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Rosuvastatin promotes benefits on induced periodontitis in hypertensive rats
Author(s) -
Messora M. R.,
Apolinário Vieira G. H.,
Vanderlei J. M. T. M. M.,
Mariguela V. C.,
Fernandes P. G.,
Palioto D. B.,
Scombatti de Souza S. L.,
Novaes A. B.,
Furlaneto F.,
Taba M.
Publication year - 2017
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12442
Subject(s) - periodontitis , proinflammatory cytokine , medicine , rosuvastatin , endocrinology , dental alveolus , acid phosphatase , ligature , fluvastatin , bone resorption , statin , matrix metalloproteinase , connective tissue , simvastatin , inflammation , chemistry , dentistry , pathology , biochemistry , enzyme
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.