Oral pain relievers, particularly nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen and aspirin, reduce inflammation by inhibiting the activity of cyclooxygenase (COX) enzymes. These enzymes, COX-1 and COX-2, are crucial in the conversion of arachidonic acid to prostaglandins, which are lipid compounds that mediate inflammation, pain, and fever. By blocking COX enzymes, NSAIDs decrease the production of prostaglandins, thereby reducing inflammation and alleviating pain.
COX-1 is involved in maintaining normal physiological functions, such as protecting the stomach lining and regulating blood platelets, while COX-2 is primarily induced during inflammatory responses. Selective COX-2 inhibitors, like celecoxib, specifically target the COX-2 enzyme, aiming to reduce inflammation with fewer gastrointestinal side effects compared to non-selective NSAIDs.
Acetaminophen (paracetamol), another common oral pain reliever, works differently. It is believed to inhibit a variant of the COX enzyme in the brain, reducing pain and fever but not significantly affecting inflammation. This makes it suitable for pain relief without the anti-inflammatory effects of NSAIDs.
These medications are absorbed into the bloodstream through the gastrointestinal tract, where they are distributed throughout the body to exert their effects. The reduction in prostaglandin synthesis leads to decreased inflammation, swelling, and pain, providing symptomatic relief for conditions like arthritis, muscle injuries, and headaches.
However, prolonged use of NSAIDs can lead to side effects such as gastrointestinal irritation, ulcers, and increased risk of cardiovascular events, due to the inhibition of protective prostaglandins. Therefore, they should be used as directed and under medical supervision when necessary.