According to a recent study, cartilage and synovial tissues may contribute to joint damage by altering the expression of proteins involved in the regulation of three major pathways.
Osteoarthritis (OA) is a very common joint disease and is a leading cause of disablement in elderly patients. While many factors are known to contribute to the development of OA, including mechanical factors, genetics and obesity, the pathophysiology behind the condition is still not fully understood. Gaining a greater understanding of the possible pathogenic role of tissues in the osteoarthritic joint, such as cartilage, synovium and subchondral bone, could lead to the development of more effective treatments, including innovative disease-modifying drugs.
In the study, protein constituents in the synovial fluid (SF) of early- and late-stage OA patient samples were analyzed and compared with age-matched samples of SF from control subjects, using 2-D difference-in-gel electrophoresis and MS. Following the analysis, 66 proteins were found to be differentially expressed in the samples of OA and healthy SF. These proteins are implicated in three major pathways; the complement pathway, the coagulation pathway and the acute-phase response signaling pathway.
Crucially, the proteins and pathways in OA SF that were found to be altered in the study, including C-reactive protein and IL-6, indicate that both cartilage and synovial tissue could contribute to joint damage in the disease. The next step for the researchers will be to gain a greater understanding of the contribution of these tissues and pathways to the progression of the disease. Further to this, the researchers hope that in the future they may be able to target these pathways with novel disease-modifying drugs, or use proteins in the pathways as biomarkers to improve treatment options and outcomes for OA patients.
Source: Ritter SY, Subbaiah R, Bebek G et al. Proteomic analysis of synovial fluid from the osteoarthritic knee: comparison with transcriptome analyses of joint tissues. Arthritis Rheum. 65(4), 981–992 (2013).