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dc.contributor.authorFrazão, Deborah Ribeiropt_BR
dc.contributor.authorMendes, Paulo Fernando Santospt_BR
dc.contributor.authorSilva, Daiane Claydes Baia dapt_BR
dc.contributor.authorMoura, João Daniel Mendonça dept_BR
dc.contributor.authorSantos, Vinicius Ruan Nevespt_BR
dc.contributor.authorSousa, José Mário Matospt_BR
dc.contributor.authorBalbinot, Gabriela de Souzapt_BR
dc.contributor.authorGuimarães, Douglas M.pt_BR
dc.contributor.authorCollares, Fabrício Mezzomopt_BR
dc.contributor.authorLima, Rafael Rodriguespt_BR
dc.date.accessioned2024-02-09T05:08:25Zpt_BR
dc.date.issued2023pt_BR
dc.identifier.issn1664-042Xpt_BR
dc.identifier.urihttp://hdl.handle.net/10183/271816pt_BR
dc.description.abstractThis study aimed to investigate if apical periodontitis in different periods changes systemic levels of the antioxidant and pro-oxidant parameters in Wistar rats. Twenty-four rats were randomly allocated into healthy animals, apical periodontitis at 14 days (AP14) and apical periodontitis at 28 days (AP28). The first mandibular molars were accessed in the AP groups, and the pulp chamber was exposed to the oral environment, inducing the apical lesion. After 14 and 28 days, the animals were anesthetized, euthanized, and hemimandibles were collected for micro-computed tomography (micro-CT) analysis to measure lesion volume, bone volume (BV), percent of bone to total tissue volume (BV/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), and trabecular space (Tb.Sp). A histological examination of the remaining bone was also performed. Finally, blood samples were collected for oxidative biochemistry analysis, investigating glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), and lipid peroxidation (TBARS). The lesion volume was greater at 28 than at 14 days, as shown by micro-CT. AP14 and AP28 had decreased BV and Tb.Th, but only AP28 showed a reduction in BV/TV. Tb.N and Tb. Sp were increased in apical periodontitis at 28 days. In the histopathological analysis, AP14 had focal regions of moderate mononuclear inflammatory infiltrate, and AP28 had an intense inflammatory infiltrate with bacterial colonies. In the biochemical evaluation, GSH, TEAC, and TBARS were increased after 14 days. However, GSH returned to control levels, TEAC was similar to AP14, and TBARS increased significantly after 28 days. Therefore, the oxidative biochemistry response was modulated according to the progression of periapical damage. After 14 days, the organism could still react to the injury. However, at 28 days, the antioxidant response decreased, associated with an increase in TBARSen
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofFrontiers in Physiology. Lausanne. Vol. 14, (2023), p. 1 - 12pt_BR
dc.rightsOpen Accessen
dc.subjectPeriodontite periapicalpt_BR
dc.subjectPeriapical periodontitisen
dc.subjectEstresse oxidativopt_BR
dc.subjectOxidative stressen
dc.subjectRatos Wistarpt_BR
dc.subjectWistar ratsen
dc.subjectMicroCTen
dc.subjectMicrotomografia por raio-xpt_BR
dc.subjectInflammationen
dc.titleModulation of blood redox status by the progression of induced apical periodontitis in ratspt_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001194679pt_BR
dc.type.originEstrangeiropt_BR


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