The effect of periodontal pathogens and their products on cardiovascular disease

Abstract

Periodontal disease is a condition in which the gums and bones surrounding the teeth are inflamed. It is a common cause of oral discomfort and tooth loss, but in recent years has been linked to a variety of systemic problems. Among them is cardiovascular disease, which is the top cause of death in the developed world. There is evidence that periodontal pathogens invade the bloodstream from the gingival pockets and contribute to the progression of disease through a variety of different mechanisms. First, they initiate the systemic inflammatory process by invading and activating vascular endothelial cells to upregulate adhesion molecules and chemokines, which then in turn activate macrophages to take up low density lipoprotein and deposit it on the luminal wall. Atherosclerotic plaque is pro-thrombotic, which increases the chances of forming blood clots and ischemic attacks. Periodontal pathogens also can induce the proliferation of antibodies that can cross-react with self-antigens, resulting in an autoimmune disease. The presence of these pathogens also causes oxidative stress through the production of reactive oxygen species, which is highly damaging.

Since these pathogens have many ways of contributing to cardiovascular diseases, it has been hypothesized that treating the periodontal problems will help prevent the progression of cardiovascular disease. Several studies show that addressing periodontitis has resulted in decreased levels of inflammatory markers like C-reactive protein, interleukin-6, and fibrinogen, lower incidences of stroke, decreased blood pressure and lipid levels, and a lower left ventricular mass.