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Osteoarthritis (OA) is the most common form of arthritis and a major cause of pain and disability in elders. It is characterised by cartilage loss and structural changes in the whole joint. Although some mechanisms involved in the pathogenesis of OA are more and more understood, several factors involved in the onset and progression of the disease remain elusive. Together with aging and genetic factors, obesity is an important risk factor for OA.1 Recent data suggest a clear role of systemic inflammatory mediators, produced by fat mass, called adipokines, in OA.2–⇓4 Actually, experimental evidences confirm the critical role of adipokines with an emphasis on old members, such as leptin and visfatin,3–⇓5 but also on new members such as chemerin.2
To this regard, several lines of evidence indicate that these factors exert pro-inflammatory and pro-catabolic actions at cartilage level.2 ,4 ,5 For instance, leptin, chemerin and visfatin trigger the expression of nitric oxide, MMPs and PGE2 in chondrocytes.2 ,4 ,5
Leptin, chemerin and visfatin have been detected in synovial fluid obtained from OA patients.6–⇓8 …
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