Synovitis is a feature of both OA and RA, and in both it may contribute to pain. OA and RA are often viewed as separate diseases, but OA may occur secondarily to, or coincidentally with RA. In both OA and RA, synovial inflammation is associated with the growth of new blood vessels. However, the mechanisms and consequences of synovial angiogenesis display both similarities and differences between diseases. Macrophages and macrophage-derived growth factors such as vascular endothelial growth factor (VEGF) are increased in the inflamed synovium of both OA and RA joints. However, biological agents such as anti-TNF therapies more convincingly reduce angiogenesis in RA than in OA. Angiogenesis is associated with sensory nerve growth. In RA, densities of both blood vessels and nerves near the synovial surface may be reduced, whereas vascular densities in OA synovium are more consistently increased, perhaps suggesting a greater contribution of vascular regression in RA synovitis. RA is associated with joint erosion, and growth of erosive pannus may be dependent on angiogenesis. However, in both OA and RA, redistribution of blood vessels from the synovial surface into the deeper synovial layers may compromise cartilage metabolism and exacerbate chondropathy. Differences between OA and RA may reflect either the intensity or underlying mechanisms of inflammation, and direct interventional studies are required to definitively dissect specific features of angiogenesis and inflammation between the 2 diseases. Better understanding the similarities and differences in blood vessel growth between OA and RA may lead to better treatments for both diseases in the future.
Disclosure of Interest None Declared