Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis

Abstract Purpose To evaluate the kinetics of apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial lipopolysaccharide (LPS) and the regulation of major enzymes and receptors involved in the...

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Main Authors: Francisco Wanderley Garcia PAULA-SILVA, Fernanda Regina RIBEIRO-SANTOS, Igor Bassi Ferreira PETEAN, Maya Fernanda MANFRIN ARNEZ, Luciano Aparecido de ALMEIDA-JUNIOR, Fabrício Kitazono de CARVALHO, Léa Assed Bezerra da SILVA, Lúcia Helena FACCIOLI
Format: Article
Language:English
Published: University of São Paulo 2020-05-01
Series:Journal of Applied Oral Science
Subjects:
Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572020000100446&tlng=en
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author Francisco Wanderley Garcia PAULA-SILVA
Fernanda Regina RIBEIRO-SANTOS
Igor Bassi Ferreira PETEAN
Maya Fernanda MANFRIN ARNEZ
Luciano Aparecido de ALMEIDA-JUNIOR
Fabrício Kitazono de CARVALHO
Léa Assed Bezerra da SILVA
Lúcia Helena FACCIOLI
author_facet Francisco Wanderley Garcia PAULA-SILVA
Fernanda Regina RIBEIRO-SANTOS
Igor Bassi Ferreira PETEAN
Maya Fernanda MANFRIN ARNEZ
Luciano Aparecido de ALMEIDA-JUNIOR
Fabrício Kitazono de CARVALHO
Léa Assed Bezerra da SILVA
Lúcia Helena FACCIOLI
author_sort Francisco Wanderley Garcia PAULA-SILVA
collection DOAJ
description Abstract Purpose To evaluate the kinetics of apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial lipopolysaccharide (LPS) and the regulation of major enzymes and receptors involved in the arachidonic acid metabolism. Methodology Apical periodontitis was induced in C57BL6 mice (n=96), by root canal exposure to oral cavity (n=48 teeth) or inoculation of LPS (10 µL of a suspension of 0.1 µg/µL) from E. coli into the root canals (n= 48 teeth). Healthy teeth were used as control (n=48 teeth). After 7, 14, 21 and 28 days the animals were euthanized and tissues removed for histopathological and qRT-PCR analyses. Histological analysis data were analyzed using two-way ANOVA followed by Sidak’s test, and qRT-PCR data using two-way ANOVA followed by Tukey’s test (α=0.05). Results Contamination by microorganisms led to the development of apical periodontitis, characterized by the recruitment of inflammatory cells and bone tissue resorption, whereas inoculation of LPS induced inflammatory cells recruitment without bone resorption. Both stimuli induced mRNA expression for cyclooxygenase-2 and 5-lipoxygenase enzymes. Expression of prostaglandin E 2 and leukotriene B 4 cell surface receptors were more stimulated by LPS. Regarding nuclear peroxisome proliferator-activated receptors (PPAR), oral contamination induced the synthesis of mRNA for PPARδ, differently from inoculation of LPS, that induced PPARα and PPARγ expression. Conclusions Contamination of the root canals by microorganisms from oral cavity induced the development of apical periodontitis differently than by inoculation with LPS, characterized by less bone loss than the first model. Regardless of the model used, it was found a local increase in the synthesis of mRNA for the enzymes 5-lipoxygenase and cyclooxygenase-2 of the arachidonic acid metabolism, as well as in the surface and nuclear receptors for the lipid mediators prostaglandin E2 and leukotriene B4.
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spelling doaj.art-1486ca9c524941ebb5f8fe83f28638412022-12-21T21:23:36ZengUniversity of São PauloJournal of Applied Oral Science1678-77652020-05-012810.1590/1678-7757-2019-0699Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitisFrancisco Wanderley Garcia PAULA-SILVAhttps://orcid.org/0000-0001-8559-532XFernanda Regina RIBEIRO-SANTOSIgor Bassi Ferreira PETEANMaya Fernanda MANFRIN ARNEZLuciano Aparecido de ALMEIDA-JUNIORFabrício Kitazono de CARVALHOLéa Assed Bezerra da SILVALúcia Helena FACCIOLIAbstract Purpose To evaluate the kinetics of apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial lipopolysaccharide (LPS) and the regulation of major enzymes and receptors involved in the arachidonic acid metabolism. Methodology Apical periodontitis was induced in C57BL6 mice (n=96), by root canal exposure to oral cavity (n=48 teeth) or inoculation of LPS (10 µL of a suspension of 0.1 µg/µL) from E. coli into the root canals (n= 48 teeth). Healthy teeth were used as control (n=48 teeth). After 7, 14, 21 and 28 days the animals were euthanized and tissues removed for histopathological and qRT-PCR analyses. Histological analysis data were analyzed using two-way ANOVA followed by Sidak’s test, and qRT-PCR data using two-way ANOVA followed by Tukey’s test (α=0.05). Results Contamination by microorganisms led to the development of apical periodontitis, characterized by the recruitment of inflammatory cells and bone tissue resorption, whereas inoculation of LPS induced inflammatory cells recruitment without bone resorption. Both stimuli induced mRNA expression for cyclooxygenase-2 and 5-lipoxygenase enzymes. Expression of prostaglandin E 2 and leukotriene B 4 cell surface receptors were more stimulated by LPS. Regarding nuclear peroxisome proliferator-activated receptors (PPAR), oral contamination induced the synthesis of mRNA for PPARδ, differently from inoculation of LPS, that induced PPARα and PPARγ expression. Conclusions Contamination of the root canals by microorganisms from oral cavity induced the development of apical periodontitis differently than by inoculation with LPS, characterized by less bone loss than the first model. Regardless of the model used, it was found a local increase in the synthesis of mRNA for the enzymes 5-lipoxygenase and cyclooxygenase-2 of the arachidonic acid metabolism, as well as in the surface and nuclear receptors for the lipid mediators prostaglandin E2 and leukotriene B4.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572020000100446&tlng=enProstaglandin E 2Leukotriene B 4Apical periodontitisLipopolysaccharideRoot canal contamination
spellingShingle Francisco Wanderley Garcia PAULA-SILVA
Fernanda Regina RIBEIRO-SANTOS
Igor Bassi Ferreira PETEAN
Maya Fernanda MANFRIN ARNEZ
Luciano Aparecido de ALMEIDA-JUNIOR
Fabrício Kitazono de CARVALHO
Léa Assed Bezerra da SILVA
Lúcia Helena FACCIOLI
Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
Journal of Applied Oral Science
Prostaglandin E 2
Leukotriene B 4
Apical periodontitis
Lipopolysaccharide
Root canal contamination
title Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
title_full Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
title_fullStr Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
title_full_unstemmed Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
title_short Root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin E 2 and leukotriene B 4 signaling in apical periodontitis
title_sort root canal contamination or exposure to lipopolysaccharide differentially modulate prostaglandin e 2 and leukotriene b 4 signaling in apical periodontitis
topic Prostaglandin E 2
Leukotriene B 4
Apical periodontitis
Lipopolysaccharide
Root canal contamination
url http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572020000100446&tlng=en
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