Immunopathogenesis of osteoarthritis

Abstract

Even though osteoarthritis (OA) is mainly considered as a degradative condition of the articular cartilage, there is increasing body of data demonstrating the involvement of all branches of the immune system. Genetic, metabolic or mechanical factors cause an initial injury to the cartilage resulting in release of several cartilage specific auto-antigens, which trigger the activation of immune response. Immune cells including T cells, B cells and macrophages infiltrate the joint tissues, cytokines and chemokines are released from different kinds of cells present in the joint, complement system is activated, and cartilage degrading factors such as matrix metalloproteinases (MMPs) and prostaglandin E2 (PGE2) are released, resulting in further damage to the articular cartilage. There is considerable success in the treatment of rheumatoid arthritis using anti-cytokine therapies. In OA, however, these therapies did not show much effect, highlighting more complex nature of pathogenesis of OA. This needs the development of more novel approaches to treat OA, which may include therapies that act on multiple targets. Plant natural products have this kind of property and may be considered for future drug development efforts. Here we reviewed the studies implicating different components of the immune system in the pathogenesis of OA.

Figure 1. Schematic representation of immunopathogenesis of OA

Several genetic, metabolic as well as environmental factors lead to the damage of cartilage resulting in the release of cartilage specific autoantigens, which in turn activate the immune/inflammatory response. There is increased infiltration of T-cells, B-cells and macrophages in the joint tissues. These immune cells along with other cells of the joint tissue get activated and release several molecules such as cytokines, chemokines and other cartilage degrading factors such as MMPs and PGE₂ resulting in further degradation in the cartilage. DAMPs: damage-associated molecular patterns