Richard H. Nagelberg, DDS
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Research is advancing rapidly on many fronts, expanding our understanding of biofilms, periodontal disease development, mechanisms of disease resolution, and how a patient’s genes affect various aspects of perio disease activity.
Among the new ideas being investigated is the effect of environmental factors on genetic activation, called epigenetics. Nutritional factors, for example, can have profound effects on gene expression. Epigenetic influences may be responsible for the subtle differences in appearance and behavior in identical twins. Recent research indicates that epigenetics may be a key factor in inflammatory and neoplastic diseases, among others.
Studies indicate an epigenetic impact in periodontal diseases. Bacterial endotoxins stimulate the release of inflammatory mediators, and as we know, chronic inflammation causes perio tissue destruction.
Research has shown that with repeated exposure to bacterial endotoxins, the genes responsible for producing inflammatory mediators are temporarily inactive, which then limits additional pathology associated with excessive inflammation. Further, there is evidence that the early inflammatory response to gingivitis influences the predominance of perio pathogens. In other words, the body may have an effect on which bacteria flourish and which diminish.
Another emerging concept involves identification of periodontal disease resolution pathways. An important difference exists between anti-inflammatory activity and disease resolution. Anti-inflammation involves pharmacologic intervention in inflammatory pathways, while disease resolution involves biologic pathways that restore periodontal health, according to researcher Thomas Van Dyke. He reports that evidence indicates that periodontitis involves a failure of resolution pathways to restore homeostasis.
In the early stages of perio disease, the acute inflammatory response prevents tissue injury; however, inadequate disease resolution results in chronic inflammation and tissue destruction. Resolution of inflammation is an active process rather than a passive diminishing of pro-inflammatory factors.
Dr. Van Dyke further indicates the traditional pharmacologic approach of diminishing pro-inflammatory pathways using agents such as NSAIDs differs from the development of therapies that address the biological disease resolution pathways. This is a promising approach to treating periodontal disease.
The interaction between host genetic factors and the microbiota was reported in a 2009 paper by Nibali et al. This interaction, called infectogenomics, has implications in many diseases, including malaria, tuberculosis, AIDS, hepatitis, and periodontal disease. The authors indicate that there is a clear relationship between infectious agents, genetic susceptibility, and tissue pathology.
In the case of periodontal disease, the predominant periodontal pathogens in an individual are determined by genetic susceptibility. The host genotype influences the immuno-inflammatory response to bacterial invasion. The authors concluded that differences in a patient’s genotype influence the composition of subgingival microbiota, and that specific genetic factors may affect bacterial proliferation leading to chronic periodontitis.
Other novel concepts deal with enhancing methods of diagnosing periodontal disease. Current protocols utilize pocket depths, bleeding, swelling, radiographs, etc. These parameters, however, represent damage that has already occurred.
Research by Giannobile et al. has shown that salivary detection of specific inflammatory mediators and bacteria provide highly accurate predictions of periodontal disease severity. A chairside test will provide an impactful risk assessment tool, facilitating proactive approaches to disease prevention. Measuring inflammation and bacterial levels by salivary testing will also provide a powerful outcome assessment.
In addition to observing clinical disease resolution, we will be able to measure reductions in bacterial and inflammatory activity. Cases in which clinical improvement do not correlate strongly with reductions in bacterial levels and/or inflammatory activity may indicate an increased risk of disease recurrence, which will impact monitoring and maintenance intervals.
It’s an exciting time to be in the dental profession. Game-changing protocols that enable us to provide individualized treatment, improve outcomes, and predict disease activity are here or coming soon.
Being able to quantify a patient’s disease risk, as well as novel approaches to disease resolution and understanding factors that influence biofilm composition, will elevate the level of care we give patients.
Dr. Richard Nagelberg has practiced general dentistry in suburban Philadelphia for more than 27 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures extensively on many topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at email@example.com.