Taking in consideration the bystander effects of articular senescence

Osteoarthritis (OA) is a whole-joint disease and one of the leading causes of chronic pain and physical disability through the world (1,2). Its prevalence is increasing drastically with the aging population (3). Causes of OA are multifactorial: genetic predisposition, alteration of joint component, aging, and mechanical factors (obesity, joint misalignment and joint trauma). OA is characterized by progressive deterioration and loss of joint cartilage combined with anatomical and molecular alterations of other joint structures. In particular, OA leads to a loss of chondrocyte function that is overcome during the repair process of cartilage damage. There is an abnormal differentiation of normal chondrocytes into hypertrophic chondrocytes. The latter contribute to the breakdown mechanisms through the production of pro-inflammatory mediators and accelerated aging.