Benign prostatic hyperplasia (BPH) is classically understood to be a disturbance in prostate homeostasis, but the underlying questions of how and why this disturbance occurs have yet to be answered definitively. An increasing body of evidence points to inflammation as a central component of the pathogenic process of BPH.
To review recent evidence regarding the association between histologic prostatic inflammation and the development and progression of BPH.
This article is based primarily on material presented at a satellite symposium entitled, “Inflammation and Prostatic Diseases: From Bench to Bedside,” held during the 2015 annual meeting of the European Association of Urology in Madrid, Spain. Current data regarding the link between inflammation and BPH were reviewed.
Evidence from a canine model of BPH and human prostate tissue has confirmed the presence of inflammation as a component of BPH. Pronounced inflammation was observed in dogs with hormonally induced prostatic hyperplasia. Longitudinal biopsy indicated that the cell-mediated and humoral immune response was preceded by hyperplasia. In surgically treated human BPH specimens, high-level inflammation was significantly associated with prostate enlargement and symptom evolution. Current opinion is that chronic inflammation and endocrine changes lead to disturbed homeostasis and tissue damage or, alternatively, that abnormal stem cell expansion and disturbed homeostasis lead to chronic inflammation and endocrine changes. Either way, a “vicious cycle” is initiated that leads to hyperplasia with fibrosis and changes in prostate tissue composition.
Increased insight into BPH pathogenesis indicates that restoring tissue endocrine metabolism and reducing chronic inflammation are prostate-specific targets for the treatment of BPH.
Increasing insight into benign prostatic hyperplasia (BPH) pathogenesis indicates that restoring tissue endocrine metabolism and reducing chronic inflammation are prostate-specific targets for treatment of BPH.
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