One example of active contracture is the end result of scar contraction. With one notable exception, scar contraction follows all injuries exceeding a certain threshold of tissue damage (mechanical, burn, radiation, infection, ischemia, or chemical) or in response to spontaneous healing of an open wound. Scar contracture is initiated by cytokines released by cell death and matrix disruption. Products of matrix degradation such as collagen fragments promote myofibroblast differentiation, and tissue stress provokes myofibroblast differentiation and contraction. A full thickness open wound lacks the normal stress shielding of intact dermis, resulting in a uniquely powerful stimulus to myofibroblast differentiation and contraction through a variety of mechanisms, including cell-matrix mechanotransduction, tension-related conformational changes in TGF-β, and others (Hinz 2007; Klingberg et al. 2014). Under maximum stimulation, myofibroblast matrix shortening of an open wound continuously advances the wound edge with velocity as great as one centimeter per month (Castella et al. 2010). Active contraction biology of an open wound continues until the wound is closed, tissue breakdown products are cleared, and matrix tension stabilizes. Although contraction is a cellular process, the matrix plays an important role, as suggested by the fact that freeze injuries, which kill cells with little or no matrix damage, do not contract unless complicated by infection or other injury (Ehrlich and Hembry 1984). Active scar contracture changes the posture or geometry of adjacent tissues.

For comparison, an example of passive contracture is post-immobilization proximal interphalangeal joint stiffness in the absence of trauma. In full extension, normal tendons and ligaments of the finger proximal interphalangeal (PIP) joints are at full length. PIP immobilization in extension may cause joint stiffness but rarely results in contracture. Stiffness is due to binding of gliding surfaces due to loss of normal synovial fluid movement, but the dimensions of the tendons and ligaments are unchanged. After PIP immobilization in extension, recovery of full range of motion is typical. PIP immobilization in flexion is different. The palmar PIP ligament complex and cruciate pulley segments of the flexor tendon sheath are lax in flexion. During prolonged immobilization in flexion, these areas undergo tissue remodeling which removes this position-related palmar slack. Following immobilization in PIP flexion, these structural changes persist, which can produce permanent flexion contracture. This is a common secondary effect of Dupuytren contracture, persisting after release or removal of shortened Dupuytren tissue. Immobilization contracture maintains the slack posture or geometry of adjacent tissues.

Three clinical observations provide evidence for passive contracture in Dupuytren contracture.