Human osteoarthritis (OA) is a heterogeneous and multifactorial disease with multiple pathogenetic mechanism implicated in its development and progression. Cartilage degradation and loss are the major features of OA; degenerative changes include fibrillation, chondrocyte proliferation into cell clusters, and matrix disruption. Although biomechanical factors are strongly implicated, it is unclear which stimuli regulate the hyperactive phenotype of OA chondrocytes, including their ability to express cartilage degrading proteinases. Recent studies have implicated the upregulation of several matrix-degrading metalloproteinases (MMPs) in OA cartilage and have suggested that chondrocyte production of MMPs in OA cartilage reflects local synthesis that varies with the extent of cartilage degeneration. The demonstration of chondrocytes producing interleukin-1 and tumor necrosis factor within the superficial zones of OA cartilage supports the concept that cytokine-MMP associations contribute to a highly catabolic state, chondrocyte apoptosis, and the resultant progressive degeneration of articular cartilage.
Surgical approaches in osteoarthritis: role of arthroscopy / Frizziero, L; Reta, M; Rizzuti, F; Zizzi, F; Frizziero, A; Facchini, A. - In: SEMINARS IN ARTHRITIS AND RHEUMATISM. - ISSN 0049-0172. - 34:6(2005), pp. 53-57.
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