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The fibroblast is one of the most abundant cell types present in the stroma. It has a variety of functions and composes the basic framework for tissues and organs. Under homeostasis, this cell is responsible for maintaining the extracellular matrix (ECM). During stress, fibroblasts adapt to their environment and have the ability to respond and send local signals. In times of injury, the fibroblast can transform phenotypes and synthesize the building blocks necessary to replace wounded tissue. During pathologic states, the extracellular matrix gets generated in excessive quantities, and collagen is deposited in a dysregulated manner often causing irreversible organ dysfunction or disfiguring appearance.

Persistence of myofibroblasts within scar tissue contributes to hypertrophic scars, keloids, and fibromatoses (Dupuytren contracture). Myofibroblasts usually disappear via apoptosis during the second week of wound healing. The failure of myofibroblast apoptosis allows for excessive matrix synthesis and contraction of normal tissue. Hypertrophic scarring, keloids, and non-healing wounds represent a pathologic healing mechanism. Delayed apoptosis results in scar hypertrophy. Hypertrophic scars are elevated, do not grow past wound boundaries, and can slowly regress over time. Keloid scars have continued growth past wound edges and expand over time.[10] Fibroblasts within keloids are an atypical subtype that is increasingly proliferative and activates surrounding fibroblasts. Comparatively, chronic non-healing wounds contain fibroblasts that have stopped proliferating or have undergone premature apoptosis with abnormal cytokine signaling.[2] Dupuytren contracture is a hand deformity that slowly forces fingers into a bent position. Due to an unknown etiology, proliferation of fibroblasts arranged in cords, nodules of myofibroblasts, and disordered collagen deposition causes disfiguration of the hand. Fibroblasts propagate this condition generating profibrotic cytokines in a prolonged manner subsequently leading to myofibroblast activation and continuous cytokine production. The pathophysiology of connective tissue contracture lies not only within the tension produced by myofibroblasts by also by the dynamic shortening of the ECM remodeling itself.[11][5][12]