Dental plaque, platelets, and cardiovascular diseases

Area of Science:

• Cardiovascular disease research
• Microbiology
• Thrombosis research

Background:

• Cardiovascular diseases like atherosclerosis and myocardial ischemia result from complex genetic and environmental factors.
• Periodontitis, an oral infection, can lead to the spread of dental plaque bacteria into the bloodstream.
• Bacteremia from periodontitis may contribute to vascular inflammation, atherosclerosis, and myocardial infarction risk.

Purpose of the Study:

• To investigate the role of dental plaque bacteria in inducing platelet aggregation and thromboembolic events.
• To determine if Streptococcus sanguis expressing platelet aggregation-associated protein (PAAP+) causes cardiac and pulmonary abnormalities.

Main Methods:

• An in vitro model of thrombosis was used to assess platelet aggregation.
• Intravenous infusion of PAAP+ Streptococcus sanguis into rabbits.
• Monitoring of electrocardiogram (ECG), heart rate, blood pressure, and respiratory rate.
• Assessment of platelet accumulation in the lungs using 111Indium-labeled platelets.

Main Results:

• PAAP+ Streptococcus sanguis induced rapid, intermittent ECG abnormalities, including left axis deviation and ST-segment depression, in rabbits.
• Infusion led to dose-dependent thrombocytopenia, tachypnea, and accumulation of labeled platelets in the lungs.
• These cardiac and pulmonary changes were consistent with myocardial infarction and thromboembolism.
• No adverse effects were observed with the PAAP- strain of Streptococcus sanguis.

Conclusions:

• PAAP+ Streptococcus sanguis interacts with circulating platelets, leading to thromboemboli formation.
• Bacteremia from PAAP+ Streptococcus sanguis and Porphyromonas gingivalis during periodontitis may increase the risk of acute thromboembolic events.
• This study highlights a potential mechanism linking oral health to cardiovascular events.