The rapid pace of research unraveling the connections between the mouth and the body has not abated. The total body of knowledge is sufficiently large and affirmed from so many independent studies that some conclusions have been drawn at this point.
There are two mechanisms of oral-systemic associations we know today. One involves the inflammatory aspects of periodontal disease. Inflammation from all sources, including periodontal disease, contributes to the total inflammatory burden. The total inflammatory burden increases the risk for vascular disease. The other mechanism is the direct effect of periodontal pathogens on the vasculature. Numerous studies have linked periodontal pathogens, such as Aa, Pg, and Fn, to vascular disease and damage. For example, in a 2011 study by Fardini et al, (Molecular Microbiology. 11/2011;82(6):1468-1480) the periodontal pathogen Fusobacterium nucleatum was found to increase endothelial permeability. The bacterium binds to endothelial cells, which form the inner lining of arteries and break down the cell-to-cell junctions. This allows the live bacteria, and anything smaller, to invade the wall of the artery where atherosclerotic plaques form. In a 2012 study by Assinger et al (Thrombosis Research. 2012;(130):e73-e78), the periodontal bacterium Porphyromonas gingivalis was found to cause platelet activation. This results in the formation of platelet/white blood cell aggregates, which support white blood cell activation, adhesion, and transmigration through the arterial endothelium. All of these processes are critical for atherosclerosis development.
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There are other pathways involved in periodontal/vascular associations, including the effect of insulin resistance. Insulin is a hormone whose function is to clear glucose from the bloodstream and move it into the cells where it is used to power the cell’s metabolic functions. Anything that interferes with the attachment of insulin to the cell surface receptor constitutes insulin resistance. When this occurs, the glucose cannot move out of the bloodstream into the cells. This creates high blood sugar levels, or hyperglycemia. The pancreas reacts to the hyperglycemia by pumping out more and more insulin until finally a gradient is created sufficient to force some of the glucose into the cells. Problems occur when insulin levels are high. High insulin levels elevate LDL (the bad cholesterol) and triglyceride levels, and decrease HDL levels (the good cholesterol). High insulin levels also elevate blood pressure, promote inflammation, and cause endothelial dysfunction. Insulin resistance is the biggest root cause of atherosclerosis as a result of the four mechanisms noted above, and periodontal disease increases insulin resistance due to the infectious and inflammatory components of the disease.
The status of other oral-systemic associations is not as well defined at this point. There is strong evidence of a link between the periodontal pathogen Aggregatibacter Actinomycetemcomitans (Aa) and rheumatoid arthritis, but further studies are needed to affirm the findings. The evidence for an association between periodontal disease and adverse pregnancy events is also waiting for further research to determine the strength of this link. The same is true for Alzheimer’s disease.
The recent study by the American Heart Association, published in the journal Circulation, concluded that causality between periodontal disease and cardiovascular disease has not been proven at this point in time, and they are correct in this conclusion. They did state that an association exists despite the lack of demonstrated causality. With much less fanfare than the original conclusions, the AHA issued a follow-up online statement in April 2012, in which they stated that there is “[Level A evidence that periodontal disease is independently associated with arterial disease.]” They further stated that the available evidence shows a trend toward reducing cardiovascular risk with periodontal therapy.
The bottom line with the AHA’s study and subsequent revision is that a lack of demonstrated causality at this time is not a reason or excuse for inaction.
The foundational knowledge and technologies we now possess allow us to treat patients individually, increasing favorable treatment outcomes. We are in a position to refer patients to their physician when we identify bacteria that are associated with an increased risk of vascular disease. We are truly affecting our patients’ health beyond the oral cavity.
