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Healthcare delivery is not immune to change. With advances in technology, consumer desires, and extensive data allowing providers to predict the potential development and progression of chronic diseases, healthcare professionals have new opportunities to offer better informed, preventive care to their patients. This is especially meaningful, as demographics indicate a shift in the type of care providers deliver, and to whom. In recent years healthcare providers have moved from treating infectious diseases experienced primarily by young children to managing the major chronic diseases of a rapidly expanding aging population, prompting them to assume responsibility for collaborating with their patients to identify better means of maintaining health.
Technological advances and access to what has been learned from massive databases have allowed healthcare providers to better predict which patient segments may be at heightened risk for chronic conditions. Coupled with consumer desires to live longer, healthier lives, healthcare providers can now better tailor health management for their patients based on information that helps to categorize their risk for certain diseases (Figure 1).
Dental professionals also have a role to play in implementing diagnostic strategies to identify at-risk patients. Dental professionals’ experience and familiarity with inflammation and chronic diseases such as periodontitis put them in an excellent position to develop customized treatment plans that provide patients with the personalized care they desire and ensure the preventive management they need. Such patient-centered strategies will prevent disease at a level that patients consider meaningful.1
Impact of Inflammation, Chronic Disease, and Other Factors on Periodontitis
Dental professionals are well positioned to educate patients about the overall health implications of chronic inflammation, particularly relating to periodontal disease. A greater understanding of the role of inflammation in various seemingly unrelated conditions allows practitioners to provide alternative strategies for prevention while resolving inflammation to reduce the risk of various systemic conditions.2
Periodontitis occurs when bacteria trigger inflammation with the release of various biochemical mediators, such as cytokines, which may lead to the destruction of gingival connective tissue and bone.3 Chronic adult periodontitis is the common form of this bacterially induced inflammatory disease, which affects a substantial number of adults and has shown to be a significant contributing factor to other systemic conditions.4 Chronic diseases such as atherosclerotic cardiovascular disease, rheumatoid arthritis, and diabetes mellitus may develop or worsen in part due to uncontrolled inflammation,5-7 but even conditions not traditionally associated with inflammation, such as Alzheimer’s disease, may also be linked.8
Periodontitis may be affected by multiple variables. Certainly accumulation of bacterial plaque deposits on teeth is required for the disease initiation and they contribute to its progression, but research indicates that not all cases of periodontitis and the individuals who experience it are alike. Risk of this disease and others is inherently dynamic and may change in response to interactions of various factors, including those that are environmental and genetic.9
As with most chronic diseases, genetics have considerable sway over disease initiation and progression, and current evidence indicates that approximately 50% of the differences in the severity of chronic periodontitis among patients is attributable to their genetics.10 Available data suggest that the clinical presentation of chronic periodontitis may result from an interaction of environmental factors and mutations in multiple genes, suggesting a significant host response component to disease initiation and severity. The most extensively studied of these genes, belonging to the family of interleukin-1 (IL-1) proteins, have patterns of genetic variations that are inherited and can lead to inflammation and increased severity of periodontitis.11
Such research on genetics—especially when combined with the known effects of smoking, diabetes, and other risk factors on periodontitis—indicates a departure from currently used approaches for the prevention and treatment of patients suffering from periodontitis and other associated inflammatory conditions. Presently, dental professionals assume that all patients are equally susceptible to plaque and therefore may use the same prevention and treatment plans for patients with periodontal disease. However, newer research indicates a more dynamic paradigm of disease development, one in which innate differences among individuals, coupled with exposure to environmental factors, may directly influence the risk and/or trajectory of inflammatory diseases.12 This implies that those who possess certain risk factors, such as smoking, diabetes, obesity, and stress, are more susceptible to the disease than those who do not, independent of bacterial plaque accumulation.
If disease initiation and progression occur on a much more individualized basis than previously believed, what does this mean for patients, the dental professionals who treat them, and the nature of the nation’s healthcare system? For dentists to provide the most comprehensive, efficient, and high quality care to their patients, a paradigm shift in preventing and treating disease should occur. This was proposed in the early 2000s, with Leroy Hood’s description of three main components—prediction, prevention, and personalization—of a more individualized healthcare approach.13,14 Given that chronic diseases, by their very nature, may be more complicated to treat, such an approach can only benefit patients suffering with these conditions and the healthcare professionals who treat them.
The Three P’s of Healthcare: Personalize, Predict, Prevent
Personalization, prediction, and prevention allow dental professionals to provide their patients with a higher standard of care by formulating treatment plans that address disease risk and preventive measures that can be taken before disease presents.
Physicians and dentists have always adjusted their treatment plans based on their knowledge of the individual patient. Personalized medicine recognizes that not all patients will respond similarly to disease development, progression, and treatment. It uses new technologies and evidence to categorize an individual’s risk more reliably. This approach provides an opportunity to establish communication with the patient about his/her personal health in general and also presents dentists with an advantage in designing an optimal treatment plan. For patients who present with risk factors, such as smoking, diabetes, and other inflammatory conditions, it is critical for dentists to inform them of their risks for severe periodontitis and modify their prevention plans accordingly.
The basis for prediction is the understanding and proper assessment of risk factors for individual patients prior to disease development. Risk factors provide an objective means by which to formulate a patient-specific prognosis (Table 1)—ie, a prediction of the future course and/or outcome of a disease, treatment, or no treatment, given current information.1 Dentists must rely on their knowledge and experiences to thoroughly evaluate a patient’s condition and his/her risks, and then make recommendations for the best future of that patient. Prognoses must be patient-specific to reap the full benefits of this principle.
Prevention builds off prediction, allowing dentists to work directly with their patients, particularly those at greater risk, to incorporate various strategies for minimizing their chances for disease development. Once patients are aware of their risks, options for prevention include lifestyle changes (eg, smoking cessation, nutritional changes) or more frequent dental visits to closely monitor for the beginning stages of disease. Such a strategy must also have a firm foundation in individualization and awareness so that patients can participate in developing the most effective treatment plan.
Implications for Periodontitis Risk Assessment & Prevention
Given what has been learned about the interactions of genetic and environmental factors as they influence a patient’s individual response to plaque, dental professionals can work to ensure that patient care is personalized. Such care should account for risk factors and be proactive, rather than reactive.
In a 10-year longitudinal study, Axelsson15 recruited a random group of 50-year-old patients, most of whom had no periodontitis at the onset of the study. These patients were monitored for 10 years, and most complied with the preventive care he established, which was adjusted in a needs-based manner based on clinical observations. At the end of the 10 years, very few of those patients who were nonsmokers and negative for IL-1 genetic variations lost two or more teeth due to periodontitis. Nearly twice as many patients who had one of those risk factors, but not both, lost two or more teeth compared to patients with neither risk factor. Almost four times as many patients who had both risk factors lost two or more teeth due to periodontitis.15
In a risk-based approach to assess tooth-loss events associated with preventive visits, Giannobile and colleagues16 classified patients based on their risk factors to determine the relationship between risk and preventive care visits. Patients were classified as high risk for progressive periodontitis if they presented with one or more of three risk factors (ie, smoking, diabetes, interleukin-1 genotype); or low risk if they presented with none of these risk factors. It was found that low-risk patients experienced tooth loss event rates of 14% to 16% over a 16-year period, which did not differ significantly among patients who consistently had two or one annual preventive visit(s), respectively; however, high-risk patients had higher tooth loss rates (17% to 22%) over the 16-year period and benefited significantly from two preventive visits annually. The researchers concluded that a personalized medicine approach combining gene biomarkers with conventional risk factors to stratify populations for preventive dentistry may provide enhanced approaches for prevention of severe periodontitis (Figure 2).16
Dentistry will likely be part of future trends in healthcare, including those initiatives to personalize preventive treatment approaches, particularly in the case of periodontitis. With evidence in the literature supporting an association between periodontitis and various risk factors, it behooves dental professionals to work with patients to undertake a more individualized approach to treatment and health management.
The author would like to thank Allison M. DiMatteo, BA, MPS, for medical writing assistance in drafting this article.
ABOUT THE AUTHOR
Kenneth S. Kornman, DDS, PhD
President and Chief Scientific Officer, Interleukin Genetics, Waltham, Massachusetts
Queries to the author regarding this course may be submitted to email@example.com
1. Kornman KS. Diagnostic and prognostic tests for oral diseases: practical applications. J Dent Educ. 2005;69(5):498-508.
2. Van Dyke TE, Kornman KS. Inflammation and factors that may regulate inflammatory response. J Periodontol. 2008;79(8 Suppl):1503-1507.
3. Ianni M, Bruzzesi G, Pugliese D, et al. Variations in inflammatory genes are associated with periodontitis. Immun Aging. 2013;10(1):39.
4. Linden GJ, Lyons A, Scannapieco FA. Periodontal systemic associations: review of the evidence. J Periodontol. 2013;84(4 Suppl):S8-S19.
5. Libby P Tabas I, Fredman G, Fisher EA. Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res. 2014;114(12):1867-1879.
6. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011;365(23):2205-2219.
7. Donath MY. Targeting inflammation in the treatment of type 2 diabetes: time to start. Nat Rev Drug Discov. 2014;13(6):465-476.
8. Mrak RE, Griffin WS. Interleukin-1, neuroinflammation, and Alzheimer’s disease. Neurobiol Aging. 2001;22(6):903-908.
9. Reynolds MA. Modifiable risk factors in periodontitis: at the intersection of aging and disease. Periodontol 2000; 2014;64(1):7-19.
10. Michalowicz BS, Diehl SR, Gunsolley JC, et al. Evidence of a substantial genetic basis for risk of adult periodontitis. J Periodontol. 2000;71(11):1699-1707.
11. Kornman KS, Polverini PJ. Clinical application of genetics to guide prevention and treatment of oral diseases. Clin Genet. 2014;86(1):44-49.
12. Kornman KS. Mapping the pathogenesis of periodontitis: a new look. J Periodontol. 2008;79(8 Suppl):1560-1568.
13. Hood L, Heath JR, Phelps ME, Lin B. Systems biology and new technologies enable predictive and preventative medicine. Science. 2004;306(5696):640-643.
14. Weston AD, Hood L. Systems biology, proteomics, and the future of health care: toward predictive, preventative, and personalized medicine. J Proteome Res. 2004;3(2):179-196.
15. Axelsson P. Diagnosis and Risk Prediction of Periodontal Diseases. Carol Stream, IL: Quintessence; 2002.
16. Giannobile WV, Braun Tm, Caplis AK, et al. Patient stratification for preventive care in dentistry. J Dent Res. 2013;92(8):694-701.