• Bernard Terlain, Nathalie Presle, Pascale Pottie, Didier Mainard, and Patrick Netter.
• Physiopathologie et pharmacologie articulaires, Faculté de médecine, avenue de la forêt de Haye, BP 184, 54505, Vandceuvre les Nancy.
• B Acad Nat Med Paris. 2006 Oct 1; 190 (7): 142114771421-35; discussion 1435-7, 1475-7.

AbstractIn addition to aging, obesity is one of the most common underlying causes of osteoarthritis (OA). Mechanical loading, together with biochemical and systemic factors linked to altered lipid metabolism, are thought to contribute to the onset of OA. It has been suggested that OA is a systemic metabolic disease associated with lipid disorders affecting joint homeostasis. These gradual changes may be due to the local effect of adipokines, and especially leptin. Indeed, their relative levels in joints differ from that found in plasma. In particular, leptin levels are increased and adiponectin and resistin levels are reduced This hypothesis is supported by--leptin overexpression in OA cartilage and its correlation with the degree of cartilage destruction,--abundant leptin synthesis by osteophytes, and--the high leptin levels found in OA joints from female patients. This link between OA and adipokines provides new leads regarding the prevention of OA and the identification of new drug targets.

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