Physiological Effects of Food Carbohydrates - ACS Publications

9 Role of Carbohydrates in Dental Caries WILLIAM H. BOWEN

Downloaded by UNIV LAVAL on July 11, 2016 | http://pubs.acs.org Publication Date: June 1, 1975 | doi: 10.1021/bk-1975-0015.ch009

Caries Prevention and Research Branch, National Caries Program, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. 20014

Dental caries results from the action of specific bacteria which colonize the tooth surface and metabolize particular compo nents of the diet. The action results in the rapid and sometimes prolonged production of acid on the tooth surface resulting in the dissolution of the enamel. Since the time of Aristotle it has been considered that car bohydrates played an essential role in the pathogenesis of dental caries. There is now an abundance of evidence accumulated from epidemiological surveys (1) and animal experimentation (2) which clearly indicates that dental caries does not develop in the absence of dietary carbohydrate. In an elegant clinical study Gustafsson, et.al. (3) showed that the incidence of caries is related to the frequency of intake of carbohydrate and not to the total amount consumed. For example, patients who in 1 year con sumed 94 kg. of sugar with meals had fewer new carious lesions than patients who consumed 85 kg., 15 of which was taken between meals.

The restriction in carbohydrate intake which occurred during World War II was followed by a dramatic f a l l in the prevalence in dental caries in many European countries. (4)(5)(6) Carbohydrates and sugar in particular apparently can also affect the maturation of enamel, a process which leads to i n creased mineral uptake in enamel post-eruptively. It was observed (7) that the teeth of rats exposed to high sugar diets showed delayed maturation and were therefore presumably more susceptible to decay. Rats bred on a diet (8) conducive to the formation of severe protein-calorie imbalance have been shown to have enhanced susceptibility to caries. The effect was ascribed to altered tooth size (9) and to alterations in salivary composition. The physical form in which sugar is ingested will also influence its cariogenicity. Powdered sugar is more cariogenic than similar sugars given in an aqueous solution. (10) The size of particles and the adhesiveness of the diet also influence the cariogenicity of the diet. (11) In general the longer a poten150 Jeanes and Hodge; Physiological Effects of Food Carbohydrates ACS Symposium Series; American Chemical Society: Washington, DC, 1975.


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t i a l l y cariogenic substance is retained in the mouth the greater is the likelihood that caries will develop. The formation of dental plaque is the earliest evidence that microorganisms and components of the diet are interacting. Dental plaque is the soft white tenacious material which occurs on tooth surfaces and is composed of microorganisms enmeshed in a matrix of carbohydrate and protein. Specific microorganisms are associated with the early formation of dental plaque and sucrose plays an important role in their establishment on the tooth surface. (12) Streptococcus mutans is a prime microbial agent in the pathogenesis of dental caries. (13)(14) It has several interesting properties; i t is found predominantly on the tooth surface and i t forms polyglucan and polyfructan from sucrose. (15)(16) Strep, mutans can become reversibly bound to the tooth surface in the absence of sucrose but following ingestion of this sugar extracellular polysaccharide is formed. (17) This substance enhances the ability of the microorganism to acThere to the tooth surface and also leads to the aggregation of other microorganisms. (18) The available evidence indicates that the predominant polyglucan in plaque is composed of material possessing mainly 1-3 linkages; substantial material possessing 1-6 linkages is also present, (19) Up to 40% of the polyglucan formed in plaque is readily metaFolizable by plaque microorganisms. (20) Although polyfructan is also found i t is metabolized very rapidly(21) by substantial numbers of the microorganisms in plaque. (22T~ Apart from the contribution that extracellular polysaccharides make to the adherence of microorganisms their precise role in the pathogenesis of dental caries is unclear. Recent evidence has shown that phosphorus is tightly bound to the polysaccharide and that the carbohydrate is charged. (23) This indicates that the polysaccharide could limit the diffusion of charged substances into and out of plaque. Acid formed within plaque could not, therefore, be readily neutralized by the diffusion of such substances as bicarbonate. It is also likely that the extracellular polysaccharide protects the microorganisms from inimical influences. Whatever the precise role they have in the pathogeneses of caries there is l i t t l e doubt that the integrity of the tooth would be enhanced by either preventing their formation or their rapid removal. There is also clear evidence which indicates that microorganisms in plaque can synthesize an intracellular polysaccharide (IPS) of the amylo pectin type from a wide variety of carbohydrates. (24)(25) This material can be catabolized by plaque microorganTsms during periods when extraneous sources of carbohydrate are lacking. This catabolism is probably responsible for the comparatively low pH values observed in plaque around carious lesions even in patients who have been fasting. (26) There is some evidence to indicate that the number of intracellular polysaccharide forming organisms in plaque is positively correlated

Jeanes and Hodge; Physiological Effects of Food Carbohydrates ACS Symposium Series; American Chemical Society: Washington, DC, 1975.


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with the number of carious lesions.(27) The results of research carried out by Kanap and Hamilton(28) indicate that both the synthesis and catabolism of IPS is influenced by the presence of fluoride. They have shown that the low concentrations of fluoride inhibit enolase and glucose-6-p formation without penetrating the cell significantly indicating that fluoride may affect the transport of sugar into the bacterial c e l l . This is probably one of several mechanisms through which fluoride exercises its cariostatic effect. Dental plaque also forms in the absence of dietary carbohydrate, (29)(30) e.g., in patients or animals who receive their completedetTby gastric intubation, but i t lacks several properties found in plaque formed under conventional circumstances. Animals fed in this manner do not develop caries.(31)In addition the plaque so formed lacks the ability to lower the pH value of topically applied sugar solutions in contrast to that formed normally, which may lower the pH value of a sugar solution to 4.5 or less in a matter of minutes. (32) It is generally considered that rapid démineraiization of the tooth surface occurs below pH 5.5. The types and proportions of acids formed in dental plaque are attracting an increasing amount of attention because i t is conceivable that the difference in the cariogenicity of plaques may reside in some measure in the different types or proportions of acids present. Gilmour and Poole (33) found that a constant relationship between the concentration of lactic acid in plaque and pH decrease was lacking. In some plaques i t was found that the concentration of lactic, propionic and acetic acids accounted for less than 50% of the titratable acidity. In a study carried out by Geddes (34) i t was observed that 'fasting plaque contained 3 X 10- m moles of acid/mg wet weight and that five minutes after exposure to sugar the concentration had increased to 5 Χ 10" m moles. The major change was to a five-fold increase in D (-) lactate and an eight-fold increase in D (+) lactate. There is a positive correlation between the frequency of sugar intake and the incidence of caries. (35) Each ingestion of sugar is followed by a rapid f a l l in pH value on the tooth sur face. The pH returns to neutrality over a 20-30 minute period. The duration for which the plaque has been allowed to accumulate will influence both the magnitude of the f a l l in pH and the time required for its recovery. (36) In general the older the plaque the greater its pathogenic potential. An extreme example of the effects of prolonged exposure to sucrose can be seen in infants who have comforters dipped in a sucrose syrup or similar solu tion. (37) These children develop rampant caries on the palatal surfaces of the upper molars and incisors. It is occasionally argued that much caries could be elimina ted i f other sugars were substituted for sucrose in the diet. Some support for this concept can be found in patients who suffer from fructose intolerance. These patients must avoid sucrose and 1

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fructose. Fructose intolerant patients have substantially less caries than normal persons but they are not caries-free. (38) Clearly such patients must alter their dietary intake consTcTerably, other than merely avoiding sucrose. Sucrose has probably been blamed as the main dietary culprit in caries causation simply because i t is the sugar which is most frequently ingested. There is no evidence that its substitution by glucose or fructose would lead to a significant reduction in dental decay in humans. Results of many experiments carried in animals clearly indicate that glucose and fructose can induce significant levels of decay. (39)(40)(41) Primates which received their complete diet by gastric Intubation with the exception of glucose or fructose (i.e. plaque was formed in the presence of these sugars) formed plaque which contained significant levels of extracellular polysaccharide and in addition this plaque could lower the pH of sugar solutions rapidly. (42) The effects of polyols such as sorbitol, mannitol and xylitol on plaque formation and the development of caries have been i n vestigated in animals and to a lesser extent in man. (43) It was observed in primates that the ingestion of sorbitol was followed i n i t i a l l y by the formation of plaque which had a syrupy consistency. It was also noted that the numbers of Strep, mutans in plaque declined markedly when sorbitol was substituted for sucrose even though Strep, mutans ferments sorbitol. Prolonged ingestion in man (44) or primates did not lead to the development of a plaque flora with an enhanced ability to metabolize sorbitol. All the available evidence indicates that sorbitol is substantially less cariogenic in animals than sugars. Xylitol was shown by Muhlemann, et. a l . (45) to be even less cariogenic than sorbitol. A possible explanation for the lower cariogenicity of sorbitol may be found in the manner in which i t is metabolized by microorganisms. The breakdown of sorbitol produces mainly formic acid and ethanol; in contrast, the metabolism of glucose results in the formation of primarily lactic acid. (46) It is possible that the extensive use ofpolyols would not be acceptable by the general public as in some persons even moderate doses have a cathartic effect. There is l i t t l e doubt that the incidence of caries would decline dramatically i f the general population would reduce the frequency of intake of fermentable carbohydrates. However the ingestion of candy is rarely associated in peoples minds with the formation of a carious lesion at some future time. Any disease which affects 95% of the population is unlikely to be controlled to a significant extent by individual effort. Effective control calls for public health measures and of these water fluoridation is the most effective.


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Physiological Effects of Food Carbohydrates - ACS Publications

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