The identification of two cyclooxygenase (COX) enzymes has been a tremendous advance in understanding the role of prostaglandins in inflammation and the actions of nonsteroidal antiinflammatory drugs (NSAIDs). COX-1 activity appears to be related to "constitutive" or "housekeeping" functions in the gastric mucosa, kidney and platelets. COX-2 activity is "inducible" and generally occurs in response to a specific stimulus to enhance inflammatory actions. Current NSAIDs inhibit both COX-1 and COX-2, although the clinical benefit of NSAIDs appears to be associated with inhibition of COX-2 activity. The inhibition of COX-1 activity by NSAIDs is related to adverse side effects in general, particularly gastrointestinal toxicity. Recently, COX-2 selective inhibitors have been developed. Current data would suggest that by inhibiting COX-2 action, these agents may have efficacy similar to that of standard NSAIDs and that by not inhibiting COX-1 activity, they may have less toxicity than standard NSAIDs. Thus, these actions indicate that COX-2 selective inhibitors will have similar clinical efficacy to the traditional NSAIDs with fewer adverse side effects.