DETECTION OF TUMOR-NECROSIS-FACTOR-ALPHA AND INTERLEUKIN-1-BETA IN THE RHEUMATOID OSTEOARTHRITIC CARTILAGE-PANNUS JUNCTION BY IMMUNOHISTOCHEMICAL METHODS

During inflammation the rheumatoid synovial membrane is invaded by a number of different cell types. When activated most of these cells produce cytokines including tumor necrosis factor alpha (TNFalpha) and interleukin-1 beta (IL-1 beta). These cytokines are believed to stimulate production of degradative enzymes and disturb the equilibrium between such enzymes and their inhibitors resulting in tissue damage. In this study we investigated the localisation of TNFalpha and IL-1 beta at the cartilage-pannus junction (CPJ). Here, cytokines are well placed to influence the integrity of articular cartilage. Tissue was derived from advanced rheumatoid (RA) and, as a comparison, osteoarthritic (OA) joints at the time of replacement surgery (arthroplasty). Antibody staining of fixed serial sections of tissue localised cells that were associated with IL-1 beta and TNFalpha. Cell markers for macrophages and endothelial cells were included to provide positive identification of the cytokine-associated cells. Anaylsis of these sections revealed that both TNFalpha and IL-1 beta were associated with macrophages, particularly those in the synovium overlying cartilage (pannus) and endothelial cells. Positive staining was seen at the CPJ in RA and in similarly located tissue in OA. The similar distribution of cytokines in OA was unexpected even if the overall numbers of tissue and infiltrating cells in the CPJ were different in the two diseases. This highlights the possible role played by endogenous inhibitors [1, 2] in influencing the degree of cytokine activity necessary to explain the different pathogenic mechanisms in RA and OA.