Pathophysiology of benign prostatic hyperplasia.

Abstract

The exact morphogenesis of benign prostatic hyperplasia (BPH) is unknown, but morphologic observations and different etiologic theories, such as the stem cell, dihydrotestosterone, and stromal-epithelial interaction hypotheses, help to explain some of the findings. For example, the initial changes in the development of BPH may result from an activation of mesenchymal clones with embryonal functions that stimulate development of the glandular component. This, in turn, induces the development and maturation of the stromal component. In areas that lack epithelial elements, such as those in the periurethral zone, the interaction stops and only embryonal small stromal nodules remain. On the other hand, the decrease in endocrine-paracrine cells may alter the normal local hormonal equilibrium of the periurethral area and may be an inducing factor in the development of BPH.