19, 20 dm_dec_clin_donley

2
19 www.dentistry.co.uk 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 response 1 . 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 persists 2 . 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 bone 3 . 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 periodontitis 4 . 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 osteoporosis 5 . 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 conditions 3 . 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 progression 6 . Yet, there is general agreement that an isolated incidence of BOP at a site is a poor predictor of disease activity at that site 7 . 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 breakdown 8 . In addition to signaling impending destructive activity, BOP is strongly correlated with gingival inflammation 9 . 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

Transcript of 19, 20 dm_dec_clin_donley

Page 1: 19, 20 dm_dec_clin_donley

19www.dentistry.co.uk

Risk-based approach to periodonticsTim Donley talks probing depths, oral inflammation and its diagnostic andtherapeutic significance in the management of periodontal disease

ClinicalThe clinical diagnosis of periodontitis historically has required evidence of loss of con-nective tissue surrounding the teeth and bone loss detected by radiography. For manyyears, clinical probing depth measurement was the primary factor used to determinewhich sites were in need of periodontal therapy. Current knowledge of the role thatinflammation plays in the etiology of many systemic diseases suggest that incorporatingother assessments into periodontal treatment decision pathways may be important.

Bacterial accumulations on the teeth are essential for the initiation and progression ofperiodontitis. This microbial infection is followed by a host-mediated destruction ofconnective and bone tissues caused by hyperactivated immune-inflammatory response1.Destruction of periodontal tissues leads to deepening of the sulci adjacent to teethresulting in the formation of periodontal pockets. Despite the awareness that inflamma-tory mediators of oral origin can affect other body disease processes, periodontal therapyhas been aimed almost exclusively on achieving and then maintaining pocket depthswhich 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 depthmay not be sufficient. Medical research underscores the important role that inflammationin the body plays in the development and progression of many of the serious, chronicdiseases 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 releasedorally in response to the pathogenic periodontal bacteria can enter the bloodstream.Inflammation of periodontal tissues can have adverse affects beyond loss of periodontalattachment and bone3. Thus, in addition to management of probing depths it seemsprudent for oral inflammation to take on added diagnostic and therapeutic significancein the management of periodontal disease. The following therapeutic approach is basedon assessment of patient, tooth and site risk factors. The intent to is more effectively targettherapy to improve patients’ oral and overall health.

Which patients to treatEnvironmental and genetic factors as well as acquired risk factors accelerate destructiveinflammatory processes in periodontitis4. The following non-oral risk factors associatestrongly with increased risk for periodontitis and disease severity: tobacco use, diabetesmellitus, family history, mental stress and depression, obesity, and osteoporosis5. Realisingthat risk factors for periodontal disease can make eradication of periodontal disease moredifficult, 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 periodontaldisease and diabetes, cardiovascular disease pre-term low birth weight deliveries, respira-tory diseases, certain cancers, kidney diseases and other systemic conditions3. It certainlyseems advisable to treat more aggressively those patients who have other risk factors forthe conditions that can be affected by periodontal inflammation. Allowing periodontalinflammation 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 patientspresenting for dental care have any of the factors indicating increased risk for periodontaldisease severity and/or any of the other known risk factors for systemic diseases that canbe affected when periodontal disease persists can be used to formulate a therapeuticapproach proportionate to the level of risk.

Which sites to treatClinical and radiographic findings are commonly used to determine a patient’s periodon-tal status. Often treatment resources are directed primarily to sites where probing depthhas increased (where disease progression has already occurred). Diagnostic findings

offering predictive value would allow the direction of treatment resources to sites at whichbreakdown was imminent. Bleeding on probing (BOP) is among the clinical signs used topredict disease progression6. Yet, there is general agreement that an isolated incidence ofBOP at a site is a poor predictor of disease activity at that site7. The predictive value of BOPincreases substantially when BOP is persistent. Sites that continue to demonstrate BOP (atsuccessive re-evaluation visits) are more likely to breakdown8. In addition to signalingimpending 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 overwhelmingevidence confirming the adverse relationship between oral inflammation and systemicdisease 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 persistentbleeding on probing or other clinical signs of inflammation should be priority candidates fortherapeutic 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 adjacentto teeth with restorations whose margins extend subgingivally all present obstacles todebridement. More aggressive therapy at such sites can increase the likelihood that inflammation will resolve.

Figure 1: Untreated persistent inflammationat interproximal areas necessitated surgicalaccess for adequate debridement. Change insoft tissue contour following resolution ofthe noted inflammation resulted inunfavourable aesthetic changes. Intervention,with a more aggressive approach earlier inthe disease process, could have preventedthe resultant adverse aesthetic changes

19, 20 DM Dec Clin Donley.qxd:DM News+Edit+lettr+FCover 2005 29/11/2010 12:39 Page 1

Page 2: 19, 20 dm_dec_clin_donley

20www.dentistry.co.uk

Clinical

There are some teeth because of their prominence in thepatient have added aesthetic importance. Interceding earlierin the disease process and/or with a more aggressiveapproach can eliminate the adverse aesthetic changes thatoccur when considerable destruction is allowed to occurbefore therapy is initiated (Figure 1). Other aestheticconcerns can affect periodontal treatment planning.

The long-term patient satisfaction of a dental prosthesisoften relies on a stable relationship between the gingivaltissue and the restoration margin. There may be merit toapplying the more aggressive approach to prostheticallyrestored teeth of aesthetic significance. Lastly, gauging thestrategic importance of involved teeth in a specific patient’sdentition may help better shape the periodontal treatmentplan.

Which treatments?Bacterial biofilm accumulations on the teeth are essential tothe initiation and progression of periodontitis10. Althoughperiodontitis begins with a microbial infection, it is thehost-mediated inflammatory response that causes clinicallysignificant connective tissue and bone destruction11. Long-term clinical studies have clearly demonstrated that the reg-ular and effective removal of bacterial biofilms on the teethcan prevent periodontitis12. Suppressing the host responsehas also been shown to play a critical therapeutic role13.

Biofilm disruption can be accomplished by mechanicalmeans (hand instrumentation and/or ultrasonic instrumen-tation), systemic and local administration of targeted antibi-otics, and laser generated energy. The chosen methodologyis most often driven by the therapist’s personal preference.The ideal debridement method should offer predictableresults independent of operator skill level, be efficient toperform clinically, well tolerated by patients, cost effectiveand low potential for adverse side effects.

While admittedly more pragmatic than scientific, a basictenet of a risk-based approach to the management of peri-odontal disease is to treat patients with a higher risk profilemore aggressively. More aggressive therapy would include:1. Intervening earlier in the disease process.2. Using adjunctive, repetitive or multiple debridementstrategies simultaneously.3. Shortening the interval between maintenance visits.

SummaryAs a basic tenet of treatment planning the level of risk for aspecific disease should influence the need for therapeuticintervention for that disease. Yet, many dental therapistscontinue to manage all of their periodontal disease affectedpatients with little variability in the approach. In addition tothe information linking periodontal inflammation withmore serious diseases, the recognised site specificity andindividual variability of periodontal disease presentationsuggests that a different approach may be advisable.

While quantitative data regarding the significance ofspecific risk factors has not yet be elucidated, it seemsreasonable to treat more aggressively those patients who aremore likely to get periodontal disease as well as patientswho are already have risk factors for the systemic diseaseswhich can be further affected when periodontal inflamma-

tion persists. Specific tooth and site specific factors shouldalso affect the treatment plan (see Table 1). Included in amore aggressive approach may be increased use of adjunc-tive therapies, intervention at an earlier stage of disease andmore frequent monitoring via maintenance care. Providingtherapy which maximises the chance for inflammation ofperiodontal origin to resolve (and then be kept at bay) canpay dividends to patients’ oral and overall health.

References1. 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 notablepast, a promising future. Williams RC. J Periodontol. 2008Aug;79(8 Suppl):1552-9.

3. Relationship between periodontal infections and systemic dis-ease. Seymour GJ, et al. Clin Microbiol Infect. 2007 Oct;13 Suppl4:3-10.

4. Determining Periodontal Risk Factors in Patients Presenting forDental Care. Schutte DW, Donley TG. J Dent Hyg. 1996 Nov-Dec;70(6):230-4.

5.The American Journal of Cardiology and Journal ofPeriodontology Editors' Consensus: periodontitis and atheroscle-rotic cardiovascular disease. Friedewald VE, et al. AmericanJournal 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 ClinPeriodontol. 2003;30:887–901.

9. Relationship of “Bleeding on Probing” and Gingival IndexBleeding” as Clinical Parameters of Gingival Inflammation. J ClinPeriodontol 1993;20(2):139-143.

10. Periodontitis An Archetypical Biofilm Disease. Schaudinn, C, etal. 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, LindheJ. J Clin Periodontol 1981;8:239–248.

13. Subantimicrobial dose doxycycline as adjunctive treatment forperiodontitis. A review. Preshaw PM, et al. J Clin Periodontol2004;31:697–707.

Dr Tim Donley is currently in the private practice of Periodontics andImplantology in Bowling Green, KY.After graduating from the University ofNotre Dame, Georgetown UniversitySchool of Dentistry and completing ageneral practice residency, he practicedgeneral dentistry. He then returned toIndiana University where he received

his masters degree in periodontics. Dr Donley is the formereditor of the Journal of the Kentucky Dental Association andis an adjunct professor of periodontics at Western KentuckyUniversity. He is a lecturer with the ADA Seminar Series.Dentistry Today recently listed him among it’s ‘Leaders inContinuing Education’. He lectures and publishes frequentlyon topics of interest to clinical dentists and hygienists.

US clinician Tim Donley returns to the UK with a full dayseminar, Better Patient Outcomes. Better Perio Incomes! Itfollows the phenomenal success of this year’s seminar thatsold out and is being hailed as a ‘must-attend’. It takes placeon Friday 11 February 2011 at the Royal College of Physicians.Delegates can gain seven verifiable CPD.For further information or to book, freephone 0800 371652or visit www.independentseminars.com. This seminar is sposnored by Oral-B – and every delegate will receive anelectric toothbrush.

Persistent inflammation with probing depth of 5mm wasnoted at the mesio-palatal surfaces of the maxillary firstmolar and the maxillary first pre-molar. Mechanicaldebridement was completed at these sites. Then, due to thesubgingival extent of the restoration margin at the molar,local antibiotic was delivered. Multiple methods ofdebridement were employed since the tooth surface riskfactor suggested an added degree of difficulty to achievingadequate debridement. Similarly, because of thedevelopmental root concavity typically noted at the mesialof the maxillary first premolar, local antibiotic was alsodelivered at this site in an attempt to maximise the chance ofachieving therapeutically effective debridement even in lightof the complex root anatomy.

The above radiographs are from a 39-year-old white malewho was a long-time smoker (one pack per day) and a less-than-ideally controlled diabetic. Mechanical debridement wassupplemented with laser debridement in an attempt tomaximise the resolution of inflammation of oral origin.Additionally, host modulation therapy was administered toaddress the host component to the noted destruction.

Example three

Example one Example two

The mandibular molars each serve as abutments for aremovable prosthesis. The loss of either of these teeth willseverely limit the prosthetic options for efficiently restoringa functional dentition. Persistent inflammation along withprobing depths of 4mm was noted at the mesial surfaces ofthese teeth. Although the noted probing depth could beconsidered ‘manageable’, adjunctive therapy (supplementingmechanical debridement with local antibiotic delivery) wasused in an attempt to increase the aggressiveness of therapydue to the strategic importance of these teeth.

Clinical application of risk-based approach

Table 1

Factors assessed prior to formulating a course oftherapy:1. The presence of inflammation at a site via probing andvisual inspection2. The probing depth at sites where inflammation is noted3. The presence of any complex root anatomy at theinvolved site4. The strategic importance of involved tooth5. The aesthetic importance of involved tooth6. The functional significance of the involved tooth7. The presence of any periodontal risk factors8. The presence of any risk factors for the systemic diseasepotentially affected by periodontal inflammation.

19, 20 DM Dec Clin Donley.qxd:DM News+Edit+lettr+FCover 2005 29/11/2010 12:39 Page 2