Fibroblasts, in particular the synovial cells, play a key role in the pathogenesis of rheumatoid arthritis. Recent evidence not only supports the concept that they are involved in the destruction of the joint tissues but also that they may migrate between joints. Far less is known about the role of fibroblasts in the other group of chronic inflammatory joint diseases, spondyloarthritis. In particular in ankylosis spondylitis, fibroblasts may be primary mediators of the disease processes. Fibroblasts-like cells in the periosteum, synovium, bone marrow and enthesis can be linked to mechano-responses and are likely producers of growth factors that stimulate cell differentiation. This may lead to the characteristic phenotype of spondyloarthritis with new cartilage and bone formation leading to ankylosis. Indeed, all these tissues were shown to contain mesenchymal stem or progenitor cell population capable of such differentiation processes. The cells may also produce chemokines and some proinflammatory cytokines linked to the further development of arthritis.
Disclosure of Interest None Declared