Abstract
For NSAIDs it has been widely accepted that prostaglandin inhibition is their mechanism of action in clinical use. Yet many other actions have been described, although it is unclear to what extent these may contribute to clinical activity. This review attempts to relate some of the experimental activities of NSAIDs to concentrations of drugs which occur in clinical use. Since it is assumed that to be effective a drug must reach its target site of action, synovial fluid concentrations for NSAIDs are considered. The resulting analysis suggests that prostaglandin inhibition is a viable mode of action for most, if not all, NSAIDs. However, some NSAIDS may rely as much, if not more, on other actions for their anti-inflammatory effect.
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