Journal of Indian Society of Periodontology (Jan 2014)

Comparative evaluation of the efficacy of the cyclooxygenase pathway inhibitor and nitric oxide synthase inhibitor in the reduction of alveolar bone loss in ligature induced periodontitis in rats: An experimental study

  • Rekha Jagadish,
  • Dhoom Singh Mehta

DOI
https://doi.org/10.4103/0972-124X.128216
Journal volume & issue
Vol. 18, no. 1
pp. 59 – 64

Abstract

Read online

Background: Alveolar bone loss is the most striking feature of periodontal disease. The aim of this study was to investigate the effect of a cyclooxygenase (COX) pathway inhibitor and nitric oxide synthase (NOS) inhibitor in the reduction of alveolar bone loss in an experimental periodontal disease (EPD) model. Materials and Methods: The study was conducted on 60 Wistar rats divided into three groups of 20 rats each and then subjected to a ligature placement around the left maxillary second molars. Group 1 rats were treated with COX inhibitor (diclofenac sodium 10 mg/kg/d), group 2 with NOS inhibitor (aminoguanidine hydrochloride 10 mg/kg/d) and group 3 served as controls, receiving only saline, intraperitoneally 1h before EPD induction and daily until the sacrifice on the 11 th day. Leukogram was performed before ligation, at 6 h and at the first, seventh and 11 th days after EPD induction. After sacrifice, all the excised maxillae were subjected to morphometric and histometric analysis to measure the alveolar bone loss. Histopathological analysis was carried out to estimate cell influx, alveolar bone and cementum integrity. Results: Induction of experimental periodontitis in the rat model produced pronounced leucocytosis, which was significantly reduced by the administration of diclofenac sodium and aminoguanidine on the 11 th day. In morphometric and histometric examinations, both the test drugs significantly (P < 0.05) inhibited the alveolar bone loss as compared with the control group. Conclusion: Both COX inhibitor and NOS inhibitor are equally effective in inhibiting the inflammatory bone resorption in an experimental periodontitis model.

Keywords