Detecção de streptococcus mutans e avaliação da expressão de marcadores teciduais em placas ateroscleróticas de pacientes com doença vascular e vasos sadios

• Ano de defesa: 2017
• Autor(a) principal: Fernandes, Clarissa Pessoa
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Aterosclerose; Streptococcus mutans; Reação em Cadeia da Polimerase em Tempo Real; Imuno-Histoquímica; Inflamação
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/22940

Over the past few years, the association between oral bacteria and atherosclerosis has been investigated, and studies have suggested that cariogenic bacteria are directly and indirectly involved in the etiopathogenesis and progression of this disease. Streptococcus mutans (SM) has demonstrated the ability to invade and cause damage to endothelial cells, favor the adhesion of leukocytes in vascular endothelium and promote the transformation of macrophages into foam cells, events directly related to the development of atherosclerosis. This microorganism has been detected in atherosclerotic plaques with variable frequency, and laboratory studies have investigated its role in the activation of inflammatory and thrombogenic markers, which are indirectly associated with the pathogenesis of this disease. However, the pathogenic mechanism of atherosclerosis is not yet fully elucidated, and the role of oral bacteria needs to be extensively investigated. The present study aimed to evaluate the association between the presence of SM and tissue and inflammatory alterations in vessels with atherosclerosis. A total of 13 atherosclerotic plaques, collected from patients with carotid stenosis or aortic aneurysm, and 10 control samples of healthy blood vessels (aortic and carotid arteries) collected during necropsy procedure, were submitted to Real-time Polymerase Chain Reaction (qPCR), histopathological analysis, histochemical analysis by Giemsa staining (GS) and immunohistochemical analysis for SM, IL-1!, TNF-", CRP, osteopontin, fibrinogen and CD61 (Streptavidin-biotin-peroxidase method). All microscopically healthy control specimens were positive for SM only through qPCR, whereas atherosclerotic plaque specimens were positive for SM through qPCR and immunohistochemistry, and showed histopathological characteristics of severe atherosclerosis (100%). Presence of fibrous tissue (100.0%) and calcification (92.3%) were the most frequent features, followed by thrombus formation (84.6%), mononuclear inflammatory cells (76.9%) and presence of core lipid (61.5%). GC showed that streptococcus colonized areas of core lipid, fibrous tissue and calcification, and was not positive in vessels of the control group. All 13 atherosclerotic plaques, immunopositive for SM, were positive for the fibrinogen, IL-1!, osteopontin and CD61 antibodies, whereas immunoexpression for CRP and TNF-" was evidenced in 12 samples (92.3%). The reactivity to IL-1!, TNF-", osteopontin and CD61 was not found in the control samples, immunonegative to SM, but in some cases, immunoexpression of fibrinogen (60.0%) and PCR (50.0%) was observed. The detection of SM in atherosclerotic plaques, in addition to the visualization of Streptococcus in areas of tissue alteration, suggests that in these samples, microorganisms found a favorable 10 environment for their proliferation. In addition, positive immunoexpression of TNF-", IL-1!, fibrinogen, CRP, osteopontin and CD61 in atherosclerotic plaque samples immunopositive to SM may suggest a possible association with atherosclerosis.