Associação entre polimorfismos genéticos, condição periodontal e niveis de mediadores inflamatórios na periodontite crônica

• Ano de defesa: 2013
• Autor(a) principal: Joice Dias Correa
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: Doença periodontal; Polimorfismo genético; Mediadores inflamatórios; Polimorfismo (Genética); Periodontite; Mediadores da inflamação
• Link de acesso: http://hdl.handle.net/1843/ZMRO-9BLNZ9

Periodontal disease (PD) results from the interaction of host defense mechanisms with the microorganisms of the oral biofilm. This interaction is regulated by cytokines that can play a protective and/or destructive role in disease progression. Some cytokines, such as IL-17, IFN- and TNF-, promote inflammation. Others, such as IL-10, present a negative role in regulating the inflammatory response. The levels of these molecules and, consequently, the course of PD can be changed by genetic polymorphisms. The aim of this study was to evaluate the presence of genetic polymorphisms of IL-17A, IL-17F, IL-10 and TNFA inpatients with chronic PD and correlate the genotypes with clinical parameters of PD and cytokine levels in periodontal tissues and serum of patients. Individuals with the allele A of IL-17 (197) and IL-10 (1087) showed increased risk for PD, whereas no differences have been detected for TNFA and IL-17F polymorphisms. Furthermore, the allele A of IL-17A was associated with worse clinical parameters, higher activity of MPO and increased expression of inflammatory mediators (IL-17A and CXCL8/IL-8). The GG genotype of IL-10 was correlated with increased levels of IL-10 and reduced expression of CXCL10 in periodontal tissues. On the other hand, the AG genotype carriers exhibited more sites with BOP and increased MPO activity. These results indicate that the IL-17A-197A allele and the IL-10- 1087A allele are associated with increased risk for PD, probably because these genotypes correlate with a pattern of exacerbated inflammatory status in periodontal tissues.