Abstract

Extreme difficulty may be met in estab­ lishing a well defined line of demarcation between so-called predisposing factors and exciting causcs in oral carcinoma. Obviously, there is much overlapping be­ tween these categories of pathogenesis, particularly with regard to those factors that continue to be in the realm of hy­ pothesis and conjecture. As indicated by clinical studies, a va­ riety of predisposing factors may be of significance in the development of lesions otherwise attributed to more direct in­ fluences such as irritation from jagged teeth, ill-fitting dentures or prolonged use of tobacco.1,2 Although this may suggest that the cited sources of chronic irrita­ tion are exciting factors acting on' a tissue already possessing an inherent tendency to cancer, it is entirely possible that they, in themselves, may predispose the mu­ cosa to malignant change. That a deficiency in vitamin A can cause epithelial metaplasia has been demonstrated many times.3,4 It is not surprising, therefore, that clinical evi­ dence points to the possible role of avita­ minosis A in the etiology of both leuko­ plakia and cancer.5 Swift, in 43 instances of vulval leukoplakia, attributed the lesions to deficient absorption of vitamin A associated with achlorhydria.6 This contention was substantiated by the bene­ ficial results which followed administra­ tion of dilute hydrochloric acid and vitamin A. Somewhat similar clinical evidence was presented by Orr7 in the case of oral cancer. Orr was interested in the prevalence in India of this malig­ nant condition and its possible relation to betel nut chewing; he concluded from studies in different geographic areas, that the incidence is related directly to states of nutrition, especially of vitamin A. Also implicated as a predisposing fac­ tor in leukoplakia and cancer is vitamin B deficiency. In this connection, other factors such as chronic alcoholism become significant as they might influence the nutritional status of an individual. Cer­ tainly, the clinically observed manifesta­ tion of lingual edema, papillary atrophy and glossitis is evidence of the consider­ able effect that vitamin B complex has on oral tissues. Although the mechanism by which these changes are brought about is not clearly understood, a possible ex­ planation is the demonstration by Adams8 of a decreased utilization of oxygen by the skin of rats rendered deficient in ribo­ flavin. Such an altered oxidative ability of epithelial tissues might well render them

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