Nutrition and dental decay

Contrary to a popularly-held view, dental decay is not a dietary disease, but one which is basically of microbial origin. Dietary carbohydrates, mainly monoand disaccharides, are absorbed into dental plaque and broken down to organic acids by the micro-organisms present in dense concentrations. The acids produced cause the equilibrium between remineralization and demineralization to shift in favour of demineralization thus initiating the carious lesion. Research in the field of dental caries using the human subject has been restricted for a number of reasons. First, dental decay is a disease of slow progression. Indeed, it has been estimated that a new lesion in a permanent tooth takes between 18 and 60 months to become clinically detectable (Parfitt, 1956). Second, once established a lesion is irreversible, thus experimental induction of caries is wholly unethical. Third, because of the length of the study period it is quite impossible to obtain dietary histories and still less is it possible to control dietary intake. Fourth, perhaps the most important, diet is but one of a large group of secondary factors which contribute to an individual’s experience of this multifactorial disease, many factors of which may be still unknown. For these reasons most of the research which relates dental caries and diet has been carried out in animals, the rat model being by far the most common. Because of the dental and other obvious differences between man and rat, the transposition of these animal findings to the human species must be carried out with great caution. Clearly it is this problem which has greatly restricted the rate of progress in our knowledge and understanding of the precise role of dietary factors in relation to dental decay. A survey of the literature would suggest that diet may influence decay experience in two ways. It may inhibit or it may promote disease. Far more is known about the latter than the former and, without question, the spearhead of prevention of caries has been directed towards restriction of caries-promoting foods rather than encouraging those which may actively inhibit. Further, diet may affect the teeth systemically while the tooth is unerupted and in its developmental or maturation phase. Alternatively, and more importantly, it may exert its effect locally after the tooth has erupted.