As part of the investigation into the burden of rheumatoid arthritis (RA) and the access to treatment, this article reviews the medical aspects of the disease. RA is mediated by a variety of pathogenic events which culminate in the activation of B-cells, T-cells and other cell populations and lead to secretion of proinflammatory cytokines. These events result in signs and symptoms of active disease, such as pain and swelling, joint damage and disability, the three cornerstones of the clinical expression of RA. Active disease leads to joint damage and both to disability, whereby joint destruction is associated with the irreversible portion of disability. The diagnosis of RA is based on characteristic clinical and laboratory features, however, these may not be obvious in early disease. Therapy aims at interfering with disease activity, ideally leading to remission, as well as at retarding, ideally holding or even healing, joint destruction. This can be achieved by using disease modifying anirheumatic drugs (DMARDs). Among the chemical DMARDs, methotrexate is the anchor drug, although there exist many more such agents. Among the biological compounds, TNF-inhibitors have been in use for more than one decade, and co-stimulation blockade and B-cell targeted therapy have been recent additions to the armamentarium. Therapeutic outcome can be predicted by clinical means.