Management of Peyronie's Disease in the Aging Male

Rany Shamloul; Anthony J Bella


Aging Health. 2011;7(1):65-78. 

In This Article


The underlying pathogenesis of PD is unknown, but is likely to be multifactorial, with an interplay between genetic predisposition, trauma and tissue ischemia. The underlying lesion of PD is a fibrous plaque(s) that contains excessive collagen, an altered framework of reduced and fragmented elastic fibers and fibroblastic proliferation, which alters penile anatomy. The fibrous plaque causes focal inelasticity and can compromise erectile function. Plaques may be fibrous, contain areas of calcification, or be completely ossified. Most authorities postulate that PD results from repeated minor blunt trauma to the penis during intercourse. PD is thought to be due to localized aberration of the wound healing process. For susceptible individuals, bleeding within the tunica albuginea, trapping of fibrin and inflammatory cells, and overexpression of matrix proteins, secondary to upregulation of cytokines and growth factors in the local environment, lead to plaque formation.[7] Excess fibrin deposition in response to microvascular injury and upregulation of TGF-1, results in one or more areas of plaque formation.[8]

Risk Factors

A family history of PD has been observed in 2% of patients.[9] In total, 21% of patients with PD may also have Dupuytren's contracture.[10] Patterns of gene expression in families with PD and Dupuytren's disease are similar, particularly in regard to collagen degradation, ossification and myofibroblast differentiation.[11] Genital and/or perineal injuries, radical prostatectomy, plantar fascial contractures, tympanosclerosis, urethral instrumentation, Paget's disease, gout and lipomas have been associated, albeit weakly, with PD.[12,13] Hypertension, smoking, hyperlipidemia and diabetes have been proposed to be risk factors, but they are more likely related to underlying ED, as current research does not show a relationship between these factors and severity of penile curvature.[13] An association with vascular comorbidities is controversial,[14] as is the role of overt trauma, such as penile fracture.[15] It needs to be emphasized that a history of penile injury is not required for a man to develop PD.

Natural History

Following diagnosis, referral to an urologist with experience treating PD is recommended.[16] Untreated PD resolves in only 12% of men, with 40–48% of men demonstrating worsening of curvature at 12 months, while curvature remains stable in the remaining patients.[17] The mean change was 15° in those in whom curvature improved; therefore, from a clinical standpoint, this degree of improvement may not be meaningful in the context of deformities, which may be either greater than 90° or corkscrew shaped, for example. The disease state may often be divided into an acute (or inflammatory) phase and a chronic phase. During the former, there may be penile pain, even when flaccid, and there are often dynamic changes of penile malformation. During the latter, pain resolves and the deformities stabilize. Although pain resolves as part of the natural progression of PD, nonsurgical treatment may shorten this time period, as well as impacting the deformity; early initiation of therapy is recommended, and there is little or no role for observation unless the deformity is minimal and does not impact sexual function.


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