Sugar and dental decay.

World Review of Nutritional and Dietetics, vol. 22, pp. 304-326 (Karger, Basel 1975)

Sugar and Dental Decay S. B. Firm and R. B. GLASS University of Alabama, Birmingham, Ala., and Harvard University and Forsyth Dental Center, Boston, Mass.

Contents I. Human Clinical Studies II. Institutional Studies III. Preschool and School Population Studies IV. War Time Population Comparisons V. Primitive Diets vs. Modern Diets VI. Mitigating Factors in Dental Caries References

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With the ever-increasing cost of foods, particularly proteins and fats, greater numbers of persons will be turning to more economical sources of food for their dally food requirements, especially their energy (calorie) requirements. As carbohydrates are the least expensive foods per calorie and require less acreage for production, it may become an economic necessity to consume greater amounts of these foods and less of others. Dental decay (dental caries) is one of the most prevalent diseases affecting mankind today, and there are indications that lead one to believe that in non-flouridated areas it may be on the increase [4]. One explanation given for its extreme prevalence is the introduction of refined sugars, principally ordinary table sugar (sucrose), into the modern diet [99]. It is, therefore, of considerable interest to review the association between sugar and dental caries and to place our present state of knowledge into proper perspective. Dental caries is a very complex disease. The scope of its many ramifications can best be appreciated if one reviews the literature of the present

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century. One is awed by the amount of research energy that has been expended in arriving at our present state of knowledge [11, 97]. Tο espouse glib generalized phrases for the total prevention of dental caries suggests a lack of understanding. It is by continued research and new knowledge that a complete and practical solution may be attainable. If the causes of dental decay were as easy to eliminate as some would have us believe, the problem would have been solved long ago.

I. Human Clinical Studies


Unquestionably, eating large amounts of sugar can increase the dental caries incidence. But there is a great deal of epidemiological evidence to indicate that it does not necessarily do so, depending upon the physical form in which it is eaten, the other ingredients of the food with which it is compounded, the amount eaten, the frequency with which it is eaten, and undoubtedly other circumstances not as yet comprehended [12, 13]. A review of many of the human clinical studies that have been conducted to date will offer a better understanding of what has actually been studied in the past and in what direction newer evidence points, so that valid judgments can be made rather than assumed [19]. Although ancient man ate no refined sugar or other refined carbohydrates, he was not completely free from dental decay [69, 84, 93]. There is evidence to suggest, however, that it was much less than in present man. Part of this reduction is attributable, not only to the lack of refined sugar in the diet, but to the early and complete wearing away of the pits and fissures on the grinding surfaces of the teeth by the coarse foods that he ate. In present man, these are generally the first and most frequent surfaces to decay. Ancient man also had dental arches that were well-formed, with properly spaced teeth. Contrast this to modern man who may have crowded and unharmonious arches and improper spacing and crowding of the teeth, which can result in greater areas of food stagnation and caries development. Human clinical studies can be divided conveniently into four general categories, as follow: 1) Institutional studies where the diets were specifically modified. 2) Preschool and school population studies where the subjects were compared relative to sugar consumption and caries prevalence.

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3) Population comparisons during periods when the normal diet was disturbed during times of war. 4) Comparison of primitive peoples prior to and after adoption of the highly refined civilized diet.

II. Institutional Studies


The Vipeholm Dental Caries Study [35] is by far the most significant institutional sugar-caries project ever undertaken. Because of its relevance to better understanding of the relationship between the quantity of sugar, frequency of eating, and physical consistency of the compounded sugar product, this study will be considered in greater detail than others. In the Vipeholm Dental Caries Study, 436 adult inmates of a mental institution in Sweden were placed on specific diets and observed over a 5-year period. These subjects were divided into 7 groups; the first 3 ate carbohydrates only at meal times, while the latter 4 groups augmented their diets by between meal eating of sweets, as follows: 1. Control group, was fed a basic diet with either 150 g or 40 g of margarine as calorie compensation for the carbohydrate added to the other diets. Even with this sugar-free diet, there occurred a yearly increase of 0.34 new carious tooth surfaces per subject. 2. Sucrose group, received 300 g of sucrose in solution for 2 test years, but reduced to 75 g the last 2 years. When this group was compared to the control group, there was no significant difference observed in the number of cavities. This suggests that there may be a threshold level of sugar ingestion at mealtimes below which caries activity is limited. The sugar in liquid form produced no new lesions in 37 0/0 of the subjects during the 5-year period. 3. Bread Group, was given 345 g of sweet bread containing 50 g of sugar. This material was rather sticky when chewed. During the first 2 years of the test, the bread was served at afternoon coffee; in the last 2 years it was served at all 4 meals. With 1 serving of the bread, no increase in decay occurred. With 4 servings at mealtimes, males showed a statistically significant increase in caries, while females showed no increase. The difference between the sexes might be attributed to the lack of toothbrushing in the males which was performed less frequently than in the females. It is interesting to note the low incidence of toothbrushing in this study population. Less than 20 °/ο brushed their teeth or had them brushed.

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In the latter 4 groups, sugars in various vehicles were given between meals. 4. Chocolate group, was given sucrose in solution in the first 2 years. During the latter 2 years, they were given 65 g of milk chocolate dally between meals. During the last 2 years, there was no significant rise in dental caries. In a collateral study on 77 institute employees receiving 54 g of the chocolate daily in unsupervised between-meal eating, no increase in caries was observed. 5. Caramel group, was given 22 caramels (70 g of sugar) between meals in 4 portions of 4 or 5 caramels each. Caries increased significantly. 6. 8 toffee group, subjects received 8 sticky toffees (60 g of sugar) between meals daily for 3 years. The toffee increased caries more than did the caramels; although the sugar content was less, caries was greater. This points to the greater stickiness and retention properties of the toffee. 7. 24 toffee group, received 24 sticky toffees between meals daily, containing 120 g of sugar. The toffee eating continued for 18 months, at which time the subjects were taken off this diet. Dental caries increased strikingly. Α number of conclusions were drawn by the authors from this study as follows: 1) The consumption of sugar can increase caries activity. 2) The risk of sugar increasing caries activity is great if the sugar is consumed in a form with a strong tendency to be retained on the surfaces of the teeth. 3) The risk of sugar increasing caries activity is greatest if the sugar is consumed between meals and in a sticky form in which the tendency to be retained on the surfaces of the teeth is pronounced, with a transiently high concentration of sugar on these surfaces. 4) Ø increase in caries activity under uniform experimental conditions varies widely from one person to another. 5) Increase in caries activity due to the intake of sugar-rich foodstuff consumed in a manner favoring caries disappears on withdrawal of such foodstuff from the diet. 6) Carious lesions may continue to appear despite the avoidance of refined sugar, and maximum restriction of natural sugars and of total dietary carbohydrates. Some collateral information suggested by this study is of interest, as follows:

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1) Oral hygiene measures appear to reduce the frequency of new carious lesions if carried out faithfully. 2) The carious lesions on a sucrose-containing diet may require a long time to develop to a clinically detectable level [77]. 3) There may be a threshold for sugar consumption below which the production of clinically significant caries does not occur. This may vary greatly among individuals. Using the same population during the Vipeholm study, LUNDQUIST [61] determined the concentration of reducing sugar present in the saliva every 15 minutes for subjects in each of the 7 groups. There was a marked difference in clearance time on the different diets. The concentration increased at mealtimes, and those given sugar supplements in between meals maintained a high level of concentration over longer periods of time, depending upon the frequency of eating. The clearance time for the various groups correlated closely with caries activity. Caries appears to be more related to the physical form of the sugar compound and to the frequency of eating rather than the total sugar consumption. MALM [63], in recent criticism of the Vipeholm study, pointed out that the `sticky sweets' which were used in the Vipeholm study did not consist only of sucrose but of a mixture of different sugars: sucrose, maltose, monosaccharides, and dextrins, and, in the case of caramels, also lactose. Sucrose actually made up less than half of the total sugar. The composition of the carbohydrate fraction of the toffee was 21.9 ο/ο dextrins, 44.4 ο/ο sucrose, 12.2 ο/ο maltose, and 9.1 ο/ο monosaccharides, and that of the caramel was 19.9 ο/ο dextrins, 19.0 ο/, sucrose, 9.3 ο/ο lactose, 10.9 ο/ο maltose, and 8.1 ο/ο monosaccharides. The `sweet' were manufactured from sugar and corn syrup, which contains dextrins, maltose and glucose. The caramels also contained milk solids, hence lactose. The fat content of toffee was low, only 2.2 0/ο, and the moisture content was 10.2 ο/ο, which is very high for this type of product which usually contains about 3 ο/ο moisture. The toffee was very sticky and was purposely made that way. Not only were the toffees very sticky but they were also purposely made so big that they could not be swallowed whole, but had to be chewed. Thus, one might say that the Vipeholm study was designed to keep a mixture of sugars in contact with the teeth for considerably longer periods of time than is the case in the ordinary eating of candies. Another institutional study concerned with diet and dental caries was that conducted on the Hopewell House group in Australia [33, 37], con-


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sisting of 81 children ranging in age from 4 to 9 years. These children subsisted on a diet of whole wheat grains, fresh and dried fruits, cooked and raw vegetables, and practically no meat, butter, cheese, eggs, milk, and fruit juices. Honey and molasses were used as sweetening agents. These foods were taken uncooked or with a minimum of preparation in order to present the food in its natural state. After 5 years on this regimen, 63 Ο/ο were without caries; 18 Ο /0 had cavities totalling 47 decayed and filled teeth. Great stress was laid on the absence of refined sugars from the diet, but there was also a lack of refined starches. This was such an unusual diet that it is difficult to imagine anyone subsisting on it voluntarily for any length of time. It is of interest to note that honey was used as a sweetening agent, the cariogenicity of which has been found in animal studies to be equal to sucrose [74]. The fact that a sugar is in a natural state does not necessarily mean that it is less cariogenic.

III. Preschool and School Population Studies


A number of studies have been made comparing the frequency and amount of sugar eaten to dental caries development [19]. ZiTA et al. [103] employed 200 children aged 5 to 13 years registered in the dental school files for their population. Upon analyzing a week's food intake, they found no correlation between the total sugar consumption and caries prevalence. However, they did find a significant positive correlation between the amount of between-meal sugar eaten and caries prevalence. Among these individuals, one-third of the total sugar consumed was from between-meal snacks, offering further confirming evidence that it is not the amount of sugar eaten but rather the frequency. A dietary study by HARGREAVES [36] on children on the Island of Lewis in Scotland in 1937 and again 30 years later revealed that a striking increase in dental caries prevalence had occurred in both the urban and rural areas. Although there was this marked increase in dental caries, the total sugar consumption had not risen. There was an increase in refined cooked cereals, however, and a decrease in consumption of fish in favour of meats. Based on a 1-day diet sample, WEISS and TRITHART [101] found that among 783 children 4 and 5 years old, there was a positive correlation between the number of between meal snacks and the severity of dental caries. Of the food items snacked, chewing gum was the most frequently

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used (35 o/o), although at least three studies have reported no increase in dental caries from sugar gum chewing [87, 94, 98]. MANSBRIDGE [65], when comparing 12- to 14-year-old children, found that only those who ate more than 8 ounces of sweets and chocolate a week had more dental caries than those who did not. In 1964, McHuGH et al. [68], using 2,652 children 13 years of age as the study population, found that they consumed between 6 and 33 ounces of sweets and chocolate per week, the average being 17 ounces. There was a significant positive correlation between the amount of sweets eaten and the number of decayed teeth. The frequency of eating sweets was not given. The words sweets and chocolates would suggest in-between-meal eating. FANNING et al. [23], in 1969, examined 1,266 secondary school children. In those schools where canteens were available where sweets could be purchased, these children had a higher caries experience than those children in schools lacking canteens. School canteens would also suggest more frequent eating of sweets. More recently, BAGRAMIAN and RUSSELL [3] gathered information from 1,486 black and white high school students from Detroit and Columbia, S. C. They report that no significant relationship could be found between the consumption of between-meal snacks containing sucrose and either low, medium, or high caries experience. Several studies have considered the effect of sugar-coated cereals on the production of dental decay. FuNi and JAMisoi [27] could find no increase in dental caries when a sugar-coated cereal was compared with natural fruit juices and dried fruits in an unrestricted but similar diet. RowE et al. [82], in a permissive cereal study employing 375 adolescents, supplied the subjects with 7 different cereals, 4 of which were presweetened. They found no statistically significant difference in caries scores compared to those who ate other breakfast regimes. No mention, however, was made of the other foods eaten during the breakfast meal. GLASS and FLEISCH [32] arrived at a similar conclusion from a population of 979 children aged 7-11 years of age who were given their choice of 8 regular and 6 presweetened cereals. They were encouraged to eat as much as they wanted, but at least 1 cereal daily. The consumption actually varied from 10 to 500 g subject week, totaling over 17,000 kg during the 2-year period. This represented a substantial exposure to both sucrose and cereal. During this period, no significant differences nor any consistent pattern of differences in caries incidence


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could be detected between those eating small or large amounts of cereal, regular or presweetened. The cereal studies presented here strongly suggest that eating sucrose during mealtime as part of a diet that may have other sugars available at mealtimes does not increase dental caries. There may be several explanations for this. Sugar foods at mealtime may be swallowed before all the sweetness is extracted and increased salivary flow at mealtime could more effectively wash away the dissolved sweets. Α series of clearance studies involving sampling of foods before they are swallowed should be done to determine the amount of undissolved sugar that is swallowed and not in contact with the teeth. Sweets consumed between meals are generally eaten slowly, devoid of other foods, and allowed to dissolve before being swallowed. This permits longer contact with the teeth. Α common practice deserving consideration at this time is the peculiar type of dental decay that develops in infants who are given the nursing bottle upon going to sleep to serve as a comforter to induce and maintain sleep. These children develop a rapid breakdown of their upper front teeth. There is some difference of opinion as to the cause of this destruction. Many clinicians feel that it can be produced by the milk alone, which is an excellent medium for bacterial growth. Others suggest that sugars must be added. Certainly, sugar teats sucked constantly by infants during sleep when the flow of saliva is negligible will produce marked decay.

IV. War Time Population Comparisons


During the two world wars, most of the involved countries suffered from food shortages. Refined sugar was in short supply, and countries that experienced a shortage of this commodity manifested a reduction in dental caries, even though sugar consumption continued at 30-40 Ο/ο of the prewar level. Under these conditions, TOVERuD et al. [97] reported that, in Norway, between-meal eating of confections practically disappeared. It must be recognized that with the loss of sugar there was also a concomitant switch to less refined flour and an increase in potatoes [66]. The relationship between reduced caries and wartime reduction in refined carbohydrates has been documented by studies done in England [42], Japan [90, 91], and Norway [88, 95, 96], among a host of other countries.

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V. Primitive Diets vs. Modern Diets When primitive peoples substitute their well-established natural diets by the softened and refined diets of civilized man, there develops a breakdown of their dentition and an increase in dental caries. When this appears, one wonders whether it is an increase in the environmental challenge or a delay in maturation of these teeth, or other host factors. Although the involvement of sugar cannot be minimized, one must rule out the lack of other protective factors which also might have influenced the resistance to decay. Such factors as fluorides and other trace elements supplied in a native diet [1], where little attention is paid to washing their food, and where even the dust accumulated on the food could supply some of these trace elements. Inadequate attention has been paid to this aspect of the primitive diet. When the Eskimo came in contact with civilization, not only did his intake of refined sugar increase, but there was a concomitant decrease in consumption of fats [80]. The protective effect of large amounts of fat in the diet has been documented, but has not been explored fully and deserves more investigation. Many primitive civilizations that have come in contact with refined foods have been studied, among them being the Bantu tribes of South Africa [76], the Eskimos [18, 81], Greenlanders [78], Malayans [24], Australian Bushman [47, 48], Maoris of New Zealand [24], and the Indians of James Bay in Northern Canada [2].

VI. Mitigating Factors in Dental Caries


Dental caries is an infectious disease produced by certain microorganisms that live on the teeth and produce acids, chiefly lactic, from sugar and starches ingested as food and drink [89]. The acid attacks the hard (enamel) surface of the teeth in specific areas of caries predilection, decalcifying and eventually destroying them. The process, however, is not that simple. Certain of these bacteria, such as Streptococcus mutans, can convert, through enzymatic action, sucrose and the simple sugars into various long-chain sugars which are very sticky and adhere to the tooth surface [39]. These long-chain sugars (glucans) entrap and can harbor continued bacterial growth to form large masses of gelatinous material identified as dental plaque [59]. The decay process originates and pro-


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gresses at the plaque-enamel interface (contact), although it may occur at any site where food stagnation is permitted to occur [5]. If one could remove the entire plaque from all surfaces of the teeth by toothbrushing and flossing at very frequent intervals, one could theoretically prevent dental decay on those surfaces adequately cleaned by this method. Unfortunately, not all areas can be cleaned by this technique, because no amount of brushing or flossing can remove the plaque deep within the pits and fissures. These must be prevented from decaying by other means such as sealing the pits and fissures with plastic sealants or prophylactic silver fillings. Three conditions within the oral cavity are essential for the development of dental caries: 1) appropriate bacteria in the oral cavity in close proximity to the tooth surface; 2) an available carbohydrate substrate sufficient to maintain the growth of these microorganisms; 3) a tooth which is susceptible to the caries-attacking forces because of indigenous factors within the tooth or its salivary environment. There is considerable indisputable research evidence to document the essentiality of each of these three conditions [62, 86, 92]. Conversely, if one could completely control any of these, dental decay could be eliminated entirely. Although the purpose of all dental caries research and education is to ultimately attain this goal, the task of completely eradicating any one of these three conditions has not been achieved for large segments of the population by present techniques or educational programs. Great strides, however, have been made in appreciably reducing the amount of dental decay in the population and in completely eliminating it among selected individuals. The numbers in which caries has been completely arrested for a lifetime is certainly minute in comparison to the relatively unmet needs of the population. To better understand the significance of each of the three requirements for the production of dental caries, some preliminary descriptive information is necessary. Although the need for bacteria has been theorized for at least a century, irrefutable proof finally came with the advent of germfree experimental animals. These animals are born and live in a completely germfree environment. Germfree rats were fed caries-producing diets containing large amounts of sugar with no resulting decay. When various specific microorganisms were introduced, decay developed. Observations disclosed that certain specific strains of microorganisms were more decay-producing (cariogenic) than others. Present thinking suggests that certain streptococci (S. mutans) are of prime importance, although the

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lactobaccili (L. casei and L. acidophilus) or other microorganisms may be involved [29, 30, 50]. The substrate (substances) upon which the bacteria feed and multiply can come from sources other than sugar or starch, e. g., the amino acids, B-vitamins, and other nutrients which are essential for their survival. The microorganisms, therefore, do not necessarily need carbohydrates, although their major source of energy comes from the sugars and starches taken into the oral cavity in the form of food and drink. The carbohydrate most commonly indicated is sugar, particularly sucrose. Research which established the essentiality of an oral substrate was conducted by feeding 2 groups of rats a decay-producing diet; 1 group received the diet directly into the stomach by a stomach-tube, the other by way of the mouth [51]. The stomach-tube fed group developed no caries, the eating group showed considerable caries. Other carbohydrates, in complex forms, appear to be less ca ogenic than sugars. Starches, however, readily break down in the mouth into sugars by the action of a constituent of the saliva, the enzyme amylase, and must be considered carogenic [31]. Many of these starches are adhesive and may cling for long periods of time to the uncleansed tooth surfaces. Recent evidence [34] suggests, that, in baboons as well as in man, sucrose may not be necessary for plaque formation. Baboons stomachtube fed for 14 days continued to form plaque; and when glucose powder was given orally, the microorganisms present in the plaque formed large amounts of extracellular polysaccharides. Upon substituting glucose for sucrose in humans, similar polysaccharides formed. Sucrose is the most frequent sugar consumed by humans. Perhaps if other sugars were eaten with the same frequency, they would be equally as ca ogenic [16, 19]. There is evidence to believe that the development of cavities may not be a continus process but, rather, an intermittent one of decalcification and remíneralization [55, 56]. On a non-carious surface, even when plaque may be present, the interface contact between plaque and enamel may be in a state of equilibrium. When sufficient plaque acid is formed, equilibrium is disrupted and the more soluble parts of the enamel are dissolved away until a state of stability is again reached. Under proper conditions, if fluorides and phosphates are available, the reaction can go in a reverse direction, producing remineralization. It is of more than passing interest to note that these remineralized areas are more resistant to future caries attack than the original enamel [79]. For this reason it would appear


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that acid production for limited periods of time could be beneficial to tooth surfaces lying beneath fluoride-containing plaques. It is unfortunate that there are no well-controlled studies conducted in water fluoridation areas to evaluate the effect of sucrose on dental caries and if there is a threshold level below which its effect has no clinical significance. This void of knowledge merits serious research effort. 'The first event to take place in the oral cavity on a perfectly cleaned enamel surface is the formation of a film called the enamel pellicle [9, 20]. This membrane forms over the tooth surface within a few hours and is derived as a modified precipitate from the saliva. It covers the entire enamel surface, is transparent, extremely thin, and is permeable to bacterially-formed acids. The oral bacteria can grow and aggregate on this pellicle to build dental plaque [10, 15]. Both caries-preventive and caries-enhancing roles have been ascribed to it. There are many host factors inherent within the oral cavity which influence the susceptibility or resistance to decay, among which are the morphology, structure, location in the mouth, and degree of chemical maturation of the teeth [58]. The physical properties of the saliva, its chemical composition, buffering capacity, rate of flow, and immunological properties may all contribute to the integrity of the tooth surface. There are those who believe, however, that any tooth, regardless of all favorable host factors, will succumb to the ravages of decay if given a formidable environment challenge. Others would disagree with this concept. Clinicians have observed patients who, in spite of a high sugar diet, remain completely free from dental caries [25]. The reason for this extreme resistance is at present not known, and one could only speculate on the possibilities. However, in one study, many completely caries-free inductees into the military developed caries after a change in their environment [49]. Heredity may play a part in caries resistance as has been shown in family and twin studies [7, 25, 52, 53, 64]. In certain hereditary diseases of the enamel (amelogenesis imperfecta), one rarely observes carious teeth [25]. It is also true, however, that in the disease, there exists hereditary fructose intolerance, a metabolic incompatibility with sugars and, when these are eaten, illness is produced. Such individuals usually eat much starchy food without sugar and develop little caries [72]. The morphology or shape of the tooth is governed by genetic factors and, in certain instances, through prenatal and postnatal input. Of major importance are the pits and fissures, defects of the enamel which most

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frequently occur within the grooves on the biting surfaces of the teeth. Because of the narrow dimension of these faults, food debris can become impacted and stagnate within these confining areas, producing carious lesions [54]. These areas are highly susceptible in contrast to those teeth which do not contain pits and fissures and which have flattened cusps [8]. If teeth are crooked and out of alignment or lack tight contact areas with adjacent teeth, they may have greater areas of food stagnation and impaction where the plaque can form and grow unmolested by the action of the tongue, cheeks, or detergent foods. The necessity for frequent flossing and brushing at these sites is obvious. Oral hygiene programs should be expanded through the public schools until the entire population is well-indoctrinated with this health habit. Before it erupts and after eruption, each tooth continues to increase in hardness through a process of maturation or increased mineralization [73]. Prenatal and preemptive maturation takes place through the blood stream that nourishes the developing tooth. Posteruptive maturation occurs locally within the oral cavity and is derived from the foods that we eat and from the saliva. The longer the teeth remain in the mouth the harder and better calcified the surface of the enamel becomes. This is one reason why decay activity decreases as one advances in age, other conditions being equal. Therefore, if one could hasten maturation and incorporate within the enamel elements which would decrease its solubility in acid, more cariesresistant teeth would result [45]. This is what fluorides do. In areas where there is a deficiency of natural fluoride in the potable water supply, the addition of approximately 1 ppm of this element reduces dental caries by about 60 ο/ο among those consuming the water during tooth formation [67]. Decay is reduced in the anterior (front) teeth by over 90 Ο/. Through water fluoridation, one markedly hastens preemptive and posteruptive maturation. The fluoride once built into the teeth is retained the entire lifetime of the individual. The cost of fluoridation amounts to approximately 25 cents/person/year. If the life span of an individual is 70 years, then for about 17 dollars his dental bills would be reduced by at least 60 Ο /ο for his lifetime. Economically, water fluoridation is certainly a good investment. In good health and reduced suffering, it has inestimable value. There is a great need for continued effort to secure fluoridation for every community that has a communal water supply. If fluoridation could be made mandatory by federal law, this achievement would be invaluable to the health of the nation. No confirmed deleterious effects have ever been documented as the result of communal water fluoridation. In areas


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where communal water supplies do not exist, school water systems can be fluoridated. Another suggested method of adding fluorides is to fortify foods such as salt, milk, and sugar. The feasibility of fluoridating sugar should be investigated thoroughly. Artifical fluoride maturation can be provided by locally applying fluoride solutions or gels to the teeth [45]. Human studies have proven the merits of direct topical fluoride applications by mouthrinses, dentifrices, and tablets. The effectiveness of these applications is not nearly as great as that obtained from water fluoridation. Bactericides, antienzymes, and antibiotics are presently receiving a great deal of attention in caries research. In the past, undesirable properties have presented problems which limited their acceptance by the public. Immunizing against dental caries would be a great achievement and is presently receiving considerable attention from investigators. One of the characteristics of the oral cavity is the presence of saliva. It is within this environment that the forces that produce dental caries must function [21, 60]. Accordingly, it is conceivable that the physical and chemical properties of the saliva do have a bearing on caries susceptibility. It has been observed that, in instances where salivary flow has been markedly decreased, as among individuals receiving radiation to the salivary glands for the treatment of tumors, rampant tooth decay is a common result. The further importance of saliva can be illustrated in experimental animals. If the salivary glands are removed in one group and left functioning in another, the desalinated animals, when placed on a cariogenic diet, show an extreme breakdown of the teeth as compared to those with intact glands [28]. It is evident that decreased salivation is conducive to increased caries and there is evidence to suggest that increased flow may be beneficial. It is of passing interest to note that the taste of sweets increases salivary flow [40] and that sweetness is the only one of the four primary tastes that is always pleasant to man [75]. One of the functions of salivary flow is to bathe the teeth and wash away food particles and soluble substances and to act as a lubricant. Salivary flow is greatest at mealtimes and only negligible during sleep. If diminished salivary flow favors dental caries, then decay should be accelerated during sleep. Certain chemical properties of saliva are important. Since acid production is associated with caries formation, the buffering capacity of the

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saliva can neutralize considerable acid before it can damage the teeth. The buffering capacity of the saliva is due primarily to the presence of bicarbonate, phosphate, protein, and mucin. In a recent study, bicarbonate was found to be the most effective buffer followed by phosphate. Reports indicate that saliva from caries-resistant individuals has a higher buffering capacity than saliva from caries-active ones [43]. This may be one explanation for the reduction in tooth decay in these individuals. Calcium and phosphorus are constituents of saliva, and it is generally believed that there is a continual exchange of these inorganic ions between the saliva and tooth surface. Both buffering capacity and inter-surface ion exchange, theoretically, should influence the resistance to decay [22]. The literature relative to the effect of carbohydrate diets on experimental-animal caries is voluminous and points to sugars and cooked starches as being the offenders [31, 41, 85]. Although most of the laboratory animal studies point to sucrose as being the most cariogenic, other sugars, such as glucose, fructose, mannitol, sorbitol, and xylotol, have recently been shown to be as destructive to the teeth when consumed in programmed feeding experiments [71]. The results of animal studies are often strictly interpreted as applying to humans; however, great differences exist between them. There are marked variations in the chemistry of the saliva, morphology (shape) of the teeth, consistency of the diet, and eating habits. These must be considered when making comparisons. The only absolute method of determining what will happen in the human mouth is by using humans as the study population. Long term studies, in many situations, are preferable, because the development of lesions occurs in a conducive environment that is established slowly rather than as an instantaneous phenomenon. Dental scientists have long sought a means of testing caries activity on tooth surfaces within the mouth. Vox DER FEHR et al. [100] used 9 daily rinsings of a 50 ο/ο sucrose solution, producing decalcifications within 23 days. During this period, there were higher plaque accumulations but the percentage distribution of plaque microorganisms remained the same. Like most cariogenic animal diets which use very high concentrations of sucrose, the concentration used to produce caries in this study was for test purposes only and was far in excess of what man would use in his regular diet. One of the most interesting approaches to caries activity testing


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within the mouth is the Intra-Oral Cariogenicity Test (ICT) devised by KouLoumDEs et al. [57], wherein a slab of enamel is placed in an oral


prosthetic appliance and worn within the mouth. The tooth slab is covered with a dacron gauze to stimulate rapid plaque growth by the bacteria present in the mouth. By dipping the appliance frequently into various sugar solutions and replacing it into the mouth for extended periods of time, or by actual mouth rinsings, it is possible to test their cariogenicity. This is accomplished by removing the slab of enamel and testing its degree of softening. With this technique, it has been found that glucose and fructose are as cariogenic as sucrose [6]. It would seem that once plaque forms, other bacteria in the plaque could easily convert the simple sugars into acid. Through continued research, the possibility should be considered of finding means of reducing the cariogenicity of sugar consumed in a sticky form between meals. One method would be to develop chemicals to add to sugar which would negate any deleterious effect, would be non-toxic, and would not alter its taste. Various phosphates have reduced dental caries when added to the diets of experimental animals [14, 38, 44, 46, 70]. Studies in humans have given equivocal results. To be most effective, it appears that the phosphate must be in contact with the sugar and with the teeth. Α chewing gum study [26], in which dicalcium phosphate was combined physically with the sugar, produced a significant reduction in dental caries when compared to a non-phosphated gum. Phosphates added to the dough of breads and pastries are apt to be swallowed as a mass of food and may not come in contact with the tooth surfaces sufficiently to allow for complete release of the phosphate. Further investigation is necessary to clarify this point. There is a tendency among some clinicians to interpret specific and limited observations into broad generalities, and to quote these as covering assumptions that the investigator did not originally intend. This has lead to slogans which may not be entirely true. General statements of this nature may be harmful because of the difficulty of the population to fulfill what is expected of them. The hackneyed suggestion to eliminate all sugars from the diet is impossible to carry out in present-day society. It would be better if the effort were placed in achieving goals that are attainable. Eating habits constitute one of the most complex facets of human behavior, and one is dealing with a highly involved behavior pattern [102]. Perhaps dentistry should establish goals that are more realistic. Recommendations to discourage frequent use of sugar-containing, sticky foods

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between mealtimes and before retiring are possible to achieve and worth an all-out effort by the dental profession. Realistic steps suggested by this review to satisfy the urgent need to reduce tooth decay are as follows: 1) Promote communal and school-water fluoridation. 2) Restrict sugar and sugar-containing products from between meal eating. 3) If one has a choice between sweets in liquid form or solids, choose the liquid form. 4) Avoid all sticky or slow-dissolving sweets. 5) Brush and floss the teeth at mealtimes and after eating sweets. 6) If brushing cannot be carried out, rinse the mouth with warm water after consuming any carbohydrate. 7) Seek dental advice regularly and develop a realistic preventive program to fit one's individual needs, including the use of fluorides and other topical measures. 8) Maintain teeth in an exemplary state of repair, for they are a part of total health. 9) Increase research effort to find effective food additives for sucrose or other sugar-containing foods to counteract any caries-producing potential. 10) Increase the number of long-term sugar studies to establish at what levels sugar is cariogenic in the different foods. 11) Sugar in moderation should not be prohibited at mealtimes as long as all nutritional requirements are satisfied. With these suggestions, it is hoped that a more meaningful program involving sugar and dental caries can be developed which will prove beneficial to the entire population.

1

2 3 4

ADEJIS, B. L. and LOSEE, F. L.: Α study of the convariation of dental caries prevalence and multiple trace element of water supplies. N. Y. St. dent. J. 36: 618-622 (1970). ARKLE, Ρ. W.: The dental condition and foods of the Indians of James Bay, Northeastern Canada. Thesis, University of Toronto (1944). BAGRAMIAN, R. Α. and RUSSELL, Α. L.: Epidemiologic study of dental caries experience and between-meal eating patterns. J. dent. Res. 52: 342-347 (1973). BARTHGLDI, W. L.; PETERSON, E. E., and CRAWhoRD, W. Η.: University of Minnesota Freshman Student Survey. J. amer. dent. Ass. 63: 868-871 (1961).


References


321


5 BLΙx, G.: Nutrition and caries-prevention; Symp. Swedish Nutr. Found. (Almgvist and Wiksell, Stockholm 1965). 6 BIDDEN, R.; KouLOURIDES, T.; KELLER, S., and MAISON-HING, L.: Sugar cariogenicity on experimental caries in humans. 52nd General Meeting of I.A.D.R., Abstr. 604 (1974). 7 BooK, J. A. and GRAHIEN, Η.: Clinical and genetical studies of dental caries. II. Parents and sibs of adults highly resistant (caries-free). Propositi. Odont. Rev. 4: 1-53 (1953). 8 BOSSER7, W. A.: Relation between the shape of the occlusal surfaces of molars and the prevalence of decay. J. dent. Res. 13: 125-128 (1933). 9 BOWEN, W. Η.: Correlation of the biochemical composition of plaque with the diet; in McHuGH Dental plaque, pp. 157-169 (D. C. Thomson and Co., Ltd., Dundee 1970). 10 Bowni, W. Η.: Effects of foods on oral bacterial populations in man and animals. J. dent. Res. 49: 1276-1281 (1970). 11 BRIsLIN, J. F. and Cox, G. J.: Survey of the literature of dental caries 19481960 (University of Pittsburgh Press, 1961). 12 CALDWELL, R. C.: The retention and clearance of food from the mouth. Evaluation of agents used in the prevention of oral diseases. Ann. N. Y. Acad. Sci. 153: 64-70 (1968). 13 CALDWELL, R. C.: Physical properties of foods and their caries-producing potential. J. dent. Res. 49: 1293-1299 (1970). 14 CALDWELL, R. C. and TιΙοµλS, J. C.: Dietary chemicals versus dental caries. Application of chemical agents for the control of dental caries. Adv. Chem., pp. 161-180 (1970). 15 CARLSSGN, J. and EGELBERG, J.: Effect of diet on early plaque formation in man. Odont. Rev. 16: 112-125 (1965). 16 CmTcm.y, P.: Effects of foods on bacterial metabolic processes. J. dent. Res. 49: 1283-1291 (1970). 17 CuRRIE, D. P. and NAVIA, J. M.: Programmed feeding/drinking system for rat caries studies, sucrose vs. fructose. I.A.D.R. Abstr. 610, General session (1974). 18 Cuιzον, M. and Cuazoi, J. A.: Dental caries in Eskimo children of the Keewatin District in the Northwestern Territories. J. canad. dent. Ass. 36: 342-345 (1970). 19 DAimms, G. N.: The significance of epidemiological studies in relation to caries resistance; in WOLSLENHOLME Caries-resistant teeth, Ciba Found. Symp., chapt. 1, pp. 7-40 (1965). 20 DAWnS, C.: The nature of dental plaque, films and calcareous deposits. Evaluation of agents used in the prevention of oral diseases. Ann. N. Υ. Acad. Sci. 153: 102-119 (1968). 21 DAWES, C.: Effects of diet on salivary secretion and composition. J. dent. Res. 49: 1263-1273 (1970). 22 Emcssoi, S. Y.: Chemistry of enamel-saliva interface. Alabama J. med. Sci. 5: 256-266 (1968). 23 FANNING, E.; GOTJAMAνοs, T., and VowLas, N. J.: Dental caries in children

322

related to availability of sweets at school canteens. Med. J. Austr. 1: 1131-1132 (1969). 24 FINN, S. Β.: Survey of the literature on dental caries, pp. 117-174 (Nat. Res. Council, Nat. Acad. Sci., 1952). 25 FINN, S. Β.: Heredity in relation to caries resistance; in WOLSLENHOLME Cariesresistant teeth, Ciba Found. Symp., pp. 41-65 (1965). 26 FiNi, S. Β. and JAMIsoN, H. C.: The effect of a decalcium phosphate chewing gum on caries incidence in children, 30 months results. J. amer. dent. Ass. 74: 987-995 (1967). 27 FINN, S. Β. and JAMISoN, H. C.: The relative effect on dental caries of three food supplements to the diet. I.A.D.R. Abstr. 667, p. 207 (1969). 28 FINN, S. Β.; KLAPPER, C. E., and VOLKER, J. F.: Intraoral effects upon experimental hamester caries. Advances in Experiment Caries. Res. amer. Ass. Adv. Sci., Washington, D. C., pp. 152-168 (1958). 29 FITZGERALD, R.: Plaque microbiology and caries. Alabama J. med. Sci. 5: 236246 (1968). 30 FITZGERALD, R.: Historical background of Streptococcus mutan. Streptococcus mutan and dental caries. Proc. Round Table Discussion, 73rd Annual Meeting, Amer. Soc. Microbiol. Nat. Inst. dent. Res., pp. 1-2 (1973). 31 FROSTELL, G. and BAER, P. N.: Caries experience of rats fed various starches for study of experimental calculus formation. Acta. odont. scand. 29: 401-413 (1971). 32 GLASS, R. L. and FLEISCH, S.: Diet and dental caries: Dental caries incidence and the consumption of ready-to-eat cereals. J. amer. dent. Ass. 88: 807-813 (1974). 33 GOLDSwοwmν, N. E.; SuLIVAN, H. R.; CAMERON, D. A., and LILIENTHAL, B.: The biology of the children of Hopewood House, Bowral, New South Wales. Med. J. Austr. Vol. 1, pp. 878-881 (1953). 34 GRΕΝΒΥ, T. H.: Dental plaque studies on baboons fed on diets containing different carbohydrates. Arch. oral. Biel. 16: 631-638 (1971). 35 GUSTAFSSON, B.; QUENSEL, C. E.; LAνκu, L.; LUNDQVIST, C.; GRAHNEN, H.; GoNow, B. E., and KRASSE, B.: The Vigeholm Dental Caries Study: The effect of different levels of carbohydrate intake on caries activity in 436 individuals observed for 5 years. Acta. odont. scand. 11: 232-363 (1954). 36 HARGREAVES, J. A.: Changes in diet and dental health of children living in the Scottish island of Lewis. Caries Res. 6: 355-376 (1972). 37 Hiuus, R.: Biology of the children of Hopewood House, Bowral, Australia. Observations on dental caries experience extending over 5 years (1957-1961). J. dent. Res. 42: 1387-1399 (1963). 38 HAa ms, R. and NAViA, J.: Influences of vehicles and routes of administration on the effectiveness of agents in the prevention of oral disease in experimental animals. Ann. N. Y. Acad. Sci. 153: 240-257 (1968). 39 HARTLES, R. L.: Dietary and environmental factors influence caries resistance; in WOLSLENHOLME Caries-resistant teeth, Ciba Found. Symg., pp. 289-312 (1965).


FINN/GLASS


323


40 ΗΕΝΚΙΝ, R. D.: The role of taste in disease and nutrition, sweetness and increased salivary flow. Borden's Rev. Nutr. Res. 28: 71-87 (1967). 41 HUXLEY, Η. G.: The cariogenicity of various percentages of dietary sucrose and glucose in experimental animals. New Zeald dent. J. 67: 67-98 (1971). 42 JAMES, P.; PARFIAr, G., and ROYDHOUSE, R.: Caries experience during a decade. Jour. Dent. Child 37: 289-295 (1970). 43 JENKINS, G.: The equilibrium between plaque and enamel in relation to caries resistance; in WOLSLENHOLME Caries-resistant teeth, Ciba Found. Symp., pp. 192-221 (1965). 44 JENKINS, G.: Diet and caries: Protective factors. Alabama J. Med. Sci. 5: 276283 (1968). 45 JENKINS, G.: In vitro studies using chemicals; in HARRIS Art and science of dental caries research, chapt. 26, pp. 331-354 (Academic Press, New York and London 1968). 46 JOHANSEN, E.: Uses of animals for evaluation of cariostatic agents. Ann. N. Y. Acad. Sci. 153: 212-222 (1968). 47 KALLIS, D. G.: Prevalence of dental caries in Australian Aboriginal children resident in Carnarvon, Western Australia. Austr. dent. J. 16: 109-115 (1971). 48 KALLS, D. G.: Dental conditions observed in Australian Aboriginal children resident in Warburton and Cundeelee Missions, Western Australia. Austr. dent. J. 16: 44-52 (1971). 49 KanνE, Η. J.; SHELAIR, I. L., and HoERMAN, K. C.: Caries immunity in naval recruits and Ancient Hawaiians; in MERGENHAGEN and SØRP Comparative immunology of the oral cavity, pp. 71-177 (U. S. Dept. Health, Education & Welfare, Bethesda, Maryland 1973). 50 KEYES, P. H. and JORDAN, H. V.: Factors influencing the initiation, transmission and inhibition of dental caries; in SοαννλaS Mechanism of hard tissue destruction, pp. 261-283 (Amer. Ass. Adv. Sci., Washington, 1963). 51 Kira, O. W.; SHAW, J. H., and SOGNNAES, R. F.: The prevention of experimental tooth decay by tube feeding. J. Nutr. 42: 89-103 (1950). 52 KLEIN, Η.: Dental caries (DMF) experience in relocated children exposed to water containing fluoride. J. amer. dent. Ass. 33: 1136-1141 (1946). 53 ΚLnτκ, H. and PALMER, C. E.: Dental caries in brothers and sisters of immune and susceptible children. Milbank Memorial Fund Quart. 18: 67-82 (1940). 54 KouIG, K. G.: Diet and caries: Cariogenic factors. Alabama J. med. Sci. 5: 267-276 (1968). 55 KOULOURmDES, T.: Experimental changes of enamel mineral density; in HARRIS Art and science of dental caries research, chapt. 27, pp. 355-377 (Academic Press, New York and London 1968). 56 KouLoumDEs, T.: Remineralization methods. Ann. N. Y. Acad. Sci. 153: 84101 (1968). 57 KouLouπτuεs, T.; Hiuscu, T., and JAMIsoN, H. C.: Effect of CaHPOa and trimetasphosphate (ΤΜΡ) on cariogenicity in humans. 52nd General Session of I.A.D.R., Abstr. (1974). 58 LARSON, R.: Tooth age and caries susceptibility; in IARus Art and science of

FINN/GLASS

324


dental caries research, pp. 257-274 (Academic Press, New York and London 1968). 59 LEac-, S. A.: Plaque chemistry and caries. Alabama J. med. Sci. 5: 247-255 (1968). 60 LEUNG, S. W.: The role of saliva in caries resistance; in WOLSLENHOLME Cariesresistant teeth, Ciba Found. Symp., pp. 266-288 (1965). 61 LuNDQντsτ, C.: Oral sugar clearance: Its influence on dental caries activity. Odont. Rev. 3: 5-121 (1952). 62 MAκινΕν, K.: The role of sucrose and other sugars in the development of dental caries: A review. Int. dent. J. 22: 363-386 (1972). 63 MALM, M.: The role of sugar in modern nutrition. Marabou Symp., Suppl. No. 9; Naringsforskning, argan 17, p. 28 (1973). 64 MANDEL, I. D. and ZENGO, A. N.: Genetic and chemical aspects of caries resistance; in MERGENHAGEN and SCκaRP Comparative immunology of the oral cavity, pp. 118-137 (I.I.D.R DREW Publication, Bethesda, Maryland 1973). 65 MANSBRIDGE, J. T.: The effects of oral hygiene and sweet consumption on the prevalence of dental caries. Brit. dent. J. 109: 343-348 (1960). 66 MARTHALER, T. M.: Epidemiological and clinical findings in relation to intake of carbohydrates. Caries Res. 1: 222-238 (1967). 67 MCCLuaa, F. J.: Water fluoridation, the search and the victory (U. S. Nat. Inst. dent. Res. 1970). 68 McHuGR, W. D.; MCEwEN, J. D., and HiTcrni, A. D.: Dental disease and related factors in 13 year old children in Dundee. Brit. dent. J. 147: 246-253 (1964). 69 MοoιιΕ, W. J. and CοRRεΤΤ, M. E.: The distribution of dental caries in Ancient British populations. Caries Res. 5: 151-168 (1971). 70 NAνιλ, J. M.: Prevention of dental caries: Agents which increase tooth resistance to dental caries. Int. dent. J. 22: 427-440 (1972). 71 Νπντπ, J. M.; LOPEZ, Η., and FISCHER, J. S.: Caries promoting properties of sucrose substitutes in foods: Mannitol, xylotol and sorbitol. I.A.D.R., Abstr. 611, General Session (1974). 72 Νεωmωi, E.: Sucrose, the arch criminal of dental caries. J. Dent. Child 36: 13-22 (1969). 73 NIKIFoRuK, G.: Posteruptive effects of nutrition on teeth. J. dent. Res. 49: 1252-1261 (1970). 74 NIzEL, A. E.; MILLER, S. A.; CLEARY, T. M., and QuINN, R. S.: Relative cariogenicity of natural and refined sugars. I.A.D.R., Abstr. 613, General Session (1974). 75 NoRDSIE C, F. W.: The sweet tooth. Amer. Scientist 60: 41-45 (1972). 76 ORANJE, P.; NoRmsmmi, J. N., and ΟSBORN, T.: The effects of diet upon dental caries in South African Bantu. Sth afr. J. med. Sci. 1: 57-62 (1935). 77 PARFIAA, G. J.: The speed of development of the carious cavity. Brit. dent. J. 100: 204-207 (1956). 78 PEDERSEN, P.O.: Investigations into dental conditions of about 3,000 Ancient


325


and Modem Greenlanders, Α preliminary report. Dent. Rec. 58: 191-198 (1938). 79 Ρκατ τuµνπκτr, P.; Κοοτοτ Rmuas, Τ., and MUNKSGAARD, E. C.: Effects of experimental cariogenesis on fluoride uptake by enamel. 52nd General Session I.A.D.R., Abstr. 443 (1974). 80 PIGMAN, W.: Carbohydrates, fats and dental caries. Adv. Chem., Ser. 94, pp. 7-22 (1970). 81 ROSEBURY, Τ. and WπυoH, L. Μ.: Dental caries among Eskimos of the Kuskokwim area of Alaska. Amer. J. Dis. Child 57: 871-893 (1939). 82 Rows, Η. Η.; ANDERSON, R. Η., and WANNINGER, L. A.: Effect of ready to eat breakfast cereals on dental caries experience in adolescent children. J. dent. Res. 53: 33-36 (1974). 83 SCHERP, Η. W.: Dental caries: Prospects for prevention. Science 173: 11991205 (1971). 84 SEDWICK, H. J.: Observations of Pre-Columbian Indian skulls unearthed in New York State. J. amer. dent. Ass. 23: 764-773 (1936). 85 SκAw, J. Η.; Κι uµινS, I., and GIBBONS, R. J.: Comparison of sucrose, lactose, maltose and glucose in the causation of experimental oral diseases. Arch. oral. Bul. 12: 755-768 (1967). 86 SHEL,AIR, I. L.: Streptococcus mutans and epidemiology of dental caries; Streptococcus mutans and dental caries. Proc. Round Table Discussion, 73rd Annu. Meeting, Amer. Soc. Microbiol., Nat. Inst. dent. Res. pp. 7-13 (1973). 87 SLACK, G. L.; DucκwοRrκ, R.; SHEER, Β.; Βaλνnr, R. S., and MAKI, C. A.: The effect of chewing gum on the incidence of dental diseases in Greek children: A three year study. Brit. dent. J. 133: 371-377 (1972). 88 SOGNNAES, R. F.: Analysis of wartime reduction of dental caries in European children. Amer. J. Dis. Child 75: 792-821 (1948). 89 SrερκAN, R. M.: Intra-oral hydrogen-ion concentrations associated with dental caries activity. J. dent. Res. 23: 257-266 (1944). 90 Τλκuυcmm, M.: Epidemiological study on relation between caries incidence and sugar consumption. Bull. Tokyo dent. Coll. 1: 58-70 (1960). 91 TAKEuCHn, M.: Epidemiological study on dental caries in Japanese children before, during and after World War II. Int. dent. J. 11: 443-457 (1961). 92 TANZER, J. M.: Sucrose metabolism of Streptococcus mutans; Streptococcus mutans and dental caries. Proc. Round Table Discussion, 73rd Annual Meeting, Amer. Soc. Microbiol., Nat. Inst. dent. Res. pp. 25-32 (1973). 93 Tum, K.: The epidemiology of dental caries in Hungary, Budapest (Akademiai Kiado 1970). 94 Toro, P. D.; RAPP, G., and O'MALLEY, J.: Clinical evaluation of chewing gum in gingivitis and dental care. J. dent. Res. 39: 750-751 (1960). 95 ΤονrnυD, G.: Decrease in caries frequency in Norwegian children during World War II. J. amer. dent. Ass. 39: 127-136 (1949). 96 TOVERUD, G.: The influence of war and post-war conditions on the teeth of Norwegian school children: Eruption of permanent teeth and status of deciduous dentition. Milbank Memorial Fund Quart. 35: 127-196 (1957). 97 TOVERUD, G.; FINN, S. B.; Cox, G. J.; BonuckuR, C. F., and Sσπw, J. Η.:

Fτκκ/Gtnss

326

Survey of the literature of dental caries. Pub. 225, Nat. Acad. Sci., Nat. Res. Council, pp. 1-54 (Washington, D. C. 1952). 98 VOLKER, J. F.: The effect of gum chewing on the teeth and supporting structures. J. amer. dent. Ass. 36: 23-27 (1948). 99 VOLKER, J. F.: What is the scope of our knowledge of the dental caries process? A symposium - Sugar and dental caries. J. Calif. St. dent. Ass. 26: 10-15 (1950). 100 Voi DER FEHR, F. R.; LoE, H., and THEILADE, E.: Experimental caries in man. Caries Res. 4: 131-148 (1970). 101 WEISS, R. L. and TRITHART, A. H.: Between-meal eating habits and dental caries, Experience in pre-school children. Amer. J. publ. Hlth 50: 1097-1104 (1960). 102 Youic, C. M.: Nutrition counseling for the pedodontic and periodontic patient. Workshop Conf. Nutr. and Preventive Dentistry, Eastman Dental Dispensary, pp. 34-42 (1960). 103 ZITA, C.; MCDONALD, R. E., and ANDREWS, A. L.: Dietary habits and the dental caries experience in 200 children. J. dent. Res. 38: 860-865 (1959).


Authors' addresses: SIDNEY B. FINN, D. M. D., M. S., Professor of Dentistry, University of Alabama, Birmingham, Ala.; and ROBERT L. GLAss, D. M. D., Dr. P. H., Associate Clinical Professor, Ecological Dentistry, Harvard University, and Associate, Forsyth Dental Center, Boston, Mass. (USA)

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