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How to explain periodontitis to your patients


It’s not always easy to explain microbial dysbiosis and inflammation, so here are some strategies for talking about these concepts with your patients.

Are you a lot like me, always searching for a creative way to explain periodontitis to a patient? Do you talk about periodontal inflammation and find the patient staring over your shoulder and looking like he’s ready to pass out from boredom? If so, you’re not alone, so let’s discuss the etiology and pathogenesis and try to find a better way to understand and explain it.

What periodontitis is NOT

Periodontitis is a chronic inflammatory condition of the periodontium and certainly not an acute bacterial infection. The inflammation of the periodontium is initiated by the presence of microbial biofilm, but it seems to be the inflammatory response that drives changes in the periodontal microbiome and amplifies the pathogenesis of this chronic condition. Periodontitis is modified by multiple host response genes in combination with lifestyle and environmental factors.1 Therefore, when introducing patients to periodontitis, it’s probably inappropriate to talk to them about killing bacteria like you would kill a fly with a fly swatter.

What is dysbiosis?

The human body, not just the oral cavity, is a host to a great number and assortment of bacteria, viruses and fungi that are beneficial to health and well-being. A community of commensal, symbiotic and pathogenic microrganisms (microbiome) share the human space and are sometimes poorly understood as elements of health and disease.

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The oral cavity is a very complex ecosystem (I call it a rainforest when talking to patients). Besides approximately 150 different species of bacteria per person, other microbe types such as archaea, fungi, viruses and protozoa can also live in a symbiotic relationship with bacteria that are in harmony and co-dependent.2 There are also commensals (microbes that act as partners that don’t hurt or help each other) that can function as a natural barrier against opportunistic or exogenous pathogens. The microbiota of the tongue and saliva are more similar but different from what’s present on teeth and root surfaces.2

Dysbiosis refers to microbial imbalance. A good example in medicine is a foodborne illness, such as E. coli. In patients with periodontitis (and peri-implantitis), a dysbiotic shift in the periodontal microbiome will elicit an unresolved inflammatory host response that damages the surrounding periodontium. Not all hosts are susceptible, but those that are affected develop periodontitis over time as a chronic inflammatory condition.

Etiology of periodontitis: polymicrobial synergy and dysbiosis

Scientists are now calling the etiology of periodontitis (and peri-implantitis) “polymicrobial synergy and dysbiosis.” (Lamont & Hajishengallis, 2015).1 According to the latest hypothesis, uncontrolled inflammation of the periodontium arises when complex microbial communities transition from commensal to pathogenic. Keystone pathogens elevate community virulence and the resulting dysbiotic community targets specific aspects of host immunity to further disable immune surveillance while promoting an overall inflammatory response. These are complex interactions and research to test this hypothesis is ongoing to further understand the various interactions between host and microbes.1 Johnson & Johnson (Listerine®) recently created a virtual reality experience (coming soon) that can take you inside biofilm and immerse you in the balance between good and bacteria inside the mouth. View these YouTube videos to see what’s coming.

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Periodontitis pathogenesis

Periodontitis is initiated by dental biofilm and some anaerobes such as P. gingivalis display destructive virulence factors, but it’s the host that seems to mediate the inflammatory response.2

A 2018 scholarly article2 states:

“Indeed, it has been demonstrated that even in health, the periodontal and peri-implant tissues are in close contact with the dental biofilm and show an active immune response, which is physiological. This low grade inflammation is complex and involves both innate and acquired immunity as well as the complement system, the major link between the two arms of the immune system. Dysregulation in the production of inflammatory mediators in response to the dysbiotic microbial challenge leads to the production of toxic products by the host cells. When produced in excess, these toxic products are responsible for tissue destruction around teeth and oral implants. Additionally, the identification of Toll-like receptors highlighted how both commensal and pathogenic bacteria can initiate innate immune responses. Finally, the discovery that most bacteria live in biofilms as tenacious multicellular communities has been important for our understanding of how microorganisms could resist the host immune response and even some conventional anti-infective approaches.”

Specific microbes are associated with periodontitis, but the presence of these microorganisms in individuals with no disease progression suggests that the inflammation is the effect of the immune response and the inflammatory processes, not the mere presence of certain pathogens.3 Immune-inflammatory mechanisms govern patient susceptibility and are modified by environmental factors.3

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Have treatment protocols for periodontitis changed?

There’s no doubt that treatment protocols for periodontitis have changed because of our growing understanding of microbial biofilms and the pathogenesis of periodontitis. The main purpose of current periodontal therapy is the control of the dysbiotic dental biofilm to restore homeostasis between the microbial community and the host.2 Initial therapy (SRP), if performed well, remains the gold standard initial treatment for periodontitis. We use fewer hand curettes and more ultrasonics, including air polishing for supra- and sub-gingival management of biofilm on teeth/roots and implants. The ADA, in 2015, published concise evidence-based clinical practice guidelines for nonsurgical periodontal therapy with and without adjuncts.

Self-care options include more emphasis on interdental brushes for wider embrasures, more sophisticated oral irrigators and powered toothbrushes. Make sure you read the literature carefully concerning clinical outcomes for self-care measures. Look at systematic reviews and meta-analyses instead of single studies and learn how to grade evidence. The ADA has a series of videos that will get you started on your journey to grade the reliability of the studies you’re looking at.

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Advanced lesions with deeper probing depths (≥ 7 mm) are less efficient, with about 15 percent showing no improvement after nonsurgical periodontal therapy, including furcation-involved teeth.2 In these cases, referral to a periodontist is justified and patients should be encouraged to see a specialist.

Unfortunately, the growth of some unscrupulous dental practices in which the nonsurgical treatment of periodontitis is viewed as a profit center has been noticed by a growing number of patients and dental professionals alike. Dental hygienists share concerns online in various chat groups about being asked to perform scaling and root planing (SRP) without adequate time and equipment. It’s not uncommon for two quadrants of SRP on patients with deep probing depths and heavy subgingival calculus to be scheduled on a daily hygiene schedule for 60 minutes or less. Instrumentation, working fast and blind, is like putting a Band-Aid on a wound without debridement. Patients such as these return in six to 12 months with little to no periodontal maintenance.

Make sure you approach periodontal therapy just as you would every other service. Clinical excellence is achievable and requires continuing education with the appropriate educator. Involve a local periodontist and schedule lunch and learns so that you can become better educated about gingival and periodontal therapy.

Dental practice takeaways

Periodontal therapy as a profit center: If a general dental practice wants to improve the periodontal health of patients, minimize the focus on profitability by giving hygienists adequate time to perform a periodontal assessment, nonsurgical periodontal therapy and periodontal maintenance. Hygienists aren’t widgets, and most dental hygiene providers will burn out quickly if you treat them like assembly line workers. If the hygienist provider requests two hours for two difficult quadrants of SRP, schedule accordingly. Be considerate and ask the RDH how much time he or she needs for a given procedure. Focus on clinical excellence, health restoration and well-being and you’ll be rewarded by being more profitable and having a patient base that trusts you and wants to return for routine care. Include your professional RDH and periodontist in developing evidence-based, ethical protocols that will benefit both the practice and the patient, and don’t ignore the entire human host in your assessment. The oral cavity is just one small part in the entire human body space and is strongly influenced by the overall health of the human host and its environment.

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Systemic antibiotics: Individuals who are promoting DNA testing and systemic antibiotic treatment (as a sole approach to treatment) for specific periodontal pathogens need to recognize limitations of this testing because, in most instances, systemic antibiotics can’t penetrate these sticky polymicrobial microbial communities. In reviewing ADA evidence-based clinical guidelines, patients with moderate to severe chronic periodontitis may consider systemic antimicrobials as an adjunct to SRP with a small net benefit expected, but the evidence to date is weak.4

Read evidence-based clinical guidelines: Be careful what you read and apply online. Make sure your protocols are supported by strong scientific evidence and keep in mind that science is constantly changing based on new emerging evidence. I regularly peruse Cochrane Oral Health Reviews, ADA Evidence-based Clinical Guidelines and the Dental Elf online.

It’s not easy to explain microbial dysbiosis and inflammation, so I use a lot of metaphors, such as Spider-Man with web shooters to describe microbial biofilm. I compare biofilm to a cobweb and talk about what purpose the web serves. I then compare a spider’s web to biofilm and make comparisons. Have fun with it!


1. Bartold PM, Van Dyke TE. An appraisal of the role of specific bacteria in the initial pathogenesis of periodontitis. Guest Editorial. J of Clin Periodontol 2018. 46(1): 6-11. 

2. Lassere JF et al. Oral health, biofilms and their role in periodontal and peri-implant diseases. Materials. 22 September 2018.

3. Cekici A. et al. Inflammatory and immune pathways in the pathogenesis of periodontal disease. Periodontol 2000. 2014 Feb. 64(1): 57-80.

4. https://ebd.ada.org/~/media/EBD/Files/ADA_Chairside_Guide_Periodontitis.pdf?la=en.


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