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Periodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesis

dc.contributor.authorSilva, Juliete Aparecida F.
dc.contributor.authorLopes Ferrucci, Danilo
dc.contributor.authorPeroni, Luis Antônio
dc.contributor.authorPaula Ishi, Eduardo de [UNESP]
dc.contributor.authorRossa-Júnior, Carlos [UNESP]
dc.contributor.authorCarvalho, Hernandes F.
dc.contributor.authorStach-Machado, Dagmar Ruth
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionInstituto Nacional de Ciência e Tecnologia de Fotônica Aplicada à Biologia Celular (INFABIC)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2015-08-06T16:12:39Z
dc.date.available2015-08-06T16:12:39Z
dc.date.issued2012
dc.description.abstractAlveolar bone resorption results from the inflammatory response to periodontal pathogens. Systemic diseases that affect the host response, such as type 1 diabetes mellitus (DM1), can potentiate the severity of periodontal disease (PD) and accelerate bone resorption. However, the biological mechanisms by which DM1 modulates PD are not fully understood. The aim of this study was to determine the influence of DM1 on alveolar bone resorption and to evaluate the role of receptor activator of nuclear factor-kappaB ligand (RANKL)/osteoprotegerin (OPG) in osteoclastogenesis in rats. PD was induced by means of ligature in nondiabetic and in streptozotocyn-induced DM1 rats. Morphological and morphometric analyses, stereology and osteoclast counting were performed. RANKL and OPG mRNA levels, protein content, and location were determined. PD caused alveolar bone resorption, increased the number of osteoclasts in the alveolar bone crest and also promoted changes in RANKL/OPG mRNA expression. DM1 alone showed alveolar bone destruction and an increased number of osteoclasts at the periapical and furcal regions. DM1 exacerbated these characteristics, with a greater impact on bone structure, resulting in a low OPG content and a higher RANKL/OPG ratio, which correlated with prominent osteoclastogenesis. This work demonstrates that the effects of PD and DM1 enhance bone destruction, confirms the importance of the RANKL signaling pathway in bone destruction in DM1 in animal models and suggests the existence of alternative mechanisms potentiating bone degradation in PD.en
dc.description.affiliationUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Diagnóstico e Cirurgia, Faculdade de Odontologia de Araraquara, Araraquara, Rua Humaitá, 1680, Centro, CEP 14801903, SP, Brasil
dc.description.affiliationUnespUniversidade Estadual Paulista Júlio de Mesquita Filho, Departamento de Diagnóstico e Cirurgia, Faculdade de Odontologia de Araraquara, Araraquara, Rua Humaitá, 1680, Centro, CEP 14801903, SP, Brasil
dc.format.extent137-150
dc.identifierhttp://www.karger.com/Article/FullText/330879
dc.identifier.citationCells Tissues Organs, v. 196, n. 2, p. 137-150, 2012.
dc.identifier.doi10.1159/000330879
dc.identifier.issn1422-6405
dc.identifier.lattes7634063102292261
dc.identifier.lattes7329430744325373
dc.identifier.urihttp://hdl.handle.net/11449/125628
dc.language.isoeng
dc.relation.ispartofCells Tissues Organs
dc.relation.ispartofjcr1.275
dc.relation.ispartofsjr0,572
dc.rights.accessRightsAcesso restritopt
dc.sourceCurrículo Lattes
dc.subjectAlveolar boneen
dc.subjectType 1 diabetes mellitusen
dc.subjectLigatureen
dc.subjectOsteoprotegerinen
dc.subjectReceptor activator of nuclear factor-kappaB ligand Aen
dc.titlePeriodontal disease-associated compensatory expression of osteoprotegerin is lost in type 1 diabetes mellitus and correlates with alveolar bone destruction by regulating osteoclastogenesisen
dc.typeArtigopt
dspace.entity.typePublication
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.lattes7634063102292261[5]
unesp.author.lattes7329430744325373
unesp.author.orcid0000-0003-1705-5481[5]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentDiagnóstico e Cirurgia - FOARpt

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