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J Dent Res 85(2):156-161, 2006
© 2006 International and American Associations for Dental Research

RESEARCH REPORT
Biological

Rosiglitazone Reduces the Evolution of Experimental Periodontitis in the Rat

R. Di Paola1, E. Mazzon1, D. Maiere1, D. Zito1, D. Britti2, M. De Majo3, T. Genovese1, and S. Cuzzocrea1,*

1 Department of Clinical and Experimental Medicine and Pharmacology, Torre Biologica, Policlinico Universitario, Via C. Valeria, Gazzi, 98100 Messina, Italy;
2 Department of Clinical Veterinary Science, University of Teramo, Italy; and
3 Department of Clinical Veterinary Medicine and Pharmacology University of Messina, Italy

* corresponding author, salvator{at}unime.it

The peroxisome proliferator-activated receptor-{gamma} (PPAR-{gamma}) receptor appears to play a pivotal role in the regulation of cellular proliferation and inflammation. Recent evidence also suggests that rosiglitazone, a PPAR-{gamma} agonist, reduces acute and chronic inflammation. We hypothesized that rosiglitazone would attenuate periodontal inflammation. In the present study, we investigated the effects of rosiglitazone in a rat model of ligature-induced periodontitis. At day 8, ligation significantly induced an increase in neutrophil infiltration, as well as of gingivomucosal tissue expression of iNOS, nitrotyrosine formation, and poly (ADP-ribose) polymerase activation. Ligation significantly increased Evans blue extravasation in gingivomucosal tissue and alveolar bone destruction. Intraperitoneal injection of rosiglitazone (10 mg/kg 10% DMSO daily for 8 days) significantly decreased all of the parameters of inflammation, as described above. Analysis of these data demonstrated that rosiglitazone exerted an anti-inflammatory role during experimental periodontitis, and was able to ameliorate the tissue damage associated with ligature-induced periodontitis.

KEY WORDS: rosiglitazone • peroxisome proliferator-activated receptor-{gamma} ligand • alveolar bone loss • reactive oxygen species • periodontal diseases






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