Caracterização da doença periodontal associada à artrite experimental em camundongos

• Ano de defesa: 2011
• Autor(a) principal: Celso Martins Queiroz Junior
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de Minas Gerais; UFMG
• Palavras-chave em Português: TNF-; Microbiota Oral; Doença Periodontal; Artrite; Biologia celular; Microbiota oral; Doença periodontal; Fator de necrose de tumor
• Link de acesso: http://hdl.handle.net/1843/BUOS-8RGJ2Q

Periodontal disease (PD) is a chronic infectious and inflammatory condition of the tooth supporting tissues, whose pathogenesis may be associated to systemic conditions, such as rheumatoid arthritis (RA). RA is a chronic systemic auto-immune inflammatory disorder, which triggers joint lesions. PD and RA share several pathogenic features and, indeed, clinical studies have suggested that RA patients are more likely to experience PD more frequently and intensively. Nevertheless, this association is not well understood. Therefore, the aim of the current study was to characterize the PD induced or exacerbated by RA, using experimental models in mice. Initially, a mouse model of chronic antigen-induced arthritis (AIA) was established and joint, periodontal and systemic parameters were evaluated. Concomitantly to joint lesion, there was significant alveolar bone loss, which was dependent on oral microbiota and was associated to enhanced expression of TNF-, IL-1, IFN-, IL-6 in maxillae, the transcription factor ROR in submandibular lymph node, serum anti-collagen I IgG, besides increased cell reactivity to this protein. Joint, oral and serum conditions triggered by AIA were ameliorated by treatment with an anti-TNF- therapy. Subsequently, the experimental AIA model was associated to a model of Aggregatibacter actinomycetemcomitansinduced PD, in order to investigate the influence of AIA on established PD. AIA exacerbated the alveolar bone loss triggered by A. actinomycetemcomitans, although the oral infection did not influence joint lesion. This process was associated to enhanced expression of the transcription factor tBET in submandibular lymph nodes, higher release of IFN- in maxillae, as well as the production of significant serum levels of IL- 6. This condition was also ameliorated by an anti-TNF- therapy. In conclusion, experimental AIA induces signs of PD and exacerbates A. actinomycetemcomitansinduced alveolar bone loss. These periodontal imbalances are dependent on oral microbiota and are attenuated by an anti-TNF- therapy