Comparison of etoricoxib and indomethacin for the treatment of experimental periodontitis in rats

Abstract

We investigated the effect of etoricoxib, a selective cyclooxygenase-2 inhibitor, and indomethacin, a non-selective cyclooxygenase inhibitor, on experimental periodontitis, and compared their gastrointestinal side effects. A ligature was placed around the second upper left molars of female Wistar rats (160 to 200 g). Animals (6 per group) were treated daily with oral doses of 3 or 9 mg/kg etoricoxib, 5 mg/kg indomethacin, or 0.2 mL saline, starting 5 days after the induction of periodontitis, when bone resorption was detected, until the sacrifice on the 11th day. The weight and survival rate were monitored. Alveolar bone loss (ABL) was measured as the sum of distances between the cusp tips and the alveolar bone. The gastric mucosa was examined macroscopically and the periodontium and gastric and intestinal mucosa were examined by histopathology. The ongoing ABL was significantly inhibited (P < 0.05) by 3 and 9 mg/kg etoricoxib and by indomethacin: control = 4.08 ± 0.47 mm; etoricoxib (3 mg/kg) = 1.89 ± 0.26 mm; etoricoxib (9 mg/kg) = 1.02 ± 0.14 mm; indomethacin = 0.64 ± 0.15 mm. Histopathology of periodontium showed that etoricoxib and indomethacin reduced inflammatory cell infiltration, ABL, and cementum and collagen fiber destruction. Macroscopic and histopathological analysis of gastric and intestinal mucosa demonstrated that etoricoxib induces less damage than indomethacin. Animals that received indomethacin presented weight loss starting on the 7th day, and higher mortality rate (58.3%) compared to etoricoxib (0%). Treatment with etoricoxib, even starting when ABL is detected, reduces inflammation and cementum and bone resorption, with fewer gastrointestinal side effects.

Treatment of experimental periodontal disease by a selective inhibitor of cyclooxygenase-2 with scaling and root planing (SRP)

“…L animals. These results are in accordance with former literature studies that demonstrated NSAIDs effectiveness upon periodontal treatment both in animals (Holzhausen et al 2002;Azoubel et al 2007;Oliveira et al 2008;Bezerra et al 2000) and in humans (Yen et al 2008;Taiyeb Ali and Waite 1993). Upregulation of RANKL has also been seen in inflamed periodontal tissues, indicating that RANKL participates in the processes of periodontal tissue destruction (Crotti et al 2003;Liu et al 2003).…”

“…Some animal studies have demonstrated that COX-2 inhibitor promotes less periodontal breakdown (Holzhausen et al 2002;Azoubel et al 2007;Oliveira et al 2008). However, clinical human studies show that non-steroidal anti-inflammatory drugs used on periodontitis treatment, showed no differences (Bissada and Ng 1998;Azoubel et al 2008) in periodontal tissue destruction.…”

Infliximab attenuates inflammatory osteolysis in a model of periodontitis in Wistar rats

“…Photographs were digitized and processed with ImageJ software (ImageJ, 1.32, National Institute of Health, Bethesda, USA) for the measurement of alveolar bone loss using a modification of the area method. 22 The alveolar bone loss was measured by the exposed molar root surface area (mm 2 ) on the buccal aspect of the maxillary left side by subtracting the total area of the left maxillae tooth and bone resorption from the right maxilla tooth area (unligated control).…”

Pharmacotherapies to Manage Bone Loss-Associated Diseases: A Quest for the Perfect Benefit-to-Risk Ratio

“…Other reports have shown that inhibition of different cellular and molecular steps of the inflammatory response to the oral bacteria or blockade of RANKL actions, may be beneficial to inhibit periodontal bone loss in animal models ( Table 5, Fig. 5) [249][250][251][252][253][254][255][256][257]. However, inhibition of MMP activity with a selective inhibitor was found to promote alveolar bone resorption [258] (Table 5, Fig.…”