It has become clear in recent years that the synovium is the primary site of inflammation and a major effector organ in a variety of joint diseases, including rheumatoid arthritis (RA). As a result, there has been increased interest in studies of the pathological changes of the synovium.1 There are, however, several caveats that need to be recognised. Many of the older studies have examined synovial tissue obtained at surgery. In these patients inflammation is not necessarily a prominent feature. Moreover, patients requiring joint surgery obviously represent a highly selective group, in whom specific pathogenetic mechanisms may be operative that are associated with the process of destruction. For instance, mutations in the tumour suppresser gene p53 were demonstrated in fibroblast-like synoviocytes from synovium of patients with RA with longstanding, destructive disease.2 It has been suggested that the resulting loss of p53 function may contribute to the autonomous progression of pannus and joint destruction. Conceivably, p53 mutations are not present in earlier, less destructive phases of the disease,3 ,4though this remains to be determined. In line with this hypothesis, intimal lining layer hyperplasia and p53 expression by fibroblast-like synoviocytes also seem to be more pronounced in tissue obtained at surgery than in arthroscopic samples.5 ,6 In addition, synovial tissue from patients with end stage, destructive RA may be distinct as a result of other mechanisms. For instance, the release of fragments secondary to the degradation of bone and articular cartilage may theoretically influence the synovial infiltrate. The advent of blind needle biopsy techniques and needle arthroscopy has created the opportunity to obtain synovial tissue samples of patients with active synovial inflammation in earlier stages …