INTRODUCTION, ETIOLOGY, AND DEFINITIONS
The integument system, also known as the human skin, is a vast organ of protection. It is the barrier that provides bodily defense between the internal and external environment. The skin's chief functions are to prevent invasion of pathogenic organisms and to keep a harmonious balance between the inside and outside of the body. When the skin is injured, it can repair itself via the mechanism called wound healing.
The normal wound-healing process can be divided into three principal stages (1) the inflammatory phase, (2) the proliferative phase, and (3) the maturation (or remodeling) phase. The inflammatory phase starts immediately at the time of injury with activation of the clotting cascade and release of certain cytokines. The release of chemotactic factors such as platelet-derived growth factor (PDGF, the major factor released by platelets during thrombus formation), prostaglandins, complement factors, and interleukins (e.g., IL-1) stimulates the migration of inflammatory cells such as neutrophils and monocytes/macrophages. The recruitment and involvement of inflammatory cells help to remove debris including bacteria and release specific growth factors. Macrophages play a role in secreting many cytokines, particularly transforming growth factors (TGF-β) and IL-6.1 These specific cytokines initiate the formation of granulation tissue, proliferation of keratinocytes, fibroblast production, and an increase in endothelial cells in the proliferative phage. This increase in cell production and migration begins approximately 4 days after initial tissue injury. Fibroblasts play a major role in the formation of provisional matrix that is composed of collagen I, collagen III, fibronectin, elastin, and proteoglycans. The keratinocytes start the epithelialization process with reconstruction of the disrupted basement membrane zone. During the maturation phase, the collagen network and proteoglycans are also remodeled. Both collagen types I and III increase during the beginning of the wound-healing process. However, when remodeling takes place, the proportion of collagen type III to collagen type I is decreased and collagen fibers are cross-linked and oriented in a more parallel arrangement, toward the direction of mechanical stress.2
Hypertrophic scars and keloids are believed to be an abnormal response during the aforementioned wound-healing process.3 Hypertrophic scars and keloids can occur in all races, but they occur much more frequently in ethnic skin, ranging from 3 to 18 times higher incidence, compared with Caucasians.4-6 The incidence has been reported to be between 4.5% and 16% in African Americans, the Chinese, and Hispanics. Patients in their second to third decade of life are more commonly affected with the same prevalence in both sexes.
There are many predisposing factors that influence the formation of hypertrophic scars and keloids, such as disruption in the integrity of the skin, location on the body, race, and genetic background.7,8 Common causes include surgery, ear piercing, tattoos, infection, vaccination, burns, and inflammatory acne. Locations that are especially prone are the jaw line, upper chest, and upper back; some patients report spontaneous scars and keloids ...