Osteoarthritis and nitric oxide.
Osteoarthritis (OA) is caused by both biochemical and mechanical factors. While the mechanisms that underlie the disease are not completely understood, investigators have characterized a number of catabolic and protective factors that have a role in the disease process. Nitric oxide (NO) and its redox derivatives appear to have a number of different functions in both normal and pathophysiological joint conditions. Until recently, NO was considered a catabolic factor that was responsible for perpetuating the OA disease process by mediating the expression of proinflammatory cytokines, inhibiting the synthesis of collagen and proteoglycans and inducing apoptosis. However, recent studies suggest that NO and its redox derivatives may also have protective effects on cartilage. This review will summarize the literature on the effects of NO on cartilage and chondrocytes as well as discuss some evidence that suggests potential protective effects of NO and/or its derivatives on other cell types. More research is needed to elucidate the role of NO and its derivatives on both normal and osteoarthritis cartilage.
Abramson
Steven B
SB
Division of Rheumatology, Faculty and Academic Affairs, New York University Medical Center School of Medicine and Hospitals Center, NYU Hospital for Joint Diseases, New York, NY, USA. stevenbabramson@nyumc.org
D000818:Animals; D017209:Apoptosis; D002358:Cartilage, Articular / Q000378:metabolism / Q000473:pathology; D019902:Chondrocytes / Q000378:metabolism / Q000473:pathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II / Q000502:physiology; D010003:Osteoarthritis / Q000473:pathology / Q000503:physiopathology*; D010084:Oxidation-Reduction
D018836:Inflammation Mediators; D016328:NF-kappa B; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II