Having just had submitted a completely revised chapter on Periodontal Microbiology for the second edition of my textbook which is due early next year, I’ve read with interest an editorial (or Perspective) by Professor Mike Curtis about a new study by Brazilian microbiologists/periodontists Perez-Chaparro et al. (2014) in the Journal of Dental Research, a systematic review of 41 studies on newly identified pathogens associated with periodontitis. As far as I understand, none was longitudinal. Curtis remembers the days (in the 1980s and 1990s) when periodontal investigators not intimately involved in what was going on in oral microbiology disrespectfully (“scornfully”) called “their microbiology colleagues – ‘The Bug of the Month Club’ – intended to convey the inappropriate promotion of this apparently bewildering array of periodontal pathogen new kids on the block.”
What is called by Perez-Chaparro et al. (2014) as “modern era” of oral microbiology, i.e. the past 12 years, was covered after the focused question had been asked, “What is the weight of evidence for the existence of newly identified periodontal pathogens based on association studies?”
As has been mentioned, the American Academy of Periodontology celebrates in 2014 her centennial. On that auspicious occasion, several themes which have shaped modern Periodontology have been identified by the Editor-in-Chief, and prominent opinion leaders asked to give brief summaries on each. The first commentary on “Bacteria [that] Play a Critical Role in the Etiology of Periodontal Disease” by Professor Niklaus P. Lang 2014 has just appeared in the February issue of the Journal of Periodontology. The title is remarkably conservative, avoiding any claims as regards periodontal diseases’ “causes”.
The brief digest summarized fifty years of oral microbiology as regards periodontal research, mentioning ground-breaking work by the Socransky group in Boston, MA; Slots in Copenhagen and later Buffalo, NY, together with Genco; as well as Loesche in Ann Arbor, MI; and Moore and Holdeman-Moore in Richmond, VA. But it also quickly focuses, in a couple of paragraphs, on the famous study on Experimental Gingivitis in Man of 1965 by one of the most eminent Norwegian periodontists, Harald Löe. Right now, the paper has been cited 2533 times, while its set-up has been repeated several hundred times for different research questions. Lang explains,
“It [the Experimental Gingivitis in Man paper] reported a straightforward, hypothesis-driven clinical experiment with only 12 volunteers, and it asked the question: Would the amount of plaque mass buildup on the teeth result in gingivitis?
During a 3-week period of no oral hygiene, all volunteers predictably developed generalized gingivitis, and upon reinstitution of oral hygiene practices, they returned to pre-experimental low levels of plaque and gingivitis. Some of the power of this study came from unique and innovative design features, including the use of healthy young human volunteers with no systemic diseases, no malnutrition, and no occlusal trauma. In addition, the participants were their own controls, so they were all taken to a healthy gingival status at baseline, induced to gingivitis solely by the absence of oral hygiene, and then returned to health solely by reinstitution of oral hygiene.”
It is worth to revisit the paper by Löe et al. (1965) after almost 40 years. Nine first-year clinical students, one teacher in Periodontology and two laboratory technicians participated in a clinical and microbiological experiment. There was no mention as regards health or occlusion. At first exam they had low, but not zero, Plaque Index (PI) scores (means between 0.00 and 0.95), which had been described the year before by Silness and Löe (1964) and low, but not zero (0.02-0.69), Gingival Index (GI) scores (Löe and Silness 1963). Although throughout scores on altogether one thousand gingival units, as the authors mention, were considered which were, according to Lang (2014) “well-defined”, Löe et al. (1965) generally averaged scores at the tooth level, groups of teeth, the area level, the subject level and the cohort level. Thus, fractions of an integer (for instance 0.60) have to be interpreted as frequencies of scores (e.g., 40% score 0, 60% score 1), since only scores were “well defined”. There was actually no preparatory phase when plaque and gingival inflammations was brought to zero. Participants, who were consistently called “patients” in the paper, withdrew from all oral hygiene and were “rechecked at varying time intervals, and a full assessment of their plaque and gingival status was carried out each time using the same criteria at the introductory eaxmination. As soon as inflammatory changes were observed and a complete index and bacteriological assessment had been made, the patients were given detailed instructions in oral hygiene methods using brush and wood massage sticks.” “At a point where the GI and PI scores approached zero, the experiment was terminated.”