Carbohydrates and dental health.

Carbohydrates, together with fats and proteins, provide the necessary energy needs for humans, and constitute, therefore, an integral part of a normal diet. An etiological model for caries that considers local and host factors is presented, highlighting the interaction of bacteria, saliva, minerals, and trace elements with food residues and with other intrinsic environmental and behavioral characteristics of the host. Consideration of this complex multifactorial etiology precludes the identification of any one factor as the only one to be singled out in prevention and management of oral disease. Sugar is, unquestionably, a risk factor for caries, and, therefore, its total substitution with energetic or nonenergetic sweeteners has been found useful. However, partial substitutions of fermentable sugars may have limited practical value in controlling caries prevalence. Caries preventive programs that take into consideration not one, but several etiologic factors, will be effective and beneficial to the general population.

A new perspective for nutrition: the health connection.

The science of nutrition has undergone a major transformation in its objectives and approaches because of the influence of new understanding in epidemiology of oral diseases in technically developed countries, as well as in developing countries with different environmental circumstances. Recent findings of biochemical, immunological, and molecular biology investigations related to oral tissues have also added a new health dimension to this understanding. The major challenge ahead is not only to continue to expand the available scientific information, but to recognize the role that nutrition has for oral tissues, which is no different than the one it has for other tissues and organ systems. Investigators in other fields have been incorporating these new concepts about nutrition in the planning of their research during the past decade, but this emphasis has been lacking in dental research and this needs to be corrected. Still, we have one more challenge ahead, and that is to transfer to the general public the information generated by research in our laboratories and clinics in a prudent and effective way. This will ensure that consumers will take advantage of nutrition information alongside oral health concepts to maintain good general health while preventing and controlling oral diseases. There is much work ahead to be done, but the following papers have already started to set up research guidelines for the future.

Nutritional status, tooth eruption, and dental caries: a review.

Animal studies have shown that early malnutrition affects tooth structure, delays tooth eruption, and results in increased dental caries. However, epidemiologic evidence in support of these findings has been elusive. Cross-sectional surveys show that populations with a higher prevalence of caries in their deciduous teeth also show a lower prevalence of caries in their permanent teeth. However, longitudinal data from individuals show exactly the opposite. Caries development is also delayed as a consequence of a delayed tooth eruption and thus the bell-shaped curve that results from plotting deciduous caries prevalence vs age is shifted to the right in malnourished children. This effect will result in an apparently negative association between caries in deciduous and permanent teeth when cross-sectional surveys are compared. Once the effect on tooth eruption is taken into account, the contribution of malnutrition to increased caries susceptibility may be observed, as demonstrated by a recent cross-sectional study involving Peruvian children.

Nutritional role of sugars in oral health.

The dental risk of dietary sugars is dependent mainly on the frequency of intake, but the prevalence of caries in a population is strongly modified by other dietary, social, and behavioral factors independent from intake of sugars. Regarding dietary factors, it must be remembered that hidden sugars in fruit as well as polysaccharides are cariogenic. The most important of the other factors is regular tooth brushing, which results in the removal of the bacterial plaque that causes caries and periodontal diseases and makes fluoride (which is contained in every advanced toothpaste) available for maintenance of the hard dental tissues and for remineralization wherever demineralization has occurred. This explains why in most highly developed countries caries prevalence has decreased markedly during the past 20 y although consumption of sugars remained high.

Chronic malnutrition, dental caries, and tooth exfoliation in Peruvian children aged 3-9 years.

A cross-sectional evaluation of dental caries in primary teeth and nutritional status was conducted involving 285 Peruvian children from low socioeconomic conditions aged 3-9 y. Forty-nine percent of the children were found to be chronically malnourished (stunted) whereas acute malnutrition (wasting) was infrequent (2%). Stunted children showed a delayed exfoliation of primary teeth. The caries prevalence curve as a function of age (ie, a plot of decayed, extracted, and filled teeth vs age) was found to be shifted to the right by approximately 15 mo in stunted children as compared with well-nourished children. Children aged 7-9 y with stunted growth showed a significantly higher percentage of carious teeth than did well-nourished children of the same age (40 and 29%, respectively; p less than 0.005). Nutritional deficits that lead to chronic malnutrition not only may affect tooth exfoliation but also appear to render the primary teeth more susceptible to caries attack later in life.

Vitamin A influence on calcium metabolism and calcification.

Vitamin A deficiency has been shown to affect vision, reproduction, cellular differentiation, and maintenance of epithelial and skeletal tissues. Different vitamin A compounds, i.e., retinol and retinoic acid, vary in their ability to fulfill these biologic functions. Aside from vision, the exact molecular mechanisms of action for retinoids are largely unexplained. High doses of vitamin A are known to increase bone resorption through stimulation of lysosomal proteolytic activity, which also leads to increased secretion of PTH. Deficiency of retinol affects bone morphology by increasing bone thickness. Using a standardized guinea pig model, bone formed entirely during a retinol-deficient (A --) period contained less calcium and took up more 35S into glycosaminoglycan (GAG) fractions in vitro than did control (A+) samples. Using rat calvaria, a pulse-chase experiment indicated that the rate of 35S loss from calvaria cultured with A -- serum was lower than in controls. Thus, retinol deficiency seems to increase the amount of sulfated GAG in bone through a defect in the degradation of GAG.

Dr. Robert S. Harris: nutritionist, oral science researcher, and visionary MIT educator.

Efforts in dental research and training have received the contribution of individuals who had no formal training in dentistry, yet they understood the dental field and the educational needs of those who would be engaged in dental research, teaching, and service in industry and academia. Dr. Robert S. Harris (1904-1983) was such a man. What follows is a personal remembrance of his character, his research accomplishments, and his successful educational endeavors in the dental field.

In vivo measurements of sulcal plaque pH in rats after topical applications of xylitol, sorbitol, glucose, sucrose, and sucrose plus 53 mM sodium fluoride.

In two series of experiments, Sprague-Dawley-derived rats were infected orally with cariogenic micro-organisms and fed caries-promoting diets. By means of an antimony electrode, resting pH values were measured in the mesial sulcus of the maxillary left first molar. 100 or 200 microL of the test solutions were applied, and the change in pH (delta pH) was recorded for three min. Test solutions were: (a) 10% sucrose, 10% glucose, 10% sorbitol, or 10% xylitol; (b) 0%, 10%, 20%, or 40% sucrose; (c) 0%, 3%, 7%, or 10% sucrose; and (d) 10% sucrose, 10% sucrose + 53 mmol/L NaF (1000 ppmF-), or 10% sucrose + 53 mmol/L NaCl. Experimental design was a 4 X 4 Latin square (a, b, c) or a cross-over design (d). Solutions of sucrose and glucose gave significantly greater decreases in pH than did sorbitol or xylitol. pH fall was maximal for 10% sucrose and significantly less for 40% sucrose during the three-minute experimental period. For sucrose solutions ranging in concentration from 3 to 10%, pH fall was highest after application of 10% sucrose when plaque was previously rinsed with water, but this pH fall did not differ significantly from that obtained using a 7% sucrose solution. Adding 1000 ppmF- to a 10% sucrose solution caused an increase in pH. Rinsing the teeth to remove saliva resulted in significantly lower resting pH values. The results of these experiments are in agreement with the results of human plaque pH measurements.

In vivo measurements of sulcal plaque pH after topical applications of sorbitol and sucrose in rats fed sorbitol or sucrose.

To test whether adaptation to sorbitol could be observed in rat plaque, we made pH measurements of rat sulcal plaque in vivo, following topical application of 10% sorbitol solution. Rat pups were inoculated orally with S. mutans 6715 and fed diet MIT 305 (5% sucrose) for 16 days. Baseline sulcal plaque pH response of these rats to topical application of 10% sorbitol solution was measured. One group of 16 rats was then fed 20% sucrose in the diet, and a second group 20% sorbitol. After 13 days' feeding of the experimental diets (four days were used for accommodation to dose, and nine days at the 20% level for sorbitol), there was a significantly greater (p less than 0.01) drop in pH following topical application of 10% sorbitol in this group than in the sucrose-fed group. There was no difference in the pH response of the two groups to topical application of a 10% sucrose solution when tested six days later. The sulcal enamel caries score was significantly higher (p less than 0.001) in the sucrose group, but buccal enamel scores were similar in both groups. Adaptation in rat plaque took place, and could be measured in vivo as an increased drop in sulcal plaque pH following topical application of sorbitol. It is not clear whether this adaptation was primarily due to selection of sorbitol-fermenting micro-organisms, or, more likely, by induction of sorbitol-specific enzymes. Relative to the sucrose-containing diet, the sorbitol diet was hypocariogenic, even under experimental conditions.

In vivo and in vitro study of the effects of vitamin A deficiency on rat third molar development.

We have examined the effect of in vivo vitamin A status on subsequent rat third molar formation and mineralization in an in vitro organ culture system. Vitamin A deficiency imposed during an eight-day in vitro period caused effects very similar to those of vitamin A deficiency imposed on rats in vivo. Analysis of the data also demonstrates that retinoic acid is capable of reversing the interference in mineralization of third molars induced by vitamin A deficiency in the organ culture system.

Sources of variability in rat caries studies: weaning age and diet fed during tooth eruption.

A factorial design (2x2) was used to study the caries effect of two diets (starch based versus stock) fed to rat dams and their litters, and also of variations in the weaning age (19 versus 25 days). Higher and reproducible caries scores were obtained in rats which were fed a purified starch-based diet, weaned at 19 days of age, and subsequently given a cariogenic challenge.

Rat caries assay of reference foods and sugar-containing snacks.

Using standard reference snack foods, we tested a method, using rats fed in a programmed feeding machine, to evaluate the caries-promoting properties of foods. Results, which were expressed in relation to a control food, indicate that the method distinguished differences in caries potential among a number of different snack foods. Buccal and sulcal caries scores of rats fed snacks foods varied in their responses. A gel diet used to provide essential nutrients for the rat growth in this approach contributed minimally to the caries response which was related principally to the food being tested.

Effects of protein deficiency and diet consistency on the parotid gland and parotid saliva of rats.

Protein deficiency results in an increased susceptibility to dental caries, suggesting that oral host-defense properties are compromised. An important component of oral host defense is salivary gland function, which is affected by both protein deficiency and diet consistency. This study describes the effects on rat parotid gland growth and secretory function induced by feeding rats diets of normal (20%) or moderately low (7%) protein content, provided in either a powdered or solid form. In addition, since protein deficiency may result in a secondary zinc deficiency which, in turn, may affect salivary gland function, the effects of these diets on liver zinc concentration were also measured. From 22 to 47 days of age, rats (18/group) were fed the following diets: normal protein, powdered; normal protein, solid; low protein, powdered; and low protein, solid. With each diet consistency, liver zinc was higher for the normal protein group. Within each protein level, liver zinc was higher for the solid diet. This latter observation suggests that food mastication and the resultant stimulation of salivary gland function may also play a role in zinc metabolism. With the normal-protein diet, parotid gland weight was higher for the solid diet; with the low-protein diet, parotid gland weight was similar for both consistencies and did not differ from that of the group fed the "normal protein, powdered" diet. For both consistencies, parotid saliva protein concentration was greater for malnourished rats.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of nutritional status on the age distribution of dental caries in the primary teeth.

A cross-sectional study of dental caries in the primary teeth as a function of nutritional status was conducted on 1481 children one to 13 years old in Lima, Perú. Forty-one percent of the children were found to be chronically malnourished (stunted), 3% were acutely malnourished (wasted), and 5% were both stunted and wasted. A plot of decayed, extracted, and filled teeth (deft) vs. age resulted in a bell-shaped curve that was shifted to the right by 2.5 years for malnourished groups, compared with normal children (p less than 0.01). The shift to the right of the age distribution of caries was associated with a delay in both the eruption and exfoliation of the primary teeth in malnourished children. Peak caries activity was significantly higher in wasted and in stunted and wasted children, when compared with normal controls. It is concluded that malnutrition delayed tooth development, affected the age distribution of dental caries, and resulted in increased caries experience in the primary teeth.

Sources of variability in rat caries studies: microbial infection and caging procedure.

Two sources of variability in rat caries experiments have been investigated: infection with two S mutans strains and two types of caging. Results indicated that strain 6715 was more virulent than was strain 10449 when 24-day-old rats were orally infected with the organism under standardized conditions. Caging of rats (2 per cage) in stainless steel, raised bottom cages resulted in higher level of caries than in plastic tubs (3 per cage) with hardwood bedding. Infection and caging conditions are two of the factors which may contribute to variability in caries pattern and severity in experimental rats.

Effect of topically-applied solutions of iodine, sodium fluoride, or chlorhexidine on oral bacteria and caries in rats.

Antibacterial levels of iodine, chlorhexidine or sodium fluoride were topically applied to the molar teeth of rats. The effect of these agents on buccal and sulcal caries, as well as on certain oral bacterial populations was assayed. All three agents exerted a significant cariostatic effect which was site specific. Buccal caries incidence and reductions appeared correlated to S. mutans counts, while sulcal caries was better correlated to total cultivable counts. These studies suggested that the simultaneous application of iodine and NaF might exert an additive cariostatic effect.

A case-control study of plasma ascorbate and acute necrotizing ulcerative gingivitis.

Data from animal studies and from studies of patients with acute necrotizing ulcerative gingivitis (ANUG) have provided suggestive evidence for an association between ascorbate deficiency and disease risk. Further, there is biological plausibility for such an association, due to the role of ascorbate in collagen synthesis and leukocyte function. A case-control study of plasma ascorbate and ANUG was performed on 60 patients with a history of ANUG infection and 60 age-race-sex-matched controls. No cases had had active lesions for at least two months prior to their vitamin assay to avoid any potential reduction of dietary intake of ascorbic acid due to the presence of painful mouth lesions. According to results obtained by use of a modification of the 2,4-dinitrophenylhydrazine method for determination of total plasma ascorbate, the mean and standard error of the mean of plasma ascorbate for all ANUG cases was 0.07 +/- 0.006 mmol/L; the mean for all controls was 0.10 +/- 0.006 mmol/L. Paired differences in plasma ascorbic acid concentrations between cases and controls were significantly different from zero (p less than 0.001). The unadjusted relative risk (RR) of ANUG as obtained by conditional logistic regression for subjects whose plasma ascorbic acid concentration was at or below the median value for controls, relative to subjects with higher values, was 7.3 (90% confidence interval, 3.0 - 17.4; one-sided p value less than 0.001). Patients with a history of ANUG ingested a daily average of 1.2 +/- 0.2 servings of dietary ascorbic acid, as compared with a daily average of 1.9 +/- 0.2 servings for healthy controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of alveolar bone in relation to nutritional status during pregnancy.

Demand for nutrients necessary for the formation of mineralized tissues increases dramatically during pregnancy to meet fetal requirements. The purpose of this clinical study was to identify short-term effects of pregnancy and dietary intakes of calcium, phosphorus, protein, and vitamin C on radiographic density and alveolar crest morphology of the mandible. Seventy-six subjects between ten and 20 weeks' gestational age were recruited from the Jefferson County, Alabama, Department of Health maternity clinic. Initially, an evaluation of their diet was done, and a single periapical radiograph was taken in the canine-premolar region of the mandible. A final evaluation of the diet and a periapical radiograph of the same teeth were obtained at a time as close to the expected date of delivery as possible. Dietary evaluation consisted of a 24-hour recall history and a food-frequency history at the two visits. Radiographs were made with a bite-block film-holding system with occlusal registration in acrylic for reproduction of projection geometry at the two visits. An aluminum stepwedge was incorporated for densitometric standardization. Measurements of plaque, and bleeding and pocket-depth probing were recorded for control of local effects on alveolar change. Standard statistical procedures of regression determined correlation of 12 nutrients and periodontal variables with bone density change and with alveolar crest morphology change. Vitamin C intakes (24-hour recall) showed a positive correlation (p = 0.033) with bone density change, and calcium intakes (24-hour recall) showed a negative, but not significant, correlation (p = 0.058) with bone density change, contributed particularly by subjects with the highest calcium intakes. The strongest relation with alveolar crest morphology change was the interproximal pocket-depth change (p = 0.086).

Effective immunity to dental caries: studies of active and passive immunity to Streptococcus mutans in malnourished rats.

The present studies suggest that rat dams passively transfer IgG to their offspring via milk. Furthermore, rat dams hyperimmunized to S mutans after intravenous administration of this bacterium have serum-precipitating antibody to S mutans group-specific antigen. This serum precipitin was also observed in serums of their offspring during the suckling period and was detectable for a week after weaning. When these offspring were infected with S mutans on the day of weaning, significantly fewer smooth surface lesions developed in them than in infected rats reared on nonimmunized mothers. These results suggest that anti-S mutans antibody, perhaps of the IgG2a class, is passively transferred from mother to offspring via the milk. Furthermore, this antibody is probably important in protection against S mutans infection. In this regard, recent studies by Lehner, Challacombe, and Caldwell have suggested that crevicular fluid transudating serum antibodies are important in the prevention of dental caries in rhesus monkeys. From our studies and others, it is becoming clear that at least two sources and classes of antibody are important in caries immunity. Secretory IgA, produced and secreted into saliva after local injection can be correlated with protection. At the same time, serum antibody (presumably IgG) either passively or actively derived also gives immune protection. Further studies must clarify the precise role of these Ig's and their possible synergistic activity with other specific immune factors in saliva in order to determine the mechanism(s) involved in effective caries immunity.

A longitudinal study of dental caries in the primary teeth of children who suffered from infant malnutrition.

A prospective, four-year longitudinal study of 209 Peruvian children was conducted to evaluate the effect of a single malnutrition episode occurring at infancy (i.e., < 1 year of age) on dental caries in the primary teeth. Children were recruited into the study at age 6-11 months after they had suffered from a malnutrition episode and were thus classified by anthropometry as either: (1) Normal; (2) Wasted (low weight for height); (3) Stunted (low height for age); or (4) Stunted and Wasted (S and W). Eruption of the primary teeth was significantly delayed in all malnourished children; however, the effect of stunting--that is, retarded linear growth--was more pronounced and lasted longer than that of wasting or acute malnutrition (i.e., 2.5 vs. 1.5 years, respectively). By age 4 years, children from group 4 (S and W) showed a significantly higher caries experience in the primary teeth than did those in any of the other three groups. In summary, this longitudinal study has confirmed previous studies in animals and indirect epidemiological evidence which had suggested a cause-effect relationship between early malnutrition and increased dental caries.

PIP: The study was conducted from 1986 through 1990 among 209 children residing in Canto Grande, a poor community located north of Lima, Peru. The children were recruited as infants, aged 6-11 months, from the outpatient population of the Canto Grande Health Center, or from two other hospitals. All children were of full-term gestation and normal birth weight ( 2500 g). Each child was assigned to 1 of 4 study groups ascertained by weight and height measurements, with the National Center for Health Statistics standards used as the reference: 1) normal; 2) wasted, indicating current acute malnutrition; 3) stunted, indicating past or chronic malnutrition; and 4) stunted and wasted, indicating malnutrition soon after birth. The data, composed of 2700 examinations, were analyzed by the Statistical Analysis System (SAS) General Linear Models (GLM) program for computation of ANOVA tables. The mean numbers of teeth at ages 1 and 1.5 years for normal children were significantly higher than those of the children who were either wasted, stunted, or stunted and wasted as infants. At age 2, normal children had significantly more teeth in the mouth than did stunted children and stunted and wasted children. At age 2.5, the number of teeth in the normal children was still significantly higher than in stunted children. At age 4, all 4 groups had their full 20 teeth. At age 4, children who were stunted and wasted during infancy showed a significantly higher number of decayed, extracted, and filled teeth (def) compared with that of the other 3 groups. When grouped into 4 def categories of low, moderate, high, and very high caries experience, the distribution of the 4th group was distinctly different from that of the other 3 groups. 17.2% of stunted and wasted children had a very high caries experience (i.e., def 13) at age 4, significantly higher than that in any of the other 3 groups (i.e., normal 9.8%, wasted 4.4%, and stunted 3.6%, respectively; p 0.001).