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Increase Toll-like receptors 2 and 4 in apical periodontitis of rats with chronic liver disease

dc.contributor.authorCantiga-Silva, Cristiane [UNESP]
dc.contributor.authorde Oliveira, Pedro Henrique Chaves [UNESP]
dc.contributor.authorFaria, Flávio Duarte [UNESP]
dc.contributor.authorJusto, Mariana Pagliusi [UNESP]
dc.contributor.authorSivieri-Araújo, Gustavo [UNESP]
dc.contributor.authorErvolino, Edilson [UNESP]
dc.contributor.authorPinheiro, Tiago Novaes
dc.contributor.authorSegura-Egea, Juan José
dc.contributor.authorCintra, Luciano Tavares Angelo [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionDental School of Amazonas State University
dc.contributor.institutionUniversity of Sevilla
dc.date.accessioned2025-04-29T20:11:53Z
dc.date.issued2025-01-01
dc.description.abstractThe aim of this study was to evaluate the influence of liver fibrosis (LF) on the expression of Toll-like receptors (TLR) 2 and 4 in apical periodontitis (AP) in Wistar rats. Forty Wistar rats were allocated in the following groups (n = 10): C—control; AP—apical periodontitis; LF—liver fibrosis; AP + LF—rats with AP and LF. LF and AP were induced by established methodologies. Histological, bacteriological, and immunohistochemical analyses were performed according to pre-established scores. For comparisons between AP and AP + LF groups, the Mann–Whitney test was used (P <.05). The livers of the LF and AP + LF groups showed generalized portal inflammatory infiltrate and collagen fibers confirming the presence of LF. Histopathological analysis in the maxilla of the AP + LF group showed areas of necrosis comprising the entire dental pulp and periapical tissue surrounded by a more intense inflammatory infiltrate than observed in the AP group (P = 0.032). A significant number of specimens in the AP + LF group showed microorganisms beyond the apical foramen adhered to the extraradicular biofilm, demonstrating greater invasion compared to the AP group (P =.008). Immunohistochemical analysis showed a large number of cells immunoreactive for TLR2 and TLR4 in the AP + LF group, compared to the AP group (P < 0.05). Liver fibrosis favors the inflammation and contamination of microorganisms in apical periodontitis and triggers the expression of TLR2 and TLR4, modulating innate immunity response in periapical lesions.en
dc.description.affiliationEndodontic Section Department of Preventive and Restorative Dentistry School of Dentistry São Paulo State University (UNESP), SP
dc.description.affiliationDepartment of Basic Science School of Dentistry São Paulo State University (UNESP), SP
dc.description.affiliationDepartment of Oral Pathology and Oral Medicine Dental School of Amazonas State University, AM
dc.description.affiliationEndodontic Section Department of Stomatology School of Dentistry University of Sevilla
dc.description.affiliationUnespEndodontic Section Department of Preventive and Restorative Dentistry School of Dentistry São Paulo State University (UNESP), SP
dc.description.affiliationUnespDepartment of Basic Science School of Dentistry São Paulo State University (UNESP), SP
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado do Amazonas
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFundação de Amparo à Pesquisa do Estado do Amazonas: 01.01.016301.000658.2018
dc.description.sponsorshipIdFAPESP: 2020/09695-5
dc.format.extent296-304
dc.identifierhttp://dx.doi.org/10.1007/s10266-024-00974-6
dc.identifier.citationOdontology, v. 113, n. 1, p. 296-304, 2025.
dc.identifier.doi10.1007/s10266-024-00974-6
dc.identifier.issn1618-1255
dc.identifier.issn1618-1247
dc.identifier.scopus2-s2.0-85197628685
dc.identifier.urihttps://hdl.handle.net/11449/308289
dc.language.isoeng
dc.relation.ispartofOdontology
dc.sourceScopus
dc.subjectApical periodontitis
dc.subjectLiver disease
dc.subjectLiver fibrosis
dc.subjectToll-like receptors
dc.titleIncrease Toll-like receptors 2 and 4 in apical periodontitis of rats with chronic liver diseaseen
dc.typeArtigopt
dspace.entity.typePublication
unesp.author.orcid0000-0003-2348-7846[9]

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