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19, 20 dm_dec_clin_donley


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19, 20 dm_dec_clin_donley

  1. 1. 19 Risk-based approach to periodontics Tim Donley talks probing depths, oral inflammation and its diagnostic and therapeutic significance in the management of periodontal disease Clinical The clinical diagnosis of periodontitis historically has required evidence of loss of con- nective tissue surrounding the teeth and bone loss detected by radiography. For many years, clinical probing depth measurement was the primary factor used to determine which sites were in need of periodontal therapy. Current knowledge of the role that inflammation plays in the etiology of many systemic diseases suggest that incorporating other assessments into periodontal treatment decision pathways may be important. Bacterial accumulations on the teeth are essential for the initiation and progression of periodontitis. This microbial infection is followed by a host-mediated destruction of connective and bone tissues caused by hyperactivated immune-inflammatory response1 . Destruction of periodontal tissues leads to deepening of the sulci adjacent to teeth resulting in the formation of periodontal pockets. Despite the awareness that inflamma- tory mediators of oral origin can affect other body disease processes, periodontal therapy has been aimed almost exclusively on achieving and then maintaining pocket depths which the therapist considers accessible to patient and professional debridement efforts. While there is little doubt that reduction in probing depth improves access to sub- gingival areas, focusing the management of periodontal disease solely on pocket depth may not be sufficient. Medical research underscores the important role that inflammation in the body plays in the development and progression of many of the serious, chronic diseases of ageing. Emerging evidence continues to suggest that the mouth can be a signif- icant source of inflammation when periodontal disease persists2 . The entrance of bacteria, bacterial byproducts and inflammatory mediators released orally in response to the pathogenic periodontal bacteria can enter the bloodstream. Inflammation of periodontal tissues can have adverse affects beyond loss of periodontal attachment and bone3 . Thus, in addition to management of probing depths it seems prudent for oral inflammation to take on added diagnostic and therapeutic significance in the management of periodontal disease. The following therapeutic approach is based on assessment of patient, tooth and site risk factors. The intent to is more effectively target therapy to improve patients’ oral and overall health. Which patients to treat Environmental and genetic factors as well as acquired risk factors accelerate destructive inflammatory processes in periodontitis4 . The following non-oral risk factors associate strongly with increased risk for periodontitis and disease severity: tobacco use, diabetes mellitus, family history, mental stress and depression, obesity, and osteoporosis5 . Realising that risk factors for periodontal disease can make eradication of periodontal disease more difficult, more aggressive therapy is considered for patients who have known periodon- tal disease risk factors. In a similar fashion, adverse associations have been identified between periodontal disease and diabetes, cardiovascular disease pre-term low birth weight deliveries, respira- tory diseases, certain cancers, kidney diseases and other systemic conditions3 . It certainly seems advisable to treat more aggressively those patients who have other risk factors for the conditions that can be affected by periodontal inflammation. Allowing periodontal inflammation to persist in such patients will only add to their systemic disease risk. Rather than applying a basic therapeutic approach to all patients, determining if patients presenting for dental care have any of the factors indicating increased risk for periodontal disease severity and/or any of the other known risk factors for systemic diseases that can be affected when periodontal disease persists can be used to formulate a therapeutic approach proportionate to the level of risk. Which sites to treat Clinical and radiographic findings are commonly used to determine a patient’s periodon- tal status. Often treatment resources are directed primarily to sites where probing depth has increased (where disease progression has already occurred). Diagnostic findings offering predictive value would allow the direction of treatment resources to sites at which breakdown was imminent. Bleeding on probing (BOP) is among the clinical signs used to predict disease progression6 . Yet, there is general agreement that an isolated incidence of BOP at a site is a poor predictor of disease activity at that site7 . The predictive value of BOP increases substantially when BOP is persistent. Sites that continue to demonstrate BOP (at successive re-evaluation visits) are more likely to breakdown8 . In addition to signaling impending destructive activity, BOP is strongly correlated with gingival inflammation9 . Gingival inflammation is typically expressed clinically as redness, edema and/or bleeding. While preventing adverse changes in pocket depth has merit, the overwhelming evidence confirming the adverse relationship between oral inflammation and systemic disease suggests that elimination of inflammation should also be a goal of therapy. In addition to sites at which increases in probing depth is noted, those sites at which persistent bleeding on probing or other clinical signs of inflammation should be priority candidates for therapeutic attention. There may also be merit to prioritising certain surfaces/teeth for more aggressive therapy. Deeper pockets, pockets in inaccessible areas, roots with complex anatomy pockets adjacent to teeth with restorations whose margins extend subgingivally all present obstacles to debridement. More aggressive therapy at such sites can increase the likelihood that inflammation will resolve. Figure 1: Untreated persistent inflammation at interproximal areas necessitated surgical access for adequate debridement. Change in soft tissue contour following resolution of the noted inflammation resulted in unfavourable aesthetic changes. Intervention, with a more aggressive approach earlier in the disease process, could have prevented the resultant adverse aesthetic changes 19, 20 DM Dec Clin Donley.qxd:DM News+Edit+lettr+FCover 2005 29/11/2010 12:39 Page 1
  2. 2. 20 Clinical There are some teeth because of their prominence in the patient have added aesthetic importance. Interceding earlier in the disease process and/or with a more aggressive approach can eliminate the adverse aesthetic changes that occur when considerable destruction is allowed to occur before therapy is initiated (Figure 1). Other aesthetic concerns can affect periodontal treatment planning. The long-term patient satisfaction of a dental prosthesis often relies on a stable relationship between the gingival tissue and the restoration margin. There may be merit to applying the more aggressive approach to prosthetically restored teeth of aesthetic significance. Lastly, gauging the strategic importance of involved teeth in a specific patient’s dentition may help better shape the periodontal treatment plan. Which treatments? Bacterial biofilm accumulations on the teeth are essential to the initiation and progression of periodontitis10 . Although periodontitis begins with a microbial infection, it is the host-mediated inflammatory response that causes clinically significant connective tissue and bone destruction11 . Long- term clinical studies have clearly demonstrated that the reg- ular and effective removal of bacterial biofilms on the teeth can prevent periodontitis12 . Suppressing the host response has also been shown to play a critical therapeutic role13 . Biofilm disruption can be accomplished by mechanical means (hand instrumentation and/or ultrasonic instrumen- tation), systemic and local administration of targeted antibi- otics, and laser generated energy. The chosen methodology is most often driven by the therapist’s personal preference. The ideal debridement method should offer predictable results independent of operator skill level, be efficient to perform clinically, well tolerated by patients, cost effective and low potential for adverse side effects. While admittedly more pragmatic than scientific, a basic tenet of a risk-based approach to the management of peri- odontal disease is to treat patients with a higher risk profile more aggressively. More aggressive therapy would include: 1. Intervening earlier in the disease process. 2. Using adjunctive, repetitive or multiple debridement strategies simultaneously. 3. Shortening the interval between maintenance visits. Summary As a basic tenet of treatment planning the level of risk for a specific disease should influence the need for therapeutic intervention for that disease. Yet, many dental therapists continue to manage all of their periodontal disease affected patients with little variability in the approach. In addition to the information linking periodontal inflammation with more serious diseases, the recognised site specificity and individual variability of periodontal disease presentation suggests that a different approach may be advisable. While quantitative data regarding the significance of specific risk factors has not yet be elucidated, it seems reasonable to treat more aggressively those patients who are more likely to get periodontal disease as well as patients who are already have risk factors for the systemic diseases which can be further affected when periodontal inflamma- tion persists. Specific tooth and site specific factors should also affect the treatment plan (see Table 1). Included in a more aggressive approach may be increased use of adjunc- tive therapies, intervention at an earlier stage of disease and more frequent monitoring via maintenance care. Providing therapy which maximises the chance for inflammation of periodontal origin to resolve (and then be kept at bay) can pay dividends to patients’ oral and overall health. References 1. The host response to the microbial challenge in periodontitis: assembling the players. Kornman KS, Page RC, Tonetti MS. Periodontol 2000 1997;14:33–53. 2.Understanding and managing periodontal diseases: a notable past, a promising future. Williams RC. J Periodontol. 2008 Aug;79(8 Suppl):1552-9. 3. Relationship between periodontal infections and systemic dis- ease. Seymour GJ, et al. Clin Microbiol Infect. 2007 Oct;13 Suppl 4:3-10. 4. Determining Periodontal Risk Factors in Patients Presenting for Dental Care. Schutte DW, Donley TG. J Dent Hyg. 1996 Nov- Dec;70(6):230-4. 5.The American Journal of Cardiology and Journal of Periodontology Editors' Consensus: periodontitis and atheroscle- rotic cardiovascular disease. Friedewald VE, et al. American Journal of Cardiology; Journal of Periodontology. Am J Cardiol. 2009 Jul 1;104(1):59-68. 6. Indices to measure gingival bleeding. Newbrun E. J Periodontol. 1996;67:555–61. 7. Bleeding on Probing. A predictor for the progression of peri- odontal disease? J Clin Periodontol 1986;13(6)590-596. 8. Clinical course of chronic periodontitis. Schätzle M, et al. J Clin Periodontol. 2003;30:887–901. 9. Relationship of “Bleeding on Probing” and Gingival Index Bleeding” as Clinical Parameters of Gingival Inflammation. J Clin Periodontol 1993;20(2):139-143. 10. Periodontitis An Archetypical Biofilm Disease. Schaudinn, C, et al. JADA 2009;140(8):978-986. 11. The Host Response to the Microbial Challenge in Periodontitis: Assembling the Players. Kornman KS, Page RC, Tonetti MS. Periodontol 2000 1997;14:33–53. 12. Effect of controlled oral hygiene procedures on caries and peri- odontal disease in adults. Results after 6 years. Axelsson P, Lindhe J. J Clin Periodontol 1981;8:239–248. 13. Subantimicrobial dose doxycycline as adjunctive treatment for periodontitis. A review. Preshaw PM, et al. J Clin Periodontol 2004;31:697–707. Dr Tim Donley is currently in the private practice of Periodontics and Implantology in Bowling Green, KY. After graduating from the University of Notre Dame, Georgetown University School of Dentistry and completing a general practice residency, he practiced general dentistry. He then returned to Indiana University where he received his masters degree in periodontics. Dr Donley is the former editor of the Journal of the Kentucky Dental Association and is an adjunct professor of periodontics at Western Kentucky University. He is a lecturer with the ADA Seminar Series. Dentistry Today recently listed him among it’s ‘Leaders in Continuing Education’. He lectures and publishes frequently on topics of interest to clinical dentists and hygienists. US clinician Tim Donley returns to the UK with a full day seminar, Better Patient Outcomes. Better Perio Incomes! It follows the phenomenal success of this year’s seminar that sold out and is being hailed as a ‘must-attend’. It takes place on Friday 11 February 2011 at the Royal College of Physicians. Delegates can gain seven verifiable CPD. For further information or to book, freephone 0800 371652 or visit This seminar is sposnored by Oral-B – and every delegate will receive an electric toothbrush. Persistent inflammation with probing depth of 5mm was noted at the mesio-palatal surfaces of the maxillary first molar and the maxillary first pre-molar. Mechanical debridement was completed at these sites. Then, due to the subgingival extent of the restoration margin at the molar, local antibiotic was delivered. Multiple methods of debridement were employed since the tooth surface risk factor suggested an added degree of difficulty to achieving adequate debridement. Similarly, because of the developmental root concavity typically noted at the mesial of the maxillary first premolar, local antibiotic was also delivered at this site in an attempt to maximise the chance of achieving therapeutically effective debridement even in light of the complex root anatomy. The above radiographs are from a 39-year-old white male who was a long-time smoker (one pack per day) and a less- than-ideally controlled diabetic. Mechanical debridement was supplemented with laser debridement in an attempt to maximise the resolution of inflammation of oral origin. Additionally, host modulation therapy was administered to address the host component to the noted destruction. Example three Example one Example two The mandibular molars each serve as abutments for a removable prosthesis. The loss of either of these teeth will severely limit the prosthetic options for efficiently restoring a functional dentition. Persistent inflammation along with probing depths of 4mm was noted at the mesial surfaces of these teeth. Although the noted probing depth could be considered ‘manageable’, adjunctive therapy (supplementing mechanical debridement with local antibiotic delivery) was used in an attempt to increase the aggressiveness of therapy due to the strategic importance of these teeth. Clinical application of risk-based approach Table 1 Factors assessed prior to formulating a course of therapy: 1. The presence of inflammation at a site via probing and visual inspection 2. The probing depth at sites where inflammation is noted 3. The presence of any complex root anatomy at the involved site 4. The strategic importance of involved tooth 5. The aesthetic importance of involved tooth 6. The functional significance of the involved tooth 7. The presence of any periodontal risk factors 8. The presence of any risk factors for the systemic disease potentially affected by periodontal inflammation. 19, 20 DM Dec Clin Donley.qxd:DM News+Edit+lettr+FCover 2005 29/11/2010 12:39 Page 2