[For himself and co-workers: MAXWELL KARSHAN and GENEVIEVE FOLEY.]
The experimental data below, coordinated with findings of other investigators, accord with the following concept : (1) Fissure caries in man is caused primarily by food particles rich in carbohydrate, and having a physical character that favors forcible impaction into fissures under relatively strong masticating pressures required to crush them. After this forcible impaction, the particles are not dislodged by subsequent excursions of other foods, and thus furnish pabulum for acid-producing bacteria, among which lactobacilli are prominent. Products of this bacterial action initiate the carious lesion in enamel. This concept supplements Miller’s theory. (2) Modifying or sec ondary phenomena affect this primary agency similarly in rats and man. Ingestion of vitamin D reduces incidence of caries without preventing it; ingestion of sugar and perhaps of any carbohydrate increases it, even if carbohydrates lack independent power to produce caries. The mechanism of vitamin-D action is unknown. Carbohydrates in general enrich the acid- yielding substrate in an impacted food mass. Other secondary phenomena in caries, indicated by experimental data, probably occur in man, but have not been demonstrated. (3) The etiology of proximal caries may be somewhat distinctive; but, since the primary agent of fissure caries in rats also causes the proximal type, the etiology of both types may follow analogous patterns. (4) It has not been shown that these data have any reference to other types of caries, such as that, most characteristic of adults, which occurs in the exposed gingival areas of teeth.
Experimental caries, histologically similar to caries in man, has been produced in young rats with diets containing coarsely ground raw rice or corn. Diets containing no coarsely ground cereal, whether nutritionally adequate or deficient in calcium and vitamin D, or high in sugar and starch, did not produce caries in rats. True caries in rats was regularly appreciable only by microscopic examination of jaw sections ; and was distinguished from other rat-tooth lesions (not analogous to caries in man, but appearing under similar dietary conditions), some of which began mechanically by fracture of tooth cusps and often became appreciable in intact jaws grossly, or under low magnification. True rat-caries could be prevented only by elimination, fine grinding, or cooking, of the primary causative food, not by dietary changes affecting only chemical composition. Diets deficient in vitamin D, calcium, phosphorus, fat and protein yielded higher incidence of rat caries than fully adequate diets. Addition to these diets, separately in different experimental groups, of normal levels of vitamin D in oil, or of normal or slightly subnormal levels of calcium and phosphorus, or of corn oil or other fatty oils or fats, or (irregularly) of protein, yielded reduced incidence of caries equivalent to that effected by simultaneous correction of several or all of these deficiencies. Whether such corrective dietary changes improved calcification, neither degree of calcification of teeth or bone as observed histologically, nor levels of calcium and phosphate in blood, showed any significant parallelism with incidence of caries. Addition of (a) sugar to the deficient caries-producing diet tended (irregularly) to induce increased incidence of caries ; (b) large amounts of foods having excess of potential alkalinity (coarsely ground raw dried lima beans, orange-lemon juice, synthetic orange-lemon juice) induced no significant reduction in incidence ; (c) finely divided silicate abrasive, causing marked attrition, yielded no reduction in incidence of caries.
Human oral and intestinal strains of lactobacilli were generally similar in their morphological, biochemical and immunological characteristics. Lactobacilli,
from human mouths having caries, produced higher effective concentrations of acid by fermentation (about pH 3.5) than other common parasitic bacteria (about pH 4.5). Enamel from human teeth was about five times as soluble at pH 3.5 as at pH 4.5. Lactobacilli were found uniformly in rat mouths irrespective of presence or absence of caries ; no qualitative difference between lactobacilli from carious mouths and those from caries-free mouths (rats) could be detected. Daily additions of freshly isolated smooth strain of human mouth lactobacilli, to deficient or adequate coarsely ground rice diets, did not in either instance increase incidence of caries in rats. Attempts to immunize rats with repeated intraperitoneal injections of living lactobacilli, using mixed human and rat strains, followed by ingestion of a coarsely ground rice diet, gave no protection against caries.
Caries among Kuskokwim (Alaska) Eskimos, although limited almost entirely to occlusal and proximal types in young persons, was clinically typical, and presented the bacteriologic picture described for caries by Bunting et al., and chemical characteristics of saliva similar to those described by Karshan. In three Eskimo communities having different caries-prevalences, there was no correlation of caries with dietary levels of carbohydrate, protein, fat, calcium or phosphorus, probable vitamin-D intake, estimated potential acidity of diets; nor with individual foods other than sugar and biscuit. Sugar was ingested mainly in solution (in tea) ; candy as such was not correlated with caries. Biscuit (pilot-bread) is chemically and physically similar to primary agents of rat caries. Three of four commercial brands of pilot-bread, in diets in which pilot-bread replaced rice or corn as the principal ingredient, produced typical caries in rats, the exception being the softest product. Incidence of caries was lower than with analogous rice or corn diets. Incidence of fissure caries was correlated with both hardness and particle size of biscuit, as with rice or corn ; but proximo-gingival caries was produced in greater degree with small than with large hard-biscuit particles. No cusp-fracture lesions (” macroscopic “) appeared in any of these biscuit animals.
References: J. Bact., 1929, 1932; J. Den. Res., 1931, 1932, 1933, 1934, 1937, 1939; J. Am. Den. Assoc., 1934, 1935; Arch. Path., 1935; Am. J. Dis. Child., 1939; Gordtn’s Dental science and dental art, Chapter VIII, 1938 (Lea and Febiger, Philadelphia).