Journal of Andrology Testis Workshop 2009
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Published-Ahead-of-Print November 19, 2009
Journal of Andrology 2009, DOI:10.2164/jandrol.109.008730

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Amelioration of Penile Fibrosis: Myth or Reality

Ahmed I. El-Sakka * and Aksam A. Yassin

* To whom correspondence should be addressed. E-mail: aielsakka{at}yahoo.com.

Several changes have been reported to occur in the cavernosal tissue as well as tunica albuginea with aging. The atherosclerosis of the penis that occurs with aging causes a decrease in penile oxygen tension. A reduction of smooth muscle cells (SMCs) has been demonstrated in relation with this change in oxygen tension. Changes in the ratio of penile collagen have also been observed and could explain the decrease in penile elasticity and compliance with aging. Chronic ischemia is, therefore, associated with fibrosis but also with nitric oxide (NO)-cyclic guanosine monophosphate reduction. The sensitivity of the alpha-adrenoceptors on the smooth muscle cells increases with aging. Furthermore, androgen deprivation produces penile tissue atrophy, alterations in dorsal nerve structure, alterations in endothelial morphology, reduction in trabecular smooth muscle content, increase in deposition of extracellular matrix (ECM) and accumulation of fat-containing cells (adipocytes) in subtunical region of corpus cavernosum. All those modifications can explain the prevalence of erectile dysfunction with aging. The aim of this review is to address the underlying etiology of corporal fibrosis especially, aging, cavernosal nerve damage, androgen deprivation in addition to tunical fibrosis. Finally we will address the proposed amelioration and reversion of fibrosis in terms of correcting, at least partially, the relative SMC loss occurring with: aging, diabetes, or cavernosal nerve damage and their impact on prevention of erectile dysfunction (ED) associated-cavernosal fibrosis.


Key words: Erectile Dysfunction • Aging • Corpora cavernosa, • Fibrosis, • Tunica albuginea,






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