Dental Caries

Dental caries consists of localized, progressive decay of the teeth, initiated by demineralization of the outer surface of the tooth. This demineralization is caused by organic acids produced locally by bacteria that ferment deposits of dietary carbohydrates. Required for production of dental caries are the presence of a susceptible tooth, an oral environment conducive to the abundant growth and implantation of cariogenic microflora and a diet providing adequate substrate for the microorganisms. Dental caries is usually a chronic disease requiring considerable time for the destructive process to become clinically evident.

EPIDEMIOLOGY OF DENTAL CARIES

There can be little question of the high prevalence of dental caries. In the Preschool Nutrition Survey, Owen et al. (1974) reported an average of 2.6 decayed, extracted or filled deciduous teeth in white children and 3.8 such teeth in black children between 4 and 5 years of age. Findings of the Ten-State Nutrition Survey (Center for Disease Control, 1972) indicate that dental caries is even more prevalent as age increases. Corresponding averages for children between 5 and 6 years of age were 3.7 and 5.1. By age 10, more than 80 percent of children have caries of permanent teeth (Downer, 1970; Palmer, 1971). In a random sample of nearly 5000 Navy recruits, only one was found to be caries-free (Newbrun, 1969). The Committee on Nutrition (1972) concluded that dental caries is the most prevalent disease for all age groups beyond infancy. But the outlook on dental caries is bright.

Dental Caries In The United States

Dental caries in children in the United States has been on the decline since 1982. Recent studies have shown that 50% of children 5 - 17 years old had no decayed, missing, or filled permanent teeth. The mean DMF of 5-year olds was 0.07.

Although there is ample evidence that dental caries in school children has been on the decline, dental caries is still a significant problem. According to 1986-87 National Caries Prevalence Survey, 50% of school children have experienced decay in their permanent teeth; by age 17 only 16 percent were caries free. The caries decline in children is characterized by differences in tooth surfaces; the impact on free smooth surfaces and proximal surfaces is more pronounced than on pit and fissure surfaces.
Studies suggest that while the total number of new lesions is decreasing, the proportion of pit and fissure lesions is growing.

Dental caries is the most common and costly of oral health problems among all age groups, and the problem increases steadily with age. DMF (decayed, missing , filled) values increase most significantly in youth and early adult years and more slowly in the later years of life. DMF in adults can be attributed to missing teeth. Improved dental care and education have resulted in adults being able to retain their original teeth throughout their lives. Only 4% of employed adults in a survey were missing all their teeth, and half had lost at most one tooth. However, complete teeth loss remains a major problem among Americans 65 and older. Forty-two percent of the seniors surveyed were missing all their teeth, and only 2% still had all 28 permanent teeth. The survey showed little difference in coronal caries between younger and older adults; employed adults had an average of 23 decayed or filled coronal surfaces out of 128 possible surfaces.

Although females generally have higher DMF scores than males, higher scores do not indicate that females are more susceptible to caries than males. The higher reported scores may have something to do with the fact that females seek dental care more frequently than males. There also was no correlation between ethnicity and race and dental caries. Even though race is not a factor in predicting the incidence of dental caries, socioeconomic patterns are a critical determinant to caries experience. Cultural dietary practices may also affect the variance among DMF scores between various population groups. Generally, the white population within the United States has better access to oral health care than do African Americans and other minority groups and, consequently, enjoys better dental health.

DIET AND CARIES

Dietary factors, especially sugar, have an influence on the prevalence of dental caries. Various studies have proven the relationship between frequent consumption of fermentable carbohydrate and incidence of dental caries. Specific bacteria present in dental plaque ferment dietary carbohydrate to produce organic acids that demineralize tooth structure. Plaque bacteria use carbohydrates to produce the sticky gel-like matrix of the plaque. On the other hand, fats and protein have no cariogenic effects. Fats may, in fact, decrease caries activity by altering surface properties of enamel. Fats also reduce sugar solubilization, are toxic to oral bacteria –all of which may result in decreased caries incidence. Fats, if they replace carbohydrates in diet, may have the indirect benefit derived from reduced consumption of carbohydrates. Proteins may reduce caries posteruptively by a direct effect on plaque metabolism, by replacement of dietary carbohydrates, or by increasing salivary urea levels. Fluoride is an essential nutrient which affects decalcification and remineralization process. Below are listed, in the order of importance, cariogenicity factors of diet habits:

a. Frequency of intake of simple sugars The more frequent the exposure to sugar, the more cariogenic the diet; six candy bars eaten at six different times during the day are more harmful in terms of acid and bacterial plaque formation than if the six candy bars were consumed at one time.

b. Form of simple sugars (liquid or retentive) Liquid sweets clear the oral cavity faster than solid or retentive sweets and therefore are less cariogenic.

c. Time of ingestion of simple sugars Combination sweets with liquids and other noncariogenic foods during a meal is less cariogenic than a concentrated expo- sure to sweets between meals as a snack.

d. Total intake of simple sugars Annual consumption of sugar for each American is over 100 pounds; 60% of the sugar intake is from processed foods (e.g., cereal), which are often called "hidden sugars".

e. Starch-rich foods that are retained on the teeth for prolonged periods of time are ultimately degraded to organic acids and can contribute to dental caries production.

f. Combining cariogenic foods with noncariogenic foods Recent studies indi cate that certain cariogenic foods (e.g., canned pears in syrup) are less cariogenic when combined with a particular noncariogenic food (e.g., cheese).

So here are the basic rules:

a. Eat a diet that is low in retentive carbohydrates.

b. Do not eat cariogenic snacks.

c. Eat a diet that is adequate in all nutrients.

d. Include foods of firm or hard texture.

Carbohydrates

Various carbobydrates serve as substrate for the microflora of the mouth. Cariogenic streptococci, such as Streptococcus mutans, anaerobically metabolize sucrose to glucose and fructose (or metabolize other simple carbohydrates to their monosaccharide components), from which long chain polymers are formed—dextrans or glucans from glucose, and levans or fructans from fructose (Makinen, 1972). The dextrans
and levans are major contributors to formation of plaques which adhere to the teeth as sticky, gelatinous masses. Because they resemble the tooth in color and are somewhat translucent, plaques are difficult to see unless they are stained with erythrocin, fast green or a similar dye. Lactic acid and other organic acids produced by the bacteria beneath a plaque are protected from the buffering effect of saliva and are therefore able to bring about demineralization of the enamel. Thus, the primary substrate for the production of plaque and of organic acids is refined carbohydrates, especially sugars. Starches are less effective substrates because of their relatively slow fermentation in the mouth.

The majority of investigators appear to have concluded that sucrose is the most cariogenic dietary carbohydrate (Newbrun, 1969; Brown, 1975). The cariogenicity of sucrose has been demonstrated in vitro and in studies of experimental animals. Rather convincing circumstantial evidence implicates sucrose as a causative agent of dental caries in human subjects. First, epidemiologic studies (Sognnaes, 1948, 1949; Toverud, 1949; Toverud et al., 1961) have demonstrated a significant decrease in the dental caries rate among school children in occupied countries during the second half of World War II and the return of the caries rate to prewar levels after the war. These changes in caries rate coincided with the wide availability of sucrose before and after the war and its relative unavailability during the second half of the war. Second, in a study conducted under controlled conditions in an institution (Gustafsson et al., 1954), frequent and long-term consumption of sticky candy was associated with increase in the dental caries rate. In Australia, children who had lived from infancy to puberty in Hopewood House, where a lactovegetarian diet with almost complete absence of refined carbohydrate was consumed, demonstrated significantly fewer decayed, missing and filled teeth than did children living under similar socioeconomic conditions in state schools but not adhering to the same dietary regimen (Harris, 1963). In a study of preschool children, frequency of consumption of between-meal snacks appeared to be correlated with dental decay rate (Weiss and Trithart, 1960). Finally, patients with the rare metabolic disorder, hereditary fructose intolerance, who develop nausea and vomiting when they consume fructose (including the fructose in sucrose), learn to avoid fructose-containing foods; these subjects are caries free or have extremely low dental caries rate (Newbrun, 1969; Scherp, 1971).

Other Dietary Considerations

Various reports in the literature suggest that certain foods, such as cow milk, cheese and fibrous foods (e.g., celery, carrot) may exert a protective effect against the action of sucrose and other cariogenic substances in the diet (Caldwell, 1970; Wei, 1974a).
Apples and other fruits contain fructose, a less cariogenie sugar than sucrose. Although excessive exposure to fructose may produce dental caries, fresh fruits are likely to be much less cariogenic than most sucrose rich snack foods consumed by small children. Phytates and phosphates (both organic and inorganic) may also exert a protective effect against dental caries. However, thus far, most studies have been conducted in vitro or with the rat as the experimental animal. There is not yet convincing evidence that in the human any foods or food components other than fluoride are protective against cariogenic substances in the diet. This is an important area for further study.

Eating Between Meals

Because refined carbohydrates exert their effect in promoting dental caries by serving as a substrate for caries-producing streptococci, it is apparent that for older children as well as for infants not only the total quantity but the form of the carbobydrate and the frequency of consumption are important. A single piece of sticky candy may adhere to the teeth for almost an hour. In the case of sugars that are not in sticky form, a specified amount consumed at one time is likely to be less conducive to formation of dental caries than the same amount consumed in small portions throughout the day.

Considerable evidence exists that between-meal snacks favor development of dental caries (Zita et al., 1959; Weiss and Trithart, 1960). Presumably, it is primarily the simple sugars that are responsible. In the case of schoolage children, it may be feasible to reduce or eliminate eating between meals, although a number of studies indicate that large infrequent meals may predispose to obesity and have other adverse effects (Fomon, 1974).

It would seem to be a sound policy to recommend that school canteens and concession stands refrain from selling sweets. Roder (1973) concluded that the motivation for selling sweets in school canteens and concession stands related to the belief that such sale was necessary in order to make a profit. It is rationalized that sweets sold in schools comprised a relatively small percentage of total daily carbohydrate intake and therefore were unlikely to be an important factor in promoting dental caries. However, the study showed a positive correlation between the availability of sweets in school canteens and the dental decay rate in primary and secondary school children. Furthermore, the study showed that canteens omitting sweets can be highly profitable.

Perhaps it is self-evident that a diet suitable for preventing one disease may contribute to development of another. Health workers need to take a broad rather than a narrow view of preventive medicine. Those dedicated to research and teaching in prevention of iron deficiency, obesity, atherosclerosis and other diseases should work jointly with those active in research and teaching in preventive dentistry. Adjustment of the diet for the purpose of prevention of dental caries should not increase the risk of other disorders.

It is evident that forbidding children to eat between meals is likely to meet with quite limited success. A better approach may be development of a list of foods to be avoided between meals and another list of foods to be permitted. Foods to be avoided are the following: sugar, honey, corn syrup, candies, jellies, jams, sugared breakfast cereals, cookies, cakes, chewing gum and sweetened beverages, including flavored milks, carbonated drinks, sweetened fruit juices and fruit or fruit-flavored drinks.

A decision may be made jointly by some families and their physicians to restrict intake of cholesterol and saturated fatty acids as a preventive measure against subsequent development of atherosclerosis. Between-meal snacks for children in such families may include fresh fruits and vegetables, breads and crackers with margarine or peanut butter, low fat (or filled milk) cheeses, lean meats and "2 percent" or skim milk. Many other foods that are neither cariogenic nor atherogenic may be added to this list according to individual preferences.

Nursing Bottle Caries

"Nursing bottle caries" refers to destruction of the anterior teeth as the result of prolonged contact of the teeth with carbohydrate-containing solutions fed by nursing bottle. When an infant is given a sugar-containing fluid as a pacifier, especially at bedtime or naptime, sucking and swallowing is infrequent, saliva flow is minimal and the sugar remains in contact with the teeth for a long time. Most seriously affected are the anterior maxillary teeth, particulary the interproximal and labial surfaces [Fig. 1]. Sometimes the entire crowns are destroyed [Fig. 2]. Usually, the mandibular incisors, which are protected by the tongue and submaxillary salivary secretions, remain free of caries.

The lactose naturally present in cow milk is probably not a major threat with respect to nursing bottle caries. Of more concern is the content of sucrose and corn syrup solids in a number of infant formulas, especially soy isolate-based and other milk-free formulas. Probably most threatening is the feeding of sweetened fruit-flavored drinks and sweetened fruit juices. It seems undesirable to feed sweetened fluids (including formula) by bottle once the teeth have erupted. The practice of permitting infants to use a bottle as a pacifier, especially at bedtime, should be discouraged.

Cleaning the Teeth

Parents should be instructed to begin cleaning the teeth of toddlers as soon as it is practical to do so. Fine gauze wrapped around the parent's finger is satisfactory at first. Brushing by the parent may be possible with some children even before 18 months of age. Toothpaste should be considered optional and its use should depend on acceptance by the child.

SUGAR CONNECTION

It is a generally accepted wisdom that sugar consumption causes dental caries. However, at least one study has found no evidence of relationship between sugar and caries in industrialized nations. This study analyzed data from 90 countries to compare the effect of sugar on caries prevalence in industrialized nations to that in developing nations, and to reexamine the role of sugar in the development of caries.

Caries scores (measured as DMFT) among 12-year-old children in each of 147 countries were obtained from the World Health Organization (WHO) Oral Disease Data Bank. Per capita annual sugar consumption was estimated from government and industrial sources. DMFT scores and sugar consumption estimates were matched by country, with complete data available for 90 nations.

For all countries and for the 61 developing nations alone, the slope of the line expressing the relationship between sugar consumption and DMFT score was significantly different from zero (Fig. 3), indicating that increased sugar intake was associated with increased DMFT scores. When the 29 industrialized nations were analyzed alone, however, the slope of the best-fitting linear model was no significantly different from zero (Fig. 4). There was no evidence of a relationship between sugar intake and caries prevalence in these countries.

Previous studies had suggested that 18.25 kg per person per year would be a "safe" level of sugar consumption, since the research showed that the countries with per capita sugar intake below that level had DMFT scores below 3.0. In the present study, however, more than half of the countries with higher levels of sugar consumption also had DMFT scores below 3.0.

The results of this analysis suggest that factors other than sugar consumption affect DMFT scores, especially in more developed nations. Exposure to fluoride, genetic effects, and other aspects of the diet may affect caries prevalence. Reducing sugar consumption to zero probably would not eliminate caries.

Source: Woodward M, Walker ARP: Sugar consumption and dental caries: evidence from 90 countries. Br Dent J 176:297-302, 1994 

FLUORIDE, REMINERALIZATION AND ROOT CARIES

A recent study examined the composition of the mineral in the tooth root, its susceptibility to dissolution, and the role of fluoride in the inhibition or reversal of this process.

There are three prerequisites for caries development: cariogenic bacteria, supply of substrate for acid production and a susceptible host. Until the early 1980s, organisms such as actinomyces were considered to be the causative agents in root caries, but several studies have shown that mutans streptococci and lactobacilli are definitely high-risk factors, as they are for enamel caries. Streptococci mutans have been found strongly cariogenic in animals. Hard surfaces are a prerequisite for their presence: organisms disappear if teeth are extracted, and would reappear with dentures. High-sucrose diet is generally associated with an increased S. mutans population. This bacteria are usually found in early stages of plaque formation. Some other forms of streptococci are S. sanguis, S. metior, S. milleri, and S. salivarius, all of which have been found cariogenic in animals.

Lactobacilli have been found cariogenic in animals but the evidence for causative role in human caries has not been definitively established. These bacteria are present in small numbers in plaque and increase in number in the mouth when the sugar content in the diet is high. Another characteristic of this organism is that it is strongly acidogenic and aciduric.

Strains of actinomyces, A. viscosus and A. naeslundii, have been known to cause root surface caries in animals. A. naeslundii is present in tongue and saliva of young children, and A. viscosus is present in supragingival plaque.

The initial stages of root caries are the acid dissolution of the apatite mineral in a similar way to the early stages of enamel caries. The acids are, of course, generated by the bacterial plaque overlying the exposed root surface subsequent to fermentable carbohydrates being ingested.

The mineral of enamel, dentin and cementum is best described as a carbonated-apatite. Pure hydroxyapatite does not exist as such in the tooth.

Carbonated apatite is much more reactive than hydroxyapatite. The carbonated apatite of dental mineral is readily dissolved by acids produced by bacterial metabolism. Cariogenic plaque, when exposed to sugar, shows a decrease in pH that is low enough to decalcify enamel within minutes; pH returns to resting levels after approximately 40 minutes; even though sugar is washed away by saliva, pH can remain at a low level for 20 minutes.

When fermentable carbohydrates are taken into the mouth, bacteria metabolize them producing weak organic acids such as acetic acid, lactic acid and propionic acid. These acids will diffuse readily through the plaque into the underlying enamel or underlying cementum/dentin finding susceptible sites on the mineral as the acids diffuse, causing mineral loss and progression of an early lesion. The demineralization process in root caries is diffusion controlled in the same way as demineralization in enamel caries is diffusion controlled. The rate of mineral loss can be up to twice as fast from the root as it is from enamel. This is much more serious in the tooth root, as there is only half as much mineral there to begin with. Consequently, the physical integrity of the root is lost much more rapidly than the physical integrity of the enamel due to the loss of the same amount of mineral.

It is well established that fluoride has an anticaries effect on bacteria. As the bacteria produce acid in the plaque as a result of carbohydrate metabolism, the drop in pH complexes the fluoride ion forming the HF molecule which can be readily transported through the cell membrane and wall of the bacteria. As the HF reaches the inside of the bacteria, the molecule dissociates producing fluoride ion inside the cell which seriously compromises the function. This has been demonstrated for enamel caries, and since the bacteria for root caries are essentially comparable, that aspect of caries inhibition will undoubtedly apply also to root caries.

Fluoride markedly inhibits demineralization of tooth enamel and synthetic apatite. Since the initial stages of root caries are essentially the same as enamel caries, it is logical to assume, therefore, that fluoride will have the same action on the inhibition of mineral loss if it is present at the surface of the crystal within the root when the acid diffuses to that surface. Consequently, it is important to have fluoride present in the plaque during the acid challenge as one of the mechanisms of inhibiting root caries.

The conclusions of this study are that fluoride-containing dentifrices would be effective in the enhancement of remineralization of root caries and that, as for enamel caries, monofluorophosphate requires hydrolysis prior to being effective. The second conclusion is that fluoride definitely works for remineralization enhancement in root caries. It is possible that higher concentrations may be more effective in root caries than they are in enamel caries.

Source: Featherstone JDB: Fluoride, remineralization and root caries. Am J Dent 7:271-274, 1994.

MEASURES FOR PREVENTING AND CONTROLLING DENTAL CARIES

Water fluoridation is the best means of preventing and controlling dental caries. In early studies children reared in a fluoridated-water community showed a 50% to 70% reduction in caries in their permanent dentition when compared to children in a non-fluoridated community. Currently, reduction in caries attributed to water fluoridation is 17% to 40% because of multiple sources of fluoride. Adjustment of the natural fluoride concentration to about 1 part fluoride to 1 million parts water is the most cost effective and efficient method of reaping the benefits of fluoride. Optimal fluoride levels range from 0.7 ppm to 1.2 ppm depending on the climate. In a warmer climate community, due to increased water consumption, the concentration is usually at the lower level whereas in the colder community the fluoride level is at the higher level.

When fluoridated water (0.7 to 1.2 mg of fluoride per liter of water) is consumed throughout life, the dental caries attack rate is reduced by 50 to 60 percent in permanent teeth (Backer Dirks, 1974) and slightly less in primary teeth (Scherp, 1971). The most likely explanation for the lesser reduction in dental caries attack rate in primary than in secondary teeth is that many infants and small children consume relatively little drinking water–suggesting the desirability of administering fluoride supplements. An excessive ingestion of fluoride causes mottled discoloration of the teeth. The index of fluorosis remains near zero with increasing fluoride concentrations in drinking water until concentrations reach values greater than 1.0 ppm. With further increases in fluoride concentration of the drinking water, the index of fluorosis rises steeply.

Increasingly it has been recognized that the benefits of water fluoridation are both systemic and topical and that the topical effect may be the more important. Small, frequent doses of topically applied fluoride appear more efficacious than yearly applications of high concentrations. In Sweden the weekly use of of sodium fluoride mouth rinses by school children was associated with reduction in caries rates comparable to those of communities with water fluoridation. Fluoride rinses are not recommended for preschool children, however, because many young children cannot control their swallowing reflexes and may swallow most of the rinse. 

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REFERENCES

1. Brown, A. T.: The role of dietary carbohydrates in plaque formation and oral disease. Nutr. Rev. 33:353, 1975.
2. Caldwell, R. C.: Physical properties of foods and their caries-producing potential. J Dent. Res. 49:1293, 1970.
3. Downer, Mc. D.: Dental caries and peiodontal disease in girls of different ethnic groups. A comparison in a London secondary school. Br. Dent. J. 128:379, 1970.
4. Ellen RP, Banting DW, Fillery ED. S. mutans and Lactobacillus detection in the assessment of dental root surface caries risk. J Dent Res 1985; 64;1245-1249.
5. Featherstone JDB. An update understanding of the mechanism of dental decay and its prevention. Nutrition Quart 1990; 14;5-11.
6. Fomon, S. J.: Infant Nutrition. 2nd ed. Philadelphia, W. B. Saunders Co., 1974.
7. Gustafson, B. E., Quensel C. E., Lanke, L. S., Lundqvist, C., Grahnén, H., Bonow, B. E., and Krasse, B.: The Vipeholm dental caries study. The effect of different levels of carbohydrate intake on caries activity in 436 individuals observed for five years. Acta Odont. Scand. 11:232, 1954.
8. Harris, R.: Biology of children of Hopewood House, Bowral, Australia. 4. Observations of dental-caries experience extending over five years. (1957-61). J. Dent. Res. 42:1387, 1963.
9. Mâkinen, K. K.: The role of sucrose and other sugars in the development of dental caries: A review. Int. Dent. J. 22:363, 1972.
10. Nelson DGA, Featherstone JDB, Duncan JF, et al. The effect of carbonate and fluoride on the dissolution behavior of synthetic apatites. Caries Res. 1983; 17;200-211
11. Newbrun, E. (ed): Fluorides and Dental Caries, Springfield, III, Charles C. Thomas, 1972.
12. Owen, G. M. Kram, K. M., Garry, P. J., Lowe, J. E., and Lubin, A. H.: A study of nutritional status of preschool children in the United States, 1968-1970. Pediatrics 53:597, 1974.
13. Nyvad B, Fejerkov O. Root surface caries: Histopathological and microbiological features and clinical implications. Int Dent J 1982; 32:312-326.
14. Nyvad B. Microbial colonization of human tooth surfaces. APMIS suppl 32, 1993: 101. Copenhagen: Munkksgaard.
15. Roder, D. M.: The association between dental caries and the availability of sweets in South Australian school canteens. Aust. Dent. J. 18:174, 1973.
16. Scherp, H. W.: Dental caries: Prospects for prevention. Science 173:1199, 1971.
17. Sognnaes, R. F.: Analysis of wartime reduction of dental caries in European children. Am. J. Dis. Child. 75:792, 1948.
18. Toverud, G.: Decrease in caries frequency in Norwegian children during World War II. J. Am. Dent. Ass. 39:127, 1949.
19. Toverud, G., Rubal, L., and Wiehl, D. G.: The influence of war and postwar conditions on the teeth of Norwegian school children. IV. Caries in specific surfaces of the permanent teeth. Milbank Mem. Fund Quart. 39:489, 1961.
20. Wefel JS. Root caries histopathology and chemistry. AM J Dent 1994; 7: 261-265.
21. Wei, S. H. Y.: The potential benefits to be derived from topical fluorides in fluoridated communities. In Forrester, D. J., and Schulz, E. M., Jr. (eds.): International Workshop on Fluorides and Dental Caries Reductions. Baltimore, Maryland, University of Maryland, 1974b, p. 178.
22. Weiss, R. L., and Trithart, A. H.: Between-meal eating habits and dental caries experience in preschool children. Am. J. Publ. Health 50:1097, 1960.