Periodontal disease and cerebral atherosclerotic disease. Translational study

Although an association has been established between periodontal disease (PD) and large vessel ischemic stroke, little is known about the relationship between PD and lacunar infarct (LI), a subtype of cerebral small vessel disease that is responsible for almost 25% of the ischemic stroke cases. Our...

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Detalles Bibliográficos
Autor: Leira Feijóo, Yago
Tipo de recurso: tesis doctoral
Fecha de publicación:2018
País:España
Institución:Universidad de Santiago de Compostela (USC)
Repositorio:Minerva. Repositorio Institucional de la Universidad de Santiago de Compostela
Idioma:inglés
OAI Identifier:oai:minerva.usc.gal:10347/17259
Acceso en línea:http://hdl.handle.net/10347/17259
Access Level:acceso abierto
Palabra clave:Materias::Investigación::32 Ciencias médicas::3207 Patología::320706 Endotoxinas
Materias::Investigación::32 Ciencias médicas::3205 Medicina interna::320507 Neurología
Descripción
Sumario:Although an association has been established between periodontal disease (PD) and large vessel ischemic stroke, little is known about the relationship between PD and lacunar infarct (LI), a subtype of cerebral small vessel disease that is responsible for almost 25% of the ischemic stroke cases. Our aim was, therefore, to investigate whether PD is linked with LI and if so, to study potential mechanisms underlying this association. In the present study we found that PD was positively associated with LI and, when present, emerged as one of the main contributors to an enhanced systemic inflammatory state promoting endothelial dysfunction with elevated levels of IL-6, PTX3, sTWEAK, and Aβ1-40 in LI patients. Moreover, moderate to severe active PD was an independent predictor of poor functional outcome in LI patients. These findings were corroborated in a preclinical in vivo study in the rodent model, in which experimental PD induced with lipopolysaccharide from Porphyromonas gingivalis was associated with a mild systemic inflammatory response with disruption of the vascular endothelial function.