Journal
JOURNAL OF PERIODONTAL RESEARCH
Volume 52, Issue 4, Pages 734-744Publisher
WILEY
DOI: 10.1111/jre.12442
Keywords
coronary heart disease(s); genetics; inflammation; periodontitis
Categories
Funding
- FAPESP [10/07007-2]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [10/07007-2] Funding Source: FAPESP
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Background and Objective: The potential benefits of statins in modulating periodontal disease is supported by in vitro and clinical studies showing statins can induce a lower expression of proinflammatory cytokines and matrix metalloproteinases. The aim of this study was to evaluate the effects of rosuvastatin (ST) on ligature-induced periodontitis in spontaneously hypertensive rats (SHR). Material and Methods: Fifty-four adult male rats were divided into three groups: SHR-C, SHR-L and SHR-L-ST (C, control; L, ligature groups). In the SHR-L-ST group, animals were treated with daily 2 mg/kg ST administration. In L groups, a ligature remained around mandibular first molars for 10 d. Each group was divided for killing at 10 or 21 d postoperatively. Microtomographic and histometric analyses were performed. Osteoclastogenesis was evaluated by tartrate-resistant acid phosphatase assay and gene expression of 84 proinflammatory mediators by polymerase chain reaction array. Results: The SHR-L-ST group showed reduced bone loss and attachment loss in comparison with the SHR-L group at both 10 and 21 d postoperatively (p < 0.05). ST decreased the amount of tartrate-resistant acid phosphatase-positive cells compared with the SHR-L group at both 10 and 21 d (p < 0.05). The SHR-L-ST group presented 14 genes differentially expressed when compared with SHR-L group, featuring a downregulated gene profile at 10 d. Conclusion: Statin therapy may promote a protective effect against alveolar bone and connective tissue attachment losses attributable to periodontitis in hypertensive rats through inflammatory gene profile modulation.
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