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Osteoarthritis (OA) is the most common joint disease and OA of the knee, in particular, is the major cause of chronic disability among people >65 years. Because nonsteroidal anti-inflammatory drugs (NSAIDs) improve symptoms in many patients with OA, it is widely considered that OA pain is due to synovial inflammation. However, OA pain may arise also from subchondral bone, the joint capsule, ligaments, tendons, entheses and periarticular muscle spasm. In many patients, the relief of OA pain and overall satisfaction with therapy may be as great with paracetamol (acetaminophen [APAP]) as with an NSAID. Cyclo-oxygenase (COX)-1-sparing NSAIDs (coxibs) are no more effective in the treatment of OA pain than non-selective NSAIDs and, although they may significantly decrease the risk of serious adverse effects related to gastrointestinal ulcers (GI) and ulcer complications, their gastroprotective effect may be reduced by concomitant administration of low-dose aspirin. Also, they may increase the risk of myocardial infarction in predisposed individuals. Because coxibs do not inhibit platelet aggregation, if prophylaxis against thromboembolic disease is required in patients being treated with a selective COX-2 inhibitor, low-dose aspirin should be used in conjunction with the coxib. Furthermore, nonselective NSAI Ds and coxibs may have adverse effects on the kidney, fracture healing and salt and water homeostasis. This paper discusses the relative positioning of APAP, NSAIDs and coxibs in the management of OA, on the basis of considerations of tolerability, efficacy and costs. [ABSTRACT FROM AUTHOR]