AbstractWound contraction is a basic mechanism for wound closure that can be lifesaving. Yet, wound contraction can also produce considerable deformity and misery in conditions as diverse as burn scar contracture, cirrhosis, Dupuytren's contracture, and contracture around silicone tissue implants. Current evidence suggests that wound contraction is a cellular function of contractile fibroblasts (myofibroblasts). These cells share the electron microscopic appearance of both fibroblasts and smooth muscle cells. Pharmacologically and immunologically, myofibroblasts have many characteristics of smooth muscle cells. Active wound contraction caused by myofibroblasts can lead to fixed, rigid scar contracture. Contracture associated with poor joint positioning can also occur passively due to collagen reorganization alone, without myofibroblast involvement.Control of contraction (and contracture) can be achieved theoretically by 3 modes of therapy. Physical means, including range of motion exercises, splinting, and full thickness skin grafting after surgical release, are used currently. Biochemical control of myofibroblast contraction by agents that affect tissue‐cultured fibroblasts has the potential of reducing wound contraction. Inhibition of collagen synthesis, inhibition of cross‐linking, or increased collagenolysis may eventually be clinically useful, and would be of value in controlling both contracture due to active wound contraction, and contracture due to passive positioning.