Perfurações experimentais de furca tratadas com MTA: Análise da resposta imune

• Ano de defesa: 2010
• Autor(a) principal: Viviane de Paula Lima
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: citocinas inflamatórias; perfuração; MTA; Cimentos dentários; Canal radicular Tratamento; Biocompatibilidade; Relação dose-resposta imunológica; Materiais restauradores do canal radicular; Citocinas
• Link de acesso: http://hdl.handle.net/1843/ZMRO-89LN6H

Furcation perforation is a mechanical or pathologic communication between the root canal system and the external tooth surface. Nowadays, MTA is the best material to treat perforation because it is biocompatible and has a good sealing ability. The aim of this study was to evaluate the expression of cytokines in the presence of MTA used to treat an induced furcation perforation in mouse. BALB/c mouse were used (n=5). The first upper molar had its furcation perforated and treated with MTA in the left side (experimental group) while in the right side, the furcation was not treated (control group). The animals were killed in 7, 14 and 21 days after the intervention. The teeth and the around tissue were extracted and mashed. Then, the RNA was extracted. The expressions of the cytokines IFN-, TNF-, IL-10, IL-4, TGF- e RANKL were investigated by real time PCR. Comparing the experimental group with the control group, only IL-4 exhibited statistical difference (p<0.05). In 07 days, there was a lower expression (p<0.05) of TNF- and IL-4 comparing to 14 days. The expression of RANKL, IFN- and TNF- demonstrated to be statistically higher (p<0.05) in 14 days comparing to 21 days. IL-10 expressed increased (p<0.05) in 21 days. The expression of TGF- did not exhibit results with statistic relevance. So, it seems that MTA favored the expression of pro-inflammatory cytokines in an intermediate phase of imuno-inflammatory response (14 days) and a reduction of these cytokines in the later phase of the response, probably due to an IL-10 imunoregulation.