dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorSpolidório, Luis Carlos
dc.creatorRamalho Lucas, Pablo Dallari
dc.creatorSteffens, Joao Paulo
dc.creatorBueno da Silva, Henrique Aparecido
dc.creatorEuzebio Alves, Vanessa Tubero
dc.creatorPalomari Spolidorio, Denise M.
dc.creatorHolzhausen, Marinella
dc.date2015-03-18T15:56:10Z
dc.date2016-10-25T20:35:23Z
dc.date2015-03-18T15:56:10Z
dc.date2016-10-25T20:35:23Z
dc.date2014-09-01
dc.date.accessioned2017-04-06T07:17:45Z
dc.date.available2017-04-06T07:17:45Z
dc.identifierJournal Of Periodontology. Chicago: Amer Acad Periodontology, v. 85, n. 9, p. 1266-1274, 2014.
dc.identifier0022-3492
dc.identifierhttp://hdl.handle.net/11449/117449
dc.identifierhttp://acervodigital.unesp.br/handle/11449/117449
dc.identifier10.1902/jop.2014.130619
dc.identifierWOS:000341580700019
dc.identifierhttp://dx.doi.org/10.1902/jop.2014.130619
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/928096
dc.descriptionBackground: Parstatin is a 41-amino acid peptide, formed by proteolytic cleavage on activation of the protease activated receptor-1, with antiangiogenic properties. The purpose of this study is to evaluate the influence of synthetic parstatin on experimental periodontal disease and repair in rats.Methods: Ligature-induced periodontitis was established in rats and the influence of parstatin administration was assessed after 8 and 15 days for periodontal disease and 24 hours and 8 days after repair after ligature removal.Results: Parstatin administration significantly inhibited gingival myeloperoxidase activity, interleukin (IL)-1 beta, tumor necrosis factor-alpha, and IL-6 levels and led to suppression of macrophages and collagen degradation. At periodontal tissues under repair, parstatin increased the gingival levels of endostatin and decreased vascular endothelial growth factor expression and blood vessel number but did not influence histologic healing. In addition, the tomographic linear bone loss was significantly reduced at 15 days of periodontitis when the rats were treated with parstatin compared to their respective phosphate-buffered saline-treated controls.Conclusions: Parstatin suppresses the periodontal tissue breakdown followed by experimental periodontitis in rats and did not impair periodontal tissue repair, despite its antiangiogenic effect. Parstatin may represent a novel approach to modulate host response in chronic periodontal disease.
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageeng
dc.publisherAmer Acad Periodontology
dc.relationJournal Of Periodontology
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectInflammation
dc.subjectneovascularization, physiologic
dc.subjectPAR-1 receptor (1-41), human
dc.subjectperiodontal diseases
dc.subjectrats
dc.subjectwound healing
dc.titleInfluence of Parstatin on Experimental Periodontal Disease and Repair in Rats
dc.typeOtro


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