Europerio 8 in London earlier this year saw the world premiere of the 3D video animation, Oral Health and General Health – The Links Between Periodontitis, Atherosclerosis and Diabetes. The movie was produced by Sunstar and Quintessence Publishing and is the fourth in a series commonly called Cell-to-Cell Communications (I had written a critical review about the first installment here; empty knowledge, Matrix-Reloaded style) and the trailer can currently be seen on the EFP website. A pumping heart gets an infarction.
Myocardial infarction. A life-threatening manifestation of a series of inflammatory changes in the walls of the coronary arteries. It is a leading cause of death in the western world. Can periodontitis or other inflammatory processes in the oral cavity contribute to the development of cardiovascular diseases and systemic conditions such as artherosclerosis or diabetes or negatively influence their course?
This is fear mongering and, to say the least, misleading the public by completely ignoring all established risk factors for cardiovascular disease (high blood pressure, high cholesterol, smoking, unhealthy diet, obesity, lack of physical activity) and diabetes as well.
As the German version of The Links will be presented at the big national dental congress in November, authors Stadlinger, Terheyden and Jepsen have published a respective essay in Zahnärztliche Mitteilungen, the German Dental Associations’ biweekly tabloid (scroll to page 38). It is strangely called “Storyboard”; and, as before in the series, biofilm and cells become actors. Apparently, Quintessence goes Hollywood. The article (unfortunately in German) is prominently featured on its cover. A careful review reveals, unsurprisingly, a remarkable mixture of undeniable facts about the well-known pathogenesis of both artherosclerosis and its sequels and diabetes, and wild speculation regarding possible contributions of periodontal pathogens. It once more seems that “visualizing the invisible” may in fact create more confusion than understanding.
Already in the fourth paragraph of Stadlinger’s essay, a long debunked myth about the size of the “periodontal wound” in periodontitis appears. As Stadlinger et al. write,
The impact of periodontitis [on the development of artherosclerosis and diabetes] at one single tooth may be small. In case of advanced generalized periodontitis one has to assume a biofilm-colonized, ulcerated wound of a size corresponding to the area of a palm which increases the influence on the body accordingly. (My translation and emphasis.)
The palm of a hand has an area of about 64 cm2 (8 x 8 cm2). Already in 2001, Hujoel et al.  had questioned this claim by presenting data. They first used published polynomials for estimating the root surface area of each tooth type which yielded a total root surface area of about 75 cm2. They then used probing depth and attachment level measurements to assess dentogingival epithelium surface areas and finally adopted these figures to certain clinical and radiographic surveys . Notably, they never found a dentogingival epithelial surface area in excess of 44 cm2.
They conclude that, “[d]epending on the population studied, periodontitis commonly leads to a mean increase in the [dentogingival epithelial surface area] of between 3 and 15 cm2. Five % of patients visiting a periodontist presented with surface areas between 30 and 44 cm2 (corresponding to the ventral area of three to four fingers).
The term “wound” is not mentioned in the entire article. Hujoel et al. rather emphasize,
The histology of the DGES [dentogingival epithelial surface area] has been studied extensively. Although the pocket surface is often considered to be ulcerated and, therefore, a wide-open portal of entry for bacteria and their products into the host tissues, the histopathology of periodontal pockets suggests otherwise (48). In its undisturbed state, the pocket epithelium forms a more or less continuous lining over the diseased soft tissues. This is particularly evident in pockets that do not bleed on probing (49). In pockets that exhibit bleeding on probing or suppuration, micro-ulcerations may be detected in localized regions, where heavy migration of polymorphonuclear leukocytes from the tissues into the pocket leaves discontinuities in the epithelial lining.
The by far worst case I have ever seen in 35 years was a 17-yr-old female patient with generalized aggressive periodontitis. The respective full-mouth survey is seen below. Hardly any tooth (maybe ##27, 37, and 47) would be considered tractable. Clinically, recession occurred but was not a prominent feature of the disease. Nevertheless, calculated exposed root surface areas would not correspond entirely with the exposed, to subgingival biofilm, soft tissue wall.
The sum of all exposed root surface areas was in fact 57 cm2. Do Stadlinger et al. really have patients like this in mind when they claim that in advanced generalized periodontitis the wound area exposed to subgingival biofilm may correspond to the area of a palm? A scientific review article about the movie will be published as a guest editorial in the Journal of Clinical Periodontology later this year. It is hoped, but not really expected, that long-debunked myths about the periodontal wound area are not repeated and wild speculations of the impact of periodontitis on both cardiovascular disease events (odds ratio of not more than 1.3 in longitudinal cohort studies; no intervention study so far has shown risk reduction after standard treatment) and diabetes mellitus (slight HbA1c reduction after standard periodontal treatment) avoided.
 Nesse et al. adopted later a similar approach when defining PISA, periodontal inflamed surface area. They considered in particular bleeding on probing as additional parameter, which would further decrease tendencies to exaggerate the impact of the “periodontal wound”. Nesse W, Abbas F, van der Ploeg I, Spijkervet FK, Dijkstra PU, Vissink A. Periodontal inflamed surface area: quantifying inflammatory burden. J Clin Periodontol 2008; 35: 668-673.
20 September 2015 @3:55 pm.
Last modified September 22, 2015.