What might lead to a Eureka! moment among our scientific and professional community should rather be seen as matter of serious concern. The two recent papers on teeth, or rather lack thereof, and possible relationship with cardiovascular events or even death have sparked the expected excitement. In one editorial of a Dutch heart journal, the editor-in-chief even trumpets in the title of his editorial, “Tooth brushing for a longer and healthier life.” He thus repeats, in other words, the notorious Floss or die! claim of 1996. I had forecast, some time ago, that relentlessly beating the drum by our thought leaders will ultimately lead to loss of any interest of the medical profession (in particular cardiologists) in the perio-systemic link, in particular as the American Heart Association had already concluded, in their comprehensive systematic review of 2012, that
[e]xtensive review of the literature indicates that PD [periodontal disease] is associated with ASVD [atherosclerotic vascular disease] independent of known confounders. This information comes mostly from observational studies, however, and therefore does not demonstrate that PD is a cause of ASVD, nor does it confirm the contention that therapeutic periodontal interventions prevent heart disease or stroke or modify the clinical course of ASVD. Although a contribution of PD to ASVD is biologically plausible, periodontal and cardiovascular diseases share multiple risk factors that are prevalent and powerful promoters of disease, including tobacco use, diabetes mellitus, and age. (Emphasis added.)
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.)