How Certain Oral Bacteria Might Contribute to Heart Condition

Endocarditis is a sometimes life-threatening infection of the inner surface of the heart and/or its valves.

Of the approximately 15,000 cases of endocarditis reported each year in the United States, many likely arise when bacteria that naturally attach to our teeth are displaced and pass into the bloodstream during a dental procedure, flossing, or even chewing food. These microbes, while relatively harmless in the mouth, have an affinity for damaged endothelial cells or blood clots in the heart, where they attach, multiply, and form larger bacterial colonies that trigger the endocarditis.

Scientists have shown that immune cells called monocytes are prominently found in early inflammatory lesions linked to endocarditis. What's been puzzling is the monocytes tend to disappear from the lesions over time without becoming macrophages, a scavenging immune cell formed from monocytes that removes debris from tissues, such as the damaged, bacteria-laden cells linked to endocarditis.

In the August 2005 issue of the journal Infection and Immunity, NIDCR grantees show that the usual monocyte-macrophage transformation rarely occurs because monocytes infected in studies with the well-known oral bacterium Streptococcus mutans instead become dendritic cells, a type of immune cell that initiates an inflammation-producing immune response upon interaction with this bacterium. This finding indicates that oral streptococci-mediated changes in a person's normal immune response can contribute to endocarditis. It also suggests that an effective future strategy to treat endocarditis might involve learning to turn off the destructive immune response and/or reprogram the monocytes to produce macrophages to clear away the disease-causing bacterial colonies from the heart.