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Use este identificador para citar o ir al link de este elemento: http://hdl.handle.net/1843/84380
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Campo DCValorIdioma
dc.creatorAline Maria do Coutopt_BR
dc.creatorAndré Oliveira Naufel de Toledopt_BR
dc.creatorCelso Martins Queiroz-juniorpt_BR
dc.creatorPatrícia Caldeira Patrícia Carlos Caldeirapt_BR
dc.creatorMila Fernandes Moreira Madeirapt_BR
dc.creatorMaria Cássia Ferreira de Aguiarpt_BR
dc.date.accessioned2025-08-14T20:36:32Z-
dc.date.available2025-08-14T20:36:32Z-
dc.date.issued2019-
dc.citation.volume33pt_BR
dc.citation.spage1pt_BR
dc.citation.epage8pt_BR
dc.identifier.doihttps://doi.org/10.1590/1807-3107bor-2019.vol33.0093pt_BR
dc.identifier.issn1807-3107pt_BR
dc.identifier.urihttp://hdl.handle.net/1843/84380-
dc.description.resumoCytokines and chemokines have a fundamental role in the maintenance of inflammation and bone response, which culminate in the development of chronic periapical lesions. Regulatory (Treg) and Th17 cytokines play a key role in regulating the immune response involved in this process. The aim of this study was to investigate the role of Treg and Th17 cells in chronic inflammatory periapical disease, by comparing the expression of the immunoregulatory mediators TGF-β, IL-10, CCL4, and the proinflammatory IL-17 and CCL20 in the periapical tissue of teeth with pulp necrosis, with and without associated chronic lesions. Eighty-six periapical tissue samples were obtained from human teeth. The samples were divided into three groups: pulp necrosis with a periapical lesion (n=26); pulp necrosis without a periapical lesion (n=30), and control (n=30). All samples were submitted to histopathological analysis and cytokine and chemokine measurement through ELISA. Statistical analyses were done with Kruskal-Wallis and Mann-Whitney tests and Spearman correlation. The group with pulp necrosis and a periapical lesion showed a higher expression of CCL4 and TGF-β in comparison with pulp necrosis without a lesion. CCL20 was higher in the group with a periapical lesion when compared to the control. In all groups there was a weak positive correlation between IL-17/CCL20, IL-10/CCL4, and IL-17/TGF-β. Both types of cytokines, pro-inflammatory and immunoregulatory, occur simultaneously in periapical tissue. However, a rise in immunosuppressive cytokines and chemokines (CCL4 and TGF-β) in periapical lesions suggests a role of these cytokines in stable periapical disease.pt_BR
dc.description.sponsorshipCNPq - Conselho Nacional de Desenvolvimento Científico e Tecnológicopt_BR
dc.description.sponsorshipFAPEMIG - Fundação de Amparo à Pesquisa do Estado de Minas Geraispt_BR
dc.description.sponsorshipCAPES - Coordenação de Aperfeiçoamento de Pessoal de Nível Superiorpt_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.departmentICB - DEPARTAMENTO DE MICROBIOLOGIApt_BR
dc.publisher.departmentICB - DEPARTAMENTO DE MORFOLOGIApt_BR
dc.publisher.initialsUFMGpt_BR
dc.relation.ispartofBrazilian Oral Researchpt_BR
dc.rightsAcesso Abertopt_BR
dc.subjectCytokinespt_BR
dc.subjectEndodonticspt_BR
dc.subjectPeriapical diseasespt_BR
dc.subjectT-lymphocytes, regulatorypt_BR
dc.subjectTh17 cellspt_BR
dc.subject.otherCytokinespt_BR
dc.subject.otherEndodonticspt_BR
dc.subject.otherPeriapical diseasespt_BR
dc.subject.otherT-lymphocytes, regulatorypt_BR
dc.subject.otherTh17 cellspt_BR
dc.subject.otherTransforming Growth Factor betapt_BR
dc.subject.otherChemokine CCL4pt_BR
dc.subject.otherChemokine CCL20pt_BR
dc.subject.otherInterleukin-10pt_BR
dc.subject.otherInterleukin-17pt_BR
dc.subject.otherDental pulp necrosispt_BR
dc.titleCytokines and chemokines associated with treg/th17 response in chronic inflammatory periapical diseasept_BR
dc.typeArtigo de Periódicopt_BR
dc.url.externahttps://www.scielo.br/j/bor/a/ghNQX5CCPQ4Dx7HC5F4jMDv/?lang=enpt_BR
dc.identifier.orcidhttps://orcid.org/0000-0003-4306-2554pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-7884-7709pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-9179-0145pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0002-1770-9978pt_BR
dc.identifier.orcidhttps://orcid.org/0000-0001-5134-3466pt_BR
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