Trauma
A long-standing theory for the etiology of PD is repeated minor sexual trauma, such as hitting or bumping of the erect penis against the pubic bone (Furey, 1957; Jarow & Lowe, 1997). Furey (1957) hypothesized that rupture of small vessels resulted in small hematomas that were replaced by fibrous tissue. More recently, histologic studies have demonstrated fibrin in the plaque tissue of 18/19 patients with PD that were biopsied but not in tunica obtained in control patients (Somers & Dawson, 1997). Somers and Dawson (1997) have also shown that PD most likely begins with buckling (bending, crumpling) trauma that causes injury to the septal insertion of the tunica albuginea. This trauma results in intravasation of blood into the tunica albuginea with activation of fibrinogen. As a sequela of the trauma, inflammatory cells, including macrophages, neutrophils, and mast cells, migrate to the area along with platelets. A variety of inflammatory mediators, including cytokines, autacoids, vasoactive factors, serotonin, platelet-derived growth factors, and transforming growth factors, are released, which lead to fibrosis. It is thought that the avascular nature of the tunica albuginea may impede the clearance of many of the growth factors, such as transforming growth factorbeta, which increases the fibrotic response (Border, & Noble 1994; Border, & Ruoslahti 1992; Davis, 1997; Diegelmann, 1997; Moreland, 1998; Mulhall, Thom, Lubrano, & Shankey, 2001; Van de Water, 1997). Down regulation (i.e., decreased function/activity) of matrix metallopreoteinase (enzyme involved in the remodeling of extracellular matrix proteins) has also been implicated as a possible mechanism for the scarring process in PD (Jordan & McCammon, 2012).
Most patients with PD, however, do not give a history of sexual trauma. Thus, although trauma may be involved, it appears that patients must also have an inherited predisposition for the disease (Hinman, 1980).