Adipokines Elicit Dose-Dependent Catabolic Responses in Cartilage and Meniscus Tissues

INTRODUCTION: The causal association between obesity and osteoarthritis (OA) has long been hypothesized to be predominantly due to biomechanical overload. However, adipose tissue produces biologically active factors known as adipokines that have been implicated in numerous inflammatory disorders, including rheumatoid arthritis [1]. Elevated levels of the adipokines adiponectin, resistin, leptin, and visfatin in both the serum and synovial fluid are associated with increased progression or severity of arthritis [2]. In vitro studies have demonstrated that each of these adipokines can induce chondrocyte expression of MMPs and pro-inflammatory markers [3, 4]. However, the role of adipokines in OA is still poorly understood and little is known on how they affect different articular joint tissues. The aim of this study was to determine if cartilage or meniscal tissue explants had catabolic responses to adiponectin, leptin, resistin, or visfatin.