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Guest Editorial
February 2012 Guest Editorial The Changing Face of Periodontal Disease Keeping up with changes and new discoveries in periodontal research can be an arduous task. Once it was easy to stay informed when new findings were reported every 10–15 years. Today, new information is estimated to double every four to five years.[1] Couple this with the research report that concluded the prevalence of periodontal disease may have been underestimated by as much as 50 percent,[2] and the implications are clear: dental hygienists have much to learn and do. Important discoveries in diagnosis, treatment and prognosis of periodontal disease have guided dental hygiene care. The Standards for Clinical Dental Hygiene Practice are based on available evidence from the periodontal and dental hygiene literature.[3] The process of care includes assessment, dental hygiene diagnosis, planning, implementation, evaluation and documentation. The rapid discoveries in diagnostic and risk assessment are exciting and could change the way we practice in the near future. Diagnosing periodontal infections is primarily based on subjective clinical examination such as periodontal pocket depth, attachment level, plaque index, bleeding on probing, and radiographic assessment. A significant drawback to these assessments is the inability to measure disease activity versus disease severity. Bleeding on probing is often used to measure disease activity but can produce false positives. The absence of bleeding on probing is a good negative predictor of disease activity.[4-6] The ability to easily and effectively identify individuals or sites that are at risk for periodontal infection may not be that far in the future. The impact on dental hygiene practice and the opportunities for advanced practitioners and researchers could be far reaching. The past 15 years have provided a clearer understanding of the pathogenesis of periodontal disease and the impact of the inflammatory process and risk factors. Research identified a link between systemic disease and periodontal disease. However, there are still many unanswered questions; primarily, can treating the periodontal disease reduce the risk of adverse outcomes, what is the treatment that is effective and will it be different for individuals or types of systemic complication, and is there a risk but no benefit from treating the periodontal infection? For instance, it can be confusing when two large intervention studies, Obstetrics and Periodontal Therapy Trial (OPT)[7] and Maternal Oral Therapy to Reduce Obstetric Risk Study (MOTOR)[8] did not show a difference in adverse pregnancies, but a systematic review of seven studies, which included the OPT, showed a reduced risk of pre-term birth.[9] The systematic review concluded that periodontal treatment reduced the risk of preterm birth, but it is important to note that the greatest benefit was seen in patients with less periodontal disease at baseline who also had no history of adverse pregnancies. This led the authors to conclude that perhaps it is more important to start off healthy than try to rectify poor oral health during the pregnancies. In other areas, such as diabetes the research has shown a bidirectional association with glycemic control. Additionally, smoking has been identified as a risk factor for periodontal disease for years, but recently the effect of environmental tobacco smoke (ETS) has been studied, and early results show a negative effect on the nonsmoker: increased periodontal disease prevalence and progression, tooth loss and increased melanin pigmentation.[10-13] Many studies that measure the impact of smoking or ETS on periodontal disease rely on self-report from the subjects, who may incorrectly report when they stopped smoking or how many cigarettes they smoke per day, thus demonstrating one of the challenges of research. The development of biomarkers for periodontal disease activity and susceptibility is the current focus of some periodontal researchers. Biomarkers can be measured in saliva, serum, subgingival plaque, tissue biopsies and gingival crevicular fluid. Commercially available diagnostic kits were introduced to the market but are not widely used today. Some of the reasons include cost and time, but one of the most important may be that the results did not translate into a change in treatment. Although the gingival crevicular fluid is ideal for evaluating each site, the challenges of adoption are many, preventing universal use by practitioners at this time. More recently, the use of saliva to measure biomarkers has been studied. This is more practical from a time and cost standpoint because it tests the whole mouth instead of each individual site. The drawback to salivary testing is the inability to fully quantify markers for specific sites. Denise Bowen’s article discusses some of the cutting edge research that looks at the inflammatory process from a different perspective and provides a glimpse into the future that may have a significant impact on dental hygiene therapy. Angela Zappone’s article on inflammation and diet takes a different look at how dental hygienists can look at reducing systemic inflammation through nutrition.
References 1. Chapple ILC. Periodontal diagnosis and treatment—where does the future lie? Periodontol 2000 2009; 51: 9-24. 2. Eke PI, Thornton-Evans GO, Wei L., et al. Accuracy of NHANES periodontal examination protocols. J Dent Res 2010; 89, 1208-13. 3. American Dental Hygienists’ Association. Standards for clinical dental hygiene practice. Available at: www.adha.org/downloads/adha_standards08.pdf 4. Lang NP, Tonetti MS. Periodontal diagnosis in treated periodontitis. Why, when and how to use clinical parameters. J Clin Periodontol 1986; 23: 199-208. 5. Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding on probing. an indicator of periodontal stability. J Clin Periodontol 1990; 17: 714-21. 6. Mordohai N, Reshad M, Jivraj S, Chee W. Factors that affect individual tooth prognosis and choices in contemporary treatment planning. Br Dent J 2007; 202: 63-72. 7. Michalowicz BS, Hodges JS, DiAngelis AJ, et al. Treatment of periodontal disease and the risk of preterm birth. N Engl J Med 2006; 355: 1885-94. 8. Offenbacher S, Beck JD, Jared HL, et al. Effects of periodontal therapy on rate of preterm delivery: a randomized controlled trial. Obstet Gynocol 2009; 114: 551-9. 9. Polyzos NP, Polyzos IP, Mauri D, et al. Effect of periodontal disease treatment during pregnancy on preterm birth incidence: a meta-analysis of randomized trials. Am J Obstet Gynecol 2009; 200: 225–32. 10. Arbes SJ, Agustsdottir H, Slade GD, Environmental tobacco smoke and periodontal disease in the United States. Am J Public Health 2001; 91: 253-7. 11. Erdemir EO, Sonmez IS, Oba AA, et al. Periodontal health in children exposed to passive smoking. J Clin Periodontol 2010; 37: 736-51. 12. Hanioka T, Tanaka K, Ojima M, Yuuki K. Association of melanin pigmentation in the gingival of children with parents who smoke. Pediatrics 2005; 116: e186-e190. 13. Nishida N, Yamamoto Y, Tanaka M, et al. Association between involuntary smoking and salivary markers related to periodontitis: a 2-year longitudinal study. J Periodontol 2008; 79: 2233-40. 14. American Dental Hygienists’ Association. Dental hygiene: focus on advancing the profession. Chicago: ADHA, 2005. Available at: www.adha.org/downloads/ADHA_Focus_Report.pdf
Deborah M. Lyle, RDH, MS is a lifelong member of ADHA, having served on the Council on Education and Task Force for Clinical Practice Guidelines, and chaired the Task Force for the ADHP curriculum development. A member of AADR/IADR and IFDH, she serves on the JDH editorial review board and is chair of the Council on Research. She is director of professional and clinical affairs at Water Pik, Inc.
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