Abstract
uman osteoarthritis (OA) is a heterogeneous andmultifactorialdiseasewithmultiplepathogeneticmech-anism implicated in its development and progression. Carti-lage degradation and loss are the major features of OA; de-generative changes include fibrillation, chondrocyteproliferation into cell clusters, and matrix disruption. Al-though biomechanical factors are strongly implicated, it isunclear which stimuli regulate the hyperactive phenotype ofOAchondrocytes,includingtheirabilitytoexpresscartilage-degradingproteinases(1).Recentstudieshaveimplicatedtheupregulation of several matrix-degrading metalloproteinases(MMPs)inOAcartilageandhavesuggestedthatchondrocyteproduction of MMPs in OA cartilage reflects local synthesisthat varies with the extent of cartilage degeneration. Thedemonstration of chondrocytes producing interleukin-1and tumor necrosis factor Theseverityofcartilagelesionshasbeenassessedusinganwithin the superficial zones ofOA cartilage supports the concept that cytokine-MMP asso-ciations contribute to a highly catabolic state, chondrocyteapoptosis, and the resultant progressive degeneration of ar-ticular cartilage (2-6).
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