Combination of etodolac and dexamethasone improves preemptive analgesia in third molar surgery: a randomized study.

OBJECTIVE: This randomized, controlled, triple-blind, crossover clinical trial aimed to investigate the use of dexamethasone (DEX) and etodolac (ETO) as preemptive analgesia before mandibular third molar extraction. METHODS: Patients were divided into three groups (n = 20 teeth each) based on the drug administered: DEX 8 mg (DEX); DEX 8 mg plus ETO 300 mg (DEX + ETO), and ETO 300 mg (ETO). Paracetamol (750 mg) tablets were administered as rescue analgesics. Pain was evaluated using the visual analog scale (VAS) at 6, 12, 24, 48, and 72 h and 7 days postoperatively. Edema and trismus were assessed 48 and 72 h postoperatively. All data were subjected to statistical analysis, where a P value < .05 indicated statistical significance. RESULTS: VAS scores and the number of rescue analgesics taken were lower in the DEX + ETO group than in the other groups (P < .001 and P = .014, respectively). At 48 h, trismus was similar among all groups; however, the ETO group showed the highest trismus 7 days postoperatively (P < .05). Edema was similar among all groups at all time points (P > .05). CONCLUSION: The combined use of the anti-inflammatory drugs, DEX and ETO, resulted in better pain control and the need for fewer rescue analgesics than the use of either drug alone, which indicated their effectiveness in mandibular third molar extractions preoperatively. CLINICAL RELEVANCE: This drug combination can lead to less pain, edema, and trismus and reduce the use of rescue analgesics in the postoperative period.

Exogenous alkaline phosphatase treatment complements endogenous enzyme protection in colonic inflammation and reduces bacterial translocation in rats.

Alkaline phosphatase (AP) inactivates bacterial lipopolysaccharide and may therefore be protective. The small intestine and colon express intestinal (IAP) and tissue nonspecific enzyme (TNAP), respectively. The aim of this study was to assess the therapeutic potential of exogenous AP and its complementarity with endogenous enzyme protection in the intestine, as evidenced recently. IAP was given to rats by the oral or intrarectal route (700U/kgday). Oral budesonide (1mg/kgday) was used as a reference treatment. Treatment with intrarectal AP resulted in a 54.5% and 38.0% lower colonic weight and damage score, respectively, and an almost complete normalization of the expression of S100A8, LCN2 and IL-1ß (p<0.05). Oral AP was less efficacious, while budesonide had a more pronounced effect on most parameters. Both oral and intrarectal AP counteracted bacterial translocation effectively (78 and 100%, respectively, p<0.05 for the latter), while budesonide failed to exert a positive effect. AP activity was increased in the feces of TNBS colitic animals, associated with augmented sensitivity to the inhibitor levamisole, suggesting enhanced luminal release of this enzyme. This was also observed in the mouse lymphocyte transfer model of chronic colitis. In a separate time course study, TNAP was shown to increase 2-3 days after colitis induction, while dextran sulfate sodium was a much weaker inducer of this isoform. We conclude that exogenous AP exerts beneficial effects on experimental colitis, which includes protection against bacterial translocation. AP of the tissue-nonspecific isoform is shed in higher amounts to the intestinal lumen in experimental colitis, possibly aiding in intestinal protection.