Imunolocalização de células positivas para a enzima diacilglicerol quinase α (DGKα) em polpas de ratos expostas à contaminação

• Ano de defesa: 2014
• Autor(a) principal: Fagundes, Gabriela Xavier
• Orientador(a): Figueiredo, José Antonio Poli de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Pontifícia Universidade Católica do Rio Grande do Sul
• Programa de Pós-Graduação: Programa de Pós-Graduação em Odontologia
• Departamento: Faculdade de Odontologia
• País: BR
• Palavras-chave em Português: ODONTOLOGIA; ENDODONTIA; INFLAMAÇÃO; RATOS - EXPERIÊNCIAS
• Área do conhecimento CNPq: CNPQ::CIENCIAS DA SAUDE::ODONTOLOGIA
• Link de acesso: http://tede2.pucrs.br/tede2/handle/tede/1257

Introduction: Dental pulp is composed of loose connective tissue, which reacts when facing a pathogenic agent, and the inflammation is the first response. DGKα is one of the key enzymes involved on inflammations cellular events. It participates on the neutrophils recruiting to the injury site and on the regulation of superoxide production. The aim of this study was to evaluate the localization of the DGKα in healthy and inflamed/infected dental pulp of rats. Methods: Were used eighteen (18) male Wistar rats. The animals were divided into three groups of six rats each. In Group 1 (control group), no cavity opening was performed. In Groups 2 and 3 dental pulp of the left first molars was exposed to oral environment for 24hours and 7 days respectively. Euthanasia was performed after the experimental periods and the jaws were dissected for histological evaluation and immunodetection of DGKα enzyme. Results: Histological analysis of the dental pulp showed that tissue exposure led to inflammatory and degenerative events, which varied in their extension according to the experimental period of time. In groups 2 and 3, DGKα immunolabeling was observed in neutrophils and abscessed areas, being detected on a greater amplitude of pulp tissue in the 24 hour period. Conclusions: DGKα is expressed on the initial stages of pulp inflammation, although there is no relation with its extent. The understanding of the DGKα role in the pathways of pulp inflammation can help the development of new therapeutic strategies to promote pulp repair.