Weak oral bacteria such as periodontal bacteria or Chlamydia pneumoniae have been observed in various arterial and venous lesions with epidemiological data reported prior to the discovery of bacterial invasion into vessels. Rich lymph vessels easily bring the bacteria from the mouth to the neck and the venous angle, which is directly open to the blood vessels. Periodontal bacteria travel within platelets and Chlamydia pneumoniae can be carried by monocytes. The transportation system of other weak oral bacteria have not been determined. Periodontal bacteria, especially P. gingivalis aggregate platelets and form thrombi. At the same time, secretions such as serotonin, various cytokines, and adhesion factors also appear in the blood. The characteristics of arterial lesions are dependent on the age of the patient and the condition of the endothelial cells. In young patients, infectious incidents occur due to embolic mechanisms in Buerger disease or adhesion to the superficial veins valves in varicose veins. In older patients, incidents result in adhesion in the proximal aorta, coronary arteries, or large arteries. The hypothesis here unifies the evidence on vessel lesion development and explains the possible discrepancy between vascular diseases.
Keywords: Buerger disease; Porphyromanas gingivalis; Treponema Denticola; platelet aggregation; weak oral bacteria.