Alkaline phosphatase activity in epithelial metaplasia.

The etiology of epithelial metaplasia and its re lation to neoplasia have been of interest for many years. Investigators have proposed (39, 41) and opposed (6j the view that metaplastic trans formations in various sites may be precancerous. It seems well established that such alterations often accompany neoplastic growths (20, 25, 27, 32). The need to distinguish metaplastic from neo plastic lesions in the genital tract has received em phasis in recent pathologic studies (7, 33, 34, 35, 43). McCullough and Dalidorf (31) have suggested that all squamous metaplasia and keratinization result from the same etiologic factor, local vita min A deficiency, regardless of the initiating stimulus (e.g., mechanical, hormonal). Investiga tions on the effects of vitamin A on estrogeninduced vaginal cornification (19, 23, 47) and on epidermal differentiation (44, 45) have given some support to this suggestion. Earlier studies sug gested that metaplastic lesions in the male rat genital tract caused by estrogen treatment and those accompanying avitaminosis-A are histologically identical (21). Such histologie identity, however, does not hold for all types of genital epithelial metaplasia in the male rabbit (9). In the male mouse, it has been shown that vitamin A deficiency intensifies the histologie response in the genital tract to minimal dosage with estro gen (15). In the course of a series of studies on the rela tion of steroids and phosphatases in the male genital tract (11, 12), it was noted that estrogen-induced epithelial metaplasia is accompanied by alkaline phosphatase activity in the replacing epithelium. This phenomenon has been investigated further in both estrogen-induced and avitaminotic-A lesions, in addition to other instances of meta plasia; results are reported herein. Differences in the histologie picture of the metaplastic proccess after estrogen treatment and in vitamin A deficiency were seen in (a) the mode of growth of