Further Update on: Eventually Dead and Buried

Evidence pyramid

One has to praise the authors of the systematic review on “The epidemiological evidence behind (sic!) the association between periodontitis and incident atherosclerotic cardiovascular disease” (Dietrich et al. 2013) [pdf] that they had managed to get the awful print-out of their paper quickly corrected, see the Corrigendum here. First I had even entertained suspicion that results of the systematic search should be rather concealed than reported. Tables in the Corrigendum are now more informative and can be scrutinized by attentive readers who are still interested in the above question (I have to admit, though, that I am more and more bored of repeatedly published “strong evidence for minor effects”).

Now, Table 3 seems in fact to reproduce Dietrich’s and coworkers’ original findings of their cohort study of 2008 [pdf] (by and large either not significant or inconclusive associations of bone loss or cumulative probing depth and incident coronary heart disease) with an important exception: figures were rounded to only one decimal place. Authors should know that rounding can only be done once, namely by the investigators of the original paper. Systematic reviews of selected papers must not produce new results by rounding. Never.

Any associations in the selected, by Dietrich et al. (2013), cohort studies (a design which might allow for at least some speculation on causation) were either not significant, inconclusive or weak at best. Authors did not attempt to do a meta-analysis. But I would bet if they had done it, the overall risk for incident atherosclerotic cardiovascular disease would be increased, based on the reviewed cohort studies, by a factor of not more than 1.3 (possibly not even significant) in case of more advanced periodontitis. A risk ratio which had been claimed already a decade or more ago.

The association in the selected case-control studies was seemingly stronger. But should they even be considered in evidence-based medicine for anything else than formulating a hypothesis which has then to be tested in well-conducted prospective cohort studies or ultimately intervention studies to eventually answer the question about causation which seems to plague a number of periodontists for more than 25 years? Actually, in the presence of new cohort studies they should no longer be considered. It is all about Sir Bradford Hill’s criteria for causation, decades old, heavily criticized but still valid. And then, if cohort studies won’t suggest strong association, then intervention studies are not justified. Keep in mind that, in any RCT, hundreds of patients with more or less severe periodontitis must be randomized and half of them be deprived of any proper periodontal therapy for years in order to prove a so far not even calculated but probably very low attributable risk.

Attributable riskSince the attributable risk, which describes the proportion of all cases of the outcome (incidence of atherosclerotic cardiovascular disease) in the target population that are attributable to the exposure (periodontitis), depends on the prevalence of the risk factor,  recent rather questionable attempts to exaggerate prevalence, extent and severity of periodontitis in the adult U.S. population by Eke et al. (2012) are directly related to the current AAP/EFP recover mission.

29 May 2013 @ 6:43 pm.

Last modified May 30, 2013.



  1. Lynne Slim

    So, Dr. Muller, when do you think the AAP and European Federation report will be corrected? It’s clear that the epidemiological evidence isn’t strong after all.


    • Muller

      Hi Lynne,
      I suppose, the evidence is in fact strong. There is overwhelming evidence that the association is but weak. In another review of the supplement, Linden et al. (2013) put it slightly differently.

      There is therefore a lack of evidence to support associations between moderate or severe periodontitis and a number of the systemic diseases and conditions reviewed [note that here associations with COPD, pneumonia, kidney disease, rheumatoid arthritis, cognitive impairment (sic!), obesity, metabolic syndrome, and cancer are reviewed]. In this context, it is worth remembering that absence of evidence is not evidence of absence (Altman & Bland 1995).

      I do not like the misleading last sentence in this context. There is plenty of evidence (mainly as evidence of absence). I like, however, another quote by Linden et al. (2013). They suggest,

      … periodontitis may be a phenotype of low socioeconomic status reflecting factors such as smoking, poverty and low education and developing in parallel with other diseases which reflect disadvantaged lifestyle.

      Research in this area is in fact much needed. Respective risk indicators can be (and should be) modified for the benefit not only of the individual but the entire society.

      What further strikes me in the paper by Dietrich et al. (2013) is when they mention the systematic review by Lockhart et al. (2012) in their Introduction section.

      Most recently, a comprehensive review was performed by an American Heart Association (AHA) working group (Lockhart et al. 2012), which concluded that “periodontal disease is associated with atherosclerotic vascular disease independent of known confounders”. It further concluded that there was no evidence for a causal link and that, therefore, statements that imply a causative association between periodontal disease and specific
      atherosclerotic vascular disease events […] are unwarranted”.

      Guess what is missing in the quote? Well, the entire sentence in Lockhart et al. (2012) should rather read,

      It further concluded that there was no evidence for a causal link and that, therefore, statements that imply a causative association between periodontal disease and specific atherosclerotic vascular disease events or claim that therapeutic interventions may be useful on the basis of that assumption are unwarranted. (My emphasis.)


  2. Lynne Slim

    Another thought~ the Dietrich et al. paper was funded by an unrestricted educational grant from Colgate-Palmolive to the European Federation of Periodontology and the American Academy of Periodontology. Why can’t an independent group of epidemiologists evaluate the evidence and publish their results in a Journal like the J of EB Dental Practice? There was already a review in the J of EB Dental Practice . . . the author reviewed the AHA Circulation paper and agreed with the AHA committee’s conclusions! So, how can we believe the AAP and the European Federation when there is clearly conflict of interest here?


    • Muller

      That the workshop and publication of the papers was sponsored by Colgate-Palmolive is one thing. That the workshops organized by the EFP every three years are under heavy influence of a very small group of individuals with their agenda is another issue. Why hadn’t people like Peter Lockhart or, say, Philippe Hujoel been invited? They might have prevented the hasty and, well, sloppy publication of some of the papers after only three days of debate. Sentences such as, “Practitioners should be aware of the emerging and strengthening evidence that periodontitis is a risk factor for developing atherosclerotic cardiovascular disease, advising patients of the risk of periodontal inflammation to general as well as oral health,” might have been abandoned in the published EFP Manifesto, which will mainly be read by practitioners.


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