Pathophysiology and Treatment of Fibroproliferative Disorders following Thermal Injury

Keloids and hypertrophic scars (HSc) are unique human dermal fibroproliferative disorders (FPD) that occur following trauma, inflammation, surgery, and burns, or possibly spontaneously.1 Keloids occur in individuals with a familial predisposition, enlarge and extend beyond the margins of the original wounds, and rarely regress. HSc are raised, erythematous, pruritic, fibrous lesions that typically remain within the confines of the original wound, usually undergo at least partial spontaneous resolution over widely varying time courses, and are often associated with contractures of the healing tissues. The development of contractures is by definition the pathologic shortening of scar tissue resulting in deformities, as opposed to wound contraction which occurs in an open wound, with the positive outcome of reducing the wound surface area. These disorders represent aberrations in the fundamental processes of wound healing, which include cell migration and proliferation, inflammation, increased synthesis and secretion of cytokines and extracellular matrix (ECM) proteins, and finally remodeling of the newly synthesized matrix. Conceptually, it is the goal of individuals caring for wounds to facilitate regeneration of the injured skin and associated structures (FIGURE 1); however, at present, adult mammalian healing occurs by the formation of scar, characterized by a disordered architecture, which in the case of HSc and keloids is also associated with excessive deposition of ECM proteins.