R heumatoid arthritis, the most common chronic polyartitular inflammatory disease, is estimated to occur in 1 to 3 percent of the population. The inflammatory process primarily involves synovial membranes, producing synovitis of both small and large joints with potential involvement of virtually any joint in the body, the periarticular bursae, tendon sheaths, and contiguous supporting structures. The systemic nature of the disease is often made apparent by a spectrum of extra-articular symptoms. These include weakness, fatigue, malaise, and weight loss, accompanied by varying degrees of anorexia, fever, and anemia. The clinical onset of rheumatoid arthritis is highly variable: it may range from an acute, almost explosive, generalized joint and extra-articular disease with prominent incapacitating constitutional symptoms, to a creeping, insidious, low-grade condition apparently confined to a few joints, and evolving slowly over several months or years. In either case, the underlying histopathology undergoes an orderly evolution from an acute to a chronic selfsustaining inflammation with characteristic synovial infiltration by lymphocytes, macrophages, and plasma ceils. Pain was recognized by Hippocrates as one of the cardinal manifestations of inflammation, along with redness, warmth, and swelling. Modern research has done much to elucidate the biochemical and cellular mechanisms of inflammation, but their relationship to pain is less well understood. Many biochemical mediators of inflammation are also thought to participate in the development of pain, such as superoxide radicals from leukocytes and macrophages, as well as cycle-oxygenase and lipoxygenase, which mediate tissue damage. As important as these individual factors may be to the inflammatory process at the cellular level, the clinical variability of pain associated with inflammation is not yet explainable. The intensity of pain varies immensely from individual to individual, and often does not correlate well with other clinical and laboratory parameters of inflammation. It is pain that motivates patients to seek medical attention for rheumatoid arthritis, and it is the relief of pain, more than any other manifestation of the disease, upon which the success or failure of treatment is judged by these patients. The treatment of rheumatoid arthritis is, therefore, directed toward suppression of pain and underlying inflammation. In the past two decades, aspirin, with its biphasic analgesic and anti-inflammatory effects, has been used as the standard against which all of the newer nonsteroidal antiinflammatory drugs are compared for efficacy and safety. Over the years, however, it has become increasingly clear that relatively few patients with rheumatoid arthritis are able to tolerate the prolonged high doses of aspirin needed to control inflammation. Recent studies suggest that traditional anti-inflammatory therapy with aspirin should be reassessed. A previously unpublished, large-scale study by Dr. Lomen and his colleagues follows. In the more than 800 patients with classic or definite rheumatoid arthritis who were evaluated, flurbiprofen was equivalent in analgesic and antiinflammatory efficacy to aspirin, and superior in tolerability.