On the Level of Periodontal Care in US American Studies

The large multi-center intervention trial by Engebretson et al. (2013), who had reported lack of any effect of non-surgical periodontal therapy on HbA1c levels in type 2 diabetes mellitus patients after 3 and 6 months, has been harshly criticized because of very moderate clinical improvements as regards pocket depth reduction (from mean 3.26 mm at baseline) of 0.4 mm (95% CI 0.4; 0.5 mm) and reduction of bleeding on probing (from mean 62%) of 19% (95% CI 15.7; 22.4). What was even more concerning was that, 6 months after seemingly intense treatment (at least 160 minutes of scaling and root planing followed by oral hygiene instruction and, for two weeks, twice daily mouthwash with 0.12% clorhexidine digluconate; then, at both 3- and 6-month follow-up examinations, further oral hygiene instructions and scaling/root planing for another hour), bleeding on probing was still seen at an average of 40% sites while, on average, 70% tooth surfaces were still covered by plaque (from 86% at baseline).

These are undeniable problems of the study. Claims that periodontal treatment was insufficient and, as a consequence, periodontal infection still present in most patients after periodontal therapy, may in fact be justified. It is the sheer size of the attack which is so appalling. Each and every editor of our professional journals and numerous further pundits, altogether 21, had joined, well, the public execution of the study’s principle investigator. Because of unwelcome results of a study with the potential of ending a story, or illusion, once and forever. And, absolutely inappropriate attempts of intimidation of scientists when writing,

“Given the inconlusive nature of these data, we recommend that the existing body of evidence in which meta-analyses consistently conclude that successful periodontal therapy appears to improve glycemic control, should instruct us until results from future studies are reported. We urge all interested parties to refrain from using this study results as a basis for future scientific texts, new research projects, guidelines, policies, and advice regarding the incorporation of necessary periodontal treatment in diabetes management.” (Emphasis added.)

So, censorship. This is absolutely unscientific. Meta-analyses are always preliminary and must incorporate new results on a continuous basis.

As regards “successful periodontal therapy” and the quality of the available evidence, consider the following example of the meta-analysis by Engebretson and Kocher (2013) which had been published a couple of months before the incrimiated large multicenter trial by Engebretson et al. (2013). Nine RCTs were identified where data of  398 test and 377 control patients could be extracted as regards possible effects of nonsurgical periodontal therapy on HbA1c levels in diabetics. The meta-analysis yielded an effect of -0.36% (95% CI -0.54; -0.19) on HbA1c. Comments by Engebretson and Kocher (2013) in Table 1 include that (1) Jones (2007) did not report (or observe?) a periodontal treatment effect. (2) In the paper by Yun et al. (2007) it was unclear whether subjects were on diabetes drugs. According to Engebretson and Kocher, the “[t]rial [was] not optimal for [the] research question because both groups received antibiotics.” Furthermore, no periodontal treatment effect was reported [or observed?]. (3) Chen (2012) did not observe an improvement of the metabolic status in either group although in both treatment groups [two different treatment regimes], periodontal conditions improved. (4) In the study by Kiran (2005) some subjects presented with HbA1c levels between 6 and 6.5% and should therefore be regarded well-controlled. (5) In the study by Katagiri (2009), HbA1c only decreased in a subgroup of patients where elevated levels of C-reactive protein decreased as well. (6) In two studies (Singh 2008, Sun 2011), changes in medication were not reported.

Any unbiased analyst of this systematic review must come to the conclusion that a meta-analysis must be regarded questionable due to the reported problems of most of the RCTs. The review had been produced on the occasion of a joint AAP/EFP workshop in November of 2012 with the clear intention of assessing any available evidence for the desired message for the public: Periodontitis is intimately connected with systemic health and disease.

Haffajee 1997

But what about the harsh condemnation of our thought leaders as regards unacceptable clinical results after non-surgical periodontal therapy? The careful re-reading of some classic papers on scaling and root planing may be worthwhile. For example, in 1997 Haffajee et al. had published a paper which has been cited so far 396 times (Google Scholar). The study employed, for the first time, so-called checkerboard DNA-DNA hybridization in a clinical trial to characterize the flora of the 40 then known most prevalent bacteria at each tooth in 57 patients with chronic periodontitis. The above picture indicates that the prevalence of three bacteria, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola had significantly decreased after non-surgical periodontal therapy (scaling and root planing, or SRP) while one bacterium, now called Actinomyces oris, had increased in prevalence. The prevalence of most other bacteria did not change.  Already in the abstract, authors mention that,

“Clinical improvement post-SRP was accompanied by a modest change in the subgingival microbiota, primarily a reduction in P. gingivalis, B. forsythus [now Tannerella forsythia] and T. denticola, suggesting potential targets for therapy and indicating that radical alterations in the subgingival microbiota may not be necessary or desirable in many patients.”

So, how impressive was “clinical improvement”? After all, scaling had been done quadrant-wise in weekly sessions and each session lasted for 45-60 minutes. Oral hygiene techniques were shown and proper home care reinforced at each treatment visit. Full-mouth maintenance scaling was done 3, 6, and 9 months after initial scaling. After 3 months sites with “gingival redness” had decreased from 68 to 57%, on average. Bleeding on probing was noticed at 58% sites before and 52% after SRP, on average. There was no significant change in the percentage of plaque-covered tooth surfaces, about 70% at either exam. Mean pocket depth decreased significantly from 3.3 to 3.1 mm three months after 3-4 hours of scaling and root planing, while the mean 0.11 mm attachment gain was not significant.

Any unbiased clinician must conclude that periodontal treatment was a grave failure. But this remained most probably almost unnoticed since the study’s “main results” fit so well with our expectations, i.e. the overwhelming importance of three possible pathogens P. gingivalis, T. forsythia, T. denticola; and the confirmation of the hypothesis of a “beneficial” organism, now called A. oris.

Meaning, results were not unwelcome, quite the opposite.

10 February 2015 @ 12:23 pm.

Last modified February 10, 2015.



  1. Muller

    Yesterday, I had the opportunity to discuss some of the above issues with Dr. Wenche S. Borgnakke, who had visited Tromsø University and gave a couple of most interesting lectures to undergraduate students and colleagues. It was a pleasant and friendly exchange of diverging opinions, absolutely professional. I mentioned my grave concern about a public “execution” of a young scientists by an armada of most eminent journal editors and Academy and Federation presidents. We agreed that a more conservative interpretation would have sufficed, but on the other hand, what authors write in the discussion section of their paper must always be regarded an opinion which they are free to express anyway.


  2. fpickett2

    I agree. Unless one agrees with the researchers (hoping to gain multi million dollar grants to study various oral/systemic links, possibly having conflicts of interest) who propose that the associations between periodontal disease and nonoral disease are “strong research”, you may be vilified by these people who have gained popularity.


    • Muller

      Dr. Borgnakke mentioned several times in her lectures the 15 mio dollars, Engebretson et al. had received for their study, a scandal in her opinion. So, the amount would only be justified if one had got the desired results. This is actually the end of science.


  3. fpickett2

    I looked at the publication by Michaelowicz et al on the secondary outcome assessment of the periodontal therapy and diabetes control study discussed above. The publication in JADA (Dec 2014 I think) states that plaque assessment data was collected as follows “They scored dental plaque at each tooth site as detectable (1) or undetectable (0, with a probe or visually) and computed it as a full-mouth percentage. ” This means that if plaque was heavy at baseline and minimal at the 3 and 6 month exams, it received the same score “detectable”. I’ve had many patients whose oral hygiene was terrible when we began therapy and at the 3 month assessment it was greatly reduced, although a small amount was still seen. This may have been the case and due to being “either” “or”, masked the reduction of plaque. They might have reported a true reflection of oral hygiene/plaque if they had used a plaque index incorporating how much of the tooth surface was covered with plaque. They also used the same method to assess BOP (yes or no) and the amount of bleeding was not considered. What if more than half the subjects in the treatment group were taking ASA? This would affect BOP results and might confuse the issue regarding the amount of BOP truly associated with inflammation.

    What do you think?


    • Muller

      By using Ainamo and Bay’s VPI (or visible plaque index) of 1975, one would have excluded all plaque which may only be detected by running a probe across the tooth, i.e. gingival index score 1 according to Silness and Löe (1964). The VPI is widely accepted index in particular here in Scandinavia. But a high percentage of paque perfectly fits with the high bleeding score, regardless of aspirin intake. It’s also a pity that, in the JADA paper by Michalowicz et al. (2014) on DPTT, plaque at 6 months was not included in (or rather intentionally excluded from) any multiple regression model for change in clinical variables pocket depth, attachment level and bleeding on probing. In my opinion, the paper creates more confusion than provides explanation for what has been found. It is a pity, but I got the impression that the authors do not want to discuss high plaque levels.
      I would agree on the following. Periodontal treatment is simply not completed after scaling and root planing, in particular if attempts to improve oral hygiene have more or less failed. In future studies in fact endpoints have to be defined and periodontal inflammation as far as possible eliminated. This is not irrational. If one wants to get definitive results, proper treatment should be provided, i.e. periodontal surgery if and when it is indicated. Remember, there were cases of advanced periodontitis among participants, but what was done was completing the hygienic phase (with probably a poor result). If the authors had actually got 15 mio dollars for their 500 participants, each participant would have cost them $30,000, an incredible amout of money.


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