Changes in articular cartilage after meniscectomy.
Hitherto, the meniscus has been regarded as a developmental remnant. However, when removed in part or in total, it alters the normal biomechanical, biochemical, and physiologic processes of the knee joint. Although the pathogenesis of osteoarthritis (OA) is unknown, accelerated rates of normal metabolism may result in failure of the articular cartilage to maintain its mechanical integrity as a result of meniscectomy. In addition, an inflammatory state within the joint cavity may result in degenerative changes, due to a perturbation of the homeostatic anabolic and catabolic processes maintaining the knee joint. Animal models reliably reproduce the focal and relatively slow degeneration seen in humans. OA degeneration after meniscectomy has been described histologically with fibrillation, swelling, fissures, cell proliferation, clustering, cell nesting, and even necrosis. Biochemical changes, however, include proteoglycan loss, proteoglycan disaggregation, and an increase in proteoglycan synthesis. In addition to increased hydration, the main structural fibers of articular cartilage, composed of Type II collagen, are exposed to increased biomechanical forces. The minor collagens, e.g., Type IX collagen, may play a role in stabilizing the proteoglycan-Type II interaction, thus providing mechanical integrity. It appears that meniscectomy produces much more than wear-and-tear arthritis.
Department of Orthopaedics, University of Washington, Seattle 98195.
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Komenda
D000818:Animals; D001696:Biomechanical Phenomena; D002358:Cartilage, Articular / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D008592:Menisci, Tibial / Q000601:surgery*; D010003:Osteoarthritis / Q000378:metabolism; D011183:Postoperative Complications / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism
D011509:Proteoglycans; D003094:Collagen