MedicalResearch.com Interview with:
Bradley F. Bale, M.D.
Texas Tech Health Science Center
School of Nursing, Lubbock, Texas
1002 Montrose Drive
Gallatin, TN 37066
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: It has been known for some time that periodontal disease is associated with higher risk for arterial disease. It was shown decades ago that the germs in the mouth frequently seed into our blood stream with simple activities such as chewing and brushing our teeth. During the last decade, it was discovered certain high risk periodontal pathogens are associated with various cardiovascular (CV) risk factors such as blood pressure, lipid levels, insulin resistance and endothelial dysfunction. These studies elucidated that the CV risk stems from the bacteria involved in the periodontal disease and not the clinical signs such as pocket depth, bleeding of gums and loose teeth.
The above knowledge demonstrated that high risk periodontal pathogens can adversely influence two of the three elements in the atherogenic triad. Those factors are concentration of apoB and endothelial inflammation and dysfunction. Then approximately two years ago it was published that the high risk pathogen
Porphyromonas gingivalis (P.g.) can enhance the third element. This portion is the transformation of contractile smooth muscle cells (SMCs) in the medial layer of artery into migratory secretory SMCs. These morphed cells enter the deep layer of the intima and enrich it with proteoglycans which are the ‘velcro’ that traps cholesterol particles in the arterial wall and initiates the formation of arterial disease.
At that point, there was solid evidence that the high risk pathogens boost every element in the triad to create atherosclerosis. With that knowledge these pathogens must be considered a
contributory cause of arterial disease. When a condition is causal it demands diagnosis and management to reduce the disease risk.
(more…)