Osteoarthritis (OA) has long been considered as a "tear-and-wear" process. In the last 15 years, the face of OA has deeply changed, now considered as a disease involving all tissues of a joint eventually leading to cartilage degradation. Among these tissues, a particular attention has been recently paid on the role of synovium in the OA process. A patchy inflammation of this tissue is described, with some kind of correlation between the degree of the synovitis and the prognostic of the disease. Whether this synovitis is a primum movens of the process or secondary to a reaction to cartilage fragments falling into the joint remains debated. Many inflammatory mediators belonging to the cytokine family, to inflammatory lipid mediators, or to matrix components play a critical role in the OA process. Interestingly, the source of these soluble mediators may be the chondrocytes themselves (via autocrine/paracrine loops), the synovial cells and the subchondral bone cells. Interestingly, all the risk factors playing a role in OA have a potential to increase the release of inflammatory mediators into the joints (adipokines for obesity/metabolic syndrome, secretory profile of senescent chondrocytes, synovitis in post-trauma). The most recent studies highlight the possibility of cross-talks between joint cells leading to communication of mediators within and between the tissues of a joint. Finally, the paradigm based on a mechanical-driven origin of the disease is not conflictual with the inflammatory hypothesis since mechanical signals are shifted into biochemical signals in chondrocytes and subchondral bone cells via mechanoreceptors leading to the release of pro-degradative and pro-inflammatory mediators.
Berenbaum, F. (2012). Osteoarthritis is an inflammatory disease. Osteoarthritis and Cartilage, 20, S5. https://doi.org/10.1016/j.joca.2012.02.621