Dental Diseases @)

m4 ——

wa

xO

Percent of Persons

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Is-24 25-29 ME34 3839 0-H 4549 50-54 $8.50 O64 bS-NO-

Age Group
w4 mn] +6 mm of |

Figure 8-3. Percent of persons by severe loss of periodontal
attachment (pocket depths measuring 4 mm or more)
and age groups as determined from the NIDR survey
of employed adults and seniors.

Source: National Institute of Dental Research 1987.

 

 

 

05 manana NCHS 1960-62
emums NIDR 1985 ee
2 40
2B
S
s 30-
c
i)
3 20
u
a.

101,

r '
35-44 45-54 55-64 65-74
Age Group

(Years)
Figure 8-4. Comparison of the percent of edentulous persons in the
1985-86 NIOR survey to that reported from the NCHS
survey of 1960-62.

Source: National institute of Dental Research 1987.

351
C Nutrition and Health

  
  
   
  
  

Fissure

Pit

Crown (Enamel)
Dentinal tubules (Dentin)
Gum

Pulp

Alveolar bone

Periodontal
ligament

Cementum

Blood vessel in
root canal

Figure 8-5. Schematic cross-section of a typical mandibular tooth. The
gums recede with age, exposing the cementum of the tooth
root.

dental organ that produces the tooth enamel and a dental papilla that
produces the tooth pulp and the dentin. Cells from the dental follicle form
the cementum and periodontal ligament after the tooth has formed.

The deciduous teeth begin forming at about 6 weeks in utero, when cells in
the primitive oral cavity differentiate to form the dental lamina—the site of
development of the tooth buds. The dental lamina is active from the second
month of embryonic development, when the first buds for the deciduous
teeth are formed, until about the age of 5 years, when the buds for the last
permanent molars are initiated.

The formation of the tooth crown begins with the secretion of a dentin
matrix containing collagen fibrils. Mineral ions then enter the matrix to
form small crystals on or between the fibrils. Successive layers of dentin
are formed. Enamel formation begins as soon as the first dentin layer has
been laid down. Cells of the enamel organ secrete successive layers of a
matrix that is chemically different from dentin matrix. Mineral crystals
appear in each layer as it is secreted and grow larger as more mineral enters
the tissue; matrix proteins and water are removed. This so-called matura-
tion of the enamel continues after the full thickness of enamel matrix has

352
Dental Diseases le

been laid down. These events occur at different times for the various
deciduous and permanent teeth, beginning from a few months before birth
until late adolescence.

As the tooth erupts into the mouth, it loses the layers of cells and blood
vessels that covered the enamel. The enamel, however. continues to
mature during the period immediately after tooth eruption and to incorpo-
rate minerals (including fluoride) into its structure from saliva, food, and
drinking fluids. Otherwise, the enamel of fully erupted teeth is not known
to have any metabolic dependence upon nutrients consumed in the diet.
The inner surface of dentin adjacent to the pulp remains lined with the cells
that formed it, and these cells continue to form secondary dentin at a very
slow rate throughout the life of the tooth.

Thus, there are different periods in the developmental history of the tooth.
During the preeruptive period when the crowns are forming in the jaws
(which, for the wisdom teeth, continues into late adolescence), the devel-
oping enamel and dentin of the crowns are subject to nutritional deficien-
cies or imbalances in the same way as other tissues. In fact, in the enamel
the preeruptive period can be divided into two phases, the secretory and
the maturation stage. Nutritional deficiencies or excesses may affect either
stage separately or both. Hypoplastic lesions in the enamel reflect distur-
bances affecting the secretory process. Hypomineralized defects, such as
the white spot lesions of fluorosed enamel, give evidence of interference
with the maturation process. After eruption, when the crown of the tooth
has emerged from the jaw and the enamel is bathed instead by the saliva as
well as exposed to micro-organisms and their byproducts, sloughed cells,
and food debris, nutritional deficiencies or excesses and dietary habits may
affect teeth in a totally different manner.

The development and maintenance of the soft tissues and bone that anchor
and support the teeth (the periodontium) are also subject to nutritional
deficiencies. The periodontium comprises the gingiva (the tissue that cov-
ers the alveolar bone process and surrounds the top of the tooth), the
periodontal ligament (the soft connective tissue that surrounds the roots of
the teeth and joins the root cementum and the alveolar bone), the root
cementum (a specialized calcified tissue that covers the tooth root), and the
alveolar bone (the bone that forms and supports the sockets of the teeth).
The bony tissue of the alveolar process is dependent on the presence of
teeth. The alveolar bone grows in response to dental eruption, is modified
by dental changes, and resorbs when the teeth are lost as a result of

353
C Nutrition and Health

advanced dental caries and/or periodontal disease. The resorption of al-
veolar bone ridges (residual ridge resorption) has been described as an oral
disease entity (Atwood 1971).

Throughout life, the oral soft tissues undergo rapid rates of turnover and
repair, and the continued presence of optimum levels of nutrients is neces-
sary to maintain proper oral health and to resist disease.

Dental Caries

Once a tooth is fully erupted, it becomes subject to the influence of
chewing, acids in the mouth, and bacterial plaque. Dental caries begins
with dissolution of the mineral surface of the tooth by acid produced from
fermentable carbohydrate (e.g., sugar) by dental plaque bacteria. Next, the
dissolution advances further into the enamel, first appearing as a white
spot, and subsequently into the dentin and eventually into the pulp. If left
untreated, the result is destruction of the crown and root system, tooth
loss, and resorption of the surrounding bone (Newbrun 1978). The decay
that begins in pits and fissures, on the smooth surfaces, or on exposed roots
of the teeth is invariably due to the combined effects of bacterial infection
and host and dietary factors over time (Wei, Fomon, and Anderson 1977;
Shaw 1978, 1987). Patients with reduced salivary flow are also at increased
risk (Mandel 1983).

Of the many bacteria found in tooth plaque, Streptococcus mutans is
considered the primary etiologic agent in coronal caries (Loesche 1986;
Shaw 1987). This bacterium is unique in that it produces enzymes that
convert table sugar (sucrose) into long sticky polysaccharides. The poly-
saccharides promote firm attachment and accumulation of the bacteria in
dental plaque (Gibbons and van Houte 1978). If not removed, the bacteria
metabolize sugars (including sucrose) and produce acids that dissolve
minerals from the teeth and begin the decay process. Root caries, decay of
tooth root cementum following recession of gum tissues, has been regarded
as an independent type of caries (Nikiforuk 1985). However, a relationship
between root caries and coronal caries has been reported recently (Vehk-
alahti 1987). Decay also occurs around restorations where plaque is diffi-
cult to remove.

Whereas sugars facilitate the action of cariogenic bacteria, saliva is a major
impediment to the pathogenesis of these bacteria (Vogel 1985; Mandel
1986). This fluid, secreted by the major and minor salivary glands, coats the
tissues of the mouth and provides protection against bacteria that cause
disease. The saliva contains molecules that when adsorbed to the tooth can
influence attachment of bacteria to this surface and, when present in the

354
Dental Diseases ie

fluid, can clump bacteria together such that they cannot attach to the teeth
but rather are cleared from the mouth by swallowing. Saliva also contains
enzymes and proteins with antibacterial activity that inhibit bacterial
growth or kill bacteria. In addition to these defense mechanisms, saliva can
contain antibodies that attack specific kinds of bacteria. Another important
function of saliva is that it supplies the calcium and phosphorus, minerals
important in the remineralization of tooth surfaces that have lost mineral
due to acid attack.

Several types of interventions might prevent tooth decay. The most impor-
tant diet-related interventions are fluoridation of drinking water and con-
trol of sugar intake, but other approaches such as oral hygiene, application
of plastic sealants, use of topical fluorides, and various chemotherapeutic
agents have also been shown to be effective (Navia 1985). The efficacy of a
caries vaccine that would prevent infection by cariogenic bacteria is under
investigation (Navia 1985; Krasse, Elmilson, and Gahnberg 1987).

Periodontal Disease

Periodontal disease encompasses pathologic changes of the gingiva, peri-
odon<al ligament, cementum, and alveolar bone that make up the attach-
ment and supporting tissues of the teeth (Lindhe 1983). The destruction of
these tissues (the periodontium) results in the loosening and loss of the
teeth. The etiology of this disease, like that of dental caries, is multifac-
torial, involving bacterial infection, host factors, diet, and duration of
infection. The accumulation of bacterial plaque near the gum line can cause
a nondestructive inflammation of the gingival tissue (gingivitis). Early
studies (Lée, Theilade, and Jensen 1965; Theilade et al. 1966) showed that
dental plaque caused clinical gingivitis and that when the plaque was
removed the disease was reversed or prevented. If the inflammation per-
sists, the disease can progress and destroy the gingival connective tissue
and underlying tissues to form a subgingival or periodontal pocket. As the
pocket depth increases, the alveolar bone (bone supporting the tooth) is
resorbed and the tooth is lost. The primary etiologic agents for periodontal
disease are subgingival bacteria (Socransky 1977).

The bacteria make and release toxic substances, destructive enzymes, and
antigenic molecules that cooperate in the destruction of periodontal
tissues. Large amounts of bacterial products can directly damage tissues or
can cause overstimulation of the immune system with resulting tissue
damage; under normal oral conditions, the immune system is protective
against bacterial challenge (Nisengard 1977; Seymour 1987). Other factors
that can decrease host defense mechanisms and, therefore, promote peri-

odontal disease are immunologic defects. metabolic problems, endocrine

355
ie Nutrition and Health

dysfunctions, and nutritional deficiencies. Reduced salivary flow is also a
risk factor (Mandel 1983).

Key Scientific Issues

® Role of Diet in Tooth Decay

@ Role of Diet in Periodontal Disease

© Role of Diet in Other Dental Conditions

© Effect of Tooth Loss on Nutritional Status

Role of Diet in Tooth Decay

Although diet is indicated as one of the main direct determinants of dental
caries, it is also linked to each of the other determinants of causation,
prevention, and treatment. Dietary factors are important for the host’s
normal tooth development, host resistance, and salivary composition; for
selection and maintenance of the microbial population; and for the amount
of time teeth are in contact with sugars and their acid byproducts (Alfano
1980). Sugars are the most important dietary factors in the causation of
dental caries; fluoride is most important in its prevention. The role of other
dietary components such as fats, protein, and minerals in modulating these
effects is also of much current interest.

Role of Sugars

Despite the complex etiology of dental caries, the causative role of dietary
sugar—especially sucrose—is well established (Keyes and Jordan 1963).
Caries-producing bacteria have a rather high need for a range of simple
sugars (glucose, fructose, lactose, maltose, and sucrose) that they readily
metabolize into acids that demineralize teeth. The unique role of sucrose,
however, depends on its ability to be converted by mouth bacteria into
extracellular polymers of glucose or fructose that adhere firmly to the tooth
surfaces (Gibbons and van Houte 1978; Doyle and Ciardi 1983). Together
with the micro-organisms that secrete them, these extracellular products
facilitate the further attachment to teeth and proliferation of bacteria.

Food sugars, such as glucose and fructose that diffuse into this plaque,
nourish the micro-organisms. Food starches are converted to a limited
extent by salivary enzymes to soluble glucose that can be used by plaque
bacteria. Although saliva readily neutralizes organic acids, it has limited
access to the acids generated at the tooth surface beneath the plaque.

356
Dental Diseases Q

Recent reviews of extensive animal studies and human epidemiologic and
clinical observations during the past 30 years have thoroughly documented
the role of sucrose and other sugars in tooth decay (Newbrun 1982; Glins-
mann, Irausquin, and Park 1986). Studies in rats, for example, have dem-
onstrated a direct relationship between the amount of sucrose in the diet
and caries incidence that reaches a plateau when the sucrose concentration
is 8 to 40 percent by weight. Such studies have also demonstrated the
importance of the consistency and composition of the diet. Sucrose has
been shown to have a greater cariogenic effect than glucose, fructose, or
other simple sugars. Caries incidence increases directly with the frequency
of sugar consumption (Bowen et al. 1983).

Despite methodological difficulties in assessing population-wide sugar
intake, human epidemiologic studies have generally indicated an associa-
tion between sugar intake and tooth decay (Sreebny 1982) as well as
increasing rates of tooth decay among populations whose sugar intake is
increasing (Burt and Ismail 1986). Human clinical studies have demon-
strated a virtual absence of tooth decay and much lower concentrations of
cariogenic bacteria in the mouths of children with inherited metabolic
disorders (e.g., fructose intolerance) that prevent sucrose consumption
(Newbrun 1982).

Other clinical studies show the importance of frequency of sugar consump-
tion and the form in which it is consumed. Sugars in solution are more
readily cleared from the mouth than sugars in solid foods and, therefore,
are more likely to have only a transient influence on plaque acidity. Foods
that adhere to the teeth are more cariogenic than those that wash off
quickly (Gustafsson et al. 1954). In addition, people eat foods in different
ways. It appears that any increase in the length of time food remains in the
mouth is likely to increase the initiation and progression of caries (New-
brun 1978).

Metabolism of sugars by mouth bacteria results in acid production con-
comitant with a pH drop in dental plaque from a level near neutral to about
5. This effect lasts 20 to 30 minutes until buffering agents in saliva restore
the normal pH. Recurrent exposures to such episodes for extended time
periods lead to dissolution of the enamel. The presence of calcium, phos-
phate, fluoride, and other minerals in the saliva permits remineralization
when the pH is neutral. Thus, the tooth is exposed to alternating cycles of
dissolution and remineralization. If the balance favors dissolution, clinical
carious lesions occur, and if it favors remineralization, early lesions are
repaired and advanced caries does not develop.

357
C Nutrition and Health

Research into the cause of caries has not entirely overcome problems in
measurement of sugar intake, the confounding effects of other dietary
components, and secular trends in dental hygiene and fluoride consump-
tion. Evidence exists that sugars as they are consumed in the average
American diet contribute to the development of dental caries. Current
average daily intake levels in the United States are 62 to 143 g, or 18 to 32
percent of total caloric intake (Glinsmann, Irausquin, and Park 1986).
Reduction of dietary sugar would be expected to reduce levels of tooth
decay in the population, in particular at the time of tooth eruption (Loesche
1985).

Nursing Bottle Caries

A special example of the importance of the duration of contact between
fermentable sugars and teeth is nursing bottle caries (Gardner, Norwood,
and Eisenson 1977; Ripa 1978; Dilley, Dilley, and Machen 1980; Kelly and
Bruerd 1987). This unique pattern of dental caries, where the upper in-
cisors become badly decayed, has been described in young children. In
severe cases, the chewing surfaces of the molars become affected, but the
lower incisors rarely develop lesions. The lesions on the upper incisors
begin as a generalized demineralization on the third of the crown next to the
gums and progress so that the tooth is encircled by a ring of decay that may
become so deep that the crown breaks off just above the gum.

This condition occurs when children are put to bed with a bottle of milk,
formula, juice, or sweetened beverages. These practices allow sugars in
milk or other fluids to remain in contact with the tooth surfaces for
extended periods. The position of the upper incisors makes them especially
vulnerable, while the lower incisors are usually protected by the tongue.
These carbohydrates are metabolized to acids by the oral micro-organisms
that are always present on tooth surfaces, and this action is compounded
by the infrequent swallowing and reduced salivary flow that occur during
sleep.

Role of Fluoride

The efficacy of fluoride in the prevention of tooth decay is well established.
It is generally assumed to prevent caries by decreasing the solubility of
tooth enamel, promoting remineralization of the enamel surface, modify-
ing the chemical interactions in plaque, or inhibiting lactic acid production
by cariogenic bacteria (Navia 1985).

Since 1945, when fluoride was first added to community water supplies,
more than 35,000 published scientific papers have attested to the efficacy,

358
Dental Diseases @)

safety, and cost-effectiveness of fluorides in prevention of tooth decay
(Richmond 1985). Many of these studies demonstrate reductions in dental
caries of 50 percent or more when fluoride is added to a community water
supply.

One focus of research in the 1930's and 1940’s was to determine the optimal
level of fluoride in drinking water. This concentration is about | ppm for
temperate regions. Current recommendations for optimum fluoride con-
centrations vary from 0.7 to 1.2 ppm, depending on regional variation in
prevailing air temperature because the amount of water consumed tends to
be less in colder climates. Caries incidence increases when drinking water
contains less than the optimum level of fluoride, but mild forms of fluorosis
(the mottling of tooth surface) can begin to occur at about twice the
optimum level. Fluorosis occurs only when developing teeth are exposed
to excess fluoride, generally over a period of months; once a tooth is fully
formed, continuing fluoride exposure may promote the remineralization
process.

For children living in areas with inadequate concentrations of fluoride in
the water, dental authorities recommend fluoride supplements at dosages
that depend on the natural fluoride content of the local water supply and the
age of the child. The dosages currently recommended by the Council on
Dental Therapeutics of the American Dental Association and the American
Academy of Pediatrics are provided in Table 8-1. The effectiveness of
prenatal fluoride supplementation, however, is uncertain because clinical
studies of its effects on subsequent caries incidence have been equivocal
(Driscoll 1981).

Table 8-1
Supplemental Fluoride Dosage Scheduled
(in mg F/day*) According to
Fluoride Concentrations of Drinking Water

 

Concentration of

 

 

Fluoride in Water (ppm)
Less Greater
Age (years) than 0.3 0.3 to 0.7 than 0.7
Birth to 2 0.25 0 0
2 to3 0.50 0.25 0
3 to 13 1.00 0.50 0

 

22.2 mg of sodium fluoride contain 1 mg of fluoride.

Source: Council on Dental Therapeutics 1984.

359
ie Nutrition and Health

Another area of uncertainty concerns current levels of fluoride intake.
When the optimal level of about 1 ppm was originally established, the
primary source of fluoride for human consumption was the water supply.
Today, fluoride is also available from toothpastes, mouth rinses, and soft
drinks and foods prepared with fluoridated water. These sources have
increased the availability of fluoride beyond that originally envisioned,
perhaps to levels that might induce fluorosis (Horowitz et al. 1984). Several
recent studies have observed an increased incidence of mild (barely notice-
able) tooth mottling among children taking fluoride supplements or living in
communities where water is fluoridated. Although there is no evidence that
this condition is harmful, these observations have led some authorities to
suggest reevaluation of previously accepted standards for optimal fluoride
use (Navia 1985; Leverett 1982).

Controversy about water fluoridation is not new. Despite the preponder-
ance of community studies conclusively demonstrating the effectiveness of
both naturally occurring and purposefully supplemented fluoride in drink-
ing water, opposition has been raised on grounds of effectiveness, safety,
and individual rights (Taves 1979; Watson and Schrotenboer 1983). How-
ever, studies have failed to show any relationship between fluoride and
increased risk for heart disease, brain lesions, liver disease, allergies,
kidney disease, mental retardation, cancer, or mutagenicity (Richmond
1985). Indeed, studies of one chronic disease, osteoporosis, suggest a
protective effect for fluoride (Simonen and Laitinen 1985; see chapter on
skeletal diseases). Based on the scientific evidence, the courts have consis-
tently ruled that States and municipalities have the right to implement
fluoridativn as a public health procedure (Block 1986; Lée 1986).

Role of Other Dietary Factors

Protein. Experimental data show certain critical periods in the develop-
ment of the teeth of young rats, during which a marginal protein deficiency
exerts striking effects (Nakamoto, Mallek, and Miller 1979a, 1979b). When
low-protein diets were fed to rats at any time throughout pregnancy and
lactation, the molars of their offspring were altered in shape and were
significantly smaller than the molars of offspring from control rats (Shaw
and Griffiths 1963; Holloway, Shaw, and Sweeney 1961). Although the
change in tooth size occurred without a reduction in enamel thickness,
minor cusps of the third molars of the offspring from these protein-deficient
females frequently did not develop, suggesting that nutritional deficiencies
can prevent normal tooth development. Caries incidence was higher in the
offspring of protein-deficient females than in control offspring when both
were fed the same caries-producing diet after weaning. The offspring from

360
Dental Diseases O

protein-depleted females had abnormalities of the salivary glands (de-
creased DNA, RNA, and protein concentrations, and decreased net
weight) and the saliva (greatly reduced salivary flow and small increase in
salivary protein concentration), which may partially explain their increased
caries incidence (Menaker and Navia 1973a, 1973b, 1974).

Supplementing the diet of pregnant and lactating rats with | percent DL-
methionine (the limiting amino acid of casein) prevented almost all of the
abnormalities, but supplementation begun at weaning was ineffective
(Shaw and Griffiths 1963). That the deficient nutrient was protein, but not
calories or other nutrients, was demonstrated when protein supplements
alone prevented these abnormalities (Menaker and Navia 1973a, 1973b,
1974).

In humans, protein-energy malnutrition is often associated with poor den-
tal health. Delayed tooth eruption and impaired tooth development are
common findings among children in developing countries where protein,
calories, and other nutrients are inadequate (Steggerda and Hill 1942;
Sweeney 1966). Abnormal lesions on the teeth of younger children in less
developed nations have been reported to be highly susceptible to tooth
decay even when children consume lesser amounts of sugar-containing
foods and consume foods less frequently than children in more highly
developed nations (Sweeney et al. 1969; Sweeney, Saffir, and de Leon
1971). Nevertheless, the permanent teeth in older children and adults in
developing countries are not more susceptible to caries than those in older
children and adults in industrialized countries (Russell 1966). At present,
there is no evidence to indicate that an increase in caries incidence accom-
panies delayed tooth eruption. Little information on the influence of pro-
tein deficiency on the rate of salivary flow or on saliva composition in
humans is available (Vogel 1985).

Fat. In animal studies, increasing the concentration of fat in a diet with the
carbohydrate concentration held constant reduces the caries-producing
potential of the diet (Shaw 1950). This may have to do with the sequence in
which foods are eaten. When dietary sugar is followed by a food such as
cheese (which is high in fat), the usual acid-forming response is blunted and
less acid is present in plaque (Edgar 1981; Edgar et al. 1982; Schachtele and
Jensen 1983). The significance of these observations for human tooth
decay, however, has not yet been established.

Vitamin A. Studies of the continuously erupting incisor of the rat showed
that a severe deficiency of vitamin A impairs tooth formation (Wolbach and

361
O Nutrition and Health

Howe 1925, 1933; Boyle and Bessey 1941; Schour, Hoffman, and Smith
1941). The observed changes resembled the effects of vitamin A deficiency
on tissues of ectodermal origin elsewhere in the body. Bones formed
entirely during a period of vitamin A deficiency contain reduced amounts
of calcium, suggesting an effect on bone mineralization and the resulting
bone structure. A deficiency of vitamin A for a limited time before tooth
eruption has been shown to increase the susceptibility of rat molars to
caries (Harris and Navia 1980; Navia and Harris 1980). Other studies, in
which the third molars of rats were cultured, showed that vitamin A
deficiency delays tooth formation and interferes with mineralization of
both enamel and dentin (Navia et al. 1984). Vitamin A deficiency has also
been observed to disrupt normal differentiation of rat tooth-forming cells
and to alter the distribution of certain molecular components of dentin and
pulp (Punyasingh et al. 1984).

Vitamin D and Calcium. In early studies of rickets, deficiencies of a fat-
soluble vitamin, later identified as vitamin D, resulted in the softening and
discoloration of the enamel of developing teeth, delayed tooth eruption,
and an irregular tooth arrangement in the jaw (Mellanby 1918, Mellanby
1919). These defects were also seen in the offspring of pregnant animals
given a vitamin D-deficient (rickets-producing) diet but not in animals that
received daily supplements of cod liver oil (Mellanby 1928). Calcium defi-
ciency resulted in less severe defects in the enamel and dentin, but deficien-
cies of both calcium and vitamin D resulted in very poorly formed enamel
and dentin (Mellanby 1923). These early studies indicated the need during
tooth development for adequate dietary intake of calcium and vitamin D.

Ina series of clinical trials in England in which children received vitamin D
supplements to their regular diet, modest reductions in dental caries were
observed both for secondary teeth that had erupted before the trials began
and for teeth that erupted during the trial (Committee for the Investigation
of Dental Disease 1936). Despite evidence for a beneficial role of vitamin D
in tooth development, clinical trials to determine whether vitamin D sup-
plements reduce dental caries have yielded varied results (Shaw 1952), and
this area remains uncertain.

A long-term study of dental abnormalities in children showed that the
inherited conditions of vitamin D-dependent rickets or hypoparathyroid
syndrome, both of which reduce levels of plasma calcium, are associated
with abnormal lesions in tooth enamel but normal dentin. Children with low
plasma levels of phosphorus but normal levels of plasma calcium developed
normal enamel but abnormal dentin. Those with low plasma levels of both

362
Dental Diseases O

calcium and phosphorus developed abnormalities in both enamel and
dentin (Nikiforuk and Fraser 1979). The implications of these observations
for dietary intake in normal children are unknown.

Phosphate. An increasing amount of phosphate in the diet reduces experi-
mental caries incidence in rats (Nizel and Harris 1964), but supplementa-
tion of the diet of children with phosphate has not been shown to produce
benefits (Stralfors 1964; Ship and Mickelsen 1964; Averill and Bibby 1964).
Phosphate supplementation of chewing gum is reported to produce a reduc-
tion in caries incidence (Baron and Bilotti 1979; Finn et al. 1978: Jamison
1979; Richardson 1979).

Trace Elements. Certain epidemiologic surveys and experimental animal
studies have suggested that some trace elements such as molybdenum,
vanadium, strontium, and iron can inhibit caries development and that
other elements such as selenium, magnesium, and cadmium can accelerate
caries development. None of these studies has demonstrated either an
independent action of these elements or an action that either augments or
decreases the influence of fluoride (Curzon 1983; Navia 1970).

Other Food Components. Foods containing salts or acids can stimulate
salivary flow, alter its buffering capacity, or decrease microbial acid pro-
duction. Food components such as lectins (Gibbons and Dankers 1981,
1982), tannins (Kashket, Paolino, and van Houte 1985), and other less well-
characterized substances (Madsen 1970) can inactivate bacteria or influ-
ence their metabolism and reproductive ability and, in these ways, may
affect caries incidence.

Alternative Sweeteners. Sucrose and other simple carbohydrates can be
replaced by polyols or non-nutritive sweeteners in many kinds of foods.
The benefits of such products must take into account the quantities of
cariogenic sweeteners that must be replaced to achieve significant caries
reduction, the relationship of a food's overall chemical composition and
physical properties to its cariogenicity, and the possibility of other nutri-
tional or health effects (Hoskins 1978).

Role of Diet in Periodontal Disease
Periodontal disease is an infection of the gums and supporting structures
caused mainly by the microbial flora that adhere to dental plaque. Like

dental caries, the etiology of this disease includes specific microbiologic,
environmental, and systemic components. The gingival sulcus (the space

363
O Nutrition and Health

between the gums and the teeth) harbors bacteria that directly and indi-
rectly affect the formation of periodontal lesions and the later destruction
of periodontal tissues and their cellular components. Environmental influ-
ences on the gums include dietary sugars and other factors that promote the
formation of plaque on tooth surfaces, entrapment of food in periodontal
lesions, and poor dental hygiene. Systemic influences on the initiation and
progression of periodontal lesions are less well defined and more difficult to
investigate, although there is considerable evidence that persons who are
diabetic, immunosuppressed, or genetically susceptible are especially
prone to periodontal disease. In general, only severe nutritional deficien-
cies or extreme endocrinologic imbalances appear to adversely affect the
resistance of the gums. Diet may influence periodontal disease not only
through its effects on plaque formation, but also through stimulation of
salivary flow, antigenic stimulation of immune mechanisms, and enhance-
ment of host repair and defense mechanisms (Alfano 1976; Navia 1985); -
however, its precise role is as yet undefined.

Role of Calcium

Calcium is a necessary mineral in the formation of all calcified tissues,
including those of the periodontium. In adult dogs, a low-calcium diet
produces radiologic evidence of loss of alveolar bone within 2 months and a
periodontal syndrome within 1 year (Henrikson 1968). When the diet was
supplemented with calcium, the periodontal disease reversed within 6

months. .

It has been proposed that periodontal disease is caused by internal resorp-
tion of bone due to an imbalance of dietary calcium-to-phosphorus ratio
(Krook et al. 1972). A more recent study (Svanberg et al. 1973) using similar
conditions failed to confirm those results. Most scientists believe that
periodontal disease is initiated by subgingival bacterial infection. Addition-
- al studies are necessary before the role of calcium in the etiology of
periodontal disease can be ascertained.

Role of Vitamin C

A diet deficient in vitamin C (ascorbic acid) causes scurvy in humans.
Advanced disease produces gingival changes and loosening of the teeth.
Scurvy and some types of periodontal disease in humans are similar to
experimental scurvy in the guinea pig and in both Old and New World
monkeys, with bleeding of the gingiva, destruction of the periodontal
membranes, and loosening and ultimate loss of teeth (Alvares et al. 1981,
Boyle and Bessey 1941; Glickman 1948). There is ample evidence that
ascorbic acid, which is required for the formation of collagen in connective

364
Dental Diseases le)

tissues, is necessary for the repair and maintenance of periodontal tissues.
Only severe deficiencies result in aggravating periodontal disease.

Role of Folate

Folate is a member of the vitamin-B complex necessary for the normal
production of red blood cells. Folate deficiency is a common type of
hypovitaminosis in humans. In experimental gingivitis studies in humans,
folate supplementation resulted in significantly less inflammation of gum
tissues (Vogel and Alvares 1985). Its role in gingivitis and periodontal
disease is under investigation.

Role of Other Nutrients

Various periodontal abnormalities have been produced in experimental
animals as a result of nutritional deficiencies of protein (Chawla and Glick-
man 1951), tryptophan (Bavetta and Bernick 1956), calcium (Becks and
Weber 1931), magnesium (Klein, Orent, and McCollum 1935), vitamin A
(King 1940), vitamin D (Becks and Weber 1931), and B-complex vitamins
(Becks, Wainwright, and Morgan 1943; Tomlinson 1939). However, in these
studies, only severe deficiencies resulted in periodontal destruction, and
most of these experiments were carried out in grown animals.

On the basis of current knowledge, nutritional deficiencies or imbalances
do not seem likely to exert major influences on the prevalence or severity of
periodontal disease in the general population. However, the ability of
individuals with nutritional abnormalities to resist the progression of peri-
odontal lesions initiated by microbiologic and environmental influences
may be reduced. Severe protein malnutrition might alter the immunologic
system in such a way as to render the host unusually susceptible to
infection.

Role of Diet in Other Dental Conditions

Residual Ridge Resorption

The alveolar ridge (the bony ridge in which teeth are positioned) is vulner-
able to the resorption or loss of mineral subsequent to tooth loss. This
process results in a progressive change in the shape and a reduction in the
size of the ridge that greatly affects the stability and retention of dentures
(Atwood 1971, 1979; Tallgren 1972). While some patients adapt to ill-fitting
dentures and contend that they can eat anything, many patients adapt by
changing their diet (Yurkstas and Emerson 1964).

365
OO) Nutrition and Health

Resorption of the residual ridge results from an imbalance of bone resorp-
tion and bone formation, as does osteoporosis, leading to speculation about
a possible relationship between these conditions. The role of calcium in the
prevention and treatment of osteoporosis, either alone or in combination
with vitamin D, estrogen, or fluoride, has received much attention, and
calcium deficiency has been reported to be a factor in both osteoporosis
and residual ridge resorption (Barzel 1979; Menczel et al. 1982). A study of
44 toothless patients found a relationship between a history of reduced
dietary calcium intake and severe accumulated ridge reduction (Wical and
Swoope 1974). Denture patients who were given daily supplements of
calcium and vitamin D in a 1-year double-blind controlled study had 36
percent less bone loss than the group that received a placebo (Wical and
Brussee 1979). However, the wide overlap of bone loss in the treatment and
control groups suggested considerable individual variation and the need for
further research in this area. Approaches available to minimize residual
ridge resorption or restore lost bone are the following: use of implants,
bone rebuilding with calcium phosphate preparations, and prevention of
tooth loss.

Oral Cancer

In its earliest stages, oral cancer is painless and may present no overt
symptoms. Because dentists see many people regularly, and because den-
tists have access to the oral cavity, they are in a unique position to provide
early identification of suspicious lesions and signs of tobacco habits that put
people at risk for oral and other diseases.

Although alcohol and chewing tobacco are known to increase risk, the role
of nutrition in oral cancer in humans is less well established (see cancer
chapter). In part, this is because epidemiologic studies on the relationship
of nutrients to cancers elsewhere in the body have not been extended to
include oral lesions. However, animal models have been developed for the
experimental production of oral cancer that take advantage of the easy
accessibility of the tongue and the mucosa of the oral pouch of the hamster
for the application of suspected carcinogens and for later observation of
their effects (Marefat and Shklar 1977; Shklar 1972).

These models permit the evaluation of nutritional influences in cancer
formation. In several studies, animals whose diets were supplemented with
derivatives of vitamin A developed oral tumors that were fewer, smaller,
and later in appearance on exposure to the carcinogen 9,10 dimethyl-1,2
benzanthracene (DMBA) than those in animals that had not received the
supplement (Shklar, Marefat, et al. 1980; Shklar, Schwartz, et al. 1980;

366
Dental Diseases )

Burge-Bottenbley and Shklar 1983). A similar test of vitamin E (DL-L-
tocopherol) produced fewer and smaller tumors in the animals that re-
ceived it (Shklar 1982; Schwartz et al, 1985; Odukoya, Hawach, and Shklar
1984). More study of these issues is needed. Similarly, results from small
studies on the influence of nutrients on the course of head and neck cancer
suggest the need for further investigation (Dwyer et al. 1986).

Effects of Tooth Loss on Nutritional Status

The loss of teeth in adulthood should not be considered a normal or an
inevitable event, but a pathologic result of disease or trauma that affects the
normal physiologic process of the jaws. teeth, muscles. and nerves of the
mouth.

Chewing Ability

The loss of natural teeth as a result of dental caries, periodontal disease, or
trauma significantly reduces the ability to chew foods, as demonstrated by
a variety of chewing-efficiency tests (Manly and Vinton 1951; Yurkstas,
Fridley, and Manly 1951; Kapur, Soman, and Yurkstas 1974; Rissin et al.
1978; Kapur and Garrett 1984; Perez, Kapur, and Garrett 1985). Other
studies suggest that tooth loss leads to reduced force in chewing such foods
as carrots, meats, raw vegetables, and peanuts, markedly lower chewing
performance (Manly and Vinton 1951; Kapur and Garrett 1984); and avoid-
ance of certain hard-to-chew foods (Yurkstas and Emerson 1964). Patients
with reduced salivary flow may be unable to wear removable dental pros-
theses due to lack of lubrication (VA 1986).

Swallowing Ability

Dentures can cause a loss of sensation in the mouth that can lead to
problems in swallowing. In a study of 584 individuals who had to have a
foreign object removed from the esophagus, the absence of natural teeth
was considered a major factor (Ray and Vinson 1958). Dentists are urged to
warn all patients provided with partial or complete dentures about this
hazard and about the need for care in the preparation and chewing of food.
Of 16 patients seen during | year because of impaction of a foreign body in
the throat, only 3 had normal teeth (Wengraf 1969).

Choking on food was reported to be the sixth most common cause of
accidental death in the United States in 1979, with 700 of 2,900 fatalities
occurring among people 75 years or older (NSC 1979). Studies of choking
victims have found that many have poor dental status (Haugen 1963:

367
e Nutrition and Health

Anderson 1977), and poorly fitting dentures are frequently suspected to be
a factor in the blockage of airways with inadequately chewed and swal-
lowed food.

Effect on Food Selection

In addition to reduced chewing efficiency, various studies have demon-
strated that loss of natural teeth, even when replaced with dentures, can
cause the following impairments: diminished ability to discriminate food
particle size and texture, such as ability to differentiate between soggy and
crisp wafers (Kapur and Collister 1970); increased flow of stimulated
salivary gland secretion (Kapur, Collister, and Fischer 1967; Kapur and
Garrett 1984); and diminished ability to perceive subtle differences in the
sweet taste of certain solid foods (Giddon et al. 1964).

Effect on Nutritional Status

Some early studies reported that inadequate dental function as a result of
toothlessness or inadequate prosthetic devices contributed to the estab-
lishment and maintenance of nutritional deficiencies (Mann, Mann, and
Spies 1945; Greene, Dreizen, and Spies 1947; Ruikka, Sourander, and
Kasanen 1967; Makila 1968, 1969a, 1969b). However, dietary intake can be
adequate in an individual with reduced chewing provided that food is
selected carefully and prepared appropriately (Geissler and Bates 1984).

Implications for Public Health Policy
Dietary Guidance

General Public

Dietary factors of principal interest in dental diseases are sugars and
fluoride. Frequent consumption of sugars, especially sucrose, promotes
formation of dental plaque, the key predisposing cause of both caries and
periodontal disease. In the United States, the daily intake of sugars ranges
on average from 62 to 143 g, or 18 to 32 percent of total caloric intake.
Evidence exists that sugars as they are consumed in the average American
diet contribute to the development of de ital caries, suggesting that the
general public should reduce its sugar consumption.

The role of fluoride in prevention of tooth decay is also well established
from animal studies and from human epidemiology and clinical trials.
Although fluoride is present in foods, the most efficient source of this
nutrient for the general public is community drinking water that naturally

368
Dental Diseases @|

contains fluoride at an optimal level or to which fluoride is added to achieve
the optimal level. Most, but not all, water supplies can be fluoridated, and
current recommendations for optimum fluoride concentrations vary from
0.7 to 1.2 ppm depending on regional variation according to prevailing air
temperature. Conclusive evidence shows that such levels of fluoride are
safe.

Although other nutrients such as vitamin A, vitamin C, calcium, and
phosphate may also be associated with prevention of dental diseases,
evidence is insufficient at this time to recommend changes in dietary
patterns on the basis of their relationship to these conditions for the general
public.

Special Populations

Persons with diminished salivary flow are at special risk for caries and
periodontal disease. They also may be unable to wear removable dental
prostheses due to the lack of lubrication by saliva. Artificial saliva prepara-
tions containing fluoride and topical fluoride gels help to prevent tooth
decay in such persons and can be recommended as an adjunct to sugar-
restricted diets and appropriate dietary counseling. Children over the age
of 6 months are at risk for nursing bottle caries, and their parents and
caregivers should receive guidance in dietary and behavioral approaches to
prevent this condition. Evidence related to the benefits of fluoride con-
sumption by pregnant women on subsequent tooth development of the
fetus and caries in the offspring is insufficient to recommend fluoride
supplementation during pregnancy. Individuals with diabetes are especial-
ly prone to periodontal infections and should take special care to use
available dietary and therapeutic means to control disease.

Nutrition Programs and Services

Food Labels

The presence and relative amount of added sugars, especially sucrose,
contained in processed foods, as indicated by ingredient lists on food
labels, should continue to play an important role in identifying dietary
factors associated with dental disease.

Food Services

Evidence related to the role of dietary factors in dental disease suggests
that food service programs should provide optimally fluoridated drinking
water and promote noncariogenic foods, especially in programs for popula-
tions at high risk for dental diseases.

369
CO) Nutrition and Health

Special Populations

Persons with an active history of dental caries or with reduced salivary flow
and parents of young children should be provided with counseling and
assistance in developing diets low in cariogenic foods and in accessing
appropriate sources of fluoride. Persons with diabetes are especially prone
to periodontal infections and should take special care to use available
dietary and therapeutic means to control their disease (see chapter on
diabetes).

Research and Surveillance

Research and surveillance issues of priority related to the role of diet in
dental diseases should include investigations into:

@ The definition of critical periods of development of dental tissues that
may be sensitive to nutrient intake.

@ The role of nutritional factors in the maintenance and repair of the
periodontium and oral tissues.

© The relationship between nutritional imbalances during tooth develop-
ment and the formation of tooth lesions or defects that may increase
caries susceptibility in children.

@ The role of nutrition and nutritional status in the etiology and patho-
genesis of dental diseases in older persons and other high-risk popula-
tions.

© The relationship between nutrition and both the immune and the
nonspecific defense mechanisms of oral tissues and fluids.

@ The most effective means to educate the public on the role of water
fluoridation, diet, and dental care in preventing dental diseases.

@ The mechanisms of fluoride action in the prevention of dental disease
or osteoporosis.

e The effect of dietary factors such as vitamin A, vitamin E, and alcohol
on the initiation and progression of oral cancers.

@ Epidemiologic methods to determine the correlation between mal-
nutrition and dental caries and/or periodontal disease.

®@ The role of calcium in the etiology and/or prevention of residual ridge
resorption and periodontal disease.

© Estimation of the levels of fluoride from all sources in the diets of
children.

e Estimation of the extent of dental fluorosis in the population.

370
Dental Diseases ie

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