Old Periodontal Paradigms... Some Things Never Die
by Shirley Gutkowski, Rdh, Bsdh And Guest Author: Bill Landers
One of the hallmarks of modern society is the fast pace of change. Science, technology, and knowledge are advancing so rapidly that what was true just yesterday is often obsolete tomorrow except, it seems, for periodontal disease paradigms developed in the 1970s. These dated concepts have been repeated so often and with such conviction, they have become accepted dogma. Like some kind of dental Dracula, they just won’t die no matter how many study stakes are pounded into their ancient hearts.
Over the last 40 years, research and discoveries have radically changed our notions of what causes periodontal disease, how to test for it, and how to treat it. Wait. That’s an overstatement. I should say that discoveries over the past 40 years have changed the way scientists think about periodontal disease. Clinical dentistry still seems locked in the 1970s. The only thing missing is a mirrored disco ball.
The Evolution of Periodontal ParadigmsPre-1970s According to Dr. Paul H. Keyes, a senior researcher at the National Institute of Dental Research, before the 1970s and for most of the 20th century, many dental professionals thought calculus caused periodontal disease (oral communications, 1983-1986). The link between calculus and inflammation seemed obvious at the time. The more calculus, the more disease. Moreover, if one removed the calculus, the patient improved. The notion was supported by studies that linked calculus deposits to inflamed and bleeding gums.1The mechanism was thought to be purely mechanical. Calculus is hard and gritty. It was compared to an irritating foreign body like a splinter. Even the word deposit is a mechanistic concept. Deposits are things that are laid down like minerals or silt. The data, however, were based on statistical associations. Koch’s Postulates (Table 1), the classic proof of causality, were never proven.
Back then, cavities were the big dental problem. Periodontal disease wasn’t very important. It was something that only happened to old people. Of course, the diagnostic methods were pretty crude. Disease had to be fairly advanced because clinicians only had x-rays, bleeding gums, and notched metal sticks as tools to measure periodontal pockets. None of which are very precise, and all of which are incapable of detecting early disease.
Curiously, the evidence that pockets aren’t the disease was there all along. Calculus seemed such an obvious and intuitive explanation; it distracted everyone from what, in hindsight, is patently obvious. As children, pretty much everyone has normal, shallow sulci, but almost all adults have some form of periodontal disease, so…disease begins in shallow sites.2,3 Disease precedes the pockets.
The 1970s4 Plaque was the new buzzword. Researchers discovered that calculus wasn’t a deposit at all. It was formed by living microorganisms in soft plaque that supposedly produced toxins called lipopolysaccharides that injured the tissue.5,6 Clinically, it didn’t make much difference. Periodontal disease began getting more attention, but the diagnostic tools didn’t change and hygienists were still busy scraping calculus off the teeth. At this time, “scrapodontics” was raised to an art form. It wasn’t enough to just remove calculus. The roots had to be as smooth as glass so no toxin-producing bacteria could attach and start forming calculus. The fact that bacteria attach chemically and not by microscopic grappling hooks wouldn’t be known for another decade.7There was more attention to home care, but the hygienist’s main job was to scrape and the patient’s job was to brush and use that miraculous high-tech tool of the age—dental floss.
The 1980s Researchers discovered that not all the microbes in plaque were bad. Only a few specific microbes were associated with disease, which led to the acceptance of the Specific Plaque Hypothesis. The generalized plaque of the 1970s was renamed the Non-Specific Hypothesis.8
Gram-negative bacteria became all the rage,9,10not that it had much impact on clinical care. “Scrapodontists” still scraped calculus off the teeth, but now there was a new and improved reason for all that scraping. They were getting rid of “Gram-Neggies.” Despite the appearance of some new microbiological tests, clinical assessment was still based on after-the-fact observations like bleeding on probing (BOP), probing depths, and x-rays. Home care began to benefit from increased use of oral irrigators, but toothbrushes and floss were still the norm.
The 1990s While most clinicians were still fixated on calculus and theories dating back to the 1970s, dental researchers were refining the Specific Plaque Hypothesis.11,12 They learned that most disease-associated microbes were anaerobes, growing best at sites with little oxygen. More importantly, it was becoming apparent that periodontal diseases had a lot in common with autoimmune diseases.13,14 While some bacteria produce toxins,15,16 the toxins are insufficient in quantity or potency to cause the destruction seen in periodontal diseases. Rather, specific microbes were found to trigger the immune system, producing a cascade of inflammatory cellular and humeral products.17 It’s the influx of these inflammatory white blood cells and enzymes, not toxins or calculus that slowly destroys the periodontium.18
The First Decade of the 21st Century The newest fact to emerge about periodontal diseases is that they are both inflammatory and contagious.19,20 Periodontal pathogens aren’t found elsewhere in nature,12 except in the mouth of mammals. Babies are born sterile, so humans have to acquire periodontal pathogens from other people or animals. Kissing and saliva are the probable transmission vectors.21 The distinction as to what causes periodontal disease isn’t just of interest to ivory tower scientists. It’s fundamentally important to clinical practice. If calculus caused disease, calculus would be the appropriate therapeutic target and “scrapodontics” would be the therapy of choice. But if periodontal disease is inflammatory and caused by specific bacteria, then those bacteria are the proper targets of therapy. Similarly, if pockets were the disease, treating pockets makes sense. But if inflammation is the disease and it begins in shallow sites, then eliminating pockets doesn’t cure the disease. The proper therapeutic targets are the bacteria that trigger the inflammation in the first place.2,22,23
The New Paradigm There’s a fundamental problem with most of the periodontal assessment methods currently in use. Table 2 explains the traditional periodontal disease measures and their limitations. They were developed in the 1900s when calculus was thought to be the primary cause of periodontal disease. They were never intended to detect pathogenic bacteria. Now that we know that periodontal diseases are caused by specific infections, it’s time to reexamine the predictive value of traditional clinical tests and whether newer microbiological tests can provide a better measure of periodontal risk.
References 1. Archambault G. Calculus formation and its effect on oral health. J Can Dent Assoc. 1967;33:82-86.
2. Riviere GR, Smith KS, Tzagaroulaki E, et al. Periodontal status and detection frequency of bacteria at sites of periodontal health and gingivitis. J Periodontol. 1996;67:109-115.
4. Simpson DM. Current concepts of the etiology and pathogenesis of periodontal diseases. NC Dental Review. 1985;3(No 2):6-11.
5. Socransky SS. Microbiology of periodontal disease—present status and future considerations. J Periodontol. 1977;48: 497-504.
6. Slots J. Subgingival microflora and periodontal disease. J Clin Periodontol. 1979;6:351-382.
7. Kalari M. Attachment Mechanisms and Properties of Bacterial Biofilms on Non-living Surfaces [dissertation]. Finland: Dept of Microbiology, University of Helsinki; 2003.
8. van Palenstein Helderman WH. Microbial etiology of periodontal disease. J Clin Periodontol. 1981;8:261-280.
9. Listgarten MA. Structure of the microbial flora associated with periodontal health and disease in man. A light and electron microscopic study. J Periodontol. 1976;47:1-18.
10. Keyes PH, Rams TE. A rationale for the management of periodontal diseases: rapid identification of microbial ‘therapeutic targets’ with phase-contrast microscopy. J Am Dent Assoc. 1983;106:803-812.
11. Loesche WJ. The antimicrobial treatment of periodontal disease: changing the treatment paradigm. Crit Rev Oral Biol Med. 1999;10:245-275.
14. Nesse W, Spijkervet FKL, Abbas F, et al. Links between periodontal disease and general health. Part 2: preterm birth, diabetes and autoimmune diseases. Dutch Journal of Dentistry. 2006;113: 191-196.
15. Holt SC, Bramanti TE. Factors in virulence expression and their role in periodontal disease pathogenesis. Crit Rev Oral Biol Med. 1991;2:177-281.
16. Simon BI, Goldman HM, Ruben MP, et al. The role of endotoxin in periodontal disease. 3. Correlation of the amount of endotoxin in human gingival exudate with the histologic degree of inflammation. J Periodontol. 1971;42:210-216.
17. Loesche WJ. The bacterial etiology of dental decay and periodontal disease: the specific plaque hypothesis. Clin Dent. 1982;2: 1-13.
18. The immune system involvement in the pathogenesis of periodontal disease. In: Miyasaki K. Periodontal Immunology [CE course]. Periodontics Information Center, University of California Los Angeles. Available at: www.dent.ucla.edu/pic/members/immunology/immunology1.html. Accessed May 25, 2006.
19. Greenstein G, Lamster I. Bacterial transmission in periodontal diseases: a critical review. J Periodontol. 1997;68: 421-431.
20. Preus HR, Zambon JJ, Dunford RG, et al. The distribution and transmission of Actinobacillus actinomycetemcomitans in families with established adult periodontitis. J Periodontol. 1994;65:2-7.
21. Zambon JJ. Familial transmission of periodontal pathogens as a risk factor for periodontal disease progression. Compend Contin Educ Dent. 1994;15:996-1000.
22. Simonson LG, Robinson PJ, Pranger RJ, et al. Treponena denticola and Porphyromonas gingivalis as prognostic markers following periodontal treatment. J Periodontol. 1992;63:270-273.
23. Renvert S, Dahlen G, Wikstrom M. Treatment of periodontal disease based on microbiological diagnosis. Relation between microbiological and clinical parameters during 5 years. J Periodontol. 1996;67: 562-571.
24. Grimes DJ. Koch’s postulates—then and now. Microbe [serial online]. May 2006. Available at: http: //www.asm.org/microbe/index.asp?bid=42390. Accessed Jun 12, 2006.
25. Lang NP, Adler R, Joss A, et al. Absence of bleeding on probing. An indicator of periodontal stability. J Clin Periodontol. 1990;17:714-721.
26. Newbrun E. Indices to measure gingival bleeding. J Periodontol. 1996;67:555-561.
27. Research, Science, and Therapy Committee of the American Academy of Periodontology. Position paper: epidemiology of periodontal diseases. J Periodontol. 2005;76:1406-1419.
Bill Landers Bill is president of Oratec Corporation, a dental company specializing in anti-infective periodontics. He is an expert on chairside microbiological risk assessment technologies and in-office antimicrobial delivery systems.
Shirley Gutkowski, RDH, BSDH Shirley is the co-author (with Amy Nieves, RDH) of The Purple Guide: Developing Your Clinical Dental Hygiene Career, which helps new and newly graduated dental hygienists make the transition to the real world of dental hygiene. She is an award-winning author and popular speaker. Shirley invites you to visit her Web site at www.shirleygutkowskirdh.com.
One of the hallmarks of modern society is the fast pace of change. Science, technology, and knowledge are advancing so rapidly that what was true just yesterday is often obsolete tomorrow except, it seems, for periodontal disease paradigms developed in the 1970s. These dated concepts have been repeated so often and with such conviction, they have become accepted dogma. Like some kind of dental Dracula, they just won’t die no matter how many study stakes are pounded into their ancient hearts. 
Search
