AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers.

作者: Thiago J. Dionísio , Gabriela P. Souza , Bella L. Colombini‐Ishikiriama , Thais F. Garbieri , Viviane A. Parisi

DOI: 10.1002/JPER.19-0064

关键词:

摘要: Background The initiation and progression of periodontitis might involve a local renin-angiotensin system in periodontal tissue. This study hypothesized that Losartan treatment could promote protection to rats submitted experimental (EP) by attenuating alveolar bone loss due reduction inflammatory cytokines, better reactive oxidant species regulation maintenance the balance between formation resorption factors. Methods One hundred thirty were EP with silk suture thread (4.0) placed around lower right first molar for 1, 3, 7, 14 consecutive days. comprised four groups: G1-control without EP; G2-animals treated water; G3-Losartan-treated animals (treatment started at same day induction), G4-animals previously 30 days followed induction continuity treatment. Results G2 had greater volume, increased number, thickness decreased separation trabeculae. On other hand, G4 showed significant improvements these parameters. Histological analysis revealed favors cell infiltration junctional epithelium, cementum crest destruction, but pretreated (G4) did not show features. Although G3 demonstrate detected G4, mRNA expression results similar. In mandibular tissue, promoted increases ACE, AT1 receptor, mediators as well decreases antioxidant enzymes. However, treatments attenuated responses addition promoting an increase markers transcription Conclusion receptor modulates progression.

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