Consider this recent story from io9:

It’s true: The idea that a tooth dropped in soda will dissolve overnight is an urban legend. But does this mean that soda doesn’t damage your teeth?

Nope. Evidence consistently shows that soft drinks erode enamel and contribute to caries (cavities; tooth decay).

And in a similar fashion, even though we can’t (yet?) say – as the American Heart Association proclaimed last week – that periodontal (gum) disease causes heart disease, it doesn’t mean there’s “no link” between the two, despite what some headlines seem to suggest.

What it means is much less interesting: correlation doesn’t equal causation.

And this is far from newsworthy – as are the findings. As Dr. Pam McClain, president of the American Academy of Periodontology, told DrBicuspid,

The conclusions of this literature review are not really any different than most other reviews. The question is, does the evidence support an association between PD and ASVD? And in fact, it does.

Periodontal disease and cardiovascular disease are both complex, multi-factorial diseases that develop over time. It may be overly simplistic to expect a direct causal link.

Indeed, as we’ve consistently noted here and in Biosis, our quarterly newsletter, the expectation of such direct causal links is one of the limitations of conventional Western medicine when it comes to dealing with complex, chronic, multifactorial conditions. Often, the most you can say is, in the words of a previous literature review on gum and heart health (PDF),

Although we know that the health of the oral cavity is not a separate component of general health, proving an association is difficult. The challenge is that the mechanism underlying chronic diseases such as cardiovascular disease and PD are not completely understood. Thus, we must rely on observational studies in order to draw inferences about the potential effect of a suspected causative factor on the development or progression of a disease. In designing studies to examine the strength of the relationship between oral and systemic diseases, a number of conditions must be met. These include biological plausibility, temporality, specificity and a dose–response gradient.

Thus, in her conversation with DrBicuspid, Dr. McClain noted two other publications:

a 2009 consensus report from the editors of the Journal of Periodontology (July 2009, Vol. 80:7, pp. 1021-1032) and The American Journal of Cardiology, which concluded that while a direct causal relationship between periodontitis and atherosclerotic cardiovascular disease has not been established, multiple studies do support two biologically plausible mechanisms:

  • Moderate to severe periodontitis increases the level of systemic inflammation, a characteristic of all chronic inflammatory diseases, and periodontitis has been associated with increased systemic inflammation as measured by hsCRP and other biomarkers. Treatment of moderate to severe periodontitis sufficient to reduce clinical signs of the disease decreases the level of systemic inflammatory mediators.
  • In untreated periodontitis, certain gram-negative bacteria may be found in periodontal pockets surrounding each diseased tooth and in approximation to ulcerated epithelium, and bacterial species found predominantly in the periodontal pockets also have been found in atheroma.

Thus, while the findings of the AHA committee do not support a causative relationship between PD and ASVD, Dr. McClain concluded, “studies have shown that if you reduce the body’s inflammatory burden, you reduce the risk of heart attack.”

And this points to why the best way to nurture and sustain good oral health is to do what nurtures and sustains your total health: Everything’s connected.

AHA Scientific Statement abstract

Image by the tattooed tentacle, via Flickr

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