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| AuthorsRobert P Sheon, MDBruce C Anderson, MD | Section EditorZacharia Isaac, MD | Deputy EditorPaul L Romain, MD |
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Dupuytren's contracture is a relatively common disorder characterized by progressive fibrosis of the palmar fascia [1]. Initial tendon thickening is painless and often goes unnoticed and undiagnosed. Joint stiffness and a loss of full extension develop insidiously over decades. As the scarring process progresses, nodules form on the palmar fascia and the finger gradually loses its flexibility, with contractures that draw one or more fingers into flexion at the metacarpophalangeal (MP) joint (picture 1) [2].
The cause of Dupuytren's contracture is unknown. The presence of CD3-positive lymphocytes and the expression of MHC class II proteins suggest the possibility of a T-cell mediated autoimmune disorder [3]. It occurs primarily in white males over the age of 50 and appears to have a pronounced genetic predisposition: 68 percent of male relatives of affected patients develop the disease at some time.
Pathologically, Dupuytren's contracture is characterized by fibroblastic proliferation and disorderly collagen deposition with fascial thickening. Nodules form due to contraction of fibroblasts in the superficial palmar fascia. Smooth muscle fibroblasts and myofibroblasts are present in the nodules; increased concentrations of prostaglandins are also found within the nodules and may influence myofibroblast contractility [4]. The flexor tendons are not intrinsically involved, but invasion of the dermis occurs and results in characteristic puckering and tethering of the skin.
Dupuytren's contracture has been observed in association with the following conditions and habits [5-12]:
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