INTRODUCTION
Scarring or scar formation is the body’s natural healing response to reestablish dermal integrity following an injury. Scars, however, are structurally different and can be functionally deficient and cosmetically less appealing than normal human skin. Pathologically, a spectrum of scars is recognized from thin almost invisible scars to stretched, depressed, and/ or contracted scars to hypertrophic and keloid scars, depending on whether or not the wound healing process was regulated correctly. Scars may also be associated with a spectrum of symptoms ranging from inflammation, erythema, dryness, and pruritus to no symptoms. Excessive scarring can cause significant cosmetic, functional, and psychological problems.1 Over the past 2 decades, research efforts have been channeled into understanding the pathophysiology of the wound healing process as well as in developing treatments for the management and prevention of scars. Consequently, a variety of treatments are currently available. While variety provides the clinician as well as the patient with choices, it also creates confusion as to how to select the most appropriate treatment for a particular type of scar.
Pathophysiology of Wound Healing
Wound healing is a complex, organized, coordinated process, which in the short-term aims to prevent infection and reestablish skin integrity and in the long-term aims to remodel and strengthen the newly formed tissue. Accordingly, wound healing may be regarded as consisting of three main stages—inflammatory, proliferative, and remodeling or maturation—that are not mutually exclusive (reviewed in Clark; Slemp et al; Eming et al; Hantash et al; Berman et al).2-6 Inflammatory PhaseThe inflammatory phase is initiated immediately following skin injury and lasts for 48 to 72 hours. It is a highly regulated process involving the nervous system, several cell types (keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets), and a network of signaling molecules (cytokines, chemokines, and growth factors) that reach the wound through vasodilation and increased blood ow to the site of injury. Clinically the inflammatory phase manifests with erythema, heat, swelling, and pain. The release of the proinflammatory cytokine interleukin-1 (IL-1) alerts surrounding cells of tissue injury and begins the reparative process. Hemorrhage from tissue damage releases blood components into the wound that activate the clotting cascade. Temporary blanching (vasoconstriction) of the wound occurs that lasts for approximately 10-15 minutes. Vasoconstriction is mediated by prostaglandins, serotonin, thromboxanes, circulating epinephrine, and norepinephrine and serves to reduce hemorrhage immediately following injury. Platelets attach and aggregate to the exposed subendothelium leading to clot formation (primary plug formation). The clot stops the bleeding, stabilizes the wound, and provides a matrix for the in ux of inflammatory cells, platelets, and plasma proteins. Platelet aggregation also activates the platelets. Activated platelets degranulate, releasing growth factors (epidermal growth factor [EGF]), platelet-derived growth factor [PDGF], and transforming growth factor-beta [TGF-β]), vasoactive agents, and proteases. Thrombin activation by the coagulation cascade results in the migration of inlammatory cells to the site of tissue injury. Mast cells produce histamine and leukotrienes, which stimulate vasodilation. Capillary vasodilation results in extravasation of serum proteins into the wound site. Polymorphonuclear (PMN) cells (neutrophils, eosinophils, and basophils) are the first inflammatory cells to arrive at the wound site. PDGF, IL-1, IL-8, and growth related oncogene play a role in attracting the PMN
