Proposal: trauma as the cause of the Peyronie's lesion

• Published in: The Journal of urology Vol. 157; no. 1; p. 285
• Main Authors: Devine, Jr, C J, Somers, K D, Jordan, S G, Schlossberg, S M
• Format: Journal Article
• Language: English
• Published: United States 01-01-1997
• Subjects: Cumulative Trauma Disorders - complications; Humans; Male; Microcirculation; Penile Induration - etiology; Penile Induration - pathology; Penis - blood supply; Penis - injuries
• ISSN: 0022-5347
• DOI: 10.1016/s0022-5347(01)65361-8

We define the cause of the occurrence of Peyronie's disease.
Clinical evaluation of a large number of patients with Peyronie's disease, while taking into account the pathological and biochemical findings of the penis in patients who have been treated by surgery, has led to an understanding of the relationship of the anatomical structure of the penis to its rigidity during erection, and how the effect of the stress imposed upon those structures during intercourse is modified by the loss of compliance resulting from aging of the collagen composing those structures. Peyronie's disease occurs most frequently in middle-aged men, less frequently in older men and infrequently in younger men who have more elastic tissues. During erection, when full tumescence has occurred and the elastic tissues of the penis have reached the limit of their compliance, the strands of the septum give vertical rigidity to the penis. Bending the erect penis out of column stresses the attachment of the septal strands to the tunica albuginea.
Plaques of Peyronie's disease are found where the strands of the septum are attached in the dorsal or ventral aspect of the penis. The pathological scar in the tunica albuginea of the corpora cavernosa in Peyronie's disease is characterized by excessive collagen accumulation, fibrin deposition and disordered elastic fibers in the plaque.
We suggest that Peyronie's disease results from repetitive microvascular injury, with fibrin deposition and trapping in the tissue space that is not adequately cleared during the normal remodeling and repair of the tear in the tunica. Fibroblast activation and proliferation, enhanced vessel permeability and generation of chemotactic factors for leukocytes are stimulated by fibrin deposited in the normal process of wound healing. However, in Peyronie's disease the lesion fails to resolve either due to an inability to clear the original stimulus or due to further deposition of fibrin subsequent to repeated trauma. Collagen is also trapped and pathological fibrosis ensues.