The document discusses a risk-based approach to periodontal treatment planning and management. It advocates assessing patient, tooth, and site-specific risk factors to determine the appropriate level of treatment. These include factors like smoking, diabetes, probing depths, bleeding, inflammation, root anatomy, tooth function and importance. The approach aims to more aggressively treat high risk patients and sites in order to better resolve inflammation and prevent further tissue destruction and systemic impacts. Multiple debridement methods and more frequent maintenance are suggested for higher risk cases to maximize the chances of controlling inflammation.

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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
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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 www.independentseminars.com. 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.
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