The underlying injury to undescended testes may be hormonal, a transient perinatal form fruste of hypogonadotropic hypogonadism characterized by blunting of the surge in gonadotropins normally seen at age 60 to 90 days. Ischemia is the underlying injury to testes associated with incarcerated inguinal hernias. To determine if the histopathology of these 2 injuries is different histomorphometric analyses were performed on semithin microscopic sections of biopsies of 21 control testes, 17 undescended testes and 13 intrascrotal testes associated with incarcerated inguinal hernias. The infants in all groups were 30 to 120 days old. The results showed that, as in previous studies, undescended testes at this age are characterized by hypoplasia of Leydig cells, normal germ cell counts and defective maturation of gonocytes into adult dark spermatogonia. In contrast, testes associated with incarcerated inguinal hernias were characterized by hyperplasia of Leydig cells, reduced germ cell counts and normal maturation of gonocytes into adult dark spermatogonia. One might conclude that the underlying injury of undescended testes, presumably the blunted surge of gonadotropins, causes a primary hypoplasia and hypofunction of Leydig cells, which in turn causes a secondary defect in transformation of gonocytes into spermatogonia. In contrast, ischemia may primarily cause a tubular epithelial lesion leaving the hypothalamic-pituitary-gonadal axis intact and allowing normal transformation of gonocytes into spermatogonia. Reduced gonadotropins and ischemia appear to produce distinctly different primary and secondary pathophysiological effects on the testes.