The article reviews the cellular mechanisms of wound contraction, focusing on the roles of fibroblasts and myofibroblasts. It begins by describing historical cases of wound contraction, such as the use of hot needles to treat shoulder dislocations in ancient Greek medicine. The process of wound closure involves epithelization, connective tissue deposition, and contraction, with each step contributing differently to the healing process. In mammals with loose skin, wound contraction leads to minimal scarring and loss of function, while in humans, it can result in significant cosmetic scarring or joint motion loss. The article then delves into the role of fibroblasts in wound contraction. Fibroblasts, which are typically quiescent, become activated after wounding, migrate to the wound site, proliferate, and synthesize a new collagen matrix called granulation tissue. Myofibroblasts, derived from fibroblasts, are responsible for force generation during contraction and exhibit features similar to smooth muscle cells. The transition from fibroblasts to myofibroblasts occurs as the wound contracts and resistance increases. In vitro models of wound contraction using fibroblasts cultured in collagen or fibrin matrices have been developed. These models show that fibroblasts in floating collagen matrices acquire tissue-like characteristics, while those in anchored matrices develop into myofibroblasts. The contraction of floating collagen matrices results in a mechanically relaxed tissue, while the contraction of anchored matrices leads to a stressed tissue. The article also discusses the role of growth factors, such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF), in regulating matrix contraction. TGF-β stimulates both floating and anchored collagen matrix contraction and promotes fibroblast differentiation into myofibroblasts. PDGF stimulates matrix contraction independently of TGF-β. Finally, the article explores the concept of stress relaxation, which represents the transition from granulation tissue to dermis or scar. This process involves a smooth muscle-like contraction and is regulated by serum factors and thrombin. The article concludes by discussing the implications of these findings for understanding wound healing and the role of mechanical forces in the process.The article reviews the cellular mechanisms of wound contraction, focusing on the roles of fibroblasts and myofibroblasts. It begins by describing historical cases of wound contraction, such as the use of hot needles to treat shoulder dislocations in ancient Greek medicine. The process of wound closure involves epithelization, connective tissue deposition, and contraction, with each step contributing differently to the healing process. In mammals with loose skin, wound contraction leads to minimal scarring and loss of function, while in humans, it can result in significant cosmetic scarring or joint motion loss. The article then delves into the role of fibroblasts in wound contraction. Fibroblasts, which are typically quiescent, become activated after wounding, migrate to the wound site, proliferate, and synthesize a new collagen matrix called granulation tissue. Myofibroblasts, derived from fibroblasts, are responsible for force generation during contraction and exhibit features similar to smooth muscle cells. The transition from fibroblasts to myofibroblasts occurs as the wound contracts and resistance increases. In vitro models of wound contraction using fibroblasts cultured in collagen or fibrin matrices have been developed. These models show that fibroblasts in floating collagen matrices acquire tissue-like characteristics, while those in anchored matrices develop into myofibroblasts. The contraction of floating collagen matrices results in a mechanically relaxed tissue, while the contraction of anchored matrices leads to a stressed tissue. The article also discusses the role of growth factors, such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF), in regulating matrix contraction. TGF-β stimulates both floating and anchored collagen matrix contraction and promotes fibroblast differentiation into myofibroblasts. PDGF stimulates matrix contraction independently of TGF-β. Finally, the article explores the concept of stress relaxation, which represents the transition from granulation tissue to dermis or scar. This process involves a smooth muscle-like contraction and is regulated by serum factors and thrombin. The article concludes by discussing the implications of these findings for understanding wound healing and the role of mechanical forces in the process.