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dc.contributor.authorEstrela, Carlos
dc.contributor.authorDecurcio, Daniel de Almeida
dc.contributor.authorSilva, Julio Almeida
dc.contributor.authorBatista, Aline Carvalho
dc.contributor.authorSouza Lima, Nathalia Caroline de
dc.contributor.authorFreitas Silva, Brunno Santos de
dc.contributor.authorChaves de Souza, Joao Antonio [UNESP]
dc.contributor.authorSouza Costa, Carlos Alberto [UNESP]
dc.date.accessioned2018-11-26T16:28:07Z
dc.date.available2018-11-26T16:28:07Z
dc.date.issued2016-03-01
dc.identifierhttp://dx.doi.org/10.1016/j.joen.2015.11.012
dc.identifier.citationJournal Of Endodontics. New York: Elsevier Science Inc, v. 42, n. 3, p. 439-446, 2016.
dc.identifier.issn0099-2399
dc.identifier.urihttp://hdl.handle.net/11449/161341
dc.description.abstractIntroduction: This study assessed the immune inflammatory profile and the expression of bone resorption activators receptor activator of nuclear factor kappa B ligand (RANKL) and inhibitor osteoprotegerin (OPG) in apical periodontitis (n = 20) that persisted after root canal retreatment. Methods: Immunohistochemistry was used to characterize lymphocyte populations (CD3(+), CD45R0(+), CD8(+), and FoxP3(+) cells), macrophages (CD68(+)), RANKL(+) and OPG(+) cells in persistent apical periodontitis (PAP) and primary periapical lesions (PPLs). By using quantitative real-time polymerase chain reaction, the mRNA expression of RANKL and OPG in PAP and periodontal ligament from healthy teeth was comparatively analyzed. The data were analyzed by Mann-Whitney, Pearson chi(2), and Wilcoxon tests (5% level). Results: PAP showed an elevated number of FoxP3(+) cells compared with PPL (P < .001). The number of CD68(+) cells was reduced in the PAP samples compared with the PPLs (P < .001). Similar number of other lymphocyte populations was observed in PAP and PPLs (P > .05 for all comparisons). No differences in the RANKL, OPG, and immune-inflammatory cells were demonstrated when comparing PAP microscopically classified as cyst with those classified as granulomas (P > .05 for all comparisons). The assessment of mRNA expression revealed higher levels of RANKL. and OPG in PAP compared with the periodontal ligament from healthy teeth (contiol) samples (P < .001). Also, a greater expression of RANKL in comparison with OPG was observed in PAP (P < .001). Conclusions: These findings indicate that PAP consists of biologically active lesions that demonstrate potential of bone resorption (higher expression of RANKL) and is characterized by an immune-inflammatory cell profile that suggests a suppressive and regulatory environment (higher number of FoxP3(+) cells and lower number of macrophages) favorable to more chronic clinical behavior.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent439-446
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofJournal Of Endodontics
dc.sourceWeb of Science
dc.subjectApical periodontitis
dc.subjectbone resorption
dc.subjectimmunological cells
dc.subjectosteoprotegerin
dc.subjectRANK ligand
dc.titleImmune-Inflammatory Cell Profile and Receptor Activator of Nuclear Factor Kappa B Ligand/Osteoprotegerin Expression in Persistent Apical Periodontitis after Root Canal Retreatment Failureen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Federal de Goiás (UFG)
dc.contributor.institutionUniversidade Estadual de Campinas (UNICAMP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationUniv Fed Goias, Dept Stomatol Sci, BR-74605220 Goiania, Go, Brazil
dc.description.affiliationUniv Estadual Campinas, Sao Paulo, Brazil
dc.description.affiliationSao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Sao Paulo, Brazil
dc.description.affiliationUnespSao Paulo State Univ, Araraquara Sch Dent, Dept Physiol & Pathol, Sao Paulo, Brazil
dc.identifier.doi10.1016/j.joen.2015.11.012
dc.identifier.wosWOS:000372559700015
dc.rights.accessRightsAcesso aberto
dc.description.sponsorshipIdCNPq: 474642/2009-7
dc.description.sponsorshipIdCNPq: 306394/2011-1
dc.identifier.fileWOS000372559700015.pdf
unesp.author.lattes4517484241515548[8]
unesp.author.orcid0000-0002-1488-0366[1]
unesp.author.orcid0000-0002-8053-2407[7]
unesp.author.orcid0000-0002-7455-6867[8]
dc.relation.ispartofsjr1,585
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