PubMed1997
PURPOSE: The understanding of the mechanism of how the plaque in Peyronie's disease causes functional distortions is presented in terms of scar formation and maturation. The repair process is important for survival. The expected biological response to tissue loss and disruption is scarring but in some situations, such as Peyronie's disease, the resultant scar creates major problems. MATERIALS AND METHODS: The development of scar involves the deposition of connective tissue which histologically can be studied in patients and in animal models as well as with in vitro models. Abnormal scarring can involve excessive connective tissue deposition. Clinically examples of excess scarring are hypertrophic scars common in healed burn patients and keloid scars seen in patients with this inherited defect in healing. In addition to excessive connective tissue deposition, another aspect of abnormal scarring is scar contracture, when the compaction of the scar tissue distorts the anatomical appearance and functional capacity of adjacent tissues and organs. The fibroblast populated collagen lattice model demonstrates the organization of connective tissue in a controlled environment and the information gained can be related to scarring. RESULTS: The compaction of scar tissue involves the reorganization of collagen fibers by resident fibroblasts using cell tractional forces rather than cell contraction forces. These findings were documented with the fibroblast populated collagen lattice model. In Peyronie's disease the distortion caused by the scar or plaque is neither related to scar contracture nor active compaction of scar tissue but, rather, the expansion of the surrounding unscarred tissue and the inflexibility of the scar tissue composing the plaque. CONCLUSIONS: Peyronie's disease plaques are rigid structures due to the organization of the deposited collagen fibers. Those fibers are independent in their connective tissue organization, which makes the plaque incompatable with adjacent structures.