There is no sound evidence as to the immediate cause of caries. That certain bacteria, including B. acidophilus, play a part in the progress of the disease seems certain, but we do not know whether they initiate it. We do not even know whether caries begins as a process of decalcification, or of disintegration of protein. We still have much to learn about the immediate as well as the predisposing causes of the disease, but to reduce its incidence it is essential to ensure that the teeth are of good structure and that they erupt in perfect alignment in well developed jaws. The author further concludes, from the results of her experimental and clinical investigations extending over a period of twenty years and from those of others, in conjunction with the distribution of caries, that predisposition to the disease is largely controlled by the original structure of the teeth. There is a definite association between tooth structure and susceptibility to caries in man. Using certain defined criteria for good (normal) and poor (hypoplastic) structure, based on evidence obtained from animal experiments rather than just from clinical impressions, the author found that extensive caries occurred in only 7 percent of well- formed teeth as compared with 74 percent of teeth with fairly severe hypoplasia. She did not find, on the other hand, that teeth with gross hypoplasia (the type usually described in text books) were more liable to become carious than average teeth without such gross defects.
The type of structure is related to the diet during the development period. The dietary factors of chief importance to the calcified dental tissues are vitamins D and A, and mineral salts—especially calcium and phosphorus. These factors are essential not only to the offspring during post-natal development, but also to the mother during pregnancy and lactation, if well-calcified teeth and jaws are to be produced. In puppies, the quality and quantity of secondary dentin deposited in response to experimental attrition also depends on the calcifying properties of the diet. This result, in con junction with the fact that secondary dentin in human teeth varies similarly in quantity and quality in response to attrition and caries, indicates that—even after eruption —diet, directly or indirectly, affects the resistance of teeth to disease.
Preliminary clinical investigations begun in Sheffield, England, eighteen years
MOORE, MARY M.: Philadelphia, Pa. (May 6, 1938).
The peak ages, both for the group having caries and for the number of cavities, are 17, 18, and 19 years. This spread of peak corresponds with individual differences between physiologic and chronologic ages. Of total caries, 20.6 percent occurs from 6 to 13 years; 79.5 percent, from 14 to 21. There is 146 percent more caries between ages 14 to 21 than would result if rate of caries from 6 to 13 had continued uniformly to age 21. Middle and later years of adolescence is the period of greatest oral evidence of caries. Control or prevention of caries has not been effected by diet, hygiene, and medical and dental care.
The author’s observations have been made on 80 patients seen on an average of three or four times a year, over fifteen consecutive years (6 to 21) ; all had not only adequate dental care but benefit of medical care and good food. At any time during the first eight years, over 50 percent of the group were free from caries. Yet observation of this same group for seven additional years showed that a belief that caries had been controlled would have been a delusion. Unless continuous observations are made during this period (6 to 21 years), and evidence of control of caries consistently obtained, it cannot be rightly assumed that any known factor or group of factors contributes to prevention of caries.
Reference: Ann. Den., 3, 77, 1936.