The age-related degeneration of joint cartilage is a strongly inflammatory condition, in which the accumulation of senescent cells plays an important role. Senescent cells produce potent inflammatory signaling that harms the local environment in a range of ways. Systemic inflammation is also thought to be a meaningful contribution to osteoarthritis, however. The immune system becomes dysfunctional throughout the body with age, becoming more active and inflammatory even as it becomes ever less capable of defending against pathogens and errant cells. Minimizing joint issues with aging will no doubt require dealing with both local and systematic sources of chronic inflammation.
Aging is an inevitable process in the human body that is associated with a multitude of systemic and localized changes. All these conditions have a common pathogenic mechanism characterized by the presence of a low-grade proinflammatory status. Inflammaging is systemic, chronic, and asymptomatic. It has a multifactorial aetiology including an increased number of proinflammatory cytokines, oxidative stress, immunosenescence, autophagy, or cellular DNA damage.
The incidence of osteoathritis (OA) is steadily increasing, especially among the elderly. The mechanism of articular cartilage degeneration is not necessarily the consequence of aging, but aging is considered to be a risk factor for the occurrence of OA. There is a close relationship between chondrocyte activity and local articular environment changes due to cell senescence followed by secretion of inflammatory mediators. Furthermore, systemic inflammaging can lead to cartilage destruction, pain, disability, and an impaired quality of life.
The term "chondrosenescence" refers to all age-dependent deterioration of chondrocytes as a consequence of replicative (intrinsic) and stress-induced (extrinsic) factors. There is a strong correlation between inflammaging, the presence of inflammasomes, autophagy, and chondrosenescence. Intrinsic factors in the aging process in association with extrinsic factors such as mechanical overload or different chemical stimuli act on articular cartilage. As a consequence, an inflammatory environment characterized by increased proinflammatory cytokines, chemokine, and activated proteinase occurs locally. All these lead to the aging process of chondrocytes (chondrosenescence), which favors the appearance of degenerative joint modifications.