Abstract

Anti-inflammatory agents have been reported to regulate bone healing. The aim of this study was to investigate the effect of a selective cyclooxygenase-2 inhibitor (meloxicam) on bone healing in calvarial defects in rats. Thirty-six adult male Wistar rats were included. After anesthesia, a linear incision was made through the skin of the scalp, a full-thickness flap was reflected and a 4 mm round defect was made with a trephine drill. The animals were randomly assigned to one of the following 4 treatment groups (9 animals each), including daily subcutaneous injections: A: saline solution for 15 days; B: saline solution for 45 days; C: 3 mg/kg of meloxicam for 15 days and D: 3 mg/kg of meloxicam for 45 days. The animals were sacrificed and the specimens, routinely processed. The bone filling was histometrically measured and statistical analysis, performed. Intergroup comparisons demonstrated that the meloxicam groups presented a significant reduction in bone healing when compared to their respective controls (group A, 44.5 +/- 5.75%, against group C, 57.5 +/- 7.25%, p < 0.05; group B, 40.25 +/- 13.75%, against group D, 52.25 +/- 17.25%). Within the limits of the present study, it can be concluded that selective cyclooxygenase-2 inhibitors may reduce bone healing in calvarial defects in rats after continuous administration.

Highlights

  • The effect of anti-inflammatory drugs on bone healing has been evaluated in several studies[1,3,11]

  • Non-steroidal anti-inflammatory drugs (NSAIDS) interfere with aracdonic acid metabolism by blocking prostaglandin synthesis through cyclooxygenase pathway inhibition, which has a fundamental role in bone healing[22,24]

  • In order to clarify the role of NSAIDS on bone healing after surgical procedures, the purpose of the present study was to evaluate the influence of meloxicam, a selective COX-2 inhibitor, on bone healing in calvarial defects in rats

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Summary

Introduction

The effect of anti-inflammatory drugs on bone healing has been evaluated in several studies[1,3,11]. Non-steroidal anti-inflammatory drugs (NSAIDS) interfere with aracdonic acid metabolism by blocking prostaglandin synthesis through cyclooxygenase pathway inhibition, which has a fundamental role in bone healing[22,24]. Selective COX-2 inhibitors have emerged with the objective of reducing stomach and renal toxicity. They can promote effects on Gurgel BCV, Ribeiro FV, Silva MAD, Nociti Júnior FH, Sallum AW, Sallum EA, Toledo S, Casati MZ. Selective COX-2 inhibitor reduces bone healing in bone defects. Braz Oral Res 2005;19(4):[312-6]

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