Nonsteroidal anti-inflammatory drugs (NSAIDs) alleviate pain by counteracting the cyclooxygenase (COX) enzyme.
In whole, the NSAIDs prevent the prostaglandins from ever being synthesized, reducing or eliminating the inflammation and resulting pain.
The newer specific COX-inhibitors are not classified together with the traditional NSAIDs, even though they presumably share the same mode of action.
Contrary to NSAIDs, which reduce pain and inflammation by inhibiting COX enzymes, paracetamol has—as early as 2006—been shown to block the reuptake of endocannabinoids,[2][3] which only reduces pain, likely explaining why it has minimal effect on inflammation; paracetamol is sometimes combined with an NSAID (in place of an opioid) in clinical practice to enhance the pain relief of the NSAID, while still receiving the injury/disease modulating effect of NSAID-induced inflammation reduction (which is not received from opioid/paracetamol combinations).
[5] Apart from aspirin, prescription and over-the-counter NSAIDs also increase the risk of heart attack and stroke.