Search

Osteoarthritis (OA) is a highly prevalent debilitating and painful pathology derived from progressive degeneration of articular joints. Obesity has long been recognized as a significant and potentially preventable risk factor for OA incidence, progression, and disability. Biomechanical loading, together with metabolic and inflammatory imbalances of the joint, strongly contributes to obesity-induced OA pathophysiology. Adipose-tissue derived cytokines—adipokines—have demonstrated roles in modulating pro/anti-inflammatory and anabolic/catabolic joint balance, with implications in cartilage and bone homeostasis. Mechanical stress may lead to considerable increases in proinflammatory mediators within the joint. Therefore, adipokines emerged as potential candidates to link mechanical, metabolic and inflammatory components of obesity-induced osteoarthritis. Herein we summarize the biology of adipokines in joint tissues, highlighting their implications in the dysregulation of joint homeostasis and, thus OA pathogenesis. Many of the aspects of the adipokine network remain largely unknown and further insights into the intimate mechanisms of adipokines activity will be of great relevance to develop disease-modifying osteoarthritis drugs, especially for obese patients.