Atherosclerosis is the developed world’s leading cause of death. New studies by Drs. Caroline Genco and James Hamilton at Boston University School of Medicine have begun to define the precise mechanisms contributing to the link between infection with Porphyromonas gingivalis and atherosclerotic disease. They report on in vivo high-resolution magnetic resonance imaging (MRI) to document P gingivalis-mediated inflammation and atherosclerosis in a mouse model. MRI allows for detailed studies of atherosclerosis progression in the same animal that can depict the narrowing of the arterial lumen and small vessel wall areas. The scientists show that P gingivalis infection accelerates inflammation and atherosclerosis in the innominate artery, an artery that has a high degree of lesion progression. Lesions in the innominate artery express traits of clinical disease in humans, including vessel narrowing characterized by atrophic media and perivascular inflammation and plaque disruption. Plaque rupture is the basis for the coronary thrombosis in acute ischemia. In humans, plaques with extensive macrophage accumulation and inflammation have a greater likelihood of disruption at their luminal surface, and formation of a life-threatening thrombus. These studies are the first to show progression of plaque in the innominate arteries by in vivo MRI, and lipid and immunohistochemical analysis following exposure to an infectious agent, and to document protection from plaque progression via immunization. It is important to question whether P gingivalis accelerates atherosclerotic plaque formation in the innominate artery leading to increased numbers of vulnerable plaques, and possibly enhanced plaque rupture. Future studies will explore this possibility and test new therapeutic strategies to prevent infection induced atherosclerotic disease.
(Source: ScienceDaily, January 4, 2011)
