Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes inflammation of joints (leading to their destruction), tissues around joints and other organ systems. The pathogenesis of RA is the subject of ongoing research, but the roles of tumour necrosis factor alpha (TNF-a), interleukin 1 (IL-1) and B cells have received increased attention resulting in several new therapeutic agents. Treatment (for pain) of RA in the first instance is with non-steroidal anti-inflammatory drugs, with second-line treatment using disease-modifying anti-rheumatic drugs (DMAR Ds). DMAR Ds are a disparate group and include methotrexate, d-penicillamine, sulphasalazine, gold salts, antimalarial drugs and immunosuppressant drugs. Methotrexate is the gold standard in terms of both efficacy and side-effect profile. The newer class of 'biological' DMAR Ds includes etanercept (TNF-a receptor-immunoglobulin (Ig) G chimera), infliximab (monoclonal anti-TNF-a antibody), anakinra (IL-1 receptor antagonist) and rituximab (an anti-CD20 antibody that depletes B cells). These 'biologicals' have, in general, good efficacy and side-effect profiles and can be combined with methotrexate.