Synovium in the pathophysiology of osteoarthritis

Osteoarthritis Osteoarthritis (OA) is the most common form of arthritis and is among the most prevalent chronic human health disorders in an aging population. It is estimated that over 50% of people aged 65 years and older show radiological signs of OA [1]. This disease mostly affects the hands, hips, knees and spine. The risk factors associated with OA pathophysiology include development-, metabolic(e.g., obesity), trauma-, age-, sexand geneticrelated triggers, which cause a cascade of events that result in the degradation of joint tissues [2]. The most common characteristics of OA include degradation of articular cartilage, osteophyte formation, meniscal degeneration, subchondral bone sclerosis, bone marrow lesions, synovial inflammation and proliferation. OA, previously believed to be a disease of cartilage, is now considered to be a disease of the whole joint, comprised of cartilage, bone and synovium [3]. While the majority of OA research is still focused on cartilage and its degradative mechanisms, advances in image ana lysis and molecular pathways involved in OA pathogenesis have revealed the critical role that synovium has in the pathophysiology of OA.