by Richard H. Nagelberg, DDS
A typical clinical presentation in every dental practice is the 30-something-year-old patient who, upon examination, is found to have periodontitis. The disease affects all four quadrants with pocket depth and clinical attachment loss measuring 5 mm, bone loss, bleeding upon probing, and a total of 15 to 20 sites. This type of patient is encountered in virtually every dental practice every day. In practices that do not treat gum disease, hopefully this patient is referred for treatment. This is also commonly the sum total of all the data collection that is considered necessary, and treatment is undertaken. Treatment typically consists of scaling, perhaps with the use of some adjunctive antimicrobial agents, perhaps not. This hypothetical patient is one whose disease does not completely respond to therapy upon reevaluation four weeks later. He still has three sites of active disease. We either consider treatment successful, or we do something else, or we refer to a periodontist. If every nonresponding site is pursued, we will eventually arrive at healing in every site. All in all, we met our responsibility and provided an acceptable level of service for this patient. Or did we? What we don’t know can hurt us.
If we had collected more data, we would have discovered that the patient had the highest recordable level of the high-risk perio pathogen Aa, which can cause disease in relatively small quantities. It is associated with aggressive forms of periodontitis, is transmittable, and is tissue invasive. Other bacteria were found to be in play as well. This hypothetical patient’s salivary test for genetic susceptibility to periodontitis was positive. We would have determined from an examination of risk elements that he never smoked, did not have diabetes, xerostomia, or a history of gum disease. In fact, no other identifiable risk elements were present, except the most important one -- high levels of a high-risk periodontal pathogen. Home care would be immediately ramped up to the patient using a power toothbrush, daily floss, a tongue scraper, and antimicrobial rinse.
With all this information impacting treatment planning for this patient, we would have achieved complete disease resolution after the first round of therapy because we would have used the correct adjunctive locally applied and systemic antibiotics, the patient would start optimizing his biofilm control immediately, and most importantly, this is not a hypothetical patient. The impact of the data collection cannot be overstated. The positive IL-1 salivary diagnostic genetic susceptibility test indicates that the patient has an exaggerated release of the tissue-destroying enzyme collagenase when responding to a lower bacterial load than he would have if his test results were negative. Couple that with the presence of a highly toxic periodontal pathogen that causes disease in low bacterial counts, and disease had to occur. The home-care regimen being practiced was inadequate to keep the bacterial levels low enough for his immune system to prevent disease manifestation. This is true for every patient who presents with periodontitis. Whatever patients are doing to control biofilm on a daily basis is not working. It is how their disease got there in the first place.
Why is all this data collection and testing necessary since we ultimately arrived at the same point clinically in both scenarios? It is because the most important aspect of this patient’s experience has not been mentioned yet -- his family health history. Examination of his family health history is the reason for all the tests, and the results guided the entire treatment plan, including the home-care regimen that was mandatory. He has a significant family history of cardiovascular disease. His maternal and paternal grandfathers both had fatal heart attacks, one at 39 years old. His father has had two nonfatal heart attacks, the first one at 45 years old, and some of his uncles had heart attacks. None of them had the benefit of the knowledge we now have at our fingertips. Postop bacterial testing revealed a reduction of Aa to nondetectable levels and Aa has been implicated in cardiovascular disease. Clinical disease resolution is not always accompanied by a dramatic reduction in bacterial levels. His monitoring and maintenance intervals are at two months for the first two years, to be reevaluated after that.
Perhaps the most important piece of information has still not been mentioned -- his two young children.
Just something to think about.
Richard Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations, and he lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at [email protected].
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