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Cutaneous wound healing in adults often leads to scarring and involves 3 major phases: 1) inflammation, 2) tissue formation, and 3) tissue remodeling. At the end of the inflammation phase of wound healing, fibroblasts and endothelial cells become some of the main protagonists of the tissue formation phase. Remodeling of the extracellular matrix (ECM) within the normal scar starts early after wounding and continues for many months until the scar takes its final shape and composition. Hypertrophic scars and keloids fail to progress through the normal and balanced stages of wound healing, demonstrating aberrant cellular responses and ECM deposition. Physiologic scarring results in the re-establishment of barrier function and local homeostasis; however, deleterious effects on sensory function, movement, adnexal function, and cosmesis result. Although multiple growth factors and cytokines are involved in wound healing and scarring, transforming growth factor beta (TGF-β) deserves special attention. The overwhelming imbalance and aberrance of growth factor and cytokine profiles ultimately result in excess collagen and cellular products. Wounds in locations of high tension such as the central chest have a higher risk of developing hypertrophic scars and keloids. The pathogenesis of atrophic scars has not been well studied, although it is presumed that destruction of collagen occurs resulting in dermal atrophy.


Loss of function of the cutaneous surface, such as barrier protection, homeostasis, or sensation due to injury, can result in disability or death. Disruption of these functions may lead to debilitating loss of perception of cues critical for interaction with the surrounding environment, inability to maintain fluid and electrolyte balances as well as temperature control, or deadly infections. Given the crucial functions of skin for survival, rapid repair to maintain homeostasis and limit immediate local disability after injury is of paramount importance. Thus, physiologic wound healing and ensuing normal scarring are essential for survival. It is estimated that approximately 100 million people acquire a scar per year.1 Scars may result from surgery, trauma, burns, or infections. The wound-healing process is a well-orchestrated, fast-acting mechanism of repair that initially aims to restore homeostasis and later attempts to optimize function by remodeling. Whereas homeostatic balance and protective barrier functions may be quickly restored by scarring fibrosis, many other functions are often permanently compromised, with loss of the normal adnexal structures such as nerves, sweat apparatus, and hair follicles. Fibrosis may also result in contractures that can limit skeletal movement and compromise function beyond the skin. Cosmesis is negatively affected with loss of contour, change in skin surface properties such as pliability, and asymmetry and deformities. Whereas the desired physiologic scars result in minor alterations in skin properties, pathologic scarring leads to hypertrophy, hypertrophy with contracture, keloids, or atrophy. As our understanding of wound-healing mechanisms grows, manipulation of this system at the molecular, cellular, and tissue levels may help in preventing unwanted or pathologic scarring while maintaining adequate repair. The current chapter will review the process of ...

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