The influence of asymptomatic inflammatory prostatitis on the onset and progression of lower urinary tract symptoms in men with histologic benign prostatic hyperplasia

Abstract

Benign prostatic hyperplasia (BPH) is a condition that greatly affects the quality of life of middle-aged and elderly men. Histopathologically, hyperplastic changes frequently occur in the prostate tissue of elderly men, the incidence of which has been reported to reach approximately 80% in men in their 70s. In clinical practice, approximately 25% of men with histologic BPH are assumed to experience lower urinary tract symptoms (LUTS) and receive some kind of treatment. In other words, there are some men with histologic BPH who do not exhibit LUTS. For that reason, many factors, such as the change in hormonal environment, the immune or autoimmune response, the alteration of gene expression, and so on, are thought to affect the onset and progression of LUTS in men with histologic BPH. One such factor that has long drawn attention is the presence of asymptomatic histological inflammation, which very often accompanies symptomatic BPH. Recent studies have suggested that asymptomatic histological inflammation causes repeated destruction, healing, and regeneration of the prostate tissue, leading to the enlargement of prostatic nodules, while at the same time causing stromal tissue-predominant remodeling of the prostate tissue, which can increase urination resistance and result in the condition changing from asymptomatic BPH to symptomatic BPH. In future, the biomolecular clarification of the significance of asymptomatic histological inflammation in the prostate tissue could help develop new treatment strategies for BPH accompanied by LUTS.

Keywords: Asymptomatic histological inflammation; Benign prostatic hyperplasia; Lower urinary tract symptoms; Prostatitis.

Figure 1

Asymptomatic histological inflammation causes the enlargement of prostatic nodules, while at the same time causing significant morphological changes to stromal tissue (remodeling), which can increase urination resistance and result in the condition changing to symptomatic benign prostatic hyperplasia.

Figure 2

The glandular/periglandular inflammatory changes from grade 1 to grade 3 (A–C) shown by immunostaining using anti-T cell (CD45RO Ab-2) as a primary antibody, reduced from × 100.

Figure 3

The stroma/epithelium ratio in prostate tissue of nonbacterial prostatitis (NBP) rats was increased with the administration of estradiol, which was estimated by Masson's trichrome staining, reduced from × 100. A: Control; B: NBP rat.

Figure 4

The anti-inflammatory effect of Eviprostat inhibited the increase in the stroma/epithelium ratio in nonbacterial prostatitis rats. *p < 0.005; **p < 0.0001.