Yesterday, new NHANES 2009-2012 data on prevalence, extent and severity of periodontitis have gone online in the Journal of Periodontology. On first sight, authors confirm findings of the previous, 2009-2010, survey in that prevalence is much larger as previously reported. So, 46% of U.S. adults have periodontitis with almost 9% having severe disease (Eke et al. 2015). The previous report (Eke et al. 2012a) contained an unclear description of how attachment loss was measured concealing that a “signed” measure of recession was used to calculate clinical attachment loss as difference of probing pocket depth and recession (from Latin, recessus, retreat). In a letter to the Editor-in-Chief of the Journal of Dental Research, Professor Giannobile, I had raised more problems in the article when I wrote,
“Teaching in particular undergraduates about how probing parameters periodontal probing depth, attachment level, and recession are measured is quite an effort but usually straightforward. In order to avoid undue exaggeration of prevalence, extent and severity of periodontitis both in the population and in patients attending a common office and to be able to assess treatment outcomes, metric periodontal probing parameters have to be properly defined. I would therefore appreciate if authors could comment on the apparent redefinition of attachment loss in their paper. When analyzing the Figure in the paper by Eke et al. (2012a), what immediately hits the eye is that there seems to be higher prevalence of attachment loss at different thresholds (a) than of pocket depth at respective thresholds (b) in all age groups. Such a pattern may actually be a result of how attachment loss had erroneously been redefined, most probably due to convenience. Just as a trivial example, a 4 mm probing depth without recession may be associated with either 0, 1, 2, 3, or 4 mm attachment loss, but the NHANES oral health data management program would have “instantly calculated” 4 mm. Based on the new case definition using attachment loss in addition to probing depth, prevalence of all periodontitis in the adult population of 30 years and older in the U.S. has now been estimated to exceed 47%, after 35% found in NHANES III during 1988-1994. This much higher prevalence may be due to the redefinition of attachment loss, too. Moreover, as to Eke et al. (2012a), mild periodontitis has a rather low prevalence in all age groups while moderate periodontitis is widespread (Figure c). The picture was different in NHANES III when severe periodontitis occurred with lowest, moderate periodontitis with intermediate and mild periodontitis with highest prevalence, a pattern which, I suppose, applies to many other widespread chronic diseases. The strange new pattern might indeed be explained partly by the redefinition of attachment loss as well, ultimately leading to a different distribution of cases.” (Emphasis added.)
Subtracting recession from periodontal probing depth makes sense only when true recession (the free gingival margin is located apical to the cemento-enamel junction) gets a minus sign. This was circumstantially explained to me in an email by the authors forwarded to me by Professor Giannobile, who never published my original letter. Eke et al. (2012a) had actually concealed that a signed recession definition was used. In the new update of NHANES 2009-2012, calculation of clinical attachment is now correctly described, including the signed recession definition. Eke et al. (2015) may also have realized that there is no complex chronic disease where moderate severity is more prevalent than its mild form. It is rather perplexing to see that authors have now abandoned the differentiation between moderate and mild periodontitis which they call “other” periodontitis (other than severe). They give the following reason,
“These subgroups [mild and moderate periodontitis] are not truly ordinal [sic] as the label suggests because many ‘moderate’ cases had insufficient pocket depth to qualify as ‘mild’ and we have therefore combined them and used the label ‘other‘ periodontitis.”
After my recent comment on the concerted action of 19 eminent and self-proclaimed eminent periodontal scientists spearheaded by Drs. Borgnakke and Chapple (2014) aiming at smashing findings of a large multicenter randomized controlled trial by Engebretson et al. 2013 on HbA1c levels in type 2 diabetics with moderate or severe periodontitis, I had honestly decided not to report any more on the issue unless an updated systematic review by the Cochrane Collaboration was published. A reader of my blog had contacted CC’s Dr. Terry Simpson who promised that, due to “logistical problem[s] including difficulties with authors not supplying vital information [sic!],” they would likely be able to publish it around the turn of the year.
Now, the final paper was published yesterday in the Journal of Evidence-Based Dental Practice with a few editorial amendments. Borgnakke’s, well, rant is remarkable since it assembles (as reviewers who are also listed as authors) in essence all editors and many members of the editorial boards of our core journals in periodontology and implant dentistry as well as the editor of Journal of Dental Research. I had reported on the history of the paper here and had noted that, after a first version had been withdrawn by the authors earlier this year, Panos N. Papapanou was no longer listed as reviewer in the version which went online on 13 August 2014. Instead, Fusanori Nishimora (an editorial board member of Journal of Periodontal Research who is involved in the so-called Hiroshima Study, see below) had joined the group. While the online early version of Borgnakke’s paper had got the title “The randomized controlled trial (RCT) published by the Journal of the American Medical Association (JAMA) on the impact of periodontal therapy on glycated hemoglobin (HbA1c) has fundamental flaws,” a slightly moderated version is now provided: “The Multi-Center Randomized Controlled Trial (RCT) Published by the Journal of the American Medical Association (JAMA) on the Effect (sic!) of Periodontal Therapy on Glycated Hemoglobin (HbA1c) Has Fundamental Problems (sic!).”
As reported before, the large muticenter intervention trial by Engebretson et al. (2013) who reported no effect of nonsurgical treatment of periodontitis on HbA1c levels in patients with type 2 diabetes mellitus has harshly been critized by our thought leaders. Last month, JAMA published a number of letters to the editor. One letter by Chapple, Borgnakke and Genco identified important problems in Engebretson’s paper including “problems with the study design, execution, data interpretation and reporting.”
“First, the periodontal therapy provided failed to clinically manage the periodontal infection and associated inflammatory burden. Residual plaque levels of 72% and bleeding scores of 42% are far below the consenus for expected outcomes [reference to van der Weijden et al., J Clin Periodontol 2002; 29(suppl 3): 55-71, 90-91]. Therefore, no conclusions can be drawn about the effect of clinicaly effective periodontal therapy on HbA1c in patients with type 2 diabetes.
Second, control of diabetes at baseline was predominantly good (mean HbA1c levels, 7.8%), with less than 60% of patients having HbA1c levels greater than 8.0% (HbA1c level <9.0% was an inclusion criterion). With the mean HbA1c value close to the therapeutic target, we would not expect an intervention to improve HbA1c substantially.
We are concerned about the reliance on statistical significance to justify a conclusion of no effect when the clinical therapy failed to deliver the expected standard of care.”
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.
The November 2012 EFP and AAP workshop on systemic health and how it is affected by periodontal disease has resulted in the joint publication of a couple of valuable systematic reviews in both Journal of Clinical Periodontology and Journal of Periodontology. I have expressed my strong opinion here on this blog that, in essence, there was not so much new or surprising. That there is strong evidence for minor effects of periodontitis on, say, cardiovascular disease and that diabetes mellitus is affected by periodontal disease while it is a risk factor for gum disease itself has been known for decades. That, what organizers had claimed, there is now a need for intervention studies to show that the risk for cardiovascular events may be reduced, has been questioned on this blog and elsewhere.
I have criticized the workshop’s Manifesto, a press release which reduced the somewhat difficult to digest information to a message for the public (and I include here in particular most of the dental profession whose members may not be able or willing to read through the pages of documents, be it but systematic reviews let alone the original cohort studies). I have also suggested a brief example (based on a gut feeling of a possible risk ratio) in which the most relevant ethical problem of not treating huge cohorts for periodontal disease was mentioned while probably a great number of patients with periodontitis had to be treated successfully (number needed to treat) in order to prevent a single cardiovascular event (if the effect was causal) which renders the whole exercise probably irrelevant.