Abstract

We have investigated the effects of WY14643, a potent peroxisome proliferator activator receptor-α (PPAR-α) agonist, in a rat model of ligature-induced periodontitis. Male Sprague-Dawley rats were lightly anaesthetized with pentobarbitone (35 mg/kg). Sterile, 2-0 black braided silk thread was placed around the cervix of the lower left first molar and knotted medially. Animals received WY14643 (1 mg/kg i.p, daily for eight days). Eighths days after placement of the ligature, we evaluated several markers of inflammation such us (1) myeloperoxidase activity, (2) a cytokines and adhesion molecules expression, (3) NF-κB expression, (4) iNOS expression, (5) the nitration of tyrosine residues, (6) activation of the nuclear enzyme poly(ADP-ribose) polymerase, (7) apoptosis, and (8) the degree of gingivomucosal tissues injury. Administration of WY14643 significantly decreased all of the parameters of inflammation as described above. These results demonstrate that WY14643 exerts an anti-inflammatory role during experimental periodontitis and is able to ameliorate the tissue damage.

Highlights

  • Periodontitis is an inflammatory lesion, mediated by accumulation of bacteria that leads to the loss of connective tissue attachment to root surface cementum and adjacent alveolar bone resulting in tooth loss [1]

  • When compared to gingivomucosal tissues sections taken from the contra lateral side obtained from vehicletreated rats (Figure 1(a)), histological examination of gingivomucosal tissues sections of ligature-operated rats showed oedema, tissue injury as well as infiltration of the tissue with inflammatory cells (Figure 1(b))

  • Masson’s trichrome stain, which is used to monitor the increase of collagen fiber, was negative in gingivomucosal tissue sections taken from the contra lateral side from vehicle when compared with gingivomucosal tissues sections of ligature-operated rats (Figures 1(d) and 1(e), resp.)

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Summary

Introduction

Periodontitis is an inflammatory lesion, mediated by accumulation of bacteria that leads to the loss of connective tissue attachment to root surface cementum and adjacent alveolar bone resulting in tooth loss [1]. Studies have demonstrated that periodontal disease affects between 10% and 15% of the world’s population [2]. The exact mechanism of periodontitis development, including the prior agents or mediators involved, is not clear. Periodontitis manifests itself as a multifactor phenomenon. It is clear that, while the etiology of periodontitis is bacteria, the pathogenesis is inflammatory. It is widely accepted that the initiation and progression of periodontitis are dependent upon the presence of microorganisms capable of causing disease.

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