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Nonsteroidal anti-inflammatory drug ingestion interferes with cessation of apoptotic events during oral mucosal ulcer healing

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image of Inflammopharmacology

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is a leading cause of gastrointestinal injury, but little is know about the effect of these agents on the integrity of soft oral tissue. We investigated the rate of buccal mucosal ulcer healing and the apoptotic processes in rats subjected to intragastric administration of NSAIDs. Groups of rats with acetic acid-induced buccal mucosal ulcers were administered orally twice daily for up to 10 days with indomethacin (5 mg/kg), or aspirin (20 mg/kg), or the vehicle, and their mucosal tissue was used for macroscopic assessment of ulcer healing rate and biochemical measurements. While in the control group the ulcer healed by the tenth day, the animals subjected to indomethacin showed only a 57.2% reduction in the ulcer area and a 54.8% reduction was attained in the presence of aspirin. The healing was reflected in a decrease in apoptosis and a decline in buccal mucosal expression of tumor necrosis factor-α (TNF-α) and endothelin-1 (ET-1), but the changes were significantly slower in the groups subjected to NSAIDs. The delay in healing in the presence of indomethacin was characterized on the tenth day by a 4.9-fold higher rate of apoptosis, a 4.6-fold higher level of TNF-α and a 2.7-fold higher expression of ET-1, while the delay in healing by aspirin was manifested by a 5.6-fold higher rate of apoptosis, a 5.5-fold higher level of TNF-α and a 2.9-fold higher expression of ET-1. Our findings are the first to demonstrate that NSAID ingestion leads to up-regulation of apoptotic events that interfere with soft oral tissue repair.


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