Pocket Monsters...The Nature of the Enemy by: Larry Burnett, DDS

Plaque consists of countless mushroom-shaped bacterial colonies in which incompatible species of bacteria not only co-exist , but actually cooperate to thrive in hostile environments. Channels through the mushrooms serve as primitive alimentary canals. This illustration appears with the permission of Dr. Maxwell H. Anderson and is derived from information from the Center for Biofilm Engineering-Montana State University.

When you read about “biofilm” in dentistry, it’s usually in an article discussing how difficult it is to clean dental waterlines. Free-floating bacteria can be easily destroyed by flushing the water system with an antimicrobial agent. But once those bacteria have time to organize into a biofilm, antimicrobial agents are virtually useless.

The best known biofilm in dentistry isn’t in your waterlines. It’s in your patient’s mouth. (1)

Bacterial plaque as a biofilm
I recently was fortunate enough to be asked by Lippincott to review preliminary copy for a book entitled Periodontal Concepts for the Dental Hygienist by Jill Nield-Gehrig, RDH, MA, (2) and I highly recommend it. Ms. Neild-Gehrig provides an excellent discussion of the biofilm called “plaque”, and I’ve borrowed freely from her chapter on plaque development as well as several research articles on the subject.

You can almost (not quite, but almost) think of plaque as a living creature in which the bacteria behave more like the specialized cells in a higher organism than as independent life forms.

By the time a patient leaves your office after a prophy and starts the engine of their car, those meticulously cleaned teeth are absorbing a molecular layer of proteins and glycoproteins from the saliva. (3) This creates a surface that’s ideal for bacterial attachment.

The first colonizers (primarily streptococci and actinomyces) connect to the protein pellicle and form the “roots” that will anchor the biofilm to the tooth. (4)

Fusobacteria serve largely as structural members. They promote co-aggregation of even more cells. As the biofilm develops, micro environments form inside the structure. Some areas are oxygen-deficient and are populated by anaerobic bacteria. In other areas variations in pH occur that appeal to specific species.

Though plaque appears to be a continuous slimy film, each micro colony really has a mushroom shape, which is connected to the tooth at a narrow base formed by those initial settlers. It branches outward as the other bacteria congregate. It’s the vast number of these microscopic colonies that create the illusion of a continuous film.

As the mushroom develops, weird stuff starts happening. Incompatible bacteria start living in intimate contact that would be impossible in a free liquid environment. The metabolism of the bacteria changes. They even begin communicating via chemical signals.

A slimy “skin” forms over the colony. This skin not only protects the bacteria from the hostile environment, but also seals off the good stuff like the oxygen and nutrients. So tunnels form through the structure to serve as primitive alimentary canals. They allow the exterior “soup” to flow through the colony so nutrients can be absorbed and distributed....and metabolic waste eliminated. In fact, the waste from one colony may be used by a different colony downstream.

If periodontal disease is a localized bacterial infection (and we all know it is, right?) why aren’t antimicrobial agents and antibiotics more effective in treating it?

Many of the early lab studies into antimicrobials and periodontal pathogens were conducted using free bacteria in petri dishes. When you can catch bacteria in the open, they’re highly vulnerable to chemical medicaments.

But it’s been estimated that 99% of all bacteria on earth exist as biofilms. (3) And bacteria in a biofilm become highly resistant to antimicrobial agents. Whether it’s in your unit’s waterline or in a 6mm pocket, bacteria in a biofilm will withstand high pH levels, antibiotics or antimicrobials that would be 100% lethal if the bacteria were exposed on their own.

In fact, studies have found that some antibiotics that kill free-floating bacteria must be increased from 50 times to as much as 1500 times (1500 times!) to be effective against the same pathogens hunkered down in a biofilm. (6)

As Jill observes in her new book, at these high doses, antibiotics would be just as lethal to the patient as to the microbes. And antimicrobial irrigants like chlorhexidine or povidone iodine don’t fair much better than antibiotics. If bacteria are suspended in liquid or if a biofilm is very young (say, 6 hours old (7), chlorhexidine is fairly effective. But in a biofilm that’s older (say, 48 hours or 72 hours)...forget it! (8) One typical study found that a 5-minute exposure to 0.2% chlorhexidene had very little effect on the viability of a mature biofilm. (9)

Don’t misunderstand me. I’m not arguing that irrigation or antibiotics aren’t effective therapies for treating periodontal disease. But they must be adjunctive therapies, not primary therapies. The most destructive of all perio pathogens are those loosely adherent or free-swimming anaerobes and they’re probably vulnerable to antimicrobial irrigants like iodine. Antibiotics like doxycycline may be indicated in refractory cases where the pathogens have invaded the lining of the sulcus. But for biofilms, you need a different strategy.

Debride, debride, debride
You can’t poison a biofilm. It’s defenses are too good for the pharmaceutical industry.

Mechanical removal remains the only way to eliminate a biofilm. And that’s one reason why debridement remains the soul of all effective periodontal therapy, both definitive treatment and maintenance therapy.

In my view the very best “hands-on” tool for removal of subgingival biofilm is the ultrasonic scaler. When I debride ultrasonically, I try like the devil to touch everything with the tip. I run it over the irregular root surfaces from different angles.

But I don’t fool myself. No matter how thorough I am, I know I’m not touching all the biofilm. Many areas of the root accessible to bacteria are not accessible to me.

Years ago, Professor Anthony Walmsley conducted some fascinating research. Walmsley found that ultrasonic debridement removed plaque in areas the tip didn’t actually touch. (10) It isn’t clear exactly why this works. It may be the “ultrasonic streaming” (that’s a technical name for the fluid turbulence created by the high frequency vibration). Or as Walmsley believed, it may be the energy released when the bubbles produced by ultrasonic vibration collapse (called “cavitation”). It doesn’t really matter.

The bottom line is this: if there’s a tool that helps me remove the biofilm I overlook or can’t reach with a conventional hand instrument, that’s the tool I want to use.

When it was originally published, the importance of Walmsley’s work wasn’t fully appreciated because the treatment of perio disease lagged substantially behind the research. But as it gradually caught up during the ‘90s, subgingival ultrasonic debridement became one of the major hygiene trends of the decade.

A new look at irrigation
And there’s also evidence that when it’s combined with ultrasonics, antimicrobial agents become more effective in treating severe periodontal cases. Again, I don’t claim to know why. It may be that the ultrasonic streaming forces the antimicrobial through the biofilm skin. Or perhaps the ultrasonic lavage breaks up the colony, and gets the bacteria running so they’re more easily poisoned. But that’s pure speculation.

It appears that the effectiveness of ultrasonic antimicrobial irrigation depends on the severity of the disease. Mild-to-moderate pockets respond well to either water or antimicrobial in an ultrasonic lavage. It’s the severe cases with 7mm pockets where iodine seems most effective. (11)

A recently-published study by researchers in Gothenburg, Sweden compared the long-term outcomes of conservative treatment with and without the ultrasonic application of povidone iodine. (12)

They selected 223 patients with advanced destructive periodontitis. To qualify for the study, at least 2 teeth in each quadrant had to have pockets of 6mm or more and demonstrate attachment loss exceeding 40%.

All the patients were given a dog-and-pony show concerning hygiene. (Incidentally, throughout the study a strong dose of re-education was administered whenever a patient seemed to be backsliding.) All patients received one phase of ultrasonic non-surgical therapy followed by 12 years of ultrasonic supportive therapy every 3-4 months.

The control group and the test group received exactly the same treatment … with just one small exception. In the test group, the irrigant used during ultrasonic debridement was 0.1% povidone iodine. In the control group, it was water.

Periodontal health data was collected frequently during the definitive treatment period at 0, 3, 5, & 12 months and then after 3, 5, and 12 years of maintenance.

Both groups showed improved gingival health, reduced pocket depth and probing attachment. (Let’s hear it for ultrasonics!) But the group that also received iodine irrigation had significantly shallower pockets and significantly greater attachment gains at every checkpoint during the initial treatment phase. That is, they got better faster.

Of course, not all the cases were successes. During the 1-3 years of maintenance about 18% of the patients had to be referred for re-treatment. However, these “losers” were not evenly distributed. Roughly 25% of the “scaling-only” patients had a relapse. Just 13% of the “scaling+iodine” patients.

In the words of the authors: “The findings from the present study demonstrated that topical application of 0.1% povidone iodine, used as a cooling liquid in conjunction with ultrasonic subgingival root debridement, established conditions which improve the outcome of non-surgical therapy.”

By the way, as in earlier studies, these researchers noted that ultrasonic administration of iodine was particularly effective in the deeper pockets.

Conclusion
In any war (and that includes the war against periodontal disease), it helps to understand your enemy. Most of the traditional techniques for treating bacterial infection simply do not apply to bacteria hunkered down in a biofilm.

Those mushroom-shaped colonies are extremely resistant to chemicals and medicaments. That’s why mechanical debridement remains the soul of effective periodontal therapy. Everything else (surgery, irrigation, systemic antibiotics) is adjunctive.

And that’s why I’m such a fan of subgingival ultrasonics. By creating fluid turbulence and cavitation, that vibrating tip mechanically blasts biofilm from surfaces even beyond those I actually touch! Furthermore, there’s growing evidence that when I deliver an antimicrobial in the ultrasonic lavage, I can improve the prognosis for deep pockets.

This article first appeared in the Parkell Today newsletter.

A graduate of the Medical College of Virginia School of Dentistry, Dr. Burnett has authored numerous articles and lectured extensively on conservative periodontal therapy throughout the US and Canada. A frequent speaker at both the ADA Annual Scientific Session and AGD meetings, he is featured in the new video-based program “Advanced Ultrasonics in General Practice.” Other articles by Dr. Burnett are available at www.parkell.com.

Dr. Burnett also conducts hands-on courses for dentists and hygienists. He can be contacted at: 2221 SW First Ave #1224, Portland, OR 97201 Tel: 503-221-4237, lburnett2@msn.com.

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Bibliography
1. Chen C. Periodontitis as a biofilm infection. J Calif Dent Assoc. 29:5, p362-9, May 01
2. Nield-Gehrig. PERIODONTAL CONCEPTS FOR THE DENTAL HYGIENIST. Lippincott, William & Wilkins - Scheduled for publication 2002
3. Marsh PD, Bradshaw DJ . Dental plaque as a biofilm. J ind Microbiol. 15(3), p169-75, Sept 95
4. Kolenbrander PE. Oral microbial communities: biofilms, interactions, and generic systems. Annu Rev Micribiol. 54, p413-37, 00
5. Nield-Gehrig
6. Nield-Gehrig
7. Zaura-Arite E, et al. Confocal microscopy study of undisturbed and chlorhexidine-treated dental biofilm. J Dent Res. 80:5, p1436-40, Ma ‘01
8. Millward TA, Wilson M. The effect of chlorhexidine on Streptococcus sanguis biofilms. Microbios. 58, p236-237, ‘89
9. Pratten J, et al. Composition and susceptibility to chlorhexidine of multispecies biofilms of oral bacteria. Appl Environ Microbiol. 64:9, p3525-9, Sept 98
10. Walmsley AD. Dental plaque removal by cavitational activity during ultrasonic instrumentation. J Periodontol. 15:9, p539-543, 88
11. Christersson, et al. Monitoring of subgingival Bacteriodes gingivalis and Actinobacillus actinomycetemcomitans in the management of advanced periodontitis. Advncs in Dental Research, 2:2, 382-388, Nov 88
12. Rosling B et al. The use of PVP-iodine as an adjunct to non-surgical treatment of chronic periodontitis. Jour Clin Perio. 28:1023-1031, 2001.

Pre-order copies of Jill S. Nield-Gehrig’s new book, Periodontal Concepts for the Dental Hygienist are available online at www.barnesandnoble.com.

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