Aetiology and pathogenesis of benign prostatic hyperplasia

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Abstract
Prostatic hyperplasia predominantly involves the stromal compartment of the gland and affects more than 70% of men of 70 years or older with or without obstructive symptoms of benign prostatic hyperplasia. A consensus view is emerging concerning the factors and control systems that modulate cell proliferation and connective tissue biology in the prostate. The purpose of this review is to discuss some of the recent work contributing to the latter in the context of the aetiology of benign prostatic hyperplasia. Studies over the last 3-5 years have identified transforming growth factor beta, fibroblast growth factor and insulin-like growth factor family members as key regulators of cell proliferation and extracellular matrix turnover with interrelated activities. Recently, oestrogens, adrenergic signalling and inflammatory processes have been shown to impact and potentially perturb the balance between the activities of the above factors. These agents are all subject to alteration with age and as such are candidates for potential triggers of the initiation of stromal hyperplasia. The current model for the control and dysregulation of prostatic stromal growth is discussed in relation to the pathogenesis of benign prostatic hyperplasia and future directions for research.