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Long-term testosterone depletion attenuates inflammatory bone resorption in the ligature-induced periodontal disease model

dc.contributor.authorGoncalves, Vincius de Paiva [UNESP]
dc.contributor.authorOrtega, Adriana Alicia C. [UNESP]
dc.contributor.authorSteffens, Joao Paulo
dc.contributor.authorPalomari Spolidorio, Denise Madalena
dc.contributor.authorRossa Junior, Carlos [UNESP]
dc.contributor.authorSpolidorio, Luis C. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal do Paraná (UFPR)
dc.date.accessioned2018-11-26T17:49:13Z
dc.date.available2018-11-26T17:49:13Z
dc.date.issued2018-04-01
dc.description.abstractBackground: Testosterone is known to affect bone in physiological and pathological conditions. The purpose of this study is to evaluate the role of testosterone in experimental periodontal disease in rats. Methods: In this study we used a ligature model of periodontal disease in rats submitted to orchiectomy (OCX, testosterone depletion) with and without testosterone replacement therapy (TR). Control animals were sham-operated and retained physiological testosterone levels. Sixty-two days after orchiectomy and sham operations, ligatures were placed around the lower first molars for 2 weeks to induce experimental periodontal disease. Negative control animals received no ligatures. The outcomes assessed in the periodontal tissues were: inflammatory cytokine expression by enzyme-linked immunosorbent assay (ELISA), stereometric analysis of the inflammatory process and quantitation of inflammatory bone resorption by microcomputed tomography (mu-CT). Results: The OCX+TR group showed the greatest increase in fibroblastic cells and blood vessels with reduced inflammatory cell numbers in the gingival tissue with induction of periodontal disease. There were no significant differences between OCX and Sham-operated groups in all the stereometric parameters assessed. Ligature placement induced inflammatory bone resorption, which was significantly attenuated in OCX animals. Experimental periodontitis induced a significant increase in interleukin (IL)-1 beta, but the lowest levels were observed in the periodontitis/OCX group. IL-6 levels were not affected by OCX, but were significantly reduced in OCX+TR animals. Conclusion: The findings of the present study suggest that testosterone depletion attenuates inflammatory bone resorption in ligature-induced periodontitis, which may be partly mediated via decreased production of IL-1 beta.en
dc.description.affiliationUniv Sao Paulo State UNESP, Araraquara Sch Dent, Dept Diag & Surg, Araraquara, SP, Brazil
dc.description.affiliationFed Univ Parana UFPR, Dept Stomatol, Curitiba, PR, Brazil
dc.description.affiliationUniv Sao Paulo State UNESP, Araraquara Sch Dent, Dept Physiol & Pathol, St Humaita,1680 Ctr, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUnespUniv Sao Paulo State UNESP, Araraquara Sch Dent, Dept Diag & Surg, Araraquara, SP, Brazil
dc.description.affiliationUnespUniv Sao Paulo State UNESP, Araraquara Sch Dent, Dept Physiol & Pathol, St Humaita,1680 Ctr, BR-14801903 Araraquara, SP, Brazil
dc.format.extent466-475
dc.identifierhttp://dx.doi.org/10.1002/JPER.17-0457
dc.identifier.citationJournal Of Periodontology. Chicago: Amer Acad Periodontology, v. 89, n. 4, p. 466-475, 2018.
dc.identifier.doi10.1002/JPER.17-0457
dc.identifier.issn0022-3492
dc.identifier.urihttp://hdl.handle.net/11449/164127
dc.identifier.wosWOS:000430670400010
dc.language.isoeng
dc.publisherAmer Acad Periodontology
dc.relation.ispartofJournal Of Periodontology
dc.relation.ispartofsjr1,408
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.subjectinflammation
dc.subjectperiodontitis
dc.subjecttestosterone
dc.titleLong-term testosterone depletion attenuates inflammatory bone resorption in the ligature-induced periodontal disease modelen
dc.typeArtigopt
dcterms.rightsHolderAmer Acad Periodontology
dspace.entity.typePublication
relation.isDepartmentOfPublicationb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isDepartmentOfPublication.latestForDiscoveryb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.lattes7634063102292261[5]
unesp.author.orcid0000-0002-6071-553X[3]
unesp.author.orcid0000-0003-1705-5481[5]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentDiagnóstico e Cirurgia - FOARpt
unesp.departmentFisiologia e Patologia - FOARpt

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