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

Autor(es)

Garcia Paula-Silva, Francisco Wanderley ^{[1, 2]} ; Ribeiro-Santos, Fernanda Regina ^{[1, 3]} ; Ferreira Petean, Igor Bassi ^[1] ; Manfrin Arnez, Maya Fernanda ^[1] ; de Almeida-Junior, Luciano Aparecido ^[1] ; de Carvalho, Fabricio Kitazono ^[1] ; Bezerra da Silva, Lea Assed ^[1] ; Faccioli, Lucia Helena ^[2]

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Fac Odontol Ribeirao Preto, Dept Clin Infantil, Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Lab Inflamacao & Imunol Parasitoses, Dept Anal Clin Toxicol & Bromatol, Fac Ciancias Farmacaut Ribeirao Preto, Ribeirao Preto, SP - Brazil

^[3] Univ Pernambuco, Arco Verde, PE - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Applied Oral Science; v. 28, 2020.
• Citações Web of Science: 0

Resumo

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 mu L of a suspension of 0.1 mu g/mu L) 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 (alpha=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 PPAR delta, differently from inoculation of LPS, that induced PPAR alpha and PPAR gamma 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. (AU)

• Processo FAPESP: 10/17611-4 - Mecanismos envolvidos na modulação da via 5-lipoxigenase na lesão periapical experimentalmente induzida
• Beneficiário: Francisco Wanderley Garcia de Paula e Silva
• Modalidade de apoio: Auxílio à Pesquisa - Jovens Pesquisadores
• Processo FAPESP: 12/01292-2 - Papel da Enzima 5-Lipoxigenase na Osteoclastogênese durante o Desenvolvimento da Lesão Periapical Experimental
• Beneficiário: IGOR BASSI FERREIRA PETEAN
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica