Scarless Wound Healing

Abstract

This chapter provides an introduction to the mechanism of adult wound healing and scar formation and also highlights regenerative healing and scar reduction theory. Adult wound healing is described as a sequence of temporally overlapping phases that include inflammation, proliferation, and remodeling. Disruption of the vascular network within cutaneous wounds results in platelet aggregation and the formation of a fibrin-rich clot, which protects from further extravasation of blood or plasma. The presence of macrophages in the wound marks the transition between the inflammatory phase and the proliferative phase of wound healing, which begins around day four to five post-injury in uninfected open wounds. Granulation tissue begins to form and is a loose network of collagen, fibronectin, and hyaluronic acid, embedding a dense population of macrophages, fibroblasts, and neovasculature. Corticosteroids are used commonly to treat symptomatic scars, and triamcinolone is the most common agent used. The mechanism of action is multifactorial. The inflammatory response is globally decreased, which secondarily decreases collagen synthesis and increases collagen degradation. Corticosteroids also inhibit fibroblast proliferation and TGF-β1 and TGF-β2 expression by keratinocytes. 5-FU has shown significant efficacy in combination with corticosteroids alone or with corticosteroids and laser therapy. The mechanism of action occurs primarily through inhibition of fibroblast proliferation and TGF-β1-induced collagen synthesis. Imiquimod 5% cream is a topical agent that enhances local production of immune-stimulating cytokines, such as tumor necrosis factor, interleukins, and interferons.