Endocarditis is an infection of the inner surface of the heart and/or its valves that can be life threatening. There are approximately 15,000 cases of endocarditis reported each year in the United States, and many of these cases likely arise when bacteria that naturally attach to teeth are displaced and pass into the bloodstream during a dental procedure, flossing, or even chewing food. These bacteria are relatively harmless in the mouth, but they 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. Research has indicated that immune cells called monocytes are prominently found in early inflammatory lesions linked to endocarditis. What has been puzzling scientists is that the monocytes tend to disappear from the lesions over time without becoming macrophages. Macrophages are a scavenging immune cell formed from monocytes that re-move debris from tissues, such as the damaged, bacteria-laden cells linked to endocarditis.
In the August issue of the journal Infection and Immunity, National Institute of Dental and Craniofacial Research (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 changes in normal immune response mediated by oral streptococci 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.
(Source: National Institute of Dental and Craniofacial Research Web site, accessed August 17, 2005)
