Arachidonic acid metabolism in inflamed gingiva and its inhibition by anti-inflammatory drugs.
Prostaglandin (PG) synthetase inhibitors are tissue-selective. Therefore, the action of four nonsteroidal anti-inflammatory drugs (NSAID) was tested against PG synthesis from 14C-arachidonic acid by gingival homogenate. Suprofen and tolmetin sodium did not significantly inhibit PGs at any of the three concentration levels used (10(-7), 10(-5), 10(-3) M), whereas flurbiprofen and zomepirac sodium did significantly inhibit PG formation at millimolar concentration. The results, coupled with our previous study on indomethacin, piroxicam and ibuprofen open the way for future tests of NSAIDs in treatment of gingival inflammation and periodontal disease.
D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001095:Arachidonic Acids / Q000378:metabolism*; D005480:Flurbiprofen / Q000494:pharmacology; D005891:Gingivitis / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D010510:Periodontal Diseases / Q000378:metabolism* / Q000503:physiopathology; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis; D013496:Suprofen / Q000494:pharmacology; D014046:Tolmetin / Q000031:analogs & derivatives / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D001095:Arachidonic Acids; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D005480:Flurbiprofen; C020549:zomepirac; D013496:Suprofen; D014046:Tolmetin