DT News - UK - Dental plaque bacteria may trigger endocarditis

Dental Tribune International

Tue. 27 March 2012

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DUBLIN, Ireland: Oral bacteria that escape into the bloodstream are able to cause blood clots and trigger life-threatening endocarditis, researchers from the Royal College of Surgeons in Ireland (RCSI) and the University of Bristol have discovered. Further research into this topic could lead to the development of new drugs to combat infective heart disease.

The researchers’ findings were presented at the Society for General Microbiology’s spring conference in Dublin last week.

Streptococcus gordonii is a common inhabitant of the mouth and contributes to plaque that forms on the surface of teeth. These bacteria can enter into the bloodstream through bleeding gums and start to wreak havoc by masquerading as human proteins.

The researchers discovered that S. gordonii is able to produce a molecule on its surface that allows it to mimic the human protein fibrinogen—a blood-clotting factor. This activates the platelets, causing them to clump inside blood vessels. These unwanted blood clots encase the bacteria, protecting them from the immune system and from antibiotics used to treat infection. Platelet clumping can lead to growths on the heart valves (endocarditis), or inflammation of blood vessels that can block the blood supply to the heart or brain.

Dr Helen Petersen, clinical lecturer at the Department of Oral and Maxillofacial Surgery at the London UCL Eastman Dental Institute, presented the findings. She stated that better understanding of the relationship between bacteria and platelets could ultimately lead to new treatments for infective endocarditis. “In the development of infective endocarditis, a crucial step is the bacteria sticking to the heart valve and then activating platelets to form a clot. We are now looking at the mechanism behind this sequence of events in the hope that we can develop new drugs which are needed to prevent blood clots and also infective endocarditis,” Petersen said.

Infective endocarditis is treated with surgery or strong antibiotics, which is becoming more difficult with growing antibiotic resistance. “About 30 per cent of people with infective endocarditis die and most will require surgery for replacement of the infected heart valve with a metal or animal valve,” according to Petersen.

Dr Steve Kerrigan from the RCSI commented: “Our team has now identified the critical components of the S. gordonii molecule that mimics fibrinogen, so we are getting closer to being able to design new compounds to inhibit it. This would prevent the stimulation of unwanted blood clots.”

The team is also trying to determine how widespread this phenomenon is by studying other bacteria related to S. gordonii.

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