Caries was experimentally produced, in rats and dogs, by disturbing their calcium-phosphorus metabolism either by excessive mobilization of Ca or P already deposited in the body, or with diet deficient in one of these elements. Since the size of the particles was the same in the diets of both control and experimental groups—in the former of which caries did not occur—size of particle could not have been a causative factor. Antenatal deficiency of vitamin D, or antenatal disturbance of Ca-P metabolism, produced changes in the dentition of the offspring resembling those that result from the postnatal influence of a rachitogenic diet, and also caused retardation of dental development.
The results mentioned above were obtained by these different procedures : (a) Diet low in calcium, high in phosphorus, and lacking vitamin D. (b) Diet low in phosphorus, high in calcium, and lacking vitamin D. (c) Daily administration of excessive amounts of (d) viosterol, or (e) parathyroid extract, or (f) radium. Caries, as thus experimentally produced, was clinically and histologically identical with the human occlusal variety. In examinations of the teeth of these animals, at various stages of development—to determine the nature and course of caries— it was found that the initial change occurred in the pulp. Following marked congestion of pulpal blood vessels, there was serous degeneration of odontoblasts and concurrent proliferation of reticular cells (fibroblasts)—especially marked immediately beneath the odontoblastic zone. Necrosis of the pulp and periapical abscesses often developed. In prolonged experiments, changes in dentin and enamel occurred. Although the affected enamel remained intact and there was no perceptible discoloration, roentgenograms revealed extensive decalcification. Although radiolucent zones, in dentin and enamel, resembled caries in radiographs, there was at first no visible surface lesion, but destruction of dentin and enamel occurred later.
References: J. Den. Res., 1932, 1937.