Sugar and human dental caries.
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Biomedical subjects
Publications and source records attributed to L M Sreebny.
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The present study, along with others, shows that when the requirement of a diet for mastication is increased, enlargement of the parotid gland occurs. This study demonstrated for the first time that the magnitude of the gland enlargement is directly related to the amount of nonnutritive bulk incorporated into the diet, and that the concentration of protein is significantly increased in the parotid saliva of rats fed such a diet. The findings show that, although the concentration of protein is increased in the parotid saliva, the composition of proteins is unchanged, leading to the conclusion that all secretory proteins are increased in parallel. A comparison of the gland enlargement observed in response to the bulk diet with that observed in response to chronic isoproterenol treatment reveals many similarities. However, the fact that the protein composition of the parotid saliva is not altered when rats are fed the bulk diet is in marked contrast to the striking changes observed following chronic isoproterenol treatment. The reason for the dissimilar response is not known. However, an investigation into the differences that exist in the gland response to these two means of inducing gland enlargement may lead to a better understanding of the factors that regulate the size of the rat parotid gland and the complement of proteins in its secretion.
This review is limited to an analysis of the relationship of the consumption of sugar to the prevalence of caries in man. The data reveal that in the human a highly forged link exists between these variables. In the absence of sugar, little decay is found; when used in large amounts over protracted periods of time, caries scores are usually high. The evidence also suggests that it is possible to reduce the incidence of caries by reducing the intake of refined sugars. Conflicting evidence exists in man, however, with regard to the influence of the total intake of sugar, the form in which it is consumed and the frequency of its consumption on the prevalence of dental decay. Moreover, little is known about the amount of sugar that individuals actually consume each day. Cause and effect conclusions should not be limited to one or another type of study. In the aggregate, the results obtained from studies in vitro, investigations in experimental animals, as well as studies in humans, all point to the existence of a powerful sugar-caries axis. More research on human subjects is needed, however, to fill the gaps in our knowledge.
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The diet and feeding patterns of developing rats were determined from feed bin weight losses and analysis of stomach contents (details in a previous report). Parotid gland development in the same rats was assessed from the specific activities of the secretory enzymes alpha-amylase, RNase and DNase, with particular attention to the occurrence of circadian variations. The results indicate that during the first week post partum, rats suckle much more by day than by night but have no circadian cycles in their parotid glands. Between 10 and 20 days, there were no consistent cycles either in feeding activity or in parotid enzymes. The progressive change from milk to stock diet between 14 and 30 days appears to promote the maturation of the parotid gland. The halfway point in the dietary change at 21 days coincides with the onset of inversely related circadian cycles in feeding and the parotid enzymes. Premature weaning at 21 days accentuates both cycles and accelerates parotid maturation. The findings indicate that the physical consistency of the diet has an imporant regulatory role in the developmental patterns of feeding activity and parotid glands of rats, but they also hint that other dietary qualities may be involved. Chronologic fluctuations in plasma corticosterone suggest an intricate relationship among this hormone, feeding behavior, and parotid glands in developing rats.
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