John J. Salley

Vitamin A deficiency in the hamster.

T HE Syrian hamster (Cricetus auratus) has steadily taken a prominent role as a laboratory animal, and it has been widely used by dental research workers. In spite of its more than 25 years of use in biologic research, there are still important facets of this animals nutritional requirements which are not known. One of these-vitamin A-will be discussed in this paper. Routh and Houchin5 cited the need by the hamster for thiamine, riboflavin, pyridoxine, pantothenic acid, and nicotinic acid, all members of the B-complex group. Cooperman, Waisman, and Elvehjem2 extended these observations to include more of the water soluble group of vitamins. Hamilton and Hogan3 published a report relating to not only the water soluble vitamins, but to the fat soluble vitamins E and K as well. They concluded that the hamster will grow at a normal rate and to normal maturation if the diet includes thiamine, riboflavin, pyrodoxine, and pantothenic acid of the water soluble group, and vitamins A, D, E, and K of the fat soluble series. In the case of vitamins A and D, no experimental evidence was presented to substantiate their conclusions. Jones5 has shown that the hamster, like the rat, does not have a requirement for vitamin D provided the calcium-phosphorus ratio of the diet consumed is adequate. Only Hirschi4 has presented a study of vitamin A deficiency in the hamster. Little information is presented in his report regarding histologic lesions characteristic of the deficiency, tissue analyses for residual vitamin A in the deficient group, mortality figures or composite weight curves; and whereas the experimental group was fed a commercially available synthetic A deficient diet, the control group was maintained on a nonsynthetic ration of laboratory chow. In light of the paucity of information available in the literature concerning vitamin A deficiency in the hamster, it was felt that such a study was indicated not only to increase our knowledge concerning its need for this particular vitamin, but also to devise a synthetic regimen with which extended observations relating to its daily requirements of other dietary elements could be carried out.

The Effect of Chronic Vitamin A Deficiency on Dental Caries in the Syrian Hamster

A RATHER well-accepted tenet among students of dental caries etiology is the inverse relationship which exists between decreased salivary secretion and caries incidence. Trimble, Etherington, and Loschl and Losch and Weisberger2 have reported increased caries experience in human beings who demonstrated decreased salivary flow. These clinical observations have been substantiated in experimental animals by Weisberger, Nelson, and Boyle3 and Cheyne4 who noted increased caries scores in rats after surgical extirpation of major salivary glands. Similar observations have been made on desalivated hamsters by Gilda and Keyes5 and Klapper and Volker.6 The development of a suitable synthetic diet for vitamin A deficiency studies in the hamster7 has made it possible to investigate the effect of this dietary deficiency on dental caries activity. In this study a constant finding among A-deficient animals was squamous metaplasia of epithelial components in salivary glands, resulting in duct obstruction, sialadenitis, and suppurative degeneration of gland parenchyma.7 These alterations of salivary gland strueture closely agreed with findings in the rat reported by Wolbach and Howe.8 Because of salivary gland degeneration with avitaminosis A, it is not unreasonable to assume that some changes in oral environment may ensue. Indeed, the fact that both major and minor salivary glands are affected in the deficient animal7 would lead to the predication that a situation somewhat analogous to gland extirpation may prevail during the deficient state. Shaw9 has speculated on this question with reference to human caries mediated through xerostoma due, in turn, to the salivary gland alterations produced by inadequate consumption or assimilation of vitamin A. In light of these corollary data and the fact that no direct experimental caries investigation has been done on vitamin A-deficient animals, it was felt that such a study should be conducted.

Epithelial carcinogenesis in the absence of accessory structures

Abstract The role of the accessory epidermal structures, sebaceous glands and hair follicles, in skin carcinogenesis has been reviewed and a comparison made between the response of epidermal and oral mucous membrane epithelium to the action of carcinogenic hydrocarbons. The rather marked susceptibility to tumor induction of an oral epithelium which is devoid of accessory structures has been pointed out. In light of this finding, as well as the reports of other investigators, 1, 2 it is suggested that epithelial adnexa acting as requisites to chemical induction of tumors may merit some re-evaluation.