Tagged: James Beck

The Literature That Shaped Modern Periodontology (V)

I have written about AAP’s centennial and the series of papers celebrating the “literature that shaped modern Periodontology” in several posts, see here and here. In this month’s contribution (in the Academy’s Journal of Periodontology), Steven Offenbacher and James Beck  attracted my attention when writing about “Changing Paradigms in the Oral Disease–Systemic Disease Relationship.” Twenty-five years after the first report by Finnish researchers on a certain risk of poor oral health for cardiovascular disease, the incredibe surge of studies all over the world (“Floss or Die!”) may have ceased, paving the way for another overdue paradigm shift.

The paper disappoints. Instead of putting the initial and long-lasting exciting in at least some relation in view of results of recent very large intervention studies which were by and large not able to confirm a postulated benefica effect of treatment of periodontal disease  on cardiovascular disease, low birth weight or diabetes, Offenbacher and Beck opened the bottom drwaer and pulled a couple of now questionable studies which, well, misled the public and thousands of researcher worldwide alike. For instance, Frank De Stefano’s paper of 1993 who, based on NHANES I follow-up data, reported a 25% increase of risk in patients with periodontitis. The data had been re-analyzed by Phillipe Hujoel in 2000 including much more careful adjustment of cofounders. They could not find an association. I have reported about the apalling letter to the editors of JAMA by Robert Genco and colleagues  here.

And then, of course, the paper by Beck et al. (1996) from the VA Longitudinal Study.

“Our paper showed that periodontal disease was a significant independent risk factor for CVD events after adjusting for traditional risk factors and displayed a dose-dependent increase in risk with increasing periodontal disease severity. Importantly, this paper described a two-component mechanistic working model that linked periodontal disease to cardiovascular disease via systemic bacterial dissemination interacting with the vasculature and activation of the hepatic acute phase response as an inflammatory trigger for CVD. We also hypothesized that there may be an underlying hyperinflammatory trait that served to increase risk for both conditions, suggesting that bacterial exposure in those susceptible individuals would result in even more risk for CVD. In addition, by placing importance on inflammation, it explained how oral infection could influence multiple conditions such as diabetes. Over the next 10 years, many studies supported this basic model. The model is now more than 15 years old, and we would modify it only by adding specific details, such as the hyperinflammatory trait likely being attributable to genetic differences in the innate immune response.” (Emphasis added.)

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How It All Began


Readers may have noticed my dismay about our “thought leaders'” recent attempts to revive the perio/systemic issue despite emerging evidence of no or very small, irrelevant, effects of periodontal treatment in large-scale intervention studies on  HbA1c in type 2 diabetes, or pregnancy outcomes.

I had yesterday discussed via email with a critical mind in the U.S. the results of another intervention study on cardiovascular events which never made it beyond a pilot study, the Periodontitis and Vascular Events, or PAVE, study. Since periodontitis patients were not randomized according to whether they received periodontal treatment but according to a community comparator (referral to community dentist with copy of x-rays and letter with diagnosis and recomendations for treatment), I had argued that such a design would not fulfil criteria of an RCT since patients who get proper periodontal treatment in the comparison group may fundamentally differ from those who won’t care. However, patients who won’t care in the test group would get the treatment anyway. So, interpretation of biased results would be difficult if impossible. Not surprising, the PAVE study did not get funding after the pilot phase (Beck et al. 2009) [pdf], which resulted in non-significant differences anyway, possibly (but not inevitably) due to lack of statistical power.

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