1.2 37 4 MSA = metropolitan statistical area. > Persons with unknown income not shown separately. Note: Data are based on household interviews of the civilian noninstitutionalized population. * = Figure does not meet the standard of reliability or precision (more than 30 percent relative standard error and numerator of percent or rate). Source: Bloom et al. 1992. 86 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL TABLE 4+.7 Estimated number and percentage of people with unmet health care wants, by selected characteristics, 1994 Medical or Number of People Dental Care Surgical Care (in millions) (percentage) (percentage) All people 259.2 8.5 5.6 Age and sex Children, 1 to 18 years 73.5 5.9 2.9 Adult men, 19 to 64 years 75.3 9.5 5.8 Adult women, 19 to 64 years 79.3 12.1? 9.3? Elderly people, 65 years and older 31.1 3.6 2.4 Race/ethnicity White 191.4 74 4.6 Black 32.2 15.07 10.2? Hispanic 23.9 8.2 6.2 Other W7 9.9 8.6 Health status Fair or poor 24.6 16.1? 11.2? Good or excellent 233.5 77 5.0 Number of chronic conditions None 158.6 73 46 One or more 100.6 10.4 7 Geographical region Northeast 478 6.9 58 Midwest 65.8 6.9 45 South 92.6 11.2? 6.1 West 53.1 74 5.9 Rural/urban status Metropolitan statistical areas 208.2 * 8.6 5.6 Nonmetropolitan statistical areas 50.5 8.1 59 Education level of head of household High school or less 117.5 9.4 6.8 Some post-high school 141.2 73 47 Family income status Less than 150 percent of the poverty level 55.7 16.4 9.12 150 percent of the poverty level or more 1743 6.3? 45 Health insurance status Private 166.6 5.9 41 Medicare 36.0 5.67 3.1? Medicaid 22.2 12.2 8.0 Uninsured 32.5 22.6 14.9 Type of private heaith insurance Health maintenance organization/ independent practice association 45.1 5.5? 5.0 Preferred provider organization 30.7 46 41 Fee-for-service 735 5.3? 3.7 The estimate differs from the percentage for the “all people” demographic at the 1 percent confidence level based ona two-tailed ¢-test of the difference in weighted estimates. Note: The standard error of each percentage is less than 30 percent of the percentage estimate. Source: Mueller et al. 1998. Access to dental care in the United States. JADA 1998 April; 129(4):429-37. Copyright 1998 by Journal of the American Dental Association. Reprinted by permission of ADA Publishing Co. Inc. (2000). ORAL HEALTH IN AMERICA: A REPORT OF T The Magnitude of the Problem prophylaxis, and 29 percent had at least one tooth filled. Edentulism is virtually nonex- istent in the active duty military population. Also, active duty mili- tary personnel have a significantly lower proportion of their decayed, missing, and filled surfaces that are untreated: this is primarily due to dramatic improvements in the oral health of active duty blacks when compared to their civilian counter- parts. Active duty whites also have somewhat better ora) health than white civilians of a similar age. The relative proportion of un- filled surfaces as a component of decayed and filled tooth surfaces in the military and civilian popula- tions is illustrated in Figure 4.25. ORAL HEALTH STATUS IN CHANGING TIMES The burden of oral diseases and conditions in the United States is extensive and affects persons throughout their life span. Birth defects such as cleft lip/palate, dental caries, and facial trauma are common in the young. Periodontal diseases, autoimmune disorders, and other chronic disabling condi- tions are seen in adults, while complete tooth loss and oral cavity and pharyngeal cancers are seen more often in older Americans. Because the most common oral disease, dental caries, is so wide- spread in the population, nearly every American has experienced oral disease. The effects of oral diseases and conditions on quality of life and well-being are discussed in Chapter 6. In sum, conditions such as cleft lip and palate and oral cancer not only involve costly and difficult surgeries and treatments, they also alter facial appearance and impair oral functioning. Pain disorders and pain as a COnse- quence of dental disease are preva- lent in certain groups and can affect daily living. HE SURGEON GENERAL 87 The Magnitude of the Problem The available trend data reveal improvements in dental health for most Americans; however, despite improvements in dental status, disparities remain. Diseases disproportionately affect some sex, income, and racial/ethnic groups, and the magnitude of the differences is striking. All the reasons for these dis- parities are not clear. Some of the most common den- tal diseases, such as dental caries, are preventable (prevention of oral diseases and conditions is pre- sented in Chapters 8 and 9). It appears, however, that not all individuals are benefiting from interventions that involve professional care, as represented by the data on dental visits. At the same time, as presented in Chapter 7, about 40 percent of the public does not receive the benefits of community water fluoridation. The emerging data on the effects of socioeconomic status on oral health are beginning to explain some, but not all, racial/ethnic differences. For other dis- eases, health disparities appear not to be related to professional services; a better understanding of the reasons for these differences is needed. This review of available data on oral diseases and conditions also reveals the lack or limitation of national or state data on oral diseases for many pop- ulation subgroups and for many conditions that affect the craniofacial structures. Information on the variables needed to explain health status differences, such as detailed utilization and expenditure data and data on services rendered, is limited as well. Data on specific services—self-care, services provided by pro- fessionals, and services that are community-based— are needed to understand the dimensions of oral health. (Some of these services are described in Chapters 7 and 8.) Although some data on expendi- tures for care and health care personnel are available to (Chapter 9) complement the statistics needed to assess oral health in the United States, almost all these data come from cross-sectional surveys that do not allow for analysis of the outcomes of disease and related care. Available state data reveal variations within and among states in patterns of oral health and disease among population groups. Having state-specific and local data that augment national data is critical in identifying high-risk populations and areas and in addressing health disparities. These data also are vital in program evaluation, planning, and policy deci- sions. Yet state and local data are almost nonexistent. In recent years, the need for state and local data has intensified as more programs are funded by local authorities and responsibilities are shifted from national to state-based levels. The nation’s health information system is under- going constant change to meet the current and future needs for health information. Consequently, many factors influence how and what data are collected and analyzed. These factors include emerging technolo- gies, legislation about how data are to be collected, and confidentiality and privacy concerns. The need for epidemiologic and surveillance data change as the understanding of specific diseases and conditions evolves and as society's goals and priori- ties change. The increasing focus on the long-term benefits of disease prevention and health promotion and the need to close the gap on disparities also affects how and what data are collected. For example, major initiatives such as the Department of Health and Human Services's Healthy People 2010 have pro- vided a framework for data collection and analysis tied to specific objectives and have helped identify needs for new health data systems. FIGURE 4.25 than for males in the U.S. military 50 45 Percentage decayed of decayed and filled surfaces 5 oe The percentage of unfilled decayed surfaces is higher for civilian males 40 35 30 The Healthy People initiative now includes objectives for the nation’s health status as well as for preven- tive interventions and objectives that would improve infrastructure and capacity building to provide the necessary services and moni- toring. This overview of the magni- tude of oral diseases and condi- tions in America raises many ques- tions still to be researched. If cer- tain oral diseases are preventable, Age group ~®> Black civilian Source: York et al. 1995. —* White civilian 18-19 20-24 25-29 30-34 35-39 ~ Black military —e White military : why do we have populations with 40-44 extensive and untreated disease? Once socioeconomic factors are controlled, why do we see differ- ences in services received? Why 38 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL are some conditions more prevalent in certain popu- lations than in others? How will the rapidly changing and projected demographics of America contribute to future trends in oral and craniofacial health and dis- ease? These and many other questions require more research, new databases, and an active and trained group of researchers. FINDINGS e Over the past five decades, major improve- ments in oral health have been seen nationally for most Americans. e Despite improvements in oral health status, profound disparities remain in some population groups as classified by sex, income, age, and race/eth- nicity. For some diseases and conditions, the magni- tude of the differences in oral health status among population groups is striking. e Oral diseases and conditions affect people throughout their life span. 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Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute; 1985. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 93 oS What Is the Relationship Between Oral Health and General Health and Well-being? The next two chapters establish that oral health is essential to general health and well-being. Chapter 5 examines multiple linkages between oral and general health. The mouth and the face reflect signs and symptoms of health and disease that can serve as an adjunct for diagnosis for some conditions. Diagnostic tests using oral cells and fluids—especially saliva—are available to detect drug abuse, hormonal changes, and specific diseases; and more are being developed. The mouth is also a portal of entry for pathogens and toxins, which can affect the mouth and, if not cleared by the many defense mechanisms that have evolved to protect the oral cavity, may spread to the rest of the body. Recent epidemiologic and experimental animal research provides evidence of possible associations between oral infections—particularly periodontal disease—and diabetes, cardiovascular disease, and adverse pregnancy outcomes, and this evidence is reviewed. The review highlights the need for an aggressive research agenda to better delineate the specific nature of these associations and the underlying mechanisms of action. Chapter 6 looks at the impact of oral health problems on the quality of life and includes examples of the kinds of questionnaires used to measure oral-health-related quality of life. Oral health is highly valued by society and individuals, and the chapter begins with a brief description of the reflections of those values in myth and folklore concerning facial appearance and the meaning of teeth. It then explores dimensions beyond the biological and the physical to examine how oral diseases and disorders can interfere with the functions of daily living, including participation in work or school, and what is known about their psychosocial impacts and economic costs, The deleterious effects of facial disfigurement and tooth loss may be magnified in a society such as ours that celebrates youth and beauty. Self-reported impacts of oral conditions on social functions include limitations in communication, social interactions, and intimacy. Research on the oral-health-related quality of life is needed to permit further exploration of the dimensions of oral health and well-being. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 95 POLPT ER See Linkages with General Health The mouth and face are highly accessible parts of the body, sensitive to and able to reflect changes occurring internally. The mouth is the major portal of entry to the body and is equipped with formidable mechanisms for sensing the environment and defending against toxins or invading pathogens. In the event that the integrity of the oral tissues is compromised, the mouth can become a source of disease or pathological processes affecting other parts of the body. It can also become a source of contagion by means of contaminated fluids or materials passed to others. This chapter explores what the mouth and face can reveal about general health, describes the role the mouth plays as a portal of entry for infection, and concludes with studies that are associating oral infections with serious systemic diseases and conditions. THE MOUTH AND FACE AS A MIRROR OF HEALTH AND DISEASE A physical examination of the mouth and face can reveal signs of disease, drug use, domestic physical abuse, harmful habits or addictions such as smoking, and general health status. Imaging (e.g., x-ray, MRI, SPECT) of the oral and craniofacial structures may provide early signs of skeletal changes such as those occurring with osteoporosis and musculoskeletal disorders, and may also reveal salivary, congenital, neoplastic, and developmental disorders. Oral cells and fluids, especially saliva, can be tested for a wide range of substances, and oral-based diagnostics are increasingly being developed and used as a means to assess health and disease without the limitations and difficulties of obtaining blood and urine. Physical Signs and Symptoms of Disease and Risk Factors A number of signs and symptoms of disease, lifestyle behaviors, and exposure to toxins can be detected in or around the craniofacial complex. Pathogens enter- ing the mouth may proliferate locally with oral and pharyngeal signs and symptoms; other pathogens may enter the bloodstream directly or through lym- phatic channels and cause generalized disease. Oral signs suspected to be indications of systemic illness may be confirmed by the presence of rash, fever, headache, malaise, enlarged lymph nodes, or lesions elsewhere on the body. Swollen parotid glands are a cardinal sign of infection with the mumps virus and can also be seen in individuals with Sjogren’s syndrome and HIV. The salivary glands are also frequently involved in tuber- culosis and histoplasmosis infections. Oral signs of infectious mononucleosis, caused by Epstein-Barr virus, include sore throat, gingival bleeding, and multiple pinpoint-sized hemorrhagic spots (pettechi- ae) on the oral mucosa. The oral signs and symptoms associated with some viral, bacterial, and fungal infections are listed in Table 5.1. There can be a large overlap in the clinical appearance of oral manifesta- tions of various diseases with different etiologies, and the clinical diagnosis often involves ancillary proce- dures, which may include laboratory tests, diagnostic imaging, and biopsy. Oral tissues may also reflect immune deficiency. For example, nearly all HIV-infected individuals develop oral lesions at some time during their illness (Greenberg 1996, Greenspan and Greenspan 1996, Phelan 1997). Other immunosuppressed individuals may have the same lesions (Glick and Garfunkel 1992). However, the presentation and the extent, sev- erity, and management of some of these lesions may reflect nuances due to variation in the underlying ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 97 Linkages with General Health TABLE 5.1 Condition Usual Location Diseases and conditions causing lesions of the oral mucosa Clinical Features Course Viral Diseases Primary acute herpetic gingivostomatitis (herpes simplex virus type 1, rarely type 2) Recurrent herpes labialis Recurrent intraoral herpes simplex Chickenpox (varicella-zoster virus) Herpes zoster (reactivation of varicella-zoster virus) Infectious mononucleosis (Epstein-Barr virus) Warts (papillomavirus) Herpangina (coxsackievirus A;also possibly coxsackievirus B and echovirus) Hand, foot, and mouth disease (type A coxsackieviruses) Primary HIV infection Lip and oral mucosa Mucocutaneous junction of lip, perioral skin Palate and gingiva Gingiva and oral mucosa Cheek, tongue, gingiva, or palate Oral mucosa Anywhere on skin and oral mucosa Oral mucosa, pharynx, tongue Oral mucosa, pharynx, palms, and soles Gingiva, palate, and pharynx Labial vesicles that rupture and crust, and intraoral vesicles that quickly ulcerate; extremely painful; acute gingivitis, fever, malaise, foul odor, and cervi- cal lymphadenopathy; occurs primarily in infants, children, and young adults Eruption of groups of vesicles that may coalesce, then rupture and crust; painful to pressure or spicy foods Smail vesicles that rupture and coalesce; painful Skin lesions may be accompanied by small vesicles on oral mucosa that rupture to form shallow ulcers; may coalesce to form large bullous lesions that ulcerate; mucosa may have generalized erythema Unilateral vesicular eruption and ulceration in lin- ear pattern following sensory distribution of trigeminal nerve or one of its branches Fatigue, sore throat, malaise, low-grade fever, and enlarged cervical lymph nodes; numerous small ulcers usually appear several days before lym- phadenopathy; gingival bleeding and multiple petechiae at junction of hard and soft palates Single or multiple papillary lesions, with thick, white keratinized surfaces containing many point- ed projections; cauliflower lesions covered with normal-colored mucosa or multiple pink or pale bumps (focal epithelial hyperplasia) Sudden onset of fever, sore throat, and oropharyn- geal vesicles, usually in children under 4 years, during summer months; diffuse pharyngeal con- gestion and vesicles (1 to 2 mm), grayish-white surrounded by red areola; vesicles enlarge and ulcerate Fever, malaise, headache with oropharyngeal vesi- cles that become painful, shallow ulcers Acute gingivitis and oropharyngeal ulceration, associated with febrile illness resembling mononu- cleosis and including lymphadenopathy Heals spontaneously in 10 to 14 days unless secondarily infected Lasts about 1 week, but condition may be prolonged if secondary infection occurs Healspontaneously in about 1 week Lesions heal spontaneously within 2 weeks Gradual healing without scarring; postherpetic neuralgia is common Oral lesions disappear during con- valescence Lesions grow rapidly and spread Incubation period 2 to 9 days; fever for 1 to 4 days; recovery uneventful Incubation period 2 to 18 days; lesions heal spontaneously in 2 to 4 weeks Followed by HIV seroconversion, asymptomatic HIV infection, and usually ultimately by HIV disease 98 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health Condition Usual Location Clinical Features Course Bacterial or fungal diseases Acute necrotizing ulcerative gingivitis (“trench mouth,” Vincent's infection) Prenatal (congenital) syphilis Primary syphilis (chancre} Secondary syphilis Tertiary syphilis Gonorrhea Tuberculosis Cervicofacial actinomycosis Histoplasmosis Candidiasis Ginaiva Palate, jaws, tongue, and teeth Lesion appears where organism enters body; may occur on lips, tongue, or tonsillar area Oral mucosa frequently involved with mucous patches, primarily on palate, also at commissures of mouth Palate and tonque Lesions may occur in mouth at site of inoculation or secondarily by hematogenous spread from a primary focus elsewhere Tongue, tonsillar area, soft palate Swellings in region of face, neck, and floor of mouth Any area in mouth, particularly tongue, gingiva, or palate Any area of oral mucosa Painful. bleeding gingiva characterized by necrosis and ukeration of gingival papillae and margins plus lymphadenopathy and foul odor Gummatous involvement of palate, jaws, and facial bones; Hutchinson's incisors, mulberry molars, glossitis, mucous patches, and fissures of corners of mouth Small papule developing rapidly into a large, painless ulcer with indurated border; unliteral lymphadenopathy; chancre and lymph nodes con- taining spirochetes; serologic tests positive by third to fourth week Maculopapular lesions of oral mucosa, 5 to 10 mm in diameter with central ulceration covered by grayish membrane; eruptions occurring on various mucosal surfaces and skin accompanied by fever, malaise, and sore throat Gummatous infiltration of palate or tongue fol- lowed by ulceration and fibrosis; atrophy of tongue papillae produces characteristic bald tongue and glossitis Earliest symptoms are burning or itching sensa- tion, dryness, or heat in mouth followed by acute pain on eating or speaking; tonsils and orophar- ynx most frequently involved; oral tissues may be * diffusely inflamed or ulcerated; saliva develops increased viscosity and fetid odor; submaxillary lymphadenopathy with fever in severe cases A solitary, irregular ulcer covered by a persistent exudate; ulcer has an undermined, firm border Infection may be associated with an extraction, jaw fracture, or eruption of molar tooth; in acute form resembles an acute pyogenic abscess, but contains yellow “sulfur granules” (gram-positive mycelia and their hyphae} Numerous small nodules may ulcerate; hoarse- ness and dysphagia may occur because of lesions in larynx usually associated with fever and malaise Pseudomembranous form has white patches that are easily wiped off leaving red, bleeding, sore surface; erythematous form is flat and red; rarely, candidal leukoplakia appears as white patch in tongue that does not rub off; angular cheilitis due to Candida involves sore cracks and redness at angie of mouth; Candida seen on KOH prepara- tion in all forms Continued destruction of tissue fol- lowed by remission, but may recur Tooth deformities in permanent dentition irreversible Healing of chancre in 1 to 2 months, followed by secondary syphilis in 6 to 8 weeks Lesions may persist from several weeks to 1 year Gumma may destroy palate, caus- ing complete perforation Lesions may resalve with appropti- ate antibiotic therapy Lesions may persist Acute form may last a few weeks, chronic form lasts months or years; prognosis excellent; actin- omycetes respond to antibiotics (tetracyclines or penicillin) but not antifungal drugs May be fatal Responds to antifungals (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 99 Linkages with General Health Condition TABLE 5.1 continued Usual Location Clinical Features Course Dermatologic diseases Mucous membrane pemphigoid Erythema multiforme (Stevens-Johnson syndrome) Pemphigus vulgaris Lichen planus Other conditions Recurrent aphthous ulcers Behcet's syndrome Traumatic ulcers Primarily mucous membranes of the oral cavity, but may also involve the eyes, urethra, vagi- na, and rectum Primarily the oral mucosa and skin of hands and feet Oral mucosa and skin Oral mucosa and skin Anywhere on nonkeratinized oral mucosa (lips, tongue, buc- cal mucosa, floor of mouth, soft palate, oropharynx) Oral mucosa, eyes, genitalia, gut, and central nervous system Anywhere on oral mucosa; den- tures frequently responsible for ulcers in vestibule Painful, grayish-white collapsed vesicles or bullae with peripheral erythematous zone; gingival lesions desquamate, leaving ulcerated area Intraoral ruptured bullae surrounded by an inflammatory area; lips may show hemorrhagic crusts: the “iris,” or “target” lesion, on the skin is pathognomonic; patient may have severe signs of toxicity Ruptured bullae and ulcerated oral areas; mostly in older adults White striae in mouth; purplish nodules on skin at sites of friction; occasionally causes oral mucosal ulcers and erosive gingivitis Single or clusters of painful ulcers with surround- ing erythematous border; lesions may be 1 to 2 mm in diameter in crops (herpetiform), 1 to 5 mm (minor), or 5 to 15 mm (major) Multiple aphthous ulcers in mouth; inflammatory ocular changes; ulcerative lesions on genitalia; inflammatory bowel disease and CNS disease Localized, discrete ulcerated lesion with red bor- der; produced by accidental biting of mucosa, penetration by a foreign object, or chronic irrita- tion by a denture Protracted course with remissions and exacerbations; involvement of different sites occurs slowly; glu- cocorticoids may temporarily reduce symptoms but do not control the disease Onset very rapid; condition may last 1 to 2 weeks; may be fatal; acyte episodes respond to steroids With repeated recurrence of bul- lae, toxicity may lead to cachexia, infection, and death within 2 years; often controllable with steroids Protracted course, may respond to topical steroids Lesions heal in 1 to 2 weeks but may recur monthly or several times a year; topical steroids give symptomatic relief; systemic glu- cocorticoids may be needed in severe cases; a tetracycline oral suspension may decrease severity of herpetiform ulcers Ulcers may persist for several weeks and heal without scarring Lesions usually heal in 7 to 10 days when irritant is removed, unless secondarily infected Source: Greenspan, in Fauci et al, 1998. Harrison's principles of internal medicine. Reprinted by permission from McGraw-Hill (2000). Copyright 2000 by McGraw-Hill. systemic condition. For example, the linear gingival erythema and necrotizing ulcerative periodontitis sometimes seen in HIV infection have been difficult to resolve with routine dental curettage and prophy- laxis (Glick et al. 1994b). The appearance of soft or hard tissue pigmentation is associated with a number of diseases and treatments. Malignant melanoma can appear in the mouth as brown or black flat or raised spots. Kaposi's sarcoma can appear as a flat or raised pig- mented lesion. Addison's disease causes blotches or spots of bluish-black or dark brown pigmentation to occur early in the disease. Congenital discrete brown or black patches (nevi) can appear in any part of the mouth. Pigmentation of the tooth crowns may be seen in children with cystic fibrosis and porphyria and those exposed to tetracycline during tooth development. The oral tissues can also reflect nutritional status and exposure to risk factors such as tobacco. The 100 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL tongue appears smooth in pernicious anemia. Group B vitamin deficiency is associated with oral mucositis and ulcers, glossitis, and burning sensations of the tongue. Scurvy, caused by severe vitamin C deficien- cy, is associated with gingival swelling, bleeding, ulceration, and tooth loosening. Lack of vitamin D in utero or infancy impairs tooth development. Enamel hypoplasia may result from high levels of fluoride or from disturbances in calcium and phosphate metab- olism, which can occur in hypoparathyroidism, gas- troenteritis, and celiac disease. The mouth also can reflect the effects of tobacco use, perhaps providing the only visible evidence of its adverse effects. Oral Manifestations of HIV Infection and of Osteoporosis The mouth can serve as an early warning system, diagnostic of systemic infectious disease and predic- tive of its progression, such as with HIV infection. In the case where oral cells and tissues have counter- parts in other parts of the body, oral changes may indicate a common pathological process. During rou- tine oral examinations and perhaps in future screen- ing tests, radiographic or magnetic resonance imag- ing of oral bone may be diagnostic of early osteo- porotic changes in the skeleton. The following sec- tions provide details. HIV Infection The progressive destruction of the body's immune system by HIV leads to a number of oral lesions, such as oral candidiasis and oral hairy leukoplakia, that have been used not only in diagnosis but also in determining specific stages of HIV infection (CDC 1992, 1994, Montaner et al. 1992, Redfield et al. 1986, Royce et al. 1991, Seage et al. 1997). Oral can- didiasis is rarely seen in previously healthy young adults who have not received prior medical therapy such as cancer chemotherapy or treatment with other immunosuppressive drugs (Klein et al. 1984). It was associated with AIDS as early as 1981 in the first report of the syndrome (CDC 1981a) and was fre- quently noted among otherwise asymptomatic HIV- positive populations (Duffy et al. 1992, Feigal et al. 1991). Oral candidiasis may be the first sign of HIV infection and often occurs as part of the initial phase of infection—the acute HIV syndrome (Tindall et al. 1995). It tends to increase in prevalence with pro- gression of HIV infection when CD4 lymphocyte counts fall (Glick et al. 1994a, Lifson et al. 1994). It also appears to be the most common oral manifesta- tion in pediatric HIV infection (Kline 1996, Leggott Linkages with General Health 1995, Ramos-Gomez et al. 1996) and has been demonstrated to proceed to esophageal candidiasis, a sign of overt AIDS (Saah et al. 1992). Both the pseudo- membranous and the erythematous forms of candidi- asis appear to be important predictors of progression of HIV infection (Dodd et al. 1991, Klein et al. 1984, 1992). Like oral candidiasis, oral hairy leukoplakia in HIV-positive persons heralds more rapid progression to AIDS (Glick et al. 1994a, Greenspan et al. 1987, Lifson et al. 1994, Morfeldt-Manson et al. 1989). Oral hairy leukoplakia is an oral lesion first reported in the early days of the AIDS epidemic (Greenspan Det al. 1984, Greenspan JS et al. 1985). Since its discov- ery, hairy leukoplakia has been found in HIV-negative persons with other forms of immunosuppression, such as organ or bone marrow recipients and those on long-term steroid therapy (Epstein et al. 1988, Greenspan et al. 1989, Itin et al. 1988, King et al. 1994, Zakrzewska et al. 1995), and less frequently among immunocompetent persons (Eisenberg et al. 1992, Felix et al. 1992). In a comprehensive review of periodontal condi- tions, Mealey (1996) noted that linear gingival ery- thema and necrotizing ulcerative periodontitis may be predictive of progression of HIV infection. Necrotizing ulcerative periodontitis, a more serious periodontal condition observed in HIV-infected per- sons, is a good predictor of CD4+ cell counts of under 200 per cubic millimeter, and in one study was a strong predictor of rapid progression to death (Glick et al. 1994a,b, Winkler and Robertson 1992, Winkler et al. 1988). In addition, the numerous ulcerative and nonulcerative conditions that affect the oral cavity (Aldous and Aldous 1991, Coates et al. 1996, Cruz et al. 1996, Gandolfo et al. 1991, Itin et al. 1993, Mealey 1996) may affect the biologic activity of HIV and are affected by its treatments. Other oral conditions, unexpected in the oral cavity, have been noted in the early stages of HIV infection. The increased incidence of Kaposis sarco- ma among young men in New York and California was one of the earliest signs of the AIDS epidemic (CDC 1981b). In addition, some conditions create a problem for differential diagnosis. For example, because involvement of the gingiva is common, early non-Hodgkin's lymphoma lesions are frequently mis- taken for common periodontal or dental infections (Epstein and Silverman 1992). The changing face of the HIV epidemic and changes in the therapies used to manage complica- tions are reflected in changes in the oral manifesta- tions, which warrant continued surveillance and research. The increasing resistance of microorganisms ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 101 Linkages with General Health to antibiotics and antifungals is challenging. On the other hand, the completion of the Candida albicans genome may yield better treatments for this oppor- tunistic infection. Osteoporosis and Oral Bone Loss With growing numbers of Americans living longer, there have been concomitant increases in the num- bers affected by age-related chronic degenerative dis- eases. Prominent among these conditions are bone and joint diseases. It is likely, for example, that some temporomandibular joint disorders are manifesta- tions of osteoarthritis, rheumatoid arthritis, or myofascial pain. Paget's disease, characterized by enlarged and deformed bone, can be particularly painful and debilitating when it affects the cranial and jaw bones. Osteoporosis, a degenerative disease character- ized by the loss of bone mineral and associated struc- tural changes, has long been suspected as a risk fac- tor for oral bone loss. In addition, measures of oral bone loss have been proposed as potential screening tests for osteoporosis (Jeffcoat 1998). Osteoporosis affects over 20 million people in the United States, most of whom are women, and results in nearly 2 million fractures per year (National Institute of Arthritis, Musculoskeletal and Skin Diseases 2000). The disease is more prevalent in white and Asian American women than in black women. Oral bone loss has been reported to be more prevalent in women than in men. Studies by Ortman et al. (1989) found a higher percentage of women than men with severe alveolar ridge resorption. This finding parallels the findings of Humphries et al. (1989), who showed that loss of bone mineral densi- ty with age in edentulous adult mandibles was more significant in women than in men. Also, the associa- tion between estrogen status, alveolar bone density, and history of periodontitis in postmenopausal women has been studied (Payne et al. 1997). Most of the studies in this area have examined bone loss in women, and most investigators have reported a correlation between oral and skeletal bone loss measured in a variety of ways. Studies of non- osteoporotic women by Kribbs et al. (1990) showed that mandibular bone mass is significantly correlated with skeletal bone mass. Dual photon absorptiometry measurements of jawbone volume in women with osteoporosis have shown that reduction in mandibu- lar bone mass is directly related to the reduction in total skeletal mass density (Kribbs and Chesnut 1984, Kribbs et.al. 1983, von Wowern 1985, 1988, von Wowern et al. 1994). Kribbs et al. (1989) further showed that mandibular mass is correlated with all skeletal measures in osteoporotic women and that the height of the edentulous ridge is correlated with total body calcium and mandibular bone mineral density. Hirai et al. (1993) found that the presence of skeletal osteoporosis strongly affects the reduction of the residual ridge in edentulous patients. A small case-control study comparing older female patients with osteoporotic fractures and non-osteoporotic women without fractures found greater periodontal attachment loss in the osteoporotic women than in the controls (von Wowern et al. 1994). Studies that have controlled for confounding fac- tors also have found correlations between oral bone loss and skeletal bone density. Controlling for pack- years of smoking, education, body anass, and years since menopause, Krall et al. (1994, 1996) found a significant positive relationship between number of teeth and bone mineral density of the spine and the radius. In a cohort of 70 postmenopausal women, Wactawski-Wende et al. (1996) measured skeletal bone mineral density at the Ward's triangle area of the femur and compared it with periodontal disease assessed by attachment loss and the height of alveo- lar bone measured by radiographs. After adjusting for age, years since menopause, estrogen use, body mass index, and smoking, the investigators concluded that osteopenia (low bone mass) is related to alveolar cres- tal height and tooth loss in postmenopausal women. Methods used to measure oral and skeletal bone loss have varied among investigators and have shown different outcomes. Kribbs (1990) found that patients in an osteoporotic group had lost more teeth, had less mandibular bone, and had a thinner bone measured at a part of the jaw (cortex at the gonion) than a comparable non-osteoporotic group. However, using periodontal attachment loss as an indicator of mandibular bone loss, they found no differences between the osteoporotic and the non-osteoporotic group. Mohajery and Brooks (1992) compared non- osteoporotic postmenopausal women with women with mild to moderate osteoporosis and found no correlation between mandibular and skeletal bone mineral density. This study raises questions about the quantification of mild and moderate osteoporosis. Defining healthy periodontal tissues as having no periodontal pockets deeper than 5 millimeters, Hildebolt et al. (1997) studied postmenopausal women with healthy periodontal tissues and found no relationship between periodontal attachment loss and postcranial bone mineral density. How- ever, preliminary studies from the oral ancillary study of the NIH Women’s Health Initiative report signi- ficant correlations between mandibular basal bone mineral density and hip bone mineral density 102 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL (r = 0.74, P < .001) Jeffcoat et al. in press). In this study, digital subtraction radiography methods were used for mandibular bone measurements, and dual- energy X-ray absorptiometry (DXA) scans were used for the hip bone measurements. The authors of this study propose the possibility that high-quality intra- oral radiographs may be used in the future for screen- ing osteopenia. Larger cross-sectional studies, as well as longitu- dinal and mechanism studies, are needed to better define the relationship between osteoporosis. osteopenia, and oral bone loss, periodontal disease, and tooth loss. The role of factors involved in the reg- TABLE 5.2 Saliva/oral fluids: sampled analytes and current FDA-approved tests Category Analytes Alcohol Amphetamines Barbiturates Benzodiazepines Methamphetamine Cocaine Opiates LSD PCP Marijuana Ethanol Nicotine Opiates PCP Antibodies? HIV HPV HHV-8/KSH C. parvum Helicobacter pylori FDA-Approved Tests Drugs of abuse? Cannabinoids Cocaine Cotinine HIV antibodies Hormanes¢ Cortisol Estriol Progesterone Testosterone Substance P Met-enkephalin Cadmium Lead Mercury Environmental toxins! Therapeutics? Antipyrine Carbamazepine Ciprofloxacin Irinotecan Lithium Methotrexate Phenytoin Phenobarbital Theophylline aCone et al. 1993, 1997. bConstantine et al. 1997. Dabbs 1993, Ellison 1993. éGonzalez et al. 1997, Joselow et al. 1968. eWilson 1993. Source: Constantine et al. 1997. Linkages with General Health ulation of bone mineral density in men as well as in postmenopausal women needs to be evaluated fur- ther with reference to oral bone loss, tooth loss, and periodontal disease. Variables such as sex, race, dietary calcium and phosphorus, vitamin D intake, exercise, body mass index, smoking, genetics, med- ication use, reproductive history, and psychosocial factors need to be assessed in depth. In addition, reli- able and valid criteria and imaging technologies for assessing osteoporosis and oral bone loss are needed to better elucidate the full relationship between skeletal and mandibular bone mineral density, peri- odontal disease, alveolar ridge resorption, and tooth loss. Oral-fluid-based Diagnostics: The Example of Saliva The diagnostic value of salivary secretions to detect systemic diseases has long been recognized (Mandel 1990), and oral fluids and tissues (buccal cells) are increasingly being used to diagnose a wide range of conditions. Saliva- and oral-based diagnostics use readily available samples and do not require invasive procedures. Researchers have detected antibodies in saliva that are directed against viral pathogens such as human immunodeficiency virus (Malamud 1997) and hepatitis A virus (O'Farrell et al. 1997) or B virus (Richards et al. 1996). Saliva is being used to detect antibodies, drugs, hormones, and environmental tox- ins (Malamud and Tabak 1993) (Table 5.2). The sim- plest tests are those that detect the presence or absence of a substance in the saliva, such as various drugs. Greater technical challenges are presented for tests that will be used for therapeutic monitoring since accurate levels of a substance and/or its metabolites are needed. In these instances the sali- va/plasma concentration ratio must be determined experimentally (Haeckel 1993). Tests beyond those listed in Table 5.2 are currently on the market, but do not yet have FDA approval. Saliva is also the fluid of choice to assess the integrity of the mucosal immune system (Mandel 1990). Most recently, oral fluids have been used as a source of microbial or host DNA. With the advent of polymerase chain reaction methods, the DNA con- tained within a single cell is sufficient for detection of viruses (e.g., Kaposi's sarcoma-associated herpes virus, Koelle et al. 1997; Epstein-Barr virus, Falk et al. 1997, mumps virus, Afzal et al. 1997) or bacteria (e.g., Helicobacter pylori, Reilly et al. 1997). Similarly, DNA extracted from sloughed buccal epithelial cells can be used to genotype persons. This has found application in forensics (Roy et al. 1997) and may be ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 403 Linkages with General Health used for diagnostic purposes in the future (van Schie and Wilson 1997). Saliva has the potential of replacing blood, the current standard for testing many diseases and conditions (e.g., diabetes, infectious disease, Parkinson's disease, alcoholic cirrhosis, Sjogren's syndrome, and cystic fibrosis sarcoidosis). Important goals for the future are the development of new diagnostic tests for early disease detection, defining individual patient risk of adverse response to drugs, monitoring therapeutic progress, and determin- ing outcomes of treatment. Key issues in the development of a new generation of saliva diag- nostics include their selectivity, sensitivity, response time, dynamic range (values of interest), rep- resentative sampling, and, perhaps most important, their reliability or stability as well their ability to assess multiple substances simultaneously. Conclusion For the clinician the mouth and face provide ready access to physical signs and symptoms of local and generalized disease and risk factor exposure. These signs and symptoms augment other clinical features of underlying conditions. Comprehensive care of the patient requires knowledge of these signs and symp- toms, their role in the clinical spectrum of general diseases and conditions, and their appropriate man- agement. Oral biomarkers and surrogate measures are also being explored as means of early diagnosis. With further development and refinement, oral- based diagnostics such as salivary tests can be- come widely used and acceptable tools for individu- als, health care professionals, researchers, and com- munity programs. The continued refinement of imaging techniques also has the potential of using oral imaging to identify early signs of skeletal bone degeneration. THE MOUTH AS A PORTAL OF ENTRY FOR INFECTION Chapter 3 provides an overview of the effects of oral microbial infections with viruses, bacteria, and fungi. More than 500 bacterial strains have been identified in dental biofilm, and more than 150 bacterial strains have been isolated from dental pulp infections. More recently, 37 unique and previously unknown strains of bacteria were identified in dental plaque (biofilm) (Kroes et al. 1999). Most oral lesions are opportunis- tic infections, that is, they are caused by microorgan- isms commonly found in the mouth, but normally kept in check by the body’s defense mechanisms. These microorganisms can induce extensive local- ized infections that compromise general well-being in and of themselves. However, they also may spread to other parts of the body if normal barriers are breached. The oral mucosa is one such barrier that provides critical defense against pathogens and other challenges (Schubert et al. 1999). Salivary secretions are a second major line of defense. Damage to the oral mucosa from mechanical trauma, infection, or salivary dysfunction with resulting derangements in lubricatory and antimicrobial functions of saliva, as a result of chemotherapy, radiation, and medications causing hyposalivation, allows a portal of entry for invading pathogens. Oral Infections and Bacteremia Oral microorganisms and cytotoxic by-products associated with local infections can enter the blood- stream or lymphatic system and cause damage or potentiate an inappropriate immune response else- where in the body. Dissemination of oral bacteria into the bloodstream (bacteremia) can occur after most invasive dental procedures, including tooth extrac- tions, endodontic therapy, periodontal surgery, and scaling and root planing. Even routine oral hygiene procedures such as daily toothbrushing, subgingival irrigation, and flossing may cause bacteremia. However, these distant infections have been seen more often in high-risk patients such as those who are immunocompromised. Oral bacteria have several mechanisms by which they invade mucosal tissues, perhaps contributing to their ability to cause bacteremias. For example, oral bacteria and their products may invade the periodontal tissues directly. Actinobacillus actino- mycetemcomitans has been found in gingival connective tissue in patients with localized juvenile periodontitis (Christersson et al. 1987a,b, Meyer et al. 1991, Riviere et al. 1991). Invasion of tissue by Porphyromonas gingivalis has also been described in vivo (Saglie et al. 1988) and in vitro (Njoroge et al. 1997, Sandros et al. 1993, 1994, Weinberg et al. 1997). Although oral bacteria can enter the blood through injured or ulcerated tissue, bacterial invasion of periodontal tissues represents another possible mechanism. In the immunocompetent individual, bacteremia originating from the oral cavity is usually transient and harmless. However, if the individual’s immune system is compromised, the normally harmless oral bacteria may pose a significant risk. The morbidity and mortality associated with oral foci of infections are hard to assess. This is due to the formidable task 104 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL of tracking the source of an infection unless the responsible pathogen is indigenous to a specific anatomic location. Viridans group streptococci (VGS) have a low degree of virulence but can be associated with mor- bidity and mortality under certain circumstances. Increased pathogenicity of Streptococcus viridans is most prominent in individuals with neutropenia (low blood counts of circulating white blood cells called neutrophils) and has been associated with a toxic- shock-like syndrome (TSLS) or viridans streptococ- cal shock syndrome (VSSS), as well as with adult res- piratory distress syndrome (ARDS) (Bochud et al. 1994). Although a high degree of morbidity is associat- ed with viridans streptococcal bacteremia, a low inci- dence of mortality has been reported (Heimdahl et al. 1989). Several studies have shown that under adverse circumstances oral flora and oral infections are associated with increased incidence of morbidity and even mortality (Engelhard et al. 1995, Lucas et al. 1998, Martino et al. 1995, Ruescher et al. 1998, Sparrelid et al. 1998, Sriskandan et al. 1995). Reduction of oral foci of infection decreases systemic complications, specifically in severely neutropenic patients undergoing chemotherapy (Heimdahl et al. 1984). In addition, hospital stays for patients with oral mucositis undergoing autologous bone marrow transplants were longer than for those without oral mucositis (Ruescher et al. 1998). Other cohorts identified at increased risk far sys- temic complications due to oral bacteria include hos- pitalized patients unable to perform adequate oral hygiene, those receiving saliva-reducing medications, and those taking antibiotics that alter the oral flora. A positive dental plaque culture for aerobic pathogens was significantly associated with the development of hospital-acquired pneumonia and bacteremia in a study of individuals in an intensive care unit (ICU) (Fourrier et al. 1998). In addition, several case reports have been pub- lished implicating indigenous oral flora in the devel- opment of brain abscesses (Andersen and Horton 1990, Andrews and Farnham 1990, Baker et al. 1999, Gallagher et al. 1981, Goteiner et al. 1982, Saal et al. 1988). This serious condition is associated with a mortality rate of almost 20 percent and full recovery in only slightly more than 50 percent of all patients (Goteiner et al. 1982). These data are based on single case reports and most probably represent rare events. However, they provide additional examples that point to the potential pathogenicity of the normal oral flora during special adverse circumstances. Linkages with General Health Oral Infections as a Result of Therapy Chemotherapy Oral mucositis can be a major dose-limiting problem during chemotherapy with some anticancer drugs, such as 5-fluorouracil, methotrexate, and doxoru- bicin. It is estimated that approximately 400,000 patients undergoing cancer therapy each year will develop oral complications (NIH 1990). Infection of ulcerated mucous membranes often occurs after chemotherapy, especially since patients are usually immunocompromised. Bacterial, fungal, and viral causes of mucositis have been identified (Feld 1997). The mechanism by which cancer-chemotherapy- induced mucositis occurs is likely associated with the rapid rate of turnover of oral epithelial cells. In addi- tion, other components likely include upregulation of pro-inflammatory cytokines and metabolic by- products of colonizing oral microflora (Sonis 1998). Chemotherapy alters the integrity of the mucosa and contributes to acute and chronic changes in oral tis- sue and physiologic processes (Carl 1995). The ulcerated mucosa is susceptible to infection by microbial flora that normally inhabit the oral cavity, as well as by exogenous organisms, and exacerbates the existing mucositis. Further, these microflora can disseminate systemically (Pizzo et al. 1993, Rolston and Bodey 1993). Compromised salivary function can further elevate risk for systemic infection of oral origin. Both indigenous oral flora and hospital-acquired pathogens have been associated with bacteremias and systemic infection (Schubert et al. 1999). Changes in infection profiles in myelosuppressed (immunosup- pressed) cancer patients tend to occur in cyclic fash- ion over many years. This evolving epidemiology is caused by multiple factors including use of antibi- otics. Gram-positive organisms including viridans streptococci and enterococci are currently associated with systemic infection of oral origin in myelosup- pressed cancer patients. In addition, gram-negative pathogens including P. aeruginosa, Neisseria spp., and Escherichia coli remain of concern. Cancer patients undergoing bone marrow radia- tion who have chronic periodontal disease may also develop acute periodontal infections with systemic complications (Peterson et al. 1987). The extensive ulceration of gingival sulcular epithelium associated with periodontal disease is not directly observable clinically, yet may represent a source for disseminat- ed infection by an extensive array of organisms. Inflammatory signs may be masked due to the under- lying bone marrow suppression. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 105 Linkages with General Health Viruses are also associated with clinically impor- tant oral disease in patients receiving chemotherapy (Rolston and Bodey 1993, Pizzo et al. 1993). Infections caused by herpes simplex virus, varicella- zoster virus, and Epstein-Barr virus typically result from reactivation of a latent virus, whereas cytomegalovirus infections can result via reactivation of a latent virus or a newly acquired virus. The sever- ity of the infection, including fatal outcome, depends on the degree of immunocompromise. Many agents and protocols have been investigat- ed to manage or prevent mucositis (Peterson 1999, Schubert et al. 1998). For example, various biologic response modifiers, including transforming growth factor B3 or keratinocyte growth factor, have been under recent study in randomized clinical trials. Allopurinol mouthwash and vitamin E have been cited as agents that can decrease the severity of mucositis, although more extensive testing is neces- sary. Prostaglandin E2 was not shown to be effective in prophylaxis of oral mucositis following bone mar- row transplant; however, more recent studies indi- cate possible efficacy when administered via a differ- ent dosing protocol. Oral cryotherapy appears to be efficacious in reducing severity of oral mucositis caused by 5-fluorouracil and related compounds (Rocke et al. 1993). Local application of capsaicin preparations may be effective in controlling oral mucositis pain as dis- tinguished from tissue injury itself (Berger et al. 1995). Capsaicin and its analogs are the active ingre- dients in chili peppers. Capsaicin’s clinical potential derives from the fact that it elevates the threshold for pain in areas to which it is applied. Radiation Therapy Radiation therapy disrupts cell division in healthy tissue as well as in tumors and also affects the normal structure and function of craniofacial tissues, includ- ing the oral mucosa, salivary glands, and bone. Oral- facial complications are common after radiation ther- apy to the head and neck. The most frequent, and often the most distressing, complication is mucositis, but adverse reactions can affect all oral-facial tissues (Scully and Epstein 1996). Radiation can cause irreversible damage to the salivary glands, resulting in dramatic increases in dental caries. Oral mucosal alterations may become portals for invasion by pathogens, which may be life- threatening to immunosuppressed or bone-marrow- suppressed patients. A less common but very serious adverse consequence is destruction of bone cells and bone death, called osteoradionecrosis (ORN). ORN can result in infection of the bone and soft tissue and can require surgery to excise the dead tissue, which can in turn leave the face badly disfigured as well as functionally impaired (Field et al. 2000). The likeli- hood of ORN is increased with trauma to the bone, including that caused by tooth extraction (Murray et al. 1980a, b). The risk is especially marked when the trauma occurs near the time of radiation (Epstein et al. 1987). Management includes elimination of acute or potential dental and periodontal foci of disease, increased patient participation in oral hygiene, use of oral topical fluorides for caries prevention, and use of antiviral, antifungal, or antimicrobial therapy for management of infections associated with mucositis. Combined Cancer Therapies Rapid developments have occurred in the use of blood cell growth factors for treatment of various conditions, including the anemia of end-stage renal disease, the neutropenia occurring with cancer care, and the bone marrow toxicity and mucositis that can follow aggressive chemotherapy or radiation therapy (Sonis et al. 1997, Williams and Quesenberry 1992). Sonis et al. (1997) found that topical application of transforming growth factor beta (TGF-B) in the ham- ster model of oral mucositis significantly reduced basal cell proliferation and reduced the severity of mucositis associated with 5-fluorouracil treatment. Other growth factors considered for use in reducing mucositis include granulocyte-monocyte colony-stimulating factor and granulocyte colony- stimulating factor. Bone morphogenetic proteins are also in development for alleviating the toxicity and mucositis that follow chemotherapy and radiation therapy. Other approaches to reducing mucositis and adverse oral effects of chemotherapy and radiation therapy include fractionating the dose of radiation, and combining chemotherapy with growth factors or with less toxic oncostatic agents. Although the oral mucositis occurring in chemotherapy and in head and neck radiation patients shares many characteristics, distinct differences also exist (NIH 1990, Schubert et al. 1998, Wilkes 1998). For example, in contrast to chemotherapy-associated lesions, radiation damage is anatomically site- specific, toxicity is localized to irradiated tissue volumes. The degree of damage depends on treatment-regimen-related factors, including the type of radiation used, the total dose administered, the fractionation, and field size. Thus, research involving both cohorts of cancer patients remains essential to enhancing patient management. Development of new technologies to prevent cancer-therapy-induced oral mucositis could 106 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL substantially reduce the risk for oral and systemic infections, oral pain, and the number of hospital days. Improvement in quality of life and reduction in health costs are also likely and desirable outcomes. The new technologies could also provide a set- ting in which novel classes of chemotherapeutic drugs, utilized at increased doses, could be imple- mented. These advances in turn could lead to enhanced cancer patient survival and lengthen the duration of disease remission. Pharmaceuticals A number of medications used to treat systemic dis- eases can cause oral complications, ranging from xerostomic effects to alterations in the surface struc- ture of the enamel or mucosa. More than 400 over- the-counter and prescription drugs have xerostomic side effects (Sreebny and Schwartz 1997). These include tricyclic antidepressants, antihistamines, and diuretics. The dimensions and impact of these side effects vary depending on the response of the indi- vidual patient and the duration of medication use. Staining of the teeth or mucosa is associated with a variety of drugs, including tranquilizers, oral con- traceptives, and antimalarials. The antibiotic tetracy- cline can cause enamel hypoplasia when taken by the mother during pregnancy and by children during tooth development. The antimicrobial mouthrinse agent chlorhexidine also can stain the teeth, but this staining is external and can be removed by dental prophylaxis. Other drugs have been associated with gingival overgrowth, including cyclosporin, which has been used as an immunosuppressant in the United States since 1984 to prevent rejection of transplanted organs and bone marrow. This drug has also been used in other countries for treatment of type 2 dia- betes, rheumatoid arthritis, psoriasis, multiple sclero- sis, malaria, sarcoidosis, and several other diseases with an immunological basis (Adams and Davies 1984). Other drugs that cause gingival overgrowth include calcium ion channel blocking agents used in the treatment of angina pectoris and postmyocardial syndrome, such as nifedipine and verapamil (Lucas et al. 1985), and phenytoin (sodium 5,5-phenylhy- dantoin), used in the treatment of epilepsy and also for management of other neurological disorders. Treatment often consists of using an alternate drug, although this is not always possible. Conservative periodontal therapy can reduce the inflammatory component of enlargement, however, surgery is often required. Oral candidiasis is typically caused by opportunistic overgrowth of Candida albicans. Drugs that cause systemic bone marrow suppression, oral Linkages with General Health mucosal injury, or salivary compromise collectively promote the risk for clinical infection. In addition, antibiotics and concurrent steroid therapy often alter oral flora, thereby creating an environment for fungal overgrowth. In high-risk cancer patients, fungal infection can cause severe morbidity and even death. Infective Endocarditis The purported connection between oral infection and a specific heart disease, infective endocarditis, has a long history. Endocarditis is caused by bacteria that adhere to damaged or otherwise receptive sur- faces of the tissue that lines heart valves (the endo- cardium) (Weinstein and Schlesinger 1974). Dental and other surgical procedures may predispose sus- ceptible patients to infective endocarditis by induc- ing bacteremias (Lacassin et al. 1995). However, bac- teremias from oral infections that occur frequently during normal daily activites, coincidental even with chewing food, toothbrushing, and flossing, con- tribute more substantially to the risk of infective endocarditis (Bayliss et al. 1983, Dajani et al. 1997, Strom et al. 1998). Oral organisms are common etio- logic agents of infective endocarditis (Bayliss et al. 1983). For example, strains of S. sanguis, as well as gram-negative oral bacteria including Haemophilus aphrophilus, A. actinomycetemcomitans, E. corrodens, Capnocytophaga spp.. and Fusobacterium nucleatum, have been associated with bacterial endocarditis (Barco 1991, Geraci and Wilson 1982, Kaye 1994, Moulsdale et al. 1980). Infective endocarditis occurs with different incu- bation periods, which differ in causative bacteria and signs and symptoms. For example, Staphylococcus aureus endocarditis may have a rapid onset and fatal course if it affects the left side of the heart. With a more indolent course, patients may often be unaware of infection and may experience fever, night chills, myalgia, and arthralgia for a considerable period of time before diagnosis. The infection is often curable if diagnosed and treated early. The classic risk factors for endocarditis include cardiac valve disorders (valvulopathies) that include theumatic and congenital heart disease, complex cyanotic heart disease in children, and mitral valve prolapse with regurgitation. Recent studies indicate that the use of certain diet drugs (fenfluramine and dexfenfluramine) has induced cardiac valvulopathy, which may in some cases be transient. Among at-risk persons, bacteremias are more likely to occur in those with periodontal disease (Silver et al. 1977). However, the oral pathogens causing periodontitis have only rarely been shown to cause endocarditis. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 107 Linkages with General Health Prevention of infective endocarditis from oral bacteria depends on limiting the entry and dissemi- nation of bacteria through the bloodstream and lym- phatic circulation. Antibiotic prophylaxis for dental procedures that are likely to provoke bacteremia has historically been recommended (Dajani et al. 1997, Durack 1995). A recent study, however, suggests that receiving dental treatment does not significantly increase the risk of infective endocarditis, even in patients with valvular abnormalities (Strom at al. 1998). Further research is necessary to determine whether some heart or valvular conditions or certain dental procedures, such as surgery or scaling, would require coverage with pre-procedural antibiotics and others would be precluded. Oral Infections and Respiratory Disease Pathogens in the oral cavity can also gain access to the airway, sometimes with serious consequences. In adults, bacterial pneumonias are strongly associated with aspiration of bacteria into the lower respiratory tract, which is normally sterile. Common respiratory pathogens such as Streptococcus pneumoniae, Streptococcus pyogenes, Mycoplasma pneumoniae, and Haemophilus influenzae can colonize the oropharynx and the lower airway. In addition, oral bacteria including A. actinomycetemcomitans (Yuan et al. 1992), Actinomyces israelii (Morris and Sewell 1994, Zijlstra et al. 1992), Capnocytophaga spp. (Lorenz and Weiss 1994), Eikenella corrodens (Joshi et al. 1991), Prevotella intermedia, and Streptococcus con- stellatus (Shinzato and Saito 1994) can be aspirated into the lower airways (Scannapieco 1998, 1999). Chronic obstructive pulmonary disease, charac- terized by obstruction of airflow due to chronic bron- chitis or emphysema and by recurrent episodes of respiratory infection, has been associated with poor oral health status (Hayes et al. 1998, Scannapieco et al. 1998). A positive relationship between periodon- tal disease and bacterial pneumonia has been shown by Scannapieco and Mylotte (1996). Although oral bacteria, including periodontal pathogens, have the potential for causing respiratory infections, the frequency and nature of such infec- tions are not known and merit further study. Oral Transmission of Infections Besides being a portal of entry for infections, the mouth is an important source of potentially patho- genic organisms and is often the vehicle by which infection is delivered to the bodies of others. Microorganisms were not discovered in the mouth until the seventeenth century, when van Leewenhoek examined dental plaque using a microscope he had constructed. In 1884, Koch demonstrated that tuberculosis could be transmitted by airborne droplets from the mouth and respiratory tract. Since that time, we have learned that many common respi- ratory infections, such as influenza, the common cold, pneumonia, and tuberculosis, can be transmit- ted from oral secretions. Before the development of effective vaccines, orally transmitted diseases such as chickenpox, measles, mumps, polio, and diphtheria were a major source of morbidity and mortality in childhood. Viral diseases such as hepatitis B, herpes labialis, acute herpetic gingivostomatitis, cyto- megalovirus, and infectious mononucleosis may also originate from oral contact. Disease-causing microorganisms can be spread by direct contact (with saliva or blood from the mouth) or indirect contact (with saliva- or blood- contaminated surfaces, including hands or lips), droplet infection (from coughing, sneezing, or even normal speech), or by aerosolized organisms. These organisms can be inhaled, ingested, or taken in through mucous membranes in the eyes, nose, or mouth or through breaks in the skin. A number of diseases can be spread via oral sexual contact, includ- ing gonorrhea, syphilis, trichomoniasis, chlamydia, and mononucleosis. As mentioned earlier, the oral mucosa and saliva provide significant defense against disease transmis- sion. Epidemiological and animal studies are provid- ing evidence, however, that the oral cavity may be the site for transmission of serious systemic infections despite the protective factors in saliva (see Chapter 2). Infection with HIV provides a case in point (Baba et al. 1996, Dillon et al. 2000, Pope et al. 1997, Ruprecht et al. 1999, Stahl-Hennig et al. 1999, Baron et al. 2000). Early in the 1980s, when AIDS was first identi- fied in the United States, concern was expressed about casual (i.e., nonsexual) transmission of HIV (CDC 1983, 1985). Detailed household studies did not demonstrate transmission of HIV, even when family members shared eating utensils and tooth- brushes with an HIV-affected member (Fischl et al. 1987, Rogers et al. 1990, Sande 1986). Similarly, sur- veillance data collected over time showed no evi- dence of casual transmission (Ward and Duchin 1997). Only one nonoccupational episode of HIV trans- mission has been attributed to blood-contaminated saliva (CDC 1997): this incident involved intimate kissing between sexual partners. There have been a few cases of HIV transmission from performing oral 108 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL sex on a person infected with HIV, and it is also pos- sible to become infected with HIV by receiving oral sex. In the San Francisco Options Study of men who have sex with men identified within 12 months of HIV seroconversion, oral transmission represented 7.8 percent of primary HIV infections (Dillon et al. 2000). Rothenberg et al. (1998) reviewed epidemio- logic studies and reports of 38 cases of oral transmis- sion of HIV in the literature. They concluded that although oral-genital contact may be less efficient than needle-sharing or anal intercourse for the trans- mission of HIV, its increased use by men who have sex with men (Ostrow and DiFranceisco 1996, Schwarcz et al. 1995) and in crack cocaine smokers (Faruque et al. 1996a,b) may increase its contribu- tion to HIV transmission over time. Several studies provide evidence that when the oral environment is compromised, the mouth can be a potential site of transmission of infectious microbes. Data from Faruque et al. (1996a,b) and Wallace et al. (1996) suggest that there is a positive association between the presence of oral lesions resulting from crack co- caine use, receptive oral intercourse, and HIV trans- mission. A case report has documented the passage of HIV from a partner who is HIV-positive to one who is HIV-negative in the presence of periodontal disease but in the absence of other risk factors (Padian and Glass 1997). Because the type, duration, and. fre- quency of oral contact in past studies may not have been specified, the risk could be somewhat higher for oral transmission of HIV than previously reported. The risk might also vary depending on factors such as viral load, infectious dose, area of exposure, and presence or absence of oral lesions. Additional stud- ies are needed to evaluate the risk of oral-genital transmission of HIV; some are under way JQ. Greenspan, K. Page-Schafer, personal communica- tion, 1999). Other sexually transmitted diseases (STDs) can occur through oral contact. For example, pharyngeal infection with Chlamydia trachomatis has been found in 3 to 6 percent of men and women attending STD clinics. Most infections are asymptomatic (Holmes et al. 1999). Another common sexually transmitted infection, herpes simplex virus, commonly infects the pharynx and is seen in 20 percent of patients with primary genital herpes. The painless chancre of pri- mary syphilis can be found in the oral cavity; howev- er, there are no data on the prevalence of this site of infection for Treponema pallidum. Among persons with gonorrhea, pharyngeal infection occurs in 3to7 percent of heterosexual men, 10 to 20 percent of het- erosexual women, and 10 to 25 percent of men who have sex with men (Holmes et al. 1999). Gonococcal Linkages with General Health infection can cause acute pharyngitis, but is usually asymptomatic. The transmission of pharyngeal gon- orthea to sex partners had been thought to be rare. However, in one study, 17 of 66 men who had sex with men who had urethral gonorrhea reported insertive oral sex as their only risk factor in the past 2 months (Lafferty et al. 1997). Conclusion The role of the mouth as a portal of entry for infec- tion presents ever-new challenges for study. Although oral tissues and fluids normally provide significant barriers and protection against microbial infections, at times these infections can not only cause local dis- ease but, under certain circumstances, can dissemi- nate to cause infections in other parts of the body. The control of existing oral infections is clearly of intrinsic importance and a necessary precaution to prevent systemic complications. ASSOCIATIONS AMONG ORAL INFECTIONS AND DIABETES, HEART DISEASE/STROKE, AND ADVERSE PREGNANCY OUTCOMES Recent studies have reported associations between oral infections—primarily periodontal infections— and diabetes, heart disease and stroke, and adverse pregnancy outcomes, but sufficient evidence does not yet exist to conclude that one leads to the other. This section characterizes the nature of these associ- ations by describing the quality of the evidence sup- porting the reports. Both observational and experi- mental studies were accepted as admissible evidence. Table 5.3 presents the hierarchy of evidence used to interpret these associations. Where there are opera- tive mechanisms proposed that support an associa- tion between oral infectious agents and the systemic conditions in question, they are introduced at the outset. These are followed by animal studies and then by epidemiologic or population-based studies. The evidence for each association is presented in the table in rank order according to the rigor of the study design. The Periodontal Disease—Diabetes Connection There is growing acceptance that diabetes is associat- ed with increased occurrence and progression of peri- odontitis—so much so that periodontitis has been called the “sixth complication of diabetes” (Lde 1993). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 109 Linkages with General Health The risk is independent of whether the diabetes is type l or type 2. Type 1 diabetes is the condition in which the pancreas produces little or no insulin. It usually begins in childhood or adoles- cence. In type 2 diabetes, secretion and utilization of insulin are impaired; onset is typically after age 30. Together, these two types of diabetes affect an esti- mated 15.7 million people in the United States and represent the seventh leading cause of death (NIDDK 1999). The goal of diabetic care is to lower blood glu- cose levels to recommended levels. Some investiga- tors have reported a two-way connection between diabetes and periodontal disease, proposing that not only are diabetic patients more susceptible to peri- odontal disease, but the presence of periodontal dis- ease affects glycemic control. This section explores the bidirectional relationship, beginning with the effects of diabetes on periodontal disease. Effects of Diabetes on Periodontitis Prevalence and Severity Several reviews have described candidate mecha- nisms to explain why individuals with diabetes may be more susceptible to periodontitis (Grossi and Genco 1998, Manouchehr-Pour and Bissada 1983, Murrah 1985, Oliver and Tervonen 1994, Salvi et al. 1997, Wilton et al. 1988). These include vascular changes, alterations in gingival crevicular fluid, alter- ations in connective tissue metabolism, altered host immunological and inflammatory response, altered subgingival microflora, and hereditary: patterns. Studies were classified by type of diabetes and age of study population (see Table 5.4). Type 1 Diabetes. Ten reports focused principally on children and adolescents with type 1 diabetes, com- paring them with groups of similar ages without dia- betes (Cianciola et al. 1982, de Pommereau et al. 1992, Faulconbridge et al. 1981, Firatli 1997, Firatli et al. 1996, Goteiner et al. 1986, Harrison and Bowen 1987, Novaes et al. 1991, Pinson et al. 1995, Ringelberg et al. 1977). All but one of the studies (Goteiner et al. 1986) reported greater prevalence, extent, or severity of at least one measure or index of periodontal disease (e.g., gingival inflammation, probing pocket depth, loss of periodontal attach- ment, or radiographic evidence of alveolar bone loss) among subjects with diabetes, even though these investigations were conducted ina variety of coun- tries across several continents. Another set of studies on the relationship between type 1 diabetes and periodontal disease included subjects with and without diabetes between the ages of 15 and 35 (Cohen et al. 1970, Galea et al. 1986, Guven et al. 1996, Kjellman et al. 1970, Rylander et al. 1987, Sznajder et al. 1978). All six studies reported greater prevalence, extent, or sever- ity of at least one measure or index of periodontal disease. A third set of studies conducted in Scandinavia looked at the relationship between periodontal dis- ease and type 1 diabetes (or diabetes reported as requiring insulin therapy without specification of diabetes type) in adults between 20 and 70 years old. Three of the four studies were cross-sectional (Glavind et al. 1968, Hugoson et al. 1989, Thorstensson and Hugoson 1993), and one was a treatment follow-up study (Tervonen and TABLE 5.3 Hierarchy of evidence used in analyzing and interpreting results Quality of Evidence Strength of Recommendation A: There is good evidence to support the recommendation. There is fair evidence to support the recommendation. moO |; Evidence obtained from at least one properly randomized controlled trial. Il-1: Evidence obtained from well-designed controlled trials without randomization. Il-2: Evidence obtained from well-designed cohort of case-control analytic studies, preferably from more than one center or research group. Il-3: Evidence obtained from multiple time series with or without the intervention. Dramatic results in uncontrolled experiments (such as the results of the introduction of penicillin treatment in the 1940s) could also be regarded as this type of evidence. Ill: Opinions of respected authorities, based on clinical experience; descriptive studies and case reports; or reports of expert committees. There is insufficient evidence to recommend for or against, but recommendations may be made on other grounds. There is fair evidence to support the recommendation that the intervention be excluded. There is good evidence to support the recommendation that the intervention be excluded. Source: Adapted from U.S. Preventive Services Task Force 1996, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health TABLE 5.4 Summary of studies of the association between diabetes and periodontal diseases, classified by strength of evidence, diabetes type, and age group Number of Measure of Subjects Ages? Periodontal Other Study Diabetes a. Diabetes a.Diabetes Disease Status: Diabetes-Related Evidence Country Design Type b. Control b. Control Diabetes Effect: Variables Considered Level! Firatli 1997 Turkey Prospective 1 a.44 a.12.2(mean) — Ging: 0s Glycemic control U-2 b.20 b.12.3 (mean) — Ppd:0s Duration of diabetes Lpa: 1s Cohen et al. 1970 USA Prospective a a.21 a. 18,35 Ging: 1s None Il-2 b. 18 b.18, 35 Lpa: 11, 1s Tervonen and Finland Prospective 1 a.36 a. 24, 36 Ging: 0e Glycemic contral I-2 Karjalainen 1997 b.10 b. 24, 36 Pod: Ir Duration of diabetes Lpa: le Diabetes complications Novaes et al. 1996 Brazil Prospective 2 a.30 a. 30,77 Ppd: 1s, ir Glycemic control I-2 b.30 b.30, 67 Lpa, 15, Ir Nelson et al. 1990 USA Prospective 2 a.720 a.15,55+ XRBL: 1i, 1p None Il-2 b. 1,553 b. 15, 55+ Taylor et al. 1998a USA Prospective 2 a.24 a. 15,57 XRBL: i, Ir None Il-2 b.338 b.15,57 Taylor et al. 19986 USA Prospective 2 a2l a. 15,49 XRBL: ti, IF Glycemic control i-2 b.338 b. 15,49 Goteiner et al. 1986 USA Cross-sectional = 1 a. 169 a.schoal ages Ging: 0s None il b.80 b.5, 18 Lpa: Op, Os PDI: 0s Harrison and USA Cross-sectional 1 a.30 a.4,19 Ging: 1s Glycemic control il Bowen 1987 b.30 b.4,19 Lpa: 1p Novaes et al. 1991 Brazil Cross-sectional 1 a.30 a.5,18 Ging: 1s None Ml “b.30 b.5,18 Ppd: Os XRBL: 1s Cianciola et al. 1982 USA Cross-sectional 1 a. 263 a.<10,>19 Ging: Ip Duration of diabetes IN b.208 b.<10,>19 Lpa: Ip XRBL: 1p, 1s JPS: 1p,1s de Pommereau France —- Cross-sectional. «= a.85 a. 12, 18 Ging: le Glycemic control tll et al. 1992 b.38 b. 12, 18 Lpa: Oe, Op, Os Duration of diabetes XRBL: Oe, Op, 0s Ringelberg USA Cross-sectional 1 a.56 a. 10, 16 Ging: 1s None Ml et al. 1977 b.41 b.10, 12 MGI: 1s Firatli et al. 1996 Turkey Cross-sectional 1 a.77 a.12.5(mean) — Ging: 0s Duration of diabetes Ml b.77 b.12.6(mean} — Ppd: 1s Lpa: is Pinson et al. 1995 USA Cross-sectional 1 a.26 a.7-18 Ging: 1s Glycemic control Ml b.24 b.7-18 Ppd: 0s Duration of diabetes Lpa:Qs Faulconbridge England Cross-sectional a.94 a.5,17 Ging: 1s Duration of diabetes Mil et al. 1981 b.94 b.5,17 Kjeliman et al. 1970 Sweden Cross-sectional = 1* a.105 a. 15,24 Ging: le Glycemic control lit b.52 b.15, 24 Ppd: Os Diabetes complications XRBL: 0s Guven et al. 1996 Turkey Cross-sectional 1 a.10 a. 18,27 Ging: le None til (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 111 Linkages with General Health TABLE 5.4 continued Number of Measure of Subjects Ages? Periodontal Other Study Diabetes a.Diabetes a. Diabetes Disease Status: Diabetes-Related Evidence Country Design Types b. Control b. Control Diabetes Effect: Variables Considered Level Rylander et al. 1987 Sweden Cross-sectional = a.46 a. 18, 26 Ging: le, 1p Diabetes complications tit b.41 b, 19,25 Ppd:0e Lpa: le, ip XRBL:Qp Sznajder et al. 1978 Argentina Cross-sectional = -1* a.20 a.9, 29 Ging: 1s None il b.26 b.9,29 Lpa: 0s Galea et al. 1986 Malta Cross-sectional = -1* a.82 a.5,29 Ppd: 1p Glycemic control tll b.unknown — b.5,29 Duration of diabetes Diabetes complications Hugoson et al. 1989 Sweden Cross-sectional = a. 154 a. 20,70 Ging: le Duration of diabetes Ill b.77 b. 20,70 Ppd: 1e, Ip, 1s XRBL: 1s Glavind et al. 1968 Denmark Cross-sectional 1* a.51 a.20,40 Ging: 0s Duration of diabetes II" b.51 b. 20,40 Ppd: Os Diabetes complications Lpa: 1s XRBL: 1s Thorstensson and Sweden Cross-sectional 1 a.117 a.40, 70 Ging: 0e Duration of diabetes ill Hugoson 1993 b.99 b.40,70 Ppd: le, 1s Onset age XRBL: 1s Morton et al. 1995 Mauritius Cross-sectional 2 a.24 a. 26,76 Ging: 1p None lil b.24 b.25, 73 Ppd: 1s Lpa: 1s Shlassman et al.1990 USA Cross-sectional 2 a, 736 a.5,45+ Lpa: Ip None ill b, 2,483 b.5,45+ XRBL: Ip Emrich et al. 1991 USA Cross-sectional 2 a.254 a.15,55+ Lpa: tp, 1s None ill b. 1,088 b.15,55+ XRBL: 1p, 1s Wolf 1977 Finland Cross-sectional = 1,2 a. 186 a. 16,60 Ging: 1s Glycemic control Ml b. 156 b. 16,60 Lpa: 1s Duration of diabetes XRBL: 1s Diabetes complications Benveniste USA Cross-sectional §=—-1,2* a.53 a.5,72 Ging: 0s None Itl et al. 1967 b.71 b.5,72° Ppd: Op, Os Finestone and USA Cross-sectional 1,2* a. 189 a. 20,79 Pl: 4s Glycemic control Mtl Boorujy 1967 b.64 b.20, 79 Duration of diabetes Diabetes complications Belting et al. 1964 USA Cross-sectional 1,2" a.78 a.20,79 Pl: 1s Diabetes severity ill b.79 b.20,79 Oliver and Tervonen USA Cross-sectional 1,2 a.114 a.20, 64 Ppd: Te, 1p None i 1993 b, 15,132 b.20, 64 Lpa: 1e, Op, Os Yavuzyilmaz et al. Turkey Cross-sectional ~=—-1,2 a1? a.25,74 Ppd: 1s None tll 1996 b.17 b, 19,29 Bridges et al. 1996 USA Cross-sectional 1,2 a.118 a. 24,78 Ging: 0s Glycemic control ill b.115 b. 24, 78 Ppd: Os Duration of diabetes Lpa: 1s Sandler and Stahl USA Cross-sectional —-1,2* a. 100 a. 20,69 PDR: le None lil 1960 b. 3,894 b. 20,69 Bacic et al. 1988 Yugoslavia Cross-sectional 1,2 a.222 a.<20, 60+ Pod: 1e, 1p, 1s Glycemic control lll b. 189 b. <20,60+ Duration of diabetes Diabetes complications Hove and Stallard USA Cross-sectional —1,2* a. 28 a.20,40+ Ging: 0s Duration of diabetes ill 1970 b. 16 b. 20, 40+ Ppd: Os Diabetes severity XRBL:0s 112 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health Number of Measure of Subjects Ages? Periodontal Other Study Diabetes a.Diabetes a. Diabetes Disease Status: Diabetes-Related Evidence Country Design Type? b. Control b.Control Diabetes Effect: Variables Considered Leveld Mackenzie and USA Cross-sectional 9 a. 124 a. 32,78 XRBL: 0s None It Millard 1963 b.92 b.32, 78 Sznajder et al. 1978 Argentina Cross-sectional 9 a.63 a. 30,49 Ging: 1s None Mt b.39 b.30, 50 Lpa: 1s Dolan et al. 1997 USA Cross-sectional = 9 Weighted a.45,75+ Lpa: 1e, 1p, 1s None itt a.107 b.45, 75+ b.554 Grossi et al. 1994 USA Cross-sectional 9 a. 1,426 All: 25, 74; Lpa: 1s, ip None Ml b.69 unknown for diabetes Tervonen and Finland Cross-sectional © 9 a.50 a. <30,40+ Ging: le Glycemic control Ml Knuuttila 1986 . b.53 b.<30,40+ Pod: 1e, 1p XRBL: 0s Campbell 1972 Australia Cross-sectional = 9 a.70 a. 17,39 Pl: Ip, 15 None il b. 102 b. 17,39 Aibrecht et al. 1988 Hungary Cross-sectional 9 a. 1,360 a.15,65+ Ging: 1s None it b.625 b.15,65+ PI: 0s Szpunar et al. USA Cross-sectional 9 a.474 a.6,65+ Pl: 1s None I 1989 (NHANES {) b. 15,174 b.6,65+ Szpunar et al. USA Cross-sectional 9 a.322 a. 15,65+ Pl: 1s, None Ul 1989 (HHANES) b.8,040 b.12,65+ dLevels of evidence are delineated in Table 5.3. aDiabetes type: 1 = type 1 diabetes mellitus; 2 = type 2 diabetes mellitus; 1,2 = both type 1 and type 2 diabetes mellitus; 9 = diabetes type not specified and not clearly ascertaina- ble from other information in the report; * = diabetes type not specified but ascertained by reviewer from other information in the report. bAges: subjects’ ages presented as minimum, maximum reported for those with diabetes and controls unless otherwise specified. < Measure of periodontal disease status. Measures used include Ging = gifigivitis or gingival bleeding; Ppd = probing pocket depth; Lpa = loss of periodontal attachment; XRBL = radiographic bone loss; JPS = juvenile periodontal score; MGl = madified gingival index; Pi = Russell's periodontal index; POR = periodontal disease rate (proportion of teeth affected by periodontal disease), The number following the measure corresponds to greater disease in those with diabetes (1) or no difference between those with diabetes and controls (0). The letter following the number corresponds to the parameter(s} assessed in the study: ¢ = extent; i = incidence; p = prevalence; s = severity; r= progression. Karjalainen 1997). All four studies reported greater prevalence, extent, or severity of at least one measure of periodontal disease. Type 2 Diabetes. There are fewer reports on the rela- tionship between type 2 diabetes and periodontal dis- ease, particularly where type 2 diabetes is explicitly identified or discernible from the ages of subjects. Seven studies limited to subjects with type 2 diabetes included a comparison group without diabetes. Two of these studies included only adult subjects (Morton et al. 1995, Novaes et al. 1996); the remaining five were large population-based studies of diabetes and periodontal disease in Pima Indians, a group with the highest known prevalence of type 2 diabetes in the world. The Pima Indian studies included subjects aged 5 years and older (Shlossman et al. 1990) or 15 and older (Emrich et al. 1991, Nelson et al. 1990, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Taylor et al. 1998a,b). All seven studies reported greater prevalence, extent, or severity of periodontal disease among subjects with diabetes for at least one measure of periodontal disease. Three of these stud- ies were longitudinal (Nelson et al. 1990, Taylor et al. 1998a,b) and showed that the progression of peri- odontal disease was greater in diabetes patients than in individuals without diabetes. In addition to finding significant differences in various measures of periodontal status between sub- jects with and without type 2 diabetes, a number of these reports also provide estimates of association and risk. Using periodontal attachment loss as the measure, Emrich et al. (1991) estimated that people with type 2 diabetes were 2.8 times more likely to have destructive periodontal disease (odds ratio, 2.8; 95 percent CI, 1.9 to 4.1). When they used radi- ographic bone loss as the measure and controlled for Linkages with General Health other important covariates, the estimate rose to 3.4 (odds ratio, 3.4; 95 percent Cl, 2.3 to 5.2). Nelson et al. (1990) quantified the increased risk of advanced periodontal disease in Pima Indians with and without type 2 diabetes, finding the prevalence of periodontal disease in subjects with diabetes to be 2.6 times greater (95 percent Cl, 1.0 to 6.6) than that of sub- jects without diabetes. Taylor et al. (1996), in anoth- er analysis of data from the Pima Indians, reported that type 2 diabetes was a significant risk factor for more severe alveolar bone loss progression (odds ratio, +.2: 95 percent CI, 1.8 to 9.9), in addition to being a significant risk factor for the prevalence of alveolar bone loss. Studies of Individuals with Type 1 or Type 2 Diabetes. Twelve reports included analyses in which subjects with type 1 and type 2 diabetes were not separated. All of these studies were cross-sectional and included adults; two studies included children or adolescents as well (Benveniste et al. 1967; Wolf 1977). Nine of the 12 studies reported greater prevalence, extent, or severity of periodontal disease among the diabetic subjects for at least one measure or index of peri- odontal disease (Bacic et al. 1988, Belting et al. 1964, Bridges et al. 1996, Finestone and Boorujy 1967, Hove and Stallard 1970, Oliver and Tervonen 1993, Sandler and Stahl 1960, Yavuzyilmaz et al. 1996, Wolf 1977). Hove and Stallard (1970) and Benveniste et al. (1967) did not find significant differences in peri- odontal disease between subjects with and without diabetes. The Hove and Stallard report included 28 subjects with diabetes and 16 without diabetes and may not have had enough statistical power to detect clinical differences, although they were able to detect a significantly higher prevalence of gingival vascular changes in subjects with diabetes. Benveniste et al. (1967) commented that their results may have been influenced by use of relatives without diabetes as the comparison group and that the subjects with diabetes were all under reasonably good control with either insulin or dietary regulation. Both factors may have minimized differences between the groups. Diabetes Type Not Specified. The final set of reports on the association between diabetes and periodontal dis- eases consists of seven cross-sectional studies in which the type of diabetes was not specified and was not easily determined from other information pro- vided. Four of the seven studies included only adults (Dolan et al. 1997, Grossi et al. 1994, Mackenzie and Millard 1963, Tervonen and Knuuttila 1986). In the other three studies, subjects ranged in age from childhood to older adulthood (Albrecht et al. 1988, Campbell 1972, Szpunar et al. 1989). Szpunar et al. (1989) presented analyses of two separate national surveys (the National Health and Nutrition Examination Survey, NHANES I, conducted between 1971 and 1974, and the Hispanic Health and Nutrition Examination Survey, HHANES, conducted between 1982 and 1984). All seven studies found subjects with diabetes to have increased prevalence, extent, and severity of periodontal disease. The statistical significance of the diabetes effect was markedly diminished in the final linear regression model used by Szpunar et al. (1989) in analysis of the NHANES I data. Two of the popu- lation-based surveys, Grossi et al. (1994) and Dolan etal. (1997), provided epidemiologic estimates of the association of diabetes and attachment loss severity with odds ratios of 2.3 (95 percent CI, 1.2 to 4.6) and 1,9 (95 percent CI, 1.3 to 3.0), respectively, while controlling for other covariates. Conclusion. Diabetes is a risk factor for the occur- rence and prevalence of periodontal diseases. Although there is insufficient evidence of a causal association, the findings of greater prevalence, sever- ity, or extent of at least one manifestation of peri- odontal disease in individuals with diabetes is remarkably consistent in the overwhelming majority of studies. Furthermore, there are no studies with superior design features in the literature to refute this assessment. The studies were conducted in distinctly different settings, with subjects from different ethnic populations and of different ages, and with a variety of measures of periodontal status. This inevitable variation in methodology and study populations lim- its the possibility that the same biases apply in all the studies. There is a need for further research using stronger designs that also control for confounding variables such as socioeconomic status. Glycemic Control Several lines of evidence support the plausibility that periodontal infections contribute to problems with glycemic control, thus compromising the health of diabetic patients. It has been reported that the chron- ic release of tumor necrosis factor alpha (TNF-a) and other cytokines such as those associated with peri- odontitis interferes with the action of insulin and leads to metabolic alterations (Hotamisligil et al. 1993, Flier 1993). Other studies have noted relation- ships between insulin resistance and active inflam- matory connective tissue diseases (Hallgren and Lundquist 1983, Svenson et al. 1987), other clinical diseases (Beck-Nielsen 1992, Beisel 1975), acute 114 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL infection (Drobny et al. 1984, Sammalkorpi 1989), and periodontal disease (Grossi et al. 1999). Grossi and Genco (1998) have proposed a model whereby periodontal infection contributes to hyperglycemia and complicates metabolic control in diabetes. Clinical Studies. The effects of periodontal infection on glycemic control have been investigated in a small number of clinical studies that looked at metabolic control at baseline and following various periodontal treatments (see Table 5.5; Aldridge et al. 1995, Christgau et al. 1998, Grossi et al. 1996, 1997, Miller et al. 1992, Seppala and Ainamo 1994, Seppala et al. 1993, Smith et al. 1996, Westfelt et al. 1996, Williams and Mahan 1960, Wolf 1977). One report is based on an epidemiological cohort study (Taylor et al. 1996). The randomized controlled trials of Grossi et al. (1997) involving populations with type 2 diabetes found that use of the systemic antibiotic doxycycline to treat periodontitis patients with diabetes resulted in a transient (3 to 6 months) improvement in glycemic control. On the other hand, the two con- trolled trials conducted in London by Aldridge et al. (1995) involving patients with type 1 diabetes found no effect. Taken together, these three studies provide inconsistent results and are limited in how well they generalize to broader populations. A small uncon- trolled study of 10 patients by Miller et al. (1992) also reported an improvement in glycemic control of diabetic patients whose periodontal disease was treated with mechanical therapy and systemic doxy- cycline. Five of the above-mentioned studies did not include control groups (Miller et al. 1992, Seppala et al. 1993, Smith et al. 1996, Williams and Mahan 1960, Wolf 1977), and four were not specifically designed to address the relationship between peri- odontal therapy and glycemic control (Grossi et al. 1996, Seppala et al. 1993, Smith et al. 1996, Westfelt et al. 1996), although the data collected allowed the investigators to address the issue. One nonrandom- ized but controlled clinical trial of nonsurgical peri- odontal therapy found no significant influence on medical data for the diabetic patients (Christgau et al. 1998). A clear relationship between improvement in periodontal health and glycemic control has not been shown. The studies seem to suggest that antibiotic treatments may help in glycemic control. A recent longitudinal study indicates inflammation may be a precursor to the onset of type 2 diabetes (Schmidt et al. 1999). Thus periodontal infection may contribute to that inflammation. Conclusion. The body of literature concerning the relationship between periodontal infection and Linkages with General Health impaired glycemic control is varied in the strength, quantity, breadth, and consistency of evidence pre- sented. The preliminary evidence, while encourag- ing, does not support a clear-cut conclusion that treating periodontal infection can contribute to man- agement of glycemic control in type 1 or type 2 dia- betes. As the table indicates, only studies using sys- temic antibiotic treatment affected glycemic control favorably. The results suggest that infections other than periodontitis may be implicated or that inten- sive treatment of periodontal infections with sys- temic antibiotics is necessary to affect glycemic con- trol favorably. Further rigorous controlled studies in diverse populations are warranted. The Oral Infection—Heart Disease and Stroke Connection During the past decade, infectious agents have become recognized as causes of systemic diseases, without fever or other traditional signs of infection. Helicobacter pylori is associated with peptic ulcers and, along with Chlamydia pneumoniae and cytomegalovirus, is now thought to be associated with increased risk for cardiovascular disease as well as malignancies (Wu et al. 2000). Studies investigating the relationship between oral and dental infections and the risk for cardiovascular disease suggest that there is potential for oral microorganisms, such as periodontopathic bacteria, and their effects to be linked with heart disease. Mechanisms of Action Infectious agents are thought to affect the risk of heart disease through several possible mechanisms. Bacteria or viruses originating in tissues such as the lungs or oral mucosa may directly infect blood vessel walls. Such infection may be largely asymptomatic, but may cause local vascular inflammation and injury, which would contribute to the development of lipid-rich plaques and atherosclerosis. Bacteria or viruses may also interact with white blood cells or platelets, both of which integrate into the developing atherosclerotic plaque. Cells of the blood vessel wall and white blood cells and platelets can release prostaglandins (especially PGE,), interleukins (espe- cially IL-1), thromboxane B2 (TBX,), and tumor necrosis factor alpha (TNF-«). Bacterial products in the blood may also stimulate liver production of other pro-inflammatory or pro-coagulant molecules such as C-reactive protein and fibrinogen. Microbes may also stimulate expression of tissue factor, which would activate coagulation. During the process of ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 115 Linkages with General Health TABLE 5.5 Effects of periodontal disease and its treatment on glycemic control: cdinical and epidemiological evidence Number of subjects Metabolic Study Diabetes a. Treatment (ages) Follow-up Control Evidence Design? Type b. Control (ages) Time Periodontal Therapy Qutcome Effects on Metabolic Control Levelt Aldridge = RCT Type 1 a. 16 (16-40) 2months — Experimental group: oral Glycated Periodontal treatment had no et al. 1995, b. 15 (16-40) hygiene instruction, scaling, hemoglobin, — effect on change in glycated Study 1 adjustment of restoration fructosamine — hemoglobin. margins, and reinforcement after 1 month; control group: no treatment Aldridge = RCT Type 1 a. 12 (20-60) 2months Experimental group: oral Glycated Periodontal treatment had no et al. 1995, b. 10 (20-60) hygiene instruction, scaling hemoglobin —_ effect on change in glycated Study 2 and root planing, extractions, hemoglobin. root canal therapy; control group: no treatment Grossiet RCT Type 2 a. 89 (25-65) 12 months Experimental groups received —Glycated The three groups receiving | al. 1996, b.24 (25-65) either systemic doxycycline or hemoglobin doxycycline and ultrasonic 1997 placebo and ultrasonic bacterial curettage showed bactericidal curettage with significant reductions irrigation using either water, (P < 0.04) in mean glycated chlorhexidine, or povidone- hemoglobin at 3 months. iodine Christgau = Treatment =‘ Type 1 a. 20 (30-66) 2months Scaling/root planing; Glycated No effect on glycated hemoglobin. —‘{l-1 et al.1998 study,non- andtype2 b.20 (30-66) subgingival irrigation with hemoglobin RCT chlorhexidine; oral hygiene instruction; and extractions Westfelt Treatment Type 1 a. 20 (45-65) 5 years Baseline oral hygiene Glycated “The mean value of HbA1c I-1 etal.1996 study,non- andtype2 b.20 (45-65) instruction, scaling and root hemoglobin between baseline and 24 months RCT planing followed by periodic was not significantly different from prophylaxis, oral hygiene that between 24 and 60 months.” instruction, localized sub- gingival plaque removal, and surgery at sites with bleeding on probing and a periodontal probing depth of >5 mm Smith Treatment Type 1 a. 18 (26-57) 2months Scaling and root planing with Glycated Found no statistically or clinically [I-17 et al.1996 — study, non- b.0 ultrasonics and curets; oral hemoglobin _ significant change in glycated RCT hygiene instruction hemoglobin. Tayior Historical Type 2 Notreatmentor 24years Not applicable Glycated Those with severe periodontitis Il-2 et al.1996 prospective control subjects hemoglobin — were ~6 times more likely to have cohort 49 (severe poor glycemic control at follow-up. periodontitis) 56 (less severe periodontitis) Miller Treatment Type 1 a.10(not given) weeks Scaling and root planing, Glycated Found decrease in glycated tll et al.1992 study, non- b.0 systemic doxycycline hemoglobin, © hemoglobin and glycated albumin RCT glycated in patients with improvement in albumin gingival inflammation (P < 0.01). Patients with no improvement in gingival inflammation had either no change or increase in glycated hemoglobin post treatment. coagulation, platelets would become trapped in the growing clot or thrombus. Microthrombus formation is one of the key factors in the development of ather- osclerotic plaques. As atherosclerotic plaques enlarge, "16 the lumen of the coronary blood vessels narrows and the blood supply to the heart muscle becomes reduced. A frank heart attack or myocardial infarc- tion results when a larger part of the coronary artery ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health Number of subjects Metabolic Study Diabetes _a. Treatment (ages) Follow-up Control Evidence Designé Type b. Control (ages) Time Periodontal Therapy Outcome Effects on Metabolic Control Level? Seppala ‘Treatment Type 1 a.38 for 1 year; 2years Scaling and root planing, Medical Reported an improvement of the MW et al.1993, study, non- 22 for 2 years‘ periodontal surgery, and history for HBA levels of the PIDD and CIDD Seppala and RCT 26 PIDD-ly (48 + 6) extractions baseline subjects (P < 0.068, t-test). Ainamo 12 CIDD-1y (43 + 5) control status; 1994 16 PIDD-2y glycosylated 6 CIDD-2y hemoglobin b.0 Al and blood glucose for assessing response to treatment Williams Descriptive Not speci- 3-7 Extractions, scaling and Insulin 7 of 9 subjects had “significant” tH and Mahan clinical fied a.9 (20-32) months curettage, gingivectomy, requirement; reduction in insulin requirements. 1960 study b.0 systemic antibiotics diabetes control (not operationally defined) Wolf 1977 Treatment Type 1 and . 8-12 Scaling and home care Blood glucose, Compared 23 subjects with lll study,non- type 2 a.117 (16-60) months instruction, periodontal surgery, 24-h urinary improved oral infections with 23 RT b.0 extractions, endodontic glucose, who had no improvement after treatment, restorations,denture insulindose —_—treatment for oral infection and replacement or repair inflammation. The subjects with 2 RCT = randomized controlled trial. otherwise in assigning the evidence levels. b Levels of evidence are delineated in Table 5.3. Note that because this body of literature is small, this review does not distinguish between “well-designed” studies and < PIDD = poorly controlled insulin-dependent diabetes; CIDD = controlled insulin-dependent diabetes. improved oral inflammation and infection tended to demonstrate diabetes control improvement (P < 0.1). However, Wolf states in discussion,“treatment of periodon- tal inflammation and periapical lesions ... does little to improve the control of diabetes.” lumen becomes occluded. Failing to receive enough blood, the heart muscle dies, resulting in an infarct. Animal Studies Bacteria originating in the oral cavity may also con- tribute to platelet clotting or thrombosis, as proposed by Herzberg et al. (1983, 1994). These investigators have suggested that the association between peri- odontal disease and cardiovascular disease may be due in part to the potential for oral bacteria such as S. sanguis and P. gingivalis to induce platelet aggrega- tion. Platelets aggregate in response to these bacteria as a result of mistaken identity: a protein structure on the surface of certain common strains of S. sanguis and P gingivalis mimics the platelet-interactive regions of collagen molecules (Erickson and Herzberg 1993, Herzberg et al. 1994). Exposure of flowing blood to collagen triggers clotting, the cen- ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL tral event in stopping blood flow. When an experi- mental bacteremia was created with a strain of S. san- guis that carried the collagen-like protein, rabbits showed changes in blood pressure, electrocardio- gram readings, heart rate, and cardiac contractility (Herzberg and Meyer 1996, 1998). Platelets also aggregated in the circulation, resulting in significant declines in platelet counts. From the electrocardio- graphic tracings, rabbit heart muscle also appeared to have suffered ischemic damage. The investigators concluded that oral bacteria carrying the collagen- like protein induced platelet aggregation or clotting in the bloodstream. These clots were of sufficient size to obstruct coronary arteries and produce ischemic heart damage, an early warning sign of a heart attack or an infarction. Because S. sanguis is present in large numbers in dental plaque and is a causative agent in infective endocarditis, it is likely that these bacteria 117 Linkages with General Health have an opportunity to induce platelet clotting dur- ing human bacteremias from oral sources. Bacteria- induced platelet clotting could contribute to microthrombosis during the development of athero- sclerotic plaques and occlusive thrombus formation with occasional myocardial infarction. Population-based Studies Any study investigating the possibility of a unique role for oral pathogens as risk factors for cardiovascu- lar disease, including atherosclerosis and the forma- tion of a blood clot in a coronary artery of the heart, which typically precedes myocardial infarction, must take into consideration such known risk factors as smoking, hypertension, obesity, diabetes, genetic sus- ceptibility, and elevated cholesterol. Genco (1998) and Beck et al. (1998) have recently reviewed studies examining the associations between oral conditions (including periodontitis) and atherosclerosis and coronary heart disease, the latter of which affects 12 million people in the United States and is the leading cause of death. These are summarized in Table 5.6. Of the ten studies cited in the table, six are prospective cohort studies, in which oral health sta- tus was established at the outset (baseline) of the study period and the subjects were followed at peri- odic intervals to a previously defined endpoint, for example, diagnosis of coronary heart disease or an acute myocardial infarction, or death. Beck et al. (1996) combined data from the Veterans Administration Dental Longitudinal Study and its parent longitudinal study, the Normative Aging Study, for a total of 203 cases and 891 noncases, to determine whether periodontal disease, judged by measuring alveolar crestal bone, is a risk factor for cardiovascular disease. After adjusting for age, blood pressure, cholesterol, and body mass index, the investigators found that subjects with periodontal disease were 1.5 times more likely to develop coro- nary heart disease over a 25-year period than controls (odds ratio of 1.5). Similarly, after adjusting for age, smoking, and blood pressure, the investigators found that veterans with periodontal disease were 1.9 times more likely to develop fatal coronary heart disease (odds ratio of 1.9). In a longitudinal study to eliminate the potential confounding effects of smoking, Genco et al. (1997) measured the incidence of periodontal disease and cardiovascular disease in 1,372 American Indians of the Gila River Indian Reservation. Although diabetes is prevalent in this population, cigarette smoking is rare in these individuals (a fact confirmed in this study), so it was considered not to be a risk factor for either cardiovascular disease or periodontal disease in this study. Periodontal disease was measured at baseline, and the incidence of cardiovascular disease was followed over the next 10 years. When the analy- sis was restricted to individuals under age 60, the risk of cardiovascular disease was 2.7 times higher in sub- jects with periodontal disease than in those with lit- tle or no periodontal infection. This association was seen even after adjusting for other risk factors for cardiovascular disease or periodontal disease such as age, sex, cholesterol, weight, high blood pressure, diabetes, and insulin use. The investigators conclud- ed that periodontal disease is an important risk fac- tor for cardiovascular disease for individuals under 60 in this group, second only to the presence of long-term diabetes. Further analysis of death due to cardiovascular disease is needed in this population to complete the study. Mattila and coworkers have conducted both prospective and retrospective studies. A prospective study (Mattila et al. 1995) showed that new episodes of myocardial infarction occurred more frequently in subjects with more extensive “dental” disease. The authors used a measure of dental disease that includ- ed a composite index that assessed caries, periodon- titis, pericoronitis, and periapical lesions. The com- posite index estimates the combined infectious load that contributes to many possible oral infections. After combining the prospective study data with data from an earlier retrospective study (Mattila et al. 1989) and adjusting for age, triglyceride levels, cho- lesterol, C-reactive protein, smoking, social class, diabetes, and hypertension, the investigators found a significant association between dental infections and acute myocardial infarction in men under age 50 (P< 0.01). A more recent study (Mattila et al. 2000) com- pared 85 patients with proven coronary heart disease and 53 matched controls. This case-control study showed that dental indices were higher among coro- nary heart disease patients than controls, but the dif- ferences were not statistically significant. Participants in the study were older, which the authors believed was the most likely reason for the results. In the first National Health and Nutrition Examination Survey, 9,670 subjects were followed for over 14 years. DeStefano et al. (1993) found that there was a 25 per- cent increased risk of cardiovascular disease in indi- viduals with periodontitis compared with those with minimal periodontal disease. The strongest associa- tion was seen in men under 50 (relative risk, 1.7). A limitation of this study, which the authors acknowl- edge, was the lack of baseline data on smoking, a major risk factor for both periodontal and cardiovas- cular disease. Morrison et al. (1999) evaluated a ret- rospective cohort study using participants in the 118 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Linkages with General Health TABLE 35.6 Summary of studies assessing the association between oral conditions, atherosclerosis, and coronary heart disease Subjects Association Study (cases/ (odds ratio or Evidence Designa controls) Oral Condition Cardiovascular Outcome Adjustments? relative risk) Levels DeStefano Prospective 1,786/7,974 Russell's periodontal Coronary heart disease . Age, sex, race, education, poverty, 1.72 (1.1-2.68) ll-2 et al. 1993 index (admission to hospital or marital status, cholesterol,BM!, (only formen death) diabetes, smoking under age 50) Mattila Prospective 52/162 Dental index (caries, New acute myocardial Smoking, hypertensian, age, sex, Yes, P< 0.01 II-2 et al. 1995 periodontal disease, infarction or death triglycerides, socioeconomic pulpal infection) status, diabetes, lipids, BMI, previous MI Joshipura Prospective 757/44,119 Periodontal disease New coranary heart Age, BMI, exercise, smoking, 1.67 (1.03-2.71) Il-2 et al. 1996 (self-reported), disease alcohol, vitamin C, family history, tooth loss due to Ml . self-reported periodontal disease Beck Prospective 203/891 —Alveolarcrestal bone New coronary heart Age, BMI, total cholesterol, 1.5 (1.04-2.14) 2 et al. 1996 loss disease, fatal coronary socioeconomic status, DBP.LDL, —1.9 (1.0-3.43) heart disease, stroke smoking, cholesterol 2.8 (1.45-5.48) Genco Prospective 68/1,304 —Alveolarcrestal bone New coronary heart Age, sex, smoking, BMI, diabetes, 2.68 (1.35-5.60) lI-2 et al. 1997 loss disease cholesterol, hypertension Morrison Retrospective 10,000 Severe gingivitis; New coronary heart Age, sex, serum total cholesterol, 1.37 (0.80-2.35) 2 et al. 1999 periodontitis; disease; cerebrovascular smoking, diabetes, hypertension —_for periodontitis edentulousness deaths 1.90 (1.17-3.10) for edentulousness for fatal CHD Joshipura Prospective 42,151 Number of teeth lost Ischemic stroke Age, smoking, obesity, alcohol, = <10 teeth 1.75 I1-2 et al. 1999 exercise, aspirin, family history, (1.03-2.99) profession, hypertension, 11-15 teeth 1.95 hypercholesterolemia (1.07-3.64) 17-24 teeth 1.48 Dental index (caries, (1.02-2.13) Mattila Case-Control 100/102 periodontal disease, Acute myocardial HDL, smoking, C-reactive protein, Yes, P< 0.01 2 et al. 1989 pulpal infections) infarctions hypertension, age, cholesterol, Dental index (caries diabetes, social class Grau Case-Control 166/166 _ periodontal disease, Stroke Diabetes, preexisting vascular Odds ratio 2.6 Ie et al. 1997 periapical infections) disease, socioeconomic status, (1.18-5.70) Dental index (caries, smoking Mattila Case-cantrol 85/53 periodontal disease, New coronary heart Age, sex, smoking, socioeconomic — i-2 et al. 2000 pulpal infections) disease class, hypertension, number of teeth, serum lipid levels the case-control studies, the first number represents the cases, and the second the controls. Levels of evidence are delineated in Table 5.3. aFor the prospective studies, the total number of subjects in the cohort is the sum of the two numbers given, the first number of which represents the subjects followed to the endpoint. For bBMI = body mass index; M! = myocardial infarction; LDL = low-density lipoproteins; HDL = high-density lipoproteins. 1970-72 National Canada Survey. In the younger cohort, those under age 69, they found that gingivi- tis, periodontitis, and edentulousness were related to fatal coronary heart disease in a statistically signifi- cant manner. However, in analyzing those over age 70, none of these dental conditions was associated with fatal heart disease. These results were adjusted for age, sex, serum total cholesterol, smoking status, diabetes status, hypertension status, and province of resi- ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL dence. This pattern of higher risk observed among younger subjects may, to some extent, reflect the rel- ative instability of risk estimates. However, it is also possible that periodontal disease, like other co-mor- bid relative risks for coronary heart disease, general- ly declines with age (Semenciw et al. 1988). Wu et al. (1999) found periodontal disease to be a potential factor for coronary heart disease and stroke based on an analysis of the first National 119 Linkages with General Health Health and Nutrition Examination Survey and its 21- year follow-up. In this analysis, periodontitis was found to be a significant risk factor for cerebrovascu- lar disease, in particular nonhemorrhagic stroke. Compared with no periodontal disease, relative risk (95 percent CI) for incident nonhemorrhagic stroke was 2.11 (1.30 to 3.42) for periodontitis. There was no significant relationship for gingivitis or edentu- lousness, which were 1.24 (0.74 to 2.08) and 1.41 (0.96 to 2.06), respectively. The increased relative risk for total cerebrovascular disease and nonhemor- rhagic stroke was not seen for hemorrhagic stroke. Similar relative risks for total cerebrovascular disease and nonhemorthagic stroke associated with peri- odontitis were seen in white men and women and African Americans. A conclusive statement about a cause-and-effect relationship between periodontitis and the risk of developing cerebrovascular disease, in particular nonhemorrhagic stroke, cannot be made at this time. The consistency of the findings in different racial groups and the strength of the association war- rant further examination of the potentially important association between these two clinical conditions, which are highly prevalent in the adult population. In the largest cohort studied, Joshipura et al. (1996) found that among a group of male health pro- fessionals who were relatively homogeneous socio- economically and who self-reported preexisting peri- odontal disease, those with 10 or fewer teeth were at increased risk of new coronary heart disease, com- pared with those with 25 or more teeth (relative risk, 1.67). These results were adjusted for standard car- diovascular disease risk factors. In a case-control study of 166 patients with acute cerebrovascular disease and 166 age- and sex- matched controls, Grau et al. (1997) found that “poor dental status” was independently associated with cerebrovascular ischemia. These results were based on a subgroup of patients and controls who completed the dental examination. A modified form of the Total Dental Index was used to measure dental status. In an 8-year follow-up of 42,151 male health professionals who were free of cardiovascular disease at baseline, Joshipura et al. (1999) reported that edentulousness was associated with an increased risk of ischemic stroke after adjusting for age, smoking, obesity, alcohol, exercise, aspirin, family history of cardiovascular disease, profession, hypertension, and hypercholesterolemia. Conclusion None of the studies reviewed to date achieves the level of rigor that can unequivocally establish peri- odontitis as an independent risk factor for cardiovas- cular disease or stroke. The methods used to measure or identify periodontal disease ranged widely from self-report, to composite indices that included dental caries experience, to precise measures of periodonti- tis severity. Nevertheless, there were consistent find- ings of increased odds ratios and significant proba- bility (P) values pointing to an association of peri- odontal and other oral infections with an increased risk for cardiovascular disease. Further studies are needed to determine whether periodontal disease alone or in the presence of other oral infections is an independent risk factor for cardiovascular or cere- brovascular disease. Research to elucidate the under- lying pathological mechanisms is also essential. Studies must also clarify the potentially confounding effects of sex, age, socioeconomic level, and race/ ethnicity. Periodontal Disease and Adverse Pregnancy Outcomes Preterm birth and low birth weight are considered the leading perinatal problems in the United States (Gibbs et al. 1992). Although infant mortality rates have decreased substantially over the past genera- tion, the incidence of low birth weight (just under 300,000 cases in 1995) has not shown a comparable decline (Institute of Medicine 1985, USDHHS 1984). Over 60 percent of the mortality of infants without structural or chromosomal congenital defects can be attributed to low birth weight (Shapiro et al. 1980). Mechanisms of Action Periodontal disease may contribute to adverse out- comes of pregnancy as a consequence of a chronic oral inflammatory bacterial infection. Toxins or other products generated by periodontal bacteria in the mother may reach the general circulation, cross the placenta, and harm the fetus. In addition, the response of the maternal immune system to the infection elicits the continued release of inflammato- ry mediators, growth factors, and other potent cytokines, which may directly or indirectly interfere with fetal growth and delivery. Evidence of increased rates of amniotic fluid infection, chorioamnion infection, and histologic chorioamnionitis supports an association between preterm birth, low birth weight, and general infection during pregnancy. It is noteworthy that the largest proportion of such infections occurred during the pregnancies of the most premature births (Hillier et al. 1988, 1995). The biological mechanisms involve bacteria-induced activation of cell-mediated immuni- ty leading to cytokine production and the synthesis 120 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and release of prostaglandins, which may trigger preterm labor (Hillier et al. 1988). Elevated levels of prostaglandin as well as cytokines (interleukin-1 (IL- 1), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-a)) have been found in the amniotic fluid of patients in preterm labor with amniotic fluid infection (Romero et al. 1993), compared with levels in patients with preterm labor without infection. Animal Models A variety of studies have used the pregnant hamster model. Some investigators have examined the effects of lipopolysaccharide, produced by oral gram-neg- ative pathogens, on cytokine production (Collins et al. 1994a). In other studies, hamsters have been infected with P gingivalis, with or without prior immunization. Collins et al. (1994b) challenged the animals with nondisseminating, low levels of P gingi- valis, introduced in a subcutaneous chamber at a dorsolumbar site. Although the doses were insuffi- cient to induce fever or wasting, the hamster litters of the infected animals showed a significant reduction in fetal weight (24 percent) in comparison with con- trol animals (P < 0.0001). This suppressive effect on fetal weight was accompanied by a proportional intrachamber rise in tumor necrosis factor alpha (TNF-a) and prostaglandin E2 (PGE}) (P < 0.0001). Immunization prior to mating did not provide pro- tection from a challenge during pregnancy, but rather potentiated the effects, indicating the potential strength of a chronic infection. In another series of hamster studies, researchers observed the effects of experimental periodontitis on pregnancy outcomes and amniotic fluid mediators (Offenbacher et al. 1998). The investigators noted a 20 percent decrease in fetal weight (P = 0.002). Periodontal infection in the pregnant hamster also was associated with a significant rise in intra-amniotic PGE, from 3.31 + 1.1 to 13.5 + 4.1 micrograms per milliliter (P = 0.03). These data suggest a link be- tween oral infection and changes in the fetal envi- ronment. Epidemiologic Studies Human case-control studies have demonstrated that mothers of low-birth-weight infants born as a result of either preterm labor or premature rupture of membranes tend to have more severe periodontal dis- ease than mothers with normal-birth-weight infants (Offenbacher et al. 1996, 1998). A case was defined as a mother whose baby weighed less than 2,500 grams and who had one or more of the following fac- tors: gestational age of infant of less than 37 weeks; Linkages with General Health preterm labor, or preterm, premature rupture of membranes. Controls were all normal-birth-weight, full-term infants. In a case-control study of 124 sub- jects, the mean clinical periodontal attachment level for the mothers of low-birth-weight babies was 3.10 + 0.74 (SD) millimeters (mm) per site (93 subjects) versus 2.80 + 0.61 (SD) mm per site (31 subjects) for mothers of normal-weight infants (P = 0.038 for all cases and controls). For a subset of mothers for whom this was the first child, the mean clinical peri- odontal attachment level for those with low-birth- weight babies was 2.98 + 0.84 (SD) mm per site (46 subjects) versus 2.56 + 0.54 (SD) mm per site for controls (20 subjects) at P = 0.041 (Offenbacher et al. 1996). This subset was analyzed separately to avoid the confounding effects of mothers With periodontal disease who had previously given birth to low-birth- weight infants but who later had normal-weight infants. Logistic regression models demonstrated that severe periodontal disease was associated with a sev- enfold increase in risk of low birth weight, after con- trolling for known risk factors such as smoking, race, alcohol use, age, nutrition, and genitourinary tract infection. This study suggests an association between periodontal disease and prematurity. In a subsequent case-control study of 44 sub- jects, additional biochemical and microbial parame- ters of periodontal disease status were studied to assess the relationship of current periodontal status to current pregnancy outcome (Offenbacher et al. 1998). Results indicate that PGE, levels in gingival crevicular fluid were significantly higher in mothers of low-birth-weight infants than in controls (131.4 + 21.8 (SE) versus 62.6 + 10.3 (SE) nanograms per mil- liliter), respectively (at P = 0.02). Furthermore, with- in the group of mothers of low-birth-weight infants there was a significant inverse association between birth weight, gestational age, and gingival crevicular fluid PGE, levels (at P = 0.023 for current births). These data suggest that the level of PGE, in gingival crevicular fluid, serving as a marker of current peri- odontal disease activity, varies inversely with birth weight, that is, the higher the PGE; level, the lower the birth weights. In this study the periodontal dis- ease was more severe in mothers with adverse preg- nancy outcomes, as determined by biochemical and microbial biomarkers, but the difference in clinical attachment levels did not reach statistical signifi- cance (P = 0.11). Studies also have been reported in other coun- tries. In the United Kingdom a preliminary analysis of 167 cases and 323 controls did not show an asso- ciation between periodontal disease and pregnancy ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 121 Linkages with General Health outcomes (Davenport et al. 1998): however, the investigators did not control for confounding factors. Dasayanake (1998) conducted a matched case-con- trol study with 55 cases in Thailand. Gingivitis was associated with a higher risk of having a growth- restricted infant (odds ratio = 0.3; 95 percent CI, 0.12 to 0.72), controlling for mothers height, prenatal care, dental caries status, and the infant's gender. Smoking was not controlled for in this study. Conclusion As a remote gram-negative infection, periodontal dis- ease may have the potential to affect pregnancy out- come. Not all the obstetric risk factors that result in babies being born too soon and too small have been fully identified (Gibbs et al. 1992, McCormick 1985). Oral infections have been investigated as a potential risk factor for preterm labor or premature rupture of membranes, which are major obstetric antecedents to spontaneous preterm births. Although the findings from animal research and case-control studies are promising, additional work, including longitudinal studies, research on mechanisms, and intervention trials, is needed to determine whether periodontitis is a risk factor and what the mechanisms of action may be for adverse pregnancy outcomes. In the United States, longitudinal and intervention studies are under way. Conclusion This critical Jook at the emerging associations among oral infections and specific conditions establishes the need for an aggressive research agenda to better understand the specific aspects of these associations and the underlying mechanisms. Prospective and intervention studies are under way and should pro- vide additional and stronger evidence of the presence and direction of an association. It is essential for such studies to include populations at known risk for the underlying conditions as well as the general popula- tion. Of the conditions reviewed, the relationship of periodontal disease and diabetes has the strongest evidence, demonstrating that the risk of periodontitis is higher in individuals with diabetes. However, the effect of periodontitis on glycemic control is less clear, a reflection of the difficulty of controlling for the effect of systemic antibiotic treatments used to manage periodontal disease in diabetic patients in clinical trials. IMPLICATIONS OF THE LINKAGES This review of oral health linkages with general health reveals implications for the clinical practice of both medicine and dentistry. The recognition of well- known and established signs and symptoms of oral diseases may assist in the early diagnosis and prompt treatment of some systemic diseases and disorders. The presence of these signs also may lead to the insti- tution of enhanced disease prevention and health promotion procedures. All health professionals, and the public, should be aware of these signs and symp- toms. Individuals, practitioners, and community pro- grams may also benefit from the accelerated develop- ment and testing of readily accessible, acceptable, and simple oral-based diagnostics. A better understanding of the role of the oral cav- ity and its components in protecting against infection is needed. This information should permit the devel- opment of interventions to enhance these compo- nents. For example, research is under way investigat- ing how to augment some of the natural antimicro- bial molecules that are present in saliva and how to use oral and nasal vaccination routes to enhance immunity. Also, host susceptibility factors contribut- ing to the dissemination of oral infections to other parts of the body should be investigated, especially in populations at high risk for disease and infection. In addition, further studies are needed to elucidate the role of the mouth as a means of transmitting infec- tious microbes. This in turn will allow the develop- ment of interventions to prevent transmission and curb the progression of infections once established. The associations between oral infections and dia- betes, heart disease and stroke, and adverse pregnan- cy outcomes warrant a comprehensive and targeted research effort. If any of these associations prove to be causal, major changes in care delivery and in the training of health professionals will be needed. Awareness of the oral complications of medica- tions and other therapies for disease management and for health promotion needs to be enhanced among health care professionals, the public, drug manufacturers, and the research community. For some of these therapies, known interventions exist and should be followed before initiating the therapy to minimize or modulate its side effects. To prevent the oral complications of other therapies, new approaches are needed. Ultimately, and ideally, the side effects of therapies should be considered in the development of new drugs and biologics. 122 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL FINDINGS e Many systemic diseases and conditions have oral manifestations. These manifestations may be the initial sign of clinical disease and as such serve to inform clinicians and individuals of the need for fur- ther assessment. e = The oral cavity is a portal of entry as well as the site of disease for microbial infections that affect general health status. e The oral cavity and its functions can be adversely affected by many pharmaceuticals and other therapies commonly used in treating systemic conditions. The oral complications of these therapies can compromise patient compliance with treatment. e Individuals such as immunocompromised and hospitalized patients are at greater risk for gen- eral morbidity due to oral infections. e Individuals with diabetes are at greater risk for periodontal diseases. e Animal and population-based studies have demonstrated an association between periodontal diseases and diabetes, cardiovascular disease, stroke, and adverse pregnancy outcomes. 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J Infect 1992 Jul;25(1): 83-7. “i2 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL CHAPTER 6 eee Effects on Well-being and Quality of Life Fifty years ago the World Health Organization (WHO) defined health as the “complete state of physical, mental, and social well-being and not mere- ly the absence of infirmity” (WHO 1948). In its defi- nition the WHO acknowledged that an individual who is technically “cured” of disease may not neces- sarily be “well” and went on to indicate three dimen- sions of well-being. Physical well-being assumes the ability to function normally in activities such as bathing, dressing, eating, and moving around. Mental well-being implies that cognitive faculties are intact and that there is no burden of fear, anxiety, stress, depression, or other negative emotions. Social well- being relates to one's ability to participate in society, fulfilling roles as family member, friend, worker, or citizen or in other ways engaging in interactions with others. The WHO declaration resonated with ongoing developments in the social sciences as theoreticians recognized the need for multiple indicators in assess- ing health and treatment outcomes (Bergner et al. 1981, Fries et al. 1982, Hunt et al. 1985, Meenan et al. 1980). These efforts led to definitions of “health- related quality of life” (Guyatt et al. 1993) as well as explanatory models. The model proposed by Wilson and Cleary (1995), for example, posits five dimen- sions by which to measure treatment outcomes: bio- logical and physiological variables, symptom status, functional status, general health perceptions, and overall quality of life. These factors are not inde- pendent but may be reciprocally connected. For example, a diabetic patient with symptoms of depres- sion may experience a rise in serum glucose as a result of less vigilant glucose monitoring; the depres- sion may then lead to a deterioration in physical and social activities. Most importantly, measures of bio- logical and physiological factors are often inconsis- tent with patients’ own reports of symptoms, ability to function, general health perceptions, and overall quality of life. In the wake of these developments in general medicine, researchers began to elaborate multidimensional models of “oral-health-related” quality of life. The efforts to understand these relationships are particularly relevant given the aging of the popula- tion. As Gift and Atchison (1995) stated, measuring health-related quality of life allows assessment of “the trade-off between how long and how well peo- ple live.” Diseases and disorders that result in dental and craniofacial defects can thwart that goal, disturb- ing self-image, self-esteem, and well-being. Oral- facial pain and loss of sensorimotor functions limit food choices and the pleasures of eating, restrict social contact, and inhibit intimacy. Oral complications of many systemic diseases also compromise the quality of life. Problems with speaking, chewing, taste, smell, and swallowing are common in neurodegenerative conditions such as Parkinson's disease; oral complications of AIDS include pain, dry mouth, mucosal infections, and Kaposi's sarcoma; cancer therapy can result in painful ulcers, mucositis, and rampant dental caries; and periodontal disease is a complication of diabetes and osteoporosis. Prescription and nonprescription drugs often have the side effect of dry mouth. The ability to measure the quality of life has the practical value of guiding policymakers, health serv- ice researchers, epidemiologists, program evaluators, and clinicians interested in the effects of interven- tions. The measures can also provide useful informa- tion to patients and family members, third-party pay- ers, and employers. For example, measures of the ability to perform activities of daily living may indi- cate areas where the patient is able and competent, as well as areas where further therapy may be helpful. This chapter reviews oral-health-related quality of life findings along functional, psychosocial, and economic dimensions, taking into consideration the ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 133 Effects on Well-being and Quality of Life influence of cultural and spiritual values. The results of studies in which investigators asked adults how they value their oral health and whether they are sat- isfied with their oral health care are included. The study of the association between oral health and quality of life is a relatively new but rapidly growing field. A variety of questionnaires have been designed to assess oral-health-related quality of life, and the chapter concludes with a discussion of their use in surveys and analytic studies, and their potential importance in outcome research, THE CULTURAL CONTEXT The determination of the health-related quality of life of an individual is implicitly made against a cultural background that includes a set of values, standards, customs, and traditions associated with a particular society. Decisions about whether to seek care from a den- tist, a physician, or other care provider may be influ- enced by cultural or ethnic perspectives and under- standing (Aday and Forthofer 1992, Andersen and Davidson 1997, Davidson and Andersen 1997, Diehnelt et al. 1990, Kiyak 1993, Lee and Kiyak 1992). Different population groups differ in the way they think about health, and in how they define a health problem, determine its seriousness, and decide whether to seek care. In one cultural setting a painful tooth may be enough to motivate care seek- ing. In another, bleeding, swelling, or fever may be necessary before care is sought. Similarly, decisions about whether to comply with a suggested treatment regimen, whether to engage in self-care, and whether to return for a follow-up appointment are also cul- turally influenced. The anthropology and ethnography literature is rich in references to the ways in which different cul- tures at different times and places have regarded the human body (Hufford 1992, Kleinman 1979). Cultural beliefs regarding the body, health, and dis- ease are often embedded in religious or spiritual traditions, which in turn may govern how diseases and disorders are regarded and treated. A brief des- cription of Western and non-Western perspectives follows. Cultural Models In the medical model typical of Western society the body is partitioned into organs and systems, each with identifiable functions. The body is seen as func- tioning well unless disease disrupts it. Diseases in themselves are understood to be invariable across cultures. The medical model has traditionally dichotomized body and mind/soul/spirit—science and magic. Such a perspective sees the body as rela- tively objective and value-free, immune to nonso- matic influences. That perspective began to change with the pio- neering work of Hans Selye in the 1930s on the importance of stress in health and disease (McEwen 1999). Research in the intervening half century has confirmed the reciprocal connections of the nervous, endocrine, and immune systems, not only in relation to stress, but also in terms of the effects of emotions and cognitive processes on health status. The model that has emerged as a new paradigm in the study of health and disease incorporates bio- logical with psychological and social factors. This biopsychosocial model is defining agendas for research in such fields as behavioral medicine and psychoneuroimmunology. Social and psychological factors are routinely incorporated into health assess- ments, the better to describe the quality of life. Other societies hold views of the body strikingly different from the medical model. In some cultures, individu- als and their care providers conceive of the body as the union of soul and soma. Illness may occur as a result of a “failure in harmony” or “an imbalance of forces.” Schools of medicine in China, India, and other non-Western societies incorporate such princi- ples into their teaching and practice (Hufford 1992). Combining Perspectives All Americans hold culturally influenced perspec- tives on healing and illness (Henderson et al. 1997), some of which come from more traditional beliefs. Some people accept pain as an inevitable part of ill- ness, a necessary evil, or even punishment for past iniquities or shortcomings and may shun pain-reliev- ing drugs (Zborowski 1952). Many pragmatically combine cultural, folk, complementary, and alterna- tive healing practices with participation in conven- tional care delivery systems. A recent survey indi- cates that over 50 percent of Americans sought non- traditional therapies for a number of ailments (Eisenberg et al. 1998). Traditional beliefs are often comforting and satis- fying to individuals (Selikowitz 1994). Certainly, Western culture and science have not always improved the quality of people’s lives (Harris et al. 1993). Dietary changes to refined foods have been associated with dental caries (Godson and Williams 1996, Navia 1994), obesity, and other deleterious health changes (Selikowitz 1994). The marketing of tobacco products has added to the burden of cancer 134 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and heart and lung problems worldwide. Migrations from traditional community rural life to urban cen- ters have been associated with family disruption and violence, drug abuse, sexually transmitted diseases, and hypertension in developing countries. On the other hand, Western science may inform some cultural groups that certain traditional child- rearing practices can be detrimental to oral health (Kolasa 1978, Scheper-Hughes 1990). Early child- hood caries is a form of tooth decay with complex etiologies. Researchers studying high rates of infant caries among some cultural groups are exploring the extent to which traditional means of soothing crying babies or handling bedtime routines play a role, as well as investigating prenatal nutrition and transmis- sion of infection from caregiver to child (Febres et al. 1997, Kelly and Bruerd 1987, Ripa 1988, Tinanoff and O'Sullivan 1997). People who hold different cultural perspectives may distance themselves from Western, scientific worldviews (Lee et al. 1993), a behavior that must be addressed in any program of health promotion and disease prevention. Health professionals who under- stand indigenous or local healing practices and con- cepts are better able to motivate patients and thereby enable them to integrate elements from various heal- ing systems (Kleinman 1979). America is undergoing major demographic changes, with the expectation that at some point before 2050 the white population will no longer represent the majority (Henderson et al. 1997). As these changes occur, cultural elements that now reflect minority groups may become more accepted and dominant. However, cultural values are neither static nor omnipotent in shaping people's lives. Furthermore, individuals within a culture manifest their cultural identity in different ways. Therefore, both the direction of these changes and their effects may be hard to predict. ORAL-HEALTH-RELATED QUALITY OF LIFE DIMENSIONS Multiple factors act and interact in determining one’s quality of life, as Wilson and Cleary (1995) and others have observed. Thus the idea of assessing quality of life along multiple “dimensions” implies a departure from a simple linear scale with excellent quality of life at one end and greatly diminished quality of life at the other. The following sections explore several dimensions, beginning with effects along functional and psychosocial dimensions and concluding with a discussion of economic effects on quality of life. Effects on Well-being and Quality of Life Functional Dimensions Investigators have reported on the effects of dental and craniofacial diseases on the ability to eat and enjoy the full range of dietary choices. The impact of less-than-optimal oral health also has been studied in relation to sleep problems, primarily in relation to oral-facial pain. Eating Both dental and systemic diseases can profoundly affect appetite and the ability to eat, and hence can compromise overall health and well-being. Because chronic illness and medications increase in aging populations, these effects may be particularly evident among the frail elderly (Ship et al. 1996). Undernutrition was observed in 50 percent of geri- atric residents in a U.S. long-term care facility, in many cases, it was linked to eating and swallowing problems (Keller 1993). Less severe oral disorders have more subtle effects on functions relating to eating, although the high prevalence of those disorders elevates their rela- tive importance among health problems. For exam- ple, data from the National Health and Nutrition Examination Survey Ill indicate that 33.1 percent of people aged 65 and older have no teeth (Marcus et al. 1996). Furthermore, clinical studies indicate that the masticatory efficiency of replacement teeth is at least 30 to 40 percent lower than that of natural teeth (Idowu et al. 1986). Consistent with these findings, surveys of elderly populations in the United States indicate that self-reported chewing problems affect significant proportions of people. For example, in California 1 percent of Medicare enrollees were unable to swallow comfortably, whereas 37 percent of senior center residents reported trouble biting or chewing foods (Table 6.1). A number of studies have indicated that having missing teeth is linked to a qualitatively poorer diet. For example, in studies of U.S. veterans (Chauncey et al. 1984), Canadians (Brodeur et al. 1993), and Finns (Ranta et al. 1987), people with impaired dentitions preferred soft, easily chewed foods that were lower in fiber and had lower nutrient density than foods eaten by people with intact dentitions. Quality of life clear- ly suffers when individuals are forced to limit food choices and the foods chosen do not provide optimal nutrition. For example, they would be hard put to comply with the healthful diet recommendation of “five-a-day” helpings of fiber-rich fruits and vegeta- bles. In the elderly, edentulousness and poor oral health may contribute to significant weight loss, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 135 Effects on Well-being and Quality of Life TABLE 6.1 Dysfunction Attributed to Oral Condition(s) Prevalence of self-reported eating dysfunction in surveys of elderly Americans Percentage of Population Group Reporting Dysfunction used to evaluate the effects of tooth loss and replacement. These measures capture aspects of eating that are not necessarily reflected in Elderly Persons in California? the clinical measures of chewing Medicare Enrollees Elderly Persons in Florida> performance with specific foods B (Demers et al. 1996). Such studies 10 of self-reported chewing ability 1 confirm several relationships already noted, including the find- Senior Center Residents Had trouble biting or chewing 37 Limited the kinds of foods eaten 23 Unable to swallow comfortably 10 Mouth sometimes dry 39 Noticed an unpleasant taste in mouth 23 Unable to chew hard things 19 Experienced change in sense of taste 9 Difficulty tasting some foods 6 Noticed change in sense of smell 5 Elderly Persons in North Carolina‘ ings that chewing ability declines as the extent of tooth loss increas- es and that removable dentures do not fully compensate for the reduction (Hildebrandt et al. 1997, Leake 1990, Slade et al. 1996, African Americans Difficulty chewing any foods 18 Felt sense of taste had worsened 13 Uncomfortable eating foods 13 Had to avoid eating some foods 10 Felt digestion had worsened 8 Had to interrupt meals 6 Wayler et al. 1984). In a study of Whites male veterans with varying levels : of tooth loss, Wayler et al. (1982) P reported that levels of taste, smell, 4 texture, perceived ease of chewing, <1 and frequency of ingestion were <1 adversely affected only among an = 1,842 elderly persons (Atchison and Dolan 1990). © = 440 persons aged 70 and older in five North Carolina counties (Hunt et al. 1995). bn = 390 dentate persons aged 65 and older living in retirement communities (Gilbert et al. 1993). people with severely compromised dentitions. However, in some stud- ies of prosthodontic treatment, self-reported chewing ability im- which may affect overall health (Blaum et al. 1995, Ritchie et al. 2000, Sullivan et al. 1993). Clinical research has demonstrated a general reduction in chewing function as the number of missing teeth increases, even when dentures are worn (Carlsson 1984, Feldman et al. 1980, Helkimo et al. 1978). However, clinical studies in Scandinavia have observed relatively good chewing performance when no more than 12 teeth are missing and the remaining 20 teeth are distributed fairly equally, providing good contact between the upper and the lower jaw (Agerberg and Carlsson 1975). This find- ing has led some researchers to advocate the concept of a “shortened dental arch” as a treatment goal for older adults, that is, retention of at least 20 well-dis- tributed teeth (Kayser 1981). A consistent finding from research into treatment of tooth loss is that removable dentures produce only partial improve- ment in chewing performance (Garrett et al. 1996, van der Bilt et al. 1994, Witter et al. 1989). Dentures anchored by implants result in significantly better chewing performance than conventional, removable dentures (Geertman et al. 1996). Self-reported measures of eating ability, satisfac- tion with eating, and avoidance of foods are widely proved following treatment, even in the absence of significant change in clinical meas- ures of chewing performance (van der Bilt et al. 1994). Impaired eating due to conditions other than tooth loss has been evaluated less frequently. In a study of dental patients with intact dentitions, Ernest (1993) correlated reduced salivary flow with decreased intake of 18 of 22 nutrients. Locker and Slade (1988) found that 6 percent of the Canadians surveyed who reported symptoms of temporo- mandibular disorders also reported problems with eating, talking, or swallowing. These conditions are often associated with limited mouth opening and severe pain, which may be constant or present when- ever jaw movements are made. The constant dry mouth of patients with Sjégren’s syndrome, a disease in which the salivary glands are progressively destroyed, is a major source of discomfort that affects speaking, chewing, and swallowing. As part of a Performance Status Scale study of oral and pharyngeal cancer patients, List et al. (1990) reported that only one third of patients achieved a perfect score on a measure of normalcy of diet and only 60 percent on a measurement of eating in pub- lic. Communication skills also suffered; only 55 per- cent scored perfectly on understandability of speech. 136 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Sleeping Sleep problems associated with oral conditions appear to be most closely related to chronic pain, either directly or indirectly in cases where pain and insomnia are exacerbated by depression. In a survey of elderly Floridians, Gilbert et al. (1993) found that 3 percent of the population reported trouble sleeping because of pain or discomfort from dental problems, whereas in a Canadian study Locker and Grushka (1987) reported that 14.2 percent of those with acute or chronic oral-facial pain (or 5.5 percent of the total population) experienced sleep disturbance related to pain. Goulet et al. (1995) assessed sleep problems not specifically attributed to pain among adults in Quebec. The prevalence of sleep problems was 13 percent for persons with no temporomandibular (jaw) pain. The proportion with sleep disturbance among persons with jaw pain increased with the severity of the pain, rising from 20 percent for those with mild pain, to 32 percent for moderate pain, and 59 percent for severe pain. Psychosocial Dimensions The social and psychological dimensions of well- being and quality of life are deeply intertwined in everyday life and so are considered together here. Findings are reported for those oral conditions where the most research has been conducted: dental dis- eases (primarily those that affect appearance or involve extensive tooth loss), pain conditions, cran- iofacial deformities (primarily clefting syndromes), and oral and pharyngeal cancers. Psychological dis- tress associated with oral health problems has been measured through individual questions (e.g., items assessing worry) and through standardized psycho- logical instruments such as the Beck Depression Inventory (Beck 1967) or the Symptom Checklist 90 (SCL-90) (Derogatis 1983). Overall, the results point to a poorer quality of life and a tendency to avoid social contact as a result of concerns over facial appearance. Persistent pain has similar isolating and depressing effects. Cultural Significance of Teeth Cultural beliefs and customs are a major influence on the psychosocial effects of dental disease on individ- uals. In a historical essay on the art of pulling teeth, Kunzle (1989) noted that “the tooth has always been accorded a special, even magical, role among all peo- ples and at all times, and has stood for power, and its loss for loss of power.” The practice of hiding or burying a lost tooth was based on the fear that its Effects on Well-being and Quality of Life recovery by an enemy could be used magically to inflict harm on the tooth owner. Remnants of that belief persist in the ritual of the tooth fairy, who res- cues the hidden baby tooth and leaves a reward. The potency of teeth is well recorded in the metaphors of language. As Ziolkowski (1976) observed, “if some- thing sets our teeth on edge or if someone casts an insult in our teeth, we can gnash our teeth in anger, show our teeth belligerently, grit our teeth resolutely, take the bit in our teeth, arm ourselves to the teeth, and fight tooth and nail in the teeth of great danger and, with luck, escape by the skin of our teeth.” The perception of healthy teeth contrasts sharply with that of diseased teeth. The sixteenth-century French surgeon Ambroise Parée remarked that “toothache was the greatest and most eternal of all pains . . . the fiery torture of the damned in hell” (Kunzle 1989); and a preacher of that time saw the root of original sin in a rotting tooth, as quoted in Kunzle (1989): “We unfortunate humans: We all have toothache and suffer ever and always from the teeth with which Adam bit the forbidden apple.” In the nineteenth century, Sir James Frazer reported that African tribal kings could not be crowned if they were symbolically emasculated by having a broken tooth, a theme Freud echoed in declaring that dreams of pulling teeth were symbols of castration (Ziolkowski 1976). The link between diseased teeth and weakness, impotence, and even moral turpitude and sin has been analyzed by scholars exploring the vast legacy of dental themes in art and literature. These authors offer a variety of political, social, psychological, and economic interpretations of diseased versus healthy teeth, attesting to the seriousness with which human- ity has invested dental pain and tooth loss. Cultures have sanctioned a variety of alterations to teeth by shaping and filing, embedding with jew- els, bleaching, capping, or providing orthodontic treatments to improve occlusion and aesthetics. These procedures have been variously designed to enhance the status, power, and attractiveness of the owner. Cultures have also dictated specific practices to indicate social position, such as the former Japanese custom of dyeing a married woman's teeth black to denote her marital status. Decisions about aesthetic surgery (Kaw 1993), the definition of what constitutes a severe malocclu- sion, and the need for dental aesthetics (Cons et al. 1986) and surgical intervention (Strauss 1985) depend on social norms. Recently, researchers have begun to examine the perceived attractiveness of the human smile in terms of tooth length, shape, and color, lip line and plumpness, and tooth exposure ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 137 Effects on Well-being and Quality of Life (Dunn et al. 1996). Although there are no reliable studies to document the proportion of people who would seek treatment for perceived defects, the growth of practitioner groups and dental supply companies that specialize in aesthetic dentistry attests to a substantial increase in cosmetic dental treatments. Follow-up studies of patients who have undergone tooth bleaching indicate high levels of sat- isfaction with the extent and stability of the color change (Haywood et al. 1994). Dental Problems and Social Function Given the importance of the mouth and teeth in ver- bal and nonverbal communication, diseases that dis- rupt their functions are likely to damage self-image and alter the ability to sustain and build social rela- tionships. The social functions of individuals encom- pass a variety of roles, from the most intimate in dat- ing and mating behaviors, to other interpersonal con- tacts, to participation in social or community activi- ties. Dental diseases and disorders can interfere with these social roles at any or all levels (Patrick and Bergner 1990). Whether because of social embarrass- ment or functional problems, people with oral condi- tions may avoid conversation or laughing, smiling, or other nonverbal expressions that show their mouth and teeth. Two surveys of different segments of the adult population in Ontario, Canada, addressed the issue of self-consciousness or embarrassment felated to oral health problems. Both inquired into the frequen- cy of such problems in the prior year. Among persons over 18 years old in North York, Ontario, 7 percent reported limiting conversation with others because of oral problems in the prior year, 15 percent reported that they had avoided laughing or smiling because of oral problems, and 19 percent reported being embar- rassed at least sometimes by the appearance or health of their teeth or mouth (Locker and Miller 1994). Among persons 50 years of age and older throughout the province, 24 percent reported being self-con- scious about their appearance at least occasionally because of problems with their teeth, mouth, or den- tures, 22 percent reported feeling uncomfortable at least occasionally, and 13 percent reported that they avoided smiling (Locker and Slade 1993). Recently, investigators have begun to develop quantitative tools to assess patterns of facial anima- tion, including normal facial expressions, in order to assess functional impairment in these movements (Trotman et al. 1998)—and ultimately to address implications for quality of life. The effects of facial expressions, particularly smiling, on social relation- ships warrant further research. The more subtle aspects of social function may also be affected by relatively common oral conditions such as tooth loss. In a study of elderly people with tooth loss in the United Kingdom, 30 percent report- ed difficulty chewing. Although only 5 percent had changed their diet, 9 percent felt uncomfortable chewing in front of others, and 13 percent reported embarrassment during social interactions (Smith and Sheiham 1979). Bergendal (1989) acknowledged tooth loss in adults to be a serious life event with a more difficult period of readjustment than retire- ment. In a study by Fiske et al. (1998), 25 percent of people without teeth reported that they had avoided close relationships because of fear of rejection when their toothlessness was discovered. The authors reported that reactions to tooth loss by the elderly include lowered self-confidence and altered self- image, bereavement, dislike of appearance, and the perception of being more advanced in age. A nation- al study surveying 3,000 homes in Great Britain regarding the effect of oral health on the quality of life was performed in 1997-98. Seventy percent of respondents reported that their oral health affected their quality of life—either positively or negatively. Older people in higher socioeconomic groups, espe- cially those who had seen a dentist within the last year, were more likely to report an enhancing effect (McGrath and Bedi 1998). In a study of older Californians, people who viewed themselves as more attractive than other people their age were more like- ly to have a greater number of natural teeth. They were also more likely to report less emotional anxiety, to rate their health as excellent or very good, and to be less likely to wear full or partial removable den- tures (Matthias et al. 1993). Less severe oral conditions may also have adverse effects on social function. Table 6.2 summa- rizes self-reported levels of impact on personal con- tact and social integration from surveys of numerous population groups within the United States. Generally, the prevalence of adverse effects ranges from 1 to 10 percent, although 20 percent of senior center residents in California reported feeling uncomfortable when eating with others. Avoidance of smiling or conversation tended to be more fre- quent than limitation of social interaction. However, the largest amount of variation appeared to be among population subgroups, even within studies. For example, within the Boston area, Veterans Affairs ambulatory care patients in the Veterans Health Study had substantially higher prevalence rates of 138 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL adverse ef men enrolled in the Normative Aging Study. fects than community-dwelling, healthy Effects on Well-being and Quality of Life general dental care, including prosthodontic care (Fiske et al. 1990). The effects on people's perceived ability to per- form their usual social roles appear to be more subtle Table 6.2). Depending on the phrasing of questions and the population subgroup surveyed, the preva- lence of limitation in social roles varied from 0 to 5 percent. although as many as 10 percent of Veterans \ffairs patients reported that their daily activities were affected because of oral conditions. There are very few studies of the effects of dental treatment on specific forms of social function. One Gooch et al. 1989. eKressin 1997. | Athi and Dolan 1990. f Hunt et al. 1995. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Intimacy Elderly Persons in North Carolina? Perceived effect of mouth on: Good Effect Bad Effect ___No€ffect_ Sex appeal 79 21 5 Kissing 78 18 4 Romantic relationships 81 V7 3 Personal contact/social integration Persons Aged 18 to 61 in Five U.S. Sites Avoid conversation 4 Personal contact/social integration Elderly Persons in Californias Reported impacts due to oral conditions: Senior Center Residents __Medicare Enrollees__ Limiting contact with people 10 1 Feeling uncomfortable eating with others 20 4 Personal contact/social integration Elderly Persons in Florida Avoid laughing or smiling 6 Avoid conversation 3 Social roles Limit activities 5 Selected Populations in Boston Areat Personal contact/social integration Normative Aging Study _ Veterans Health Study Women’s Health Project Avoidance of conversation 2 10 7 Social interaction affected 1 9 7 Social roles Daily activities affected 1 10 10 Elderly Persons in North Carolinat Personal contact/social integration African Americans Whites Avoided smiling 10 3 Unable to enjoy people's company 5 1 Avoided going out with others 3 0 Less tolerant of others 3 0 Social roles Difficulty doing jobs 1 0 Unable to work 3 0 Strauss and Hunt 1993. 4 Gilbert et al. 1993. 139 Effects on Well-being and Quality of Life compared pain in the temporomandibular region to back pain, headache, chest pain, and abdominal pain on a number of dimensions. The usual intensity of temporomandibular disorder (TMD) pain (4.3 on a 10-point scale) was similar to that of chest pain (4.3) and back pain (4.7); abdominal pain and headache were rated as more intense (5.1 and 5.9, respective- ly). TMD pain and back pain were more persistent than other pains, with 28 percent of persons with TMD pain (and 29 percent of those with back pain) reporting pain on more than half of the days in the prior 6 months. The daily duration of pain was also relatively high for TMD pain, with 27 percent report- ing pain for 9 or more hours per day; this proportion was roughly the same as for headache and back pain. In this setting, persons with TMD pain sought care for their pain at about the same rate as persons with other pain, with about one quarter having sought care in the past 6 months and about 60 percent hav- ing sought care at some time in the past. Locker and Grushka (1987) reported that more than 70 percent of persons with all types of acute and chronic pain worried about their dental health. Using scales of the Symptom Checklist 90 (SCL-90), age- and sex-standardized to the population under study, persons in the general population who reported TMD pain had substantially higher levels of anxiety and depression than those without a current pain condi- tion (Von Korff et al. 1988). In the same study, items from the SCL-90 were used to assign an algorithm for diagnosis of depression. The percentage of persons with TMD who met the criteria for a possible diag- nosis of major depression was 11 percent, compared with 2 percent among those without a current pain condition and 3 to 5 percent in the general popula- tion. Recent studies suggest that depression in TMD patients follows the onset of symptoms and reflects uncertainty about the cause(s) and the lack of effec- tive treatments. Social Responses to Facial Appearance Just as cultural considerations color an individual's response to dental disease and tooth loss, so, too, does culture play a major role in the psychosocial impact of craniofacial deformities. More than any other body part, the face bears the stamp of individ- ual identity, a fact neurobiology confirms in identify- ing an area of the brain that is dedicated to the recog- nition of faces. In ancient Greece the face was seen as the mortal reflection of the gods, and those faces deemed most beautiful were also judged to be morally superior. Although cultures differ in the details, there appear to be some invariant factors in the judgment of facial beauty and deformity (Stafford et al. 1989), and they are learned early in life. One U.S. study concluded that perceptions of what does and does not constitute an attractive face are established by age 7 (Cross and Cross 1971). Aristotle also thought that the face, because of its position in the uppermost part of the body, pointed to the highest, most spiritual parts of the cosmos. Something of this mystical belief is preserved in lin- guistic traditions that regard what is “higher” and “ascending” as nobler than what is “lower” and “descending,” whether in reference to body parts, human feelings, or classes and castes in society. But if facial beauty is the mark of truth, moral superiority, nobility, and the soul, what of the oppo- site? Faces judged ugly or disharmonious, or those marred or scarred by birth defects or injury, have been associated with defects in character, intelli- gence, and morals. There is a long tradition of read- ing character on the basis of facial and head shapes according to one or another school of “physiog- nomics.” Some schools likened human faces to ani- mal species, such as cats, monkeys, or horses, endowing the human with the traits of the animal in question. Others constructed facial geometries that purported to show which races were nobler, which closer to animal ancestors. During the nineteenth century, Cesare Lombroso, an Italian physician and criminologist, developed a measuring scheme linking certain facial types to criminality (Magli 1989). Given such a tradition, it is not surprising that people continue to “judge a book by its cover.” A large body of research indicates that attractiveness has an important effect on psychological develop- ment and social relationships (Berscheid 1980). Noteworthy among early social psychological studies was the demonstration that physical attractiveness plays a key role in social expectations (Clifford and Walster 1973). Schoolteachers who were asked to evaluate the educational potential of students from school records and facial photographs judged attrac- tive students to have higher educational potential and social ability than unattractive students. This finding has been replicated in a variety of school set- tings and grade levels. The process of attributing positive characteristics to physically attractive persons is called the “beauty is good hypothesis.” The positive impact of attractive appearance has been demonstrated to influence a wide range of social activities, from legal proceedings (Sigall and Ostrove 1975) to psychotherapeutic prog- nosis. This body of research indicates that appear- ance affects social expectations not only in educa- 140 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL tional performance, but also in vocational, marital, legal, and health care endeavors. However, the con- cept may not apply to all personal attributes. Bennett and Stanton (1993) found that appearance may have little effect on perceptions of intelligence or honesty. Discrimination and stigmatization have histori- cally characterized social responses to deformities. People whose appearance is significantly different from what society considers “normal” continue to be stigmatized. Examples in literature abound, in fable and myth, novels, movies, and plays (e.g., Beauty and the Beast, The Elephant Man, The Hunchback of Notre Dame, The Phantom of the Opera, and Scarface). Goffman (1963) provided a theory of stigmatization useful in understanding social responses to human differences and health conditions (Ablon 1981). Persons seen as deviant experience social devaluation associated with prejudices about the causes and con- sequences of congenital and acquired deformities (Macgregor 1974). Ethnographic studies of. facial deformities demonstrate marked variation in how birth defects are explained and treated (Cheng 1990, Meyerson 1990, Scheper-Hughes 1990, Toliver-Weddington 1990). Many cultures have regarded birth defects and the appearance of multiple births as ill omens, with the infants fated to be abandoned or killed. Even today, when it is understood that birth defects may result from an inherited genetic disorder, decisions about what that means and what if anything should be done about it are affected by religious or spiritual beliefs (Strauss 1988). Progress in dentistry, medicine, and surgery has raised expectations that deformed or injured persons can be treated to enhance their appearance. Although critics have objected to the high value that U.S. soci- ety places on attractiveness and youthful appearance, and on how this emphasis influences opportunity, advocates of remediation counter that social values are hard to change and that individuals must adapt to a society's norms and stereotypes. Corrective surgery does produce positive assessments from others (Berscheid and Gangestad 1982). People in postoper- ative photographs following reconstructive and plas- tic surgery were seen as kinder, more sexually appeal- ing, more likely to be better marriage partners, and more employable and successful than the same indi- viduals in preoperative views. Effects on Well-being and Quality of Life Cleft Lip/Palate and Malocclusion Persons with cleft lip/palate have a variety of prob- lems related to appearance, eating, and speech. Studies of self-concept (Broder and Strauss 1989, Kapp-Simon 1986), psychosocial development (Richman and Eliason 1982, Richman et al. 1988), and social perception by peers (Schneiderman and Harding 1984, Tobiasen 1987), parents and teachers (Mitchell et al. 1984, Schneiderman and Auer 1984), and the public (Middleton et al. 1986) highlight the psychosocial problems of children with cleft lip/palate (Broder and Richman 1987). These problems often continue into adolescence, with appearance and speech remaining problematic (Richman et al. 1985), even when the individual has had comprehensive care (Strauss et al. 1988). Studies show an association between cleft lip/palate and the increased reporting of conduct problems at home (Tobiasen and Hiebert 1984) and of behavioral and learning problems at school (Tobiasen et al. 1987). Although children with cleft lip/palate have not been shown to suffer from a negative self-concept (Kapp 1979, Richman 1983) or psychological disorders, they often become socially inhibited and self-con- scious (Richman and Eliason 1982). Adolescent girls with cleft lip/palate have higher rates of social adjustment problems, particularly related to appearance (Leonard et al. 1991). Using psychological projection methods, one study (Pillemer and Cook 1989) also concluded that chil- dren with facial deformities may have inhibited per- sonality styles as well as reduced expectations for success in social interactions. Kapp-Simon (1986) found that social relationships negatively influence overall self-esteem and that adjustment of adoles- cents is associated with the degree of inhibition (Kapp-Simon et al. 1992). Many of the earliest studies of the consequences of oral disease examined the impact of developmen- tal disorders such as facial clefts and malocclusion on personal contact and social integration. There are few outcome studies that demonstrate how social, mari- tal, and occupational status may be affected in adults with facial deformities or cleft lip/palate. In studies dating from the 1970s, persons with cleft lip/palate achieved greater educational levels than did their fathers, but did not exceed their fathers’ occupation- al status (McWilliams and Paradise 1973). Persons with cleft lip/palate were less upwardly mobile than their siblings and achieved lower adult incomes (Peter et al. 1975). Although persons with cleft ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 141 Effects on Well-being and Quality of Life lip/palate had higher occupational desires, they had lower income expectations than did controls; adults felt socially inept and had a tendency to shy away from group activities (Van Demark and Van Demark 1970). Subtle forms of discrimination and stigmati- zation were experienced among adults with cleft lip/palate (McWilliams 1970). Studies of marital status have indicated that per- sons with cleft lip/palate are less likely than nonaf- fected peers to date (Peter et al. 1975) or marry (McWilliams and Paradise 1973), and that when they marry, they marry later (Heller et al. 1981, Peter and Chinsky 1974). Persons with cleft lip/palate were also more likely to remain childless or have fewer children (Peter and Chinsky 1974), The evidence concerning anatomical misalign- ments of the jaws (e.g., overbite, open bite, crossbite) is less consistent, with some early studies showing no clear relationship between the malocclusion and job opportunities or social discrimination (Shaw et al. 1980a). However, people with severe malocclusions are likely to be teased and to have difficulty interacting socially. These problems improve following orthodontic and orthognathic treatment (Cunningham et al. 1996, Helm et al. 1985, Shaw et al. 1980b). Oral and Pharyngeal Cancers Surgical treatment for oral and pharyngeal cancers can result in functional impairment as well as per- manent disfigurement. Problems may include the loss of part of the tongue, loss of taste, loss of chew- ing ability, difficulty in speaking, and pain. Furthermore, in addition to concerns about their function and their future, oral and pharyngeal cancer patients must cope with an altered appearance. In a study of patients who were disease-free from 6 months to 8 years following surgical tumor removal, Gamba et al. (1992) reported that those with more pronounced disfigurement had greater changes in self-image, a worsened relationship with their part- ner, reduced sexuality, and increased social isolation. A study by Bjordal and Kaasa (1995) also noted that 30 percent of oral and pharyngeal cancer patients were still experiencing psychological distress 7 to 11 years after treatment. Depression, too, is frequent in cancer patients. Patients with oral and pharyngeal cancers are at an even greater risk for depression than other cancer patients, due to surgeries that alter their appearance (Gritz et al. 1999). Because oral and pha- ryngeal cancers are also frequently associated with chronic alcohol and tobacco use, depression may be related to withdrawal from these substances or to preexisting psychopathology. Persistent pain, as noted earlier, may also be a contributing factor to depression. Gritz et al. (1999) conducted a prospective analysis of changes in quality of life over time with the aim of identifying which factors might be predic- tive of future improvements or declines. Participants were 186 oral and pharyngeal cancer patients, all smokers or recent former smokers, diagnosed with primary carcinomas of the oral cavity, pharynx, or larynx. The patients were tested at baseline, at 1 month after radiation and/or surgery, and 1 year later (for a subset of 105 patients available for follow-up). Measures used included the Karnofsky Performance Scale, which uses expert judgments of functional per- formance scored from O to 100; the Cancer Rehabilitation Evaluation System Short Form, in which patients rate their quality of life along physi- cal, psychosocial, marital, sexual, and medical inter- action scales; the previously mentioned Performance Status Scale for Head and Neck Cancer Patients (which includes scales for eating and speaking); and the Profile of Mood States, in which patients rate their feelings over the previous week, yielding analy- ses that enable scaling along six mood states: tension- anxiety, depression-dejection, anger-hostility, confu- sion-bewilderment, and vigor-activity. Results indi- cated that in spite of functional improvement on some scales over time, there was continued dysfunc- tion in speech and eating. Patients also reported declines in marital and sexual functioning, as well as an increase in alcohol use. Interestingly, the best pre- dictor of quality of life 1 year after treatment was the scores obtained after initial smoking cessation advice was given, while the patients were undergoing treat- ment and in recovery. Other predictors were treat- ment type (quality of life was generally poorer for radiation patients) and score on the vigor subscale of the Profile of Mood States. The investigators con- cluded that medical follow-up must integrate tailored psychological and behavioral interventions to achieve better quality of life for oral and pharyngeal cancer patients. Indirect Economic Costs The financial impact of oral disease on quality of life is easiest to quantify in terms of direct per capita costs of oral disease and treatment as well as the costs of publicly supported dental care programs. The Health Care Financing Administration includes these costs in its annual total health care expenditure reports. These expenditures are presented in Chapter 9, and the related data on utilization of care are given 142 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL in Chapter 4. Estimating the indirect costs associated with oral health conditions and treatments, such as disability days or lost productivity, is more difficult. Several methodologies are used to estimate these costs, although relatively few studies have actually estimated the indirect costs associated with mortality or lost productivity due to dental conditions or treat- ments (Reisine and Locker 1995). The annual National Health Interview Survey routinely collects data on disability days associated with selected conditions. As shown in Table 6.3, there were 3.7 days of restricted activity per 100 employed persons 18 years and older reported in the United States in 1996 associated with an acute dental condition, as defined by a dental symptom or treat- ment visit. Restricted activity days were most preva- lent among adults aged 18 to 24 years, women, blacks, and individuals with annual incomes of less than $10,000. Compared to the 624.0 restricted activity days per 100 persons per year for all acute conditions, the 3.7 restricted activity days for dental conditions represent a relatively small loss on an individual basis. They do, however, add up to a siz- able number of days lost from work or school every year for the population as a whole. In addition, Table 6.3 presents the number of bed days and work-loss days per 100 employed persons aged 18 and older. Also, for youths 5 to 17 years of age, 3.1 days of school were lost per year. An important aspect of identifying the specific health-related quality of life burden of oral disease will be to acquire more data on how the overall health-related quality of life of persons with oral dis- ease differs from that of healthy persons, those with other diseases and activity limitations, and those with co-morbid oral and general health problems. The CDC’s “Healthy Days” measures and population Effects on Well-being and Quality of Life data—used by all states since 1993 on the Behavioral Risk Factor Surveillance System (BRFSS) and recent- ly added to the National Health and Nutrition Examination Survey (NHANES)—offer the potential of examining quality of life outcomes in relation to oral health and other disease measures used in these surveys (Gift 1996). These productivity-related measures ask about the number of recent days when physical health was not good, mental health was not good, and activities were limited. These measures were found to be valid in use with general popula- tions and among older persons and adults with dis- abilities (Moriarty and Zack 1999). Related measures on activity limitations and recent days of pain, depression, anxiety, sleeplessness; and vitality are also asked by about half of all BRFSS states and— when used with oral disease measures—could help to identify the impact of oral disease prevention pro- grams at the state and local levels. In the 1996 National Health Interview Survey, the percentage of all acute conditions that are med- ically attended for all ages is 67.9 percent. “Medically attended” is defined as having contacted a physician (or other provider) or having a condition that causes a person to cut back on activities for at least half a day. For acute dental conditions, 59.6 percent are medically attended for all ages (NCHS 1996). The most dramatic oral diseases by virtue of their high mortality rates are oral and pharyngeal cancers. The Centers for Disease Control and Prevention esti- mated in 1988 that 16.2 years of life were lost per person dying of cancer of the oral cavity and pharynx (CDC 1991). This exceeds the average for all cancer sites, which was 15.4 years lost. Researchers are beginning to assess costs associ- ated with chronic craniofacial conditions such as periodontal diseases, pain syndromes, and congeni- tal anomalies. These estimates may also include the costs to care- TABLE 6.3 givers who take time off from Disability days due to all acute conditions and acute dental conditions, work to attend to these needs or United States, 1996 to take children to the dentist. All Acute Conditions Acute Dental Conditions Recent estimates put the lifetime Total Days Days per Total Days Days per costs of multiple surgeries and the (inthousands) 100 Persons (in thousands) — 100 Persons other medical, dental, and rehabil- School-loss days® 152,305 296.9 1611 3.18 itation therapies typical of the Work-loss days* 358,377 384.0 2,442 1.90 team approach to the habilitation Bed days? 717,868 YAW 4,602 17> of individuals with cleft lip or Restricted activity? 1,648,932 624.0 9,705 37 palate at a minimum of $101,000 2 Youths 5 to 17 years of age. > Figure does not meet NCHS standard of reliability or precision. “Currently employed persons 18 years and alder. 4 Persons of all ages. Source: NCHS 1996. (Waitzman et al. 1996). Overall costs of chronic pain conditions in America are estimated to be $79 billion (Bonica 1990). Given the prevalence of headaches and ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 143 Effects on Well-being and Quality of Life temporomandibular disorders, the amount repre- senting chronic oral-facial pain would certainly be in the billions. RATINGS OF ORAL HEALTH Researchers use two ways to assess how individuals rate their oral health: global ratings and satisfaction ratings. Global ratings employ a ranking scale, with excellent health at one end and poor health at the other. Satisfaction ratings are more akin to oral- health-related quality of life measures insofar as they ask individuals how satisfied (or dissatisfied) they are with their oral health status in relation to symptoms, physical function, appearance, social function, and psychological status. Global Ratings The dental survey conducted in connection with the International Collaborative Survey II (ICS I) asked younger (35 to 44 years) and older adults (65 to 74 years) of various ethnic groups at three sites in the United States to rate their oral health from 1 (excel- lent) to 6 (poor). The vast majority of younger and older white adults rated their oral health as good to excellent (82 and 80 percent, respectively, in Baltimore, and 71 and 68 percent, respectively, in San Antonio). In contrast, American Indians, Hispanics, and African Americans were more likely to rate their oral health as fair or poor. More detailed analysis found a significant relationship between oral health ratings and perceived general health, dentate status, importance of oral health, income, oral pain, symp- toms, and dental visits (Chen et al. 1997). Studies in the United States (Bloom et al. 1992, Chen et al. 1997, Gift et al. 1997, Matthias et al. 1995) have related global ratings of oral health to demographic, clinical, and psychosocial factors. A special supplement on oral health in the National Health Interview Survey in 1989 asked participants to rate their oral health as excellent, very good, good, fair, or poor (Bloom et al. 1992). The majority of peo- ple (67 percent) rated their oral health as excellent or very good, 23 percent rated it good, and only 10 per- cent rated it fair or poor. Men, younger people, and more frequent users of dental services tended to rate their oral health better than women, older adults, and less frequent users. African Americans, Hispanics, and American Indians were less likely to rate their oral health positively than were whites in similar geo- graphic locations (Atchison and Gift 1997). A study of Medicare participants in California (Matthias et al. 1995) also found that when asked to rate oral health as excellent, very good, good, fair, or poor, most people rated it as good or above (74 per- cent). Interestingly, the relationship between self- rated global oral health and clinical measures used to rate the severity of dental caries or periodontal dis- ease was weak. The finding of such inconsistency has been confirmed in other studies (Gooch et al. 1989, Reisine and Bailit 1980, Rosenberg et al. 1988) and was noted by Wilson and Cleary (1995). The most important correlates of self-rated oral health were worry about teeth and appearance, race, education, general health status, and depression scores. Satisfaction Ratings According to Jokovic and Locker (1997), “expres- sions of satisfaction and dissatisfaction are important oral health status indicators since they synthesize objective health states, subjective responses, and cul- turally based values and expectations.” ICS I repre- sented an early effort at assessing satisfaction with dental status (Armlijot and WHO 1985). Specifically, it looked at satisfaction with teeth and gingiva among adults and adolescents in metropolitan and non- metropolitan areas in 10 countries. With the excep- tion of Japanese participants, satisfaction with teeth and gingiva among adolescents was fairly high, but the percentage of adults satisfied with teeth among participants from all countries was relatively low. A decade later, ICS I] (Chen et al. 1997) again assessed whether younger and older adults were satisfied with the way their teeth looked. American Indians were the least satisfied with the appearance of their teeth. Other community surveys of satisfaction (Barenthin 1977, Gilbert et al. 1994, Jokovic and Locker 1997, Murtomaa and Laine 1985, Rosenoer and Sheiham 1995, Van Waas et al. 1994) show that most people are satisfied with the performance and appearance of their teeth. ORAL-HEALTH-RELATED QUALITY OF LIFE MEASURES Much of the research on oral health and quality of life focuses on the negative impact of craniofacial dis- eases and disorders, diverting attention from the pos- itive effects of good oral health. Although it could be argued that the benefits are self-evident, few studies have investigated how people value oral health. Strauss and Hunt (1993) found that older adults in North Carolina felt that the presence of teeth enhanced their appearance, ability to eat, and enjoy- ment of food, and that teeth also had a positive effect on comfort, confidence, speech, enjoyment, and 144 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL longevity. More generally, a large multisite study in the United States found that most adults across eth- nic groups believe in the seriousness of oral disease and the importance of oral health for general health (Davidson et al. 1996, Nakazono et al. 1997). During the last decade, researchers have identi- fied and described specific effects of oral disease on quality of life, and there are now at least 11 ques- tionnaires designed to measure oral-health-related quality of life (Slade et al. 1998). These range from the three-item Rand Dental Health Index (pain, worry, conversation) to the 49-item Oral Health Impact Profile, which includes items relating to func- tion, pain, physical disability, psychological disabili- ty, social disability, and handicap. Other researchers have used generic quality of life questionnaires (Reisine and Weber 1989) or ana- lyzed oral health survey data, statistically summariz- ing clinical measures with self-reported symptoms, perceptions, and behaviors to create scales of oral- health-related quality of life (Gift et al. 1997, Gilbert et al. 1997). An essential requirement for these analyses is the establishment of theoretical models that describe and distinguish among quality of life dimensions. Although the questionnaires have been used in population studies, there is increased emphasis on the need to incorporate concepts of quality of life into outcome research, using the questionnaires in longitudinal or intervention studies to examine changes in quality of life following provision of den- tal care. Individual items from the questionnaires can be used in describing the impact of oral health status on specific functions. For example, the ques- tions concerning eating dysfunction presented in Table 6.1 are derived from such questionnaires. Multidimensional indicators also can be used to pro- duce quantitative scores that indicate the severity of the impact caused by oral health problems. Because there are seldom any reference values or population norms to indicate thresholds at which such scores represent “abnormal” or “severe” impacts on quality of life, the results are more valuable for analytic studies examining trends and associations than for describing impacts of oral health within populations. Surveys in the United States and elsewhere have used multidimensional questionnaires and have revealed consistent correlations between reduced quality of life and poorer clinical oral status and reduced access to dental care. Table 6.4 provides an overview of these studies, their populations, and descriptions of the assessment tools used. In the studies using varied tools, there are consistent rela- tionships between quality of life and standard epi- Effects on Well-being and Quality of Life demiological indices of missing teeth, decayed teeth, and periodontal disease—conditions that are linked to a lack of dental care. In several studies, infrequent dental visits and problem-motivated dental visits were found to be independently associated with reduced quality of life in multivariate models (Gilbert et al. 1997, Slade and Spencer 1994a). Lower socio- economic status was an additional explanatory factor in five studies (Atchison and Dolan 1990, Gilbert et al. 1997, Gooch et al. 1989, Leao and Sheiham 1995, Locker and Slade 1994). All of the studies in Table 6.4 used cross-section- al designs to analyze associations with quality of life; it is thus not possible to infer a causal link between quality of life and the factors. under study. Information about change in quality of life from those questionnaires is available from only two population-based longitudinal studies. In one, a study of elderly Floridians, small and statistically nonsignificant changes in the Geriatric Oral Health Assessment Index were observed following an oral health promotion program (Dolan 1997). In the sec- ond, a 2-year longitudinal study of elderly South Australians, change in quality of life was measured using the Oral Health Impact Profile. The study did not find that regular dental attendees had consistent- ly better patterns of change than episodic dental attendees (Slade and Spencer 1994b). In contrast, some information from experimental studies of carefully selected clinical samples indicates effects of specific dental treatments on quality of life. Using the Sickness Impact Profile in a U.S. study of 30 patients treated for TMDs, Reisine et al. (1989) found significant improvements for rest/sleep, home tasks, work, and leisure following treatment. A ran- domized clinical trial of 63 Canadians treated for TMDs compared changes in quality of life, measured using visual analog scales. The investigators found equivalent improvements in quality of life, which mirrored improvements in pain ratings, in all three treatment groups (Dao et al. 1994). A German study by Schliephake et al. (1996) reported improvements in quality of life, measured using a 22-item scale, among 85 patients following tumor removal and reconstructive surgery. Two multidimensional scales have been specifi- cally designed to assess global disability (e.g., disabil- ity days, pain interference with daily activities) relat- ed to recurrent or chronic pain. Both the Graded Chronic Pain Scale (Von Korff et al. 1992) and the Multidimensional Pain Inventory (Kerns et al. 1985) have been used to assess disability related to TMDs, as well as back pain and headache. Although TMD patients are generally found to have lower mean levels ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 145 Effects on Well-being and Quality of Life of disability than patients with other types of pain using these scales, both scales can discriminate the full range of disability in TMDs. For example, the Graded Chronic Pain Scale is an ordinal scale that assigns persons with pain to hierarchical grades indi- cating low-intensity, nondisabling pain (grade 1); high-intensity, nondisabling pain (grade II); high- disability, moderately limiting pain (grade III); and high-disability, severely limiting pain (grade IV). In a sample of HMO patients with TMDs, 41 percent were grade I, +3 percent grade Il, 11 percent grade III, and 5 percent grade IV (Von Korff et al. 1992). That is, about 16 percent of patients seeking care for TMDs were moderately or severely limited by their pain. HEIGHTENED EXPECTATIONS Advances in public health and biomedical research in the late twentieth century have transformed our lives remarkably, adding years to the life span, providing cures for many diseases and disorders, and promising a new era of genetic medicine and bioengineering. The new field of science aimed at formulating con- cepts and methods for determining health-related quality of life is a reflection of these advances. People living in societies that enjoy the benefits of this progress are responding with heightened expecta- tions: They want to live long and live well, free of infirmity, impairment, disability, and handicap; they want an optimal quality of life and well-being. In terms of oral health, new social norms and cultural values now dictate that teeth should be retained over the lifetime, and oral pain and dysfunction forever banished. Quality of life measures applied to oral health outcomes will be used to further those goals. FINDINGS Examination of efforts to characterize the functional and social implications of oral and craniofacial dis- eases reveals the following findings: e Oral health is related to well-being and qual- ity of life as measured along functional, psychosocial, and economic dimensions. Diet, nutrition, sleep, psychological status, social interaction, school, and work are affected by impaired oral and craniofacial health. TABLE 6.4 Studies of multidimensional quality of life measures Numbers of Population Studied individuals Assessment Tool Description of Assessment Tool Gooch et al. 1989 U.S. insured adults aged 902 female Rand Dental Heaith index Three dental questions written to represent 18-61 years 756 male factors contributing to adverse effects of dental disease Atchison and Dolan —_ California Medicare 1,000 female Geriatric Oral Health A series of 12 questions measuring patient-reported 1990 recipients aged 65+ 755 male Assessment Index (GOHAI) oral functional problems Hunt et al. 1995 N.C. elderly aged 70+ 440 Oral Health Impact Profile A comprehensive measure of self-reported {OHIP) dysfunction consisting of 49 questions Kressin et al. 1996 Male veterans aged 47+ 1,242 male Oral Health-related Quality A brief global assessment of the impact of oral conditions Of Life (QHQOL) consisting of three items Gift et al. 1997 US. aged 18+ 760 female 1981 Health Resources and Multidimensional concept using data from a large 555 male Services Administration study national sample Gilbert et al. 1997 Floridians aged 45+ 491 female Oral Disadvantage Assessment Eight self-reported measures of avoidance in daily 383 male activities due to decrements in oral health Locker and Miller Canadians aged 18+ 299 female Subjective Oral Health Five oral health status indicators based on WHO's 1994 244 male Status Indicators International Classification of Impairments, Disabilities and Handicaps Locker and Slade Canadians aged 50+ 168 female Oral Health Impact Profile A comprehensive measure of self-reported 1994 144 male (OHIP) dysfunction consisting of 49 questions Slade and Spencer Australians aged 60+ 660 female Oral Health Impact Profile A comprehensive measure of self-reported 1994b 557 male (OHIP) dysfunction consisting of 49 questions Leao and Sheiham Brazilians aged 35-44 303 female Dental Impact on Daily Thirty-six questions that assess the oral heaith impacts 1995 359 maie Living (DIDL} on daily living Coates et al. 1996 Australian dental patients 635 (+795 Oral Health Impact Profile A comprehensive measure of self-reported previously (OHIP) dysfunction consisting of 49 questions surveyed) 146 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL e Cultural values influence oral and craniofa- cial health and well-being and can play an important role in care utilization practices and in perpetuating acceptable oral health and facial norms. e® Oral and craniofacial diseases and their treat- ment place a burden on society in the form of lost days and years of productive work. Acute dental con- ditions contribute to a range of problems for employed adults, including restricted activity, bed days, and work loss, and school loss for children. In addition, conditions such as oral and pharyngeal can- cers contribute to premature death and can be meas- ured by years of life lost. e Oral and craniofacial diseases and condi- tions contribute to compromised ability to bite, chew, and swallow foods; limitations in food selection; and poor nutrition. These conditions include tooth loss, diminished salivary functions, oral-facial pain condi- tions such as temporomandibular disorders, alter- ations in taste, and functional limitations of prosthet- ic replacements. e Oral-facial pain, as a symptom of untreated dental and oral problems and as a condition in and of itself, is a major source of diminished quality of life. 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For example, some 40 percent of the U.S. population resides in communities that do not have optimal fluoride levels in their water supply. Chapter 7 reviews the evidence for current prevention measures. Community water fluoridation remains an ideal public health measure, which benefits individuals of all ages and all socioeconomic strata. Other methods to deliver fluoride are reviewed, as is the use of dental sealants in caries prevention. The prevention of periodontal diseases and conditions such as oral and pharyngeal cancers and craniofacial injuries is at an early stage. Surveys of the knowledge and practices of the public and care providers reveal opportunities for enhanced education. Attaining and maintaining oral health require a commitment to self-care and professional care. Chapter 8 highlights both individual responsibilities and emerging roles for health care providers. With greater understanding of the pathophysiology of oral diseases, providers can incorporate new preventive, diagnostic, and treatment strategies. These include developing risk assessment approaches for individual patients and adopting new strategies for the control of infections. Care providers are well positioned to instruct patients on tobacco cessation, appropriate dietary practices during pregnancy, and other healthful behaviors. The professional provision of oral health care in America involves contributions from the dental, medical, and public health components. These are reviewed in Chapter 9, which focuses primarily on the dental component. A number of factors limit the capacity to improve the nation’s oral health. Public assistance programs as currently designed are not meeting the oral health needs of eligible populations. A troubling lack of diversity exists in the oral health workforce, along with continued shortfalls in the number of men and women attracted to positions in oral health education and research. Correcting these limitations would contribute to increased access to care for underserved populations, enhanced preparation of future practitioners, and an expanded ability to pursue the many research questions generated in this report. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 153 PT eee Community and Other Approaches to Promote Oral Health and Prevent Oral Disease The remarkable improvements in oral health over the past half century reflect the strong science base for prevention of oral diseases that has been developed and applied in the community, in clinical practice, and in the home. This chapter presents the evidence for key preventive measures for those oral conditions that pose the greatest burden to ULS. society. Because the emphasis given to each condition discussed here reflects the extent of the evidence for the associated preventive measures, the chapter is heavily weighted toward the prevention and control of dental caries, for which multiple effective preventive modalities have been developed. The dental profession has long championed dis- ease prevention and health promotion approaches to oral health, The initial observations in the 1930s that people living in communities served by naturally fluoridated water had lower dental caries inspired the trailblazing clinical prevention studies of the 1940s and 1950s. Researchers compared whole cities agree- ing to fluoridate their water supplies to control cities whose drinking water contained only trace amounts of fluoride. Five years into the studies, follow-up with schoolchildren who had been examined at base- line revealed dramatic reductions in dental caries in the children drinking fluoridated water, as compared to controls. The overwhelming success of the studies led to a widespread adoption of community water fluoridation in the United States as a high-benefit, low-cost preventive method that benefited old and young, rich and poor alike. It also provided momen- tum for health practitioners, researchers, industry, and public health directors to consider other kinds of community-wide, provider-based, and individual strategies aimed at improving oral and general health. Most common oral diseases can be prevented through a combination of community, professional, and individual strategies. The strategies selected here include disease prevention and health promotion interventions directed toward the public, practition- ers, and policymakers to create a healthy environ- ment, reduce risk factors, inform target groups, and improve knowledge and behaviors. They were select- ed on the basis of the significance of the health prob- lem they were designed to prevent, whether in terms of prevalence, incidence, severity, cost, or impact on quality of life (see Chapters 4 and 6). Table 7.1 sum- marizes the strategies for the primary prevention of caries, periodontal diseases, oral and pharyngeal can- cers, inherited disorders, and trauma, distinguishing among those that can be implemented community- wide, through health professionals, or through the exercise of individual responsibility. Some strategies can be applied at multiple levels. Box 7.1 provides a glossary of terms related to community health programs. This chapter also includes a discussion of knowl- edge and practices of the public and health care providers regarding the three oral conditions about which we have the most knowledge. The purpose of this discussion is not to outline specific health pro- motion strategies to enhance knowledge and prac- tices but to indicate the opportunities and needs for both broad-based and targeted health promotion pro- grams and activities. WEIGHING THE EVIDENCE THAT INTERVENTIONS WORK Researchers, policymakers, and practitioners make judgments about whether a health intervention works based on estimates of its efficacy or effective- ness. Estimates of an interventions efficacy are best based on randomized controlled trials, which may be conducted under ideal circumstances. Evidence for whether an intervention works when applied in the community at large is referred to as its effectiveness ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 155 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease (O’Mullane 1976). The distinction between efficacy and effectiveness is often blurred in dental public health programs because the studies and their set- tings can be very similar. Nevertheless, the major dif- ference between the two lies in the degree of control exerted over factors that can affect results. Effectiveness studies more accurately reflect results that may be expected from the implementation of interventions. The current trend in health care and public health is to base recommendations on evidence derived from systematic reviews of the literature and an assessment of the quality of evidence. The U.S. Preventive Services Task Force (1996) and the Canadian Task Force on the Periodic Health Exam- ination (Ismail and Lewis 1993, Lewis and Ismail 1995) are examples of groups that have used system- atic reviews to establish the evidence of efficacy or TABLE 7.1 Community Strategies Professional Strategies Community, provider, and individual strategies for primary prevention of key oral diseases and conditions Individual Strategies Dental caries Community-wide health promotion interventions? Fluoride use Community water fluoridation School-based dietary fluoride tablets School-based fluoride mouthrinse School-based and school-linked sealant programs Schooi-linked screening and referral Counseling to follow measures to reduce risk of disease Fluoride use Prescriptions for fluorides (supplements or rinses) Gels and other high-fluoride topicals Topical remineralization solutions Fluoride-containing restorative materials Provision of sealants Prescriptions for antimicrobial agents Individualized recall schedule Being informed about strategies to prevent disease Fluoride use Dentifrice Mouthrinse, over the counter Asking about sealants Use of antimicrobial agents Self-initiated use of dental services Periodontal diseases Community-wide health promotion interventions? School-based personal hygiene, reinforcement of personal oral hygiene habits in Headstart or primary schoo! classrooms Schooi-linked screening and referral Oral and pharyngeal cancers Community-wide heaith promotion interventions? Cancer screening programs (such as health fairs) Counseling to follow measures to reduce risk of disease Control of plaque bacteria by mechanical means (prophylaxis or scaling) Chemical plaque control Chemotherapeutic agents Monitoring and early detection of disease Professional education and patient counseling on risk factors Routine soft-tissue oral examination for early detection of precancerous lesions Being informed about strategies to prevent disease Oral hygiene measures Toothbrushing and flossing Toothbrushing with dentifrices Plaque control Self-initiated use of dental services Being informed about strategies to prevent disease Avoidance of tobacco use Reduction of alcohol use Use of sunscreen and lip protector Self-initiated use of dental services Request for cancer screening Inherited disorders Early detection programs Interdisciplinary early detection programs Trauma Community-wide health promotion interventions? Mouth protector fittings for entire team Professional education and patient counseling on risk factors Fabrication of mouth protectors Being informed about strategies to prevent trauma Use of mouth protectors and helmets ®Community-wide health promotion interventions (education, political, regulatory, and organizational) are directed toward the public, practitioners, and policymakers to create a healthy environment, reduce risk factors, inform target groups, and improve knowledge and behaviors. vit aj ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Dise BOX 7.1 Glossary: The Nature of Community Health Programs Community health programs are defined as health promotion and disease prevention activities that address health problems in populations. Community health programs often provide a level of organization and resources beyond those available to an individual. The programs thus com- plement personal care and professional services. Many programs target populations with limited access to professional services or limited resources to pay for services. Government agencies, religious organizations, charities, schools, foundations, and other private and public groups may spearhead such programs, tapping into the expertise, enthusiasm, and knowledge of community values of staff and volunteers. Some programs are sponsored by national, state, and local dental societies and their members. Five terms related to community health programs—community, health promotion, health literacy, health education, and disease prevention—have been further articulated by experts in the field. Community. According to Last (1995), a community is“a group of individuals organized into a unit, or manifesting some unifying trait or common interest.” The unit can be a town, a geographic area, the state, nation, or body politic (Last 1995). The unit may also be a selected subgroup, such as disadvantaged children living in a large city or women urged to have mammograms according to specified schedules. In designing and implementing community programs, planners must take into consideration that no two communities are identical. In a classic expression of this concept, McGavran (1979) wrote that a community is“an entity different from every other community as an individual is different from his neighbor: different in its physical makeup, its geographic and demographic limitation, different in its social structure, its power structure, its governmental and legal structure, different in mental and emotional patterns, in its ethnic groups, its mores, its religious and nutritional patterns, and different in its educational procedure, its institutions, and its community organization.” On the other hand, communities may have similar risk factors for poor oral health, allowing common solutions to similar problems. Lessons learned in one community may be applicable to those with sim- ilar characteristics. In recent years, investigators have begun to examine characteristics of communities, noting that some communities provide an environment that contributes to the overall health and well-being of the members, whereas others appear to be detrimental. All communities, however, have both pos- itive and negative influences on health and well-being—the challenge is to minimize the negative factors and maximize the positive in each com- munity, Healthy communities have been characterized as having a degree of openness and cooperation—neighbors helping neighbors. Healthy communities also are ones in which there are less extreme separations of individuals by social class (Wilkinson 1996). Health Promotion. Health promotion is “any planned combination of education, political, regulatory, and organizational supports for action and conditions of living conducive to the health of individuals, groups, or communities” (Green and Kreuter 1999). Examples of broad-based health pro- motion activities include programs encouraging people of all ages to stop using tobacco, regulations requiring the use of mouthguards in contact sports, laws to prohibit tobacco sales to minors, and labels that indicate the amount of sugar ina product. Health Literacy. Health literacy is “the capacity of individuals to obtain, interpret, and understand basic health information and services and the competence to use such information and services in ways which enhance health” (Joint Commission on National Health Education Standards 1995). Health literacy is correlated with general literacy, and both vary by educational achievement, socioeconomic status, race, and ethnicity. This is an important concem in a society that is becoming more diverse in terms of language, religion, culture, race, and ethnicity. Programs intending to serve, immigrants, for example, must attend to ensuring that information, programs, and systems are accessible, understandable, and culturally sensitive, particularly if the target audience for health information and services does not speak English, if there are unique cultural and religious beliefs at vari- ance with those of the dominant culture, or if living arrangements are such that individuals lack access to sources of health information and care. Health Education. Health education is an important part of health promotion. It is defined as “any planned combination of learning experiences designed to predispose, enable, and reinforce voluntary behavior conducive to health in individuals, groups, or communities” (Green and Kreuter 1999). Examples include the multiple campaigns to prevent tobacco use among youth. An example at the statewide level is Arizona's promotion of the use of dental sealants with an educational campaign that says “Sealants Are in the Groove.” Disease Prevention. The term prevention embodies the goal of promoting and preserving health and minimizing suffering and distress. Community health programs generally focus on either primary prevention—removing or reducing risks or providing protection from disease before it occurs—or secondary prevention—screening and early detection and intervention to arrest the progress of disease after it occurs. Tertiary pre- vention—rehabilitating and restoring structure and function—is provided in some community-based programs, such as clinical dental care organ- ized and delivered under conditions determined by the community. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL ase 157 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease effectiveness of clinical preventive services for the purpose of making recommendations. Similar reviews of the evidence of effectiveness for commu- nity preventive services are currently under way by the Task Force on Community Preventive Services (2000). These reports provide clear statements about the evidence and recommendations for or against a given strategy. The discussion in this chapter is more illustrative than comprehensive. Readers are encouraged to seek specific guidance from the reports of the U.S. Preventive Services Task Force where available. Furthermore, because of the interest in community preventive services, “expert opinion” about the mer- its of community interventions is included, even though the work of the Task Force on Community Preventive Services has not been completed. Expert opinion is formed by less systematic reviews of the literature or addresses interventions to be applied in settings other than those previously studied. In particular, suggestions are offered for several interventions intended to reduce oral disease and promote oral health that reflect the opinion of experts who contributed to this report. Until findings from additional research are available, expert opinion remains the best guidance for community interven- tions where only efficacy studies have been done or where they were applied to populations with differ- ent attributes or risk factors than those of current interest. Also, expert opinion has been used where there is an interest in criteria that were not consid- ered in previous efficacy studies, such as cost-effec- tiveness and practicality. Readers interested in more detailed information about interventions in areas such as control of tobac- co use or motor vehicle safety are directed to the upcoming report of the Task Force on Community Preventive Services (2000). Interventions included in this chapter (and high- lighted in Table 7.1) are those that have been shown to be effective in certain settings, but which can be applied in other settings. The anticipated benefits may be difficult to determine. In general, the per capita cost of an intervention is lower for communi- ty interventions and is usually a function of the num- ber of people reached for a given level of profession- al effort. Effectiveness, however, is often a function of the risk characteristics of a given individual in the group receiving the intervention. Such risk factors are often easier to target by individual practitioners than by community programs. In the absence of con- temporary data, the promotion of strategies deemed to be more cost-effective than others relies on the opinion of experts. Individual decision making regarding self- or provider care further reflects the subjective value placed on the outcome of care. Therefore, it is not possible to make general state- ments about the superiority of any given approach. _PREVENTION AND CONTROL OF DENTAL CARIES Although many caries prevention strategies, notably community water fluoridation and use of a fluoride- containing dentifrice, benefit adults and children alike, most of our understanding of the effectiveness of these strategies comes from the study of children, during a life stage when caries incidence is high. Caries prevention programs have been designed and evaluated for children and have used a variety of flu- oride and dental sealant strategies applied separately and together. Because these strategies are comple- mentary, their use in combination has the potential of virtually eliminating dental caries in all children. However, dental caries is a problem for all ages. Although direct evidence of caries preventive strate- gies in adults is limited, the evidence that does exist is consistent with expected effects based on experi- ence with children. The Centers for Disease Control and Prevention (CDC) recently convened an expert work group to develop recommendations for modal- ities to prevent and control dental caries based on a review of publications selected by the work group and other experts. The resulting recommendations are summarized in Table 7.2, where they are organ- ized according to quality of evidence, strength of rec- ommendation, and target population in accordance with criteria adapted from the U.S. Preventive Services Task Force (CDC in press). Fluoride Fluoride reduces the incidence of dental caries and slows or reverses the progression of existing lesions (i.e., helps prevent cavities). Today, all Americans are exposed to fluoride to some degree, and there is little doubt that widespread use of fluoride has been a major factor in the overall decline in recent decades in the prevalence and severity of dental caries in the United States and other economically developed countries (Bratthall et al. 1996). Fluoride is the ionic form of the element fluo- rine, the thirteenth most abundant element in the crust of the Earth. Because of its high affinity for cal- cium, fluoride is mainly associated with calcified tis- sues (i.e., bones and teeth). The ability of fluoride to inhibit, and even reverse, the initiation and progres- sion of dental caries is well known. Fluoride’s mech- 158 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease anisms of action include incorporation of fluoride into enamel preeruptively, inhibition of demineral- ization, enhancement of remineralization, and inhi- pition of bacterial activity in dental plaque. 4 variety of theories regarding fluoride’s mecha- nisms of action account for the range of fluoride products available (Burt and Eklund 1999, Stookey and Beiswanger 1995). The initial theory of action was based on the belief that incorporation of fluoride into the hydroxyapatite of developing tooth enamel in the preeruptive phase reduced the mineral’s solu- bility, thereby increasing enamel resistance. Because of the length of time the tooth is at risk of caries dur- ing the posteruptive phase, however, the topical effects of fluoride are considered to predominate (Clarkson et al. 1996). These effects are based on flu- oride’s role in the aqueous phase around the tooth, both in saliva and in dental biofilm (plaque). Fluoride in plaque contributes to the remineraliza- tion of demineralized enamel when bound fluoride is released during an acid challenge, resulting in a more acid-resistant enamel surface structure. Fluoride also has been shown to inhibit the process of glycolysis by which fermentable carbohydrates are metabolized by cariogenic bacteria to produce acid. All these effects occur after the tooth erupts, while it is functioning in the mouth, enabling fluoride to prevent caries over a lifetime in both children and adults. The first use of fluoride for caries prevention was in 1945 in the United States and Canada, when the fluoride concentration was adjusted in the drinking water supplying four communities (Arnold et al. 1962, Ast and Fitzgerald 1962, Blayney and Hill 1967, Hutton et al. 1956). This public health approach followed a long periad of epidemiologic studies of the effects of naturally occurring fluoride in drinking water (Burt and Eklund 1999). The success of the community water fluoridation trials in reducing dental caries led to the develop- ment of other important fluoride-containing prod- ucts, such as dietary supplements and, most notably, fluoride-containing dentifrices, in the early 1960s. Fluoride-containing gels, solu- | FABLE 7.2 Quality of evidence, strength of recommendation, and target population of recom- mendation for each modality to prevent and control dental caries tions, pastes, and varnishes were also developed for topical use, either applied by professionals or self-applied at home or in other aged >16 years. 2Assume that the modalities are used as directed in terms of dosage and age of user. efficacy or effectiveness. ing of orthodontic appliances or prostheses. dAssessment of risk is based on both patient and tooth-specific factors. Source: Modified from CDC in press, and ASTDD 1995. N.A.= no published studies of effectiveness of fluoride supplements in controlling dental caries among persons >The quality of evidence for targeting some modalities to persons at high risk is grade tll, representing the opinion of respected experts, and is based on considerations of cost-effectiveness that were not included in the studies establishing © Groups believed to be at high risk for caries are members of families of low socioeconomic status (SES) or with low levels of parental education; those seeking dental care on an irreqular basis; and persons without dental insurance or access to dental service. Individual factors contributing to increased risk are currently active dental caries; a history of high caries experience in older siblings or caregivers; exposed root surfaces; high levels of infection with cariogenic bacteria; impaired ability to maintain oral hygiene; reduced salivary flow due to medications, radiation treatment, or disease; and the wear- Quality of Strength of settings. All of these products were Evidence Recommendation Target tested for safety and effectiveness Modality? (grade) (code) Population’ in reducing caries. Products Community water fluoridation t+ A All areas designed for professional use gen- School water fluoridation -3 ¢ Rural, nonfluoridated areas erally have higher concentrations Fluoridated dentifrices | A All persons and are used at less frequent inter- Fluoride mouthrinses | A High risk: vals than those designed for self- Fluoride supplements 5 ati application. Pregnant women | E None wo: . ; a Controlled clinical trials from Children aged <6 years N-3 C High risk he 1940s th h the 1970s d Children aged 6 to 16 years A High risk the s through the 1710s coc: Persons aged > 16 years NA. C High risk umented the benefits of profes- Fluoride gels | A High tisk sionally applied fluoride in reduc- Fluoride varnishes ] A High risk ing dental caries, and several Dental sealants | A High riské excellent reviews are available Notes: Criteria for quality of evidence and strength of recommendation designations are adapted from USPSTF as (Horowitz and Ismail 1996, Table 53. Johnston 1994, Ripa 1990, Stookey and Beiswanger 1995). Professional application of fluoride is inherently more expensive than self-applied methods, so the use of such an approach for groups and individuals at low risk of dental caries is unlikely to be cost-elfec- tive. For patients at high risk of dental caries, however, profession- ally applied fluoride is still consid- ered cost-effective. It is not clear whether fluoride varnishes and ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 159 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease gels would be most efficiently used in clinical pro- grams targeting groups at high risk of dental caries or whether they should be reserved for individual high- risk patients. The U.S. Preventive Services Task Force (Greene et al. 1989, USPSTF 1996) and the Canadian Task Force on Periodic Health Examination (Lewis and Ismail 1995) affirm that there is strong evidence to support the major methods for providing fluoride to prevent dental caries. The safety of fluoride is well documented and has been reviewed comprehensively by several scien- tific and public health organizations (Institute of Medicine (IOM) 1997, National Research Council (NRC) 1993, Newbrun 1996, U.S. Department of Health and Human Services (USDHHS) 1991, World Health Organization (WHO) 1984). When used appropriately, fluoride has been demonstrated to be both safe and effective in preventing and controlling dental caries. The IOM (1997) classified fluoride as a micronutrient, citing it, along with calcium, phos- phorus, magnesium, and vitamin D, as an important constituent in maintaining health. Appropriate use of fluoride products can mini- mize the potential for enamel fluorosis, a broad term applied to certain visually detectable changes in the opacity of tooth enamel associated with areas of flu- oride-related developmental hypomineralization. There are also many developmental changes in enamel that are not fluoride-related (Fejerskov et al. 1990). Most enamel fluorosis seen today is of the mildest form, which affects neither aesthetics nor dental function. Cosmetically objectionable enamel fluorosis can occur when young children ingest higher than optimal amounts of fluoride, from any source, while tooth enamel is forming (up to age 6). Its occurrence appears to be most strongly associated with the total cumulative fluoride intake during the period of enamel development, but the condition’s severity depends on the dose, duration, and timing of fluoride intake. Specific recommendations have been made to control fluoride intake by children during the years of tooth development (USDHHS 1991). Fluoridation of Drinking Water For more than half a century, community water fluor- idation has been the cornerstone of caries prevention in the United States; indeed, CDC has recognized water fluoridation as one of the great public health achievements of the twentieth century (CDC 1999). All water contains at least trace amounts of fluoride. Water fluoridation is the controlled addition of a flu- oride compound to a public water supply to achieve a concentration optimal for dental caries prevention. In the 1940s, Dean et al. (1941) concluded that 1 ppm (part per million) fluoride was the optimal con- ’ centration for climates similar to that of the Chicago area; this concentration would significantly reduce the prevalence of dental caries with an acceptably low prevalence of enamel fluorosis. Current U.S. Public Health Service (USPHS) recommendations for fluoride use include an optimally adjusted concen- tration of fluoride in drinking water ranging from 0.7 to 1.2 ppm, depending on the mean maximum daily air temperature of the area (Galagan and Vermillion 1957, USDHEW 1962). A lower fluoride concentra- tion is recommended for communities in warmer cli- mates than cooler climates, because it is assumed that persons living in warmer climates drink more tap water, Effectiveness Numerous studies in naturally fluoridated areas pre- ceded the field trials. There are no randomized, double-blind, controlled trials of water fluoridation because its community-wide nature does not permit randomization of people to study and control groups. Similar results have been derived from numerous well-conducted field studies by various investigators on thousands of subjects in different parts of the world. Conducting a study in which individuals are randomized to receive or not receive fluoridated water is unnecessary and is not feasible. In 1945, Grand Rapids, Michigan, became the first city in the United States to fluoridate its water supply; the oral health of its schoolchildren was peri- odically compared with that of schoolchildren in the control city, Muskegon, Michigan. Dramatic declines in dental caries among children in Grand Rapids and three other cities conducting studies shortly there- after led to fluoridation in many other cities. In an extensive review of 95 studies conducted between 1945 and 1978, Murray et al. (1991) reported the modal caries reduction following water fluoridation to be between 40 and 50 percent for primary teeth and 50 and 60 percent for permanent teeth. Newbrun (1989) reported on more than 60 studies conducted during the 1970s and early 1980s, limiting his review to those with concurrent control groups because of the continuing decline in dental caries in both fluor- idated and nonfluoridated areas. Comparisons of flu- oride-deficient and fluoridated communities in the United States, Australia, Britain, Canada, Ireland, and New Zealand have consistently demonstrated the ORAL HEALTH EIN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease continued effectiveness of water fluoridation. Caries reductions ranged between 15 and 40 percent in fluoridated, as compared with fluoride-deficient, communities (USDHHS 1991). Fluoridation also benefits middle-aged and older adults. Benefits to adults include reductions in both coronal and root caries. These benefits are important because older people typically experience gingival recession, which results in exposed root surfaces, which are susceptible to caries. In addition, tooth retention in older U.S. cohorts has increased in recent decades, so that the number of teeth at risk for caries in older age groups is also increasing. Finally, many medications used to treat chronic diseases common in aging have the side effect of diminished salivary flow, depriving teeth of the many protective factors in saliva. Other evidence of the benefits of fluoridation comes from studies of populations where fluorida- tion has ceased. Examples in the United States, Germany, and Scotland have shown that when fluor- ;dation is withdrawn and there are few other fluoride exposures, the prevalence of caries increases. In Wick, Scotland, which began water fluoridation in 1969 but stopped it in 1979, the caries prevalence in 5- to 6- year-olds with limited exposure to other sources of fluoride increased by 27 percent between 1979 and 1984. This was despite a national decline in caries and increased availability of fluoride-containing den- tifrices (Kugel and Fischer 1997, Seppa et al. 1998, Stephen et al. 1987). . Costs and Cost-effectiveness The increase in other fluoride exposures since water fluoridation was first introduced in 1945—particu- larly from fluoride-containing dentifrices, mouth- rinses, and foods and beverages processed using fluoridated water—has led to smaller differences in the prevalence of dental caries between people in fluoridated and those in nonfluoridated communities than in the past. Most public health experts believe that water fluoridation continues to be a highly cost- effective strategy, even in areas where the overall caries level has declined and the cost of implement- ing water fluoridation has increased (Burt 1989, CDC 1999). Compared to the cost of restorative treatment, water fluoridation actually provides cost savings, a rare characteristic for community-based disease pre- vention strategies (Garcia 1989). The mean annual per capita cost of fluoridation ranges from $0.68 for systems serving populations greater than 50,000 (large systems) and $0.98 for systems serving between 10,000 and 50,000 (medium systems), to $3.00 for systems serving less than 10,000 (small sys- tems) (reported in 1999 dollars) (Ringelberg et al. 1992). In 1992, approximately 60 percent of the U.S. population receiving fluoridated water was served by large systems, 31 percent by medium systems, and 9 percent by small systems (USDHHS 1993). Access to Optimally Fluoridated Water in the United States The most recent national data on the extent of com- munity water fluoridation reflect the status of fluori- dation in 1992 (see Figure 7.1 and Table 7.3). About 145 million people, or 62 percent of the population served by public water supplies, consume water with optimal fluoride levels. Of the 50 largest cities in the United States, 43 are fluoridated (Table 7.4). Residents of the seven unfluoridated cities in the group are among the almost 100 million persons in the United States who lack this method of caries prevention. Although many states and large cities had been quick to implement fluoridation programs in the 1950s and 1960s, the trend then began to level off. In the absence of legislative mandates in most states and categorical federal funding, fluoridation decisions are left to the states, and frequently to local governments and city councils. Thus expansion of fluoridation in the United States is not simple and requires decisions at many levels. The national health promotion and disease prevention objectives in Healthy People 2010 (USDHHS 2000) call for increasing the percentage of Americans on public water supplies drinking fluori- dated water from 62 to 75 percent—a 21 percent improvement (see Figure 7.1). This would mean adding 30 million people served by well over 1,000 community water systems to those who currently have access to fluoridated public water systems (USDHHS 1993). Summary: Community Water Fluoridation Epidemiological studies carried out during the last five decades provide strong evidence supporting the effectiveness of water fluoridation in preventing coronal and root caries in children and adults. Further support of effectiveness comes from studies that indicate that caries experience increases in com- munities that no longer fluoridate the water supply (and where there are few other exposures 10 fluo- rides). Given the modest cost of less than 1 dollar per person per year to fluoridate water systems serving most people, community water fluoridation is rec- ommended as a very effective and cost-effective ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 161 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease FIGURE 7.1 Percentage of U.S. population by state served by fluoridated public water supply, 1992 24.0 57.4 MA 57.0 RI 100.0 85.9 the children were present for only portions of the day and year. Although the strategy shares some of the advantages of community water fluorida- tion—serving rich and poor alike and requiring no action 13.0 a Source: USDHHS 1993. 21 Y 95.2 Ord 87.9 ae 58.4 . 100.0 i aa oo Sas, ob Healthy People 2010 Goal of 75 Percent [J Goal not attained HEBD Goal attained or exceeded 16.2 on the part of the children (other than drinking the water)—a number of disadvan- tages were evident from the outset. These included the lim- itations inherent in beginning exposure to fluoride only when children were of school age and then providing only inter- mittent exposure. Also, the possibility that the exposure would not confer benefits after the children left school was a TABLE 7.3 Population served by fluoride-adjusted and naturally fluoridated water, United States, 1992 Number of Number of Type of Fluoridation Population Systems Communities Adjusted 134.6 million 10,567 8,572 Natural 10.0 million 3,784 1,924 Both 144.6 million 14,351 10,496 Source: USDHHS 1993. method of preventing coronal and root caries in chil- dren and adults. Moreover, water fluoridation bene- fits all residents served by community water supplies regardless of socioeconomic status. Few barriers to its implementation exist, with the important excep- tion of the political opposition that the measure often engenders and certain technical difficulties and costs involved in fluoridating very small water systems. School Water Fluoridation During the 1960s, 1970s, and 1980s, programs were initiated to bring the benefits of fluoride in drinking water to children living in homes supplied by well water and whose schools had independent water sup- plies. The idea was to adjust the fluoride content of the water supplies of the schools these children attended, especially consolidated rural schools, to levels higher than those that would be used for com- munity water fluoridation, taking into account that concern. Practical considera- tions included the cost of operations, personnel, logistical difficulties, and mandatory water testing (CDC 1995). Moreover, the intervening decades have seen increased school consolidations, increased cov- erage of schools by community-wide water systems, declining numbers of children who could benefit from such programs, and a continuing general decline in dental caries in children. Another concern is that schools increasingly enroll preschoolers into daycare programs for which school water fluorida- tion at higher levels than for community water sys- tems is not appropriate. Only four intervention stud- ies evaluating the effectiveness of school water fluor- idation have been published. Summary: School Water Fluoridation Given the limitations of the evidence for effec- tiveness, as well as the difficulties of implementation and operation, school water fluoridation has limited application. Decisions to initiate or continue school fluoridation programs should be based on an assessment of present caries risk in the target school(s), alternative preventive modalities that may be available, and periodic evaluation of program effectiveness. Dietary Fluoride Supplements Dietary fluoride supplements are available as tablets that are swallowed or chewed, drops that are swal- lowed, and lozenges that dissolve slowly in the 162 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL mouth, They can provide topical and systemic fluoride for children in the absence of optimally fluori- dated drinking water. In the United States, supplements are available by prescription only, to he used once 4 day beginning at 6 months and ending at age 16. According to a 1986 National Health Interview Survey (NHIS), slightly more than 16 percent of children younger than 2 years used fluoride dietary supplements (Nourjah et al. 1994). The fluoride supplement dosage schedule in use in the United States was last revised by the American Dental Association (ADA) in 1994 (Table 7.5) (ADA 1995). This schedule, based on the level of fluoride in the com- munity water supply and on the age of the child, has also been endorsed by the American Acad- emy of Pediatric Dentistry and the American Academy of Pediatrics. Fluoride supplements should not be prescribed for individuals living in optimally fluoridated communities. Effectiveness of Home Use The current fluoride supplement dosage schedule does not recom- mend prescribing fluoride for infants younger than 6 months. A double-blind study of fluoride sup- plements conducted to ascertain the effects of fluoride administered to the mother during the last 6 months of pregnancy followed by 5 years of supplements to the child after birth found no additional benefits from prenatal fluoride use (Leverett et al. 1997). In a ran- domized, double-blind, controlled trial in which supplements were administered from birth, Hennon et al. (1967) had found statistical- ly significant 4-year reductions in caries in primary and permanent teeth of 65 and 41 percent, respec- tively. Beyond this study, which was conducted when other sources Community and Other Approaches to Promote Oral Health and Prevent Oral Disease TABLE 7.4 Water fluoridation status of top 50 U.S. cities Population Estimate Size Rank Fluoride/ (7/1/96) 1996 No Fluorides New York, New York 7,380,906 1 F Los Angeles, California 3,553,638 2 F Chicago, Illinois 2,721,547 3 F Houston, Texas 1,744,058 4 F Philadelphia, Pennsylvania 1,478,002 5 F San Diego, California 4,171,121 6 NF Phoenix, Arizona 1,159,014 7 F San Antonio, Texas 1,067,816 8 NF Dallas, Texas 1,053,292 9 F Detroit, Michigan 4,000,272 10 F San Jose, California 838,744 Vl NF Indianapolis, Indiana 746,737 12 F San Francisco, California 735,315 B F Jacksonville, Florida 679,792 14 F-nat Baltimore, Maryland 675,401 15 F Columbus, Ohio 657,053 16 F El Paso, Texas 599,865 7 F-nat Memphis, Tennessee 596,725 18 F Milwaukee, Wisconsin 590,503 19 F Boston, Massachusetts 558,394 20 F Washington, D.C. 543,213 21 F Austin, Texas 541,278 22 F Seattle, Washington 524,704 23 F Nashville-Davidson (remainder), Tennessee 511,263 24 F Cleveland, Ohio 498,246 25 F Denver, Colorado 497,840 26 F Portland, Oregon 480,824 27 NF Fort Worth, Texas 479,716 28 F New Orleans, Louisiana 476,625 29 F Oklahoma City, Oklahoma 469,852 30 F Tucson, Arizona 449,002 31 NF Charlotte, North Carolina 444,297 32 F Kansas City, Missouri 441,259 33 F Virginia Beach, Virginia 430,385 34 F Honolulu, Hawaii 423,475 35 NF Long Beach, California 421,904 36 F Albuquerque, New Mexico 419,681 37 F Atlanta, Georgia 401,907 38 F Fresno, California 396,011 39 NF Tulsa, Oklahoma 378,491 ct) F Las Vegas, Nevada 376,906 4 F Sacramenta, California 376,243 42 F Oakland, California 367,230 43 F Miami, Florida 365,127 44 F Omaha, Nebraska 364,253 45 F Minneapolis, Minnesota 358,785 46 F St. Louis, Missouri 351,565 47 F Pittsburgh, Pennsylvania 350,363 48 F Cincinnati, Ohio 345,818 49 F Colorado Springs, Colorado 345,127 50 F af = fluoride, NF = no fluoride, and F-nat = natural, nonadjusted fluoride in the water supply. bYoted but not yet started. Source:T. Reeves, CDC Division of Oral Health, personal communication, April 18, 2000. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 163 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease of fluoride were not as widespread as today, there are no well-designed clinical trials of home-based administration of postnatal supplements. As Murray and Naylor (1996) noted, many studies are difficult to interpret, either because of small size, short exper- imental period, or inadequate reporting. The studies are further complicated by problems in self-selection bias, in choosing comparable control groups, and in compliance to the daily regimen. Notwithstanding the paucity of true randomized controlled clinical trials to demonstrate efficacy of supplement use in children, at least 60 studies have reported on the effectiveness of fluoride tablets or drops in home- or school-based programs (Driscoll 1974, Murray and Naylor 1996, Stephen 1993). However, none used the current prescribing sched- ule. Altogether, the evidence for using fluoride sup- plements to prevent and control dental caries is mixed. Although many studies have reported that the use of fluoride supplements by infants and children before their permanent teeth erupt reduces caries in permanent teeth, many other studies have reported that it does not (CDC in press). For children aged 6 to 16 who take supplements after most teeth have erupted, the evidence is much clearer that fluoride reduces caries experience (DePaola and Lax 1968, Driscoll et al. 1978, Stephen and Campbell 1978). Most of the supplements taken at home are prescribed by physicians and dentists in private practice, with physicians prescribing the larger share. Two difficulties are associated with home use. First, the provider may prescribe incorrectly; second, compliance with home-based tablet programs can be very poor. More public and professional education is needed to overcome the difficulties inherent in following recommended regimens for home use of fluoride supplements, which require motivation and adherence on the part of children, parents, and prescribers. Effectiveness of School-based Programs Most community fluoride supplement programs are school-based. Each schoo! day, participating students receive a tablet, which they chew under supervision, swishing the resultant solution between the teeth for 30 seconds before swallowing. Supplement programs in schools have been shown to be effective in preventing caries in perma- nent teeth when administration is tightly controlled and children are instructed to let the tablet dissolve slowly, to ensure as much topical fluoride exposure as possible. Under these conditions, randomized con- trolled trials in the United States reported caries reductions of 20 to 28 percent over periods of 3 to 6 years (DePaola and Lax 1968, Driscoll et al. 1978). In a randomized, double-blind, 3-year study of Scottish schoolchildren who were 5.5 years of age at the start of the study, a much higher percentage reduction in caries in permanent teeth was observed (Stephen and Campbell 1978). In this study, teachers were specifi- cally requested to encourage children each school day to let the sodium fluoride tablet dissolve slowly. These children were from lower socioeconomic groups and may not have had access to fluoride-con- taining dentifrices and other sources of fluoride, fac- tors that most likely put them at high risk for caries. Costs of School-based Programs The costs of a school-based tablet program are low because equipment is not necessary, the procedure does not take long, and an entire classroom of chil- dren can participate at once. A 1988 survey of five programs ranging from 7 to 49 schools and 657 to 10,751 children found an average direct cost of approximately $2.53 per child per school year (Garcia 1989). The costs ranged from $0.81 to $5.40, depending on whether paid personnel or volunteers supervised the procedure. The economic benefits of a fluoride supplement program were assessed in ran- domized controlled clinical trials in Manchester, England, and results showed overall health and cost benefits for the experimental group (O’Rourke et al. 1988). Summary: Dietary Fluoride Supplements For children not exposed to optimal fluoride concen- tration in their water supply, the evidence from stud- ies conducted prior to the 1980s supporting the effectiveness of home use of daily dietary fluoride supplements in preventing dental caries in school- aged children is weak. However, the evidence of the effectiveness of school-based fluoride supplement programs is strong. Such programs require highly TABLE 7.5 Dietary fluoride supplement dosage schedule Fluoride Dosage (milligrams per day) at Fluoride in Water Concentration of Age of Child 0.6ppm Birth to 6 months None None None 6 months to 3 years 0.25 None None 3 years to 6 years 0.50 0.25 None 6 years to 16 years 1.00 0.50 None Source: ADA 1995. 164 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease motivated teachers and students, a requirement that likely has limited their widespread adoption. Experts recommend that school-based dietary fluoride sup- plement programs are likely to be effective in provid- ing topical fluoride protection for children at high risk for dental caries in settings where supervising personnel are highly motivated (CDC in press, Clarkson 1992, Ismail 1994, WHO 1994). Under these conditions, such programs may also be cost- effective. Fluoride Mouthrinses Several different formulations of fluoride mouth- rinses are available, differing in the amount of fluo- ride and suggested frequency of use. Rinses with low fluoride concentrations (0.05 percent neutral sodium fluoride or 0.1 percent stannous fluoride) are designed for daily use and are available over-the- counter. Higher-concentration rinses (0.2 percent sodium fluoride) are designed for weekly use and are available only by prescription or in public programs. School-based Programs Fluoride mouthrinses were developed in the 1960s as a public health measure for use primarily in schools. They were conceived as a way of avoiding the high costs associated with professional applications of gels and other topical fluoride products in school settings and the poor acceptance by children of brush-on flu- oride pastes. For children in the first grade and up, the proce- dure consists of vigorously rinsing with 10 milliliters (ml) of solution for 60 seconds. After the rinsing, the fluoride solution is expectorated into a cup, a napkin is inserted to absorb the solution, and both are dis- posed. Kindergarten children rinse with only 5 ml of solution. Effectiveness School-based fluoride mouthrinse programs have been evaluated extensively during the past three decades and have been the subject of numerous reviews (Adair 1998, Birkland and Torell 1978, Bohannan et al. 1985, Petersson 1993, Ripa 1991, Stamm et al. 1984, Torell and Ericsson 1974). Of the many studies during the 1970s and 1980s, 13 satis- fied the strict criteria of randomized controlled clini- cal trials. Caries reductions ranging from 20 to 50 percent were observed, firmly establishing their effi- cacy. No recent controlled trials have been done. After the efficacy of fluoride mouthrinses was estab- lished, a 17-site national school-based demonstration program showed that a protocol involving weekly rinsing with 0.2 percent sodium fluoride was emi- nently practical. Most studies done after efficacy was established used a before-and-after design with no concurrent comparison group. This design might over- estimate the caries reduction effects. On the whole, however, the programs appear to have been effective. A survey conducted in 1984 found fluoride mouthrinsing programs in 48 states, with 3.2 million children participating (Bednarsh and Connolly 1984). A later study by CDC reported that 3.25 mil- lion schoolchildren were participating in mouthrins- ing programs at 11,683 sites in 1988 (Burt 1989), although there are reports that some states have recently curtailed use of these programs (R. Kuthy, personal communication, 2000). Cost-effectiveness The cost of the procedure in 1988 ranged between $0.52 and $1.78 per child per school year, depending on whether paid or volunteer adult supervisors were used (Garcia 1989). An extensive study during the late 1970s, when downward trends of caries rates were noted, questioned the cost-effectiveness of rinse programs (Klein et al. 1985). Fluoride mouthrinses may be more cost-effective when targeted to school- children with high caries activity (Bawden et al. 1980, Leverett 1989, Torell and Ericsson 1965). Summary: School-based Fluoride Mouthrinse Programs Sufficient evidence exists from studies conducted before 1985 to support the effectiveness of 0.2 per- cent sodium fluoride mouthrinses in preventing coronal caries in school populations. There is evi- dence that with a declining prevalence of dental caries, the cost-effectiveness of these procedures is reduced. Experts recommend that school-based rins- ing once a week with 0.2 percent sodium fluoride is likely to be effective if used in schools and class- rooms where students are at high risk for caries and if applied consistently over time (CDC in press). Fluoride mouthrinse programs are not recommended for preschool children in the United States, and pro- grams for kindergarten children should use only 5 ml of solution. Fluoride Varnishes Fluoride varnishes have not been approved for use in the United States with an anticaries indication. However, the U.S. public health community has begun to investigate the use of fluoride varnishes, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 165 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease which became available in this country in 1994. The varnishes are viscous, resinous lacquers painted onto teeth. Because the varnish adheres to enamel surfaces for up to 12 hours or more, fluoride retention in the mouth is greater than with solutions or gels. Varnishes have been used in Europe for 30 years. No data are available on the use of varnishes in children under 3 years, and, although the results were positive, only two randomized clinical trials have been conducted abroad using preschoolers (Holm 1979, Peyron et al. 1992). Many fluoride rins- ing programs in Finland have been replaced with flu- oride varnish application programs (Seppa 1991, Sundberg et al. 1996). Studies conducted in Canada (Clark et al. 1987) and Europe (de Bruyn and Arends 1987, Helfenstein and Steiner 1994, Twetman et al. 1996) have found that fluoride varnish is efficacious in preventing dental caries. Applied semiannually, this modality is as effective as professionally applied fluoride gel (Seppa et al. 1995). Some researchers advocate application of fluoride varnish up to 4 times per year to achieve maximum effect, but the evidence of benefits from more than two applications per year remains inconclusive (Mandel 1994, Seppa 1991, Seppa and Tolonen 1990). Other studies have shown that three applications in 1 week, once a year, may be more effective than the more conventional biannual regimen (Petersson et al. 1991, Skold et al. 1994). European studies have shown that fluoride varnishes prevent decalcification (a very early stage of dental caries) beneath orthodontic bands (Adriaens et al. 1990) and slow the progression of existing enamel lesions (Peyron et al. 1992). Findings on cost-effec- tiveness are mixed (Kirkegaard et al. 1986, Koch et al. 1979, Seppa and Pollanen 1987, Vehmanen 1993). Dental Sealants The pits and fissures that characterize the biting sur- faces of posterior teeth provide a haven for food debris and decay-causing bacteria. Not surprisingly, these sites are often the first and most frequent to be affected by decay in children and adolescents. The width of most pits and fissures is narrower than a sin- gle toothbrush bristle, making cleaning of their deep- est recesses almost impossible. According to national estimates, as much as 90 percent of all dental caries in schoolchildren occurs in pits and fissures (Kaste et al. 1996). The teeth at highest risk by far are perma- nent first and second molars. Enamel bonding, a technology introduced in the mid-1950s, led to the development of sealants. These are clear or opaque plastic resinous materials designed for professional application to the pit-and- fissure surfaces of teeth. The material hardens within 60 seconds or so into a thin, hard, protective coating. Sealants were introduced in the late 1960s and received the American Dental Association Seal of Approval in 1976 (ADA 1976). Most of the dozen products approved by the ADA do not contain a ther- apeutic agent, but work by providing a physical bar- rier that prevents microorganisms and food particles from collecting in the pits and fissures (ADA 1997). First-generation sealants used ultraviolet light to harden or “cure” the material; improved second- and third-generation sealants cure by chemical or visible light activation, respectively. Sealant placement requires meticulous attention to technique, but they can be successfully provided in “field” settings using portable dental equipment. To be most effective, sealants should be placed on teeth soon after they erupt, but they can be applied across a wide age range. Not only does the risk for caries continue across the life span, but an individ- uals risk can increase for any number of reasons. Sealants are particularly helpful for persons with medical conditions associated with higher caries rates, children who have experienced extensive caries in their primary teeth, and children who already have incipient caries in a permanent molar tooth. Efficacy Initial clinical trials using a random half-mouth design and first- or second-generation sealant materi- als established their efficacy. Several comprehensive reviews and a meta-analysis of the amount of caries prevented testify to the utility of these materials (Llodra et al. 1993, Ripa 1993, Weintraub 1989). Llodra et al. (1993) used a systematic process to select and review studies of one-time sealant place- ment on permanent teeth in subjects unexposed to other preventive measures. Pooled results from 17 studies meeting their selection criteria found that second-generation sealants reduced caries over 70 percent. These early trials firmly established retention as essential to preventing caries; a sealant is virtually 100 percent effective if it is fully retained on the tooth (NIH 1984). Mertz-Fairhurst (1984) reported 92 to 96 percent retention rates in second-generation sealants after 1 year, with 67 to 82 percent retention after 5 years. A review of studies of long-term reten- tion of second-generation sealants showed 41 to 57 percent intact after 10 years (Ripa 1993). The longest-running study of a one-time application of a first-generation sealant indicated a reduction in pit- and-fissure caries by 52 percent after 15 years 166 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL _Simonsen 1991). Retention results for third-genera- non sealants are similar to those for second-genera- ton systems (Ripa 1993). Effectiveness Administrators of school-linked sealant programs Collins et al. 1985, Sterritt and Frew 1988) and of school-based programs with either fixed clinics Ismail et al. 1989, Messer et al. 1997, Whyte et al. 1987) or portable equipment (Bravo et al. 1996, Calderone and Davis 1987, Calderone and Mueller 1083, Hardison 1983, Kumar et al. 1997, Morgan et al. 1998) have reported on their experiences with these programs. These studies, using second-genera- tion sealants, have shown effectiveness results com- parable to those of clinical trials, regardless of the physical delivery site or personnel used for sealant application. Complete retention after approximately \ year varied from 83 to 94 percent (Calderone and Mueller 1983, Hardison 1983, Ismail et al. 1989, Sterritt and Frew 1988, Whyte et al. 1987). A Consensus Development Conference spon- sored by the National Institutes of Health concluded that “an extensive body of knowledge has firmly established the scientific basis for the use of sealants” (NIH 1984). The panel urged the development of educational materials to enhance public and profes- sional acceptance as well as third-party reimburse- ment, Consensus on the value of sealants is reflected by the inclusion of sealant objectives in Healthy People 2000 and Healthy People 2010 (see Table 7.6). In addition, sealant placement is supported in federally funded programs for women and children, and sealants are covered services in all state Medicaid programs. A Workshop on Guidelines for Sealant Use has made recommendations for sealant use in both community and individual care programs (ASTDD 1995). Community Dental Sealant Programs Several community-based public health initiatives have arisen to promote sealant use among private practitioners and through community-based pro- grams. These activities include reaching dentists through continuing education courses (Bader et al. 1987, Callanen et al. 1986, Siegal et al. 1996); direct- ing large-scale promotional activities to consumers, community leaders, and third-party payers (Siegal et al. 1997a); and providing sealants directly to children in school programs. Community programs that provide sealants directly to schoolchildren generally target vulnerable populations less likely to receive private dental care, ORAL HEALTH IN AMERICA: Community and Other Approaches to Promote Oral Health and Prevent Oral Disease such as children eligible for free or reduced-cost lunch programs. School-based programs are usually conducted entirely on site. School-linked programs conduct some portion of the program in schools, such as patient selection and parental permission, but generally provide the sealants at an off-site pri- vate practice or clinic. Nationally, 88 community- based sealant placement programs were in operation in the 1992-93 school year. These programs served children in 1,636 schools (Siegal et al. 1997b). Combining Sealants with a Fluoride Program Dramatic evidence of the impact of a combined fluo- ride and sealant program is provided by a program in Guam (Sterritt et al. 1990). For many years the chil- dren on this island had experienced dental caries rates more than double those of their U.S. mainland counterparts. In 1984 a school-linked pit-and-fissure sealant program was added to an existing school- based fluoride mouthrinse program. More than 15,000 children participated annually in the sealant program. After 8 years of fluoride mouthrinsing (from 1976 to 1984), mean decayed, missing, and filled surface (DMFS) scores declined by 1.79 sur- faces per child. Only 7 percent of that decline was due to prevention of caries on surfaces that can ben- efit from sealants. With the addition of the sealant program to mouthrinsing, overall DMFS scores decreased an additional 2.34 surfaces per child in only 2 years. Most of this decline took place on pit- and-fissure surfaces. For the 10-year period a reduc- tion of 4.13 DMFS per child was seen—a decline from 7.06 DMFS per child at baseline to 2.93 DMFS in 1986. At the end of the 10 years, participating chil- dren on Guam had caries rates close to those of main- land schoolchildren. The National Preventive Dentistry Demonstra- tion Program, a large project conducted in 10 US. cities between 1976 and 1981 to compare the costs and effectiveness of combinations of caries preven- tion procedures, found that the inclusion of sealants was critical to the cost-effectiveness of prevention strategies (Disney et al. 1989, Klein et al. 1985). In another combined program, Morgan et al. (1998) found that a 3-year sealant program and a fluoride mouthrinse program for secondary schoolchildren incurred a low cost for each tooth surface saved from caries. The incremental cost-effectiveness ratios com- paring the intervention to the control group varied from a cost of $35.60 per tooth surface spared to a net savings of $7.00, depending on the assumptions used in the analysis. A REPORT OF THE SURGEON GENERAL 167 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Sealing Incipient Caries Heller et al. (1995) evaluated the effect of sealants placed as part of a school-based program on perma- nent first molar teeth after 5 years. Sealants were applied to both sound teeth and those with incipient carious lesions (where the fissure is stained but not yet cavitated). For the initially incipient carious sur- faces, the 5-year decay rate was 10.8 percent for sealed surfaces and 51.8 percent for unsealed sur- faces. Initially sound surfaces had a decay rate of 8.1 percent for sealed surfaces and 12.5 percent for unsealed surfaces. Initially sound tooth surfaces were unlikely to become decayed in 5 years and did not benefit greatly from the application of sealants. The study showed potential efficiencies in targeting teeth with incipient caries for sealants. Cost-effectiveness of Sealant Programs Studies suggest that sealants are an efficient use of resources when used in populations with higher- than-average disease incidence rates and when selec- tion methods limit sealants to teeth at highest risk of disease. Weintraub et al. (1993) demonstrated cost savings or improving cost-effectiveness with time in a sealant study at a children’s dental clinic for low- income families. A strategy of identifying children with prior molar restorations (an indicator of high risk) and sealing the remaining molars showed cost savings within 4 to 6 years. Summary: Dental Sealant Programs Studies carried out during the last 20 years provide strong evidence to support the effectiveness of sealants in preventing the develop- ment of caries in tooth pits and fis- TABLE 7.6 sures. Economic analyses suggest Baseline data for Healthy People 2010 objective 21-8a & b: increase the proportion that community sealant programs of children who have received dental sealants on their molar teeth are cost-effective and may even Percentage of Children Who Have Received Sealants provide cost savings when used in high-risk populations. Experts rec- Aged 8 Years Aged 14 Years ommend that programs should be to ‘ 8.9 4 baseline . * limited to high-risk children and ‘ high-risk teeth. Race and ethnicity American Indian or Alaska Native (1999) 7 26 ‘sion or Pacific Islander Om ne PREVENTION AND sian . Native Hawaiian and other Pacific islander DNC DNC CONTROL OF Black or African American el 5 PERIODONTAL White 26 _ 19 DISEASES Hispanic or Latino DSU DSU Periodontal diseases, caused by Nottignantntay : en specific bacteria in dental plaque, Black or African American - 5 affect most adults at some point in White 29 18 their lives. The mildest and most common form of periodontal dis- Gender 4 14 ease is gingivitis. Over time, peri- Male 2 16 odontitis, the more severe form of Education level (head of household) penodontal disease, can lead to the Less than high school 7 4 destruction of the soft tissue and High schoo! graduate 12 6 bone that anchor the teeth into the Atleast some college 35 28 jaw. Lacking support, teeth can Disability status loosen and be lost. Persons with disabilities DNC DNC Periodontal diseases can be Persons without disabilities ONC DNC prevented and controlled through Selected populations an array of mechanical and chemi- Third-grade students 26 NA cal means (Ismail and Lewis 1993, @DNA = data have not been analyzed. DNC = data are not collected. DSU = data are Statistically unreliable. NA = not AAP 1996). Conscientious oral applicable. hygiene and professional oral Data are for IHS service areas. cleanings to reduce plaque can ean Heaith and Nutrition Examination Survey (NHANES), NCHS, CDC: Oral Health Survey of Native reverse gingivitis (Lée et al. 1965). Source: USDHHS 2000. 768 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Methods for personal oral hygiene include tooth- brushing and flossing, which may be augmented by over-the-counter and prescription mouthrinses with antimicrobial action. Community Programs to Prevent Gingivitis \With the confirmation of specific bacteria in dental plaque as the cause of gingivitis, public health offi- cials began to seek ways to educate the public about plaque control in community settings, primarily in schools. These efforts have had equivocal results. Although knowledge and attitudes were enhanced in demonstration programs, improvements in plaque levels and gingivitis were short-lived in clinical trials (Horowitz et al. 1980). Prevention of Periodontitis Tobacco use is a major risk factor for the develop- ment and progression of periodontal diseases, and proven strategies aimed at reducing tobacco use should aid in the prevention of periodontitis. The following section on oral and pharyngeal cancers includes a discussion of such intervention strategies. Until recently, most interest in controlling tobacco use reflected concerns about oral cancers. As appre- ciation of the role of tobacco in the progression of periodontal diseases and tooth loss increases, atten- tion to these oral health effects may increase atten- tion to tobacco cessation in primary oral health care. Periodontitis can also be a complication of poorly controlled diabetes. (See Chapters 3 and 5 for a dis- cussion of other periodontal risk factors; Chapter 5 discusses the connection between periodontal dis- ease and diabetes.) Some efforts have been directed at alerting dental practitioners to the need to educate patients about diseases affecting the periodontal tissues (Bader et al. 1990, Brown and Spencer 1989). These efforts have met with some success, but they tend to reach only those people who already use dental services. Currently, there are no broad community-based inter- vention programs that address periodontal diseases. Summary Gingivitis can be controlled with available methods, and its control is the principal way to prevent peri- odontitis. However, the currently available methods are individually or professionally based and require conscientious oral hygiene practices and regular den- tal visits. Although some schools instruct children in ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Promote Oral Health and Prevent Oral Disease proper methods of oral hygiene, no community methods, other than programs designed to discour- age tobacco use, are available for preventing gingivi- tis or periodontitis in the general population. PREVENTION AND CONTROL OF ORAL AND PHARYNGEAL CANCERS The term oral and pharyngeal cancers refers to a diverse group of tumors affecting the oral cavity and pharynx, the majority of which are squamous cell carcinomas. Usually included are cancers of the lips, tongue, pharynx, and oral cavity. These malignan- cies are among the most debilitating and disfiguring of all cancers. More than 30,000-new cases of oral and pharyngeal cancers are diagnosed each year, and more than 8,000 people die annually from these dis- eases. The overall 5-year survival rate (52. percent) has not changed in the past four decades (Murphy et al. 1995, Silverman 1998). Primary risk factors for oral cancers in the United States are the use of tobacco and alcohol products and, for lip cancer, exposure to sun. Tobacco and alcohol independently increase the risk of oral and pharyngeal cancers and also act synergis- tically, so that persons who use both are at much higher risk than those who use only one. Other risk factors include insufficient fruits and vegetables in the diet, failure to use ultraviolet protection, and infection with certain viruses (Winn et al. 1998). In 1996 CDC convened the National Oral Cancer Strategic Planning Conference to develop strategies for preventing and controlling oral and pharyngeal cancers in the United States. The confer- ence, which was co-sponsored by the National Institute of Dental and Craniofacial Research and the ADA, included over 125 experts in oral and pharyn- geal cancer prevention and control, treatment, and research (CDC 1998). These experts developed rec- ommendations concerning public advocacy, collabo- ration, and coalition building, public education; pro- fessional education and practice; and data collection, evaluation, and research. An ongoing multidiscipli- nary subgroup from that conference, the Oral Cancer Working Group, met in 1997 and again in 1999 to share information on progress made and to discuss steps to implement a national plan. This group's work will augment existing interventions directed at the reduction of tobacco use, for which several commu- nity-based interventions have already been shown to be effective. The group is also developing several statewide models for the prevention and early detec- tion of oral and pharyngeal cancers. 169 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Many recommendations from the 1996 Strategic Planning Conference relate to the inclusion of pri- mary prevention (i.e., reducing risk factors) and early detection. These include a recommendation that because people at high risk for oral cancers are more likely to visit a physician than a dentist, and because physicians may be less likely than dentists to perform an oral cancer examination on such patients, all pri- mary care providers should assume more responsibil- ity for counseling patients about behaviors that put them at risk for developing these cancers; should per- form oral cancer examinations on all patients who are at high risk for developing the disease because of tobacco use or excessive alcohol consumption; and should refer patients to the appropriate specialist for management of suspicious oral lesions (CDC 1994c, Elwood and Gallagher 1985, Lynch and Prout 1986, Prout et al. 1990, Yellowitz and Goodman 1995). Further research is needed to better define screening parameters. Comprehensive education of medical and dental practitioners in diagnosing and promptly managing early lesions was recommended to facili- tate the multidisciplinary collaboration needed to detect oral cancers in their earliest stages. Furthermore, because of the public’s lack of knowl- edge about the risk factors for oral cancers and because these diseases can often be detected in the early stages, it is also recommended that programs to raise the public's awareness of oral cancers (including their risk factors, signs, and symptoms) be increased. Community-based Interventions Community-based interventions for oral and pharyn- geal cancer prevention have depended on tobacco control programs. School-based Prevention Programs On average, more than 3,000 children and teenagers become regular smokers each day (USDHHS 1994). Prevention efforts aimed at young people are extremely important because nearly all initiation of tobacco use in the United States occurs by age 18. Moreover, the finding that the earlier that smoking begins the more likely it is to lead to heavy use in adulthood makes preventing tobacco use among school-age youth all the more critical (CDC 1994a). Programs identifying the social influences that foster tobacco use in schoolchildren and teaching skills to resist such influences have yielded consis- tent and significant results. Reductions or delays in adolescent smoking have been documented, ranging from 25 to 60 percent and persisting from 1 to + years (CDC 1994b). The interventions were based on a CDC review of published research, including the conclusions of the National Cancer Institute's (NCI) Expert Advisory Panel on School-based Smoking Prevention Programs and findings from the 1994 Surgeon General's report, Preventing Tobacco Use Among Young People (CDC 1994b). The Guidelines for School Health Programs to Prevent Tobacco Use and Addiction cites seven recommendations (CDC 1994a,b): 1. Develop and enforce a school policy on tobacco use. 2. Provide instruction about the short- and long-term negative physiologic and social conse- quences of tobacco use, social influences on tobacco use, peer norms regarding tobacco use, and refusal skills. 3. Provide tobacco-use-prevention education in kindergarten through 12th grade; this instruction should be especially intensive in junior high or mid- dle school and reinforced in high school. 4. Provide program-specific training for teachers. 5. Involve parents or families in support of school-based programs to prevent tobacco use. 6. Support cessation efforts among students and all school staff who use tobacco. 7. Assess the tobacco-use-prevention program at regular intervals. A major part of most successful interventions has been the decrease of illegal sales to minors. This strategy has been accomplished by increasing mer- chant education and enforcement of laws prohibiting tobacco sales to minors under 18 and increasing the cost of cigarettes (CDC 1994a,b, Lewit et al. 1997, Lynch and Bonnie 1994). All 50 states and the District of Columbia have laws prohibiting the sale of tobacco, including smokeless (spit) tobacco, to minors. In recent years, attempts to prevent and reduce the use of spit tobacco have increased. These infor- mational and educational efforts have largely target- ed baseball clubs, Little League baseball teams, and 4- H Club members. A major new initiative, the National Spit Tobacco Education Program, has been launched by Oral Health America, with support from NIH and CDC and funding largely from the Robert Wood Johnson Foundation in collaboration with the Major League Baseball Players Association, to help break the link between spit tobacco and Major League Baseball. 170 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Other Program Models The majority of community programs designed to prevent Or reduce the use of tobacco products have focused on cigarette smoking. Initially, NCI funded randomized trials of interventions to prevent smok- ing in adolescents and promote cessation in adults. The value of multiple interventions delivered through multiple channels was confirmed in NCTIs Community Intervention Trial for Smoking Cessation (COMMIT 1995a,b). Findings from more than 100 intervention trials continue to provide important information about how to reach smokers and potential smokers. A major conclusion from these studies is that large- scale reductions in smoking prevalence are unlikely when interventions focus on the individual, but that interventions can be effective when community- based. Further, researchers found a statistically sig- nificant difference in the proportion of light-to-mod- erate (but not heavy) smokers who quit in the inter- vention communities compared with control com- munities (COMMIT 1995a,b, Klausner 1997, NCI 1995). Findings from COMMIT and other studies in the United States and abroad led to planning for ASSIST (American Stop Smoking Intervention Study for Cancer Prevention). In 1990, California adopted the ASSIST model, and early success in the California Statewide Tobacco Control Program clearly showed an impact on per capita cigarette consumption in that state compared with consumption in the United States as a whole (Manley et al. 1997a.b, Shopland 1993). The ASSIST model uses surveillance systems that allow for time-series analysis designs comparing intervention and control communities. Media-led tobacco control campaigns, as well as efforts to increase state excise taxes on cigarettes and thereby discourage teenagers from smoking, are included in the model. There are now dedicated tobacco-control coali- tions in all 50 states, and the Agency for Healthcare Research and Quality (formerly Agency for Healthcare Policy and Research) has developed clini- cal practice guidelines on smoking cessation to aid health professionals in interventions with patients (Fiore 1997). Although the major focus in reducing the risk for oral and pharyngeal cancers has been on tobacco ces- sation programs, reduction in alcohol use is clearly indicated. Currently, alcoholic beverages carry the Surgeon General's warning label stating that pregnant women should not drink because of the risk of birth defects and admonishing that alcohol impairs the ability to drive and operate machinery and may cause other health problems. Many communities have pro- grams that stress responsible drinking by adults relat- ed to the use of motor vehicles and completely dis- courage drinking among young drivers. Community approaches have also been developed to discourage drinking among young people. Targets are youth and adults who are at risk for alcohol-related problems, such as college students who may need to develop skills to avoid binge drinking, or women attending women’s clinics who might not know the risk of fetal alcohol syndrome. Because alcohol use, like tobacco use, usually begins in adolescence, development and testing of community- and school-based programs that provide youth with the skills’to avoid alcohol use are warranted. Early Diagnosis of Oral and Pharyngeal Cancers Primary care providers can counsel patients about lifestyle behaviors that increase the risk for oral can- cers. Dental as well as medical personnel have pro- vided successful tobacco control programs in their offices (see Chapter 8). Generally, Americans are ill- informed about the risk factors as well as the signs and symptoms of oral cancers (Horowitz and Nourjah 1996, Horowitz et al. 1995). The mass media have paid little attention to the topic, and health education textbooks are nearly devoid of dis- cussion (Canto et al. 1998b, Chung et al. 2000, Gold and Horowitz 1993, Horowitz et al. 1998). The scant attention that has been paid to oral cancers has focused on the role of spit tobacco. At present, the principal test for oral and pha- ryngeal cancers is a comprehensive clinical examina- tion that includes a visual/tactile examination of the mouth, full protrusion of the tongue with the aid of a gauze wipe, and palpation of the tongue, floor of the mouth, and lymph nodes in the neck. The U.S. Preventive Services Task Force concluded that there was insufficient evidence to recommend for or against routine screening for oral cancers, but noted that clinicians should remain vigilant for signs and symptoms of oral cancers and premalignancy in peo- ple who use tobacco or regularly use alcohol (USPSTF 1996). The Canadian Task Force on Periodic Health Examination (1997) states that although there is insufficient evidence to include or exclude screening for oral cancers from the periodic health examination for the general public, those at high risk (smokers and heavy drinkers) over 60 warrant an annual oral cancer exam by a physician or dentist (Lewis and ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 171 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Ismail 1995). The American Cancer Society recom- mends annual examinations for individuals 40 and older and for individuals who are exposed to known risks. Nevertheless, a 1992 national survey showed that only 15 percent of U.S. adults reported ever hav- ing had an oral cancer examination (Horowitz and Nourjah 1996). There are large gaps in knowledge of the efficacy of oral cancer examinations and the effectiveness and cost-effectiveness of community approaches to early detection of oral cancers. Methodologies and settings differ across studies. Moreover, these studies do not provide definitive evidence supporting the oral can- cer exam, and there have been no controlled clinical trials for defining the effectiveness of screening pro- grams. Further research is thus needed. Summary Although no school- or community-based interven- tions specifically designed for the prevention or early detection of oral and pharyngeal cancers are now in place, scientists representing the agencies in the newly formed oral cancer consortium have begun to develop statewide model protocols, beginning with the state of Maryland. In the meantime, any program that aims at eliminating tobacco use will reduce the primary risk factor for oral and pharyngeal cancers, along with other tobacco-related diseases. The evi- dence on the effectiveness of school-based programs to prevent tobacco use and addiction among children and adolescents provides strong support for their use as part of the school health education curriculum. Further, other community-based interventions such as COMMIT and ASSIST are recommended because they have demonstrated effectiveness in getting light- to-moderate smokers to quit. After reviewing the evi- dence, an expert panel convened by AHCPR (now the Agency for Healthcare Research and Quality) rec- ommended that all primary care clinicians be trained to provide smoking cessation activities (see Chapter 8). In addition, providers should perform oral cancer examinations on high-risk persons regularly. The rec- ommendation to use all of these interventions to pre- vent or cease tobacco use in communities is based on expert opinion. Oral cancers occur in sites that lend themselves to early detection by most primary health care providers and, to a lesser extent, by self-examination. Heightened awareness in the general population could help with early detection and could stimulate dialogue between patients and their primary health care providers about behaviors that may increase their risk. Recent advances in understanding the molecular events involved in developing cancer might provide the tools needed to design novel pre- ventive, diagnostic, prognostic, and therapeutic regi- mens to combat oral cancers. Acquiring greater knowledge of the biology, immunology, and patholo- gy of the oral mucosa may also help reduce the mor- bidity and mortality from these cancers. PREVENTION AND CONTROL OF CRANIOFACIAL BIRTH DEFECTS The causes of craniofacial birth defects are often complex and multifactorial—the result of gene-envi- ronment interactions occurring’from the time of con- ception to birth. Even when a mutation in a single gene has been discovered as the cause of a particular syndrome, there can be considerable variation in sus- ceptibility, with some infants showing little or no sign of a problem and others experiencing multiple organ defects. The work to complete the mapping and sequenc- ing of the human genome will undoubtedly shed light on the hundreds of genes involved in craniofa- cial development and provide details on when and how they function in development. This knowledge may in turn lead to gene therapies that restore or “rescue” the function of a defective gene and thus prevent the anomaly. Craniofacial defects also may occur because the susceptible embryo or fetus was exposed to an envi- ronmental teratogen, a diminished oxygen supply, or a deficit in an essential nutrient. Chapter 5 reports an association between low-birth-weight, premature babies who may show other subtle craniofacial anomalies and mothers with chronic oral infectious disease. In addition, diets poor in folic acid increase the risk of spina bifida and possibly clefting syn- dromes. Clinical trials using vitamin supplementa- tion with varying levels of folic acid are under devel- opment to determine if they can lower the risk of clefts in high-risk pregnancies. Outcomes of clinical trials of nutrient supplementation in pregnancy may lead to new nutritional guidelines and the develop- ment of enriched food products, which can form the basis for community-wide health promotion and dis- ease prevention programs. Given the array of variables affecting prenatal growth and development, the key to public health programs aimed at preventing birth defects lies pri- marily in health promotion and education cam- paigns. Individuals need to be made aware of known risk and protective factors in pregnancy. Such pro- grams should emphasize the importance of good nutrition, avoidance of tobacco and alcohol use, and 172 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease renatal care. Education includes knowledge about the teratogenic effects of prescription drugs, such as the antiepileptic drug phenytoin and the retinoic acid drugs used to treat cystic acne. Summary As information from developmental biology, genetics, and epidemiologic and clinical studies accrues, den- tal care providers are better positioned to provide counseling. The public is best served by health pro- motion and disease prevention campaigns that com- municate findings about risk and protective factors in pregnancy. PREVENTION AND CONTROL OF INTENTIONAL AND UNINTENTIONAL INJURY Intentional and unintentional injuries are related to behaviors and are thus amenable to prevention. As studies of motor vehicle and sports injuries have de- monstrated, injuries are frequently due to a sequence of predictable events, and a public health approach can be successful in injury prevention and control. The interventions that have proved to be most effective in controlling injuries have been passive; that is, they do not require the individual to partici- pate. Examples include the use of environmental controls such as vehicle and roadway design, speed limits, passenger restraints, and airbags to prevent injuries from motor vehicle collisions (Karlson 1992, Smith and Falk 1987). Passive measures such as these are more easily implemented at the state or fed- eral level. However, many preventive measures for oral-facial injuries have been directed at the individ- ual and professional health service levels, rather than at the population at large (see Table 7.7). Craniofacial Injuries The principal causes of craniofacial injuries are motor vehicle collisions, falls, assaults, and sporting activities. Except in relation to sports, injuries to the craniofacial region have received little attention. These injuries are hardly insignificant, however, and efforts to prevent them are gaining acceptance. For example, to increase public awareness of the impor- tance of facial protection, the inaugural National Facial Protection Month was celebrated in April 3000. This national campaign, providing information to the media and the public, was sponsored by the American Association of Oral and Maxillofacial Surgeons (AAOMS 2000). Motor vehicle collisions are the leading cause of death during the first three decades of life in the United States and the leading cause of death from injury over most of the life span (Baker et al. 1992). Data from multiple sources indicate that craniofacial injuries account for a substantial subset of these injuries annually (USDOT 1998). Even though it is likely that passive measures enacted to reduce fatali- ties have reduced nonfatal craniofacial injuries, no supporting data exist. Various sources report the number of motorcy- cle- and pedal-cycle-related craniofacial injuries. Data from the National Electronic Injury Surveillance System indicate that head injuries account for 50 per- cent of all pedal-cycle-related injuries; of those, bicy- cle-related events accounted for 19 percent of all facial injuries within the study period (McDonald 1994). In similar studies, tricycle-related incidents were found to be responsible for up to 61 percent of injuries to the head, face, or mouth (CDC 1987, USCPSC 1986). Motorcycle injuries are a major source of fatal and nonfatal head trauma in the United States (Rivara et al. 1988). Helmet use reduces head and facial injuries among bicyclists (Acton et al, 1995, Grimard et al. 1995, Rivara et al. 1997) and motorcyclists (Bachulis et al. 1988, Johnson et al. 1995, Lee et al. 1995) by up to 50 percent. Health promotion efforts have increased acceptance at the community level for hel- met use by bicyclists, however, helmet use regula- tions vary by state (Sacks et al. 1996) and with the public whim (Sosin et al. 1990). Over a dozen states currently have bicycle helmet laws, and half of the states have motorcycle helmet laws (NCHS 1992). Many authors have described craniofacial injuries related to sports. Information is usually obtained from community or regional surveys of injuries or mouthguard use and effectiveness. Craniofacial injuries sustained during sporting activ- ities are a major source of nonfatal injury and dis- ability (Baker et al. 1992), possibly accounting for up to one third of all sports injuries (Cathcart 1982, Meadow et al. 1984). The increasing participation of women in competitive sports means that young women should be alerted to the risks and advised of the need for additional protective gear as appropriate. The most comprehensive data on the effectiveness of protective equipment have been collected by agen- cies such as the National Alliance of Football Rules Committee, the National Collegiate Athletic Association, and the U.S. Consumer Product Safety Commission. Data on craniofacial injuries from par- ticipation in football before and after the enactment of mandatory mouthguard regulations indicate 4 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 173 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease TABLE 7.7 Restraints and Airbags Community-based interventions for the prevention and control of craniofacial injuries Helmets Mouthquards Guidelines for use Public policies Utilization rates Type of evidence for effectiveness and PHS ratings Evidence for effectiveness Combination of manual lap and automatic shoulder restraints plus airbag; emphasis on passive systems to overcome noncompliance Restraints: Mandatory use required by jaw in 48 states Airbags: All late model vehicles required to have driver-side airbags, and future models to add passenger-side airbags; National Traffic and Motor Vehicle Safety Act legislates policies Restraints: Compliance with seatbelt laws ranges from 29 to 74 percent (Reinfurt et al. 1991); current use may be as high as 67 percent (NCHS 1992) Airbags: Utilization may become an issue if on-off switch is implemented + Hospital and trauma registry studies (Sutyak et al. 1997, Orsay et al. 1990) * Modeling from insurance studies (Sorenson 1993) * Case-control study (Marine et al. 1994) Restraints: Use reduces facial injuries by 30 percent (Orsay et al. 1990) Airbags: Projected facial injury harm reduction of up to 90 percent for airbag added to restraint (Sorenson 1993): report of facial injuries may increase with airbags due to a decrease in fatalities and more severe injuries (Blacksin 1993) Cyclists, both motorized and nonmotorized, wear approved protective helmets, preferably with a full face mask for motorcyclists * 3 states have bicycle helmet laws; 25 have motorcycle helmet laws + Post-law bicycle helmet use rates increase by up to 50 percent among children (National Center for Injury Prevention and Control 1995) * States with helmet use laws have higher rates of helmet use Bicycle: Approximately half of bicyclists awn a helmet, and half of those consistently wear it (Sacks et al. 1996); 62 percent of motorcyclists and 17.6 percent of bicyclists wear helmets (NCHS 1992) + Hospital and trauma registry studies (Bachulis et aJ. 1988, Johnson et al. 1995) + National survey (Sacks et al. 1996) * Case-control study (Thompson et al. 1996) Motorcycle: A twofold decrease in incidence of maxillofacial trauma in helmeted versus nonhelmeted motorcyclists (Bachulis et al. 1988); nonhelmeted 3 times more likely to have facial fractures than those with helmets (Johnson et al. 1995) Bicycle: Hemet wearers have a 65 percent reduction in upper- and mid-face injuries (Thompson et al. 1996); head injuries decreased 67 percent in children concomitant with rate of helmet use increase of 35 percent following educational campaign (Rivara et al. 1994); helmets with face protection decrease facial injuries by a factor of 3 (Vaughan 1977); helmet wearing alone is not sufficient to prevent serious injury and fatality (Rivara et al. 1997) Football: Wear helmet with face mask and use mouthguard Hockey: Wear helmet with face mask and use mouthguard because face shields do not prevent injury to lower face Football: Requirement since 1962 for mandatory mouthguard use in football accompanied by significant decline in inci- dence of oral-facial injuries Hockey: Mandatory requirement for full facial protection in Canada has reduced facial injuries among youth (Rampton et al. 1997) Football: 72 percent of children wear head- gear and mouthguards Baseball/softball: 35 percent of children wear headgear; 7 percent consistently wear mouthguards Soccer: 4 percent of children wear headgear; 7 percent of children wear mouthguards (Nowjack-Raymer and Gift 1996) Basketball: 4 percent of respondents report- ed wearing mouthquards (Maestrello- deMoya and Primosch 1989) * Hospital and trauma registry studies * Questionnaire (baseball and basketball) * Before and after NFA rule in 1962 + Descriptive survey (Maestrello-deMoya and Primosch 1989) Football: Face mask reduces oral-facial injury by 50 percent; addition of a mouth- guard reduces risk to less than 1 percent (AAHPER 1960) Hockey: Full-face protection reduced chance of upper facial injury; haif visor same as no face protection (Rampton et al. 1997) Baseball and basketball: 60 times more likely to sustain oral injury without mouth- guard (McNutt et al. 1989); 30 percent reduced risk of oral-facial injury for those wearing mouthguards (Powers et al. 1984) 174 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Risks Costs and effectiveness Recommendations Community and Other Approach yes to Promote Oral Health and Prevent Oral Disease Restraints and Airbags Restraints: + [mproper car seat design and use for infants Airbags: + Concern regarding higher risk for death in children and small women + Case report of facial desquamation from ruptured airbag Airbags and restraints: U.S. costs are calculated for all injuries or fatalities, not craniofacial injuries; Australian report estimated savings of 108 million (Australian) dollars per year due to facial injury reduction (Sorenson 1993) + Extend safety belt laws to all 50 (abstracted from CDC states 1987, USDHHS 2000) + Increase airbag efficacy and safety research for craniofacial injuries Helmets + No injuries have been documented secondary to the helmet itself; helmets do not decrease risk of injury to lower face, mandible, and mouth Bicycle: Hospital treatment costs for bicyclists estimated at $1 billion annually— includes mortality and morbidity (Sacks et al. 1996) + Helmets should meet recommended industry manufacturing standards {mplement national mandatory helmet requirement law for motorcyclists in all states + (mplement national mandatory helmet requirement law for child bicyclists in all states——strongly recommend heimet use for adult bicyclists Combine heimet use with education and health promotion and environmental controls (e.g., separation of cyclists and motor vehicles, features to make cyclist more visible) State and local health departments should engage in health promotion for helmet use, develop and work for legislation for mandatory helmet use, and evaluate programs Mouthguards Costs are high because mouthguards should be fabricated for each individual by a health professional Hockey: Direct costs: 3 mtiltion (Canadian) dollars annually (Rampton et al. 1997) + Extend mandatory mouthguard use for all team sports sponsored by organizations, agencies, and institutions * Utilize health promotion and education of trainers, athletes, and parents to increase use of protective sporting equipment significant decline in crani 1988). Further, the U.S. Con ofacial injuries (Sane sumer Product Safety unintentional injuries from falls in the home. These include installing adequate lighting and handrails, Commission's review of National Electronic Injury Surveillance System data showed that mouth in- juries were more frequent in baseball than in any other sport monitored (USCPSC 1981). These com- bined reports were instrumental in implementing policies for protective equipment use in these two sports. (See Box 7.2, Sports Injuries and Oral-Facial Trauma.) Research on elderly and disabled individuals has led to the development of safety measures to prevent using nonskid materials on floors and in bathrooms, and positioning furniture to reduce the risk of trip- ping. Wider distribution and adoption of such safety measures should lower the risk of oral and craniofa- cial injuries due to falls for the general population as well, not only in the home but also in the workplace and other settings. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 175 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Summary: Prevention of Craniofacial Injuries Health education and injury prevention campaigns addressing the need for pro- tective gear in sports and cycling activ- ities can increase awareness and use. More rapid adoption can occur through legislation or regulation. Greater dis- semination of safety measures for home and workplace can similarly lower the risk of falls and other unintentional injuries. With regard to reducing inten- tional injuries in the United States, cur- rent and ongoing policy discussions, legislative proposals, and research efforts are necessary first steps toward appropriate programs. ORAL HEALTH PROMOTION AND DISEASE PREVENTION KNOWLEDGE AND PRACTICES To take full advantage of emerging sci- ence-based health and health care prac- tices, individuals, health care providers, and policymakers need to be sufficient- ly informed that they can take appro- priate actions for themselves, for those for whom they have responsibility, and for the community at large. For the individual, these actions include brush- ing with a fluoride-containing denti- frice for caries prevention, brushing and flossing to prevent gingivitis and periodontal diseases, and avoiding tobacco and other substances that are detrimental to health. Lack of knowledge can affect care. If parents are not familiar with the importance and care of their child's pri- mary teeth or if they do not know that dental sealants exist, they are unlikely to take appropriate action or seek pro- fessional services. If the public is not aware of the benefits of community water fluoridation, public referenda and funding for such interventions are not likely to be supported. Similarly, if individuals do not know that an oral cancer examination exists, they may not ask about the need for one. However, it is well established that BOX 7.2 Sports Injuries and Oral-Facial Trauma The national concern regarding oral-facial injury is addressed in the Healthy People 2010 objective 15-31, which is to increase the proportion of public and private schools that require use of appropriate head, face, eye, and mouth protection for students participating in school- sponsored physical activities. The National Youth Sports Safety Foundation estimates that more than 3 million teeth will be knocked out in youth sporting activities this year, an injury almost completely preventable by wearing a mouthguard. Even more significant, oral-facial trauma from sports injuries will result in facial bone fractures, concussion, permanent brain injury, temporomandibular dysfunction, blinding eye injuries, and even death. Currently, no systematic monitoring for oral-facial injuries exists in the United States. Progress toward a more broadly targeted Healthy People 2000 objective proved to be diffi- cult to track because of the data requirements of monitoring all organizations, agencies, and institutions sponsoring sporting and recreational events that pose risk of injury. By focusing on-schools, not only should the monitoring of progress be feasible, but healthy habits will be formed early. The hope is that by the time the athletes reach young adulthood they will rec- ognize the hazards posed by their athletic interests and, perhaps, be more comfortable using protective devices than they would be without them. It is estimated that as many as one third of all dental injuries are sports-related. A particu- larly high proportion of all baseball injuries (41 percent) is estimated to occur to the head, face, mouth, or eyes. Nowjack-Raymer and Gift (1996) reported that in 1991 more than 14 million U.S. school-aged youngsters participated in at least one sport that was listed on the 1991 National Health Interview Survey questionnaire, with more than 9 million of these children in organized baseball or softball. Baseball and softball are the most popular organized sports, with nearly one quarter of the school-aged population playing. Unlike football, not all baseball/softball leagues or teams require the use of safety equipment. In many cases, only selected positions such as catchers and batters are covered by rules. Thus only 35 percent of players reported that they wore headgear all or most of the time, and only 7 percent wore mouthguards all or most of the time. Further analysis of the interview data revealed a variety of socioenvironmental differences in the wearing of headgear and mouthguards. Forty percent of males who played baseball or softball reported wearing protective headgear “all or most of the time,” compared with only 25 percent of females. Differences were also found by poverty level, with 36 percent of those at or above poverty level wearing headgear, compared with 24 percent of those below. Better educated parents were somewhat more likely than less educated parents to have responded that their child wore headgear “sometimes” (45 percent versus 38 percent) and non-Hispanics reported occasional use more than Hispanics (43 percent versus 30 percent). Parents of a greater percentage of baseball or softball players of high school age (12 percent) than elementary school-aged players (6 percent) reported that their child wore a mouth- guard “all or most of the time.” Also, more black (17 percent} than white (6 percent) children reported the use of mouthguards. These socioeconomic differences might be greater were it not for the safety efforts of school athletic programs. Still, many parents and coaches are not as proactive as they could be and are not aware that facial injuries also occur in sports that are not considered high contact. For example, basketball players typically do not wear mouthguards. Yet approximately 34 percent of all injuries to basketball players involve teeth and/or the oral cavity. Examples of community-based interventions to prevent sports-related, oral-facial trauma include the development of rules and regulations for the use of headgear and mouthguards in sports where craniofacial injury is a risk; efforts to alert players, parents, sports officials, and organizers to the potential for injury; better product design; and the creation of sup- portive environments for sports-related equipment and recreation areas. 176 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease knowledge alone will not necessarily lead to appro- priate practices. For example, even if individuals know that tobacco use is unhealthful and that it con- tributes to multiple life-threatening illnesses, some continue to smoke. The majority of people who need such information most—those in low-income groups and those with lower levels of education—also are the ones who lack the information and skills (oral health literacy) to ask for and obtain specific preven- tive services or treatment options. Health profession- als are in an ideal position to provide up-to-date health information and care to their patients. They also have an opportunity to enhance their knowledge and practices as well as increase their communica- tion to patients about the procedures they provide and the reasons for these procedures. Few national studies of public and professional knowledge, attitudes, and practices exist. Highlights from these as well as from state and local studies that evaluated the prevention of dental caries, periodontal diseases, and oral cancers are provided below. Generally, the public is unable to discriminate between methods that prevent dental caries and those that prevent periodontal diseases (Corbin et al. 1985, Gift et al. 1994). This confusion has been attributed to the prevailing marketing message that refers to them as “plaque diseases” preventable by thorough tooth cleaning with a toothbrush and floss. In addition, the general public and health care providers are not fully informed about the relative value of fluoride and the appropriate recommended applications of regimens to prevent dental caries (Corbin et al. 1985, Gallup 1992, Gift et al. 1994, (Neil 1984). More work is needed to improve knowledge and practices related to oral cancer pre- vention as well. As with other areas of investigation, additional survey research is needed to better understand findings to date and to develop tailored interventions. Research is ongoing to improve the design of survey instruments and the wording of questions to address cultural and ethnic differences and interpretations. Dental Caries Prevention The Public Most members of the general public, regardless of socioeconomic level, tend to believe that the best way to prevent dental caries is by brushing their teeth (Corbin 1985, Gift et al. 1994, O'Neil 1984). In the 1990 National Health Interview Survey (NHIS), respondents were asked the purpose of adding fluoride to public drinking water. About two thirds of the respondents 25 to 65 years of age knew that water fluoridation helps prevent caries, compared with only 51 percent and 49 percent of those 65 and older and 18 to 24 years of age, respectively. Blacks and Hispanics were less likely to know the value of this preventive procedure than whites. In the same sur- vey, when asked to indicate the one best way to pre- vent tooth decay from five answers (limiting sugary snacks, using fluorides, chewing sugarless gum, brushing and flossing the teeth, and visiting the den- tist every 6 months), only 7 percent of the respon- dents answered correctly that fluoride was the most effective (Gift et al. 1994). More than two thirds said tooth brushing and flossing were the most effective. These results paralleled those of earlier studies (Gift et al. 1994, O'Neil 1984). A lower perceived value of fluorides by the public in preventing dental caries also was seen in the 1985 NHIS (Corbin et al. 1985). In a survey of knowledge and beliefs of the public, dentists, and dental researchers about the best way to prevent dental caries, the public and the dentists identified tooth brushing, whereas dental researchers unanimously ranked fluorides, as most important (O'Neil 1984). A small study among Latina mothers showed that they believed that brushing with baking soda is a good way to prevent dental caries; they knew little about brushing with a fluoride-containing dentifrice (Watson et al. 1999). Dental sealants and appropriate use of fluoride are critical for caries prevention. In the 1990 NHIS, about 32 percent of the public had heard of dental sealants, but among those only three fourths knew the purpose of this preventive measure (Gift et al. 1994). In 1991 the Gallup Organization conducted a poll for the American Academy of Pediatric Dentistry among a national sample of 1,200 parents of children 16 years and younger. The results indicated that only 58 percent believed fluoride to be very important to a child’s oral health; another 36 percent considered it to be somewhat important. Eight of 10 parents did not know when a child should be prescribed fluoride supplements, and virtually no one knew when sup- plements should be stopped. Only 25 percent of par- ents in nonfluoridated communities reportedly give their children fluoride supplements (Gallup 1992). Health Care Providers In a national survey of U.S. dental hygienists’ knowl- edge, opinions, and practices regarding dental caries etiology and prevention, over 90 percent agreed that “adults benefit from the use of fluorides” and that “root surface caries is an emerging problem.” A little ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 177 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease less than one third did not provide fluoride treat- ments to adults. This same survey found that only 57 percent of the respondents recognized remineraliza- tion as fluorides most important mechanism of action; rather, flossing was selected as the most effec- tive procedure for preventing caries in adults. Also, only 18 percent reported providing the recommend- ed time for acidulated phosphate fluoride (APF) gel treatment (Forrest 1998). A city-based survey of den- tists and dental hygienists found that nearly 70 per- cent of the offices used lower than recommended topical fluoride application times and that some of the fluoride products reportedly used had not been clinically tested (Warren et al. 1996). Periodontal Disease Prevention The Public In the 1990 NHIS the majority of household respon- dents (79 percent) could identify one common sign of “gum” disease. Level of education was directly related to knowledge of gum disease. Eighty-nine percent of those with more than a high school level of education were able to name a common sign of gum disease, compared with 79 percent of those with a high school education and 60 percent of those with less than a high school education (Gift et al. 1994). A Roper report on oral health surveyed more than 1,000 adults 18 and older. Eighty percent reported that they did not believe they have had peri- odontal disease. However, 70 percent reported hav- ing experienced at least one symptom of gum dis- ease—bleeding gums; swollen, painful, or receding gums; a change in bite; or loose teeth. Although 41 percent of the respondents said that losing their teeth was their greatest fear regarding oral health, only 38 percent who had bleeding gums said they told their dentists about the problem. Further, only 30 percent of the respondents who had experienced warning signs of gum disease were worried about developing periodontal problems in the future. Fifty-eight per- cent knew that plaque is the main cause of gum dis- ease and that flossing alone will not prevent gum dis- ease, whereas 77 percent knew that brushing alone would not prevent gum disease. The majority (90 percent) knew that gum disease could strike anyone at any age (Roper Report 1994). In a recently reported study on the oral hygiene practices of a convenience sample of 34,897 users and nonusers of tobacco products who obtained den- tal care in 75 dental practices, 74 percent reported brushing twice a day and 36 percent reported flossing once daily (Andrews 1998). Tobacco users brushed and flossed much less frequently than nonusers. Patients with more than a high school education were less likely to use tobacco products and more likely to brush at least 2 times a day and floss daily than were those with less education. A 1996 study of 1,000 U.S. adults showed that nearly one third (29 percent) of respondents were extremely or very concerned about getting gum dis- ease. Concern was highest among younger respon- dents 18 to 49 years of age and those who very or somewhat frequently experienced bleeding gums. Only 6 percent said they frequently suffered from bleeding gums (2 percent very frequently and 4 per- cent somewhat frequently). Gnly 13 percent said a dental professional had diagnosed them with any kind of periodontal disease (gingivitis, pyorrhea, and periodontitis). Older respondents were somewhat more likely than younger ones to have been diag- nosed with gum disease, and 17 percent reported experiencing gingival bleeding occasionally (Andrews 1998). Health Care Providers Studies of dental professionals regarding periodontal disease prevention practices are limited. In 1989, Dental Products Report launched a study to deter- mine the involvement of general practitioners in periodontal care. Overall, general dentists and their hygienists have become more involved in the peri- odontal exam phase of patient treatment. This posi- tive trend suggests that periodontal diagnosis and treatment are well integrated into general practice. For example, when asked “what phases of periodon- tal treatment are you providing at present?” 100 per- cent reported gingival exam and evaluation, 97 per- cent reported pocket probing, and 88 percent report- ed providing patient education. The majority of den- tists (67 percent) used as many as six measurement sites per tooth. Nearly all (93 percent) reported hav- ing a referral relationship with a periodontist (Dental Products Report 1996). Oral Cancer Prevention and Early Detection The Public USS. adults generally are ill-informed regarding risk factors for and signs and symptoms of oral cancers. Further, a 1990 national survey found that only 14 percent of adults 40 and older reported that they had ever had an oral cancer examination. Of those, only 7 percent had had an exam within the last year 178 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Horowitz et al. 1995). In a statewide survey in \farvland. 85 percent of the adults claimed to have heard of oral or mouth cancer, but only 28 percent reported ever having an oral cancer examination Horowitz et al. 1996), A state-based study of veter- yns—a population at high risk for oral cancers— ‘ound that they were ill-informed and misinformed about these cancers (Canto et al. 1998a). Finally, a study among Latino youths who reported use of tobacco and alcohol found that they, too, were not knowledgeable regarding risk factors for oral cancers Canto et al. 1998b). Health Care Providers 4 recent national pilot survey of U.S. dentists found that the respondents’ knowledge regarding risk fac- tors for and signs and symptoms of oral cancers and their reported practice of examination procedures were limited (Yellowitz et al. 1998). Most respon- dents believed they were adequately trained to pro- vide oral cancer examinations, and 70 percent pro- vided annual oral cancer exams to patients 40 and older. Seventy-four percent reported their knowledge of oral cancers to be current, yet only 30 percent cor- rectly identified the age cohort most frequently diag- nosed with oral cancers. Further, less than 50 percent correctly identified the stage at which most oral can- cer lesions are diagnosed, and nearly one third of respondents could not identify the two most com- mon sites of these lesions. Although 86 percent claimed to assess their patients’ current tobacco use, only 50 percent assessed current alcohol use; rela- tively few dentists assessed past alcohol or tobacco use. There was a modest amount of misinformation as well. For example, 65 percent believed, incorrect- ly, that ill-fitting dentures and partials were a risk fac- tor for oral cancers, and 47 percent believed, also incorrectly, that poor oral hygiene was a risk factor. Further, although the majority of dentists claimed to provide oral cancer examinations to the majority of their patients, a large proportion did not palpate the lymph nodes—part of a comprehensive oral cancer examination. These results confirm an earlier study conducted among a convenience sample of Maryland dentists and physicians in that both groups believed their knowledge and skills related to oral cancer pre- vention and early detection to be wanting (Yellowitz and Goodman 1995). A recent national survey among U.S. dental hygienists found that although 98 percent agreed that oral cancer examinations should be provided annual- ly for adults 40 and older, only 6+ percent reported performing such an exam 100 percent of the time, and nearly 17 percent reported not performing an exam at any time (Forrest 1998). Further inconsis- tencies were found between knowledge of risk factors and performance. For example, although 94 percent correctly identified alcohol use as a risk factor for oral cancer, only 49 percent asked about alcohol use. Less than a majority (45 percent) reported their knowledge of oral cancers to be current. A majority (61 percent) believed they were adequately trained to palpate lymph nodes; still, only 24 percent reported routine palpating of lymph nodes, while 51 percent indicated they did not do so at any time. Summary Findings from national surveys, together with those from local studies, suggest that there are opportuni- ties for enhanced educational efforts for both the public and health professionals to improve oral health. These studies focus on the public and the dental profession for selected diseases. New research is needed to assess knowledge, attitudes, and prac- tices of all health professionals and for other condi- tions and risk factors related to oral health as well. BUILDING UPON SUCCESS As research and technology advance our understand- ing of the causes of major craniofacial diseases and disorders and lead to improved methods of diagnosis, treatment, and prevention, opportunities for new community-based prevention programs will grow. Ultimately, the application of any preventive inter- vention is driven by a combination of individual behaviors, community interventions, and profession- al practice. Only a few studies have taken into account all three spheres of action in determining health outcomes in a community (Arnijot et al. 1985, Chen et al. 1997). Our knowledge of the effects of multiple interventions is limited because most inter- ventions were developed and tested singly. In the past half century, however, advances in our understanding of oral diseases and the applica- tion of multiple preventive measures have resulted in continuing declines in the prevalence and severity of both dental caries and periodontal diseases for a size- able majority of Americans. For dental caries, for example, experts now believe that most people can maintain a low risk of the disease by a combination of drinking fluoridated water and brushing daily with a fluoride dentifrice. They recommend that addition- al provider- and community-based dental prevention programs be targeted to high-risk individuals and groups. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 179 Community and Other Approaches to Promote Oral Health and Prevent Oral Disease Many of the studies reviewed in this chapter were conducted when higher rates of caries pre- vailed, community water fluoridation was less wide- spread, and use of fluoride dentifrices and supple- ments was not as common as today. These facts must be taken into consideration in contemporary deci- sion making by public health professionals and poli- cymakers. The validity and reliability of recommen- dations will benefit from the systematic reviews of the scientific evidence by the Task Force on Community Preventive Services (2000) to be includ- ed in a Guide to Community Preventive Services. Oral health promotion strategies are among those current- ly being evaluated. Future innovations include implementing pro- grams in new settings, such as workplaces, senior centers, and nursing homes, where individuals at high risk can be reached. Even if these programs are more expensive, the yield may be worth it if they reach those at high risk for disease. Similarly, focus- ing community-based interventions on populations at greatest risk will make optimal use of available resources. However, continued research to under- stand risk and improve ways to measure it is equally important for the success of these ventures. A review of progress in reaching the Healthy People 2000 oral health objectives reveals relatively little gain across many of the objectives (Table 7.8). Progress in the next decade will require diligent efforts to identify public health problems, mobilize resources, and ensure that the necessary conditions are in place and crucial services received. Public health agencies will be instrumental in carrying out these functions, and state arrd local dental directors can perform a leadership role. Box 7.3 describes the public health services that are essential if a commu- nity is to realize fully the benefits of available disease prevention and health promotion interventions. TABLE 7.8 Progress in meeting Healthy People 2000 oral health objectives Age Baseline Data HP 2000 Goal Final Data Summary 13.1 Reduce dental caries in children 6-8 54% 35% 52% Prog Reduce dental caries in adolescents 15 78% 60% 61% Prog +++ 13.2 Reduce untreated dental decay in children 6-8 28% 20% 29% Reversed Reduce untreated dental decay in adolescents 15 24% 15% 20% Prog ++ 13.3 Increase adults who have never lost a 35-44 31% 45% 31% No Change permanent tooth 13.4 Reduce adults who have lost all their teeth 65+ 36% 20% 30% Prog ++ 13.5 Reduce gingivitis among adults 35-44 41% 30% 48% Reversed 13.6 Reduce destructive periodontal disease 35-44 25% 15% 22% Prog + 13.7 Reduce oral and pharyngeal deaths in males 45-74 13.6% 10.5% 10.3% Met Reduce oral and pharyngeal deaths in females 45-74 4.8% 4.1% 3.5% Met 13.8 Increase sealants in children 8 11% 50% 23% Prog ++ Increase sealants in adolescents 14 8% 50% 24% Prog ++ 13.9 Increase persons on public water receiving 61% 75% 62% Prog fluoridated water 13.10 Increase topical/systemic fluorides among 50% 85% No data No data nonfluoridated 13.11 Increase caregivers using feeding 55% 75% No data No data practices that prevent early childhood caries 13.12 _ Increase oral health screening, referral, follow-up, 66% 90% 75% Prog ++ first time school attendee 13.13 For long-term care, oral exam and services No data 100% No data No data provided within 90 days 13.14 Increase use of oral health care system 35+ 54% 70% 63% Prog ++ (adults) 13.15 Increase states with system for recording 11 states 40 states 23 states Prog ++ and referring orofacial clefts 13.16 Extend use of protective head, face, eye, No data No data No data No data and mouth equipment 13.17 Reduce smokeless tobacco use among males 12-17 6.6% 4% 3.7% Met 18-24 8.9% 4% 6.9% Prog ++ Source: Adapted from NCHS 1999, 180 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Community and Other Approaches to Promote Oral Health and Prevent Oral Disease BOX 7.3 Essential Public Health Services for Oral Health The Association of State and Territorial Dental Directors’ Guidelines for State and Territorial Oral Health Programs (ASTDD 1997) identi- fies the following essential public health services to improve oral health: |. Assessment A. Assess oral health status and needs so that problems can be identified and addressed. B, Analyze determinants of identified oral health needs, including resources. C._ Assess the fluoridation status of water systems, and other sources of fluoride. D. Implement an oral heath surveillance system to identify, investigate, and monitor oral health problems and health hazards. I. Poticy Development A. Develop plans and policies through a collaborative process that support individual and community oral health efforts to address oral heaith needs. B. Provide leadership to address oral health problems by maintaining a strong oral health unit within the health agency. (. Mobilize community partnerships between and among policymakers, professionals, organizations, groups, the public, and others to identify and implement solutions to oral health problems. Hl. Assurance A. Inform, educate, and empower the public regarding oral health problems and solutions. B. Promote and enforce laws and regulations that protect and improve oral health, ensure safety, and assure accountability for the public’s well-being. C._ Link people to needed population-based oral health serv- ices, personal oral health services, and support services and assure the availability, access, and acceptability of these services by enhancing system capacity, including directly supporting or providing services when necessary. D. Support services and implementation of programs that focus on primary and secondary prevention. E. Assure that the public health and personal health workforce has the capacity and expertise to effectively address oral health needs. F. Evaluate effectiveness, accessibility, and quality of popula- tion-based and personal oral health services. G. Conduct research and support demonstration projects to gain new insights and applications of innovative solutions to oral health problems. FINDINGS e Community water fluoridation, an effective, safe, and ideal public health measure, benefits indi- viduals of all ages and socioeconomic strata. Unfortunately, over one third of the U.S. population (100-million persons) are without this critical public health measure. e Effective disease prevention measures exist for use by individuals, practitioners, and communi- ties. Most of these focus on dental caries prevention, such as fluorides and dental sealants, where a combi- nation of services is required to achieve optimal dis- ease prevention. Daily oral hygiene practices such as brushing and flossing can prevent gingivitis. e Community-based approaches for the pre- vention of other oral diseases and conditions, such as oral and pharyngeal cancers and oral-facial trauma, require intensified developmental efforts. e Community-based preventive programs are unavailable to substantial portions of the under- served population. e There is a gap between research findings and the oral disease prevention and health promotion practices and knowledge of the public and the health professions. e Disease prevention and health promotion approaches, such as tobacco control, appropriate use of fluorides for caries prevention, and folate supple- mentation for neural tube defect prevention, high- light opportunities for partnerships between commu- nity-based programs and practitioners, as well as col- laborations among health professionals. e Many community-based programs require a combined effort among social service, health care, and education services at the local or state level. 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Watson MR, Horowitz AM, Garcia I, Canto MT. Caries conditions among 2-5 year old immigrant Latino children related to parents’ oral health knowledge, opinions and practices. Community Dent Oral Epidemiol 1999;27:8-15. Weintraub JA. The effectiveness of pit and fissure sealants. J] Public Health Dent 1989;49(5 Spec No):317-30. Weintraub JA, Stearns SC, Burt BA, Beltran E, Eklund SA. A retrospective analysis of the cost-effectiveness of dental sealants in a children’s health center. Soc Sci Med 1993 Jun;36(11):1483-93. Whyte RJ, Leake JL, Hawkey TP. Two-year follow-up of 11,000 dental sealants in first permanent molars in the Saskatchewan Health Dental Plan. J Public Health Dent 1987 Fall;47(4):177-81. Wilkinson R. Unhealthy societies: the afflictions of inequality. London: Routledge; 1996. Winn DM, Sandberg AL, Horowitz AM, Diehl SR, Gutkind S, Kleinman DV. Reducing the burden of oral and pharyngeal cancers. J Calif Dent Assoc 1998 Jun;26(6):445-51,454. World Health Organization (WHO). Fluorine and fluo- rides: environmental health criteria 36. Geneva: World Health Organization; 1984. World Health Organization (WHO). Fluorides and oral health. Geneva: The World Health Organization; 1994. Yellowitz JA, Goodman HS. Assessing physicians’ and dentists’ oral cancer knowledge, opinions and prac- tices. ] Am Dent Assoc 1995 Jan;126(1):53-60. Yellowitz JA, Horowitz AM, Goodman HS, Canto MT, Farooq NS. Knowledge, opinions and practices of general dentists regarding oral cancer: a pilot survey. J Am Dent Assoc 1998 May;129(5):579-83. 188 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL ee Personal and Provider Approaches to Oral Health Oral health is not a given. It takes conscious and repeated efforts on the part of the individual, care- givers, health care providers, and the community. For ihe individual, daily hygiene routines and healthy lifestyle behaviors provide a frontline defense in dis- vase prevention and health promotion. Equally important are periodic professional assessments of the individual's oral health status, which may include diagnostic, preventive, and therapeutic services and counseling. Community activities complement per- sonal and provider approaches to oral health. As dis- cussed in the previous chapter, these include water fluoridation, dental sealant applications for children, tobacco cessation campaigns, the use of mouth- guards in sports, and a variety of other school- and community-based oral health promotion and disease prevention activities. The interaction of these com- ponents is critical to oral health, as it is to overall health. In particular, there is now a better under- standing of the relationship of individual health to the health of the community in which the individual lives, and the importance of this relationship is one of the underlying premises of Healthy People 2010. This chapter discusses actions individuals can take to maintain their oral health and prevent disease, and reviews emerging approaches taken by dentists and other health care providers to promote oral health, assess risks, and prevent disease. INDIVIDUAL RESPONSIBILITY: PERSONAL APPROACHES TO ORAL HEALTH Sound personal hygiene practices and adherence to a healthy lifestyle are the mainstays of personal approaches to oral health. Long before the germ the- ory of disease, the need for tooth cleaning was recog- nized—if only to rid the mouth of food debris, elim- inate odor, and improve appearance. Tools developed for this purpose have ranged from primitive tooth sticks and picks, still used in parts of the world, to the water irrigators and electronic toothbrushes available in industrialized societies. An impressive array of oral care products greets the shopper in supermarkets and pharmacies today. Beyond the dozens of toothbrush shapes and sizes, there are flavored and textured dental flosses, floss holders, rubber tips, toothpicks, small brushes for cleaning between teeth, scores of dentifrices, and a range of fluoride-containing, antitartar, and antiseptic mouthrinses. Daily oral hygiene efforts contribute to the prevention of dental caries and periodontal diseases. The biofilm on tooth and root surfaces (dental plaque) can be disrupted to a large extent by the mechanical action of brushing and flossing. Daily efforts are necessary, not only because of food intake, put also because dental plaque is never completely removed. It starts to build up even after the most assiduous cleaning (or prophylaxis) in the dental office and even after the application of a potent antimicrobial mouthrinse. The oral and dental tissues and structures thus require more intensive daily care than do other body areas exposed to the environment. Daily Hygiene and Dental Caries Prevention The use of a fluoride-containing dentifrice is critical for dental caries prevention. Even more beneficial than the physical removal of plaque in toothbrushing is the delivery of a small amount of fluoride to the tooth surfaces. Investigators have conducted numer- ous clinical trials on fluoride dentifrices using rigor- ous designs and including randomized groups, dou- ble-blind designs, and placebo controls. All together, these studies provide strong evidence that using a ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 189 Personal and Provider Approaches to Oral Health fluoride dentifrice is effective (Clarkson et al. 1993, Lewis and Ismail 1995, Stookey et al. 1993). Fluoride dentifrices account for more than 90 percent of the market in the United States, Canada, and other devel- oped countries (Levy 1994). A fluoride dentifrice is an effective means of reducing the prevalence of dental caries for all per- sons. Although children’s teeth should be cleaned daily from the time they erupt, parents and caregivers should consult a dentist or other health care provider about the use of a fluoride dentifrice for children under the age of 2. For children under 6, fluoride dentifrices should be used in small amounts to mini- mize swallowing of the product. Mild enamel fluoro- sis can result from excessive dentifrice use, because children under 6 do not have adequate control of the swallowing reflex or may intentionally swallow a fla- vored dentifrice. Experts recommend that for chil- dren under 6, the parent or caregiver should super- vise toothbrushing, apply a pea-sized amount (0.25 gram) of dentifrice to the toothbrush, and encourage the child to spit out the excess (Bawden 1992). Because the topical benefits of fluoride have been shown to be highly effective, and daily exposure to small amounts of fluoride can reduce the risk of den- tal caries in all age groups, experts recommend that all persons drink water with an optimal fluoride con- centration in addition to brushing daily with a fluo- ride dentifrice (Bawden 1992, CDC in press). This combination provides a cost-effective and easy way to prevent dental caries and is an excellent example of the individual-community partnership. For persons at low risk of dental caries, these two exposures to fluoride may be the only ones necessary. For persons at moderate or high risk of dental caries, additional fluoride may be helpful and can come from daily use of another fluoride product. These can include mouthrinses, prescribed supplements, and _profes- sionally applied topical fluoride products (CDC in press). Daily Hygiene and the Prevention of Periodontal Diseases Toothbrushing and flossing also play a critical role in the prevention of periodontal diseases. Unlike dental caries prevention, prevention and control of gingivi- tis and periodontitis are achieved directly through the mechanical removal and disruption of dental plaque (Genco and Newman 1996). Some dentifrices also contain chemical therapeutics to control the for- mation of tartar (calculus) (Mandel 1995) and to reduce plaque formation and gingival inflammation (Hancock 1996). Both manual and electric tooth- brushing are effective at removing plaque and pre- venting gingivitis (Walsh et al. 1989, Axelsson et al. 1991). Interproximal (between the teeth) cleaning is also important in maintaining gingival health (Lang et al. 1994). In one short-term evaluation of adults, the addition of flossing to the daily regimen of brush- ing resulted in an almost twofold reduction in gingi- val inflammation (Graves et al. 1989). Because pre- ventive measures in periodontics rely mainly on the removal of bacterial plaque and calculus, methods typically include personal oral hygiene measures combined with professional diagnostic and prophy- lactic measures (ie., regular €xam and cleaning). Periodic professional care for removal of plaque and calculus deposits has also been demonstrated to improve the periodontal health of participants (Cutress et al. 1991, Ronis et al. 1993). Healthy Lifestyles There is more to the individual’s role in promoting oral health and hygiene than brushing and flossing. Other behaviors that have an influence on oral health include use of tobacco and/or alcohol products, diet, oral habits such as bruxing and clenching the teeth, and use of helmets, mouthguards, or other protective devices. Table 8.1 summarizes selected behaviors that have an effect on oral, dental, and craniofacial health status. These are described more fully in Chapters 3, 7, and 10. Individuals can obtain credible information regarding oral health from various sources, including health care providers, professional organizations, government agencies, and patient advocacy groups. Increasingly, the World Wide Web is a source for health care information. For example, the National Oral Health Information Clearinghouse offers infor- mation on oral health, with an emphasis on special care patients and their health care providers. Care Seeking In addition to self-care, individuals also need to seek professional health care—both dental and medical— on a regular basis and whenever a problem manifests. The recall interval is based on the provider's assess- ment of the individual’s dental and medical history and lifestyle behaviors, among other factors. In the case of children and dependent adults, parents and caregivers are responsible for teaching and encourag- ing healthy behaviors and seeking timely and appro- priate care. As noted at the outset, it is only through the combination of individual and professional care, reinforced by community-based health promotion 790 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health and disease prevention programs, that optimal oral and general health can be achieved. The remainder of this chapter focuses on the role of the professional in oral health care. PROVIDER-BASED CARE The range of conditions and diseases that affect the craniofacial complex is extensive and can provide clinicians with important indications about the patient's general as well as oral health status. Management of the oral health-general health inter- face calls for interdisciplinary and coordinated care and an enhanced role for primary care providers. Dentists, oncologists, dermatologists, infectious dis- ease specialists, hematologists, endocrinologists, plastic surgeons, and rheumatologists are just a few of the specialists who may be involved in the diagno- sis and management of conditions affecting the cran- iofacial complex. Dentists, their allied staff, and medical and nurs- ing personnel are in a unique position to incorporate new approaches for prevention,’ diagnostic, and treatment strategies in their practices. Advances in oral science are providing the basis for a shift in emphasis from the repair and restoration of damaged tissues to earlier diagnoses, control of infections, and remineralization and regeneration of lost tissues. The application of risk assessment strategies and inter- ventions tailored to individuals and groups is systemic nutrition. (See Chapter 10, Box 10.1.) Oral hygiene and home care practices (are seeking all oral and craniofacial health. Parafunctional habits using behavioral strategies. Tobacco use Alcohol use defects and mental retardation. injury control practices calorie malnutrition, deficiencies of vitamin A, asco Linear enamel hypoplasia and hypomineralization ous and permanent teeth. The physical consistency, been linked to the development of caries. Reduced clinical signs of nutritional deficiencies and eating with clenching and other oral habits such as frequent tion. Treatment may begin with making the individua TABLE 8.1 Selected individual behaviors affecting oral, dental, and craniofacial health Behavior Effect Diet and nutrition Nutrition and diet contribute to oral and craniofacial development and to the maintenance of these tissues throughout life. Nutritional deficiencies during pregnancy can affect tooth size, enamel solubility, time of tooth eruption, salivary gland function, saliva composition, epithelial tissue, and susceptibility to dental caries. Deleterious effects specific to the dentition include protein- rbic acid, vitamin D, calcium, phosphorus, iron, and iodine, and excessive fluoride. during the first year of life increase susceptibility to dental caries in both decidu- sequence, and frequency of carbohydrate intake (primarily refined sugars) have calcium intake is associated with greater levels of periodontal disease. Early disorders are often seen in and around the mouth. Oral lesions may also affect Regular toothbrushing with a fluoride-containing dentifrice prevents dental caries. Rinsing with fluoride mouthrinse can aid in reducing caries and in the remineyalization of tooth structure. Requiar toothbrushing and proper flossing can prevent gingivitis. Seeking health care—both dental and medical—on a regular basis and whenever a problem manifests is important. In the case of children or dependent adults, it alls for the caregivers to teach and encourage healthy behaviors and to seek appropriate care from a variety of care providers. Prenatal care, as well as oral health care prior to major treatments such as chemotherapy, is critical to over- Habitual grinding (bruxism) and/or clenching teeth are farms of abnormal motor behavior. These habits often occur during sleep. As gum-chewing, bruxism can cause tooth wear and affect muscles of mastica- | aware of the problem, providing an occlusal splint to prevent tooth wear, and The use of tobacco in all forms increases the risk for oral and pharyngeal cancers, and smoking is a leading risk factor for periodontal diseases. Increased risk for dental caries has been associated with spit tobacco use. In HIV-infected individuals, tobacco use is a risk factor contributing to increased risk of the development of oral candidiasis. (See Chapter 10, Box 10.2.) Alcohol alone, as well as acting synergistically with tobacco, greatly increases the risk for oral and pharyngeal cancers. independently, alcohol in excess is associated with circulatory and neurological problems, liver disease, and other organ-specific dis- eases and disorders. Alcohol use in pregnancy can lead to birth defects, such as fetal alcohol syndrome and its associated craniofacial Proper use of helmets, mouthguards, safety belts, and other protective devices helps prevent injuries to the head, neck, and mouth. _ ‘The term prevention, as used in this chapter, includes interventions aimed at reducing the incidence of disease in relatively healthy patients. It includes both health promotion and specific protection to control one or more risk factors. Some strategies, such as the prevention of tobacco use, are applicable to many odontal diseases, whereas other strategies are specific, such as t ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL oral diseases, including oral cancer, oral candidiasis, and peri- he use of dental sealants and fluorides for caries prevention. 191 Personal and Provider Approaches to Oral Health expanding with the increased understanding of risk factors and the development of biomarkers that sig- nal host resistance, susceptibility, and the presence and progression of disease. The changing demographics of the U.S. popula- tion and a greater understanding of the relationship between oral health and general health are presenting . new challenges. Making clinical decisions for patients requires integrating a range of interacting biological, psychological, social, cultural, and envi- ronmental factors. In order for disease to manifest, the etiologic agent(s) must be present, the host must be susceptible, the environment conducive, and suf- ficient time available for the factors to interact (Figure 8.1). Early diagnosis and prompt treatment require an understanding of the pathology and of the diagnostic, prevention, and treatment modalities available. As genetic information accumulates, clini- cal judgments will increasingly be informed by knowledge of an individual's genetic susceptibility or resistance to particular diseases and disorders. The development of tailored treatment plans will require incorporating all these factors together with input from the patient's health providers, taking into con- sideration the patient's interests and needs. The fol- lowing sections provide an overview of emerging approaches to clinical management and highlight selected diseases as examples. Risk Assessment Given the greater understanding of disease etiology, epidemiology, patient characteristics, and genetic information, it is becoming increasingly possible to determine an individual's risk of disease and tailor treatments accordingly. Risk assessment for dentistry has been defined as “the use of knowledge of factors FIGURE 8.1 Factors involved in disease Etiolagic Agent(s) Environment and Behavior Patient Susceptibility that are associated with dental disease to determine which patients are more or less likely to prevent or control their dental disease” (Douglass 1998). The factors can include co-morbidities, medications used, and patient characteristics such as sex, age, and lifestyle behaviors, among others. By compiling such factors and sorting them by risk category, patients can be classified into high- or low-risk groups, enabling providers to make more comprehensive diagnoses and identify patients who would benefit from more aggressive prevention strategies. Such analyses conducted during the early stages of disease can result in treatments that reverse or contain the disease process (Douglass 1998). Knowledge of risk factors for oral and craniofacial diseases and disor- ders allows other health care providers to screen for these risk factors and contribute to improving oral health. Risk assessment and disease prediction studies have focused primarily on dental caries and peri- odontal diseases (Genco 1996, Page and Beck 1997, Pitts 1998, Powell 1998). In addition, risk factors for oral and pharyngeal cancers have been explored Johnson 1991). The evidence base for risk assess- ment is developing from population-based studies. It involves a research process in which a suspected risk factor is related in a multivariate model to other fac- tors and confounders (Beck 1990). The resulting model is tested in a second group of subjects, and a targeted intervention study is conducted to confirm the predictive validity of the risk factor. Although the application of research findings of risk assessment has begun in some practices, the pre- diction of future disease at the individual patient level has not yet been extensively studied. Douglass (1998) has posed six clinically oriented questions that need to be addressed if risk assessment is to be adopted into routine clinical practice: 1. Does the scientific theory or biologic logic of the risk factor fit with our current body of knowledge about the disease in question? 2. Has the technical merit of identifying the risk factor (such as imaging technologies and bacter- ial assays) been evaluated? 3. Has the efficacy of the risk factor in predicting disease been evaluated in terms of sensitivity, specificity, and positive and negative predictive values?” 4. Has the potential effect of the risk factor on the disease management decision been explored? Can knowledge of the presence of a particular risk factor or pattern of risk factors alter the treatment plan? 192 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health 5, Has the influence of the risk factor on oral health outcomes been assessed? 6. Has the cost-effectiveness of collecting risk factor data from each patient been evaluated? Is the added expense justified either by increased effective- ness or by avoiding other expenses? Diagnostic Tests \Whereas risk assessment aims to predict future dis- ease and disease progression, diagnostic tests evalu- ate a patients current status with regard to a specific disease or disorder. They enable the provider to for- mulate, in cooperation with the patient, a treatment plan. In relation to dental caries and periodontal dis- cases, the diagnosis ideally should not only detect the presence of disease, but also distinguish between active and arrested disease. Today, most diagnostic tests for oral conditions are based primarily on anatomic clinical evidence. However, microbiological, pathological, immunolog- ical, genetic, and tissue metabolite tests are increas- ingly available and valuable. Table 8.2 cross-refer- ences diseases with categories of diagnostic tests available. The following sections describe elements of a general health assessment and highlight risk assess- ment, diagnosis, and prevention of selected diseases and conditions. Oral Health Assessment An oral health assessment involves an evaluation of an individual's overall health status, including any risk factors and personal needs that can affect health and treatment options. For the majority of craniofa- cial conditions, this assessment and subsequent care are coordinated with a range of health care providers, with the intent of enhancing the patient's overall health and well-being. The information gathered for the assessment is derived from patient information, extraoral and intraoral clinical examinations, and imaging and other diagnostic tests as needed. The patient provides demographic and lifestyle behavior information and a medical and dental history, including current come- plaints, if any. Symptom analysis entails an addition- al series of questions that explore symptom onset, characteristics, and course. Figure 8.2 provides an example of a medical history form used in dental practice. The clinician will take into consideration the patient’s general appearance and ability to function, as noted by characteristics of facial symmetry or asymmetry and speech. In addition, the patient's vital signs may be assessed, and a thorough examination of the head, neck, temporomandibular joints, and other structures will be conducted. The intraoral por- tion of the examination involves an extensive assess- ment of the tissues: the lips and labial mucosa, buc- cal mucosa and mucobuccal fold, the floor of the mouth, tongue, hard and soft palate, oropharynx, muscles of mastication, salivary glands and saliva, gingiva, periodontium, and teeth. Depending on the needs of the patient, the initial physical examination is usually augmented by sup- plementary data from radiographs and sometimes by other diagnostic tests, including tissue biopsies and samples of oral cells and fluids. Such samples can be used to type specific bacteria, viruses, or fungi or to detect elevated levels of tissue metabolites or [rs BLE 8.2 Categories of diagnostic methods for selected oral, dental, and cran Diagnostic Periodontal Oral Procedure Caries Diseases Infections Interview Patient history Sa Sg a Physical Clinical examination ° So o Probing/caries ° Probing/periodontal o Imaging a Sd Biologic —_-Histology/cytology o Microbiology o o o Genetics/DNA o iofacial diseases and disorders Mucosal Temporomandibular Craniofacial Diseases Disorders Defects Oral Cancers Cd od ¢ Oo aa CY ° « o o Sa o o ° o ° OO Sensitivity is a measure of how often the test is positive when applied to patients known to have a particular disease or condition; specificity is a measure of how successful the test is in judging the absence of a disease or condition. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 193 Personal and Provider Approaches to Oral Health FIGURE 8.2 Medical history form for use in dental practice Medical History Form Date Name Home Phone (___} Address _ Business Phone (___) City State Zip Code Occupation Social Security No. Date of Birth ss / /___ Sex MF Height Weight Single Married Name of Spouse Closest Relative Phone (___) if you are completing this form for another person, what is your relationship to that person? Referred by For the following questions, circle yes or no, whichever applies. Your answers are for our records only and will be considered confidential. Please note thaf during your initial visit you will be asked some questions about your responses to this questionnaire and there may be additional questions concerning your health. 1. Are you in good health? Yes No 2. Has there been any change in your general health within the past year? Yes No 3. My last physical examination was on 4. Are you now under the care of a physician? Yes No If so, what is the condition being treated? 5S, The name and address of my physician(s) is 6. Have you had any serious illness, operation, or been hospitalized in the past 5 years? Yes No If so, what was the illness or problem? 7. Are you taking any medicine(s) including non-prescription medicine? Yes No Ifso, what medicine(s) are you taking? 8. Do you have or have you had any of the following diseases or problems? a. Damaged heart valves or artificial heart valves, including heart murmur or rheumatic heart disease Yes No b. Cardiovascular disease {heart trouble, heart attack, angina, coronary insufficiency, coronary occlusion, high blood pressure, arteriosclerosis, stroke) Yes No 1, Do you have chest pain upon exertion? Yes No 2. Are you ever short of breath after mild exercise or when lying down? Yes No 3. Do your ankles swell? Yes No 4. Do you have inborn heart defects? : : Yes No 5. Do you have a cardiac pacemaker? Yes No «Allergy Yes No d. Sinus trouble Yes No e. Asthma or hay fever Yes No f. Fainting spells or seizures Yes No g. Persistent diarrhea or recent weight loss Yes No h. Diabetes Yes No i. Hepatitis, jaundice, or liver disease Yes No j. AIDS or HIV infection Yes No k. Thyroid problems Yes No t. Respiratory problems, emphysema, bronchitis, etc. Yes No m. Arthritis or painful swollen joints Yes No n. Stomach ulcer or hyperacidity Yes No 0. Kidney trouble Yes No p. Tuberculosis Yes No q. Persistent cough or cough that produces blood Yes No r. Persistent swollen glands in neck Yes No s. Low blood pressure Yes No t. Sexually transmitted disease Yes No u. Epilepsy or other neurological disease Yes No vy. Problems with mental health Yes No w. Cancer Yes No x. Problems of the immune system Yes No 9. Have you had abnormal bleeding? Yes No a. Have you ever required a blood transfusion? Yes No 194 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health eee +9. Do you have any bload disorder such as anemia? ........ Yes No +1, Have you ever had any treatment for a tumor or growth? Yes No “2. Are you allergic or have you had a reaction to: a, _ Local anesthetics 7” . . a . . Yes No b. Penicillin or other antibiotics epwiseeereeees Yes No «Sulfa drugs ..... Yes No g, _Barbiturates, sedatives, OF sleeping pills . eoeeee . Yes No e. Aspirin. + Yes No §HOdiMe i nsnnensnnnnnrnnnninnt EET Yes No g. Codeine or ther Narcotics nenwsnsewemnnrsnnnnnnenennninrnnnrann LSS SET eee Yes No h. Other ; 13. Have you had any serious trouble associated with any previous dental treatment? .......-.-s-se . Yes No if-so, explain 14. Do you have any disease, condition, or problem not fisted above that you think | should KNOW BDOUL? ..sssseessecenseeerssneentee Yes No If so, explain 15. Are you wearing contact a Yes No 16, Are you wearing removable dental appliances? .nevnesseneeneatnnnnrermnneare eS Tpeeeeene . Yes No 17. Do you currently u Yes No Ifso, which type? : 18, Are youa former tabacco user? i Yes No Ifo, which type of tobacco? 19, How many years have/did you use tobacco? 20. How much tobacco do/did you use a day? _ 21. Ifyou have stopped using tobacco products, how long ago did you stop? 22. Have you ever used alcoholic DeVEraGeS? .asentsceeseenessrnetntnntnnncentenesty Yes No 23. How long ago did you stop using alcoholic beverages? 24, Do you currently u vecensaasanssaravansnennearsssnansnneesteet . . Yes No If'so, which type? 25, How many times a week do you use alcoholic beverages? Women 26. Are you pregnant? ......... vescueseasssanessanensnysensbitessaneeonseQQ@sQeew0e™ Yes No 27. Do you have any problems associated with your menstrual POTIOG? aseeeeeeseseens Yes No 28. Are you nursing? pennssceeseees - . + Yes No 29. Are you taking birth control Pills? escnseneeeneesnetemtnnnnarnnrrannn Yes No Chief Dental Complaint ae { certify that I have read and understand the above. acknowledge that my questions, if any, about the inquiries set forth above have been answered to my satisfaction. twill not hold my dentist, or any other member of his/her staff, responsible for any errors or amissions that | may have made in the completion of this farm. Signature of Patient For completion by the dentist. Comments on patient interview concerning medical history: Significant findings from questionnaire or oral interview: ee ental management considerations: i Oate Signature of Dentist Medical history update: Comments Signature Oe Source: Adapted from American Dental Association, as reproduced in Rose and Steinberg 2000. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 195 Personal and Provider Approaches to Oral Health immune system factors associated with disease. The number of such tests is increasing and will be sup- plemented by genetic tests to indicate an individual's susceptibility to specific diseases. Currently, the assessment of oral and craniofacial health and disease involves intraoral radiographs as well as radiographic imaging, including arthrogra- phy, motion-based tomography, and computed tomography (Jeffcoat 1992). Intraoral radiographs permit detection of lesions between teeth and are the only widely available clinical test that can assess peri- odontal bone support in situ (Jeffcoat et al. 1995). Radiographs are an essential tool for treatment plan- ning of complex prosthetic reconstructions as well as a diagnostic method to assess periodontal progres- sion. However, the mere presence of bone loss on a radiograph does not imply progressive osseous destruction, although it does increase the patient’ risk of future bone loss (Armitage 1996, Genco 2000). Radiographs have high specificity for disease progression, and low sensitivity. Because all radi- ographic examinations expose the patient to some, albeit small, level of ionizing radiation, current guidelines indicate that radiographs should not be taken routinely (FDA 1987), but should be pre- scribed after an initial assessment by the dentist. Image processing techniques, such as digital radiography, enhance the clinician's ability to detect small intraoral osseous changes over time and aid in the detection of small changes in skeletal tissues between examinations. Direct digital radiography uses an intraoral detector to capture a radiographic image of the diagnostic area of interest (Ellwood et al. 1997, Matsuda et al. 1997). Several proposed meth- ods for quantitative estimation of lesion mass or vol- umetry using digital subtraction radiography exist (Armitage 1996). A recent multicenter validation study has indicated that simulated lesions as small as 1 mg in mass may be detected with better than 90 percent sensitivity and specificity Qeffcoat et al. 1996). These techniques are currently in use in clin- ical trials. New diagnostic methods are also becoming available as adjuncts to existing methods for caries diagnosis. Comparing data between bite-wing radi- ographs of potential occlusal fissure lesions, Lussi et al. (1995) found that electrical resistance measure- ment may provide a substantial improvement in caries diagnosis. Other imaging approaches are used to assess craniofacial anatomy, temporomandibular joints, maxillary sinuses, and other associated tissues, and in the assessment of the size and quality of bone to receive dental implants. Magnetic resonance imaging (MRD is also receiving increased attention for cran- iofacial applications, such as for the assessment of the temporomandibular joints. Finally, light-based imaging of teeth and associated structures, using a small intraoral camera, gives both the patient and the provider a wide-screen view of the oral cavity, aiding in patient education. In the course of conducting a general assess- ment, the clinician notes disease-specific signs and symptoms. While examining the teeth, the clinician may detect signs of relatively rare hereditary diseases such as ectodermal dyplasias, or more common destructive habits such as bruxism, where the enam- el and at times the dentin may be abraded. Examinations of the face and oral cavity may reveal the effects of intentional and unintentional injuries. With the results of the general assessment in hand, the clinician will classify the patient's general and oral health status and make treatment and/or referral recommendations. A classification system adopted in 1962 by the American Society of Anesthesiologists, used to cate- gorize a patient’ risk on the basis of physical status, also has been applied, along with the patient's gener- al and oral health risk assessment, to determine the need for coordinated multidisciplinary referral and whether care in a hospital is indicated rather than in the dental office (Bricker et al. 1994) (Table 8.3). Changing Approaches to Selected Diseases and Conditions The science and technology base is providing new approaches to risk assessment, diagnosis, prevention, and treatment. Highlights of selected diseases and conditions follow. Dental Caries Dental caries is caused by a transmissible microbial infection that affects tooth mineral. A number of fac- tors play a role in the initiation and progression of the disease, including bacterial biofilm, specifically the presence of mutans streptococci and species of lactobacilli; the frequency of simple sugars in the diet; the flow and composition of saliva; the avail- ability of fluoride; the structure of tooth mineral in a given individual; and oral hygiene behaviors. Sound caries management takes all these factors into account (Figure 8.3) (Burt and Ismail 1986). Today there is the prospect that clinicians will be able to bal- ance protective and pathologic factors and work with the patient to control disease (Anderson et al. 1993, Edelstein 1994, Featherstone 1996). 196 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health Risk Assessment. Reviews of caries risk prediction models conclude that clinical variables, especially past caries experience, are the best predictors of new wanes experience (Newbrun and Leverett 1990, Powell 1998). Table 8.4 shows a timeline summariz- ing the strongest predictors of caries incidence based on a review of the modeling literature. At the time of initial tooth eruption, the presence of mutans strep- tococci appears to be the primary predictor of future caries. With continued tooth eruption, this variable disappears as a primary predictor and is replaced by the status of the most recently exposed or erupted tooth surface. For example, the ——— TABLE 8.3 American Society of Anesthesiologists—medical risk categories and associated dental considerations ASA Classification Dental Consideration presence of carious lesions in the primary incisors has been found to be the best predictor of caries in the later-erupting primary molars (Powell 1998). Physical status 1 A patient without systemic dis- ease; a normal, healthy patient Physical status 2 A patient with mild systemic disease medical consultation) Physical status 3 A patient with severe systemic dis- ease that limits activity but is not incapacitating considerations Physical status 4 A patient with incapacitating sys- temic disease that is a constant threat to life special considerations Routine dental therapy without modification Routine dental therapy with possible treatment limitations or special considerations (e.g., duration of therapy, stress of therapy, prophylactic consideration, possible sedation, and Dental therapy with possible strict limitations or special Emergency dental therapy only, with severe limitations or Despite recent declines, dental caries is a prevalent disease, with some age and pépulation groups particularly vulnerable (see Chapter 4). A guide for the identi- fication of vulnerable patients and the treatment of caries as an infec- tious disease has been developed (ADA 1995). Figure 8.4, from that guide, proposes questions to be considered at an initial examina- tion. These questions, together with information gathered at recall examinations, allow classification of child and adult patients into high-, moderate-, and low-risk dis- ease categories (Table 8.5). This Source: Genco 2000. Risk factors for periodontal disease. In Rose LF, Genco RJ, Cohen DW, Mealey BL. Periodontal medicine. Hamilton:B.C. Decker Inc. 2000:35-43. Copyright 2000 by B.C. Decker Inc. Reprinted by permission of B.C. Decker Inc. (2000). approach has been incorporated in a variety of caries risk assessment FIGURE 8.3 Multifactorial model of dental caries Host Enamel crystal structure { Enamel minerals: Agent i GPF §. mutans | Saliva quantity Lactobacilli \ Saliva quality Other bacteria \, Immune response Host behavior Host attitudes Environment Plaque quantity Plaque quality Enzymes Minerals Bacterial substrate Protective factors Socioeconomics Culture Source: Burt and Ismail 1986. Copyright 1986 by Journal of Dental Research. Reprinted by permission of Journal of Dental Research (2000). forms adopted by some dental schools and managed care programs (C.W. Douglass, personal communication, 1999). Studies are needed to determine the validity and reliability of such approaches for different patient populations and practice settings. The use of tests to assess caries risk to determine the activity status of preclinical disease is becoming more widespread. A range of diagnostic aids for caries activity testing are available. Microbial tests can detect the presence and quantify the levels of lactobacilli and mutans streptococci. The develop- ment and use of these tests are based on studies that have associated these microbes individually and together with different types of carious lesion devel- opment. Measurements of plaque and salivary pH have been used to evaluate the oral environment overall and to note the changes in pH that occur after eating various foods. Salivary flow and compo- sition analyses add another dimension. Decreased flow has been related to caries susceptibility, as have increases in viscosity. These factors warrant further study to determine their sensitivity and specificity. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 197 Personal and Provider Approaches to Oral Health Diagnosis. Clinical signs, patient-derived history, and radiographic images remain the primary means of dental caries diagnosis. Tooth surface pitting and cavitation, white and/or brown spots, areas soft to tactile probing, and radiolucencies are used to detect the effects of this disease. The most common diagnostic approaches include visual inspection, the use of an explorer (a probelike instrument) to determine the integrity of the tooth surface, the use of a light source to detect difference in reflectance across tooth structure (transillumination), and radiographs. Table 8.6 compares the reported sensitivity and specificity of selected methods. No single method stands out as superior with regard to both sensitivity and specificity for all tooth surfaces. The most basic diagnostic methods—visual alone and visual examination with an explorer—have limited sensitivity, but excellent specificity. The visu- al examination may be combined with a radiograph- ic series for the initial assessment. Bite-wing radiographs are frequently used to diagnose inter- proximal caries (between teeth) and for these sur- faces provide excellent sensitivity and specificity. Radiographic examination allows examination of otherwise inaccessible areas. Specifically, the depth of a lesion and its relationship to the pulp chamber can be evaluated for interproximal lesions. However, radiographs are of little value in detecting caries on the occlusal surfaces of the teeth. For these surfaces, a negative radiographic diagnosis does not imply lack of a carious lesion in enamel. Precavitated carious lesions and caries in restored teeth pose an additional diagnostic chal- lenge. A review of the literature on the clinical diag- nosis of precavitated carious lesions concluded that visual detection of these lesions has low sensitivity and moderate specificity (Ismail 1997). It is difficult with these lesions to determine whether there is no caries or whether only the enamel or outer layer of dentin is involved. Carious lesions forming around restorations are seen more frequently at the approxi- mal and cervical margins of these restorations (Mjor 1985). Distinctive color changes around a restoration alone are not diagnostic of active caries (Kidd 1990). Currently, the progression of carious lesions is the most definitive diagnostic parameter for disease activity. Progression can be determined over specific time intervals only by professional assessment. Prevention. The primary prevention of dental caries starts with adequate prenatal and perinatal nutrition to ensure normal development of the teeth and sup- porting structures. It continues with interventions aimed at preventing transmission of cariogenic microbes from caregivers to infants, and proceeds with specific strategies employed across the life span. These approaches include the provision of sufficient fluoride, the use of dental sealants, the adoption of healthy behaviors, including avoiding unhealthy dietary practices and practicing appropriate oral hygiene, and the timely use of care services. Although many factors are brought to bear on the primary prevention of dental caries, the combination of fluoride in its multiple forms and dental sealants is the foundation (as described in Chapter 7). Fluoride is available in a variety of products that can be used by health professionals, individuals, and public programs. Topical solutions and gels, mouthrinses, and dentifrices are available for daily, weekly, or as-prescribed frequency. In addition, TABLE 8.4 Timeline of strongest clinical predictors of caries incidence Age (years) 0 1 2 3 4 ~=«°55 6 7 8 9 0 4H 12. «1301421 22-45 >45 Dentition — Primary Mixed Early Mature permanent permanent Event Eruption primary molars Eruption first Eruption second Progression of gingival recession permanent molar permanent molar Predictor Mutans dmifs, especially dmfs, especially DMFS, especially first Incipient Not studied Coronal and root streptococci’ primary incisors primary molars permanent molars smooth DMFS Mutans streptococci First molar occlusal First motar occlusal surface lesions Number of teeth and lactobacilli morphology morphology DMFS Periodontal DMFS Incipient smooth disease surface lesions Note: dmfs = decayed, missing, or filled primary tooth surfaces; DMFS = decayed, missing, or filled permanent tooth surfaces. Source: Powell 1998. Caries prediction: a review of the literature. Community Dentistry and Oral Epidemiology 1998; 26:361-71. Copyright 1998 by Munksgaard International Publishers Ltd., Copenhagen, Denmark. Reprinted by permission of Munksgaard International Publishers Ltd., Copenhagen, Denmark (2000). 198 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health FIGURE 8.+ Caries risk questions for initial examination INITIAL VISIT—QUESTIONS TO CONSIDER |s there current caries activity? Are there indications that yield potential for development of caries within the next year? « Prior DMFS (decayed, missing, or filled surfaces) + Tooth morphology + Medications that decrease saliva flow and/or affect viscosity of saliva « Medical condition or treatment(s) What is the individual's caries risk? * Low + Moderate * High What are the modifiable risk factors that may be responsible for or may contribute to this caries activity? » Insufficient systemic and topical fluoride + Medications * Poor oral hygiene habits or skills « Deep pits and fissures without sealants + Poor dietary habits What can be done to prevent new caries or caries progression within the next year? + Sealants + {Increase fluoride use * Oral hygiene instruction/education * Dietary counseling + Monitor bacterial count + Antimicrobial agents « Conservative restorative techniques—to minimize removal of tooth structure What is the prognosis for successful intervention? + Patient compliance * Clinician skill (diagnosis, intervention counseling) + Prevention modalities are accepted/applied + Severity at onset Are there other considerations that may affect the decision process that cannot be changed? (effect modifiers, confounders) + Age + Socioeconomic considerations * Medicatly and/or physically compromising conditions Source: American Dental Association Council on Access, Prevention and inter- professional Relations 1995. Caries diagnosis and risk assessment. A review of preventive strategies and management. JADA; 126: 15-245. Copyright 1995 by American Dental Association. Reprinted by permission of ADA Publishing Co. Inc. (2000). fluoride-containing prophylactic pastes are available for professional application (see Chapter 7). Clinical judgment of risk factors determines the type and frequency of interventions needed. Although there is general agreement on the over- all value of topical fluorides in reducing dental caries (ADA 1986, 1994, Moss 1976, Stookey et al. 1993), comparative clinical trials are needed to determine which of the existing fluoride formulations (acidulat- ed phosphate fluoride, stannous fluoride, amino- fluoride, or sodium fluoride) and which delivery sys- tem (gel, varnish, dentifrice, or solution) are most efficacious. A second line of defense is through control of the etiologic agent. Chemotherapeutic agents (including the antimicrobial mouthrinse agent chlorhexidine and fluoride) can be used to reduce plaque. Dietary measures aimed at reducing the frequency and quan- tity of sugars and the substitution of sugars by sugar- free sweeteners may effectively starve the bacteria. The process of tooth demineralization and re- mineralization has received significant attention over the past four decades (Geiger et al. 1992, Koulourides et al. 1961, Larsen and Fejerskov 1987, Linton 1996, Silverstone et al. 1981, White 1988), although the concept was documented in the early 1900s (Head 1912) (see Chapter 3). Investigators are studying the effectiveness of therapeutic agents for arresting carious lesions and remineralizing enamel in populations at high risk for dental caries. For example, a combined chlorhexidine-fluoride solution can enhance remineralization of incipient lesions and arrest caries in patients who suffer from radiation- induced caries (Katz 1982). The use of a twice-daily rinse with 0.05 percent sodium fluoride to prevent demineralization and induce remineralization in sub- jects with radiation-induced hyposalivation has also been found to be effective (Meyerowitz et al. 1991). This study also addressed the effects of chlorhexidine use alone, which has been associated with tooth staining, alterations in taste, and potential hypersen- sitivity reactions (Ohtoshi et al. 1986, Okano et al. 1989). Schaeken et al. (1991) showed that the appli- cation of 40 percent by weight chlorhexidine varnish every 3 months enhanced remineralization of root caries more than fluoride varnish, although both treatments were associated with fewer filled root sur- faces than the control group after 1 year. A chlorhex- idine varnish has not yet been approved in the United States, and large-scale, double-blind, placebo-con- trolled clinical trials are not yet available to test the effects of specific regimens in relation to caries risk. Studies also are evaluating interventions to pre- vent mutans streptococci transmission. Find- ings from cross-sectional studies indicate that infants are initially infected by their parents, specifically mothers, around the time the teeth erupt (Berkowitz et al. 1975, Caufield et al. 1993, Kohler and Bratthall 1978). A longitudinal study using DNA fingerprint- ing demonstrated that mothers were the source of the ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 199 Personal and Provider Approaches to Oral Health TABLE 8.5 Caries risk classification guidelines Age Category for Recall Patients? Risk Category Child/Adolescent Adult Low No carious lesions in last year No carious lesions in last 3 years Coalesced or sealed pits and fissures Adequately restored surfaces Good oral hygiene Good oral hygiene Appropriate fluoride use Regular dental visits Regular dental visits Moderate One carious lesion in last year One carious lesion in last 3 years Deep pits and fissures Exposed roots Fair oral hygiene Fair oral hygiene Inadequate fluoride White spots and/or interproximal White spots and/or interproximal radiolucencies radiolucencies {regular dental visits {rreqular dental visits Orthodontic treatment Orthodontic treatment High >? carious lesions in last year >? carious lesions in last 3 years Past smooth surface caries Past root caries; or large number of exposed Elevated mutans streptococci count roots Deep pits and fissures Elevated mutans streptococci count No/little systemic and topical fluoride Deep pits and fissures exposure Poor oral hygiene Poor oral hygiene Frequent sugar intake Frequent sugar intake Irregular dental visits Inadequate saliva flow Inappropriate bottle feeding or nursing (infants) Inadequate use of topical fluoride Irregular dental visits {nadequate saliva flow aAt initial visit for new patient, if time of last caries experience cannot be determined, a person with no decayed, missing, or filled surfaces (DMFS = 0) would be classified as low risk. A person with past caries experience (DMFS > 0) and/or one active lesion would be classified as moderate risk. A person with past caries experience and/or two active caries or one smooth surface lesion would be classified as high risk. Parents of young children and expectant parents need additional counseling on inappropriate nursing or bottle feeding practices that can lead to the development of early childhood caries. Parents and caregivers should be advised to introduce children to a cup in an effort to discontinue use of the bottle by the age of 1 year. Also, parents and caregivers should be advised never to place anything other than plain water in a naptime or nighttime bottle. Children should not be allowed to bottle feed at will and should be weaned from the bottle by the age of 1 year. Many medically compromised individuals are likely to be assessed in the higher risk categories because of their use of certain medications and possible xerostomia. Source: American Dental Association Council on Access and Interprofessional Relations 1995. Caries diagnosis and risk assessment. A review of preventive strategies and management. JADA 1995; 126: 15-245. Copyright 1995 by American Dental Association. Reprinted by permission of ADA Publishing Co. inc. {2000}. TABLE 8.6 Sensitivity and specificity of selected dental caries diagnostic procedures Sensitivity Specificity bacteria in their infants and the degree of matching to maternal strains was higher for female infants than for males (Li and Caufield 1995). Based on a study of child-mother pairs (with the child initially at 1 year of age), the application of a 1.0 percent chlor- hexidine rinse alternated with a 0.2 percent sodium fluoride gel to the mother’s teeth (3 times per day on 2 consecutive days, twice per year for 3 years) delayed, and in some cases prevented, the colo- nization of their children’s teeth by mutans streptococci (Tenovuo et al. 1992). Timing of colonization has been shown to be correlated with caries prevalence. In a longi- tudinal study that followed chil- dren in 4-month intervals from 15 months to 4 years of age, children who were infected earlier had a higher caries prevalence than those in whom the infection was detected at later ages. Studies also have been aimed at reducing the levels of cariogenic bacteria in the infants themselves. Work continues on the devel- opment of a caries vaccine. One approach focuses on the produc- tion and release of antibodies against cariogenic bacteria anti- gens (Russell et al. 1995). Specific antigens have been purified and synthesized. Another approach involves biological replacement therapy, where nonpathogenic bacteria, instilled in the mouth, prevent pathogenic bacteria from colonizing (Hillman et al. 2000). Yet another approach employs pas- sive immunization in which anti- bodies, produced outside the body (in cultures, animals, eggs, oT plants), are applied to the teeth and oral tissues to protect against disease. A recent study indicated that “plantibodies” painted on the teeth could prevent mutans strep- tococci colonization for 120 days, the period of the experiment (Ma (percentage) (percentage) References Visual examination of noncavitated fissures 12-31 70-99 Lussi 1993, Ketley and Holt 1993 Examination using explorer 14-24 70-99 Penning et al. 1992, Lussi 1993 Radiographs of approximal lesions 50-90 85+ Grindahl 1989, Benn and Watson 1989 et al. 1998). 200 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health Treatment. Prompt UWeatment of early carious lesions permits the preservation of tooth structure through conservative approaches. A 10-year study reported that caries did not progress under a dental sealant placed over cavitated lesions where the lesions were no more than halfway through the dentin (Mertz- Fairhurst et al. 1998). Materials that can bond to enamel and to dentin continue to be refined and improved. Glass ionomer cements have contributed to materials that can bond to enamel and dentin, release fluoride, and increase remineralization in adjacent teeth (Mount and Hume 1998, Qvist et al. 1997). These cements, together with polymeric resin composites and hybrids of these two materials, are now available for tooth restoration with other materials. Based on the available materials and emerging techniques, such as air abrasion and laser ablation (Featherstone et al. 1998, Kantorowitz et al. 1998), restoration procedures are more conser- vative than ever before (Mount and Hume 1997). A proposed categorization of carious lesions for the purpose of conservative management places lesions into three categories: lesions where no treat- ment is advised, lesions where preventive care is advised, and lesions where restorative treatment is advised (Pitts and Longbottom 1995). This approach, using caries as an infectious disease para- digm, resulted in a marked reduction of operative procedures in Danish schoolchildren (Thylstrup et al. 1995) and has been proposed as a means to pre- serve tooth structure and maximize appropriate care in the United States (Ismail 1997). New imaging and laser technologies are emerg- ing as tools for early diagnosis and prompt treatment of dental caries. For example, quantitative light- induced fluorescence is showing promise (de Josselin de Jong et al. 1996) for dental caries diagnosis. Two different methods, the quantitative infrared laser flu- orescence method and electrical conductance meas- urements, are currently commercially available. At present, these methods are being used to augment conventional diagnostic tools but are not yet part of routine practice. However, they could potentially be used for close monitoring of the lesions and for patient motivation (Angmar-Mansson et al. 1996). Laser treatments for soft tissue surgery have been used in dentistry in recent years. Currently, in vitro studies are under way for the application of lasers for hard tissues, specifically to prevent dental caries by altering tooth mineral and inhibiting progression of artificial caries-like lesions (Featherstone et al. 1998, Kantorowitz et al. 1998). Despite the best efforts of the individual and health care provider, caries may progress. Advances in materials science over the last two decades have fortunately led to major improvements in dental restorative materials, resulting in a wide range of aes- thetically pleasing, longer-lasting restorations that can be placed with less trauma. Traditional materials such as amalgam fillings and gold crowns are now augmented by aesthetic materials, including bonded composite resins, porcelain fused to metal crowns, and facings. When teeth have been lost, the options for reha- bilitation include a range of prosthetic devices. Removable full and partial dentures and fixed bridges provide aesthetic and serviceable restorations for many patients. Still another option is the use of den- tal implants. These are used not onty in patients who have lost teeth due to caries and periodontal diseases, but also to restore form and function in patients treated for trauma, craniofacial cancers, hereditary tooth defects, and other abnormalities. The evidence base for the survival of the endosseous dental implants, an implant that is placed directly into a tooth socket, is extensive and has been recently reviewed (Cochran 1996, Fritz 1996). The predictability of endosseous dental implants in fully and partially edentulous patients has been clearly demonstrated in longitudinal studies (Albrektsson 1988, Albrektsson et al. 1988, Buser et al. 1991, Spiekermann et al. 1995). Many implant designs and surfaces have shown high success rates (often exceeding 95 percent in good-quality bone and 85 percent in poorer-quality bone, such as the posterior maxilla) (Buser et al. 1988, Cochran 1996, Fritz 1996). Rehabilitation of lost tooth structure or even the whole tooth itself may be revolutionized in the next century, based on discoveries of the natural repair and regeneration mechanisms the body uses. The new sciences of biomimetics and tissue engineering combine engineering principles and materials sci- ence with rapidly growing knowledge of the progen- itor cells and molecules that give rise to specific tis- sues such as skin, bone, teeth, and cartilage. Already it is possible to generate new cartilage and bone of a prescribed shape to replace tissue lost from injury or disease (Reddi 1995). Eventually, it may be possible to use a patient's own oral cells and cell products to generate new tooth enamel, dentin, and cementum for the natural repair of carious lesions. Periodontal Diseases Periodontal diseases are caused by microbial infec- tions, and are plaque-related complex diseases like dental caries, presenting as several clinical variants ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 201 Personal and Provider Approaches to Oral Health (see Chapter 3). The mildest form is gingivitis, char- acterized by inflammation of the gingiva with a marked loss of gingival collagenous material (Page and Schroeder 1976, Schroeder et al. 1973). In a more advanced disease, periodontitis, there is involvement of the soft tissue and bone that support the teeth. If untreated, periodontitis may progress and result in abscesses, mobile teeth, and tooth loss. Periodontitis also may be associated with certain sys- temic diseases and conditions (see Chapter 5). Gram-negative anaerobic bacteria in plaque are implicated as causative agents in periodontitis. However, host immune system factors, specifically, a chronic inflammatory response, are now considered to be the primary determinants of disease progression and outcome (Page 1998). The disease process is very similar across the different types of periodontal disease and involves interactions between infectious agents and their virulence factors and host defense mechanisms, operating within a context of environ- mental, acquired, and genetic risk factors specific to a given individual. Figure 8.5 illustrates the patho- genesis of these diseases (Page and Beck 1997). Risk Assessment. Sufficient knowledge of demograph- ic and systemic risk factors and indicators has been acquired to guide clinical decisions in the manage- ment of periodontal diseases (Genco 1996, 2000, Page and Beck 1997, Papapanou 1998). Table 8.7 provides an overview of the strength of the associa- tions of local and systemic factors with destructive periodontal diseases (Genco 1996, 2000). Table 8.8 presents the odds ratios derived from studies that investigated the likelihood of developing periodontal disease given a specific risk factor, indicator, or mark- er/predictor (Jeffcoat et al. 1997, Page and Beck 1997). The presence of pathogenic bacteria, poor oral hygiene, tobacco smoking, diabetes mellitus, and preexisting periodontal disease are some of the fac- tors that contribute to the likelihood of disease pres- ence, progression, and treatment outcomes. A systematic identification of risk factors, indica- tors, and predictors has been proposed as the first step in diagnosing and managing periodontal dis- eases (Genco 1996, Page and Beck 1997, Papapanou 1998). Clinicians can weigh the known risks for indi- vidual patients and devise treatment plans appropri- FIGURE 8.5 Anew paradigm for the pathobiology of periodontitis Antigens Lipopoly- saccharide virulence factors Environmental and acquired (behavioral) risk factors Antibody Cytokines & prostanoids . Polymorpho- Host Connective Clinical Microbial nuclear immuno- tissue signs of challenge neutrophils inflammatory and bone disease and response metabolism progression Matrix metallo- proteinases Genetic risk factors Source: Page and Kornman 1997. The pathogenesis of human periodontitis: an introduction. Periadontology 2000 1997; 14:9-11. Copyright 1997 by Periodontology 2000. Reprinted by permission of Munksgaard International Publishers Ltd., Copenhagen, Denmark (2000). 202 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health TABLE 8.7 The strength of association of local and systemic factors with destructive periodontal disease Case Report Case-Control Cross-sectional Longitudinal Factor Studies Studies Studies Studies Intervention Studies Specific bacteria P gingivalis Yes Yes " Yes Yes Yes B. forsythus Yes Yes Yes Yes Yes Pintermedia Yes Yes Yes Yes Yes Sex Male Yes NR Yes NR NR Age Yes Yes Yes No (to 7th decade) NR Diabetes mellitus Type 2 Yes Yes Yes Yes Yes (treatment reduces glycosylated hemoglobin) Type 1 Yes Yes Yes NR NR Smoking NR Yes Yes Yes Yes (smokers heal poorly) Osteoporosis Yes Yes Yes NR NR Stress, distress, coping Yes Yes Yes NR NR Polymorphonuclear disorders Yes Yes NR Yes (case series) NR Genetic factors (IL-1 polymorphisms) - NR Yes NR NR NR Dietary calcium NR Yes Yes NR NR Preexisting periodontal disease Yes Yes Yes Yes Yes Note: NR = not reported, or not relevant. Source: Genco 2000. Copyright 1996 by Journal of Periodontology. Reprinted by permission of the Journal of Periodontology (2000). TABLE 8.8 Risk of periodontal disease Strength af Association With Odds Ratio Demographic characteristics Age, 35-44 years alvealar bane loss 2.60 Age, 65-74 years alveolar bone loss 24.08 Risk factors Smoking, light periodontal disease 2.05 alveolar bone loss 1.48 Smoking, heavy periodontal disease 475 alveolar bone loss 7.28 Bacterial risk factors Pear oral hygiene periodontal disease 20.52 P gingivalis periodontal disease 3.60 A. actinomycetemcomitans periodontal disease 2.50 Clinical measurement Bleeding on probing? progression of periodontitis 27 aMeta-analysis (Armitage 1996). Sources: Jeffcoat et al. 1997, Page and Beck 1997. ate to their risk category. These same factors and the outcomes of treatment can also be used to assess prognosis upon completion of therapy. Studies are under way to determine the feasibility and validity of assessing a complex of risk factors to predict states of ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL periodontal health and disease (Genco 1996, 2000, Genco et al. 1999, Papapanou 1998). Most recently, putative genetic markers for sus- ceptibility for oral disease have been studied. In par- ticular, a specific genotype of the polymorphic IL-1 gene cluster has been shown to be associated with severe periodontitis in nonsmokers (Kornman et al. 1997). IL-1 is of interest because the proinflamma- tory cytokines are key regulators of the host immune response to microbial infection and extracellular matrix catabolism and bone resorption. Functionally, this polymorphism is associated with high levels of IL-1 production, and high levels of IL-1 have been associated with progressive periodontal breakdown (Cavanaugh et al. 1998). A consensus has been reached by a specialty organization that all patients in general and specialty care should be screened for periodontal disease (AAP 1996). The recommended approach is to apply the Periodontal Screening and Recording examination (PSR). Related screening tests include the Com- munity Periodontal Index of Treatment Needs (CPITN) (Ainamo et al. 1982) and the Basic Periodontal Examination. Diagnosis. The strengths and weaknesses of the range of tests and methods used to diagnose periodontal wd oo } Personal and Provider Approaches to Oral Health diseases are presented in Table 8.9. Most diagnostic tests for periodontal diseases rely on a physical examination to note any swelling, redness, gingival bleeding, or tooth mobility. Periodontal probing, radiographs, and microbiologic and_ histological examinations of biopsied tissue provide important - additional information. These tests indicate the presence, extent, and severity of gingival and periodontal tissue destruction; they do not indicate the cause of disease or whether it is quiescent or actively progressing. Gingival inflammation may be assessed using a variety of methods, including bleeding on probing and the use of indices such as the gingival index (Lée and Silness 1963) to grade redness and bleeding. In adult periodontitis, the absence of inflammation is associated with a lack of disease progression, but the presence of inflammation does not indicate inevi- table progression to destruction (Armitage 1996, Halazonetis et al. 1989, Okamoto et al. 1988). Longi- tudinal studies have also been conducted in patients who participate in maintenance programs. The absence of gingival bleeding, especially at recall vis- its, has been shown to be a valid indicator of gingival health in these patients (Lang et al. 1986). Measurement of probing depths (also termed pocket depths) is an integral part of the periodontal examination. Longitudinal studies have shown that shallow probing depths and minimal loss of attach- ment are associated with lack of disease progression. The mere presence of a pocket does not herald pro- gressive periodontitis at that site. Although teeth with moderate to deep probing depths are at higher risk for additional destruction, a single examination cannot determine the fate of the tooth with certainty (Armitage 1996, Haffajee et al. 1983, Halazonetis et al. 1989, Okamoto et al. 1988). Radiographs are used to obtain a visual image of the bony support around a tooth or dental implant. They are an essential tool in planning complex pros- thetic reconstructions, as well as a necessary diag- nostic aid in assessing periodontal progression. At least 15 different organisms have been associ- ated with adult periodontitis. The 3 species most and recording (PSR) practice Probing pocket depths _ All patients TABLE 8.9 Strengths and weaknesses of tests and methods used to diagnose periodontal diseases Application Strengths Weaknesses Type of Evidence Periodontal screening —_ All patients in every Cost-effective, quick, easy; detects Does not provide a tooth-by-tooth Epidemiologic studies patients with periodontal disease, Shallow probing depths are associated with lack of future disease progression. assessment for later comparison during maintenance. A full periodontal examination is needed for this purpose. Moderate to deep pockets in single probing depth examination will not distinguish with certainty which teeth will undergo progressive periodontal destruction. Longitudinal studies Gingival inflammation Radiographic evidence of bone loss Microbial/plaque tests Biochemical profiles in gingival crevicular fluid Assessed in all patients At-risk patients as determined by PSR screening or periodontal examination High-risk or refractory patients Not yet determined Absence of inflammation is associated with a lack of future progression. In treated patients, bleeding on probing is associated with an increased risk for pragressive loss of attachment. Absence of bone loss is associated with a lower risk of future progression. Absence of supragingival plaque is associated with lack of disease progression. In compromised or refractory patients, may be useful in determining the presence of pathogens. A number of biochemical markers may identify individuals at risk. Presence of inflammation will not distinguish with certainty which teeth will undergo progressive periodontal destruction. Presence of bone loss ona single radiograph will not distinguish with certainty which teeth will undergo progressive periodontal destruction. At this time, routine testing offers limited benefit in adult periodontitis. At present, there are no specific biochemical profiles that characterize specific periodontal diseases. Longitudinal studies Longitudinal studies Cross-sectional and Longitudinal studies Case reports Cross-sectional and Longitudinal studies 204 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health strongly linked are Porphyromonas gingivalis, Bacteroides forsythus, and Treponema denticola. Actinobacillus actinomycetemcomitans is most strong- ix linked to early-onset periodontitis (Haffajee and socransky 1994). No single bacterial species has been shown to satisfy Koch's postulates (Moore 1987, socransky and Haffajee 1992), leading some investi- wators to suspect that periodontitis is a mixed infec- o tion (Ranney 1993). As a result, diagnostic tests for periodontal diseases have included assessments of the presence and amount of several putative microbes in the subgingival plaque. Routine bacterial testing of patients with adult periodontitis is not usually necessary and indeed is not supported by the preponderance of the evidence (Armitage 1996, AAP 1996). In formulating treat- ment programs for special patient populations and as 4 research tool, however, the tests can be very help- ful. Such patients include those refractory to previous therapy, patients with rapidly progressive or early- onset periodontitis, and certain medically compro- mised patients. The traditional method for assessing the subgin- gival flora is by culturing samples extracted from the site of infection. Culturing allows the clinician to determine the antibiotic sensitivity of the organisms, but it is technique-sensitive: scrupulous care is required when sampling the periodontal pocket. This is especially true for microbes that are strict anaer- obes, because they are killed by even brief exposure to air. The requirement that bacteria have time to grow also precludes chairside testing. With the advent of molecular biology, bacterial species can be identified by their DNA (Moncla et al. 1988, Savitt et al. 1988, 1990) or by unique antigenic components (Zambon et al. 1986). Either method will detect putative periodontopathic bacteria quick- ly and with a high degree of sensitivity and specifici- ty, usually above 90 percent. The tests do not indicate whether there is actual disease, however. Nor do the tests reveal anything about the antibiotic sensitivity of the detected bacteria. Because DNA is very stable, the tests can be applied to nonliving plaque samples, simplifying the collection process. Kits are available that allow DNA testing to be performed in the dental office; otherwise the samples are sent to a reference laboratory. Other tests are available for the detection of groups of putative periodontopathic bacteria (Loesche 1986). The BANA test detects a trypsin-like enzyme that is present in P gingivalis, T. denticola, and B. forsythus (Loesche et al. 1990). Somewhat less accurate than the tests described above, the BANA test is 92 percent sensitive and 70 percent specific in detecting these groups of bacteria. Once a periodontal infection is established, tell- tale metabolic changes occur in the body as a result of inflammation, injury, or death of tissue. A sample of fluid exudate from the gingiva (gingival crevicular fluid) in an affected pocket can be analyzed for these changes. They include elevated levels of prostaglandin E, (Cavanaugh et al. 1998, Offenbacher et al. 1986), interleukin 1 and inter- leukin 6 (Cavanaugh et al. 1998, Geivelis et al. 1993, Masada et al. 1990, Tsai et al. 1995), tumor necrosis factor (Rossomando et al. 1990), B-glucuronidase (Lamster et al. 1994, 1995), aspartate aminotrans- ferase (Chambers et al. 1991, Persson and Page 1992), elastase (Armitage et al. 1994, Palcanis et al. 1992), and collagenase (Lee et al. 1995). Most of these analyses are based on inserting a filter paper strip into the isolated pocket to collect the fluid and testing for the metabolite of interest. A positive result usually indicates that inflammatory or destructive pathways have been triggered, but provides no clues concerning the etiologic factor or factors. Because of differences in experimental designs in the clinical studies, it is difficult to compare the sensitivity and specificity of each metabolite in detecting disease. Prevention. Because periodontal diseases are plaque- associated infections, prevention and management of the early signs of these diseases depend on effective plaque control. This can be accomplished using both mechanical and chemotherapeutic approaches (Table 8.10). The prophylaxis performed in the dental office on periodontally healthy patients reduces plaque and removes stains and calculus. How often patients should be recalled for such preventive procedures is based on an assessment of risk factors such as the patients age, oral hygiene, personal habits (e.g., smoking and diet), and a medical history indicating a heightened risk of infection (such as noted with dia- betes or HIV infection) (Hancock 1996, Mealey 1996). Chemical plaque control has become an impor- tant part of the clinician's armamentarium and may be prescribed for patient care at home (Table 8.10). Reviews of the literature by Hancock (1996) and Drisko (1996) provide detailed supporting evidence. Significant reductions in gingival inflammation have been demonstrated for chlorhexidine, triclosan co- polymer when used in conjunction with a fixed com- bination of essential oils, and stannous fluoride. The magnitude of gingival inflammation reduction was greatest for chlorhexidine. The evidence supporting ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 205 Personal and Provider Approaches to Oral Health these effects includes multiple randomized, double- blind, controlled clinical trials. Treatment. Once periodontal disease is established, the resultant bone and connective tissue loss may be quiescent or actively progressing. The goal of treat- ment is to determine whether the disease is active in order to prevent further tissue loss. This entails pro- fessional plaque removal and careful instruction of the patient on scrupulous self-care. The concept of management of a patient's risk factors as part of treatment is reasonably well docu- mented for individuals who smoke and those who are diabetic and may be important for other risk fac- tors such as stress (Genco et al. 1999) and low dietary calcium (Nishida et al. in press). Several stud- ies have shown that treatment of periodontal disease in smokers is not as successful as in nonsmokers (Grossi et al. 1996). Thus, the management of smok- ing as a risk factor will contribute to the success of periodontal therapy. Furthermore, it appears that treatment of diabetic patients with periodontal dis- ease may require more intense therapy since several studies have shown that antibiotic therapy is suc- cessful not only in reducing periodontal disease, but also in reducing glycated hemoglobin (Grossi and Genco 1998). Professional plaque removal typically employs scaling and root planing, in which hardened deposits _ of plaque and other debris are removed from the peri- odontal pocket and the tooth root surface is smoothed over. The effectiveness of scaling and root planing has been demonstrated repeatedly in longi- tudinal, cohort, and randomized clinical trials and was reviewed by Cobb (1996). Demonstrated bene- fits include decreased gingival inflammation, decreased probing depth, and facilitation of mainte- nance of clinical attachment level. The evidence indi- cates that similar results may be obtained with ultra- sonic and sonic instruments as with manual instru- ments. Regardless of the methods used, meticulous attention to detail is required to achieve optimal results (Cobb 1996). TABLE 8.10 Periodontal diseases: mechanical therapy and chemotherapeutics Category of Treatment Treatment Professional mechanical therapy—used in the treatment of gingivitis and periodontitis Scaling and root planing with Manual instrument Ultrasonic and sonic scaling and used as an adjunct to brushing —_ gingivitis Sustained release anti- intrapocket resorbable or non- Strengths Decreases gingival inflammation Requires attention to detail by 40 to 60 percent Decreases probing depth Facilitates gain in clinical attachment level Results are similar to manual Significant reductions in gingival No clear evidence that there is root planing scaling and root planing Chemical plaque control == Chlorhexidine with mouthrinses and Triclosan co-polymer or triclosan inflammation dentifrices zinc-citrate Essential oils Stannous fluoride Irrigation Supra- and subgingival irrigation Aids in the reduction of When used as an adjunct to Weaknesses Type of Evidence Numerous longitudinal, cohort, and randomized clinical trials Longitudinal, cohort, and randomized clinical trials Randomized double-blind a substantial long-term clinical trials benefit for periodontitis except to control co-existing inflammation Randomized double-blind clinical trials No clear evidence that there is a substantial long-term benefit for periodontitis Few reported side effects Randomized double-blind microbials resorbable delivery systems scaling and root planing, gains in include transient discomfort, clinical trials containing a tetracycline clinical attachment level and erythema, recession, allergy, antibiotic decreases in probing depth and —_ and rarely candidiasis bleeding Systemic antibiotics Tetracyclines, metronidazole, May be useful to treat aggressive Not indicated for gingivitis Assessment of risk-benefit spiromycin, clindamycin, and destructive periodontitis Not indicated for most adult ratio combinations such as periodontitis patients Randomized double-blind metronidazole and amoxicillin clinical trials Randomized double-blind clinical trials, longitudinal assessment of patients 206 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Personal and Provider Approaches to Oral Health Topical administration of antimicrobial agents contributes to the control of gingival inflammation Table 8.10). Supragingival irrigation (e.g., applying a jet of water under pressure) may be used as an adjunct to toothbrushing and has been shown to aid in the reduction of gingival inflammation. However, no clear substantial long-term benefits for the treat- ment of periodontitis have been shown if irrigation is applied subgingivally. Surgical therapy is employed to provide access to root surfaces and bony defects for debridement and root planing. Surgery can facilitate regeneration, augment the gingiva, and promote root coverage Table 8.11). It is also necessary in placing dental implants. Palcanis (1996) reviewed the evidence regarding surgical therapy. The overall goal is to make plaque control easier for the patient, thereby reducing dis- ease progression. Many surgical techniques are avail- able. Extensive randomized clinical trials and longi- tudinal studies form the basis of the evidence for the efficacy of these procedures (Kaldhal et al. 1996, Knowles et al. 1979, Pihlstrom et al. 1983, Ramfjord et al. 1987). All procedures decrease pocket depth, and, with the exception of gingivectomy, all increase clinical attachment level. A caveat to be noted, how- ever, is that procedures designed to reduce probing depth may increase gum recession, exposing the root and possibly compromising aesthetics. Thus, selec- tion of a particular surgical procedure must always be based on the individual needs of the patient. Regardless of the approach selected, maintenance is important to long-term success. Systemic administration of antibiotics, including the tetracyclines, metronidazole, spiromycin, and clindamycin, has been extensively studied and reviewed (Drisko 1996). The risk of generating antibiotic resistance in bacteria precludes the use of systemic agents in treating simple gingivitis (AAP 1996). Similarly, systemic antibiotics should not be used for the routine first-line treatment of common forms of adult periodontitis (AAP 1996, Drisko 1996). The preponderance of evidence from well- controlled, randomized, blinded clinical trials indi- cates that the agents do not offer sufficient benefit to overcome risks of either drug sensitivity or the emer- gence of antibiotic-resistant pathogens. The situation is different in cases of aggressive forms of periodontitis, such as early-onset, rapidly progressive, or refractory periodontitis, which affect less than 10 percent of periodontitis patients. Randomized, double-blind clinical trials, as well as longitudinal assessments, indicate that the use of sys- temic antibiotics can slow disease progression in these patients (AAP 1996, Drisko 1996). To circumvent the problems of systemic therapy, investigators have applied antimicrobial agents directly into the pocket. Antimicrobials incorporat- ed into either resorbable and nonresorbable inter- pocket delivery systems have been studied in ran- domized, double-blind, controlled clinical trials and are now FDA approved and on the market (Goodson et al. 1991, Jeffcoat et al. 1998). When used as an adjunct to scaling and root planing, gains in clinical attachment level and decreases in probing depth and gingival bleeding were demonstrated. Because control, and enhances width. TABLE 8.11 Periodontal disease: selected surgical procedures Category and Goal Procedures Strengths Weaknesses Type of Evidence Pocket therapy— Modified Widman Flap to All procedures decrease pocket depth. Procedures designed to Randomized clinical trials provides access to root provide access to roots and With the exception of gingivectomy, all reduce probing depths Longitudinal studies surfaces and bony bony defects for increase clinical attachment level may increase recession. defects, reduces probing debridement Lack of i a After 5 years, greatest reduction in probin ack of professional depths, facilitates plaque Apically repositioned flap years, 9 maintenance and depth with osseous Tecontouring. ‘ ; with or without bony . . . restorative and cosmetic recontouring Apically repositioned flap with or without dentistry . bony recontouring used in crown- Gingivectomy lengthening procedures to provide biologic patient compliance can be detrimental to long- term success. ee 3Certain systemic tetracyclines, notably doxycycline, are safe an d effective in low doses for prevention of bone loss associated with periodontitis. Doxycycline hyclate (20-mg capsule) is approved for twice-a-day use for up to 9 months for this indication. At these low doses, the doxycycline appears to reduce the elevated collagenase activity, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL rather than function as an antimicrobial. 207 Personal and Provider Approaches to Oral Health these delivery systems are relative- ly new, there is a paucity of evi- dence addressing their long-term effectiveness. For patients who have lost sig- nificant bone and/or connective tis- sue, there are a number of regener- ation procedures to facilitate the growth of new periodontal liga- ment, cementum, and alveolar bone over previously diseased root surfaces. The evidence base for bone-grafting techniques using either natural or synthetic bone materials has been reviewed by Garrett (1996). Natural bone grafts may use autografts, in which bone is transferred from one site to another in the same patient; allo- grafts, which use bone grafts from a human donor, and xenografts, which use tissues from other species. Limited case report evi- dence shows that extraoral auto- genous bone, such as hip grafts, has high potential for bone growth (Garrett 1996). Extraoral sites require a second surgical site, and in some cases fresh grafts may be associated with root resorption. Case report evidence indicates bone fill exceeding 50 percent of the osseous defect may be achieved (Garrett 1996). Controlled studies comparing grafted to nongrafted sites report significant improve- ments in clinical attachment levels and bone gain, but the magnitude of gain is less than that indicated in case reports. Freeze-dried demineralized bone represents one of the most frequently used and well-studied bone graft materials in periodon- tics. Freeze-dried demineralized bone is an allograft material, har- vested, prepared, and demineral- ized prior to grafting. The deminer- alization step is important because it retains the activity of bone mor- TABLE 8.1l2a Odds ratios for risk factors for oral and pharyngeal cancers Both Sexes Males — Females Cigarettes: Never 1.0 1.0 Ever 19 3.0 Smoking status, adjusted for alcohol drinking? None 1.0 1.0 Short duration/former 14 4.0 1 to 19 per day for 20+ years 1.6 3.0 20 to 39 per day for 20+ years 2.8 4.4 40+ per day for 20+ years 44 10.2 Cigars? Never 1.0 _ Ever 2.8 _ Pipes? Never 1.0 _ Ever 18 _— Smokeless tobacco among nonsmokers! Never _ 1.0 Ever _— 6.2 Number of drinks of beer per week, adjusting for smoking? <1 10 1.0 1to4 1.2 2.2 5to 14 17 29 15 to 29 3.4 23 30+ 47 18.0 Number of drinks of hard liquor per week, adjusting for smoking? 0.2 3.1 14 42 (28 16 034338 <0,5% 0.3% 0.2% 0.3% 3% 1.5% <0.2% <0.1% Sources: Data from PHS Oral Health Coordinating Committee, personal communication, 2000, Public Health Functions Steering Committee 2000. 226 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL demiologic and other public health expertise .ASTDD 3000). Similar gaps occur in many local public health departments that lack adequate oral health programs OT appropriately trained personnel “USDHHS 2000). Public health agencies at all levels have identified disparities in oral health and access to care, in terms af both population subgroups and geographical areas. In 1998, there were 1,036 dental Health Professional Shortage Areas (HPSAs), which required 3.98+ dentists. Of 686 consolidated Community Health Center grantees, 385 (or 56 percent) provide dental services (j. Anderson, HRSA, personal com- munication, 1999). Community Health Centers provide preventive and basic dental care to 1.2 million patients nation- wide (HRSA 1998). Health Centers are located in medically underserved urban and rural areas and tar- get low-income, migrant, homeless, and other disad- vantaged populations. Individuals pay for dental services on a sliding fee scale adjusted by their abili- ty to pay. Health Centers are a primary source of care for 2.84 million Medicaid-eligible individuals, who make up 33 percent of Health Center clients. An additional 3.55 million uninsured patients represent 41 percent of their clients (HRSA 1998). Health Centers that provide oral health care include it as part of an integrated primary care system. In addi- tion, federal programs such as the National Health Service Corps offer scholarships and loan repayment opportunities to encourage newly licensed dentists to locate in underserved areas. Areas of Overlap The various components of oral health care work together in diagnosis, prevention, and treatment services. AS mentioned above, dental and medical specialists work on teams treating patients with cran- iofacial birth defects. Oncologists, radiologists, oto- laryngologists, plastic surgeons, and surgeons spe- cializing in head and neck surgery similarly may part- ner with oral and maxillofacial surgeons and prostho- dontists in treating oral and pharyngeal cancers and other tumors of the oral cavity and pharynx. Dentists also are active members of general oncology teams. They participate in the examination of patients about to undergo chemotherapy, radiation, or bone marrow transplantation, for example, to ensure that proven preventive measures are taken before treatment to minimize the effects of the therapy on the oral mucosa, salivary glands, and dentition. Private medical and public health professionals often collaborate in implementing immunization Provision of Oral Health Care programs and other preventive strategies to reduce a specific disease or to change risk behaviors. Similarly, dental personnel in the private and public sectors cooperate in the implementation of mouthguard pro- grams for sports injury prevention, statewide pro- grams to apply sealants to the teeth of low-income children, and the promotion of oral health self-care behaviors. Private practitioners can deliver care that is paid for by public programs or can work as con- tractors to Migrant and Community Health Centers and local health departments, among others. Finally, all three components can work together to promote programs that address cross-cutting issues such as tobacco cessation and the prevention and control of HIV disease, oral and pharyngeal cancers, and early childhood caries. EXPENDITURES FOR ORAL HEALTH CARE The $1.1 trillion spent in the United States on health care services in 1998 includes the cost of hospital care, physician and dental services, home health care, nursing home care, prescription drugs, medical equipment, private health insurance, public health activities, and research and represents an increase of 5.6 percent from 1997 (HCFA 2000b). Analysts proj- ect that this amount will double by 2007 to total more than $2.1 trillion (HCFA 2000a). Expenditures for dental services in the United States in 1998 were $53.8 billion, a 5.3 percent increase from 1997 and 4.7 percent of the total spent on health care that year (Table 9.3 and Figure 9.2). This figure is an undercount, however, because it rep- resents only those costs associated with care deliv- ered by dentists in practice settings. A generation ear- lier, in 1960, $2 billion was spent on dental care, which represented 7.3 percent of that year’s total | 5 IGURE 9.2 Dental services as a percentage of total U.S. health care expenditures by type of service, 1997 Dental Services Nursing Home Care | 8% Drugs and Other Hospital Care Medical Nondurables : 34% 10% Physician Services 20% Other Source: HCFA 2000a. 23% ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 227 Provision of Oral Health Care health care expenditures. During the 1970s, dental expenditures grew at approximately the same rate as personal health care expenditures, with both exceed- ing the growth of the economy overall. But starting in 1978, dental expenditures began to flatten and, until 1994, increased more slowly than expenditures for personal health care. Since 1994, dental expenditures have increased at a higher rate than personal health care expenditures (Levit et al. 1998). Real per capita dental care expenditures (1995 dollars) are currently at about the level they were in the early 1980s, and in some years have declined (Figure 9.3) (ADA 1997b, Beazoglou et al. 1993, Beazoglou 1998). The American Dental Association estimated that $174.12 was spent per capita in 1995 for dental services (ADA 1997b); HCFA estimated the same year's per capita consumer expenditures for dental services at $164 (U.S. Bureau of the Census 1998). The annual percentage change in fees for med- ical, physician, and dental services as measured by the Consumer Price Index (CPI) has generally exceeded that for the index as a whole (U.S. Bureau of Labor Statistics 1999) (Table 9.4 and Figure 9.4). Percentage changes in the dental CPI have generally followed those for other medical services; since 1983, however, prices for dental services have increased at a rate faster than those for physician and all medical services. These trends signal different market forces for dental care services as compared to other health services. In addition to dental care expenditures for serv- ices provided by dentists in practice settings, the full cost of oral health care in the United States must take into consideration the breadth of oral, dental, and craniofacial conditions for which services are provid- ed in hospital and other institutional settings, often by nondentists. For example, the Healthcare Cost and Utilization Project (2000) estimated inpatient hospital charges for diseases of the mouth and disor- ders of the teeth and jaw to be $451 million in 1996. Estimates for the management of severe early child- hood caries range from $1,500 to $2,000, depending on whether hospitalization is necessary (Griffin et al. 2000, Kanellis et al. 2000). In lowa the average cost of treating this condition in a hospital operating room was estimated to be $2,578 (Damiano et al. 1996). In California, the lifetime cost per case for cleft lip/palate repair is estimated at $101,000 (Waitzman et al. 1996). TABLE 9.3 U.S. national health expenditures by source of funds and type of expenditure, 1998 (S billions) Private Government Consumer All Private Out of Private State and Total Funds Total © Pocket Insurance Other Total Federal Local National health expenditures 1,149.1 626.4 574.6 199.5 375.0 518 522.7 376.9 145.8 Health services and supplies 4,113.7 613.4 574.6 199.5 375.0 38.8 500.4 360.4 140.0 Personal health care 1,019.3 $74.5 536.5 199.5 337.0 37.9 444.9 343.6 101.3 Hospital care 382.8 149.9 130.9 12.8 118.0 = 19.1 232.9 187.4 45.5 Physician services 229.5 156.2 151.7 35.7 116.0 45 7333 60.8 12.4 Dental services 53.8 51.5 51.3 25.8 25.5 0.2 23 13 1.0 Other professional services 66.6 52.4 474 27.2 20.2 5.0 14.2 11.2 3.0 Home health care 29,3 137 10.0 6.0 40 37 15.5 3.1 2.4 Drugs and other medical nondurables 121.9 103.1 103.1 55.4 478 — 18.8 10.7 8.1 Vision products and other medical durables 15.5 9.0 9.0 8.2 0.8 — 6.5 6.4 0.1 Nursing home care 87.8 34.8 33.2 28.5 47 1.6 53.0 35.4 177 Other personal health care 32.1 3.8 _ _— _ 3.8 28.3 17.1 11.2 Program administration and net cost of private health insurance 577 38.9 38.0 _— 38.0 0.9 18.8 12.6 6.2 Government public health activities 36.6 _ _ _ _-_ = 36.6 42 32.4 Research and construction 35.3 13.0 _ —_ — 130 22.3 16.5 5.8 Research 19.9 1.6 _— _— _— 1.6 18.3 15.5 2.8 Construction 15.5 11.5 —_ _— — 115 40 1.0 3.0 Note: Research and development expenditures of drug companies and other manufacturers and providers of medical equipment and supplies are excluded from research expenditures, but are included in the expenditure class in which the product falls. Numbers may not add to totals because of rounding. Source: HCFA 2000b. 228 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL FINANCING AND REIMBURSEMENT Dental care is financed principally through private eources, either as out-of-pocket payments made directly to the dentist or through employment-based dental insurance benefits. Since 1960, these two sources have financed over 93 percent of all dental expenditures (Figure 9.5). Table 9.5 shows the change in contributions for dental expenditures from 1970 to 1996. The proportion of dental expenditures that private dental insurance covers has increased over the past two decades. Dental insurance now contributes about 48 percent of dental expenditures, 4s compared to 50.1 percent contributed by medical insurance for physician services. In contrast, the per- centage of out-of-pocket payments for dental servic- es is over 3 times that for physician services (Figure 9.6). Sharp differences are also evident in terms of federal, state, and local government contributions to the cost of dental care as compared to physician serv- ices. Only 4.0 percent of dental care costs, or $2.3 bil- lion in 1998, is financed publicly (largely through federal-state Medicaid programs), compared to 32.2 percent for medical care. Few hospital dental servic- es are reimbursed by Medicare, and state Medicaid programs may provide low reimbursement for dental Provision of Oral Health Care services. In contrast, public sources pay a large part of hospital costs for medical care. Insurance Insurance is a major determinant of dental utiliza- tion: 70.4 percent of individuals with private dental insurance reported seeing a dentist in the past year, compared to 50.8 percent of those without dental insurance (Bloom et al. 1992). Private dental care benefits are available to most full-time employees (59 percent) in medium-sized and large businesses. Fewer small businesses offer dental benefits. For the 22.6 million employees with employer-provided den- tal benefits, dental care may be offered as part of a comprehensive medical and dental plan or as a sepa- rate plan. Firms often offer employees a choice of medical plans as well as a separate dental plan that can accompany any medical plan. For employees with employer-provided dental benefits, 81 percent received care through fee-for-service plans, 11 per- cent from preferred provider organizations, and 8 percent from health maintenance organizations (HMOs) in 1998 (EBRI 1998). FIGURE 9.3 Per capita dental expenditures in current and real (1995) dollars, United States, 1970 to 1995 180 160 140 120 5 100 ‘eo a 80 60 40 20 0 TT T T T T T T T T T T T T = = x 2 2 3 oS oS 3 =) a S a = = = = = = i = = = = = = Year —» Per Capita Expenditures = Real (1995) Per Capita Expenditures Sources: U.S. Bureau of the Census 1998, U.S. Bureau of Labor Statistics 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 229 Provision of Oral Health Care Most participants in employer dental plans receive benefits through a fee-for-service plan, which reimburses patients or providers after services are received. Such plans are commonly obtained through a commercial insurer, or are self-insured (the firm sets aside funds to meet expected charges), or are a combination of the two. Among self-insured plans is a type of dental plan called direct reimbursement, which enables patients to pay the dentist directly based on what they have been charged. The patients are reimbursed by the plan based on their expendi- tures, up to a predetermined limit for total expendi- tures, but not according to the type of service they receive. Dental insurance plans that reimburse dentists by type of service performed typically cover technical procedures but not counseling services, treatment planning, or disease management. Diagnostic and preventive care usually includes dental examinations, prophylaxes, sealants, and radiographs. Restorative procedures may be limited to fill- ings, but may include crowns. TABLE 9.4 Other services that may be covered Consumer Price Index for dental services, physician services, all medical care, and all include périodontal care, endo- items, United States, 1960 to 1997 dontic care, prosthetics, and oral All All Dental? ~—s«Dental/-~—sCDental/ surgery. Orthodontic care 15 Cov- Dental Physician Medical Items Physician All Medical All Items ered less often by dental plans than 1960 27.0 19 23 296 1B 121 091 are other procedures. In addition, 1961 mA 22.4 229 29.9 121 1.18 0.91 most plans limit orthodontic cov- 1962 27.8 23.1 235 30.2 1.20 1.18 0.92 erage to dependent children and 1963 28.6 23.6 24.1 30.6 121 1.19 0.93 set maximum allowable payments. 1964 29.4 242 246 31.0 121 1.20 0.95 Dental implants, cosmetic proce- 1965 30.3 25.1 25.2 315 1.21 1.20 0.96 dures, and some preexisting condi- 1966 313 26.5 26.3 32.4 1.18 1.19 0.97 tions typically are not covered. 1967 32.8 28.4 28.2 33.4 4.15 1.16 0.98 Dental insurance plans are 1968 34.6 30.0 29.9 34.8 1.15 1.16 0.99 similar to medical plans in defin- 1969 37.1 32.1 19 36.7 1.16 1.16 1.01 ing the terms of payment on a fee- 1970 39.2 345 34.0 38.8 1.14 1.15 1.01 for-service basis. Typically, they 1971 41] 36.9 36.1 40.5 1.13 1.16 1.03 may pay a percentage of the fee: 1972 434 38.0 73 418 1.14 1.16 1.04 - , 1973 448 39,3 38.8 44.4 1.14 1.15 1.01 they may pay up to a specified dol- 1974 48.2 429 424 49,3 1.12 1.14 0.98 lar amount using a table of 1975 53.2 48.1 475 53.8 W 112 0.99 allowances; they may require the 1976 56.5 53.5 52.0 56.9 1.06 1.09 0.99 patient to pay initial costs up to a 1977 60.8 58.5 57.0 60.6 1.04 1.07 1.00 fixed amount (a deductible); or 1978 65.1 63.4 618 65.2 1.03 1.05 1.00 they may pay a varying percentage 1979 70.5 69.2 67.5 72.6 1.02 1.04 0.97 of dental charges, based on a 1980 78.9 76.5 74.9 82.4 1.03 1.05 0.96 patient's past use of dental services. 1981 86.5 84.9 82.9 90.9 1.02 1.04 0.95 In all cases, the patient pays the 1982 93.1 92.9 92.5 96.5 1.00 1.01 0.96 difference. Copayments are a larg- 1983 99.4 100.1 100.6 99.6 0.99 0.99 1.00 er percentage of the total cost of 1984 107.5 107.0 106.8 103.9 1,00 1.01 1.03 1985 1142 133 «135 ~—*1076 1.01 1.01 1.06 dental care than is the case for 1986 120.6 121.5 122.0 109.6 0.99 0.99 1.10 medical care. 1987 128.8 130.4 130.1 113.6 0.99 0.99 1.13 Dental coverage varies by 1988 137.5 139.8 138.6 118.3 0.98 0.99 1.16 race/ethnicity, income, and 1989 146.0 150.1 149.2 124.0 0.97 0.98 1.18 educational levels. Whites (41.8 1990 155.8 160.8 162.8 130.7 0.97 0.96 1.19 percent), people with 13 years or 1991 167.4 170.5 177.0 136.2 0.98 0.95 1B more of education (51.4 percent), 1992 178.7 181.2 190.1 1403 0.99 0.94 1.27 and families with annual incomes 1993 188.1 1913 2014 144.5 0.98 0.93 1.30 of $35,000 or more (60.8 percent) me tment a | have the hight prea o 1996 2165 164 2282 156.9 1.00 0.95 1.38 demographic categories (F veut 1997 226.6 229 234.6 160.5 1.02 0.97 141 9.7). Hispanic individuals have the Source: U.S. Bureau of Labor Statistics 1999. lowest percentage of coverage 230 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Provision of Oral Health Care Source: U.S. Bureau of Labor Statistics 1999. Sources: HCFA 200 BLE 9 (29.7 percent), followed by blacks TABLE 9.5 ; - (32.4 percent), a pattern seen in y.5. national expenditures on dental services, 1970 to 1996 ($ millions) medical insurance as well. Because Total Dental Out-of-Pocket Private Health Other Private Public Funds private dental insurance is Expenditures Payments Insurance Funds (Medicaid, etc.) typically an employment-related 1970 4,669 4,240 12 0 27 benefit, some individuals lose their 1971 5,181 4,672 248 0 261 dental coverage when they retire. 1972 5,516 4,934 292 0 290 As a consequence, people 65 and 1973 6,323 5,605 378 4 336 older reported the lowest levels of 1974 7,076 6,130 550 7 389 coverage (NCHS 1992). 1975 7,956 6,530 939 a 475 Although over 14 percent of "9 woes - ro , a children under 18 have no form of 197 A : : : : ' ' rivate or public medical insur- 978 10,957 7918 2,508 2 7 vce more Chan ewice that man 1979 11,893 8,237 3,072 27 557 a ‘thon children, fh 4 x 1980 13,323 8,833 3,811 27 652 ‘ million children, have no aenta 1981 15,698 10,082 4,839 39 738 insurance (Vargas et al. 2000). Over 1982 16,953 10,547 5,737 rr) 626 15 percent of persons 18 and older 1983 18,271 11,010 6,578 44 639 have no form of medical insur- 1984 19,833 11,578 7,613 51 591 ance, but 3 times as many, over 85 1985 21,650 12,243 8,682 B 653 million persons, have no form of 1986 23,108 12,658 9,677 81 693 dental insurance (NCHS 2000). 1987 25,343 13,118 11,409 86 730 1988 27,460 13,845 12,758 94 763 1989 29,496 14,485 14,115 110 786 The Changing Market 1990 31,566 15,389 15,134 124 919 . : . 1991 33,348 16,139 15,948 134 1,127 Increasingly, private dental insur- 1992 37,013 17,782 17,686 143 1,402 ance plans are entering into con- 1993 39,099 18,647 18,398 154 1,900 tractual agreements with dentists. 1994 41,665 19,727 19,798 167 1,974 The purpose of these agreements is 1995 44,695 21,007 21,477 173 2,038 to shift some or all of the financial 1996 47,551 22,116 23,166 183 2,086 tisk to the clinician, the benefici- Source: HCFA 2000b. ary, or both. These alternative FIGURE 9.4 FIGURE 9.5 Ratio of dental services CPI to physician services CPI, all medical Percentage of total U.S. dental expenditures by care CPI, and all items CPI, 1960 to 1997 source and year, 1960 to 1996 1.60 100 ammeguie 1.40 5 90 Pac Ser eel 1.20 4 80 1.00 4 am 70 Eu US CLG So S 0804 gz, 60 ce a 060 4 e 50 Out of Pocket 0 & 4 020 4 30 20 0.00 TTTTTTITITT!I TYTTTrTTtTTY! TITTTTTIT I TTTTTT! SSESSLATLRSSSSSRRES 10 RRRRRRTRARRSSSAS ASS Year 0 . 3S z 3 & a Dental Services -e Dental Services -e- Dental Services x a Ss s 2 CPI/All tems CPI CPI/All Medical cPl/Physician Year Care CPI Services CPI 0b, U.S. Bureau of the Census 1998,U.5. Bureau of Labor Statistics 1999. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 231 Provision of Oral Health Care reimbursement systems have been labeled “managed dental care.” As defined by the Physician Payment Review Commission (1997), managed care is “any system of health services payment or delivery arrangements where the health plan attempts to con- trol or coordinate use of health services by its enrolled members in order to contain health expen- ditures, improve quality, or both.” In dentistry the primary alternative reimburse- ment systems in place are the dental health mainte- FIGURE 9.6 Source of funds for dental and physician services, United States, 1997 Out of pocket Private insurance Federal State and local 0 10 20 30 40 50 60 Percentage @ Dental Service Source: York et al. 1995. Wi Physician Service nance organization, dental preferred provider organi- zation (PPO), and dental referral network. Between 1995 and 1996, dental HMO enrollment grew 17.7 percent; it grew another 8.6 percent between 1996 and 1997, for a total enrollment of approximately 26.5 million people: Dental PPO enrollment grew 30.9 percent in 1996 and 32.6 percent in 1997 toa total of about 24.5 million people (Table 9.6). Dental indemnity increased by 10.1 percent in 1996 and 2.6 percent in 1997 to about 90.6 million persons (NADP 1998). By comparison, the Health Care Financing Administration reported an increased shift of employers and employees from indemnity to man- aged care health plans, in the past several years. According to HCFA, 86 percent of all insured work- ers were covered by managed care health plans in 1998, an increase of 54 percent over 1993 (HCFA 2000b). The rapid changes in the health care environ- ment have emphasized the development of perform- ance measures that can be used by both public and private purchasers of care, consumers, and health care professionals. Specifically, health care quality oversight has focused on the collection and use of data that provide the basis for assessing and moni- toring care delivery performance. These performance FIGURE 9.7 Dental insurance coverage, United States, 1989 Percentage of persons aged 2 and older who are covered by private dental insurance, by sex Male 41.4 Female 39.6 i T T T T T T 1 0 10 20 30 40 50 60 70 Percentage of persons aged 2 and older who are covered by private dental insurance, by race/ethnicity White 418 Black 32.4 Hispanic 297 Qo —_ Qo Ww Oo w Qo in Qo nn oOo — Qa Sources: ADA 1997b, NCHS 1992. Percentage of families with private dental insurance with an annual income of <$10,000 $10,000 to $19,999 $20,000 ta $34,999 $35,000+ 0 10 20 30 40 50 60 70 Percentage of persons with private dental insurance with an education level of Less than 9 years 9 to 11 years 12 years 13 years or more 70 232 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL or outcome measures require development and test- ing to determine their reliability and validity, and depend on enhanced data collection and information eystems for their application. An example of per- jarmance measures 1s the Health Plan Employer Data and Information Set (HEDIS), a set of standardized measures developed by the National Committee for Quality Assurance. Recently, pediatric oral health measures have been reviewed and additional meas- ures proposed for HEDIS consideration (Crall et al. 1999). A framework for the development of outcome measures for oral health care has been proposed along four dimensions: biologic, clinical, psychoso- cial, and economic. This schema is designed for potential use by patients, health care providers, pur- chasers of care, and the public (Bader and Ismail 1999). Efforts are needed to proceed with the devel- opment and testing of reliable and valid outcome measures in all four dimensions for oral health care and their incorporation into practice and programs. Federal and State Programs Medicaid The Medicaid program, established as Title XIX of the Social Security Amendments of 1965, was designed to provide health care for all indigent and medically indigent persons, with funding shared between federal and state governments. Although states differ in eligibility rules and expenditures for services provided, amendments to the Medicaid pro- gram instituted in 1968 required all states to include dental care for individuals under 21 years of age as part of the Early and Periodic Screening, Diag- nostic, and Treatment (EPSDT) service. In addition, the Omnibus Budget Reconciliation Act of 1989 required the provision of all medically needed dental services for EPSDT beneficiaries beyond what is cov- ered under the state's Medicaid plan. Medicaid funds Provision of Oral Health Care dental care for low-income individuals and persons with disabilities at usual and customary fees, or the Medicaid fee schedule rate, whichever is lower. Although some states have increased their medical reimbursement to 80 percent of usual and customary fees, the norm is 47 percent (Colby 1994). In 1998, total governmental outlays for dental services were $2.3 billion ($1.3 billion federal, $1.0 billion state and local). Of this total, $2.0 billion rep- resented dental Medicaid expenditures, which is approximately 1.25 percent of the $159.6 billion des- ignated for all Medicaid personal health care expen- ditures, a proportion that is much lower than it was in the early years of the Medicaid program (HCFA 2000b). Some states have tightened their eligibility requirements and have reduced the range of covered dental services for adults. States have not been able to meet the mandatory components of the EPSDT den- tal program, partly because of low levels of reim- bursement to providers and difficulties regarding access to care for eligible enrollees. Eligibility for Medicaid, as with any form of insurance coverage, does not ensure receipt of ade- quate dental care. A 1996 report by the USDHHS Inspector General estimated that 80.3 percent of eli- gible infants, children, and youth up to 20 years of age, for whom disease levels are known to be high (see Chapter 4), did not receive preventive dental services (USDHHS 1996). The report stated that the reasons were complex and included the following factors: few dentists see Medicaid patients, Medicaid families give dental services low priority, and the youngest patients are the least likely to obtain care. The State Children’s Health Insurance Program Legislation passed by Congress in 1997 created the State Children’s Health Insurance Program, which provides billions of dollars to states (supplemented by required state contributions) to extend coverage for health care to uninsured children. For a child to be eligible, family income may be TABLE 9.6 ket sector and year, United States, 1995 to 1997 Source: Data from NADP 1998. Estimated number of dental plan members and annual percentage change by mar- as high as twice the federal pover- ty level, exceeding eligibility for Medicaid. The states must cover immunizations and well-child care Number of Members Percentage Percentage within specified program require- thang 1995 Change 1996 ments, but are otherwise free to Year End 1995 Year End 1996 Year End 1997 to 1996 to 1997 decide how the money is spent. By Dental HMO 20,697,452 24,359,434 26,457,650 WwW] 8.6 midsummer 1999, only 1.3 million Dental PPO 14,085,181 18,442,216 24,460,062 30.9 32.6 of the 10 million uninsured chil- Dental referral 1,920,330 5,033,866 5,453,264 8.3 dren had been enrolled in SCHIP Dentalindemnity 80,255,346 88,323,803 90,640,826 2.6 with some states using the funds to Total/average 116,958,309 136,159,319 147,011,802 16.4 8.0 expand Medicaid coverage and _ ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 233 Provision of Oral Health Care others designing new programs that may or may not snclude dental care (see Chapter 10 for more details). Medicare Dental services covered under the Medicare program are limited. Unlike Medicaid, Medicare (Title XVIII of the Social Security Amendments of 1965) is financed totally by the federal government, it was originally designed to provide physician and hospital services for all persons 65 and older, rich and poor alike, Medicare is split into hospital insurance (Part A) and physicians’ services (Part B), the latter being a voluntary supplemental insurance program paid for by the individual. Medicare was not designed to insure routine dental care. Rather, as an exception to the statutory exclusion from Medicare of dental services, it covers dental services needed by hospitalized patients with specific conditions. These include dental services in connection with jaw fractures or with preparation of patients for radiation in cases of oral and pharyngeal cancers or as part of a comprehensive workup prior to renal transplant surgery (Table 9.7). Total Medicare payments for dental services in 1998 were $0.1 billion (HCFA 2000b). Recently, the Institute of Medicine (IOM) was asked to study the short- and long-term benefits and costs to the Medicare program of extending coverage to include “medically necessary dental care” to bene- ficiaries for a limited number of conditions. In the Medicare program, the term “medically necessary dental services” is used narrowly to mean care that occurs as the direct result of an underlying medical condition or its treatment or that has a direct effect on such a condition. Under this definition, care for serious periodontal disease would not be “medically necessary” unless, for example, it threatened the health of someone with leukemia or was caused by the disease or its treatment (and could otherwise be health threatening if untreated). The 1OM report noted that such a restrictive definition may suggest that “periodontal or other tooth-related infections are somehow different from infections elsewhere” and “imply that the mouth can be isolated from the rest of the body, notions neither scientifically based nor constructive for individual or public health.” The IOM committee concluded that it is reason- able for Medicare to cover both tooth-preserving care and extractions for patients undergoing radiation for oral and pharyngeal cancers, and a dental examina- tion, cleaning of teeth, and treatment of acute infec- tions of the teeth or gingiva for a leukemia patient prior to chemotherapy. The report suggested that fur- ther study would enable recommendations to be made—on a condition-by-condition basis—for cov- erage of effective dental services needed in conjunc- tion with surgery, chemotherapy, and radiation for other conditions (Field et al. 1999). FACTORS AFFECTING THE CAPACITY TO MEET ORAL HEALTH NEEDS The nation’s capacity to provide care that is accessible and acceptable to address the oral health needs and wants of Americans in the next century is challenged by numerous factors. Among them are concerns about a declining dentist-to-population ratio, an inequitable distribution of oral health care providers, a low number of underrepresented minorities TABLE 9.7 Current Medicare coverage for dental services Clinical Condition Covered Service Part A (hospital) Part B (physician) Underlying medical condition and clinical status require Inpatient hospital services only X hospitalization for dental care Severity of dental procedure requires hospitalization for Inpatient hospital services only X dental care Any oral condition for which nondental services are covered All dental services if incident to and an integral part of X covered procedure or service Neoplastic jaw disease Extractions prior to radiation X Renal transplant surgery Oral/dental examination on an inpatient basis Xx X (if dentist is on (outpatient staff at hospital payment for where service physicians only) is provided) Source: HCFA 2000b. 234 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL applying to dental schools, the effects of the cost of dental education and graduation debt on decisions to pursue a career in dentistry, the type and location of practice Upon graduation, current and expected shortages 10 personnel for dental school faculties and oral health research, and an evolving curriculum with an ever-expanding knowledge base. Numbers of Dental Personnel The ratio of dentists to the total population is declin- ing: in 1996, there were approximately 58.4 profes- sionally active dentists per 100,000 people in the United States, down from 59.1 in 1990. The current ratio equates to one dentist for every 1,700 people (HRSA 1999). The dentist-to-population ratio is a very crude measure of dental care capacity, because it does not consider dentist productivity (affected by hours worked, use of auxiliary personnel, and mix of services provided) or location of practices relative to underserved populations; there is no agreement on the number that is optimal. Nevertheless, this ratio does indicate trends. By 2020 the dentist-to- population ratio is expected to drop to 53.7 per 100,000 (Figure 9.8). Moreover, it appears that the absolute number of active dentists will decline after 2000. In part, this drop reflects the retirement of older dentists (estimated to range from 2,500 to over +4300 per year between 1996 and 2021 (HRSA 1999) ° with insufficient numbers of new graduates (estimat- ed at about 4,000 per year) replacing them (ADA 1999). In comparison, the ratio of active physicians to population has been increasing; it was 251.6 per 100,000 in 1997, up from 226.1 in 1990 (HRSA 1999), The trend in the reduction of the dentist-to- population ratio and the absolute number of dentists Provision of Oral Health Care implies a shortage of dentists in the future. This trend may, however, be offset by innovation in dental prac- tice. However, if the impact of future technology changes is similar to that produced by changes over the past 20 to 30 years, it will not substantially affect the projections. The entering supply of dentists and dental hygienists depends on the number of graduates from dental and dental hygiene schools. The number of applicants to dental schools almost doubled between 1989 and 1997. However, the number of applicants declined by 4 percent in 1998, with further declines of 8 to 10 percent expected for 1999 and 2000. Based on the sharp decline that has occurred in the number of individuals taking the Dental Admissions Test, similar declines may continue into the early 2000s. During the 1989-97 time period, dental school first- year enrollment increased only about 9 percent. Little further growth in enrollment is anticipated because the current infrastructure in dental education has limited ability to expand, coupled with the declines occurring in dental school applicants. Along with concerns about a possible shortage of dentists, there is concern that the pool of qualified applicants may not be sufficient to supply a dental workforce that meets the needs of society, as well as the needs of dental education and research. In contrast, the number of dental hygiene pro- rams and students has increased almost 18 percent since 1990. The number of first-year dental hygiene students currently stands at 6,000, more than recov- ering from the 15 percent decline that occurred in these programs during the late 1970s through the mid-1980s. The last 4 years has seen a steady 11 per- cent growth in dental hygiene positions. The numbers of dentists and sites of health pro- FIGURE 9.8 Dentists per 100,000 U.S. population, 1950 to 2020 70 60 50 40 30 Number of dentists 20 10 0 1950 1960 1970 1980 1990 2000 = 2005 Sources: HRSA 1999, ADA 1996. fession education programs have been influenced by government policies and social factors. During the late 1950s an emerging short- age of health care providers (including dentists) was expected arising from the “baby boom” that began in the late 1940s. Beginning in the early 1960s, the federal government supported an expansion in the number of med- ical and dental schools and in class sizes. By the mid-1970s, the number of dental schools had grown from 47 to 60. First-year enrollments grew from 3,612 to 2020 6,301. By the mid-1970s, a possi- ble oversupply of physicians and 2015 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 235 Provision of Oral Health Care dentists became a concern. Government support for all health profession education was substantially reduced. Through the 1980s, dental schools reduced their enrollment by 37 percent. By 1993, six dental schools, all affiliated with private universities, had closed. Following the growth in dental school enroll- ments that has occurred since 1989, the 1998-99 first-year enrollment stood at 4,268 in 55 dental schools located in 33 states, the Commonwealth of Puerto Rico, and the District of Columbia. One more dental school (at Northwestern University) is sched- uled to close in 2001. One is scheduled to open in 2001, at the University of Nevada at Las Vegas (ADA 1996). Total dental school enrollment in 1998-99 was 17,033 students, down from a peak of 22,842 in 1980-81. Sex and Racial/Ethnic Composition of Dental Personnel The number and percentage of women in the dental and medical professions have continued to increase. Thirty years ago, women represented 1.3 percent of first-year enrollment in dental schools. By 1988, that proportion had risen to 35.7 percent, a level that has been relatively constant over the past 10 years. Recent trends indicate that the proportion of women in dentistry will continue to increase: by 2000, more than 26,000 women will be active practitioners, this is almost twice the number in 1990 (HRSA 1993, 1999). However, data from 1990 show that the pro- portion of dentists who were women (9.5 percent) was smaller than the proportion of female physicians (17.0 percent), female pharmacists (28.9 percent), and female optometrists (14.6 percent). The percent- age change in the numbers of first professional degrees conferred to women by health field of study and race/ethnicity from 1981 through 1990 shows that although dentistry is second lowest (next to allo- pathic medicine), the percentage changes for Hispanic women and American Indian/Alaska Native (AIAN) women in dentistry were among the highest (46.7 percent and 500.0 percent, respectively), even though the actual numbers were low (HRSA 1993). The participation of racial and ethnic minorities in dentistry does not mirror the dramatic increase in the entrance of women into the profession in the course of a single generation. The demographic pro- file of the U.S. population is changing rapidly, and is likely to continue to do so, with continued increases in racial and ethnic minority groups in comparison to whites. However, these trends and projections are not reflected in the dental or medical workforce. The overall percentage of minority students has increased significantly, to the point that, in 1998, a little over 34 percent of the first-year students were members of a minority group. This overall percent- age is up from 13 percent in 1980. However, the pri- mary increase has come among Asian/Pacific Islander students, increasing from about 5 percent of enroll- ment in 1980 to almost 25 percent in 1998. At the same time, the proportion of black/African American, Hispanic/Latino, and American Indian students, together, has shown only a small percentage point increase since 1980, from about 7.5 percent to nearly 10 percent. The percentage of first-year enrollment in 1998 for black/African American students was 4.4 percent. It was 4.9 percent for Hispanic/Latino stu- dents and 0.4 percent for American Indians. These percentages for black/African American, Hispanic/ Latino, and American Indian students are far less than their percentages in the U.S. population. In addition, a specific look at black dental school grad- uates during the 1980s and 1990s showed that although the number of black female graduates had increased, the increase was insufficient to offset the decline in black male graduates (HRSA 1993). In 1996, African Americans made up 12.0 per- cent of the general population, but only 2.2 percent of active dentists (Brown and Lazar 1999). Similarly underrepresented were Hispanics, who accounted for 10.7 percent of the population, but only 2.8 percent of active dentists. The Hispanic population is the fastest-growing segment of the population and by 2002 will exceed the number of blacks (U.S. Bureau of the Census 2000). American Indians, 0.7 percent of the population, represented only 0.2 percent of active dentists. Table 9.8 shows the 1996 dentist-to- population ratios by race/ethnicity of the dentist. As has been shown in Chapter 4 and elsewhere in this report, oral health problems disproportionate- ly affect disadvantaged populations among underrep- resented minority groups. This disparity will not be ameliorated through technology improvements or increases in clinical productivity. Moreover, recent data show that underrepresented racial and ethnic minority dentists are more likely to provide care to minority populations. In 1996, black dentists report- ed that 61.8 percent of their patients were black, and Hispanic dentists reported that Hispanic patients made up 45.4 percent of their practice; 76.6 percent of white dentists’ patients were white (Brown and Lazar 1999). A recent study of the role of black and Hispanic physicians in the provision of care for underserved populations demonstrated that these physicians practiced in communities with a higher percentage of their racial or ethnic group (Komaromy 236 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL et al. 1996). Also, black physicians saw more \fedicaid patients, and Hispanic physicians more uninsured patients, than other physicians. If this pat- tern of treatment of Medicaid patients and the un- insured. is similar for dentists, the underrepresenta- aon of minority dentists may also contribute to the unmet needs of minority patients. This issue war- rants further research. Regarding the importance of reaching parity in the dental profession, the American Association of Dental Schools comments, “The production of underrepresented minority [URM] dentists is totally out of synch with projected U.S. demographics. The US. population is expected to increase by 60 percent, reaching 394 million by 2050. At that time, nearly half (48 percent) of the population will be constitut- ed from racial and ethnic minority groups. Strategic measures are needed to increase the number of URM dental graduates that will improve access to care for minorities throughout the nation” (AADS 1999). Recruitment and retention of underrepresented minorities and women into the health professions will continue to be a challenge in the coming years. Activities such as enrichment programs in science and mathematics for grades K-12 and precollege are designed to increase the interest and capacity of all students, including women and underrepresented minorities, in health professions and science careers. These efforts will require careful design, implementa- tion, and evaluation. Student Indebtedness and Its Effects The American Association of Dental Schools reports that in 1998 graduates of dental schools had incurred, on average, over $84,000 in educational debt (G. Luke, AADS, personal communication, 1999). Average debt ranged from $71,000 for graduates of public schools to $98,000 for private/state-related schools and $108,000 for private schools. This was over 14 percent more than the educational debt of graduating medical students. Specialty education Provision of Oral Health Care may result in additional debt. Setting up an office involves additional costs. In the end the burden of debts to be repaid is a driving force in decision mak- ing for many new graduates regarding career direc- tion and practice site. Fewer dentists establish practices in low-income communities. The National Health Service Corps (NHSC) was created in 1970 as a program of the U.S. Public Health Service to provide financial assistance to health professionals who agree to locate in a Health Professional Shortage Area (HPSA). The NHSC offers programs for both students and clini- cians, including scholarships, loan repayment pro- grams, and rotations in Community Health Centers. Currently, there are approximately 2,526 clinicians, including 306 dental care providers, delivering care to more than 4.6 million people through these pro- grams. Only about 6 percent of the dental need is currently being met in the approved 1,198 dental HPSAs with a population of 25.9 million. It is esti- mated that an additional 4,873 dental care providers are needed to meet the current demand. In fiscal year (FY) 1999 the NHSC provided 139 new and contin- uing dental loan repayment awards, valued at $9 mil- lion, In FY 1998, there were 308 dental NHSC schol- ars, a 40 percent increase since 1994. Outreach and program development are critical to foster growth and create opportunities for placing dentists in underserved areas, where the needs are great. In addition to the NHSC, the Indian Health Service operates a loan repayment program to identi- fy health professionals who will practice full-time at an IHS facility or approved tribally managed site in exchange for repayment of their eligible health pro- fessions educational loans. Funding for this program has remained level for the past 8 years, in spite of the fact that student debt has nearly doubled during that time. Primary care dental residency programs support- ed by Health Professions Training Funds also play a role in meeting the oral health care needs of the nation. An evaluation performed for the USDHHS Source: HRSA 1999. TABLE 9.8 U.S. dentist-to-population ratios by race/ethnicity of the dentist, 1996 Asian/Pacific American Total Black Hispanic Islander Indian White "U.S. population 265,189,000 31,933,000 28,092,000 9,181,000 1,954,000 194,029,000 Active dentists 154,900 5,201 5,178 10,693 194 133,634 Number af dentists per 100,000 population 58.4 16.3 18.4 116.5 99 68.9 Number of people per dentist 11,712 1:6,140 135,425 1:859 1:10,072 131,452 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 237 Provision of Oral Health Care found that 87 percent of General Dentistry trainees remain in primary care practice and over 30 percent of General Dentistry program graduates receiving federal support over the last 4 years entered practice in underserved communities. The issue of indebtedness not only is an impor- tant consideration for the graduate in deciding where. to practice, but also has become an obstacle to col- lege students contemplating a career in dentistry and other health professions. Moreover, it can affect the choices graduates make about whether they will pur- sue careers in academia or research. The National Institutes of Health created three loan repayment programs to attract health care professionals to research in its facilities. In addition, innovative loan repayment incentives, such as awarding “extramural” loan repayment to researchers working in dental edu- cation institutes, have been proposed to overcome the current critical shortage of dental faculty/ researchers. Personnel Needs for Faculty and Clinical Research The education and training of dentists and allied den- tal health personnel are essential to the countrys capacity to meet its oral health needs. Dental educa- tion institutions and their allied academic health cen- ters play a critical role in providing the infrastructure for oral, dental, and craniofacial research and contin- uing education for dental professionals. A task force report on the future of dental school faculty shows that the number of faculty vacancies in the clinical sciences has more than doubled in recent years, ris- ing from 139 in 1992-93 to more than 300 in 1999 (AADS 1999). The task force projects that retire- ments will rapidly increase in the coming decade given the average age of the faculty (47 percent of all faculty members are aged 50 and older, and 19 per- cent are 61 and older). Kennedy (1990) estimated that dental institutions need at least 208 to 218 new faculty members each year, based on a faculty turnover rate of approximately 33 percent every 3 years. Curriculum Needs New technologies such as telehealth, bioinformatics, and virtual reality, as well as databases specifying human, animal, and microbial genomes, are altering public awareness, attitudes, and behavior regarding health issues. The new knowledge and tools available are also changing dramatically how health care pro- i) tg w fessionals are taught, how they learn, how they prac- tice, and how they retain clinical practices. These developments, along with new paradigms for the treatment of oral, dental, and craniofacial dis- eases and disorders, have led to several recent studies of oral health professional education and curricula (Field 1995). A 1995 Institute of Medicine study on the future of dental education called for greater inte- gration and collaboration of dental schools with the parent university and academic health center, a com- mitment to research programs and the building of research capacity, and an enrichment of the curricu- lum to incorporate new scientific knowledge and its transformation into clinicalapplications. The report's first strategic policy principle affirmed that “oral health is an integral part of total health, and oral health care is an integral part of comprehensive health care, including primary care.” Ideally, curricu- la for all health professional schools should reflect this principle by integrating knowledge and manage- ment of oral and medical health and disease. ’ Work is beginning on revisions to educational materials necessitated by these advances in research and technology. Initial steps are being taken to increase emphasis on interdisciplinary training, clin- ical research, and orientation to cultural competency in health professional education. The National Coalition for Health Professional Education in Genetics is promoting the incorporation of genetics, genomics, and proteinomics into predoctoral pro- grams to prepare future health professionals to inte- grate genetics into practice. Other developments that need to be addressed include HIV disease and other emerging and reemerging infectious diseases, in- creased understanding of gender health issues, man- agement of chronic pain, and the growing numbers of aging baby boomers and older Americans with complex and chronic health problems. For example, instruction on the special needs of individuals whose oral health is compromised by systemic diseases or disease treatments and on the heightened quality-of- life expectations of young and middle-aged adults should be incorporated into the curricula. In addi- tion, in Area Health Education Centers in some states, health profession students work together to care for patients in underserved, rural, or disadvan- taged populations. The HIV/AIDS Dental Reimbursement program assists dental education programs in meeting the HIV/AIDS community’ significant need for oral health care services. This program trains dental students and residents in the care and treatment of those living with this chronic disease. A federal- ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL institutional partnership provides funds to dental education institutions to partially reimburse for the -osts of providing oral health care services to people living with HIV and AIDS. As the health professional curriculum evolves, so must efforts in K-12 education and beyond to improve the public's health literacy. Efforts directed toward improving science and health knowledge and attitudes and at implementing health-promoting practices have begun; these can contribute to an enhanced partnership between patients and their health care providers. Taking Care of Those Most in Need The capacity to care for those most in need requires not only an adequate number of individuals to pro- vide the care, but also an equitable distribution of providers to ensure the availability of care. In addi- tion, sufficient financial resources must be available to support the delivery of and reimbursement for care provided to those most in need. Attention must also be given to a quality of care that ensures that the serv- ices provided fulfill the needs and functional require- ments of the patients. Although the proportion of the population that uses dental services continues to increase, disparities remain (see Chapter 4). A recent review of the literature related to access to care has identified many of the factors associated with these disparities. The lack of dental insurance emerged as a highly significant factor (Isman and Isman 1997). A series of reports demonstrates that privately insured individuals of all ages are more like- ly to get dental care when they need it than are the uninsured (Bloom et al. 1997, Cohen et al. 1997, Simpson et al. 1997). Lack of insurance was found to be an even more significant barrier to gaining pri- mary care access for children than either poverty or minority status (Newacheck et al. 1997). Once access to care has been established, there 1s greater likelihood that individuals will adopt preven- tive practices. Although a causal relationship has not been established, Wagener et al. (1992) found that brushing with a fluoride dentifrice and using dietary fluoride supplements were more frequent among pre- school children who had had a dental visit in the past year than among those who had not. In contrast, as discussed in Chapter 4, one of the most common rea- sons cited by individuals in all income and education groups for not having made a dental visit was that they did not perceive that they had a problem. This implies a lack of awareness that attaining and main- taining good oral health and preventing disease Provision of Oral Health Care require not only self-care but also professional oral health care. Federal and state statistics show strong and con- sistent racial and ethnic disparities among U.S. chil- dren in disease occurrence and severity, untreated dental disease, access to dental care, and use of pre- ventive services (see Chapter 4). Vulnerable child populations as well as the elderly, individuals with disabilities, people with HIV, migrant workers, and homeless persons pose an additional set of chal- lenges. These populations require health care providers sensitive to cultural and social issues who are capable of addressing complex problems that demand integrated dental and medical care. The oral, dental, and craniofacial and medical care curricula are vital in preparing dental and other health care providers to coordinate and integrate care for these individuals. The issues of oral health and the underserved have been addressed in a policy paper, Oral Health for All: Policy for Available, Accessible and Accept- able Care (Warren 1999). This report makes recom- mendations regarding financial barriers to care, integration of oral health services into health care delivery, capacity to meet oral health needs, cultur- al competency of health care providers, and educa- tion and oral professional practice requirements to meet the oral health care needs of underserved populations. A survey of dental care reported that more than half of the responding private practice dentists pro- vided some charitable care to low-income popula- tions in 1996 (ADA 1998b). Although access-to-care dental programs for low-income populations are sup- ported by many dental societies, this generosity falls well short of meeting the needs of these populations, which also require community-based programs (Waldman 1999) (see Chapter 7). Programs such as Community and Migrant Health Centers serve hard- to-reach populations. In 1996, more than half of such centers provided dental services, serving more than 1 million people J. Anderson, personal communica- tion, 1999). TWENTY-FIRST CENTURY CHALLENGES: WHAT LIES AHEAD? The United States is witnessing unprecedented changes in demography, patterns of disease and disorders, and the nature of health care. The imperative to keep abreast of advances in science and technology is already evident in dentistry and medicine, aided by access to multiple information ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 239 Provision of Oral Health Care systems. In addition to the Internet and continuing dental education, the new century will see continued growth in imaging systems, computer-assisted technology, teledentistry and telemedicine, improved diagnostics and therapeutics, and new biomaterials and other biotechnology products. Genetic information will play an increasing role in assessing a patient's risk for disease and in planning treatments. Although some information is available on the effectiveness, cost-effectiveness, and outcomes asso- ciated with health care treatment, further research will be needed to determine “best practices*"—which treatments work for which patients, under what cir- cumstances, and at what cost. Treatment planning will incorporate outcome measures and patient pref- erences. Systematic reviews of the existing literature will help promote an evidence-based approach to dental and medical care. In addition, comprehensive diagnostic and treatment codes, as well as a process by which new technologies can be incorporated appropriately, will be needed. The dental profession has been at the forefront of efforts to prevent disease and enhance general health and the quality of life. Efforts such as community water fluoridation, over-the-counter fluoride prod- ucts, and dental sealants represent a preventive ori- entation that has been associated with the dental pro- fession for half a century. Dentistry is continuing to be responsive to the ever-rising expectations of patients. Increases in the provision of fee-for-service cosmetic dentistry, adult orthodontics, and dental implants are among the trends already in evidence and expected to grow. As the knowledge base regarding the relation- ships between oral health and general health increas- es, so too will the need for greater coordination of dental and medical services. Efforts to improve car- diac care, for example, may include treatment of periodontal diseases. Prenatal care may come to include a dental evaluation and treatment to reduce the risk of preterm, low-birth-weight deliveries. Regular oral examinations and periodontal treatment for diabetic patients may become an important com- ponent in disease control. Partnerships will need to be expanded and new ones created among the private dental, medical, and public health components. A challenge facing the health professions will be to expand community-based disease prevention and personal oral health care to meet the needs of popu- lations. Questions of access and barriers to care must be addressed and satisfactory solutions found to ensure that there is care for all who seek it. The extent to which these predicted structural, organizational, and thematic changes will affect the nation’s capacity and commitment to provide oral health care is not certain. The nation’s health promo- tion and disease prevention objectives, which include oral health objectives, serve as a critical guide. How successful a changed care system will be in address- ing the oral health needs and wants of the nation can be measured in several ways. These include reduc- tions in health disparities in the population, decreas- es in the overall incidence and prevalence rates of diseases for the entire population, improved func- tional status, lower costs, reduced mortality rates, and enhanced health and quality of life. FINDINGS e Dental, medical, and public health delivery systems each provide services that affect oral and craniofacial health in the U.S. population. Clinical oral health care is predominantly provided by a pri- vate practice dental workforce. e Expenditures for dental services alone made up 4.7 percent of the nation’s health expenditures in 19908—$53.8 billion out of $1.1 trillion. These expenditures underestimate the true costs to the nation, however, because data are unavailable to determine the extent of expenditures and services provided for craniofacial health care by other health providers and institutions. e The public health infrastructure for oral health is insufficient to address the needs of disad- vantaged groups, and the integration of oral and gen- eral health programs is lacking. e Expansion of community-based disease prevention and lowering of barriers to personal oral health care are needed to meet the needs of the population. e Insurance coverage for dental care is increasing but still lags behind medical insurance. For every child under 18 years old without medical insurance, there are at least two children without dental insurance; for every adult 18 years or older without medical insurance, there are three without dental insurance. e Eligibility for Medicaid does not ensure enrollment, and enrollment does not ensure that individuals obtain needed care. Barriers include patient and caregiver understanding of the value and importance of oral health to general health, low reim- bursement rates, and administrative burdens for both patient and provider. 240 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL e Anarrow definition of “medically necessary gental care” currently limits oral health services for many insured persons, particularly the elderly. e The dentist-to-population ratio is declining, creating concern as to the capability of the dental workforce to meet the emerging demands of society and provide required services efficiently. e Anestimated 25 million individuals reside in areas lacking adequate dental care services, aS defined by Health Professional Shortage Area (HPSA) criteria. e Educational debt has increased, affecting both career choices and practice location. e Disparities exist in the oral health profession workforce and career paths. The number of under- represented minorities in the oral health professions is disproportionate to their distribution in the popu- lation at large. e Current and projected demand for dental school faculty positions and research scientists is not being met. A crisis in the number of faculty and researchers threatens the quality of dental education; oral, dental, and craniofacial research; and, ultimately, the health of the public. e Reliable and valid measures of oral health outcomes do not exist and need to be developed, val- ;dated, and incorporated into practice and programs. REFERENCES American Association of Dental Schools, (AADS). Report of the AADS President's Task Force on Future Dental School Faculty. Washington: American Association of Dental Schools; 1999. American Dental Association (ADA), Survey Center. 1990 survey of dental services rendered. Chicago: American Dental Association; 1990. American Dental Association (ADA). Dental manpower model: 1995-2020. 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Trends in child- hood use of dental care products containing fluoride: United States, 1983-89. Adv Data 1992 Nov 20:(219):1-15. Waitzman N, Scheffler RM, Romano PS. The cost of birth defects: estimates of the value of prevention. Lanham (MD): University Press of America; 1996. p. 262. Waldman HB. Why not Medicaid dentistry. NY State Dent J 1999 Nov;42-4. Warren RC. Oral health for all: policy for available, accessible, and acceptable care. Washington: Center for Policy Alternatives; 1999 Sep. p. 33. York AK, Poindexter FR, Chisick MC. 1994 Tri-Service comprehensive oral health survey, active duty report. 1995 Jun. NDRI Report no. PR-9503. TAZ ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL PERT What Are the Needs and Opportunities to Enhance Oral Health? Many factors have been implicated in determining oral health; and they have varying effects across the life stages. These factors are discussed in Chapter 10, where the incorporation of determinants of health in major public health initiatives such as Healthy People 2010 is highlighted. Essential factors include individual biology and lifestyle, the physical and social environment (including whether a community supports health-promoting measures such as water fluoridation), and the organization of health care. These factors are not independent but interact. An individual with no inherent health problems and a healthy lifestyle also needs to live in a healthy environment with ready access to and ability to pay for health care services. Studies of oral health over the lifetime highlight the interaction of these factors. The chapter focuses primarily on Americas most vulnerable populations—children and the elderly—where issues of access, insurance, and reimbursement are critical in determining oral health and limit the delivery of care for individuals with special needs and those residing in institutions. Chapter 11 focuses on the future and the promise of research born of the revolutions in genetics, biotechnology, and biomimetics—the new science of tissue repair and regeneration. Global demographics and technologic innovations signal the need for health literacy and universal access to care if we are to enhance oral health for all Americans. Chapter 12 highlights the major findings and recommendations of the report. Everyone— individuals, communities, policymakers, health care providers, educators, and researchers—has a role in improving and promoting oral health. The major conclusion of the report is that oral health is essential to general health and well-being. A National Oral Health Plan will facilitate the means to improve the nation’s oral health. The chapter concludes with five actions proposed toward that end: strengthen understanding of oral health and disease by the public, practitioners, and policymakers, accelerate building the science and evidence base; enhance health infrastructure and program integration, reduce barriers to oral health care, and increase public-private partnerships to address health disparities. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 243 ( POT 0 Factors Affecting Oral Health over the Life Span When the World Health Organization (WHO) expanded the definition of health in 1948 to mean a complete state of physical, mental, and social well- being, and not simply the absence of infirmity, the move stimulated research to define the major factors affecting health and well-being. Investigators devel- oped model systems of “health-related quality of life” and “oral-health-related quality of life.” Chapter 6 describes such models and provides examples of indices and instruments used to measure quality of life. What these models have in common are factors that include biological or physiological measures of health, but also take into consideration an individ- ual's ability to function normally in the routines of daily living, experience symptom relief, and fulfill usual roles in personal relationships and in family, work, civic, and social interactions. The researchers note that the factors are not mutually exclusive, but interact, feeding back on one another. Often the measurements include an individual's subjective assessment of quality of life before and after the onset of the disease or disorder and its treatment. In the context of a broadened concept of health, there is clearly more to attaining and maintaining good health and quality of life than seeking regular medical and dental checkups and performing daily personal hygiene routines. Other factors that are important have been incorporated in a number of models of “determinants of health,” which are described in the next section. These models recog- nize that the determinants themselves are subject to change with changes in society and also vary in their salience over the lifetime of an individual. The con- cluding sections of the chapter illustrate this variabil- ity by examining oral health at successive stages of the life span, from childhood to old age. The vulner- abilities of selected subpopulations within each age group are highlighted, with particular emphasis on the plight of poor children and many older Americans. HEALTH IN THE CONTEXT OF SOCIETY Thinking about what makes people healthy has inspired philosophers and historians over the cen- turies. Following is a brief overview that points to commonalities among the models proposed. Historical Models As early as the fifth century B.C., Hippocrates con- sidered it essential that physicians know each patient's way of life, habitation, work, and dietary habits (Porter 1997). He counseled those who were considering a new city of residence to take into account the geography, water supply, and behavior of the citizens, specifically whether they drank and ate excessively, were lazy, or enjoyed exercise and hard work (Rose 1993). Recent accounts of the history of medicine and public health similarly recognize the roles of envi- ronment, lifestyle, and the health care provider in determining health. Pine (1997) has described four phases in the history of public health. Phase 1, from the middle to the late 1800s, was characterized by urbanization and industrialization that significantly contributed to suboptimal living conditions for workers. Sanitary reforms were the hallmarks of pub- lic health achievement during this period. In addi- tion, epidemiological studies began to demonstrate causal relationships between compromised health status and conditions such as malnutrition and poor hygiene. The second phase, between 1880 and 1930, was characterized by advances in bacteriology and immunology. Increasingly, the prevention of disease was being applied to populations as well as individu- als. The third phase, from 1930 through 1974, was a therapeutic period. The hospital became the essential base and focus for medical services, and medical treatment grew more complex. With the development ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 245 Factors Affecting Oral Health over the Life Span of vaccines and antibiotics, along with the success of surgical procedures, people began to rely on medical interventions as the source of health. The biomedical approach became paramount, and people began to believe that health was delivered to them by health professionals. The contributions of hygiene, sanita- tion, and living conditions to health were dimin- , ished. Doyal and Doyal (1984) point out that success depended on the maximal compliance of the patient. Contemporary Models The fourth phase of public health, 1974 to the pres- ent, ushered in the modern era, referred to as “the new public health” (Ashton 1993). This phase devel- oped out of a realization that health care costs were spiraling and there were few cures for an increasing burden of chronic diseases. The biomedical approach FIGURE 10.1 Aconceptual model of influences on health in sodety and factors that affect health through the life stages RCs Flere ue LUC "4 We uel Lea ba wee ae cae 4 Age,sex, and hereditary factors at eerie Source: Dahigren and Whitehead 1995. Reprinted by permission of Transaction Publishers. Figure 11.2, influences on health by Bernzeval, Judge and Whitehead 1995. Copyright 1995 by Transaction Publishers; all rights reserved. alone could not solve all health problems. Rene Dubos (1979, 1990) stated that theories of specific etiology provided only a partial explanation for the development of diseases; they could not explain under what conditions a specific cause of disease could be determined and was able to flourish. McKeown (1979) cited three factors he believed were responsible for the major reductions in disease: the environment, economics, and behavior. His analysis of data from numerous countries confirmed that the achievements of medicine alone could not explain improvements in health. The decline in mor- tality from many diseases, including tuberculosis, whooping cough, measles, scarlet fever, diphtheria, and smallpox, had begun well before the develop- ment of specific vaccines and therapies. He conclud- ed that “the misinterpretation of the major influences, particularly personal medical care, on past and future improvements in health has led to misuse of resources and distortion of the role of medicine” (McKeown 1976). ‘Taking a similar critical view, Cochrane (1971), the physician in whose honor the Cochrane Collaboration of clinical trials was established, chal- lenged the medical establishment to test medical pro- cedures, including those long believed to be effective, with rigorous randomized controlled trials, paying particular attention to cost-benefit analyses. Long- held traditions of dental care have also been ques- tioned, resulting in increased emphasis on clinical trials, systematic reviews of the oral health literature, and evidence-based practice (Chapter 8). In 1974, Marc Lalonde, then Minister of Health of Canada, released a report that clearly articulated that human biology and health care organization are not the sole factors that determine health (Lalonde 1974). What is now known as the Lalonde Report, or FIGURE 10.2 Relationships between the strategies in health services, health protection, and health promotion, the process of change they seek to set into motion, the determinants of health they can influence, and the ultimate social and health benefits they are expected to yield Community or population Processes of change Health field health strategies {immediate objectives) objectives Social and health benefits Health Organizing Access to _ Reduced morbidity services resources health services - and mortality Policies, Technology, / t : { } Increased longevity Health . Healt Predisposing, enabling, . Lifestyle ae onan promotion and reinforcing behavior — > enhancement Healthier people nancing, Regulation Health t ' { { Improved quality of life protection Regulating Environmental ; environment changes Reduced social costs Source: Green and Otteson 1999. Community and population health. Copyright 1998 by The McGraw-Hill Companies. Reprinted by permission of The McGraw-Hill Companies (2000). 246 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL the Health Field Concept, emphasized that lifestyle nd environment were of critical importance. Lalonde defined four elements as determinants of health: human biology, lifestyle, environment, and the organizauon of health care. These elements were -onsidered interdependent, and it was their dynamic interactions over the course of a lifetime that deter- mined the level of health and well-being attained by an individual. As well, the elements and their inter- ction have implications for the level of health wuained by larger aggregations of people—from neighborhoods to nations. Lalonde stated that most of society’s efforts to improve health, and the bulk of direct health expenditures, have been focused on the fourth element—the organization of health care, yet the main causes of sickness and death are rooted in the other three elements. At a subsequent WHO meeting in Ottawa, Canada, a set of five actions to promote health and quality of life, based on the four determinants, was proposed. Implementation of these actions clearly required going beyond the confines of a hospital, a medical office, or a home. Specifically, the Ottawa Charter for Health Promotion (WHO 1986) called for 1) creating supportive environments, 2) building healthy public policy, 3) strengthening community Factors Affecting Oral Health over the Life Span action, 4) developing personal skills, and 5) reorient- ing health services. In a model proposed by Dahlgren and Whitehead (1995), the individual is surrounded by lifestyle fac- tors, social and community influences, living and working conditions, and general socioeconomic, cul- tural, and environmental conditions (Figure 10.1). Green and Ottoson (1999) integrate the Lalonde Health Field Concept into a framework of population health strategies, processes of change, determinants of health, and ultimate social and health outcomes (Figure 10.2). Cohen and Gift (1995) acknowledge the role of multiple determinants and quote the medical histori- an, Henry Sigerist, who, in the mid-1940s, stated, “Health is promoted by providing a decent standard of living, good labor conditions, education, physical culture, means of rest, and recreation. The coordinat- ed efforts of large groups are needed to this end, of the statesman, labor, industry, of the educator and of the [health care provider] who as an expert in mat- ters of health must define norms and set standards” (Sigerist 1946). McGoldrick (1997) provides an overview of sev- eral health behavior models in current use (Table 10.1). Some of these models have been applied to TABLE 10.1 Examples of theories and models in health behavior oral-health-related behavioral research. Using the Health Belief Basic Theories Group-Dynamic Model Social Learning Theory Theory of Reasoned Action Theory of Planned Behavior Self-Efficacy Theory Health Belief Model Health Action Model Theory of Social Behavior Precede Framework Sense of Coherence Theory Health Promotion Model Authors Lewin, 1947, 1951 Rotter 1954, Bandura 1969, 1977 Ajzen and Fishbein 1977, 1980 Schifter and Ajzen 1985 Bandura 1982 Rosenstock 1966, 1974, Becker and Maiman 1975, Becker et al. 1974 Tones 1987, Tones et al. 1990 Triandis 1979 Green et al. 1980 Antonovsky 1979a,b Pender 1987 Major Elements Role-playing approach Identification, reinforcement, feedback, and reward Attitude-behavior relations Perceived behavioral control Behavior determined by cognition of individuals about their behavior Behavior determined by psychological readiness to take action Interaction of knowledge, beliefs, values, attitudes, drives, and normative pressures Behavioral intention Predisposing, reinforcing, and enabling causes in educational diagnosis and evaluation Salutogenic paradigm—focus on successful coping Cognitive-perceptual factors Source: Adapted from Pine 1997. Model in a study of dental patients, for example, Kuhner and Raetzke (1989) reported that motivation and perceived severity of the con- dition were the primary predictors of compliance with oral hygiene instruction. Perceived benefits and experience were also important. The United States published a first set of national health goals for 1990 in 1979. The goals focused on the reduction of mortality in four different age groups and emphasized increased independ- ence for older adults. Since then, national health goals have been established by the U.S. Depart- ment of Health and Human Services for each decade and published under the title “Healthy People.” For Healthy People 2010 the broad goal is to increase the quality and years of healthy life. The concep- tual framework, illustrated in Figure 10.3, features at the center determinants comparable to the ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 247 Factors Affecting Oral Health over the Life Span elements in the Lalonde Report. They include the interaction of individual biology, behavior, and the social and physical environment amidst policies, interventions, and access to quality health care. The United States has invested heavily in ele- ments of human biology and health care organiza- tion, but the nation has also readily embraced the notion that lifestyles influence health. Physical fit- ness and self-care are concepts that mesh with the individualistic spirit of U.S. society. Much attention has been given to health education, behavior change, and “healthy living.” Applications to Oral Health Within oral health, the self-care approach is best illustrated by the use of fluoride products for the reduction of dental caries. The successful adoption of FIGURE 10.3 Conceptual framework from Healthy People 2010 fora systematic approach to health improvement —— Goals © __ Objectives —— Determinants of Health Policies and Interventions rm : 4 — , Behavior el Physical a Social Environment Individual Environment t_, . a Access to Quality Health Care < RRR NEE are a’ Health Status Biology . — Mie aed or a Source: USDHHS 2000. self-care regimens has been reinforced through the efforts of parents, caregivers, health educators, health professionals, advertisers, manufacturers, and early childhood programs such as Head Start that include oral health initiatives. The Andersen Model. The oral health research com- munity has begun to assess the behavior/lifestyle determinants of oral health as well. Andersen and colleagues point out that over the years concepts of health behavior have broadened from the biologic to the psychosocial (Andersen et al. 1988, Gochman 1988). Andersen has been a pioneer in the develop- ment of models of health determinants. The most recent refinement of the Andersen Behavioral Model (Figure 10.4) proposes that interactions among four major categories are critical to understanding the determinants of health. The first is the environment, described as the broader context in which popula- tions live and behaviors occur. It includes the exter- nal environment and health care systems. The sec- ond category, population characteristics, includes three subsets: predisposing characteristics such as sociodemographic features, enabling resources such as those that enable the individual to pursue and achieve good health, and the need for care, which is defined by the individual's perceptions of necessary preventive interventions or treatments. The third cat- egory is the health behaviors themselves, and the fourth category, outcomes, includes perceived and evaluated health status and consumer satisfaction (Andersen 1995). In weighing the contributions of the various determinants of oral health, Andersen et al. (1995) suggest that the external environment, relating to both specific and general health, is the primary determinant of oral health behaviors and outcomes. Oral-health-specific environmental determinants FIGURE 10.4 An emerging model—Phase 4 of the Andersen behavioral model | Environment Population characteristics Health behavior Outcomes Health Care Personal System — Health Practice ; Predisposing Enabling alti B ractices External Characteristics Resources Use of Environment Health Services ee Source: Andersen 1995. Copyright 1995 by Journal of Health and Social Behavior. Reprinted by permission of the American Sociological Association (2000). 248 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL range from positive factors such as water fluoridation i negative factors such as lack of food policies to geal with frequent sugar and carbohydrate intake. Thev define general environmental factors as those that deal with the relative wealth of the society, gen- eral economic “climate,” and the political and societal norms that affect the delivery of oral health services. Workplace Effects. Several researchers (Karasek and Theorell 1990, Marmot and Theorell 1988, Marmot et al. 1984, Syme 1996) have found an association between the level of control and flexibility people have in their work setting and the types of health conditions they develop and the subsequent levels of severity of those conditions. Abegg et al. (1999) looked at the relationship between oral hygiene per- formances and levels of flexibility of work schedule. They found a highly statistically significant relation- ship between flexibility of work schedule and tooth- cleaning frequency, range of oral hygiene aids used, and level of dental plaque. These associations remained even after adjusting for age, sex, socioeco- nomic status, and marital status (Abegg et al. 1999). Effects of Income Inequality Investigators are also studying how socioeconomic status affects oral health (Chapter 4). The degree of income inequality between the richest and the poor- est within a country, state, Or neighborhood con- tributes to the overall health of the population (Kawachi et al. 1997, Kennedy et al. 1996). There is conjecture from this research that increased income inequality leads to decreased levels of social cohesion and trust, or what has been described as a “disinvest- ment in social capital” (Kawachi et al. 1997). This is defined as “features of social organization, such as civic participation, norms of reciprocity, and trust in others, that facilitate cooperation for mutual ben- efit.” Results of other studies indicate that lower lev- els of social trust are associated with higher rates of coronary heart disease, cancer, stroke, and infant mortality. However, study of healthy versus unhealthy communities is a relatively new field and offers an opportunity for oral health to be included. Additional research is needed to determine the attrib- utes of a community that either favor or diminish the health of residents, what factors influence their development, how attributes can be changed to improve the health of a community, and how com- munities can build social capital. There are indicators of differentials in oral health status when poor and nonpoor populations are compared. Factors Affecting Oral Health over the Life Span Across numerous indicators, the poor are more likely to have oral diseases, disorders, and condi- tions. Poor children are less likely to have dental sealants. In addition, the poor are less likely to visit a dentist or dental hygienist in the course of a year. The differentials in oral health status between the poor and nonpoor cross the life span and are major social indicators of the current status of oral health in America today and provide a challenging baseline against which improvements can be measured. CHANGING VULNERABILITIES THROUGHOUT LIFE As all models of health determinafits recognize, the health of individuals and of society at large is not static. Vulnerabilities and risks for diseases and dis- orders change over a lifetime and are affected by chance events as well as deliberate actions of individ- uals and communities, of the sort proposed in the Ottawa Charter. The remainder of the chapter describes how oral health plays out across major life stages and identifies selected aspects of biology, behavior, environment, and the organization of health care that affect oral health. The plight of vul- nerable subpopulations, in particular, children and older Americans, are highlighted. The information presented includes data from national surveys, such as those presented in Chapter 4, as well as studies of convenience populations. Children In general, society gives special attention to the developing years of childhood, acknowledging that much of what happens to affect the health of a child bears directly on the health and well-being of the adult that child will become. In the case of oral health, there is enough known about health promo- tion and disease prevention to improve the oral health and well-being of all children, beginning with prenatal care. Adequate nutrition during pregnancy, including adequate folate intake, avoidance of sub- stances of abuse and therapeutic agents that have ter- atogenic potential, and the elimination and control of microbial infections in the mother increase the likeli- hood of an infant’s healthy start. (See Box 10.1 on the effects of nutrients on oral health.) As more becomes known about how the health of mothers and other caregivers can affect the oral health of children, addi- tional services may be warranted during the prenatal period (Chapter 5). Subsequent nurturing of the infant includes the home and health professional care necessary to promote health and interventions that ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 249 Factors Affecting Oral Health over the Life span limit the infant's exposure to infections that con- tribute to oral diseases. Throughout the first two decades of growth and development, children and young people are deeply influenced by the social and environmental opportu- nities and constraints imposed by families, commu- BOX 10.1 The Role of Nutrition in Oral Health General malnourishment impairs normal growth, development, and maintenance of the body's tissues and organs and impairs immune responses and wound healing, Reduced resistance of oral tissues to dis- ease can lead to increased colonization by oral pathogens and more sustained and severe oral infections. Clinical signs of malnutrition often appear first in the oral cavity. Craniofacial Development. Adequate maternal intake of folic acid dur- ing pregnancy has been shown to be essential in preventing neural tube defects (incomplete fusion of the neural tube in embryo), which results in spinal cord defects after birth (Botto et al. 1999). Folic acid also appears to be important in preventing clefting syndromes (in which there is incomplete fusion in utero of paired labial or palatal tis- sues at the midline) (Tolarova and Harris 1995). Tooth Development. Protein/calorie malnutrition and deficiencies in ascorbic acid, vitamins A and D, calcium, phosphorus, and iodine affect the human dentition (DePaola et al. 1999). These deficiencies in devel- opment can lead to tooth defects after teeth erupt, manifesting as enamel hypoplasia and hypomineralization, either of which can increase susceptibility to dental caries, Premature and very-low-birth- weight infants frequently show enamel defects (Seaw 1987). Since tooth enamel is acellular, and hence not subject to turnover and repair, enamel defects in development are permanent (Jonasson et al. 1999, Jeffcoat 1998, Talbot and Craig 1998, Payne et al. 1999). Supporting Bone. Adequate calcium intake, along with vitamin D and other essential vitamins and minerals, is needed not only to build but also to maintain healthy teeth and bones. The teeth are supported in the jaws by projections of maxillary and mandibular trabecular bone known as alveolar processes. When teeth are lost, alveolar bone resorbs, reducing the height of the bony ridge supporting the teeth. When serum calcium levels fall, withdrawal of calcium from alveolar bone to meet other tissue needs may precede calcium withdrawal from skeletal bone elsewhere in the body. Hence reduction in alveolar bone mass may be an early indication of skeletal osteopenia (reduced bone volume) or frank osteoporosis (Jeffcoat 1998, Jeffcoat et al. 2000). Oral Soft Tissues. Oral mucosa undergoes rapid turnover. In particular, the gingival lining between the gums and the teeth (the suicular epithelium) is replaced every 3 to 7 days. Thus the tissue requires a steady supply of nutrients to support DNA, RNA, and protein synthesis (Alfano 1976). Diets poor in folate, ascorbic acid, iron, and zinc are asso- ciated with increased permeability and decreased integrity of the sul- cular epithelium. Protein, vitamins A and C, and zinc are important for synthesis of connective tissue (largely collagen), which constitutes part nities, and society. Although every healthy newborn has the potential for success and good health, there are profound disparities in children's experiences and opportunities, which often manifest in inequities in oral and general health, education, and well-being. Many children achieve excellent oral health—sound of the attachment apparatus supporting the teeth in the jaw (Alvares and Siegel 1981, Vogel et al. 1986). The classic signs of scurvy, caused by severe vitamin C deficiency, include gingival bleeding, tooth mobility, and loss of connective tissue attachment. Painful oral lesions, including inflammation and cracks at the corners of the mouth and vertical fis- suring of the lips, are changes associated with riboflavin, iron, or pro- tein deficiency. Inflammation, a burning sensation, and tenderness of the tongue or palate are associated with deficiencies in B-complex vitamins, protein, or iron. Oral Defense Mechanisms. Chronic deficiencies of ascorbate and iron may impair the function of white blood cells (especially polymor- phonuclear leukocytes) in moving to sites of infection and initiating immune defense mechanisms. Zinc is a component of many enzyme systems and is also important in leukocyte activity (Hsu et al. 1991). General Oral Health. Foods rich in fiber aid digestion and stimulate sali- vary secretion. Salivary flow is important in initiating the digestion of starch, in facilitating food tasting and swallowing, and in ensuring a ready supply of components in the oral cavity that protect and main- tain the orai tissues. Nutrients Associated with Specific Diseases Dental Caries. The role of sugars and other carbohydrates is critical. Nearly all carbohydrates have caries-promoting properties. Most sweet foods contain a mixture of sugars (predominantly sucrose) and starch- es, which can be fermented by cariogenic bacteria to dissolve tooth mineral, Bacteria also use sucrose to generate glucans—sticky extra- cellular molecules that promote their attachment to tooth surfaces. The physical consistency, frequency of consumption, and the order in which foods are eaten affect cariogenicity. For example, following a sweet with a nonsweet food such as an aged cheese may counteract the acid attack on enamel. The presence of calcium and phosphates in the cheese also is beneficial (Jensen 1999, Rugg-Gunn 1993). Caries in tooth roots is produced by the same process as in tooth crowns and involves the same dietary etiology (Papas et al. 1995), but may occur more rapidly because the root mineral, cementum, and underlying dentin are more soluble than enamel. Periodontal Disease. Several studies have implicated deficiencies in ascorbate and folate with severity of gingivitis (Leggot et al. 1991, Pack 1984}, but in general the role of nutrients in periodontal disease appears to be related to conditions that lead to increases in dental plaque, impaired host defenses, and weakened integrity of the peri- odontal tissues. More recently, surveys indicate that calcium intake for a large segment of the population is below recommended daily amounts (NHANES III) and that reduced calcium intake is associated with greater levels of periodontal disease in both men and women 230 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL (Nishida et al. 2000). This is consistent with the findings of Krall et al. (1997), who showed that calcium supplementation in postmenopausal women with deficient calcium intake protected against tooth loss. Oral and Pharyngeal Cancers. High intakes of pickled vegetables, salted meat and fish, spicy foods, charcoal-grilled meat, and beverages served at very high temperatures have been found to be associated with oral cancers in some countries (Winn 1995). Malnutrition has also been found in association with the diagnosis of oral and pharyngeal cancers (Bassett and Dobie 1983). Whether the malnutrition was the cause or the effect is not clear. Oral Cancer Prevention. A consistent finding across numerous studies is that a diet high in fruit and vegetables is associated with a reduced risk of oral cancer even when smoking and alcohol intake are taken into account (Steinmetz and Potter 1996).In a case-control study, risk of sec- ond primary tumors in oral and pharyngeal cancer patients was reduced in those with a high vegetable intake (Day et al. 1994). Fruits and vegetables contain fiber, carotenoids, and vitamin C, which may be important in cancer chemoprevention. Vitamin C may act as an antiox- idant, protecting cell membranes and DNA from oxidative damage. Lack of vitamin C may interfere with collagen synthesis and permit tumor growth. Green leafy vegetables contain lutein, a carotenoid, xantho- phyll, an antioxidant, and folic acid. Folic acid deficiency may interfere with DNA methylation and DNA repair (Winn 1995). The only prospec- tive cohort study of diet and oral cancer (>25,000 persons in Maryland) showed that high serum total carotenoids and alpha tocopherol (vita- min £) reduced the risk of oral cancer, but high serum gamma toco- pherol and selenium increased cancer tisk (Zheng et al. 1993). The use of retinoids and 8-carotene in controlled therapeutic doses shows pro- tective effects. Fewer new primary tumors in persons with previous oral cancers and reversal or reduction in size of premalignant lesions have been reported (Khuri et al. 1997, Papadimitrakopoulou and Hong 1997). For example, high doses of 13-cis-retinoic acid, though causing significant toxicities, have been effective in the treatment of oral leuko- plakia (Hong et al. 1990). References Alfano MC. Controversies, perspectives and clinical implications of nutri- tion in periodontal disease. Dent Clin North Am 1976;20:519-48. Alvares 0, Siegel |. Permeability of gingival sulcular epithelium in the development of scorbutic gingivitis. J Oral Pathol 1981;10:40-8. Bassett MR, Dobie RA. Patterns of nutritional deficiencies in head and neck cancer. Otolaryngol Head Neck Surg 1983;91:119-25. Botto LD, Moore CA, Khoury Mi, Erickson JD. Neural-tube defects. N Engl J Med 1999;341:1509-19. Day GL, Shore RE, Blot WJ, McLaughlin JK, Austin DL, Greenberg RS, Liff JM, Preston-Martin S, Sarkar S, Schoenberg JB, et al. Dietary factors and second primary cancers: a follow-up of oral and pharyngeal cancer patients. Nutr Cancer 1994;21:223-32. DePaola DP Faine MP. Palmer CA. Nutrition in relation to dental medi- cine. in: Shils ME, Olson JA, Shike M, Ross CA, editors. Modern nutri- tion in health and disease. Baltimore: Williams & Wilkins; 1999. p. 1099-124. Hong WK, Lippman SW, Itri LM, Karp DD, Lee JS, Byers RM, Schantz SP, Kramer AM, Lotan R, Peters LI, et al. Prevention of secondary pri- mary tumors with isothetincin in squamous-cell carcinoma of the head and neck. N Engl J Med 1990;328:15-20. Hsu DJ, Daniet JC, Gerson SJ. Effect of zinc deficiency on keratins in buc- cal epithelial cells. Arch Oral Biol 1991;365:759-63. Jeffcoat MK. Osteoporosis: a possible modifying factor in oral bane loss. Ann Periodontol 1998;3:312-21. , Jeffcoat MK, Lewis CE, Reddy MS, Wang CY, Redford, M. Post- menopausal bone loss and its relationships to oral bone loss. Periodontol 2000; in press. Jensen ME. Diet and dental caries. Dent Clin North Am 1999;43:615-33. Jonasson G, Kiliaridis S, Gunnarsson R. Cervical thickness of the - mandibular alveolar process and skeletal bone mineral density. Acta Odontol Scand 1999;57:155-61. Khuri FR, Lippman SM, Spitz MR, Lotan R, Hong WA. Molecular epidemi- ology and retinoid chemoprevention of head and neck cancer.) Natl Cancer Inst 1997;89:199-211. Krall EA, Dawson-Hughes B, Hannan MT, Kiel DP. Postmenopausal estro- gen replacement and tooth retention. Am J Med 1997;102:536-42. Leggott PJ, Robertson PB, Jacob RA, Zambon JJ, Walsh M, Armitage GC. Effects of ascorbic acid depletion and supplementation on peri- odontal health and subgingival microflora in humans. J Dent Res 1991;70:1531-6. Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ.Calcium and risk for periodontal disease. Periodontol 2000;70(7):in press. Pack AR. Folate mouthwash: effects on established gingivitis in peri- odontal patients. J Clin Periodontol 1984;11:61 9-28. Papadimitrakopoulou VA, Hong WK. Retinoids in head and neck chemoprevention. Proc Soc Exp Med 1997;216:283-90. Papas AS, Joshi A, Palmer CA, Giunta JL, Dwyer JT. Relationship of diet to root caries. Am J Clin Nutr 1995;61(Suppl):4255-95. Payne JB, Reinhardt RA, Nummikoski PV, Patil KD. Longitudinal alveolar bone loss in postmenopausal osteaporotic/osteopenic women. Osteoporos Int 1999;10:34-40. Rugg-Gunn AJ. Nutrition, diet and dental public health. Community Dent Health 1993;10(Suppl 2):47-56. Seow WK, Humphrys C, Tudehope DI. Increased prevalence of develop- mental defects in low birth-weight, prematurely born children: a controlled study. Pediatr Dent 1987;9(3):221-5. Steinmetz KA, Potter JD. Vegetables, fruit and cancer prevention: a review. | Am Diet Assoc 1996;96:1027-37. Talbot L, Craig BJ. Osteoporosis and alveolar bone floss. Probe 1998;32:11-3. Tolarova M, Harris J. Reduced recurrence of orofacial clefts after peri- conceptual supplementation with high dose folic acid and multivi- tamins. Teratology 1995;51:71-8. Vogel RI, Lamster 1B, Wechsler SA, Macedo B, Hartley L, Macedo JA.The effects of megadoses of ascorbic acid on PMN chemotaxis and experimental gingivitis. J Periodontol 1986;57:472-9. Winn DM. Diet and nutrition in the etiology of oral cancer. Am J Clin Nutr 1995;61 (Suppl):4375-455. Zheng W, Blot WJ, Diamond EL, Norjus EP Spate V, Morris JS, Comstock GW.Serum micronutrients and the subsequent risk of oral and pha- ryngeal cancer. Cancer Res 1993;53:795-8. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Factors Affecting Oral Health over the Lile span Factors Affecting Oral Health over the Life Span teeth, firm gums, healthy soft tissues, well-function- ing bites, and beautiful smiles—but many do not. One in every four U.S. children today is born into poverty (U.S. Bureau of the Census 1998b) with all of its associated barriers and constraints. Poverty is a key indicator of poor oral health status among children (Litt et al. 1995). Poor children suffer twice as much dental caries as their more affluent peers (Vargas et al. 1998). Studies have shown that the children with the most advanced oral disease are primarily found among America’s most vulnerable groups: the poor, American Indians and other minorities, homeless and migrant populations, chil- dren with disabilities, and children with HIV (sman and Isman 1997). If untreated, oral diseases in children frequently lead to serious general health problems and significant pain, interference with eating, overuse of emergency rooms, and lost school time (Edmunds and Coye 1998). It has been estimated that 51 million school hours per year are lost because of dental-related illness alone (Gift 1997). The Institute of Medicine reports that 70 percent of U.S. children are generally healthy and require only regular preventive and intermittent medical services. Twenty percent experience chronic prob- lems, which may impose significant limitations on their ability to function effectively and require regu- lar treatments for their conditions. Only the remain- ing 10 percent suffer from severe chronic conditions necessitating intensive health services (Edmunds and Coye 1998). Similarly, the vast majority of America’s children today enjoy excellent oral health, but a significant subset of children experience a high level of oral dis- ease. Although it is no longer unusual to see children smiling with a full set of unmarred teeth, millions of other children have little to smile about. For them, the daily reality is persistent dental pain, endurance of dental abscesses, inability to eat comfortably or chew well, embarrassment at discolored and dam- aged teeth, and distraction from play and learning. Like asthma, learning difficulties, and social problems, dental caries is highly correlated with low income, limited education, and social disadvantage. In this regard, it may serve as a sentinel disease for other pediatric conditions that are related to inade- quate diet and hygiene and to family conditions and a social environment that do not support healthy lifestyles. Some oral conditions, like other childhood ill- nesses, affect children randomly, regardless of social or economic status. Such conditions include cleft lip and palate and other craniofacial developmental dis- orders, malocclusion, and unintentional injuries. Other oral conditions in children such as mucosal lesions may be a sign of risk behaviors such as tobac- co use. All oral conditions may be exacerbated in children with other special health care needs. Adults concerned about the health of children, particularly low-income and minority children, are regularly confronted by the reality and consequences of unmet oral health care needs. Although often viewed as innocuous by those who enjoy excellent dental health or have ready access to dental care, den- tal and oral problems impact the very life experience of affected children. Chronically poor oral health is associated with diminished growth in toddlers (Acs et al. 1992, Ayhan et al. 1996) and compromised nutrition (Acs et.al. 1999). Dental disease in children also takes a personal and social toll. Observing dis- advantaged inner-city schoolchildren, Kozol (1991) noted, “although dental problems don’t command the instant fears associated with low birth weight, fetal death, or cholera, they do have the conse- quences of wearing down the stamina of children and defeating their ambitions.” In addition to the millions of children with extreme dental problems, many times more encounter more modest disease. For example, the review of the Healthy People 2000 objectives found that more than half of all second graders, children aged 6 to 8, still experience cavities (USDHHS 1997). Dental caries remains the single most common dis- ease of childhood that is neither self-limiting, like the common cold, nor amenable to a simple course of antibiotics, like an ear infection (Edelstein and Douglass 1995). The numbers of poor and minority children are increasing faster than other socioeconomic subsets of US. children (Waldman 1996), and dental caries is common in these children. Twenty-five percent of these children have never visited a dentist before entering kindergarten (USDHHS 1997), despite widespread understanding that the dental caries process is established before age 2 and the recom- mendation of experts that children as young as 1 may benefit from a dental visit (AAPD 1997, Green 1994, USDHHS 2000). Parents are consistently concerned about the dental needs of their children (Simpson et al. 1997), and studies conducted in hospital emer- gency rooms have found extensive dental needs among children (Sheller et al. 1997, Unkel et al. 1989, Wilson et al. 1997). Dental care has recently been noted as the most prevalent unmet health need among American children (Newacheck et al. 2000). These conditions are evident despite the advances in the oral health sciences and the growing capacity of 252 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL oral health care providers to prevent common pedi- anc oral diseases. Children with disabilities present unique prob- tems and are at increased risk for oral infections, delavs in tooth eruption, periodontal disease, enamel irregularities, and moderate-to-severe malocclusion {sman and Isman 1997). Their exposure to certain medications and therapies, special diets, and their difficulty in maintaining daily hygiene further com- promise their oral health (Casamassimo 1996). Also, access to professional care is a particular problem for these children (see Chapter 4). Guides for dental pro- fessionals serving children with special health care needs are under development (USC 1999). The Role of Insurance in Children’s Oral Health Disparities also occur in access to care. Medical insurance is a strong predictor of access to dental care. Children with no medical insurance are 2.5 times less likely than insured children to receive dental care (Bloom et al. 1992, Monheit and Cunningham 1992, Newacheck et al. 1997). Children with no dental insurance were 3.0 times more likely to have an unmet dental need than their counterparts with either public or private insurance (Newacheck et al. 2000, Waldman 1998). Dentists daily observe that insured children are more likely to obtain comprehensive, continuous, and coordinated care and are more likely to be followed regularly for semiannual preventive visits. It has long been recog- nized that dental plans with low cost-sharing requirements are likely to improve the oral health of young people, especially those with the poorest oral health (Bailit et al. 1985). Children’s general health also affects access to dental care. Children with “fair or poor” general health have nearly twice the unmet dental needs as children with “good or excellent” health, according to their parents (Simpson et al. 1997). As income rises, unmet treatment needs drop off dramatically. Children from families with annual incomes of $10,000 to $20,000 have 10 times more unmet den- tal needs than children whose families earn more than $50,000 per year (Simpson et al. 1997). White children are more likely than children in other ethnic and racial groups to have private dental insurance coverage. When last surveyed nationally in 1989, about half (52 percent) of white children had dental insurance, compared to only 39 percent of black children and 32 percent of Mexican American children. As family incomes increase, children are more likely to be covered by dental insurance (USD- HHS 1992). Factors Affecting Oral Health over the Life Span In the United States, most health insurance is provided through the workplace, and about 60 per- cent of children are covered by private health insur- ance through their parents’ plans (U.S. Bureau of the Census 1998a). A smaller percentage, about 31 per- cent, enjoy dental insurance as well. There are at least > 6 children without dental insurance for each child without medical insurance (Vargas et al. 2000). Over the last decade, employer-based coverage for children has eroded, while publicly funded health insurance through Medicaid and the State Children’s Health Insurance Program (SCHIP) has expanded to cover over 25 percent of all children (U.S. Bureau of the Census 1998a). The Congressional Budget Office estimates that 2.5 million children will be insured through SCHIP. However, even with this increase many children will remain without dental coverage. Properly funded dental insurance works. When commercial-style, state-funded dental coverage became available to modest-income families in west- ern Pennsylvania, the percentage of previously unin- sured children (uninsured for more than 6 months) who saw a dentist during one year of coverage increased from 30 to 64 percent. The percentage of parents who reported that their child had a regular source of dental care increased from 51 to 86 percent. The percentage of parents who claimed that their children had unmet or delayed dental needs decreased from 52 to 10 percent. In addition, the number of dental visits fell as children’s acute and episodic care decreased and they began programs of regular preventive and maintenance care (Lave et al. 1998). Publicly Funded Insurance for Children Medicaid. Although publicly funded programs such as Medicaid have succeeded dramatically in provid- ing a “medical home” and regular medical care to children from low-income families (Newacheck et al. 1997), Medicaid’s record of ensuring regular access to dentists and providing effective dental care is less successful. Fewer than one in five Medicaid-covered children received a single preventive dental visit dur- ing a recent year-long study period, according to the U.S. Inspector General (USDHHS 1996). The study indicated that three fourths of states provided pre- vyentive services to fewer than 30 percent of eligible children, and no state provided preventive dental care to more than 50 percent of all eligible children. More disturbing is the finding that few Medicaid chil- dren who receive dental care get any services beyond a cleaning and fluoride treatment, despite their need for dental repair and fillings (Solomon 1998). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 253 Factors Affecting Oral Health over the Life Span Federal legislation enacted over three decades ago established a guarantee of dental care to Medicaid-eligible children through the Early and Periodic Screening, Diagnostic and Treatment Service (EPSDT; PL. 90-284). Final regulations, effective in early 1972 (U.S. Bureau of the Census 1998a), ensure comprehensive dental services—prevention, diagno- sis, and treatment for “teeth and associated structures of the oral cavity and disease, injury or impairment that may affect the oral or general health of the recip- ient”—and promise children access to dental servic- es of sufficient “amount, duration, and scope” to ensure oral health. Federal law also requires provi- sion of enabling services such as transportation and translation. In addition, revisions to the Social Security Act in 1989 (OBRA 89) made several changes to EPSDT services. States are now required to set a distinct periodicity schedule for the provision of dental services after consultation with recognized dental organizations involved in child health care. States are also required to provide any medically nec- essary dental service coverable under Medicaid to an EPSDT eligible child even if the service is not avail- able to individuals age 21 and older under the Medicaid state plan. Despite these laws and regula- tions, inadequate funding, chronically poor pay- ments to dentists, administrative burdens, and bene- ficiary utilization patterns have limited the effective- ness of this program (USDHHS 1996). Increasingly, states are electing to purchase den- tal care for low-income populations through man- aged care organizations rather than to pay providers directly for Medicaid. As states take on the role of purchasers of care rather than claims payers, their focus has turned to a concern for health outcomes. However, participation of dentists in managed care programs is low (AAPD 1997, ADA 1998b, NADP 1998), and the effort to move dental Medicaid care into managed care programs may further constrain the availability of care. A 1998 survey of state Medicaid authorities by the National Conference of State Legislatures report- ed that, on average, only 16 percent of dentists in the 35 responding states participate actively in Medicaid (i.e., were compensated more than $10,000 in the preceding 12 months for dental care to Medicaid- enrolled patients). In 24 of these 35 states, fewer than 20 percent of active dentists participate actively (Guiden 1998). The study also raised awareness that common Medicaid payment rates for five typical children’s dental procedures rarely exceed 65 to 70 percent of dentists’ usual fees (Guiden 1998), a per- centage that represents dentists’ typical overhead costs in delivering those services (ADA 1998b). A 1998 federally sponsored national meeting, “Building Partnerships to Improve Children's Access to Medicaid Oral Health Services,” also identified inad- equate payments to dentists among multiple barriers in Medicaid program administration. Barriers identi- fied by the conference were categorized as financing and funding issues, Medicaid policies and adminis- trative procedures, supply and distribution of providers, parental valuation of oral health, and lack of a systematic approach to identifying and promot- ing successful interventions (Spizak and Holt 1999). Medicaid expenditures for dental care are low. On average, state Medicaid agencies contribute only 2.3 percent of their child health expenditures to den- tal care (Yudkowsky and-Tang 1997), whereas nationally, the percentage of all child health expendi- tures dedicated to dental care is more than 10 times that rate, almost 30 percent (Lewit and Monheit 1992). A 1998 actuarial study of health care costs for children (AAP 1998) calculated that 21 percent of expenditures for a comprehensive package of health services (including inpatient, outpatient, mental, dental, vision, hearing, and pharmacy services, but excluding orthodontic care) should be dedicated to dentists’ services. This study suggests that fully $21.35 per child per month must be expended in order to meet the dental care needs of covered chil- dren. A similar study conducted by the Reforming States Group (1999) determined that $17 to $18 per child per month is a necessary expenditure for dental care, assuming that providers accept a modest discount on their fees when serving low-income children. In FY 1995, Medicaid expended only $4.44 per enrolled child per month (Yudkowsky and Tang 1997). Although states vary widely in the percentage of children covered by Medicaid and in the income lev- els they require for eligibility, all states must entitle child beneficiaries to comprehensive dental services under EPSDT. A review of 15 state oral health and dental access surveys (Tinanoff 1998) noted the fol- lowing recurrent themes about Medicaid in relation to children’s oral health: e States show similar dental care issues for Medicaid-enrolled children: high disease prevalence, low provider participation, and insufficient funding. e Children at the highest risk of having dental caries are the least likely to have access to regular dental care. e Barriers to provider participation include low reimbursement rates in a health care environment that has high overhead; perception of administrative 254 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL roblems with Medicaid programs, and patients who do not fit the expectations of the dentist. e Medicaid payments for dental care account for less than 3 percent of total state Medicaid child health expenditures in these states. e The percentage of EPSDT eligibles with a dental visit (an initial measure of access to care) fails to reflect the insufficiency of reparative care to meet children’s acute dental health needs. e Lack of access to dental services for Medicaid recipients is perceived as the greatest pedi- atric health care problem in many states. e Untreated dental problems get progressively worse and ultimately require more expensive inter- ventions, often in a hospital emergency room OF operating room. State Childrens Health Insurance Program. Thirty years after enacting Medicaid, the U.S. Congress in 1997 addressed the lack of medical coverage for over 10 million additional children by passing the State Children’s Health Insurance Program (SCHIP). The Congressional Budget Office anticipates that this pro- gram will extend health insurance to at least 2.5 mil- lion more children and in the process will identify many additional children who are eligible for, but not enrolled in, Medicaid. SCHIP complements the Medicaid program by providing health insurance to children whose family income is above Medicaid eli- gibility standards, generally up to 200 percent of the federal poverty level. SCHIP differs from Medicaid in that it is not an individual entitlement, and states have broad latitude in designing and implementing insurance programs for modest-income children. The law provides no direct mandate regarding services to be covered beyond immunizations and well-baby, well-child care. Dental coverage is specifi- cally cited as one of 28 services that can be funded with SCHIP dollars. Although states are not required to provide dental coverage, congressional report lan- guage and presidential pronouncements are explicit in emphasizing the need for dental care (ADA 1998a,b). Prior to signing the bill in August 1998, President Clinton stated, “it is important that we have an adequate benefit package for children, recog- nizing that there are some problems that children have in a way that is more profound than adults, including problems with vision, with hearing and with dental health.” Upon signing the bill, he said, “Because we have acted, millions of children all across the country will be able to get medicine, and have their sight and hearing tested and see dentists and doctors for the first time.” Factors Affecting Oral Health over the Life Span States can elect to apply federal SCHIP funds to expand Medicaid or they may use one of four options to provide services under a separate SCHIP program: 1) develop a new state program based on benchmark coverage, which is state employee coverage; 2) pro- vide coverage under the SCHIP using benchmark- equivalent health coverage, which requires the use of an actuarial report to determine that coverage is at least equivalent to one of the benchmark plans; 3) apply existing comprehensive state-based coverage available in New York, Florida, and Pennsylvania, and +) seek Secretary-approved coverage. Only 2 (Delaware and Colorado) of 56 states and territories have not included substantial dental care for most children covered by SCHIP’ States implementing SCHIP have expanded access to dental care services through a variety of mechanisms. Expanding cover- age through Medicaid ensures that newly enrolled children are entitled to dental coverage, although these children face the same barriers as other Medicaid children, as discussed previously. Even with current levels of commercial dental insurance and improved access through Medicaid and the new SCHIP program, almost one quarter of children will remain without dental coverage. The Social and Professional Environment for Prevention Although science continues to reveal new opportuni- ties to prevent disease and promote health, sufficient understanding already exists to significantly reduce common oral diseases for all children. One of the most critical findings is that effective prevention requires an early start. The American Academy of Pediatric Dentistry (AAPD 1997), the American Dental Association (ADA 1997), and the Bright Futures health supervi- sion consensus project (Green 1994) all recommend that a toddler be seen by a dental professional at 12 months of age for an initial examination and risk assessment for common oral diseases and injuries. This first visit provides an opportunity for parents to learn about multiple oral health issues—dental caries, periodontal health, injury prevention, dental development, oral habits, common soft tissue sores, and bite development—as well as how to promote their child’s complete oral health (Nowak 1997). Despite professional guidance and a Healthy People 2000 goal that 90 percent of children be seen by a dentist before entering kindergarten, only 63 percent of children have a dental visit before starting school (USDHHS 1997). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 255 Factors Affecting Oral Health over the Life Span Because growth and development is so pre- dictable, it can be anticipated and guided through education and carefully timed interventions. Applied to oral health, “anticipatory guidance” allows par- ents, children, and institutions to learn the stages of oral, facial, and dental development and how to care for the next stage of development (Nowak and Casamassimo 1995). Tables 10.2, 10.3, 10.4, and 10.5 provide examples of the risk and risk reduction methods related to periodontal diseases, dental caries, malocclusion, and injury, respectively (Casamassimo 1996). Physical, behavioral, socioen- vironmental, and disease and treatment-related fac- tors are addressed. Anticipatory guidance allows the parent, dental team, other health care providers, and institutions that care for the child to ensure a child's good oral health, avoiding preventable pitfalls and problems by knowing how a child’s mouth changes over time. For example, prevention of early child- hood caries requires guidance to tribute to the infant’s or toddler's general and oral health. Current investigations suggest that pathogen- ic exposures can be limited, children’s resistance to acquiring disease-causing bacteria can be enhanced, physical and chemical barriers to transmission can be erected, and early-stage disease can be reversed with medications. Importantly, there is no one-size- fits-all solution to disease prevention and suppres- sion. Most acquired dental and oral disease of child- hood is preventable. The challenge today is to bring the promise of prevention to the most vulnerable of our children and youth. Meeting the challenge will require enhancing programs such as the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC), Head Start, along with early child care, and community and school-based centers. Families have the capacity to support healthy oral health practices, as well as to support and caregivers before the child's teeth erupt to prevent or limit the trans- mission of microbial infections from mother to child and to pro- TABLE 10.2 Risk Factors Risk and protective factors for periodontal diseases Risk Reduction Methods mote appropriate feeding prac- tices even before the child has any teeth in place (Grindefjord et al. 1995, Kohler et al. 1984, 1988, Li Physical Examples and Caufield 1995, Tanzer 1995). ruber Similarly, anticipatory guidance Pregnancy for oral health extends to safe- Mouthbreathing guarding a house to prevent oral burns and injuries and to teach parents about the dangers of for- eign objects in the mouths of tod- dlers and preschoolers. Anticipat- ing a young persons interest in sports requiring mouth guards or head protection, discouraging smoking and smokeless tobacco before they are first used, and encouraging teens to adopt hy- giene practices that prevent peri- odontal disease initiation also are examples of guidelines that need to be addressed by all individuals and organizations responsible for the child. There is promise for further Lefevre syndrome} Behavioral Examples Inadequate oral hygiene Tobacco use Poverty Injury hypophosphatasia) treatment) Anatomical variations (e.g., frenum) Malpositioned and crowded teeth Genetic predisposition (e.g., Down or Papillon Socioenvironmental Examples Poor oral health and hygiene Disease- or Treatment-related Examples Nutritional deficiencies (e.g., vitamin C) Metabolic disease (e.., diabetes, Neoplastic disease (e.g., leukemia or its Infectious disease (e.g., HIV/AIDS) Surgical correction Orthodontic care Treatment of disease Preventive measures to address oral effects Preventive measures to address oral effects Management of mouthbeathing Preventive intervention to minimize effects Improved oral hygiene Tobacco cessation Access to care and improved oral hygiene Access to care Use of age-appropriate safety measures and treatment of injury Healthy eating habits Treatment of disease Treatment of disease and preventive intervention to minimize effects Treatment of disease and preventive intervention to minimize effects eradication of common childhood dental and oral infections. Edu- cation regarding oral infections in mothers and caregivers can con- 256 Medications (e.g., Dilantin) Poor-quality restorations Unrestored carious lesions Preventive intervention to minimize effects Restoration of carious lesions Properly contoured and finished restorations Source: Modified from Casamassimo 1996. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL encourage behaviors conducive to health and well- being, no matter their income. Communities that recognize children’s oral health as an important pub- lic good can provide resources and ensure services, ranging from sealant programs, school education, and fluoridation programs to candy-free aisles in gro- cery stores and merchant campaigns to combat teen smoking and drinking. At the state and federal levels, however, the good intentions of legislation have fallen short of adequate implementation. Nevertheless, by linking the power of growth and development with health promotion activities, the nation has the potential to bring excel- lent oral health to all children. Health promotion covers a spectrum of efforts: anticipating problems, preventing them from occur- ring, and suppressing them when they first occur. These efforts can be targeted to individual children or entire communities of children, particularly children at high risk for dental and oral problems. Factors Affecting Oral Health over the Life Span Adolescents and Young Adults Data regarding oral health during adolescence and young adulthood are not abundant. However, most teenagers and young adults live healthy and active lives. Indeed, these years represent a peak period of biological fitness. This also is a time when individu- als are exposed to and begin behaviors that may place them at risk, such as tobacco and alcohol use and poor dietary practices. For 12- to 17-year-olds who use smokeless (spit) tobacco, for example, 34.9 per- cent of current snuff users and 19.6 percent of cur- rent chewing tobacco users had tobacco-related oral lesions (Tomar et al. 1997). (See Box 10.2 on the effects of tobacco on oral health.) Adolescents become more mobile, traveling independently in cars, motorcycles, and other vehicles, where the use of safety belts and helmets is needed. Sexual prac- tices begin during this time, further exposing indi- viduals to infections that predispose them to general and oral health problems. Ideally, TABLE 10.3 Risk and protective factors for dental caries Risk Factors Risk Reduction Methods the prevention of risk behaviors begins earlier in life, but this stage of life brings such a cascade of events that even the most informed and well-supported adolescent may Physical Examples Variations in tooth enamel; deep pits and fissures; anatomically susceptible areas Sealants (if possible) or observation find it difficult to adhere to prac- tices recommended by caregivers and institutions. Gastric reflux High mutans streptococci count Special health needs Previous caries experience History of baby bottle tooth decay Behavioral Examples Bottle used at night for sleep or “at will” while awake Frequent snacking Inadequate oral hygiene Eating disorders, including self-induced vomiting (bulimia) Socioenvironmental Examples Inadequate fluoride Poor oral health and hygiene Poverty High parental levels of bacteria (mutans streptococci) Diseases or Treatment-related Examples Special carbohydrate diet Frequent intake of sugared medications Reduced saliva flaw from medication or irradiation Orthodontic appliances Management of condition Reduction of mutans streptococci Preventive intervention to minimize effects Increased frequency of supervision visits Increased frequency of supervision visits Prevention of bottle habit and weaning from bottle by 12 months Reduction in snacking frequency Improved oral hygiene Referral for counseling Optimal systemic and/or topical fluoride Access to care and improved oral hygiene Access to care Good parental oral health and hygiene Preventive intervention to minimize effects Alternate medications or preventive intervention to minimize effects Saliva substitutes Good oral hygiene for appliances Source: Modified from Casamassimo 1996, This period of life also is marked by rapid change as individuals move from school to work to marriage and parenting, possibly relocating far from their birthplace. Many young persons who were fortunate to have health insurance lose their coverage after they leave college or are no longer “dependents.” Health status is largely determined by lifestyle behaviors and socioeconomic factors reflecting education, career, and income. About one third of 15-year- olds have experienced dental caries in their permanent teeth, and another 20 percent have untreated dental decay. Poor adolescents have higher disease rates and more untreated disease. Periodontal dis- eases, as defined by having 4 mm or more of attachment loss, are seen in about 3 percent of 18- to 24-year-olds, although it is in the ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 257 Factors Affecting Oral Health over the Life span Variations in development (e.g., tooth eruption delays and malpositioned teeth) Muscuiar imbalances Familial tendency for malocclusion Conditions associated with malocclusion (e.g., cleft lip/palate) Behavioral Examples Nonnutritive sucking habits Disease- or Treatment-related Examples Injury Acquired problem from systemic condition or its therapy Loss of space due to caries Musculoskeletal conditions (e.g., cerebral palsy) Skeletal growth disorders (e.g., renal disease) TABLE 10.4 Risk and protective factors for malocclusion Risk Factors Risk Reduction Methods Physical Examples Congenital absence of teeth Early intervention Mouthbreathing Management of mouthbreathing Early intervention Early therapy Early intervention Early intervention Elimination of habit Use of age-appropriate safety measures (e.g, car safety seats, safety belts, stair gates, mouth guards) and treatment of injury Dental intervention as a part of medical care Early intervention for caries Dental intervention as a part of medical care Dental intervention as a part of medical care Source: Modified from Casamassimo 1996. TABLE 10.5 Risk and protective factors for injury Risk Factors Risk Reduction Methods Physical Examples Lack of protective reflexes Poor coordination Protruding front teeth Behavioral Examples Failure to use safety measures appropriate for infant/child/adolescent (e.g., car safety seats, stair gates, mouth guards, safety belts) Participation in contact sports Socioenvironmental Examples Substance abuse in family Substance use by child or adolescent Child abuse or neglect Multiple family problems Disease- or Treatment-related Examples Overmedication Hyperactivity Referral for appropriate therapy Referral for appropriate therapy Orthodontic care Use of age-appropriate safety measures Use of protective gear Referral for counseling Referral for counseling Referral for counseling Referral for counseling Adjustment of medications Management of condition Source: Modified from Casamassime 1996. adolescent years that early-onset periodontitis is first diagnosed. Young non-Hispanic blacks have twice the proportion of periodon- tal disease than either white or Mexican Americans aged 30 to 49 years. Complete tooth loss is low in this age group, with only an estimated 0.4 percent of individu- als aged 18 to 34 years having no teeth (see Chapter 4). These years also mark the period of life when intentional and unintentional injuries take their greatest tell, Because many of these injuries affect the oral-facial region, they have special relevance to oral health. In particular, the example of oral-facial sports injuries illustrates the roles of behavior and socioeconomic envi- ronment as determinants of health, as well as pointing to several actions, such as use of protective head gear and mouth guards, that can serve as correctives. Midlife Adults Adults between 35 and 65 have been aptly called “the sandwich generation”—caring simultane- ously for aging parents and dependent children, while trying to maintain their own health, careers, and family structure. This population cohort is growing in numbers in parallel with the ever- increasing numbers of the elderly. Although many older Americans will be self-sufficient for the rest of their lives, about one third will require higher levels of care because of chronic or terminal illness. The demographic nature of these middle-aged adults is com- plex. In many families, both spouses work and have moved from their birthplaces. Many oth- ers have divorced, remarried, moved again, lost or changed jobs, and experienced a variety of midlife crises. Adding to the 258 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL BOX 10.2 The Effects of Tobacco on Oral Health The use of tobacco products—cigarettes, cigars, pipes, and smokeless (spit) tobacco products (snuff and chewing tobacco) —has emerged as 3 major preventable risk factor for a number of oral diseases and disorders. Oral and Pharyngeal Cancers Cigarettes. Tobacco smoke contains over 4,000 compounds, some of which are carcinogenic, toxic, or mutagenic (USDHHS 1989). An exten- sive review of the literature has clearly established a causal relationship between cigarette smoking and oral cancer (USDHHS 1982, 1989). Indeed, about 90 percent of oral cancer deaths are attributable to smoking (Shopland 1995, USDHHS 1989}, and smoking cessation can significantly reduce the risk (USDHHS 1999). : Smokeless (Spit) Tobacco. These products are causally linked to oral and pharyngeal cancers (IARC 1985, Nash 1986, USDHHS 1986). About 30 carcinogens have been found in spit tobacco, including tobacco-specif- ic N-nitrosamines, benzo[alphalpyrene, and formaldehyde (Hoffman and Djordjevic 1997). Spit tobacco users have an oral cancer risk 4 to 6 times that of nonusers (Blot et al. 1988, Winn et al. 1981). Characteristic mucosal lesions are associated with spit tobacco use (Axéll et al. 1976, Holmstrup and Pindborg 1988, Peacock et al. 1960, Pindborg and Renstrup 1963) and can be found even among adolescent users (Greer and Poulson 1983, Offenbacher and Weathers 1985, Poulson et al. 1984, Tomar et al. 1997b, Wolfe and Carlos 1987). They are considered poten- tially premalignant (USDHHS 1986). Cigars and Pipes. Cigar smoke contains the same toxic and carcinogenic compounds found in cigarette smoke (Hoffmann and Hoffmann 1998). Arecent review of case-control and cohort studies also shows a consis- tent elevation in risk for oral and pharyngeal cancers among cigar smokers, with cigar smokers having 2 to 22 times the risk of non-smok- ers of cigars (USDHHS 1998). The risk of oral and pharyngeal cancers increases with the number of cigars smoked per day and the depth of inhalation. Although data for pipe smoking and oral cancer risk are more limited than data for use of other forms of tobacco, relative risk estimates from longitudinal studies are similar for pipe smokers and cigarette smokers (USDHHS 1982, 1989). Periodontal Diseases Reviews of the literature have long implicated cigarette smoking as a risk factor for periodontal diseases. More recent studies such as Grossi et al. (1994, 1995) showed that smoking was a major risk factor for periodontal disease in a group of 1,500 adults. Measured either by radiographic bone height or probing attachment level, and after adjusting for age, sex, socioeconomic status, and plaque and calculus levels, the investigators found that smokers were 7 times more likely to develop periodontal disease than nonsmokers. They also found a direct linear dose-response relationship between the level of smoking, assessed by pack years (number of cigarettes smoked per day times years smoked), and destructive periodontitis. Smoking is also a prognostic indicator: current smokers are at a significantly greater risk for further loss of periodontal attachment than are nonsmokers, with an odds ratio of 5.4 (95 percent confidence interval of 1.5 to 19.5). Mechanisms explaining the association suggest that smoking depress- es immune responses (Holt 1987, Sasagawa et al. 1985), including diminishing white blood cell activity (Gala et al. 1984, Kenney et al. 1977). Toxic and vascular effects as well as effects on the subgingival flora are also suggested. In addition, smokers do not heal as well as nonsmokers after periodontal disease therapy and experience less reduction in levels of periodontal pathogens (Grossi et al. 1997). The negative effects of smoking can be reversed with cessation of tobacco use. After 10 years, former smokers appear to be no more likely than nonsmokers to have severe loss of periodontal attaghment (Tomar and Marcus 1998). Spit Tobacco. Reports indicate that oral tobacco use results in gingival recession at the usual site of snuff or chewing tobacco placement. Ina study of adolescent males, Offenbacher and Weathers (1985) found that 60 percent of users had gingival recession, compared with 14 per- cent of nonusers. Dental Caries The strongest evidence for an association of tobacco use and risk for dental caries relates to the use of chewing tobacco and increased risk for root caries. The causative factor relates to the sugar content of the product. Several popular brands of chewing tobacco have high levels of ~ fermentable sugars (between 30 and 60 percent by weight). In a cross- sectional study of older adults in North Carolina, chewing tobacco users had a higher number and percentage of root surfaces affected by caries than those who used other forms of tobacco or had never or formerly used tobacco (Tomar et al. 1997a). This finding was confirmed in an analysis of data from NHANES Ill (Tomar and Winn 1998). Trends in Tobacco Use In 1995, 47 million adults—25 percent of the U.S. adutt population— were smokers (CDC 1997). This figure represents a steady decline from the 52 percent of the population reported to be smokers in 1965, the year following the release of the first Surgeon General's Report on Tobacco (Giovino et al. 1995). The prevalence of smoking in women was 34 percent in 1965, 30 percent in 1979 (Giovino et al. 1994), and 23 per- cent in 1995 (CDC 1997). in contrast, cigarette smoking in adolescents has been increasing. Daily smoking among high school seniors increased from 17 percent in 1992 to 22 percent in 1996 (Johnston et al. 1997). High school students who reported smoking in the preceding month increased from 27.5 percent in 1991 (USDHHS 1994) to 36 percent in 1997 (CDC 1998}. Spit tobacco use has also increased. Sales of moist snuff—the most popular form of spit tobacco used by young people (Tomar et al. 1995)—have increased every year since the mid-1970s (FIC 1997, Maxwell 1992, USDA 1997). About 20 percent of male high school stu- dents reported using spit tobacco during the previous month (CDC (continues) ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Factors Affecting Oral Health over the Life Span 259 Factors Affecting Oral Health over the Life Span 260 BOX 10.2 continued 1996, Johnston et al. 1997). About 6 percent of adult males use spit tobacco (CDC 1993). Nearly all regular users are male. Aggressive marketing has also led to explosive growth of sales and con- sumption of cigars. Between 1993 and 1997, cigar consumption increased nearly 50 percent (Gerlach et al. 1998).In 1997, 22 percent of high school students smoked at least one cigar in the preceding 30 days (CDC 1998). Implications of Trends For Oral and Pharyngeal Cancers. The increases in spit tobacco and cigar use among young people do not bode well for the oral and general - health of coming generations of Americans. Over the past 35 years the decline in the incidence and mortality rates of oral cancer has been attributable to dectines in cigarette smoking primarily in adult white males. Cigarette smoking among African American males over the same time period was higher. This practice contributed to the higher rates of oral cancer among black males during these years. However, recent studies indicate precipitous declines in smoking among black males, so that their smoking rates are approaching the rates seen in white males (USDHHS 1998). Indeed, figures on smoking among ado- lescent and younger African American adults have even been lower than those for their white counterparts. These trends could result in substantial reductions in the risk for oral cancer among African Americans, were they to continue. Unfortunately, there is recent evi- dence that cigarette smoking among African American high school stu- dents is increasing (CDC 1998). For Periodontal Diseases. The growing popularity of cigar smoking may counter the declines in cigarette smoking and maintain the percentage of periodontal disease attributable to tobacco use. References Axéll T, Mornstad H, Sundstrom B. The relation of the clinical picture to the histopathology of snuff dipper’s lesions in a Swedish popula- tion. J Oral Pathol 1976;5:229-36. Blot W!, McLaughlin JK, Winn DM, Austin DF, Greenberg RS, Preston- Martin S, Bernstein L, Schoenberg JB, Stemhagen A, Fraumeni JF Jr. Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 1988;48:3282-7. Centers for Disease Control (CDC). Use of smokeless tobacco among adults—United States, 1991. MMWR Morb Mortal Wkly Rep 1993(a};42:263-6. Centers for Disease Control and Prevention (CDC). Tobacco use and sources of cigarettes among high school students—United States, 1995. MMWR Morb Mortal Wkly Rep 1996;45(20):413-8. Centers for Disease Control and Prevention (CDC). Cigarette smoking among adults—United States, 1995. MMWR Morb Mortal Wkly Rep 1997;46:1217-20. Centers for Disease Control and Prevention (CDQ). Tobacco use among high school students—United States, 1997. MMWR Morb Mortal Wkly Rep 1998;47:229-33. federal Trade Commission (FTC). 1997 smokeless tobacco report to Congress. Washington: Federal Trade Commission; 1997. Gala D, Kreilick RW, Hoss W, Matchett S. Nicotine-induced membrane perturbation of intact human granulocytes spin-labeled with 5- doxylstearic acid. Biochim Biophys Acta 1984;778:503-10. Gerlach KK, Cummings KM, Hyland A, Gilpin EA, Johnson MD, Pierce JP. Trends in cigar consumption and smoking prevalence. In: National Cancer Institute. Cigars: health effects and trends. Smoking and Tobacco Control Monograph 9. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National institutes of Health; 1998. p. 21-53. NIH Pub. no. 98-4302. Giovino GA, Schooley MW, Zhu BP. Chrismon JH, Tomar SL, Peddicord JP. Merritt RK, Husten CG, Eriksen MP.Surveillance for selected tobacco- use behaviors—United States, 1900-1994. MMWR Morb Mortal _ Wkly Rep 1994;43(SS-3):1-43. Giovino GA, Henningfield JE, Tomar SL, Escobedo LG, Slade J. Epidemiology of tobacco use and dependence. Epidemiol Rev 1995;17:48-65. Greer RO, Poulson TC. Oral tissue alterations associated with the use of smokeless tobacco by teen-agers. Part I. Clinical findings. Oral Surg 1983;56:275-84. Grossi SG, Zambon JJ, Ho AW, Koch G, Dunford RG, Machtei EE, Norderyd OM, Genco RJ. Assessment of risk for periodontal disease. |. Risk indicators for attachment loss. J Periodontol 1994;65:260-7. Grossi SG, Genco RJ, Machtei EE, Ho AW, Koch G, Dunford R, Zambon JJ, Hausmann EE, Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontal 1995;66:23-9. Grossi SG, Zambon J, Machtei EE, Schifferle R, Andreana S, Genco RI, Cummins D, Harrap G. Effects of smoking and smoking cessation on healing after mechanical periodontal therapy. J Am Dent Assoc 1997;128:599-607. Hoffmann D, Djordjevic MV. Chemical composition and carcinogenicity of smokeless tobacco. Adv Dent Res 1997;11:322-9. Hoffmann D, Hoffmann |. Chemistry and toxicology. In: National Cancer Institute. Cigars: health effects and trends. Smoking and Tobacco Control Monograph 9. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health; 1998. p. 55-104. NIH Pub, no, 98-4302. Holmstrup P, Pindborg JJ. Oral mucosal lesions in smokeless tobacco users. CA Cancer J Clin 1988;38:134-41. Holt PG. Immune and inflammatory function in cigarette smokers. Thorax 1987;42:241-9. International Agency for Research on Cancer (IARC). Tobacco habits other than smoking; betel-quid and areca-nut chewing; and some related nitrosamines. IARC Working Group. Lyon, 1984 Oct 23-24. IARC Monogr Eval Carcinog Risk Chem Hum 1985 Sep;37:1-268. Johnston LD, Bachman JG, 0’Malley PM. Monitoring the future: ques- tionnaire responses from the nation’s high school seniors, 1995. Ann Arbor (MI): Survey Research Center, Institute for Social Research, University of Michigan; 1997. Kenney EB, Kraal JH, Saxe SR, Jones J. The effect of cigarette smoke on human oral polymorphonuclear leukocytes. J Periodont Res 1977;12:227-34. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Maxwell JC Jr. The Maxwell consumer report: the smokeless tobacco industry in 1991.Richmond (VA): Wheat, Butcher, and Singer; 1992. Nash DB. Health implications of smokeless tobacco: a National Institutes of Health Consensus Development Conference. Ann Intern Med 1986;104:436-7. Offenbacher S, Weathers DR. Effects of smokeless tobacco on the peri- odontal, mucosal and caries status of adolescent males. J Oral Pathol 1985;14:169-81. Peacock EE, Greenberg BC, Brawley BW. The effect of snuff and tobacco on the production of oral carcinoma: an experimental and epi- demiological study. Ann Surg 1960;151:542-50. Pindborg JJ, Renstrup G. Studies in oral leukoplakias. Il. Effect of snuff on oral epithelium. Acta Derm Venereol 1963;43:271-6. Poulson TC, Lindenmuth JE, Greer RO. A comparison of the use of smokeless tobacco in rural and urban teenagers. CA Cancer J Clin 1984;34:248-67. Sasagawa S, Suzuki K, Sakatani 7, Fujikura T. Effects of nicotine on the functions of human polymorphonuclear leukocytes in vitro. J Leuk Biol 1985;37:493-502. Shopland DR. Tobacco use and its contribution to early cancer mortali- ty with a special emphasis on cigarette smoking. Environ Health Perspect 1995; 103(Suppl 8):131-42. Tomar SL, Marcus SE. Cigarette smoking and periodontitis among U.S. adults. J Dent Res 1998;77(Spec No B):830 (abstract 1585]. Tomar SL, Winn DM. Coronal and root caries among U.S. adult users of chewing tobacco. J Dent Res 1998;77(Spec No A):256 [abstract 1205}. Tomar SL, Giovino GA, Eriksen MP. Smokeless tobacco brand preference and brand switching among US adolescents and young adults. Tob Control 1995;4(1):67-72. . Tomar SL, Weintraub JA, Gansky SA. Coronal and root caries among long-term users of chewing tobacco. J Dent Res 1997a;76(Spec No):372 [abstract 2872]. Tomar SL, Winn DM, Swango GA, Giovino GA, Kleinman DV. Oral mucos- al smokeless tobacco lesions among adolescents in the United States. J Dent Res 1997b;76(6):1277-86. U.S. Department of Agriculture (USDA). Tobacco situation and outlook report. TBS-239. Washington: U.S. Department of Agriculture, Commodity Economics Division, Economic Research Service; 1997. U.S. Department of Health and Human Services (USDHHS). The heaith consequences of smoking: cancer. Rockville (MO): U.S. Department demands of a spouse and children, the care of older parents contributes yet another strain to caregivers “in the middle.” These caregivers are predominantly female and may be dependent on their own income. They may be single and faced with dealing with their own “passages” (Sheehy 1984). The baby boomers will be the first U.S. genera- tion to age while maintaining their natural dentition. They are the first to benefit from the caries preventive effect of widespread community water fluoridation and fluoride dentifrices. As a result, the baby Factors Affecting Oral Health over the Life Span of Health and Human Services, Public Health Service, Office on Smoking and Health; 1982. DHHS Pub. no. PHS 82-50179. U.S. Department of Health and Human Services (USDHHS). The health consequences of using smokeless tobacco: a report of the Advisory Committee to the Surgeon General, 1986. Washington: U.S. Department of Health and Human Services, Public Health Service; 1986. NIH Pub. no, 86-2874. U.S. Department of Health and Human Services (USDHHS). Reducing the health consequences of smoking: 25 years of progress. A report of the Surgeon General. Rockville (MD): U.S. Department of Health -and Human Services, Centers for Disease Control, Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1989. DHHS Pub.no. CDC 89-8411.” U.S. Department of Health and Human Services (USDHHS). The heaith benefits of smoking cessation: a report of the Surgeon General. Atlanta:U.S. Department of Health and Human Services, Centers for Disease Control, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1990. DHHS Pub. no. CDC 90-8416. U.S. Department of Health and Human Services (USDHHS). Preventing tobacco usé among young people: a report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 1994. US. Department of Health and Human Services (USDHHS). Tobacco use among U.S. racial/ethnic minority groups: African Americans, American Indians and Alaskan Natives, Asian Americans and Pacific Islanders, and Hispanics. A report of the Surgeon General. Atlanta: J.5. Department of Heaith and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 1998. Winn DM, Blot WJ, Shy CM, Pickle LW, Toledo A, Fraumeni JF. Snuff dip- ping and oral cancer among women in the southern United States. N Engl J Med 1981;304:745-9. Wolfe MD, Carlos JP. Oral health effects of smokeless tobacco use in Navajo Indian adolescents. Community Dent Oral Epidemiol 1987;15:230-5. boomers bring to the aging process higher expecta- tions about oral health throughout the lifecycle. Maintaining the family’s oral health may require as many individual solutions as there are sandwich generation members (Sanders 1997, Stern 1994, Warner 1995). Healthy lifestyle decisions combined with preventive measures at home will be as impor- tant as regular professional care. In addition to their own oral hygiene practices, a key component of maintaining the oral health of midlife Americans is the availability of dental bene- ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 261 Factors Affecting Oral Health over the Life Span fits. Six of 10 full-time employees are offered dental benefits by their employers, according to a survey by the U.S. Bureau of Labor Statistics (www. e-dental.com/Virtual Community for the Dental Industry, 12/30/99). These data are from a 1997 sur- vey of firms with 100 or more employees in private nonagricultural industries and are representative of benefits available to 46 million workers. The dental benefits, one of the less prevalent benefits for employees, vary by occupation group and are higher for professional and technical employees (64 per- cent) than for blue-collar or service employees (56 percent). Among the estimated 22.6 million employ- ees with employer-provided dental benefits, most employees (81 percent) receive their care from tradi- tional fee-for-service plans; 11 percent, from pre- ferred provider organizations; and 8 percent, from health maintenance organizations. Ensuring the oral health of the middle-aged gen- eration must take into account the shifting patterns of need and the family’s ability to cope, the education and training of health care workers about geriatric and family issues, general comprehensive communi- ty education programs about aging, estate and taxa- tion issues, housing, and social policies and pro- grams that support all individuals in their quest for self-sufficiency and individual responsibility. Older Americans Continued growth of the population 65 and older will have profound effects on health care in the twenty-first century (National Institute on Aging 1997). By 1994 the number of persons 65 and older had grown to 33.2 million and represented 13 percent of the population. Although the total US. population is expected to increase by 42 percent over the next half century, the number of men and women 65 and older will increase by 126 percent, those 85 and older by 316 percent, and centenarians by 956 percent—nearly 10 times the present number. The baby boom generation currently makes up almost one third of the U.S. population. By 2011, when these men and women reach 65, they will swell the ranks of older Americans and significantly bur- den health care programs and organizations respon- sive to the needs of older Americans (National Institute on Aging 1997). Although members of this generation can look forward to continued good oral and general health, the challenge will be in providing effective oral health care for those who are not in good health, especially the oldest old, and those with limited financial support. Oral Health Status Chapter 4 provides selected oral health data for older Americans as a whole. There is great heterogeneity in oral health status among older Americans. The extent and severity of oral conditions varies across subpop- ulations of this age group, and many have unmet treatment needs. Even so, older Americans are retain- _ing their teeth more than ever before and hence remain subject to oral diseases and disorders (Douglass et al. 1998). Indeed, with more teeth at risk, there will be an increase in coronal and espe- cially root caries among the elderly, as well as peri- odontal diseases and inadequate or absent prostheses (Burt 1992). Oral and pharyngeal cancers are prima- rily diagnosed in older Americans. For a closer look at the oral health of both insti- tutionalized and homebound elderly, Dolan and Atchison (1993) compiled data based on a compre- hensive review of the literature. Although the long- term care population is easily accessible in large groups, oral examinations for research purposes can be challenging. Patient consent and antibiotic pre- medication are issues, as well as the fact that conven- ience samples must be used because many patients are unable to cooperate. The authors’ summaries of oral health status and perceived needs based on the most comprehensive homebound and long-term care oral health surveys are shown in Tables 10.6 and 10.7, respectively. Table 10.6 describes eight studies, with 31 to 289 patients, with edentulous rates ranging from 23.8 to 62 percent. In these studies use of dental services within the past year ranged from 8 to 100 percent. In a 1994 Home Health and Hospice sur- vey, only 1 percent of patients reported having a dental visit during that year (Dey 1996). Forty- three to 83 percent of persons in six of the home- bound studies in Table 10.6 recognized that they had dental problems. In the long-term care studies listed in Table 10.7, 45 to 65 percent of those surveyed were completely without their natural teeth. One study found that 17 percent required immediate or emergency dental care. By any standards in the United States, a high degree of dental disease and dental care needs was recognized in all four studies presented. Daily oral care is an important and easily neg- lected service that should be offered to this popula- tion. Unlike many of the inevitable declines the frail elderly face with their various diagnoses, the decline in oral health can be stayed with good daily oral care. Nursing staff participation in the daily oral care of long-term care patients is crucial. Mouth care is often 262 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL considered an unpleasant task and is often delegated to nursing auxiliaries, who have even less oral health training than registered nursing staff. Seventy percent of patients in long-term care facilities had unaccept- able levels of oral hygiene (Kiyak et al. 1993, Mcintyre et al. 1986). Barriers to such needed care include lack of knowledge about oral care by the nursing staff, per- ceived lack of time for care, and lack of perceived need for daily oral care by both caregivers and patients. The resulting failure to provide daily oral Factors Affecting Oral Health over the Life Span care will often doom oral health that had been previ- ously well maintained. Data on the oral health status of hospice patients are scarce. Although not all hospice patients are eld- erly, data from the 1994 Home and Hospice Care Survey showed that 19.8 percent of those in hospice care wore dentures. The terminally ill often suffer from taste alterations, oral soreness, oral dryness, and oral candidiasis or thrush (Aldred et al. 1991). In most cases, the caregiver will perform daily oral care and palliative oral care measures. Palliative care can TABLE 10.6 Summary of published reports and abstracts on the oral health status and barriers to dental care for homebound elders of homebound persons in Kentucky Sample Sample Mean Dental Percentage Size Description Age (years) Utilization Edentulous Findings Steitel et ai. 1979 64 Two nonprofit Approx.75 25% visit in past Approx. 60% 60% reported dental needs, visiting nurse year dentate subjects more likely to services, Seattle seek care , Barrier: transportation Yellowitz et al. 1988 107 Recipients of visiting NA 34% visit in past NA >50% reported mouth [abstract] nurse services, Utah year discomfort, painful tongue, dry mouth, difficulty chewing Kaste et al. 1989 289 Homebound, >65 82.5 50% with no visit 62% 43% perceived dental need [abstract], Marcus et years, recipients of in 10 years Barriers: transportation, cast, al. 1989 [abstract] home care services, needed physical assistance Boston Aponte-Merced et al. 50 Recipients of home 79.0 8% visit in past 59% 37% had dental complaint; 1990 [abstract] health services, year 60% perceived dental need; county health 28% no visit in 84% wanted treatment departments, 20 years Alabama Strayer et al. 1990 67 Clients of urban NA Not reported 44% 80% perceived dental need [abstract], Strayer et social service Barriers: transportation, cost, al. 1997 [abstract] agency, 60% physical impairments homebound Yellowitz et al. 1991 123 Recipients, veterans 72.2 40% visit in past 33% 50% reported dental health {abstract} hospital-based home year fair/poor; 50-83% perceived cafe, Denver and dental need Minneapolis Barriers: 53% no perceived need; 25% had no dentist; 22% transportation; 22% cost Strayer and Ibrahim 34 Chart audit, patients 748 100% 23.8% 59.7% had 1991 treated at Ohio State periodontal/preventive/ University operative needs; Williams and Butters Statewide survey to 68.6 53.8% visit in NA 27.3% prosthodontic needs; 1992 identify the number past year 46.8% surgical needs; 2.7% of Kentucky households have a homebound resident Source: Dolan and Atchison 1993. Copyright 1993 by American Association of Dental Schools. Reprinted by permission of American Association of Dental Schools (2000). ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 263 Factors Affecting Oral Health over the Life Span include oral moisturizers such as artificial saliva, ice chips, a water atomizer, daily oral-cleaning or swab- bing, and, if needed, treatment for yeast to relieve oral pain. Americans have the potential to experience a life- time of oral health rather than a lifetime of oral restorative care. Each of the following questions can be applied to the major oral problems of the elderly, TABLE 10.7 Empy et al. 1983 California Dental Association (CDA) 1986 Veterans Administration (VA) 1989 Kiyak et al, 1993 Mean Age (years) Sample Description 242 residents of 12 skilled 81 nursing facilities; stratified random sample; Washington state 286 residents of a stratified 81 random sample of nursing homes , 634 residents of six VA 7] facilities: Florida, Illinois, Massachusetts; regional convenience sample 1,063 residents of 31 nursing homes in Washington state range 72 to 98 Dental Utilization mean time since last dental visit: 4,9 years 22% visit in past year Not reported Not reported Percentage Edentulous 65.3% 57% 50% 44.8% Summary of four published reports on the oral health status and barriers to dental care for nursing home residents Findings Needing denture treatment: urban, semirural, rural; 63, 46, 39%, respectively Mean number of decayed teeth: 1.8, 3.0, 2.4, respectively Mean number of periodontally involved teeth: 1.9,0.7, 1.1, respectively 80% who did not intend to visit dentist felt “no need” Median age of dentures: 15.5 years 17% had immediate dental needs Dentate residents: mean number teeth: 17 12.9% carious 7.0% fractured 49.6% periodontal disease 75.8% needed 1+ quadrants scaling Prosthodontic needs: 25% maxilla, 28% mandible Reasons for not seeking care: 52% felt no need; 24% transportation; 9% finances, 9% illness; 43% oral mucosal disease Dentate residents: 3.7 decayed coronal surfaces (DFS = 18.6) 4.8 decayed root surfaces (DFS = 6.5) Average periodontal attachment loss: 2.5 mm, 27% pockets >4 mm Prosthodontic needs: 35% maxilla, 28% mandible 40% denture-related oral lesions Dentate residents: oral problems: 72% poor oral hygiene 36% root caries 26% coronal caries 24% retained root tips 18% significant tooth mobility 11% swelling, soft tissue lesions 10% dry mouth Edentulous residents: oral problems: 46% loose dentures 18% sore ar bleeding gums 15% poor oral hygiene 10% dry mouth 5.4% soft tissue lesions 63.8% had dental treatment needs Source: Dolan and Atchison 1993. Copyright 1993 by American Association of Dental Schools. Reprinted by permission of American Association of Dental Schools (2000). 264 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL including coronal and root caries, periodontal dis- eases, oral cancer, oral-facial pain, tooth loss, salivary gland dysfunction, and oral mucosal diseases: e How do we best identify elders at greatest risk for oral diseases? Who is not at risk? How can we improve diagnostic accuracy? When is increased accuracy not related to improved outcomes? e Can these diseases be prevented or delayed? Which measures are most effective? Which have the greatest benefit for the least cost? e Once a person has the disease, which treat- ments are most effective? When measuring effectiveness, care should be taken to consider the proximal outcomes, that is, effects at the tissue level, as well as ultimate out- comes, that is, how the overall effects of the treat- ment affect a person's ability to function and be a pro- ductive, contributing member of society. An important consideration in treating oral health problems in the elderly is the relationship between oral and general health. Too often, oral health care is ignored or takes second place in light of the high prevalence of such chronic and life-threat- ening conditions as heart disease, stroke, cancer, osteoporosis, and diabetes. Yet the evidence present- ed in Chapter 5 speaks to associations linking oral infectious diseases such as periodontitis to the increased risk for cardiovascular, cerebrovascular, and lung disease, to exacerbations of diabetes, and as an early indicator of osteoporosis. In turn, to ignore oral health care in the course of cancer radiation and chemotherapy predisposes the patient to serious oral infections, mucositis, severe pain, bone loss, and potential abscesses. The 1988 Surgeon General's Workshop on Health Promotion and Aging stated that all health care providers should be educated in the importance of oral health to overall health and well-being (USDHHS 1988). Insurance Issues. In light of the oral care needs of the elderly and their vulnerability to systemic diseases, the lack of dental insurance poses a serious barrier (Jones et al. 1990, Niessen 1984). Medicare funds cover only a negligible and select amount of care. Many elders lose their dental insurance at retirement (Niessen 1984). The situation may be worse for older women. Because women overall have lower incomes than men, lack of insurance and high copayments for dental services may represent formidable obstacles to care. In addition, women assume a disproportionate burden as caregivers for family members of all ages: the young, the sick, and the elderly (Niessen 1984). This often disrupts employment and, consequently, insurance coverage. Factors Affecting Oral Health over the Life Span Thus, the majority of dental care rendered to older patients is paid for out of pocket. Medicaid pro- grams fund dental care for low-income and disabled adults, including elders, in some but not all states (ADA 1998b, Jones et al. 1990), but reimbursements are scant, even in emergency situations. Where there is reimbursement, it is often low and slow, adding yet another disincentive for provision of oral care. Medicaid funds the costs of the majority of patients in long-term care, which means that they either have spent their life earnings or were in poverty prior to admission. This lack of dental coverage is occurring at a time when more and more of the new elderly will be dentate and both want and need care (Ettinger and Beck 1982). Thus, funding dental care for elders is a major obstacle. Social Services. Decreased functional status and increasing levels of dependence add barriers to den- tal care for elders. It will be increasingly important for community and social service programs to respond to older residents’ needs for assistance, including transportation to meet their oral care needs. For example, programs administered by the Administration on Aging (AOA) that integrate oral health into general health programs for the elderly raise awareness about the benefits of good oral health and its contribution to nutritional status and quality — of life (National Policy and Resource Center 1998). For patients in long-term care settings, access to den- tal care is even more problematic. Lack of adequate compensation has been a barrier to increasing the number of dentists who choose to pursue this type of dental practice. Trends Despite advances in modern medicine that have greatly increased life expectancy in the twentieth century, there will be an increase in the number of persons with acute and chronic diseases, including arthritis, diabetes, osteoporosis, and senile dementia (U.S. Bureau of the Census 1998b). As always, it is necessary to distinguish between healthy elders who age normally and remain active and community dwelling and the frail elderly (Niessen and Jones 1991). Most community-dwelling elders take both pre- scription and over-the-counter drugs (Chrischilles et al. 1992). Approximately 30 percent of all medica- tions prescribed in the United States are for persons over the age of 65, with an average of 8.1 medications per patient in a long-term care facility (Gurwitz et al. 1990, Lamy 1989). Seventy-five to 94 percent of ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 265 Factors Affecting Oral Health over the Life Span patients taking medications are taking at least one drug that may have an oral side effect (Baker et al. 1991, Levy et al. 1988, Lewis et al. 1993). The most common of these side effects is dry mouth, or xeros- tomia. Others include abnormal homeostasis, soft tis- sue lesions or reactions, taste changes, altered host resistance, gingival overgrowth, burning oral sensa- tions, increased caries due to high sugar content, and involuntary oral movements. At any given time, approximately 5 percent of the population 65 and older live in a long-term care facil- ity, and an estimated 43 percent of these elders will require long-term care placement at some point in their lives (Murtaugh et al. 1990). As discussed earli- er, one result of elders’ increased disability and dependency is that middle-aged family members are confronted with increased parental care concerns and needs (U.S. Bureau of the Census 1990). Determining the oral health status of home- bound and hospice populations is challenging. Statistics are reported by evaluating persons who seek services for either home or hospice care. Obviously, this underrepresents both populations by leaving out those who refuse, are not aware of, or do not qualify for services. As with long-term care, most homebound are women, although the average age is younger than for those in long-term care facilities. This may represent a step in the continuum of care before long-term care is necessary. Fifty-five percent of women are hospice patients, and hospice patients are a much younger population than either the homebound or those in long-term care. Table 10.8 lists the 10 chronic conditions seen most frequently in the frail elderly. These health problems are important in relation to oral health because they, or their treatments, may worsen oral health or in turn be worsened in the presence of oral disease (see Chapter 5). Long-term: care residents have an average of 3.3 chronic conditions per person (Adams and Marano 1995). Although it is difficult to evaluate dementia patients following strict research protocol, several studies have noted high caries rates, poor oral hygiene, and a high percentage with unmet dental needs (Chapman and Shar 1991, Gordon 1988, Jones et al. 1993). Patients with dementia depend heavily on caregivers to provide daily oral care, and dental care can be most challenging. The Impact on Women Redford (1993) examined the effects of biological, behavioral, and societal factors on women’s oral and general health and treatment needs. Throughout their lives, American women report more acute symptoms, chronic conditions, and short- and long- term disabilities than men; women’s activities are limited by health problems 25 percent more days each year than men’s (Verbrugge 1984, 1990). The TABLE 10.8 Most common diagnoses of frail elderly (>65) in nursing homes, receiving home health (homebound) and hospice care by percentage of the population, 1994 to 1995 Rank Nursing Home Resident Homebound Hospice 1 Diseases of circulatory system Diseases of the circulatory system Neoplasms 2 Mental disorders Endocrine, nutritional, metabolic, Diseases of the circulatory system and immunity disorders 3 Diseases of nervous system and sense organs Diseases of musculoskeletal Diseases of the nervous system and and connective tissue systems sense organs 4 Injury and poisoning injury and poisoning Diseases of the respiratory system 5 Endocrine, nutritional, metabolic, and immunity Diseases of the respiratory system All other diagnoses disorders 6 Diseases of the respiratory system Neoplasms AIDS and infectious or parasitic diseases* 7 Diseases of the musculoskeletal and connective \\-defined conditions AIDS and infectious or parasitic diseases? tissue systems 8 Diseases of the digestive system Diseases of nervous system and sense organs 9 Diseases of the genitourinary system Disease of skin and subcutaneous tissue 10 Neoplasms Diseases of the digestive system a Rates of the two categories are equal. Sources: Data are from 1994 Home and Hospice Care Survey and 1995 National Nursing Home Survey (Dey 1996, 1997, Haupt 1997). 266 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL “gender gap” in physical disability widens with advancing age (U.S. Bureau of the Census 1990). Women in nursing homes or personal care facilities outnumber men three to one (NCHS 1991). In the course of aging, significant numbers of women experience compromised functional status, physical confinement, medical conditions, and cog- nitive impairments. The literature indicates that these factors have placed women's oral health at risk. At the same time, they may limit a woman's ability to maintain oral hygiene self-care regimens, seek professional dental services, tolerate dental treat- ment, and comply with postoperative instructions Factors Affecting Oral Health over the Life Span time during which employment and responsibility for caring for others play a critical role. Overlying the age spectrum are other sociodemographic factors that intensify the need to address each group and each health issue in a manner that optimizes health outcomes. In the overview of special populations presented in Chapter 4, the impact of race and ethnicity, socioeconomic status, and issues in relation to the health of women and individuals with disabil- ities clearly cut across all life stages. The nation’s social and welfare programs, the organization of our private systems of health care, and the values of the many cultures that make up America contribute to (Gift 1998). Pharmacologic regimens common among women can TABLE 10.9 promote xerostomla, thereby in- | summary: Healthy People 2010 objectives—oral health creasing the risk of caries, periodontal diseases, and atro- Objective Age(s) 2010 Baseline 2010 Goal phic/disease changes in oral 21.1 Reduce dental caries experience in children 24 18% 11% mucosa (Atkinson and Fox 6-8 52% 42% 1992). As a consequence of 15 61% 51% chemotherapy for breast cancer, 21.2 Reduce untreated dental decay in children and adults 2-4 16% 9% women may suffer inflammation 6-8 29% 21% and ulceration of the oral 15 20% 15% mucosa, oral infection, hemor- 35-44 27% 15% rhage, neurotoxicity, and salivary 21.3 Increase adults with teeth who have neverlast atooth 35-44 31% 42% Saran Ana (MeCartity 21.4 Reduce adults who have lost all their teeth 65-74 26% 20% an illings 1992, Nationa ge . , 21.5a Reduce gingivitis among adults 35-44 48% 41% Institutes of Health Consensus 5 : : ° Development Conference State- 21.5 Reduce periodontal disease among adults 35-44 22% 14% ment: Oral Implications of 21.6 Increase detection of Stage | oral cancer lesions all 35% 50% Cancer Therapies 1990). 21.7 Increase number of oral cancer examinations 40+ 9% 35% 21.8 Increase sealants in 8-year-old first molars 8 23% (a Ist) 50% ACHIEVING ORAL and in 14-year-old first and second molars 14 15% (a 1st&2nd) 50% : as . ‘ HEALTH THROU GHOUT 21.9 Increase persons on public water receiving fluoridated H,0 all 62% 75% LIFE 21.10 Increase utilization of oral health (OH) system 2+ 44% 56% Each life stage brings a unique set 21.11 _ Increase preventive dental services for poor children 2-17 20% 57% of issues and considerations. 31.12 _ Increase number of school-based Health Centers with K-12 developmental Ultimately, this overview identi- OH component unknown fies the need for research on 21.13 Increase number of Community Health Centers and all 56% 75% health services, health promo- local health departments with OH component tion, and disease prevention spe- 21.14 Increase utilization of dental service for those all 17% 25% oe to populations at different in long-term facilities, e.g., nursing homes ue “. and throughout the i 21.15 Increase states with system for recording all 23 51 span. ur nations young anw° and referring orofacial clefts exemplify the complexities of the re : . 71.16 Increase the number of states with all 0 51 individual, family, community, . tates . . state-based surveillance systems and institutional interactions that shape health and well-being. The 21.17 Increase the number of state and local dental all developmental middle years are not without programs with public health trained directors unknown complexities, but represent a aBased on self-report, National Health Interview Survey, 1996 (NCHS 1996). Source: USDHHS 2000. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 267 Factors Affecting Oral Health over the Life Span the current status of health, including oral health, and are the basis for further improvements. The models described at the beginning of this chapter provide a structure for designing strategies to improve and promote health. Any one approach can be used as a framework for action. The Healthy People 2010 objectives provide a useful template for driving many age-specific and disease/condition-spe- cific outcomes. The multiple oral-health-related objectives outlined there emphasize the importance of risk behaviors and comorbidities that need to be addressed in order to further improve oral, dental, and craniofacial health (USDHHS 2000) (Table 10.9). Recurrent themes in this chapter and other parts of the report underscore the importance of access to health care and health care services, the adoption of healthy behaviors, and the role of individuals and all health care providers in contributing to oral health. Public policies, institutional care guidelines, and community programs can reinforce what individuals can do by providing a health-promoting environ- ment. Toward that end, a recently published report from the Center for Policy Alternatives (Warren 1999) examines and recommends health policies and related actions to improve the oral health status of the poor and underserved. Focus is placed on five dimensions of oral health—finance, sustainability of services, capacity to provide services, cultural com- petency of care providers, and infrastructure to sup- port professional practice. Policy recommendations and proposed action steps are presented in terms of the availability, accessibility, and acceptability of care. Dental care services are emphasized over other aspects of oral health maintenance, because much of the unmet need warrants dental services for preven- tion and treatment. Health care providers, program administrators, local, state, and government administrators, educa- tors, scientists, and leaders, among others, have pro- posed ways of promoting health and preventing dis- ease that respond to the principal health determi- nants presented in the chapter. Thus, efforts can be directed toward changing the environment to make it more life-enhancing; establishing new public health policies; enhancing health literacy to encourage healthy behaviors and lifestyles; working at the microlevel of neighborhoods and communities on health-related measures; and orienting health care to meet the needs of a changing society. Building on programs and structures already in place that have contributed to the improvements in oral health is essential. Further advances in the oral health of all Americans cannot be made unless the health needs of the underserved and vulnerable pop- ulations are addressed. The inability of federal and state programs that are the primary source of funding for services to these populations, specifically, Medicaid, SCHIP, and Medicare, to cover and ade- quately reimburse for dental services has been duly noted. The current review of access to dental care by the Government Accounting Office should add to an earlier review of EPSDT and further address barriers to access and other issues that warrant attention. The Institute of Medicine (IOM) study on the extension of Medicare services to include medically necessary dental services is an additional source of recommen- dations to better address the health needs of vulnera- ble populations and enhance health overall (Field et al. 1999). Other critical reviews of the problems entailed in addressing the nation’s oral health needs and proposing solutions include the 1989 Public Health Service Workshop on the Oral Health of Mothers and Children (USDHHS 1989). Recommendations covered the areas of public education, professional education, coalitions, advocacy and collaboration, health policy, and data collection, evaluation, and research. These recommendations formed the basis for the 2000 Surgeon General’s Workshop on Children and Oral Health. Similarly, the 1988 Surgeon General’s Workshop on Health Promotion and Aging (USDHHS 1988) provided guidance for steps to be taken to improve the oral health of the nation’s elders, all of which are still relevant. This workshop provided the impetus to add objectives on oral health status in nursing homes to Healthy People 1990. Ideally, organizations and agencies working together can resolve the issue of barriers to care. Concentrated efforts such as those focused on improving the access of children to Medicaid oral health services by the Health Care Financing Administration, Health Resources and Services Administration, American Dental Association, and National Center for Education in Maternal and Child Health are an example of how national organizations can unite to make a difference. Still, activities are needed at the local community level. The efforts of Milgrom and colleagues provide one such example for children eligible for Medicaid, with a focus on early childhood caries (Milgrom and Weinstein 1999, Milgrom et al. 1999). In implementing these efforts, however, the capacity of current national, state, and local programs as well as legislative mandates to meet the oral health needs of all Americans must be reviewed and strengthened, as necessary. 268 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL FINDINGS e The major factors that determine oral and general health and well-being are individual biology and genetics; the environment, including its physical and socioeconomic aspects; personal behaviors and lifestyle; access to care; and the organization of health care. These factors interact over the life span and determine the health of individuals, population groups, and communities—from neighborhoods to nations. e The burden of oral diseases and conditions is disproportionately borne by individuals with low socioeconomic status at each life stage and by those who are vulnerable because of poor general health. e Access to care makes a difference. A complex set of factors underlies access to care and includes the need to have an informed public and policymakers, integrated and culturally competent programs, and resources to pay and reimburse for the care. 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Sociodemographic distribution of pediatric dental caries. NHANES III 1988-1994. Hyattsville (MD): National Center for Health Statistics; 1998. Vargas CM, Isman RE, Crall JJ. Comparison of children’s medical and dental insurance coverage by socioeco- nomic characteristics, U.S. 1995. Submitted for pub- lication, 2000. Verbugge LM. A health profile for older women with comparisons to older men. Res Aging 1984;6(3). Verbugge LM. Pathways of health and death. In: Apple RD, editor. Women, health, and medicine in America. A historical handbook. New York: Garland Publishing Inc.; 1990. Waldman HB. Mid-1990's profile of U.S. children and the conditions in which they live. J Dent Child 1996 Jul-Aug;63(4)285-90. Waldman HB. More children are unable to get dental care than any other single health service. J Dent Child 1998 May-June;65(3):204-8. Warner KL. The rewards of the sandwich generation. J Pract Nurs 1995;45(4):16-20. Warren RC. Oral health for all: policy for available, accessible, and acceptable care. Washington: Center for Policy Alternatives; 1999. Wilson S, Smith GA, Preish J, Casamassimo PS. Nontraumatic dental emergencies in a pediatric emergency department. Clin Pediatr 1997;36:333-7. World Health Organization (WHO). Ottawa charter for health promotion. Geneva: World Health Organization; 1986. Yudkowsky BK, Tang SFS. Medicaid state reports—-FY 1995. Elk Grove Village (IL): American Academy of Pediatrics; 1997. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 273 kk S Facing the Future The challenges for oral health in the twenty-first cen- tury are formidable. First and foremost is the need to ensure that all people have access to health care and can acquire the health literacy necessary to make use of health promotion and disease prevention informa- tion and activities. The century offers the promise of a new era for health wrought by the convergence of six cultural movements, any one of which would be sufficient to transform the human condition: e = The biological and biotechnology revolutions. e A redistribution of the worlds people by rapid and sizable migrations within countries and across borders. e Changing demographics in industrialized as well as developing nations. e Changing patterns of disease. ineluding the emergence and reemergence of infectious diseases, and changes in the organization of health care. e Instant worldwide communication through the Internet, cable, satellite, and wireless technology. e A continuing exponential rate of growth in information technology, specifically in computer speed, memory, and complexity. These global currents are changing the way we live now and will have profound implications for the future of the oral and general health and well-being of all people. THE PAST AND PRESENT AS PROLOGUE The Pioneers The history and intellectual activity of the eighteenth and nineteenth centuries set the seeds for the flower- ing of biology in the twentieth and early twenty-first centuries (Porter 1997). The scientific and techno- logical discoveries of the early anatomists and embry- ologists—the founders of cell theory and brain research—were followed by the brilliant innovations of Pasteur, Koch, and Ehrlich, who established the new fields of microbiology and immunology. The cumulative achievements of these pioneers set the foundation for the diagnostic and therapeutic science and art of dentistry, medicine, nursing, and pharma- cology in the twentieth century. The seeds were also sown for the convergence of chemistry, physics, and biology in the field of molec- ular biology, as well as the convergence of Darwinism, fruit fly genetics, and population genetics into the modern evolutionary synthesis. These convergences inspired the current quest to identify all 100,000 genes of the human genome and to assign functional meanings to the motifs that are encoded within them. Vital Statistics The growth of the world population and the transcontinental movements of people are proving a dominant force for change. The twentieth century began with increased European and Asian migrations to the United States. By 1900 the U.S. population had reached 90 million residents and the Earth’s popula- tion was approaching 1 billion people. Life expectan- cy in the United States was 47 years of age. Acute viral and bacterial infections were the primary caus- es of infant morbidity and mortality. Being edentu- lous, or “toothless,” was a normal expectation for mature adults. For most of recorded human history and the 100,000 years of human prehistory, life expectancy was very low. Life expectancy at the time of the Roman Empire was approximately 28 years of age. From the beginning of the first millennium A.D. to 1900, each year of history saw an average gain of 3 days in life expectancy. Each year since 1900, ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 275 Facing the Future however, has seen a gain of 110 days in average life expectancy (Rowe and Kahn 1998). Life expectancy at birth in the United States has increased from 47 years in 1900 to approximately 76 years today. While the entire population of the United States has tripled since 1900, the absolute number of older persons, currently 33 million, has increased elevenfold (Finch and Pike 1996, Rowe and Kahn 1998, p. +). The U.S. population is 270 million and will reach 300 million in the next few decades. The Earth’s population dou- bled by 1950, doubled again by 1975, and currently is 6 billion. Health Improvement Measures such as improved sanitation and housing, prenatal care, immunizations, health education and promotion, community water fluoridation, and den- tal sealants have greatly improved oral health for the majority of the population. Advances in science and technology, health professional education, the sci- ence of public health and clinical practice, and the health literacy of the public will continue to improve the health and well-being of Americans in the com- ing years (Kevles 1997, Schwartz 1998). Ever larger numbers of senior adults expect to retain a full or nearly complete dentition and to live well into their 70s, 80s, and 90s free of pain and discomfort (Slavkin 1997a). DIVERSITY OF DISEASES AND PATIENTS Those seeking care in the decades ahead will present with a wide range of diseases and disorders, uneven- ly distributed across populations. The very youngest patients include children with complex hereditary or congenital craniofacial defects in need of expert mul- tidisciplinary teams to repair and restore form and function. Early childhood caries, one of the most severe forms of the disease, is especially prevalent among poor children in some racial/ethnic groups in America, such as American Indians and Mexican Americans. Young adults are particularly vulnerable to unintentional and intentional craniofacial injuries. Middle-aged and older generations typically experi- ence chronic diseases affecting the heart or lungs as well as cancers, diabetes, and the various degenera- tive diseases of joints and bones and the nervous sys- tem, all of which may affect or be affected by oral dis- eases and their treatments. TRANSFORMING TREATMENTS The cultural movements that are changing the human condition will likely transform treatments for many of the complex disorders just described. The instrumentation used to detect subtle genetic varia- tions in each of the 100,000 genes in the human genome will inexorably reveal which gene or genes are defective in hundreds of inherited and acquired craniofacial diseases or syndromes. On the horizon are promotion measures to enhance health and elim- inate exposures to teratogens, as well as surgical techniques to correct the defects in utero, obviating the need for costly multiple surgeries and rehabilita- tion programs for affected children. We are entering the “golden age of molecular oral health” with gene-based diagnostics, therapeu- tics, and biomaterials. Risk assessment for disease will be based in part on understanding the genetic variations that affect resistance or susceptibility, but also will be determined in part by environmental fac- tors, socioeconomic status, personal behaviors, and lifestyle. The risk for early childhood caries is likely to be determined by a combination of all these fac- tors, as well as cultural beliefs and practices within some populations. Elimination of all infections, whether in the oral cavity or elsewhere, will be seen as a critical part of health promotion. Prevention of injuries will call for approaches that are both culturally and age sensitive, in addition to the coordinated efforts of policymakers and legis- lators to mandate protective gear in sports and other safety measures when necessary. Gene therapy will be applied to treat oral and pharyngeal cancers and also will be used for the oral and systemic delivery of endogenous and synthetic molecules to treat salivary gland disorders, oral infec- tions, and systemic disease. Highly specific drugs will be developed for the management of chronic facial pain such as trigeminal neuralgia and Bell's palsy. Should additional evidence in the early years of the twenty-first century further indicate that oral infections actually cause some cases of heart disease, pulmonary disease, and stroke, or trigger the birth of premature, low-birth-weight babies, treatment approaches will be radically altered. TRANSFORMING HEALTH PROFESSIONAL EDUCATION The scientific and technological bases of dentistry, medicine, nursing, and pharmacy are expanding rap- idly in parallel with the changing demographics of 276 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL the nation, the public's expectations for an enhanced quality of life, and changes in the management and financing of health care. Health professional schools, often organized around academic health science centers, are responding to these challenges and opportunities. Students and clinicians alike need to be prepared to adopt evidence-based health care. Today and tomorrow, students must be well versed in epidemi- ology, biometry, bioinformatics, molecular biology, bioengineering, and much more. In addition, they must be prepared to adopt and implement new pre- ventive strategies and comprehensive and molecular- based diagnostics and therapeutics, to support cost-effective community-based health programs: and to anticipate all the challenges that promotion of health entails. Clinical science or scientific evidence in the new millennium will continue to evolve in molecular dentistry and medicine with attendant opportunities for addressing the social, legal, and ethical implications. We must prepare clinicians for the nuances and complexities of modern clinical research-based results. The previous chapters of this report provide the documentation that can be used to assess health pro- fessional education. Major progress in health promo- tion, disease prevention, diagnostics, therapy and therapeutics, and the socioeconomic and behavioral factors that influence oral, dental, and craniofacial health will further contribute to the transformation of health professional education. TRANSFORMING HEALTH CARE We are currently witnessing a significant transforma- tion in the financing and management of health care, which is affecting all the health specialties. Care providers are assuming new responsibilities and functions, and changing employment patterns. Traditionally, the management of health care has been centered on the providers of services and hospi- tals. Recently, the center has enlarged to include addi- tional marketplace stakeholders, the purchasers of health care and health care plans, and increasingly all segments of society. The interactions among all these participants will shape health and health care for the foreseeable future. Risk assessment models are also being developed and used to design treatment options tailored to communities and to individual patients. Increased use of information technology, greater efforts to con- duct community needs assessments, and greater emphasis on enhanced quality of life expectations of Facing the Future patients, families, and communities are also in evidence (USDHHS 2000). The responsibility for oral and craniofacial care involves all health professionals, so coordinated care delivery and reimbursement will be critical. Evidence-based systematic assessments and guide- lines will contribute to clinical and public health decision making. In addition, the linkage between health care professions and public health and social service activities will need to be strengthened. These trends are complemented by greater understanding of the psychosocial-behavioral aspects of oral diseases and disorders. These advances will continue to influence the nation’s capacity to address the breadth and depth of diseases and conditions affecting oral health across the life span and their relationship to general health and well-being. Access to the Internet and increased health and science reporting in print and broadcast media have created a more knowledgeable public motivated to understand the value of healthy choices. However, increasing numbers of patients are also questioning traditional practices and seeking alternative and complementary approaches. ORAL HEALTH—NOT YET FOR ALL Demographers predict that by 2050 there will be no single racial/ethnic majority in the United States. Rather, we will become an increasingly diverse nation with diverse patterns of disease and levels of health. This is especially evident for African American, Latino, Asian and Pacific Islander, and American Indian communities (Pamuk et al. 1998). Disparities in educational advancement, job opportunities, income and wealth, housing and neighborhood char- acteristics, health access and status, and involvement in the criminal justice system for various subpopula- tions will remain unless steps are taken to reverse the trends (Council of Economic Advisers 1998). The proportion of school-aged children who are caries-free in their permanent teeth has more than doubled during the last 20 years. However, in states such as California, Texas, Louisiana, Alabama, Florida, and Georgia the trends are different; fewer than one third of the children are caries-free in their permanent dentition. One attempt to come to the aid of poor children is the State Children’s Health Insurance Program (SCHIP), federal legislation designed to help individ- ual states meet the health needs of children (Council of Economic Advisers 1998, NRC 1998). As of 1998, more than 11 million children in America—| in 7 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 277 Facing the Future children—are estimated to be uninsured. Most of these children live in families with working parents who have jobs that do not provide health insurance and who are unable to purchase health care insur- ance (NRC 1998). Nationally, 1 in 6 African American children and 1 in 4 Hispanic children are uninsured, compared with 1 in 10 white children (Council of Economic Advisers 1998, NRC 1998). This limited health care access is particularly signifi- cant in relation to oral health. HOPE FROM SCIENCE AND TECHNOLOGY The biological and biotechnology revolutions will accelerate, inspiring theory building and new models of miniaturization and speed that can be applied to improve oral health. The Human Genome Project will be completed no later than 2003. The entire human genetic lexicon will be accessible through the Internet. To date, more than several hundred mutat- ed craniofacial regulatory and structural genes have been found to cause abnormal formation of oral, den- tal, and craniofacial tissues and structures. In addition, the genomes of many significant viruses, bacteria, yeast, parasites, plants, and animals are currently being deciphered, and these are revolu- tionizing how we think about biology and human diseases (Bodmer and McKie 1995, Chambers 1995, Collins et al. 1998). At present, research is under way to decipher the genetic lexicon of 60 microbes, 6 of which are important oral pathogenic bacteria or fungi. The evolution of this knowledge will yield innovations in areas from clinical prevention to drug and biomaterials discovery. Figure 11.1 presents a model of the possible interface between genomics and molecular dentistry. Perhaps with the sole exception of trauma, all human diseases have a genetic component. Genetic dentistry and medicine are based on the paradigm that changes or mutations in individual nucleotides within genes or alleles result in variations or poly- morphisms. These mutations are either inherited or “acquired after birth. For example, inherited muta- tions in the amelogenin gene located on the human X (and Y) chromosome can produce X-linked domi- nant or recessive amelogenesis imperfecta, a painful disease characterized by defective tooth enamel (Backman 1997), and mutations in the fibroblast growth factor receptor 2 gene can produce serious craniofacial birth defects such as Crouzon’s disease and other syndromes with premature fusion of cra- nial bones (craniosynostosis) (Cohen 1997). Mutations in a number of transcription factors that regulate development produce other craniofacial syn- dromes (Slavkin 1999). The human genome contains approximately 100,000 genes or alleles. The genome consists of 3 billion nucleotides or bases. Mutations changing one or more bases, in one or more genes, can result in dis- eases or disorders. Many environmental factors termed mutagens, carcinogens, or teratogens can cause mutations in one or more genes resulting in human disease such as neoplastic diseases. The com- pletion of the Human Genome Project in the next 2 years will afford an unprecedented opportunity to advance our understanding of inherited as well as acquired human diseases and disorders. Scientific discoveries are rapidly defining single- gene mutations, mapping these individual genes in their precise positions on each of FIGURE 11.1 Interfaces between genomics and molecular dentistry Oral Diseases with Genetic Component Oral Pathogen » Map /y Diagnostics Clone ' Understand » Preventive Function Genomes Gene(s) Gene(s) Genome of Oral, Dental, and Craniofacial Tissues TIME the 46 human chromosomes. These findings are being used to diagnose inherited and acquired clinical phenotypes as well as “at- risk populations” throughout the human life span. These remarkable advances in human molecular genetics are identifying candidate genes for developing targeted gene-mediated therapeutic approaches to many oral health diseases, ranging from passive immunization for dental caries, induction of new bone and cartilage tissue, and regeneration of periodontal tissues, to the arti- ficial synthesis of saliva for pat- ients suffering from xerostomia. Health Promotion Dentistry Therapeutics * gene therapy * gene therapeutics 278 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Gene mutations also define the virulence of microbes (viruses, bacteria, yeasts, and parasites), as well as the fidelity of the human immune system. Microbial as well as human genes are extremely sen- sitive to environmental stress and can and do mutate, resulting in antibiotic resistance. The genetic vari- ance within microbial genomes such as the genome of the yeast Candida albicans may be closely aligned with the host changes associated with immunologi- cally compromised patients. The HIV viral genome is another particularly useful model for considering viral mutation frequency during pathogenesis (Slavkin 1996a). These discoveries provide the foun- dations for gene-based diagnostics for disease detec- tion: therapeutic drug development, and individual predictors of drug response during the management of chronic facial pain, osteoarthritis as related to tem- poromandibular joint disease, and osteoporosis asso- ciated with periodontal diseases. We are beginning to understand that polymor- phisms (variations) in multiple genes confer suscep- tibility or resistance to chronic and disabling diseases and disorders such as osteoporosis, periodontal dis- eases, and temporomandibular disorders (Slavkin 1997b). In these examples, multiple genes and mul- tiple gene-environment and gene-gene interactions are associated with the molecular etiology and pathophysiology of the disease process. The function of most genes must inevitably be studied and understood at the level of their encoded proteins and protein-protein interactions, for these are the biologically active players of life. An enor- mous number of genes encode protein information that is highly conserved, that is, found in almost identical form in such diverse organisms as fruit flies and humans. Further scrutiny and analysis have determined that specific motifs encoded in larger domains of each protein serve as the “business” por- tion of the protein, binding to a cell surface, aggre- gating with other proteins, serving to catalyze a chemical reaction, binding to zinc or calcium ions, or serving other crucial functions in cell biology. The functional motifs are also being characterized in terms of structural biology. The scientific and educa- tional communities are building large databases and then mining this information by using sophisticated information technology. These genomic databases provide remarkable opportunities for the identification, design, and pro- duction of a new generation of biomarkers for diag- nostics; innovative biomaterials for repair and regen- eration: and the development of highly sensitive and specific drugs and vaccines to improve the health of all people (Baum et al. 1998, Slavkin 1996b,c, Facing the Future 1997a). Genomics has emerged as a major driver to realign academic, industry, and government science and technology to foster health, pharmaceutical, biotechnology, agricultural, food, chemical, environ- mental, energy, and computer science applications (Kaku 1997, Rifkin 1998). Many of these applica- tions profoundly influence oral health (Slavkin 1996d, 1998a,b). This epic period will also herald the advent of “biochemistry on a chip,” used in connection with body fluids such as saliva, cells, and tissues to diag- nose diseases and disorders. The so-called chip tech- nology will enable identification, quantitation, and complex analyses on surfaces no larger than one-cen- timeter square coupled to laser optical-reader systems and computer-assisted informatics. Prototypes are already available to be tested against samples of sali- va, cervical fluids, buccal mucosal cells, and blood (Slavkin 1998b). This technology should revolution- ize saliva-based diagnostics and prognostics in oral health (Table 11.1). Major progress is also anticipat- ed in bioengineering through nanotechnology, minia- turization, and the innovations of design and fabrica- tion of biomaterials. Anticipated advances include the repair and regeneration of cartilage, bone, mus- cle, nerve, salivary glands and saliva, and teeth (cementum, dentin, enamel, and periodontal liga- ment) (Slavkin 1996d, 1998a,b). Additional scientific progress in the neuro- sciences will have broad implications for the diagno- sis and treatment of diseases and disorders of the craniofacial complex including neuromuscular-relat- ed conditions (e.g., facial and dental trauma, brux- ism, autism, Mobius syndrome, Bell's palsy, temporo- mandibular joint disorders, trigeminal neuralgia, Parkinson's disease, and disorders of speech, smell, and taste), the habilitation of craniofacial syndromes, and the management of facial pain. The field of biomimetics is an example of the translation of human genomics into innovative developments in biotechnology. The idea is to use biological strategies to solve human diseases and dis- orders, essentially mimicking biological processes in the design and fabrication of new biomaterials to replace body parts or synthesize new drugs or reagents. For example, biological cartilage can now be designed and produced in artificial systems that present three-dimensional forms for nose and ear replacements as required in craniofacial birth defects, head and neck trauma, and oral and pharyngeal can- cer patients (Slavkin 1996b, 1998a,b). Another approach is to design and fabricate bioceramics to be used in the replacement of human enamel or dentin on the surfaces of teeth. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 2793 Facing the Future A FRAMEWORK FOR ORAL HEALTH At the most basic level, local, state, and national health care policies will continue to strive to improve the health status of all Americans. Major reforms will improve public health competency. Enlightened health literacy will continue to influence quality of life expectations. Many social, economic, and politi- cal influences will continue to influence local, state, and national priorities for health policies (Isaacs and Knickman 1999). Included in these reforms will be efforts to improve the oral and craniofacial health of the American people. Oral and craniofacial health issues will continue to be diverse and complex. In this context, two major themes remain: the need and demand for oral and craniofacial health services: and the role, functions, and mix of health professionals (Casamassimo 1996, USDHHS 1998). First, need and demand will continue to be the two drivers of the health service requirements of our society. Need is an epidemiologically based and clinically derived measure of the amount of disease and adverse conditions that require treatment in order for the population to be healthy. Demand measures a population's health literacy, willingness, and capacity to utilize and finance health services. Public health literacy or competency and proactive oral health education will increase demand as well as delineate functions of oral health professionals for 2000 and beyond. Often, biomedical research advances in terms of new pharmaceuticals, devices, and procedures popularized in the media influence quality of life expectations, demand for health services, and the economy (Pardes et al. 1999). They can also lead to the creation of new types of health providers. Research also has the potential to reduce the need, demand, and costs for health services (McRae 1994). Thus outpatient surgery obviates the need for hospitalization: immunization or anti- biotics control infections; and community water fluoridation, other fluorides, dental sealants, and related oral health policies help prevent dental caries. Second, the major changes in demography, pat- terns of disease, and management of health care will continue to shape the roles and functions of health professionals. For example, significant increases in the numbers of senior citizens (65 years and older) with chronic facial pain, osteoarthritis, temporo- mandibular joint disorders, type 2 diabetes, demen- tia, osteoporosis, and oral and pharyngeal cancers will challenge health care providers for the next 50 years. These conditions will necessitate interdiscipli- nary and multidisciplinary approaches to care. Coordination of professional care with that of indi- viduals, caregivers, and the com- munity will be needed to control TABLE 11.1 Examples of saliva fluid diagnostics costs and ensure early diagnosis and prompt treatment. Measles Hepatitis A HIV-1 Mumps Hepatitis B HIV-2 Rubella Detection of exposure to viruses by measuring antibodies specific for a viral antigen To ensure that all people have access to health care and can acquire the health literacy neces- sary to make use of oral and craniofacial health promotion Direct antigenic detection of microbes and biomarkers Influenza A and B (neuraminidase) Streptococcus group A (N-acetylqlucosamine) Salivary estradiol (pre-term labor indicator) (A-15, EGFR, cathepsin-D, and Waf 1 (proposed breast cancer biomarkers) Zinc-binding cystic fibrosis antigen (proposed biomarker) Glutamic acid decarboxylase autoantibody (proposed predictive biomarker in type-1 diabetes) and disease prevention informa- tion and activities, a complete assessment of the nation’s capacity to achieve access for all is warrant- ed. Federal, state, and local gov- ernment programs, legislation, Culture of microbial organisms Streptococcus mutans—dental caries Lactobacillus acidophilus—dental caries Candida albicans—oral candidiasis and regulation; health professional societies and organizations, pro- fessional schools, colleges within universities, and K-12 education; patient groups; the private sector, Examples of hormones and drugs identified and measurable in saliva aldosterone progesterone phenytoin antipyrine cortisol testosterone theophilline estrogens carbamazepine caffeine insulin lithium cocaine melatonin methadone continine and the larger society have the ethanol responsibility to achieve access to manjuana oral health care for all. opiates Sources: Derived from Malamud 1992, AGD 1996, Malamud and Tabak 1993. 280 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL REFERENCES AGD. Saliva: a spitting image of the body. AGD Impact 1996;24(8):10-5. Backman B. Inherited enamel defects. 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Hyattsville (MD): U.S. Department of Health and Human Services, National Center for Health Statistics, 1998. U.S. Department of Health and Human Services (USD- HHS). Healthy People 2010: understanding and improving health. Washington: U.S. Department of Health and Human Services; 2000. Available from: US GPO, Washington, DC. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 281 DO A Call to Action The major message of this Surgeon General's report is that oral health is essential to the general health and well-being of all Americans and can be achieved by all Americans. However, not all Americans are achiev- ing the same degree of oral health. In spite of the safe and effective means of maintaining oral health that have benefited the majority of Americans over the past half century, many among us still experience needless pain and suffering, complications that can devastate overall health and well-being, and financial and social costs that diminish the quality of life and burden American society. To maintain the health and well-being of Americans already enjoying good oral health and to address the gaps in oral health status of others require actions at all levels of society, from individu- als and neighborhoods to the nation as a whole. A coordinated effort can overcome the educational, environmental, social, health system, and financial barriers that have created vulnerable populations whose oral health is at risk. MAJOR FINDINGS Following are the major findings of the report. They reflect the detailed findings highlighted at the end of each chapter as well as the broad themes presented in Chapter 1. Oral diseases and disorders in and of themselves affect health and well-being throughout life. The burden of oral problems is extensive and may be particularly severe in vulnerable populations. It includes the common dental diseases and other oral infections such as cold sores and candidiasis that can occur at any stage of life, as well as birth defects in infancy and the chronic facial pain conditions and oral cancers seen in later years. Many of these conditions and their treatments may undermine self- image and self-esteem, discourage normal social interaction, cause other health problems, and lead to chronic stress and depression as well as incur great financial cost. They may also interfere with vital functions such as breathing, food selection, eating, swallowing, and speaking and with activities of daily living such as work, school, and family interactions. Safe and effective measures exist to prevent the most common dental diseases—dental caries and periodontal diseases. Community water fluoridation is safe and effective in preventing dental caries in both children and adults. Water fluoridation benefits all residents served by community water supplies regardless of their social or economic status. Professional and individual measures, including the use of fluoride mouthrinses, gels, dentifrices, and dietary supplements and the application of dental sealants, are additional means of preventing dental caries. Gingivitis can be prevented by good personal oral hygiene practices, including brushing and flossing. Lifestyle behaviors that affect general health such as tobacco use, excessive alcohol use, and poor dietary choices affect oral and craniofacial health as well. These individual behaviors are asso- ciated with increased risk for craniofacial birth defects, oral and pharyngeal cancers, periodontal dis- ease, dental caries, and candidiasis, among other oral health problems. Opportunities exist to expand the oral disease prevention and health promotion knowl- edge and practices of the public through community programs and in health care settings. All health care providers can play a role in promoting healthy lifestyles by incorporating tobacco cessation pro- grams, nutritional counseling, and other health pro- motion efforts into their practices. There are profound and consequential oral health disparities within the U.S. population. Disparities for various oral conditions may relate to income, age, Sex, Tace OT ethnicity, or medical status. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 283 A Call to Action Although common dental diseases are preventable, not all members of society are informed about or able to avail themselves of appropriate oral-health-pro- moting measures. Similarly, not all health providers may be aware of the services needed to improve oral health. In addition, oral health care is not fully inte- grated into many care programs. Social, economic, and cultural factors and changing population demo- graphics affect how health services are delivered and used, and how people care for themselves. Reducing disparities requires wide-ranging approaches that tar- get populations at highest risk for specific oral dis- eases and involves improving access to existing care. One approach includes making dental insurance more available to Americans. Public coverage for dental care is minimal for adults, and programs for children have not reached the many eligible beneficiaries. More information is needed to improve America’s oral health and eliminate health dispari- ties. We do not have adequate data on health, dis- ease, and health practices and care use for the U.S. population as a whole and its diverse segments, including racial and ethnic minorities, rural popula- tions, individuals with disabilities, the homeless, immigrants, migrant workers, the very young, and the frail elderly. Nor are there sufficient data that explore health issues in relation to sex or sexual ori- entation. Data on state and local populations, essen- tial for program planning and evaluation, are rare or unavailable and reflect the limited capacity of the U.S. health infrastructure for oral health. Health serv- ices research, which could provide much needed information on the cost, cost-effectiveness, and out- comes of treatment, is also sorely lacking. Finally, measurement of disease and health outcomes is need- ed. Although progress has been made in measuring oral-health-related quality of life, more needs to be done, and measures of oral health per se do not exist. The mouth reflects general health and well- being. The mouth is a readily accessible and visible part of the body and provides health care providers and individuals with a window on their general health status. As the gateway of the body, the mouth senses and responds to the external world and at the same time reflects what is happening deep inside the body. The mouth may show signs of nutritional defi- ciencies and serve as an early warning system for dis- eases such as HIV infection and other immune sys- tem problems. The mouth can also show signs of general infection and stress. As the number of sub- stances that can be reliably measured in saliva increases, it may well become the diagnostic fluid of choice, enabling the diagnosis of specific disease as well as the measurement of the concentration of a variety of drugs, hormones, and other molecules of interest. Cells and fluids in the mouth may also be used for genetic analysis to help uncover risks for disease and predict outcomes of medical treatments. Oral diseases and conditions are associated with other health problems. Oral infections can be the source of systemic infections in people with weakened immune systems, and oral signs and symp- toms often are part of a general health condition. Associations between chronic oral infections and other health problems, including diabetes, heart dis- ease, and adverse pregnancy outcomes, have also been reported. Ongoing research may uncover mech- anisms that strengthen the current findings and explain these relationships. Scientific research is key to further reduction in the burden of diseases and disorders that affect the face, mouth, and teeth. The science base for dental diseases is broad and provides a strong foundation for further improvements in prevention; for other craniofacial and oral health conditions the base has not yet reached the same level of maturity. Scientific research has led to a variety of approaches to improve oral health through prevention, early diagnosis, and treatment. We are well positioned to take these pre- vention measures further by investigating how to develop more targeted and effective interventions and devising ways to enhance their appropriate adop- tion by the public and the health professions. The application of powerful new tools and techniques is important. Their employment in research in genetics and genomics, neuroscience, and cancer has allowed rapid progress in these fields. An intensified effort to understand the relationships between oral infections and their management, and other illnesses and con- ditions is warranted, along with the development of oral-based diagnostics. These developments hold great promise for the health of the American people. A FRAMEWORK FOR ACTION All Americans can benefit from the development of a National Oral Health Plan to improve quality of life and eliminate health disparities by facilitating collaborations among individuals, health care providers, communities, and policymakers at all levels of society and by taking advantage of existing initiatives. Everyone has a role in improving and promoting oral health. Together we can work to broaden public understanding of the importance of oral health and its relevance to general health and well-being, and to ensure that existing and future preventive, diagnostic, and treatment measures for 284 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL oral diseases and disorders are made available to all Americans. The following are the principal components of the plan: Change perceptions regarding oral health and dis- ease so that oral health becomes an accepted com- ponent of general health. e Change public perceptions. Many people consid- er oral signs and symptoms to be less important than indications of general illness. As a result, they may avoid or postpone needed care, thus exacerbating the problem. If we are to increase the nation’s capacity to improve oral health and reduce health disparities, we need to enhance the public's understanding of the meaning of oral health and the relationship of the mouth to the rest of the body. These messages should take into account the multiple languages and cultur- al traditions that characterize America’s diversity. e Change policymakers’ perceptions. Informed pol- icymakers at the local, state, and federal levels are critical in ensuring the inclusion of oral health serv- ices in health promotion and disease prevention pro- grams, care delivery systems, and reimbursement schedules. Raising awareness of oral health among legislators and public officials at all levels of govern- ment is essential to creating effective public policy to improve Americas oral health. Every conceivable avenue should be used to inform policymakers— informally through their organizations and _aiffilia- tions and formally through their governmental offices—if rational oral health policy is to be formu- lated and effective programs implemented. e Change health providers’ perceptions. Too little time is devoted to oral health and disease topics in the education of nondental health professionals. Yet all care providers can and should contribute to enhancing oral health. This can be accomplished in several ways, such as including an oral examination as part of a general medical examination, advising patients in matters of tobacco cessation and diet, and referring patients to oral health practitioners for care prior to medical or surgical treatments that can dam- age oral tissues, such as cancer chemotherapy or radiation to the head and neck. Health care providers should be ready, willing, and able to work in collabo- ration to provide optimal health care for their patients. Having informed health care professionals will ensure that the public using the health care sys- tem will benefit from interdisciplinary services and comprehensive care. To prepare providers for such a role will involve, among other factors, curriculum changes and multidisciplinary training. A Call to Action Accelerate the building of the science and evidence base and apply science effectively to improve oral health. Basic behavioral and biomedical research, clinical trials, and population-based research have been at the heart of scientific advances over the past decades. The nation’s continued investment in research is critical for the provision of new knowl- edge about oral and general health and disease for years to come and needs to be accelerated if further improvements are to be made. Equally important is the effective transfer of research findings to the pub- lic and health professions. However, the next steps are more complicated. The challenge is to understand complex diseases caused by the jnteraction of multi- ple genes with environmental and behavioral vari- ables—a description that applies to most oral dis- eases and disorders—and translate research findings into health care practice and healthy lifestyles. This report highlights many areas of research opportunities and needs in each chapter. At present, there is an overall need for behavioral and clinical research, clinical trials, health services research, and community-based demonstration research. Also, development of risk assessment procedures for indi- viduals and communities and of diagnostic markers to indicate whether an individual is more or less sus- ceptible to a given disease can provide the basis for formulating risk profiles and tailoring treatment and program options accordingly. Vital to progress in this area is a better under- standing of the etiology and distribution of disease. But as this report makes clear, epidemiologic and sur- yeillance databases for oral health and disease, health services, utilization of care, and expenditures are lim- ited or lacking at the national, state, and local levels. Such data are essential in conducting health services research, generating research hypotheses, planning and evaluating programs, and identifying emerging public health problems. Future data collection must address differences among the subpopulations making up racial and ethnic groups. More attention must also be paid to demographic variables such as age, Sex, sexual orientation, and socioeconomic fac- tors in determining health status. Clearly, the more detailed information that is available, the better can program planners establish priorities and targeted interventions. Progress in elucidating the relationships between chronic oral inflammatory infections, such as peri- odontitis, and diabetes and glycemic control as well as other systemic conditions will require a similar sntensified commitment to research. Rapid progress ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 285 A Call to Action can also occur with efforts in the area of the natural repair and regeneration of oral tissues and organs. Improvements in oral health depend on multidisci- plinary and interdisciplinary approaches to biomed- ical and behavioral research, including partnerships among researchers in the life and physical sciences, and on the ability of practitioners and the public to apply research findings effectively. Build an effective health infrastructure that meets the oral health needs of all Americans and inte- grates oral health effectively into overall health. The public health capacity for addressing oral health is dilute and not integrated with other public health programs. Although the Healthy People 2010 objec- tives provide a blueprint for outcome measures, a national public health plan for oral health does not exist. Furthermore, local, state, and federal resources are limited in the personnel, equipment, and facilities available to support oral health programs. There is also a lack of available trained public health practi- tioners knowledgeable about oral health. As a result, existing disease prevention programs are not being implemented in many communities, creating gaps in prevention and care that affect the nation’s neediest populations. Indeed, cutbacks in many state budgets have reduced staffing of state and territorial dental programs and curtailed oral health promotion and disease prevention efforts. An enhanced public health infrastructure would facilitate the develop- ment of strengthened partnerships with private prac- titioners, other public programs, and voluntary groups. There is a lack of racial and ethnic diversity in the oral health workforce. Efforts to recruit members of minority groups to positions in health education, research, and practice in numbers that at least match their representation in the general population not only would enrich the talent pool, but also might result in a more equitable geographic distribution of care providers. The effect of that change could well enhance access and utilization of oral health care by racial and ethnic minorities. A closer look at trends in the workforce disclos- es a worrisome shortfall in the numbers of men and women choosing careers in oral health education and research. Government and private sector leaders are aware of the problem and are discussing ways to increase and diversify the talent pool, including eas- ing the financial burden of professional education, but additional incentives may be necessary. Remove known barriers between people and oral health services. This report presents data on access, utilization, financing, and reimbursement of oral health care; provides additional data on the extent of the barriers; and points to the need for public-private partnerships in seeking solutions. The data indicate that lack of dental insurance, private or public, is one of several impediments to obtaining oral health care and accounts in part for the generally poorer oral health of those who live at or near the poverty line, lack health insurance, OF lose their insurance upon retirement. The level of reimburse- ment for services also has been reported to be a prob- lem and a disincentive to the participation of providers in certain public programs. Professional organizations and government agencies are cognizant of these problems and are exploring solutions that merit evaluation. Particular concern has been expressed about the nation’s children, and initiatives such as the State Children’s Health Insurance Program, while not mandating coverage for oral health services, are a positive step. In addition, indi- viduals whose health is physically, mentally, and emotionally compromised need comprehensive inte- grated care. Use public-private partnerships to improve the oral health of those who still suffer disproportionately from oral diseases. The collective and complementa- ry talents of public health agencies, private industry, social services organizations, educators, health care providers, researchers, the media, community lead- ers, voluntary health organizations and consumer groups, and concemed citizens are vital if America is not just to reduce, but to eliminate, health disparities. This report highlights variations in oral and general health within and across all population groups. Increased public-private partnerships are needed to educate the public, to educate health professionals, to conduct research, and to provide health care serv- ices and programs. These partnerships can build and strengthen cross-disciplinary, culturally competent, community-based, and community-wide efforts and demonstration programs to expand initiatives for health promotion and disease prevention. Examples of such efforts include programs to prevent tobacco use, promote better dietary choices, and encourage the use of protective gear to prevent sports injuries. In this way, partnerships uniting sports organiza- tions, schools, the faith community, and other groups and leaders, working in concert with the health com- munity, can contribute to improved oral and general health. 286 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL CONCLUSION The past half century has seen the meaning of oral health evolve from a narrow focus on teeth and gin- giva to the recognition that the mouth is the center of vital tissues and functions that are critical to total health and well-being across the life span. The mouth as a mirror of health or disease, as a sentinel or early warning system, as an accessible model for the study of other tissues and organs, and as a potential source A Call to Action of pathology affecting other systems and organs has been described in earlier chapters and provides the impetus for extensive future research. Past discover- ies have enabled Americans today to enjoy far better oral health than their forebears a century ago. But the evidence that not all Americans have achieved the same level of oral health and well-being stands as a major challenge, one that demands the best efforts of public and private agencies and individuals. ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 287 Index Page numbers followed by italicized b, f, and t indicate boxes, figures, and tables, respectively. A Access barriers to for elderly, 263, 265 insurance and, 12-13, 268 children and, 253 elderly and, 265 as reason for nonutilization, 84t-86t removal of, 4, 12-13, 19, 268, 286 and dental care utilization, among military vs. civilian population, 83, 87, 88f ACE See Administration for Children and Families Acids and caries, 37-38 saliva and, 27 and tooth surfaces, 31 Actinobacillus actinomycetemcomitans and adult periodontitis, +0 and bacteremia, 104 and early-onset periodontitis, 42, 205 and periodontal disease, 203t Administration for Children and Families (ACF), 226, 226t Adolescents/young adults, 257-258. See also Children Adult periodontitis, 40-42 bacterial activity in, 40, 203t, 204-205 diagnosis of, 204-205, 204t immune response to, 40—41 progression of, 40 rapidly progressing, 40, 41, 207 refractory, 42 susceptibility factors, 41 systemic antibiotics for, 207 Adult respiratory distress syndrome (ARDS), 105 African Americans. See also Race/ethnicity cancer in incidence of, 68, 68f survival rates for, 68-69, 69f children, insurance coverage of, 253, 278 congenital malformations in, 72, 72f dental care among nonutilization of, 83, 84t utilization of, 80t, 81-82, 81t dental caries in, 63-64, 63f, 64f as dental personnel, 236-237, 237t oral and pharyngeal cancers in diagnosis of, 69, 69f by sex, 68, 68f oral health status of, 74-75 periodontal disease in, 65-66, 66f and ratings of oral health, 144 tobacco use by, 260b tooth loss in, by economic status, 67, 67f toothaches among, prevalence of, 73 Age and canker sores, prevalence of, 71, 71f and dental care nonutilization, 83, 84t utilization, 80-81, 80t and dental caries, by economic status and race/ethnicity, 63-64 and injuries, 72—73 and insurance coverage, 231 and oral-facial pain, prevalence of, 73, 73f oral health data on, 2-3 oral health vulnerabilities according to, 249-267 and oral herpes lesions, prevalence of, 70-71, Tif and periodontal disease, 65-66, 65f, 203t adult periodontitis, 41 by race/ethnicity, sex, and economic status, 65-66 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 289 Index Age (continued) and ratings of oral health, 144 and tooth loss, 66 Agency for Healthcare Research and Quality (AHRQ), 171, 172, 213, 225, 226t Aging, and craniofacial complex, 31-32 AHRQ. See Agency for Healthcare Research and Quality AIDS. See also HIV infection Candida infections with, 43 esophageal candidiasis with, 101 and oral cancer, 46 Alcohol, 191t community programs, 171 as general health risk factor, 10 in mouthwash, and oral cancer, 210 and oral cancer, 44-45, 46, 169, 208t, 209, 209t tobacco and, combination of, and oral cancer, 45, 208t, 209 Allodynia, 52 Allografts, 208-209 Alloplasts, 209 Allopurinol mouthwash, and mucositis, 106 Alpha tocopherol, 47, 251b Alveolar bone. See also Jaw; Oral bone aging and, 31-32 loss of, 32 osteoporosis and, 102-103 risk factors for, 203t smoking and, 41 nutrition and, 250b regeneration of, 208-209 Amelogenesis imperfecta, 49, 278 American Indians/Alaska Natives children of, oral health of, 76-77 as dental personnel, 236, 237t oral and pharyngeal cancers and, by sex, 68, 68f oral clefts, 72 oral health status of, 76-77 Pima tribe, in diabetes-periodontal disease study, 113-114 and precancerous lesions from smokeless (spit) tobacco, 70 and ratings of oral health, 144 American Society of Anesthesiologists, classification of patient's risk, 196, 197t Americans Stop Smoking Intervention Study for Cancer Prevention (ASSIST), 171 Anaerobes, gram-negative, 39 Andersen behavioral model, 248-249, 248f Anodontia in ectodermal dysplasias, 50 hereditary, 49 Antibiotics and disruption of oral homeostasis, oral candidiasis and, 42 systemic, for periodontitis, 206t, 207 Antibodies. See also IgA antibody; Immunoglobulins in adult periodontitis, 40-41 in mucosal immune system, 28 oral fluids in diagnostic tests for, 103, 103t Anticipatory guidance, for children, 256 Antigenic components, in identification of periodontopathic bacteria, 205 Antimicrobial agents, for periodontal diseases, 206t, 207 Antimicrobial components, in saliva, 27 Antioxidants, +7 Apert’s syndrome, 49 Aphthous ulcers, recurrent, lesions caused by, 100¢ Apoptosis and oral cancer, 45, 46 Sjogren's syndrome and, 51 ARDS. See Adult respiratory distress syndrome Arthritis, jaw manifestations of, 52 Ascorbate, and gingivitis, 250b Asians/Native Hawaiians/Pacific Islanders. See also Chinese Americans; Vietnamese Americans as dental personnel, 236, 237t oral and pharyngeal cancers and, by sex, 68, 68f oral health status of, 76 Aspartate aminotransferase, in adult periodontitis, 205 Assaults. See Violence ASSIST. See American Stop Smoking Intervention Study for Cancer Prevention Association of State and Territorial Dental Directors (ASTDD), 226-227 ASTDD. See Association of State and Territorial Dental Directors Autografts, 208 Autoimmune disorders, 212 Sjogren's syndrome, 51 B B cells, 28 Bacteremia infective endocarditis and, 107-108 and microthrombosis, 117-118 and oral infection, 104-105 Bacteria. See also specific bacteria in adult periodontitis, 40, 41, 204-205 in dental caries, 37-38 in early-onset periodontitis, 42, 205 in gingivitis, 39 gram-negative, and adult periodontitis, +0 in heart disease, 117-118 290 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL lesions caused by, 99t in periodontal disease, 202, 203t, 204-205 in refractory periodontitis, 42 Bacteroides forsythus in adult periodontitis, 40, 205 in periodontal disease, 203¢ BANA test, in identification of periodontopathic bacteria, 205 Behcet's syndrome lesions caused by, 100t and RAU, 44 Benzpyrene, 45 Betel nuts, and oral cancer, 45 Biofilm, 26, 37, 104. See also Plaque and gingivitis, 39 Biomarkers future of, 279 for oral cancer, 210 Biomimetics, 279 Biopsy for mucosal disease diagnosis, 212 for oral cancer diagnosis, 210 Birth control medication, and gingivitis, 39 Birth defects, craniofacial, 47-50 clinical management of, 210-211 cultural reactions to, 141 point mutations and, 31 prevalence of, 71-72 prevention and control of, 172-173, 210-211 strategies for, 156t secondary to other developmental disorders, 49 Bone grafts, 208-209 Bone loss. See Alveolar bone, loss of: Oral bone, loss of Boston-type craniosynostosis, 49 Brain abscesses, oral flora and, 105 Branchial arch(es), 29 altered morphogenesis of, birth defects caused by, 47-48 Bruxism, 52, 190, 191t Burkitt's lymphoma, viral causes of, 45 C Calcium metabolism of, disturbances in, oral manifestations of, 101 and periodontal disease, 203t, 250b-251b Calcium channel blockers, and gingivitis, 39,107 Calculus and adult periodontitis, 40 and gingivitis, 39 Campylobacter, and gingivitis, 39 Index Canadian Task Force on the Periodic Health Examination, 156-158 Cancer. See also specific type oral and pharyngeal, 44-47, 209 health care providers’ knowledge about, 179 HPV and, 43, 45-46, 208t, 209, 210 prevention and management of, 47, 169-172 community-based interventions, 170-171 early diagnosis in, 171-172 nutrition in, 210, 251b provider-based, 210 strategies for, 156t public knowledge about, 178-179 quality of life with, 136, 142 risk factors in, 44-47, 208t, 209-210, 209t nutrition and, 251b statistics on incidence rates, 67, 68, 68f, 74 mortality rates, by state, 70, 70t site-specific, 69-70 sources for, 62 stage of diagnosis of, by race/ethnicity, 69, 69f survival rates, 67-69, 74 tobacco and, 259b, 260b therapies. See also Chemotherapy, Radiation treatment combined, and oral mucositis, 106-107 types of incidence rates for, 68, 68f survival rates for, 69, 69f Candida albicans and oral cancer, 46, 209 and oral candidiasis, 42 Candida infections, 42-43 Candidal angular cheilosis, +3 Candidiasis esophageal, 101 lesions caused by, 99t oral, 42-43 with HIV, 42, 43, 71, 101 prevalence of, 71 Canker sores, 43-44. See Recurrent aphthous ulcers (RAU) prevalence of, 71, 71f Capnocytophaga, and prepubertal periodontitis, 42 Capnocytophaga ochracea, and localized juvenile periodontitis, 42 Capsaicin, 25 for oral mucositis pain, 106 Carbamazepine, and tic douloureux, 52 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 291 Index Cardiovascular disease, oral infection and, 115-120 animal studies, 117-118 mechanisms of action in, 115-117 population-based studies, 118-120, 119t Caries. See Dental caries Carious lesions, precavitated, in restored teeth, diagnosis of, 198 Carotenoids, +7, 251b Cavities, 37. See also Dental caries CDC. See Centers for Disease Control and Prevention Celiac disease, oral manifestations of, 101 Cements, glass ionomer, in dental caries treatment, 201 Center for Policy Alternatives, 268 Centers for Disease Control and Prevention (CDC), 225, 226t . Cervical cancer, human papillomavirus (HPV) and, 43, 45 Cervicofacial actinomycosis, lesions caused by, 99t Chediak-Higashi syndrome, and periodontal disease, 41 : Chemotherapeutic agents, in plaque reduction, 199 Chemotherapy oral candidiasis and, 42 oral infections from, 105 oral ulcers and oral mucositis from, 26 Chickenpox, oral lesions with, 98t Children anticipatory guidance for, 256 craniofacial birth defects in. See Birth defects, craniofacial dental caries in, 2, 38, 252 by economic status and race/ethnicity, 63-64 dental risk and protective factors for, 257t dental sealants for, 167-168, 168¢ with disabilities, 79, 253 enamel fluorosis in, 160 fluoride for in dietary supplements, 162-165, 164t in mouthrinses, 165 in school water, 162 from supplement programs, 164-165 future of oral care and, 277-278 injuries and, 258t, 722 insurance coverage, 231, 253, 277-278 Medicaid, 2, 253-255, 268 State Children’s Health Insurance Program, 13, 233-234, 255, 277 malocclusion in, risk and protective factors for, 258t oral health of, 2, 249-253 barriers to, 13, 286 preventive environment for, 255-257, 256t, 257t, 258t periodontal diseases in, risk and protective factors for, 256t poverty and, 2, 252 violence and abuse, 51 Chinese Americans, nasopharyngeal cancer incidence and mortality, 76 Chlorhexidine to limit gingival inflammation, 205, 206t to prevent mutans streptococci transmission, 200 and remineralization, 199 teeth stains from, 107 Chronic and disabling oral conditions, 51-53, 73 Cigarettes, and oral and pharyngeal cancer, 259b. See also Tobacco Cigars. See also Tobacco and oral and pharyngeal cancer, 259b and oral cancer, 208t, 209 trends in smoking, 260b Cleft lip/palate, 47-48 cost of, 228 prevalence of, 72, 72f quality of life with, 141-142 in Waardenburg syndrome, 50 Cleft palate, +7-48 Clefting abnormalities from altered branchial arch morphogenesis, 47-48 incisive foramen and, 30 Cleidocranial dysplasia, 50 Cochrane Collaboration, 213, 214t, 246 Collagenase, in adult periodontitis, 205 COMMIT. See Community Intervention Trial for Smoking Cessation Community Health Centers, 227, 237 Community health programs. See also Public health programs for craniofacial birth defects, 172-173 for dental caries, 158-168 evidence of effectiveness of, 155-158 glossary of terms, 157b for injury, 173-176 for oral and pharyngeal cancers, 169-172 for periodontal diseases, 168-169 strategies used, 156t Community Intervention Trial for Smoking Cessation (COMMIT), 171 Corticosteroids, and disruption in oral homeostasis, oral candidiasis and, 42 Cosmetic dentistry, increased demand for, 137-138 Coxsackievirus, oral lesions with, 98t Cranial bones, birth defects involving, 48-+9 292 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Craniofacial complex aging of, 31-32 contact and communication in, 23-25 diagram of, 22 functions of, 1, 17 oral cavity in, 25-28 origins and development of, 28-31 early development of, 29-30 genetic controls in, 30-31 nutrition in, 250b research on, 4, 19 sensory functions of, 23 Craniofacial defects. See Birth defects, craniofacial Craniosynostosis, 49, 278 and gene mutations, 31 Crohn's disease, and RAU, 44 Crouzon's disease, +9, 278 Cryotherapy, for mucositis, 106 Cuban Americans, oral health of, 75 Cyclosporin, and gingivitis, 39, 107 Cytokines, 28 and adult periodontitis, 40-41 and periodontal diseases, 203 and pregnancy, 120-121 Cytomegalovirus, and chemotherapy, 106 D Demineralized bone, freeze-dried, in bone grafts, 208-209 Dental appliances, 201 and chewing function, 135-136 and oral candidiasis, 43, 71 Dental care. See also Oral health care system active personnel in, 223-224, 224t, 235-236, 235f composition of, by sex and race/ethnicity, 236-237, 237t annual expenditures on, 223, 228, 228t, 231f, 231t per capita, 228, 229f vs. total health care expenditures, 227, 227f, 228f costs of indirect, 142-144, 143t per capita, 228, 229f as reason for nonutilization, 83, 84t-86t vs. other medical services, 228, 230t, 231f disciplines in, 224 evidence-based, 213, 246, 277 expenditures on, 227-228 by source 1960-1996, 231f 1998, 228t Index vs. total health care expenditures, 227f, 228t financing and reimbursement for, 228t, 229-234, 231f, 231t, 232f managed, 231-233, 233t, 254 among military personnel, vs. civilian population, 83, 87, 88f nonutilization of, reasons for, 83, 84t-86t population-to-dentist ratio, 224, 224f for underserved populations, 239 unmet needs in, 83, 87t for children, 252-253 utilization of, 80-81, 190-191 by sex, race/ethnicity, income, and insurance, 80t, 81-82, 81t variation by oral health status, 82, 82t Dental caries, 37-39 changing clinical approach to, 196-201 diagnosis of, 198, 200t multifactorial model in, 196, 197f prevention of, 198-200, 200t tisk assessment in, 197, 198f, 198t, 199t, 200t treatment of, 201 in children, 2, 38, 252 by economic status and race/ethnicity, 63-64 risk and protective factors for, 257t classification of, 201 nutrition and, 250b prevalence of by age, economic status, and race/ethnicity, 63-65 prevention of community approaches to, 158-168 dental sealants, 166-168 dietary fluoride supplements, 162-165 fluoridated drinking water, 160-162 fluoride mouthrinses, 159t, 165 fluoride varnishes, 165-166 school water fluoridation, 162 fluoride in, 2-3, 10, 18, 27, 38, 155, 158-160 health care professionals’ knowledge about, 177-178 provider-based, 198-201 public's knowledge about, 177 saliva and, 27, 38 strategies for, 156t target population for, 159t daily hygiene, 39, 189-190 progression of, 198 rate of, 38-39 smokeless (spit) tobacco and, 39, 259b ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 293 Index Dental caries (continued) susceptibility to, 39 tobacco and, 259b vaccine for, 200 Dental hygienists, 235 knowledge of dental caries prevention, 177-178 knowledge of periodontal disease prevention, 178 Dental implants, 201 Dental plans. See Insurance Dental plaque. See Plaque; Biofilm Dental practice, 223-224 Dental schools curriculum needs of, 237-238 enrollment, 235 of minorities, 236 faculty vacancies, 237 graduate indebtedness, 237-238 Dental sealants, 38, 166-168 for children, 167-168, 168¢ combined with fluoride use, 167 cost-effectiveness of, 168 in dental caries treatment, 201 effectiveness of, 159t, 166-167 prevalence of use, by race/ethnicity, 82 Dentrifice, 159t, 176, 177, 179, 189-190 Dentinogenesis imperfecta, 49 Dentists availability of, 224 charitable care by, 239 compensation of from elderly in long-term care, 265 from Medicaid, 254 increased importance of, 191-192 knowledge of dental caries prevention, 177-178 knowledge of periodontal disease prevention, 178 numbers of, 223-224, 224t, 235-236, 235f visits to. See also Dental care, utilization of and susceptibility to adult periodontitis, 41 Denture sore mouth, 43 Denture stomatitis, 43, 71 Depression atypical facial pain with, 52 with cancer, 142 with TMD, 140 Dermatologic diseases, lesions caused by, 100t Developmental disorders, 47-50 clinical management of, 210-211 cultural reactions to, 141 prevalence of, 71-72 prevention and control of, 172-173 strategies for, 156t dfs, definition of, 62b dft, definition of, 62b Diabetes mellitus and adult periodontitis, 41 and periodontal disease, 2, 17, 109-115 research used in, 110¢, 111t-113¢ treatment of, 206 type 1, and periodontal disease, 41, 110-113, 114, 203t type 2, and periodontal disease, 113-114, 203t Diagnostic codes, dentistry, 216 Diagnostics, saliva and oral fluids in, 103-104, 103¢, 279, 280t Diet. See also Nutrition effect on oral health, 191t’ and oral and pharyngeal cancer, 209t poor, as general health risk factor, 4, 10, 18 DiGeorge syndrome, 48 Digital radiography, 196 Dilantin, and gingivitis, 39 Disability days, due to dental conditions, vs. other conditions, 143, 143t Disabled population, oral health of, 78-79 DMFS, definition of, 62b DMFT, definition of, 62b DNA in identification of periodontopathic bacteria, 205 saliva as source for, 103—104, 103t Down syndrome, and periodontal disease, 41 Drug abuse, oral fluids for diagnosis of, 103, 103t Dry mouth. See Xerostomia and dental caries, 38 and chewing function, 136 and Sjogren's syndrome, 51, 136 Dysplasia, +6 E Early and Periodic Screening, Diagnostic and Treatment Service (EPSDT), 254 Early childhood dental caries (ECC), 38, 228 Early-onset periodontitis, 42 bacteria linked to, 205 by sex and race/ethnicity, 66 systemic antibiotics for, 207 Eating problems, and quality of life, 135-136, 136¢ ECC. See Early childhood dental caries Ectodermal dysplasias (EDs), 49-50, 211 Edentulism by age, economic status, sex and race/ethnicity, 66-67 by economic status, 82 and heart disease, 119 by state, 67t 294 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL and stroke, 120 EDS. See Ectodermal dysplasias Education level and dental care wants, 87t and dental visits, 802, 81, 81t and insurance coverage, 231. 232f and knowledge of periodontal disease, 178 and susceptibility to adult periodontitis, 41 Educational debt, 237-238 Efficacy, of health programs, vs. effectiveness, 155-156 EGE See Epidermal growth factor Egg polarity genes, 30 Eikenella corrodens and adult periodontitis, +1 and prepubertal periodontitis, +2 Elastase, in adult periodontitis, 205 Elderly adults. See also Age chronic health problems of, 266, 266t eating problems of, 135-136, 136t oral health of, 3, 262-266, 263t, 264t. trends in, 265-266 © research on, 262, 263t, 26+t sleep problems of, 137 social functioning of, 138-139, 139t women, 266-267 Electrical resistance measurement, 196 Enamel age and, 31 demineralization of, 38, 199 remineralization of, 199 fluoride and, 159 saliva and, 27, 31, 38 Enamel fluorosis, 160 Enamel hypoplasia, 101 from tetracycline, 107 Endocarditis, infective, oral infection and, 107-108 Endocrine system and disruption in oral homeostasis. oral can- didiasis and, 42 and immune system, 28 nicotine and, and oral and pharyngeal cancers, 46-47 Environment importance of, 248-249, 248f improvement of, 268 for children, 255-257, 268 Epidemiologic data, need for. See Data Epidemiology, definition of, 62b Epidermal growth factor (EGF), 27 and oral and pharyngeal cancers, 46 Epidermolysis bullosa-recessive dystrophic type, 49 Epithelial cells. cancers of. See Squamous cell carci- nomas, oral ORAL HEALTH IN AMERICA: Index Epithelium, 25-26 aging and, 32 nutrition and, 250b EPSDT. See Early and Periodic Screening, Diagnostic and Treatment Service Epstein-Barr virus and chemotherapy, 106 and oral cancer, 45 and oral lesions, 98t Erythema multiforme, lesions caused by, 100t Erythroplakia lesions, 209 and squamous cell carcinoma, +4 Estrogen replacement therapy, and adult periodonti- tis, 41 Ethnicity. See Race/ethnicity Evidence-based practice, 213, 246, 277 Explorer, visual examination with, for dental caries diagnosis, 198, 200t F Face. See also Craniofacial complex appearance of, social responses to, 140-141 embryonic formation of, 29 as reflection of general health, 97-104 Falls, 50, 72-73. See also Injury FDA. See Food and Drug Administration Federal oral health infrastructure, 226-227, 226t Federal support for dental school programs, 235-236 for educational debt, 237 Fibromyalgia, jaw manifestations of, 52 Fillings. See also Restorations materials used in, 201 Flossing, 39, 176, 190 and bacteremia, 104 and dental caries prevention, 178 dental professionals’ knowledge of, for dental caries prevention, 178 public knowledge of for dental caries prevention, 177 and gum disease, 178 by tobacco users vs. nonusers, 178 Fluoride, 155, 158-160 dental professionals’ knowledge about, 177 in dentifrices, 159t, 176, 177, 179, 189-190 in dietary supplements, 162-165 dosage of, 163, 164t effectiveness of, 159t, 163-164 public knowledge of, 177 in drinking water, 2-3, 18, 159t, 160-162 access to, 161, 162f, 162t, 163t costs of, 161 effectiveness of, 159t, 160-161 A REPORT OF THE SURGEON GENERAL 295 Index Fluoride (continued) history of, 159 public knowledge of, 177 recommended concentration levels, 160 in schools, 159t, 162 enamel hypoplasia from high levels of, 101 in mouthrinses, 159t, 165 professionally applied, 159-160, 198-199 public knowledge about, 177 and rate of dental caries progression, 38-39 safety of, 160 in saliva, dental caries protection from, 27, 38, 159 in varnishes, 159t, 165-166 Folate, and gingivitis, 250b Folic acid birth defects and, 47-48, 172 cancer and, 251b Food and Drug Administration (FDA), 225, 226t Fungal diseases, lesions caused by, 99t Fusobacterium nucleatum and gingivitis, 39 and smoking, 41 G Gastroenteritis, oral manifestations of, 101 Gene therapy, 276 Genes and periodontal disease, 203, 203t and resistance to dental caries, 39 Genetic derangements. See also Developmental disorders and clefting abnormalities, 48 and oral cancer, 46 and periodontal disease, 41 Genetics and control of embryonic development, 30-31 and future of oral health, 276, 278-279, 278f and understanding craniofacial development, 28 Genomic databases, 279 Geographical region. See also Residence, place of and dental care wants, 87t Germ cell layers, in craniofacial development, 29 Gingiva bleeding and inflammation of, as diagnostic test, 204, 204t lesions of, diseases and conditions causing, 98t-99t recession of, age and, 31 surface of, 25 Gingival crevicular fluid, periodontal infection and, 204t, 205 Gingival erythema, linear, and HIV, 101 Gingivitis, 39-40 with adult periodontitis, +0 and heart disease, 119 from medication, 107 and pregnancy, 122 prevention of, 10, 168-169, 190, 191t, 205-206 by race/ethnicity, 66 Global ratings, of oral health, 144 Glossary, 62b B-glucuronidase, in adult periodontitis, 205 Glutathione, +7 Glycemic control, affected by periodontal disease, 114-115, 116t-117t Gonorrhea lesions caused by, 99t pharyngeal, 109 Growth factors, 27 and oral cancer, 46-47 in reducing mucositis, 106 Guided tissue regeneration, 209 Guidelines, for clinical practice, 213-214, 215t Guidelines for School Health Programs to Prevent Tobacco Use and Addiction (CDC), 170 Gum disease, prevention of, public knowledge of, 178. See also Gingivitis; Periodontal disease Gums. See Gingiva H Hand, foot, and mouth disease, oral lesions with, 98t HCFA. See Health Care Financing Administration Head Start, 226 Health biopsychosocial model of, 134 broadened meaning of, 2, 17-18 cultural perspectives on, 134-135 determinants of, theories and models of, 246-248, 246f historical trends in life expectancy, 275~276 science and technology, 275 World Health Organization (WHO) definition of, 133 Health care evidence-based, 213, 246, 277 expenditures on, 227-228 Consumer Price Index for, 230t, 231f per capita, 229f by source of funds, 228t by type of service, 227f, 228t, 230t federal and state programs for, 233-234 296 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL oral care in. See Dental care; Oral health care system personnel in, collaboration with dental care providers, 225, 227 trends in, 277 unmet needs in, 83, 87t utilization of, 190-191 Health Care Financing Administration (HCFA), 225 Health Field Concept, Lalonde’, 247 Health maintenance organizations (HMOs), 229, 232, 233t Health Plan Employer Data and Information Set (HEDIS), 233 Health professional schools, future of, 276-277. See also Dental schools Health Professional Shortage Area (HPSA), 227, 237 Health Resources and Services Administration © (HRSA), 225, 226t Healthy People 2000, progress in meeting objectives of, 180t Healthy People 2010, 4, 19, 247-248, 248f objectives of, by age, 268t Heart disease. See Cardiovascular disease HEDIS. See Health Plan Employer Data and Information Set Herpangina, oral lesions with, 98t Herpes labialis lesions location, features, and course of, 98t prevalence of, by race/ethnicity, 71 Herpes simplex virus, 43 and chemotherapy, 106 lesions from, by population group, 70 and oral cancer, 45—+6, 209, 210 oral lesions with, 98t as pharyngeal infection, 109 type | (HSV-1), 43 lesions from, 70, 71f and oral cancer, 45 type 2 (HSV-2), 43 Herpes zoster, oral lesions with, 98t Herpetic gingivostomatitis, primary acute, oral lesions with, 98t Herpetic stomatitis, primary, 43 Herpetiform recurrent aphthous ulcers, 44 HHANES. See Hispanic Health and Nutrition Examination Survey Hispanic Health and Nutrition Examination Survey (HHANES), 75 Hispanics. See also Cuban Americans, Mexican Americans; Puerto Ricans children of insurance coverage of, 278 oral health of, 75 Index dental care among nonutilization by, 84t-85t utilization by, 80t, 81-82, 81t as dental personnel, 236-237, 237t oral and pharyngeal cancers and, by sex, 68, 68f oral health status of, 75-76 and ratings of oral health, 144 toothaches among, 73 Histoplasmosis, lesions caused by, 99t HIV/AIDS Dental Reimbursement program, 238-239 HIV infection human papillomavirus (HPV) and, 43, 71 and oral candidiasis, 42, 43, 71, 101 oral lesions with, 98t, 101-f02 oral manifestations of, 97, 101-102 oral transmission of, 108-109 and periodontal disease, 41 and RAU, 44 and trench mouth, 40 HMOs. See Health maintenance organizations Hodgkin's lymphoma, 46 Hom genes, 30 Homeotic genes, 30 Hormones, oral fluids in diagnostic tests for, 103, 103t Hospice patients, 263, 266, 2606t Hospitalized patients, and systemic complications due to oral bacteria, 105 Hospitals, oral health care at, 225 Hox genes, 30 HPSA. See Health Professional Shortage Area HPV. See Human papillomavirus HRSA. See Health Resources and Services Administration HSV-1. See Herpes simplex virus, type 1 HSV-2. See Herpes simplex virus, type 2 Human genome, in understanding craniofacial development, 28 Human Genome Project, 53, 278 Human immunodeficiency virus. See HIV infection Human papillomavirus (HPV), 43 and oral cancer, 43, 45-46, 208t, 209, 210 prevalence of, 71 Hypodontia in ectodermal dysplasias, 50 hereditary, 49 Hypoparathyroidism, oral manifestations of, 101 I IFN-y. See Interferon ‘y IgA antibody, 32 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 297 Index IHS. See Indian Health Service IL-1. See Interleukin 1 IL-1B. See Interleukin 1B Imaging technologies, 196 for dental caries diagnosis and treatment, 201 for oral cancer diagnosis, 210 for TMD, 212t Immune cells in adult periodontitis, 40-41 and oral cancer, growth factors and, 46-+7 types of, 28. See also B cells; T cells Immune system, 27-28 disorders of, Sjogren's syndrome, 51 and disruption in oral homeostasis, oral candidiasis and, 42 microbial genome research and, 279 mucosal, 27-28 nutrition and, 250b and RAU, 44 Immunoglobulins, 28. See also IgA antibody smoking and, 41 Immunosuppression and bacteremia, 104-105 oral signs of, 97-100 Immunosurveillance and control, loss of, and oral cancer, 46 Implants. See Dental implants Incidence, definition of, 62b Incidence rate, definition of, 62b Incisive foramen, embryonic formation of, 29-30 Income and adult periodontitis, 41 and children dental caries and, 63-64, 63f, 64f and insurance coverage, 253 oral health and, 2, 252 dental care and nonutilization of, 85t-86t utilization of, 80¢, 81-82, 81t wants, 87t and dental caries, 63-64, 63f, 64f and edentulism, 82 and insurance coverage, 231, 232f for children, 253 low-income communities dentists in, educational debt and, 237 expansion of care to, 239 and oral health, 249 among Hispanics, 75 and periodontal disease, 65-66, 66f and toothaches, 73 Indemnity plans, 232, 233t Indian Health Service (IHS), 76-77, 225, 226t loan repayment program, 237 Infection, oral. See also Mucosal infections; Periodontal disease bacteremia and, 104-105 from cancer therapy, 105-107 infective endocarditis and, 107-108 protection against. See also Immune system by mucosal immune system, 27-28 by saliva, 26-27 respiratory disease and, 108 Inflammation, gingival. See Gingivitis Injury, oral-facial, 50-51. See also Falls, Trauma in adolescents, 258 in children, 2, 72, 258t prevalence of, 72-73 prevention and control of, 191t community-based, 173-176, 174t-175t future of, 276 helmet use, 173, 174t-175t, 176b from sports, 50, 73, 173-176, 174t-175t, 176b, 258 in young adults, 258 Insurance changing market in, 231-233 coverage, 12-13, 229-231 by age, 231 for children, 2, 253-255, 277-278 and dental care nonutilization, 86t and dental care utilization, 80t, 81-82, 81, 229 among children, 253 and dental care wants, 87t by education level, 231, 232f for elderly, 265 employer-provided, 229-231, 261-262 children and, 253 future goals in, 286 by income, 231, 232f by sex and race/ethnicity, 230-231, 232f Medicaid, 87t, 229, 233 for children, 2, 253-255, 268 for elderly, 265 Medicare, 234, 234t, 265 performance measures in, 232-233 as source of expenditures on dental services, 228t, 231f, 231t State Children’s Health Insurance Program, (SCHIP) 2, 13, 233-234, 255, 277 and utilization, 81t, 82 Interferon ‘y (IFN-y), and adult periodontitis, +1 Interleukin 1 (IL-1) and adult periodontitis, +1, 205 and periodontal disease, 203 298 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Interleukin 18 (IL-18) and adult periodontitis, +1 and periodontal disease, 203 Interleukin 6, and adult periodontitis, 205 Interleukins, and heart disease, 115 Irrigation, to control gingival inflammation, 206t, 207 J Jaw (mandible and maxilla). See also Alveolar bone; Oral bone aging and, 31-32 bone loss in, osteoporosis and, 102-103 K Kaposis sarcoma, 46,101 Keratin, 25 Keratin genes, mutations in, and epidermolysis bullosa, +9 Keratinocytes, and oral cancer, +6 Killer cells, and oral cancer, +6 L Lacrimal glands, Sjogren's syndrome and, 51 Lalonde Report, 246-247 Langerhans cells, and immunosurveillance, 46 Language mechanisms of, 25 skills, of oral and pharyngeal cancer patients, 136 Laser technologies, in dental caries diagnosis and treatment, 201 Leukoplakias, 44, 209 Lichen planus, lesions caused by, 100¢ Life expectancy, 275-276 Lifestyle of adolescents/young adults, 257-258 as determinant of health, 190, 1911, 246f, 247-248 Lip cancer incidence of, 69, 70 risk factors, 208t, 209t, 210 sun exposure, 169 Lips, lesions on, diseases and conditions causing, 98t, 100t LJP. See Localized juvenile periodontitis Local public health departments, 226, 286 Localized juvenile periodontitis (LJP), 42 Lymphocytes, and immunosurveillance, +6. See also B cells; T cells ORAL HEALTH IN AMERICA: Index M Macrophages, cytotoxic, and immunosurveillance, 46 Magnetic resonance imaging (MRI), 196 Malocclusions prevalence of, 72 quality of life with, 141-142 risk and protective factors for, 258¢ Mandibulofacial dysostosis, 48 Marijuana, oral cancer and, 45, 208t, 209t Masseter muscle, 26 Mastication, muscles of, 26 Mechanoreceptors, 24 Medicaid, 229, 233 for children, 2, 253-255, 268 dental vs. other health expenditures for, 254 and dental care wants, 87t for elderly, 265 Medical care, in oral health care system, 225 Medicare, 234, 234t, 265 and dental care wants, 87 Medications and dental caries, 38 and disruption in oral homeostasis, oral candidiasis and, 42 and elderly oral health, 265-266 and gingivitis, 39 oral complications of, 107 Men and adult periodontitis, susceptibility to, 41, 65, 65f cancer in oral and pharyngeal, by race/ethnicity and sex, 68, 68f types of, by race/ethnicity, 68, 68f and dental care nonutilization, 84t and injuries, 73 and pain, 25 prevalence of, 73, 73f and periodontal disease, 203t Metabolites, in detection of periodontal disease, 205 Mexican Americans children insurance coverage of, 253 oral health of, 75 dental care utilization by, 80t, 81-82, 8lt and dental caries, susceptibility to, 63-64, 63f, 64f tooth loss by, by economic status, 67, 67f Microbes genome research on, 279 oral transmission of, 108-109 A REPORT OF THE SURGEON GENERAL 299 Index Microbes (continued) protection against. See also Immune system by saliva, 26-27 Micronutrients. See also Nutrition and cancer prevention, +7 fluoride as, 160 Military personnel, dental care among, vs. civilian population, 83, 87, 88f Mononucleosis, infectious, oral lesions with, 98t Mortality rate, definition of, 62b Motor vehicle collisions, 50, 73, 173 Mouth. See also Craniofacial complex; Oral cavity elements of, 1, 17, 25 embryonic formation of, 29 as gateway, 37 for infection, 104-109 lesions in, diseases and conditions causing, 98t-100t as reflection of general health, 1-2, 10-11, 17, 97-104, 284 Mouthguard use, 173-175, 174t-175t, 176b Mouthrinses, fluoride, 159t, 165 MRI. See Magnetic resonance imaging Mucins, 27 aging and, 32 Mucosal immune system, 27-28 Mucosal infections, 42-44, 70-71, 212 by race/ethnicity, socioeconomic status, and sex, 70-71 Mucous membrane pemphigoid, lesions caused by, 100t Multiple sclerosis, and tic douloureux, 52 Mumps, swollen parotid glands with, 97 Mutans streptococci, 37, 38 median age of acquisition of, 39 mother as source of, 199-200 as primary predictor of dental caries incidence, 196-197, 198t Mutations and craniofacial syndromes, 31, 278-279 in keratin genes, and epidermolysis bullosa, 49 and oral cancer, 46 and periodontal disease, 41 N Nasopharyngeal carcinoma, 45, 76 National Facial Protection Month, 173 National Health and Nutrition Examination Survey (NHANES), 61, 62 National Health Interview Survey (NHIS), 61 National Health Service Corps (NHSC), 237 National Institute for Dental and Craniofacial Research (NIDCR), 213 National Institutes of Health (NIH), 225, 226t National Oral Cancer Strategic Planning Conference, 169-170 National Oral Health Plan, 21, 284-286 components of, 11-13, 284-286 National Preventive Dentistry Demonstration Program, 167 Necrotizing ulcerative gingivitis, acute, lesions caused by, 99t Necrotizing ulcerative periodontitis, and HIV, 101 Nervous system, and immune system, 28 Neural crest, 29 defective development of, Treacher Collins syndrome and, 48 ” Neural tube, 29 Neutrophils in adult periodontitis, 40-41 smoking and, 41 in early-onset periodontitis, 42 NHANES. See National Health and Nutrition Examination Survey NHIS. See National Health Interview Survey NHSC. See National Health Service Corps Nicotine, endocrine effects of, and oral and pharyngeal cancers, 46-47. See Tobacco NIH. See National Institutes of Health NIDCR. See National Institute of Dental and Craniofacial Research 4-nitroquinoline-N-oxide, 45 Nitrosamines, 46 N-nitrosonornicotine, 45 Nociceptors, 24 Non-Hodgkin's lymphoma, 46 misdiagnosis of, 101 Sjogren’s syndrome and, 31 Nonneuronal tissues, 29 Nose. See also Olfactory system embryonic formation of, 29 Notochord, 29 Nursing homes, in oral health care system, 225 Nutrition, 191t, 250b. See also Diet and birth defects, 47-48, 172, 211 and cancer prevention, 47, 169, 251b and dental caries, 250b micronutrients in cancer prevention properties, 47 fluoride as, 160 and oral cancer prevention, 209t, 210, 251b oral tissue as reflection of, 100-101 and periodontal disease, 250b-251b prenatal and perinatal, 198 and quality of life, 135-136, 136t and RAU, 44 300 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL O Olfactory system, 24 aging and, 32 Oncogenes discovery of, 45 and oral and pharyngeal cancer, 46 Oral, definition of, 1, 17 Oral bone, loss of, osteoporosis, 102-103 Oral cavity. See also Mouth elements of, 25-28 manifestations of systemic disease in, 37, 97-101, 98t-100t Oral flora, 37 and brain abscesses, 105 Oral fluids, diagnostic value of, 103-104, 103t, 279, 280 Oral health barriers to, removal of, 4, 12-13, 19, 286 broad definition of, 2, 17-18, 133-134 costs of, 4, 19, 227-228, 227f, 228t, 229f, 230t indirect, 142-144, 143t determinants of, 248-249 income inequality, 249 lifestyle, 190, 191t, 246f, 247-248, 283 workplace effects, 249 disparities in, 1, 4, 10, 17, 19, 88, 239, 284 enhancement of, 267-268 for adolescents and young adults, 257-258 for adults, 258-262 for children, 249-257 insurance and, 253-255 social and professional environment and, 255-257 for elderly adults, 262-267, 263t-264t for elderly women, 266-267 expenditures for, 227-228, 227f, 228t financing for, 228t, 229-234, 231f, 231t, 232f vs. total health care expenditures, 227, 227f, 228t future of, 280 diversity of diseases and patients in, 276 National Oral Health Plan, 284-286 new treatments in, 276 and general health, 2, 4-5, 10-11, 17-18, 19, 53, 285-286 in elderly, 265 implications of linkages between, 122 risk factors in, 4, 10, 18 historical trends and, 275-276 meaning of, 5, 17-21, 20 of military personnel, vs. civilian population, 83, 87, 88f Index objectives for, 267-268, 267¢t personal approaches to, 189-191 care seeking, 190-191 daily hygiene, 189-190 among elderly, 262-263 healthy lifestyle, 190, 191¢t prevention measures, 3-4, 7-9, 10, 18. See also Oral health care system in public health programs, 12 ratings of, 144 status of, 35-93 and dental care wants, 87t trends in, 87-89 Oral health care system. See also Dental care active personnel in, 223-224, 224t, 235-236, 235f, 286 by sex and race/ethnicity, 11, 236-237, 237t, 286 community approaches in for craniofacial birth defects, 172-173 for dental caries, 158-168 effectiveness of interventions by, 155-158, 156t glossary of terms for, 157b for injury, 173-176 for oral and pharyngeal cancers, 169-172 for periodontal diseases, 168-169 expanding base of, 216 future of, 239-240 capacity to meet needs in, 234-239 molecular, and genomics, 278, 278f, 279 individual approaches in care seeking in, 190-191 daily hygiene in, 189-190 among elderly, 262-263 healthy lifestyles in, 190, 191t, 246f, 247-249, 248f knowledge of and practice in, 176-179 professional components of dental care, 223-224 medical care, 225 overlap among, 227 public health programs, 225-227 progress in, 179-180, 180t provider-based care in, 191-212. See also Provider-based care diagnostic tests in, 193, 193t future of, 212-216 oral health assessment in, 193-196, 194f-195f, 197t risk assessment in, 192-193 public-private partnerships in, 13, 286 strategies for, 156t underserved in, 239 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 301 Index Oral hygiene, 189-190, 191t and bacteremia, 104 and dental caries, 39, 189-190 among elderly, 262-263 and gingivitis, 39 and periodontal disease, 168-169, 190, 191t, 203t public practices survey, 178 workplace effects on, 249 Oral mucosa, 25-26 aging and, 32 lesions of, diseases and conditions causing, 98t-100t nutrition and, 250b staining of, 107 ORN. See Osteoradionecrosis Osteogenesis imperfecta, 49 Osteoporosis and adult periodontitis, susceptibility to, 41 and oral bone loss, 102-103 and periodontal disease, 203t Osteoradionecrosis (ORN), 106 Ottawa Charter for Health Promotion, 247 P Pain facial, atypical, 52 oral, chronic, 24 oral-facial, 24-25, 52 clinical management of, 211 control of, 24 impact of, 139-140 prevalence of, 73, 73f sex differences, 25, 77 sleep problems with, 137 Palate, 25 embryonic formation of, 29 lesions of, diseases and conditions causing, 98t-100t Papillae, as oral mucosa, 25 Papillomavirus, oral lesions with, 71, 98t Papillon-Lefevre syndrome, and periodontal disease, 41 Parotid glands, 26 aging and, 32 swollen, 97 Pathogens, protection against. See also Immune system by saliva, 27 Pathology, systemic, craniofacial disease as model of, 53 Pemphigus vulgaris, lesions caused by, 100t Periodontal attachment loss of by age, sex, race/ethnicity, and income, 65-66 definition of, 62b osteoporosis and, 102 Periodontal disease, 39-42 adult periodontitis. See Adult periodontitis by age, sex, race/ethnicity, and income, 65-66 from bone marrow radiation, 105 and cardiovascular disease, 115-120 clinical management of, 201-209 diagnosis of, 203-205, 204t, 278 prevention of, 205-206, 206t risk assessment in, 202—203, 203t treatment of, 206—209, 206t diabetes and, 2, 17, 109-114 glycemic control affected by, 114-115, 116t-117t research used in, 110t, 111t-113t early-onset. See Early-onset periodontitis heart disease and stroke with, 115-120 animal studies, 117-118 mechanisms of action in, 115-117 population-based studies, 118-120, 119t nutrition and, 250b—251b pathogenesis of, 202 preexisting, as risk factor, 202, 2031 and pregnancy, adverse outcomes in, 120-122 prevention of, 10, 168-169, 256t daily oral hygiene and, 168-169, 190, 191t, 203t dental professionals’ knowledge about, 178 history of, 3, 18 provider-based, 205-206, 206t public’s knowledge about, 178 strategies for, 156t risk and protective factors for, 256t tobacco and, 259b, 260b Periodontal ligament regeneration procedures for, 208 sensitivity of, 24 teeth in, 26 tissue turnover in, 31 Periodontitis adult. See Adult periodontitis and heart disease, 118-120 as mixed infection, 205 necrotizing ulcerative, and HIV, 101 pathobiology of, 202, 202f and stroke, 119-120 Perioral skin, lesions of, diseases and conditions causing, 98t Pfeiffer’s disease, 49 PGE). See Prostaglandin E, 302 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL pH in dental caries risk assessment, 197 saliva and, 27 Phagocytes, in adult periodontitis, smoking and, 41 Pharmaceuticals. See Medications Pharyngeal cancer. See Cancer, oral and pharyngeal Pharynx, 25 herpes simplex virus and, 109 lesions of, diseases and conditions causing, 98t, 100t Phenytoin, and gingivitis, 39, 107 Phosphate metabolism, disturbances in, oral manifestations of, 101 Pierre Robin syndrome, 48 Pigmentation, of soft or hard disease, 100 Pipe smoking, and cancer, 208t, 259b Plaque, 37, 104. See also Biofilm control of, 39, 205-206, 206t chemical, 205 with daily hygiene, 190 professional, 206 , fluoride in, 159 public knowledge about, 178 subgingival, 40 Pocket depths, and periodontal disease diagnosis, 204, 204t Point mutations, birth defects and, 31 Polymeric resin composites, in dental caries treatment, 201 Population, trends in, 275-276, 280 Population groups characteristics of, as determinant of health, 248, 248f data on, 10, 61-62, 88 disabled, oral health of, 78-79 diversity of, future of oral care and, 277 oral health disparities among, 1, 4,10, 17, 19, 88, 239, 283-284 oral health services targeted to, 225, 239 racial/ethnic minorities. See Race/ethnicity, specific minority group women. See Women Porphyromonas gingivalis in adult periodontitis, 40, 41, 205 in adverse pregnancy outcomes, 121 and bacteremia, 104 in heart disease, 117 in periodontal disease, 203t Poverty, 249. See also Income children in, oral health of, 2, 252 and dental care utilization, 80, 80t, 81 and dental caries, susceptibility to, 63-64 and tooth loss and edentulism, 66, 67f oral tissue, as sign of ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Index and toothaches, 73 PPOs. See Preferred provider organizations Precancerous lesions HPV and, 45 and oral cancer, 44-45 and smokeless (spit) tobacco, 70. 70f Precavitated carious lesions, in restored teeth, diag- nosis of, 198 Preferred provider organizations (PPOs), 229, 232. 233t Pregnancy adverse outcomes of, periodontal disease and, 120-122 and dietary fluoride supplements, 163-164 gingivitis in, 39 Prenatal care, 172, 198, 210-211 Prenatal syphilis, lesions caused by, 99t Prepubertal periodontitis, 42 Prevalence, definition of, 62b Prevalence rate, definition of, 62b Prevotella intermedia in adult periodontitis, 40, 41 in periodontal disease, 2031 in prepubertal periodontitis, 42 smoking and, +1 Private practice, 223-224, 227 Probes/instrumentation, sensitivity of, +0 Probing depths, and periodontal disease diagnosis, 204, 204t Prostaglandin(s) and adult periodontitis, 40-41 and heart disease, 115 and pregnancy, 121 Prostaglandin E, and adult periodontitis, 40-41, 205 and mucositis, 106 and periodontal disease, and low birth weight. {2) Proto-oncogenes discovery of, 45 and oral cancer, 46 Provider-based care, 191-212 changing approach by to birth defects, 210-211 to dental caries, 196-201 to oral and pharyngeal cancers, 209-210 to periodontal diseases, 201-209 for chronic craniofacial pain and sensorimotor conditions, 211 diagnostic tests in, 193, 193t dental caries, 198, 200t oral and pharyngeal cancer, 210 periodontal diseases, 203-205, 204t future of 303 Index Provider-based care (continued) broadening base in, 216 clinical practice guidelines, 213-214, 215t evidence-based practice, 213 science and technology contributions, 216 for mucosal and autoimmune diseases, 212 oral health assessment by, 193-196, 194f-195f, 197¢ prevention by of birth defects, 210-211 of dental caries, 198-200 of oral and pharyngeal cancer, 210 of periodontal diseases, 205-206, 206t risk assessment by, 192-193 of dental caries, 197, 198t, 200t of oral and pharyngeal cancer, 208t, 209-210, 209t , of periodontal diseases, 202-203, 203t for temporomandibular disorders, 211-212 Pseudomembranous candidiasis, 43 Pterygoid muscle, 26 Puberty gingivitis, 39 Public knowledge, attitudes, and practices of, 177-179, 239, 280 perceptions of, 11, 285 Public health programs. See also Community health programs; Medicaid; Medicare for elderly, 265 essential services for, 181b in oral health care system, 12, 225-227, 286 Public-private partnerships, 13, 286 Puerto Ricans, oral health of, 75 Pulmonary disease, obstructive, and oral health, 108 Pulp tissue infections in, 24, 38 tissue turnover in, 31 Q Quality of life cultural perspectives on, 134-135 heightened expectations of, 146 oral health in, 133-134 functional dimensions of eating problems and, 135-136, 136t sleep problems and, 137 indirect costs of, 142-144, 143t need for measurement of, 133—134 psychosocial dimensions of, 137-142 cleft lip/palate and malocclusion, 141-142 facial appearance, 140-141 oral and pharyngeal cancers, 142 oral-facial pain and, 139-140 social function and, 138-139, 139t research on, 144-146, 146t R Race/ethnicity. See also specific minority group and adult periodontitis, 41 and congenital malformations, 72, 72f and dental care nonutilization, 84t-85t utilization, 80t, 81-82, 81t wants, 87t and dental caries, susceptibility to, 63-64, 63f, 64f future of oral care and, 277 and insurance coverage, 230-231, 232f and malocclusions, 72 in oral health workforce, 12, 236-237, 237t, 286 and periodontal disease, 41, 65-66, 66f Radiation treatment oral candidiasis and, 42 oral infections from, 106 oral ulcers and oral mucositis from, 26 periodontal disease from, 105 Radiographs, 196 bite-wing, 198, 200t in periodontal disease diagnosis, 204, 204t Rapidly progressive periodontitis, 40, +1 systemic antibiotics for, 207 Ratings, of oral health, 144 RAU. See Recurrent aphthous ulcers Recurrent aphthous ulcers (RAU), 43-44 prevalence of, 71, 71f Refractory adult periodontitis, 42 systemic antibiotics for, 207 Reimbursement, direct, 230. See also Dental care, financing and reimbursement Relative survival rate, definition of, 62b Remineralization, 27, 38, 159, 199 Research. See also Science base current, 4, 5, 11, 19, 20 in evidence-based practice, 213, 246 federal studies of oral health, 268 need for expansion of, 285-286 on quality of life, 144-146, 146t surveys used for health data, 61-62 trends in, 214-216 Respiratory disease, oral infections and, 108 Restorations precavitated carious lesions in, diagnosis of, 198 procedures for, 201 Retinoids, 47 304 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL Rous sarcoma virus (RSV), and oral cancer, 45 RSV. See Rous sarcoma virus Rural/urban status, and dental care wants, 87t Ryan White Comprehensive AIDS Resources Emergency Act, 225 S S-IgA, 28 Saethre-Chotzen syndrome, 49 Saliva, 26 aging and, 32 and cariogenic bacteria, 38 decreased flow of in dental caries risk assessment, 197 and chewing function, 136 diagnostic value of, 103-104, 103t, 279, 280t fluoride and, 27, 38, 159 . functions of barrier and buffering properties, 27 dental caries prevention, 27 tissue protection, 26-27 wound healing, 27 and general health, 1, 17 immunoglobulins in, smoking and, 41 Salivary glands, 26 and aging, 32 and general health, 1, 17 involvement in infections, 97 Sjogren's syndrome and, 51 Satisfaction ratings, of oral health, 144 Scaling and root planing, for plaque removal, 206, 206¢ SCHIP See State Children’s Health Insurance Program School-based programs. See also Dental schools, Health professional schools dental sealant programs in, 167 dietary fluoride supplements in, 164-165 fluoridated drinking water in, 159t, 162 fluoride mouthrinses in, 165 oral and pharyngeal cancer prevention programs in, 170 strategies employed by, 156t tobacco prevention programs in, 170 Science base. See also Research and evidence-based practice, 213, 246 need for expansion of, 11-12, 285-286 in oral health, 5, 19-20 Scientific worldviews, 134-135 Scurvy, oral signs of, 101 Sealants. See Dental sealants Secretory leukocyte protease inhibitor (SLPI), 27 Self-care. See Oral health care system, individual Index approaches in Senses, 23-25, 32 Sex and adult periodontitis, susceptibility to, 41, 65, 65f and dental care nonutilization, 84 utilization, 80t, 81-82, 8lt wants, 87t of dental personnel, 236-237 and injuries, 73 and insurance coverage, 231, 232f and oral and pharyngeal cancers, by race/eth- nicity, 68, 68f and oral clefts, 72 and oral health, 77-78 ratings of, 144 and pain, 25, 77 prevalence of, 73, 73f and periodontal disease, 203t and Sjogren's syndrome, prevalence of, 73 and taste, 78 and TMDs, prevalence of, 73 and tooth loss, 66 Sex hormones and adult periodontitis, susceptibility to, 41 pain and, 25 Sexually transmitted diseases (STDs), oral transmis- sion of, 109 Single-gene defects, 49-50 Sjogren's syndrome, 31 prevalence of, 73 swollen parotid glands with, 97 Skin, lesions of, diseases and conditions causing, 98t, 100t Sleep problems, and quality of life, 137 SLPI. See Secretory leukocyte protease inhibitor Smell aging and, 32 development and function of, 23, 24 Smokeless (spit) tobacco. See Tobacco Smoking. See also Tobacco and birth defects, 48 cessation of, 210 community intervention models, 171 and oral cancer, 46 and periodontal disease, 203t, 206 school-based intervention models, 170 and trench mouth, 40 Social function, and dental problems, 138-139, 139t Socioeconomic status. See Income Sonic instruments, for plaque removal, 206, 206t Spinal chord, early development of, 29 Spirochetes, and trench mouth, 40 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 305 Index Sports injuries, 50, 73, 173-176, 174t-175t, 176b, 258 Squamous cell carcinomas, oral, +4 HPY and, 43, +5 Stannous fluoride, to limit gingival inflammation, 205, 206t State Children’s Health Insurance Program (SCHIP), 2,13, 233-234, 255, 277 States data from, need for, 10, 88, 28+, 285 on edentulism, 67t income of, and population-per-dentist ratio, 224, 224f on mortality rates for oral and pharyngeal cancer, 70, 70t public health systems in, 226-227, 286 STDs. See Sexually transmitted diseases Steroid hormones, and gingivitis, 39 Stevens-Johnson syndrome, lesions caused by, 100t Streptococci, 39. See also Mutans streptococci Streptococcus sanguis, in heart disease, 107, 117 Streptococcus viridans, oral infections from, 105 Stress and immune system, 28 and periodontal disease, 203t. 206 Stroke, oral infection and, 115-120 animal studies, 117-118 mechanisms of action in, 115-117 population-based studies. 118-120, 119¢ Student indebtedness, 237-238 Sublingual glands, 26 Submandibular glands, 26 aging and, 32 Submucous fibrosis, and oral cancer, 45 Sugars and dental caries, 38, 250b intake reduction of, 199 in smokeless (spit) tobacco, 39 Surveillance data, 61-62 need for, 12, 88-89 on quality of life, 144-146, 146¢ surveys used for, 61-62 Survival rate, definition of, 62b Svphilis. lesions caused by, 99t, 109 T T cells, 28 smoking and, 41 Tar. tobacco carcinogens in, +5 dysplasia and, +6 Tartar. and gingivitis, 39. See also Calculus Task Force on Community Preventive Services, 158, 180 Taste development and function of, 23-24 sex differences in, 78 Tear glands, Sjégren’s syndrome and, 51 Technology, future of, 278-279 Temperature, sensitivity to, 24-25 Temporalis muscle, 26 Temporomandibular disorders (TMDs), 52-53 and chewing function, 136 clinical management of, 211-212 diagnosis of, 211-212, 212t pain from, impact of, 139-140 prevalence of, 73 and quality of life, 145-146 treatment for, 212 Temporomandibular joint, 26 Teratogens, 47-48 Tetracycline, enamel hypoplasia from, 107 TGF-ca. See Transforming growth factor a Therapeutics, oral fluids in diagnostic tests for, 103, 103t Thermoreceptors, 24 Thrombosis, from oral cavity bacteria, 117 Thromboxane B2, and heart disease, 115 Thrush, 43. See Candidiasis prevalence of, 71 Tic douloureux, 52 TMDs. See Temporomandibular disorders TNF-a. See Tumor necrosis factor « Tobacco, 191t among adolescents, 259b and adult periodontitis, susceptibility to, 41 and alcohol, combination of and oral cancer, 45, 208t, 209 and dental caries, 259b as general health risk factor, 4, 10, 18 and oral and pharyngeal cancer, 259b, 260b and oral cancer, 44-45, 169, 170, 208t, 209, 209t and oral candidiasis, 42 oral effects of, 101 and oral mucosal lesions, 70 and periodontal diseases, 169, 259b, 260b and saliva, 27 smokeless (spit) tobacco among adolescents, 257 and dental caries, 259b and oral and pharyngeal cancer, 44-45, 208t, 259b and oral mucosal lesions, 70, 70f and periodontal diseases, 259b 306 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL prevention programs for, 170 and tooth decay, 39 trends in use of, 259b-260b Tongue cancer in, 70 lesions of, diseases and conditions causing, 98t-100t Tooth/teeth, 26 aging of, 31 birth defects involving, 48-49, 50 clenching of, 190, 191t, 212 conically shaped, in ectodermal dysplasias, 50 cultural significance of, 137-138 decay in. See Dental caries embryonic development of, 30 grinding of, 52, 212 loss of by age, socioeconomic status, sex, and race/ethnicity, 66-67 and chewing function, 135-136 malocclusions. See Malocclusions nutrition in development of, 250b pain in, 24 primary, 26 restored. See Restorations staining of, 107 thermal sensitivity in, 24 trauma to from falls, 50 prevalence of, 72 Toothbrushing, 39, 176, 179, 190 and bacteremia, 104 public knowledge of for dental caries prevention, 177 for gum disease prevention, 178 public practices, 178 Toothaches, prevalence of, 73, 73f Toothpaste. See Dentifrice Touch, sense of, in mouth, 24 Toxic-shock-like syndrome (TSLS), 105 Toxins, saliva and, 27, 103, 103 Transforming growth factor a (TGF-a), and oral and pharyngeal cancers, 46, 47 Trauma. See also Injury, and oral-facial prevention of, strategies for, 156t and RAU, 44 Traumatic ulcers, lesions caused by, 100¢ Treacher Collins syndrome, 48 Treatment(s). See also specific disease future of, 276 outcomes as determinant of health, 248, 248f measurement of, 133 Index Trench mouth, 40 lesions with, 99t Treponema, and gingivitis, 39 Treponema denticola, in adult periodontitis, 40, 205 Triclosan copolymer, to limit gingival inflammation, 205, 206t Trigeminal ganglion, oral herpes and, 43 Trigeminal neuralgia, 52 TSLS. See Toxic-shock-like syndrome Tuberculosis, lesions caused by, 99t Tumor necrosis factor a (TNF-a) and adult periodontitis, 41, 205 and glycemic control, 114 and heart disease, 115 and pregnancy, 121 Tumor suppressor genes, mutations of, in oral and pharyngeal cancer, 46 U Ulcerative colitis, and RAU, 44 Ultrasonic instruments, for plaque removal, 206, 206t U.S. Department of Agriculture, 225 U.S. Department of Defense, 225 U.S. Department of Health and Human Services (USDHHS), 225, 226, 226¢ U.S. Department of Justice, 225 U.S. Department of Transportation, 225 U.S. Department of Veterans Affairs, 225 U.S. Preventive Services Task Force, 156-158 USDHHS. See U.S. Department of Health and Human Services Vv Van der Woude syndrome, 48 Varicella-zoster virus and chemotherapy, 106 oral lesions with, 98t Vascular endothelial growth factor (VEGF), 27 VEGE See Vascular endothelial growth factor Veillonella parvula, and gingivitis, 39 Velocardiofacial syndrome, 48 Venereal warts, 71 VGS. See Viridans group streptococcei Vietnamese Americans, nasopharyngeal cancer inci- dence and mortality, 76 Vincent's infection, 40 lesions caused by, 99t Violence, 51, 72-73 Viridans group streptococci (VGS), 105 Viridans streptococcal shock syndrome (VSSS), 105 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL 307 Index Viruses. See also specific virus chemotherapy and, 106 lesions caused by, 98t oral cancer and, 45-46 Vitamin B deficiency, oral signs of, 101 Vitamin C deficiency and cancer, 251b oral signs of, 101 Vitamin D deficiency, oral signs of, 101 Vitamin E, 47 cancer and, 251b and mucositis, 106 VSSS. See Viridans streptococcal shock syndrome WwW Waardenburg syndrome, 50 Warts, viral, 43 oral lesions with, 98t Water fluoridation. See Fluoride, in drinking water Well-being and oral diseases, 10, 11 and oral health, 2, 4-5, 18, 19 in World Health Organization (WHO) definition of health, 133 Western scientific worldviews, 134-135 WHO. See World Health Organization WIC. See Women, Infants, and Children program Wolinella recta, in adult periodontitis, +1 Women and adult periodontitis, susceptibility to, 41, 65, 65f and dental care nonutilization, 84f as dental personnel, 236 in dentistry, 223-224, 224t elderly, risk factors for, 266-267 and injuries, 73 and oral and pharyngeal cancers, 68, 68f and oral bone loss, 102—103 oral health of, 77-78, 266-267 areas of study in, 78, 78f and pain, 25, 77-78 prevalence of, 73, 73f TMDs, 52, 73 and Sjogren's syndrome, prevalence of, 73 Women, Infants, and Children (WIC) program, 225, 256 Workplace effects, on oral health, 249 World Health Organization (WHO) 18, 133 X Xenografts, 208 Xerostomia. See Dry mouth and dental caries, 38 and oral candidiasis, 42 Xerostomic side effects, of medication, 107 Y Yeast. See Candida albicans 308 ORAL HEALTH IN AMERICA: A REPORT OF THE SURGEON GENERAL