RT Book, Section A1 Moioli, Eduardo K. A1 Bolotin, Diana A2 Alam, Murad A2 Dover, Jeffrey S. A2 Waibel, Jill S. A2 Arndt, Kenneth A. A2 Kim, John Y. S. A2 Thomas, J. Regan A2 Gaball, Curtis W. A2 Chan, Rodney K. SR Print(0) ID 1176876471 T1 Basic Science of Scars T2 Treatment of Scars From Burns and Trauma YR 2021 FD 2021 PB McGraw Hill PP New York, NY SN 9780071839914 LK dermatology.mhmedical.com/content.aspx?aid=1176876471 RD 2023/06/10 AB 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.