Rheumatoid arthritis (RA) shares some features with osteoarthritis (OA); in terms of synoviocyte activation, synovial hyperplasia and release of proinflammatory cytokines in the synovial fluid, OA seems a quantitatively dampened down variant of RA rather than a totally different entity.1 Moreover, lesions of deep cartilage and subchondral bone have been identified in RA prior to other defects.2

Recently, an association of a functional GDF5 polymorphism with OA was reported.3 GDF5 (growth differentiation factor 5) is a secreted prochondrogenic growth factor detected in regions of future joints during early development. Mutations in mouse and human GDF5 cause defective joints,4 several skeletal dysplasias have been described. RA pathogenesis was speculated to involve an attempt to recapitulate the embryonic limb development programme.5 We hypothesise that RA may share with OA an …