The role of androgens and estrogens in the pathogenesis of experimental nonbacterial prostatitis

Abstract

The etiology and pathogenesis of nonbacterial prostatitis remains unclear. This study provides evidence that genetic background, advancing age, and hormonal imbalance are important etiologic factors for prostatitis in rats. It also demonstrates that Lewis and Wistar rats develop a spontaneous nonbacterial prostatitis with advancing age, making them good animal models for the laboratory investigation of this disease. Spontaneous nonbacterial prostatitis is much more common in Lewis rats (72%) than in Wistar rats (27%, p less than .05), and does not occur in Sprague-Dawley rats. The incidence of spontaneous prostatitis is significantly higher in older animals than in younger animals (72% old adult Lewis rats vs. 30% young adult Lewis rats, p less than .05). Administration of exogenous 17 beta-estradiol increases the incidence and severity of prostatitis in old Wistar rats (100% treated vs. 27% control, p less than .01). Castration has a similar effect. Testosterone can block the effect of estradiol on prostatitis, however treatment with an anti-estrogen or an aromatase inhibitor to block estrogen action does not improve prostatitis in the rat. The major finding of this study is the demonstration that severe prostatitis can be induced in young adult Wistar rats by neonatal treatment with 17 beta-estradiol followed several months later in adulthood by testosterone administration. The results of this study suggest that genetic background, advancing age, and hormonal imbalance contribute to the pathogenesis of nonbacterial prostatitis in rats.