Leptin in osteoarthritis: Focus on articular cartilage and chondrocytes

Abstract

Osteoarthritis (OA) is a complex joint disorder with a number of underlying physical, biochemical, biomechanical and genetic causes. Obesity is considered to be one of the major risk factors for the development and progression of OA. It actively contributes to the inflammatory status and to cartilage degradation in the OA joints. Recent data suggests that metabolic factors produced by white adipose tissue, such as leptin, may provide a mechanistic link between obesity and OA, providing an explanation for the high prevalence of OA among obese and over-weight individuals. The unbalanced production of catabolic and anabolic mediators by chondrocytes, the only cell type present in cartilage, determines cartilage degradation, which is the central pathological feature of OA. Evidence is accumulating to support a key role for leptin in the pathogenesis and/or progression of OA. The goal of this focused review is to summarize the current knowledge on the role of leptin in OA with particular emphasis on the effects of this adipokine in cartilage and chondrocyte pathophysiology.