Compliance vs. patient selection: Trays provide an option in countering periodontal microbes

Anne Guignon, RDH, explores how trays provide an option in countering periodontal microbes.

By Anne Guignon, RDH, MPH, CSP

Dental hygienists seem to be particularly hardwired to the concept of patient compliance, often judging their professional worth on whether or not a patient follows instructions or proceeds with recommend treatment. Not a day goes by that there isn't some kind of online discussion revolving around compliance issues. Often the comments about the patients are judgmental and occasionally quite harsh.

After a frustrating day in the clinical setting, it is really tempting to blow off steam. However, it's helpful to step back a bit and look at the situation without all the emotional fog. First of all, if there were no patients, we would not have a job. Dental hygienists serve people. We are health-care providers, and we provide preventive services as well as appropriate treatment for disease.

While dental hygienists are limited to providing diagnostic evaluations in the realm of dental hygiene services, we are educators and, along with the doctors, shoulder the responsibility to provide information about all treatment options. The information given to the patient should include both the risks and the benefits for all options, including no treatment.

In our fast-paced world, it is easy to shorten the list to the option we personally feel is best for the patient, but this approach is fraught with problems. Some very nurturing caregivers may inadvertently think they know the patient so well that certain treatment protocols are never presented.

If a clinician is strapped for money or finds it hard to spend dollars on something they deem to be over-the-top, it's easy to let emotions cloud one's judgement. Quite simply, it is unfair to assume a patient does not have adequate resources to pay for a certain type of treatment just because they drive an old car or come dressed in old clothes. It's also unfair to assume that a patient will not accept treatment recommendations based on a past history of refusing treatment. It is not our job to diagnose their pocketbook or past behaviors.

But providing all treatment options can get tricky, especially if you fall back into the trap of "that's not what I learned in school." Since I graduated in 1971 and was initially trained much like Irene Newman, an approach like this would be downright ludicrous.

What are you doing to keep current? Are you taking courses, reading articles or reviewing scientific papers? Are you engaging in online dialogues with other dental professionals? The online world is easy and information can be seductive or even false, especially in casual chats where participants chime in with one-line anecdotal reports without any scientific substantiation.

Here are some wise words about compliance from veteran hygienist, Lisa Nelson Derlau, RDH:

"When you give up needing to be right and decide people have the right to their own decisions, relationships improve. Patients will be more compliant about getting healthy. Patients know when you think they are being stupid. It shuts them down, and you out. When patients know you are on their side, they will open up and listen. Then you can begin educating."

Role of Pathobionts

For years we have known that anaerobic organisms are the predominate players in periodontal disease lesions. With the advent of molecular genetics, scientists are now finding DNA fragments of microbes that have never been cultured. New information is coming to light about the role of known microbes, such as Porphyromonas gingivalis in periodontal disease.1,2 Current studies show P. gingivalis is a key player and has recently been identified as a keystone pathogen responsible for initiating the development of dysbiotic microbial communities.1-5 Dysbiosis by definition is a microbial community that is exactly opposite of homeostasis. Dysbiotic communities do not contain sufficient levels of beneficial microbes, have low microbial diversity, and demonstrate a substantial increase in pathobionts over what is found in a healthy microbiome.6-8

P. gingivalis is considered a low abundance microbe; in other words, even small quantities can wreak havoc. P. gingivalis is very aggressive microbe and present in early, middle, and late stages of periodontal disease.4 It is known to interfere with a patient's immune system response, recruit commensal microbes to become pathobionts, and has the capacity to upregulate the virulence of the entire inflamophilic microbiological community.6,7P. gingivalis thrives when inflammation is present and has the ability to cover itself with a sugar coating, which makes the microbe undetectable to the immune system.9

Three different studies, published in 2016, are shedding light on the potential role of P. gingivalis, and other periodontal pathogens, on the development of pancreatic cancer,10 esophageal squamous cell cancer,11 and atherosclerosis.12 None of these papers demonstrate causality, but there is mounting evidence that a relationship exists between P. gingivalis and other periodontal anaerobes indicating these microbes may be disease markers,13 associated with the progression of a specific disease or possibly increase susceptibility to inflammation. Bottom line: P. gingivalis and associated anaerobic pathogens are the enemy.

Organism Stabilization

Since it is difficult and expensive to culture anaerobes, it is unlikely that scientists will be able to identify all periodontal pathogens even in the near future. Expecting to reverse this biofilm-based process using antibiotics is not a tenable solution. Today's antibiotic preparations do not penetrate the extracellular polysaccharide slime (EPS) matrix that protects the pathogens.14 There is growing concern about developing antibiotic-resistant bacterial strains since microbes can mutate and change genetic expression in remarkably short periods of time.

Our clinical focus needs to be on homeostasis. The challenge is how to achieve that goal over a long period of time. The two keys are: patient compliance and finding an effective protocol that that creates a balanced, healthy environment. Anaerobes can't survive the oxygen levels present when a patient is stable and healthy. Hydrogen peroxide is an antiseptic that debrides wounds and helps reduce inflammation and products, with a concentration of of 3% or less, and are approved by the FDA for oral use. Hydrogen peroxide has a profound effect on biofilm by degrading the EPS slime, lysing bacterial cell walls and releasing large quantities of oxygen.15

The key is finding a system that delivers a sustained concentration of hydrogen peroxide for a period of time sufficient to kill pathogens while creating an oxygen-rich environment that does not foster future anaerobic growth. Research shows 15 minutes of direct contact with hydrogen peroxide is needed to achieve these goals.16 While 3% hydrogen peroxide kills microbes, the liquid has a rapid oxygen spike making it impossible to maintain a constant subgingival concentration for the appropriate amount of time. In addition, over the counter hydrogen peroxide is very acidic with the pH level of 3.

Tray System

As dental health care providers, we are responsible to offer viable solutions and treatment options. Unless you practice in a perfect world, each one of us has patients who experience chronic bleeding, or who do not opt for periodontal scaling or surgical treatment, and we also have those who are classified as downright hopeless. The PerioProtect system was developed over a decade ago to help manage gingivitis and periodontitis and is backed with well-thought-out studies.17-18 Patients wear an FDA-cleared prescription tray filled with a 1.7% hydrogen peroxide gel for 15-minute increments.

These are not bleaching trays, but custom trays that create a seal delivering the peroxide gel into sulcus depths as deep as 9mm. The sealing system keeps the gel in place long enough to oxygenate the micro environment.

At this low concentration, the ideal therapeutic time point is 15 minutes. Initially patients may need to wear the custom trays two to three times a day, but once gingival health is stable most only need a single daily application to maintain optimal results. Patients who use the trays on a regular basis experience fresher breath and whiter teeth-beneficial side effects for most people.

Even though I am low risk for periodontal disease, the system intrigued me. Last fall, I was fitted for prescription trays, which are much more comfortable than anticipated. The gel has a mild wintergreen flavor and is easy to dispense. My one personal challenge is a quick gag reflex, so I wear each tray separately. I put the trays in, set the timer on my phone and go about my daily routine. It's not any harder than that.

Let's circle back to the issue of patient compliance. Periodically questions about PerioProtect come up on internet chats. The two most frequent comments involve patient compliance and cost. PerioProtect is an easy system to adopt for a patient willing to commit to a daily regimen. It's easy to wear the trays while showering, getting dressed, driving to work, or folding the laundry. Individual practices set the fee for the trays, which are fabricated to last around five years. Most patients use a tube of gel every six weeks, with an annual expense of approximately $200 a year.

Is PerioProtect a beneficial system? Absolutely, but is not the right option for a patient who wants a quick fix. It works for people who are committed to being part of the solution. It works for hopeless patients who want another chance.

If you don't know about this option, it's time to learn where this fits into patient care. From an ethical standpoint we need to provide all of the options, including the attendant risks and benefits, to our patients, not just the choices we like or the treatments we think they will choose. RDH

References

1. Wade WG. Has the use of molecular methods for the characterization of the human oral microbiome changed our understanding of the role of bacteria in the pathogenesis of periodontal disease? J Clin Periodontol. 2011 Mar;38 Suppl 11:7-16.
2. Wade WG. The oral microbiome in health and disease. Pharmacol Res. 2013 Mar;69(1):137-43
3. Zhu Y, Dashper SG, Chen YY, Crawford S, Slakeski N, Reynolds EC. Porphyromonas gingivalis and Treponema denticola synergistic polymicrobial biofilm development. PLoS One. 2013 Aug 26;8(8): e71727.
4. Periasamy S, Kolenbrander PE. Mutualistic biofilm communities develop with Porphyromonas gingivalis and initial, early, and late colonizers of enamel. J Bacteriol. 2009 Nov;191(22):6804-11.
5. Könönen E, Müller HP. Microbiology of aggressive periodontitis. Periodontol 2000. 2014 Jun;65(1):46-78.
6. Hajishengallis G, Lamont RJ. Beyond the red complex and into more complexity: the polymicrobial synergy and dysbiosis (PSD) model of periodontal disease etiology. Mol Oral Microbiol. 2012 Dec;27(6):409-19.
7. Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response. Trends Immunol. 2014 Jan;35(1):3-11.
8. Hajishengallis G. The inflammophilic character of the periodontitis-associated microbiota. Mol Oral Microbiol. 2014 Dec;29(6):248-57.
9. Singh A, Wyant T, Anaya-Bergman C, Aduse-Opoku J, Brunner J, Laine ML, Curtis MA, Lewis JP. The capsule of Porphyromonas gingivalis leads to a reduction in the host inflammatory response, evasion of phagocytosis, and increase in virulence. Infect Immun. 2011 Nov;79(11):4533-4. 10. Jacob JA. Study Links Periodontal Disease Bacteria to Pancreatic Cancer Risk. JAMA. 2016 Jun 28;315(24):2653-4.
11. Gao S, Li S, Ma Z,et al. Presence of Porphyromonas gingivalis in esophagus and its association with the clinicopathological characteristics and survival in patients with esophageal cancer. Infect Agent Cancer. 2016 Jan 19;11:3.
12. Bale BF, Doneen AL, Vigerust DJ. High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis. Postgrad Med J. 2016 Nov 29. pii: postgradmedj-2016-134279.
13. Krishnan K, Chen T, Paster BJ. A practical guide to the oral microbiome and its relation to health and disease. Oral Dis. 2016 May 24.
14. Schaudinn C, Gorur A, Keller D, Sedghizadeh PP, Costerton JW. Periodontitis: an archetypical biofilm disease. J Am Dent Assoc. 2009 Aug;140(8):978-86.
15. Marshall MV, Cancro LP, Fischman SL. Hydrogen peroxide: a review of its use in dentistry. J Periodontol. 1995 Sep;66(9):786-96.
16. Dunlap T, Keller DC, Marshall MV, Costerton JW, Schaudinn C, Sindelar B, Cotton JR. Subgingival Delivery of oral debriding agents: A proof of concept. Jour Clin Dent. 2011, Nov; XXII(5):149-158.
17. Putt MS, Mallatt ME, Messmann LL, Proskin HM. A 6-month clinical investigation of custom tray application of peroxide gel with or without doxycycline as adjuncts to scaling and root planing for treatment of periodontitis. Am J Dent. 2014 Oct;27(5):273-84.
18. Cochrane RB, Sindelar B. Case Series Report of 66 Refractory Maintenance Patients Evaluating the Effectiveness of Topical Oxidizing Agents. J Clin Dent. 2015;26(4):109-14.


ANNE NUGENT GUIGNON, RDH, MPH, CSP, provides popular programs, including topics on biofilms, power driven scaling, ergonomics, hypersensitivity, and remineralization. Recipient of the 2004 Mentor of the Year Award and the 2009 ADHA Irene Newman Award, Anne has practiced clinical dental hygiene in Houston since 1971, and can be contacted at anne@anneguignon.com.

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