Bale/Doneen/Nabors response to the AHA and ADA statements regarding Periodontal Disease and Cardiovascular Disease

The issue of the relationship between chronic inflammatory periodontal disease (PD) and cardiovascular disease has, and continues to be, a subject of intense research as well as much debate. While the literature continues to show an independent relationship between these two diseases, the issue of causation was addressed in a recent and important article by the American Heart Association. http://circ.ahajournals.org. The Circulation AHA article examined 537 peer- reviewed studies that addressed the relationship between periodontal disease and cardiovascular disease. Concluding remarks from this intense analysis were as follows: “Observational studies to date support an association between PD and asymptomatic vascular disease (ASVD) independent of known confounders. They do not, however, support a causative relationship.” The American Dental Association (ADA) Council on Scientific Affairs agrees with these conclusions.

Albeit the American Heart Association (AHA) does acknowledge the value of good oral health and hygiene, they stop short of suggesting that a direct relationship between the two conditions exists. This article provides the opportunity to investigate the objective data to determine the positive aspects of the analysis. Bradley Bale, MD, Amy Doneen, MSN, ARNP, and Thomas W. Nabors, DDS, FACD have the following response to the paper and position statement of the AHA and ADA. In light of the science presented in their article coupled with the substantial burden CVD places upon our society, we cannot afford to wait for the acquisition of causality data to incorporate assessing and treating PD in an effort to minimize CV risk.

We must acknowledge that cardiovascular disease (CVD) remains the leading cause of death and disability in this country and is projected to have substantial growth in monetary expenditures and morbidity in years to come. It is well established that systemic inflammatory diseases contribute to the potential for plaque rupture/erosions which create thrombotic events resulting in plaque growth patterns, microvascular thrombus activity that manifests itself with end stage diseases such as vascular dementia and peripheral vascular disease or major symptomatic events such as heart attacks and strokes.*

In light of this recent AHA publication, we must investigate the data that establishes the relationship of periodontal disease (PD) and cardiovascular disease (CVD). Current data establishes PD as a variety of and continuum of inflammatory conditions. These infections of the gingival tissues and alveolar processes exhibit classic demonstration of chronic inflammation of varying degrees and potential systemic dissemination of pathogenic oral bacteria.

A significant challenge in evaluating a cause and effect relationship between these two diseases is that PD is not consistently nor universally defined. This results in substantial variation in definitive clinical diagnoses. An objective and uniform definition of PD from its biological phenotype would be helpful in order to establish a formal cause and effect relationship with CVD. In the recent AHA article, the interpretation of the data in various studies has been limited to a subjective definition of PD which creates a tenuous platform of relating PD to CVD. More recent definitions of PD that includes DNA determination of pathogen burden are widely accepted and appear to add great value to determining severity of PD. Contrarily, the antibody titers of oral pathogens are highly variable as PD is a group of distinct diseases vs. a single disease. Additionally, PD (as defined by oral pathogen burden), demonstrates a trend in CV benefit when PD is effectively treated. In regards to defining if PD therapy reduces ASVD risk or CVD events, an additional obstacle for any cause and effect therapeutic study will be to control for all known confounding CV risk factors. There needs to be no statistically significant difference at baseline and at end of study with all of the known risk factors in the treatment group and the control group. Due to the huge number of known risk factors, this will be a daunting task.