ABSTRACT
Peyronie’s disease is characterized by the development of fibrosis within the tunica albuginea of the corpora cavernosa. This scar or plaque restricts the elasticity of the involved tunical segment and may lead to erectile curvature. The most accepted etiology of Peyronie’s disease to date is that repetitive penile trauma is responsible for the tunical injury. During erection, the penis remains relatively straight as the elastic corpora cavernosa fill with blood. The septal strands become taut between the dorsal and ventral tunica albuginea, contributing to the axial rigidity of the penis. When the erect penis is subjected to loading and some degree of bending occurs, stress is focused at the junction of the septal strands and tunica albuginea.1 Bending of the penis during intercourse may be exaggerated by age-related changes in erectile function and rigidity. In addition, it has been shown that the concentration of elastic fibers within the tunica albuginea decreases with time.2 It has been postulated that a combination of these factors may lead to delamination of the inner circular and outer longitudinal layers of the tunica albuginea at the site of attachment of the septal strands, resulting in hemorrhage and local inflammation. Fibrin may become trapped within the hypovascular tunica, leading to persistent inflammation and subsequent fibrosis.1 The process can extend laterally, leading to a more extensive or even circumferential plaque. Obviously the initial aspects of this process occur in many men, more than those with clinical Peyronie’s disease, indicating that some inherent predisposition to excessive scar formation may exist.
