aNew York University Hospital for Joint Diseases Orthopaedics Institute, The New York University School of Medicine, 301 East 17th Street, New York, NY 10003, USA bDepartment of Orthopaedic Surgery, The Mount Sinai School of Medicine, 5 East 98th Street, Box 1188, New York, NY 10029, USA
Motion-limiting arthrofibrosis has been described in numerous joints, including the knee [1-4], ankle [5,6], shoulder [7-10], and elbow [11,12]. Clinically, arthrofibrosis is characterized by limited joint motion and pain . Although less well described, arthrofibrosis also occurs in the wrist joint [14,15]. The normal range of motion of the wrist is 70 degrees of extension and 80 degrees of flexion, 30 degrees of ulnar and 20 degrees of radial deviation, 80 degrees of pronation and 80 degrees of supination . However, less than half of total wrist motion permits almost all of functional range of motion. Palmer and associates  determined that functional ranges of wrist motion for most activities of daily living are 5 degrees of flexion, 30 degrees of extension, 10 degrees of radial deviation, and 15 degrees of ulnar deviation, and Morrey and associates  determined that forearm rotation of 50 degrees of supination and 50 degrees of pronation was necessary for most activities. More recent studies have reported that most activities could be performed with 40 degrees of wrist flexion and extension, 10 degrees radial deviation, and 30 degrees ulnar deviation [19,20]. Arthrofibrosis is characterized by pain and
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E-mail address: [email protected] (S.K. Lee).
limitation of motion beyond that required for most daily activities, as defined above.
Stiffness and decreased range of motion are common following trauma or surgery to the wrist. This usually resolves with physiotherapy. Arthro-fibrosis is defined as pain and stiffness that does not allow functional range of motion and is due to adhesions or contracture of the joint. The etiology of contracture of a joint can be classified into either intraarticular or extraarticular . Arthrofibrosis is due to an excessive fibrotic response during the repair process, which leads to fibrotic tissue deposition, within or around the joint, and progressive loss of motion of the joint .
The mechanism is initiated by an excessive synovial inflammatory response with activation and proliferation of fibroblast cells and a significant increase in the deposition of extracellular matrix proteins [23,24]. It is believed that the pathophysiology first involves inflammation of the synovium, then subsynovial fibrosis, leading to capsular thickening, and ultimately contracture of the affected joint [9,23-26].
Although the etiology is still unknown, there are alterations of the extracellular matrix with an increase of collagen type VI expression similar to other local or systemic fibrotic disorders . A chronic inflammatory process may play a crucial role in the mechanism of primary arthrofibrosis, and may indicate an immune response . Association with human leukocyte antigens and dysregu-lation of cytokine release have been demonstrated to be involved in its pathogenesis [29-32].
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