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Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/82274
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Campo DCValorIdioma
dc.creatorJoão Luiz Guilherme Netopt_BR
dc.creatorSandra Yasuyo Fukada Alvespt_BR
dc.creatorLucas Gabriel Rodrigues Venturinipt_BR
dc.creatorAyda Henriques Schneiderpt_BR
dc.creatorThaise Mayumi Tairapt_BR
dc.creatorLetícia Fernanda Duffles Rodriguespt_BR
dc.creatorFlávio Protásio Veraspt_BR
dc.creatorSicília Rezende Oliveirapt_BR
dc.creatorTarcília Aparecida da Silvapt_BR
dc.creatorFernando de Queiroz Cunhapt_BR
dc.date.accessioned2025-05-14T19:21:15Z-
dc.date.available2025-05-14T19:21:15Z-
dc.date.issued2023-11-
dc.citation.volume49pt_BR
dc.citation.issue11pt_BR
dc.citation.spage1514pt_BR
dc.citation.epage1521pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.joen.2023.07.027pt_BR
dc.identifier.issn1878-3554pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/82274-
dc.description.resumoIntroduction: Neutrophil extracellular traps (NETs) have been described as structures composed of DNA and proteins, such as elastase and myeloperoxidase, that are able to kill bacteria extracellularly. The aim of the present study was to evaluate the role of NETs in bone resorption observed in pulp infection-induced apical periodontitis in mice. Methods: Apical periodontitis was experimentally induced by exposing the dental pulp of the mandibular first molar of mice to the oral microenvironment. The expression of NETs was evaluated by immunofluorescence in mice and biopsies of apical periodontitis. Mice were treated with vehicle or DNase I to degrade NETs, and the samples were collected after 7 days. The size of the apical lesion and the osteoclast number were determined in hematoxylin-eosin- and tartrate-resistant acid phosphatase-stained sections, respectively. Osteoclast differentiation and function markers were evaluated by quantitative polymerase chain reaction. The level of NETs in the serum was determined by the myeloperoxidase-DNA PicoGreen assay. Results: We first confirmed the presence of neutrophils and NETs at the site of the lesion in mice and in biopsies of patients with apical periodontitis. The treatment of mice with DNase I reduced the level of NETs in the serum and led to a reduction in apical lesion size and alveolar bone resorption. This effect was associated with a reduction of local inflammatory infiltrate and a reduced number of osteoclasts. We found that the increased expression of Acp5, Ctsk, and Rankl genes associated with osteoclast formation and function were abrogated by the absence of NETs. Conclusions: Our data highlight NETs as an important player in the pathogenesis of apical periodontitis with regard to the local inflammation and consequent bone resorption after pulp infection.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPESP - Fundação de Amparo à Pesquisa do Estado de São Paulopt_BR
dc.format.mimetypepdfpt_BR
dc.languageengpt_BR
dc.publisherUniversidade Federal de Minas Geraispt_BR
dc.publisher.countryBrasilpt_BR
dc.publisher.departmentFAO - DEPARTAMENTO DE CLÍNICApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofJournal of Endodonticspt_BR
dc.rightsAcesso Restritopt_BR
dc.subjectApical periodontitispt_BR
dc.subjectBone resorptionpt_BR
dc.subjectNeutrophil extracellular trapspt_BR
dc.subjectNeutrophilspt_BR
dc.subjectOsteoclastspt_BR
dc.subject.otherPeriapical periodontitispt_BR
dc.subject.otherBone resorptionpt_BR
dc.subject.otherExtracellular trapspt_BR
dc.subject.otherNeutrophilspt_BR
dc.subject.otherOsteoclastspt_BR
dc.subject.otherEvaluation studypt_BR
dc.subject.otherDeoxyribonuclease Ipt_BR
dc.subject.otherInfectionspt_BR
dc.subject.otherGene expressionpt_BR
dc.subject.otherTartrate-resistant acid phosphatasept_BR
dc.subject.otherRANK ligandpt_BR
dc.titleNeutrophil extracellular traps aggravate apical periodontitis by stimulating osteoclast formationpt_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.sciencedirect.com/science/article/pii/S0099239923005034?via%3Dihubpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6589-4784pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7585-7709pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-2474-2773pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-3719-9503pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-2781-9986pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-6222-4064pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-8164-2122pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-9623-7835pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4755-1670pt_BR
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