Report of the Joint Committee of the American Academy of Pediatrics and the American Society of Dentistry for Children Dental Caries and a Consideration of the Role of Diet in Prevention

DENTAL CARIES AND A CONSIDERATION OF THE ROLE OF DIET IN PREVENTION T HE FOUNDATION for dental health is established early in life. The greatest single cause of dental disease is caries which, in turn, is largely a disease of the first two decades of life. The deciduous teeth are no less susceptible than the permanent ones, and disease in them is not without serious consequence for the permanent dentition. Since those physicians caring for children should be informed of current knowledge concerning the relation between diet and caries prevention, representatives of the American Academy of Pediatrics and the American Society of Dentistry for Children met to prepare a joint statement on this problem. The report which follows represents a summary of the position taken by this Committee. This report has been reviewed by the Committee on Nutrition of the American Academy of Pediatrics; it has endorsed those portions which relate specifically to Ilutrition. The dental aspects, particularly the pathogenesis of caries, are the responsil)ihty of dentists. Since there is significant (lifference of opinion on these problems, even among experimental pathologists in dentistry, the burden of responsibility must he borne by those assisting in the preparation of this report. Anyone interested in a broad survey on the pathogenesis of dental caries may find a comprehensive statement in a publication of the National Research Council, Control of Tooth Decay, from the Committee on Dental Health, Food and Nutrition Board (N. R. C., Washington, D.C., 1953). Dental caries is a disease of the calcified tissues of the teeth. It is generally believed to be caused by acids resulting from anaerobic glycolysis by microorganisms, is characterized by decalcification of the inorganic portion, and is accompanied or followed by disintegration of the organic substance of the tooth. The lesions tend to occur in particular regions of the teeth, i.e., the occlusal fissures of the molar teeth, the contact areas between adjacent teeth, and, in cases of rampant caries, the cervical areas near the gingiva. These are areas which are not self-cleansing. Lactic acid, which has been demonstrated in areas of initial caries activity (Fancher et al,’ Muntz,’) and advanced caries (Armstrong et al.,’ Miller,4) is the principal acid involved in the caries process.5 It is derived from bacterial action upon a carbohydrate substrate. Any microorganism, or combination of microorganisms, capable of producing an acidity of about pH 5, which is sufficient to decalcify enamel, can initiate dental decay.6 The time that the acid must be in contact with the tooth in order to produce decalcification is not precisely known, but from in-vitro studies of adult teeth, may be as short as 10 to 15 minutes. Whether or not the acid formed will decalcify the enamel of a tooth is dependent on the concentration of the acid, its protection against dilution, and its duration of contact with the tooth. There are natural factors in the mouth which contribute to the dissipation of acids formed on the tooth surface, such as the amount of saliva and the buffering capacity of the saliva. Specific inhibitory factors may play a part. Of course, variations in the inherent re-