The Verdict

The first withdrawn manuscript by Drs. Wenche Borgnakke and Iain Chapple and each and every editor of our hardcore periodontal journals as well as otherwise eminent individual in Periodontology, which had proclaimed that “[t]he 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” about the paper by Engebretson et al. (2013), see [pdf], went online today in the Journal of Evidence-Based Dental Practice.

I had wondered before why it had been withdrawn but couldn’t figure that out. Interesting may be that the withdrawn paper had listed all 19 authors, while the current version does not. Maybe that Borgnakke and Chapple are only pawns in a worldwide political enterprise launched by our “thought leaders”. It may also be that more “evidence” (see below), possibly (but rather not) suitable for putting findings by Engebretson et al. (2013) into perspectve, needed to be included in what is almost a revile.

The paper by Engebretson et al. (2013) had been heavily criticized from the beginning for more than modest periodontal improvement after nonsurgical therapy of moderate or advanced periodontitis in type 2 diabetics. In particular rather high proportions of sites bleeding on probing (40% after 3 and 6 months, on average) and tooth surfaces covered by plaque (65% after 3 months, even 71% after 6 months, on average) despite after all at least 160 min scaling, on average, is in fact disturbing. When Borgnakke, Chapple et al. (2014) compare these results and reported mean periodontal probing depth reductions (attachment gains are not compared; see below) with those expected in nondiabetic patients with chronic periodontitis (based on previous systematic reviews) one might actually ask whether that was justified. I would have expected a quick systematic review of published results after nonsurgical therapy of periodontally diseased diabetics in the first place. More serious is selected reporting, for instance, about a systematic review by van der Weijden and Timmerman (2002). In their Table 2, Borgnakke, Chapple et al. (2014) claim an expected decrease of periodontal probing depth after nonsurgical treatment of periodontitis in diabetics of 1.18 mm as compared to 0.4 mm achieved in the paper by Engebretson et al. (2013) which at least looks substantially less. However, while the latter reported means about all sites, the former calcuated an effect for only deep sites of 5 mm or more. If Borgnakke, Chapple et al. (2014) had read the paper by van der Weijden and Timmerman (2002) more carefully, they would have noted that these authors did another meta-analysis of 2 studies where all sites had been assessed before and after scaling. The mean attachment gain was then 0.22 mm, somewhat less than the 0.35 mm in the study by Engebretson et al. (2013). Ironically, the first author of one of these two studies was, yes, Iain Chapple.

Engebretson et al. (2013) were not able to demonstrate an effect of nonsurgical periodontal therapy on HbA1c levels of diabetics which seemingly contradicts recent reports after systematic reviewing the literature. Borgnakke, Chapple et al. (2014) list the results of these systematic reviews in Table 1. Despite the impression that the evidence must be overwhelming with 6 out of 7 systematic reviews reportig significant HbA1c reductions of between 0.36% and 0.65% after nonsurgical periodontal therapy, one has to conclude that most considered the same, basically small-scale, single-center, poorly designed intervention studies. In some studies adjunct antibiotics were used, in most not. When checking the RCTs it becomes clear that clinical periodontal improvements have often been modest, to say the least.

And finally, obesity. As a matter of fact, patients in the study by Engebretson et al. (2013) were very obese, on average, with a BMI of 34,7 +/- 7,5 kg/m2. Borgnakke, Chapple et al. (2014) criticize (and the following bumpy circular reasoning and distraction is worth to be quoted at length) that,

“A third significant flaw is that the chronic, low-grade inflammatory state elicited by the prominent obesity in the treatment group […] would have masked any anti-inflammatory effect of successful periodontal treatment. It is the decrease in inflammation due to periodontal infection that leads to the decrease in blood glucose levels, and thus we would not expect to be abe to measure any significant decrease in glycated hemoglobin levels, even after successful periodontal treatment in such obese subjects. The Hiroshima Study demonstrated that HbA1c levels improve by resolution of the perodontal infection-related systemic inflammation, but only in subjects with initially elevated levels of the acute-phase inflammatory marker C-reactive protein, measured with high sensitivity (hs) CRP. [Reference to Munenaga et al. April 2013] In fact, the initial hsCRP level is a significantly important indpendent variable influencing HbA1c reduction rates, and the greatest reduction in HbA1c level is experienced by the group with the highest hsCRP reduction following periodontal treatment. Importantly, the subjects in [the] Hiroshima study were nonobese subjects with type 2 diabetes. An earlier US study called Atherosclerotic Risk in Communities (ARIC) already reported that, when the BMI of the subjects was in the range of twenties, there was a predicted 2-fold difference in hsCRP between sever and no/mild periodontitis groups, b the difference decreased with increasing BMI and became negligible when BMIs reached 35 kg/m2. [Reference to Slade et al. 2003] In the current study, although the effect of periodontal therapy on the reduction in the systemic inflammaory burden was not evaluated, it is possible that most of the subjects were resistant to the elimination of periodontal disease-related systemic inflammation due to overwhelming influence of their obesity-related systemic inflammatory load.”

Would have, could have, would not, could not. And everything is possible. But more important, what which must not cannot be. The most constructive advice for Drs. Borgnakke and Chapple would be to apply for research money and figure it out.

When the data by Engebretson et al. (2013) and those of another small-scale intervention study are added to data considered in the systematic review by Engebretson & Kocher (2013) [pdf] he weighted mean difference of HbA1c after nonsurgical periodontal therapy was reduced to -0.26% (95% CI -0.43; -0.09) in a random effects model. Significant (p=0.04) and substantial heterogeneity was observed (I2= 44%).

14 August 2014 @ 8:24 pm.

Last modified August 22, 2014.



  1. Frieda Pickett

    The only design error I found in the Engebretson et al study was subjects were allowed to take low dose ASA but the groups were not randomized for this parameter. There are several studies reporting low dose ASA will result in BOP and one author commented this result could affect clinical studies measuring BOP in the effects of the study. So the lack of effect or poor effect of BOP could be due to the taking of low dose ASA rather than lack of reduction of inflammation.
    Frieda Pickett, RDH, MS


    • Muller

      The paper in JEBDP is worth to be read very carefully. It is a reviling rant aiming at blemishing the paper by Engebretson as irrelevant because of apparent irrelevance (so that it must not be included in future meta-analyses). I would have expected that Borgnakke et al. would first check whether their numerous issues with Engebretson’s study (it’s not only about modest periodontal effects of periodontal treatment) would apply also to the other (small-scale, single center) papers on the topic. After all, there are now 4(!) recent SRs on perio tx on HbA1c levels.
      I have encouraged students and colleagues time and again to do their own SRs and meta-analyses and get an idea about the evidence when in doubt. I really do not need to be told by 19 “thought leaders” what kind of clue I should have. This seems to be political and highly dogmatic.


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