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PennWell designates this activity for 2 Continuing Educational Credits

Published: April 2011
Expiry: March 2014
Earn
2 CE credits
This course was
written for dentists,
dental hygienists,
and assistants.
Instrumentation for
the Treatment of
Periodontal Disease
Peer-Reviewed Publication
Written by Timothy Donley DDS, MSD
This course has been made possible through an unrestricted educational grant. The cost of this CE course is $49.00 for 2 CE credits.
Cancellation/Refund Policy: Any participant who is not 100% satisfied with this course can request a full refund by contacting PennWell in writing.
2 www.ineedce.com
Educational Objectives
The overall goal of this course is to provide the reader with
information on nonsurgical periodontal therapy and instru-
mentation of periodontal sites. Upon completion of this
course, the clinician will be able to do the following:
1. List and describe the prevalence of periodontitis in the
population
2. Describe the periodontal disease process
3. List and describe the associations between oral and
systemic health
4. List and describe therapeutic options for the treatment
of periodontal disease
5. List and describe the mechanism by which ultrasonic
instrumentation works
6. List and describe insert tip selection for periodontal
sites and the rationale for their selection
Abstract
The initiation and progression of periodontal disease re-
quires the presence of bacterial accumulations. Once peri-
odontal disease exists, its progression depends on the host
response. In order to treat periodontal disease, the bioflm
must be disrupted and all hard and soft deposits removed
from the tooth surfaces. In order to thoroughly remove
deposits and debris without removing excessive tooth
structure, instruments must be selected that are suitable for
the intended site and technique. The selected debridement
method should offer predictable results independent of
operator skill level; be effcient to perform clinically, well
tolerated by patients and cost effective; and have a low po-
tential for adverse side effects.
Introduction
Periodontitis is common, with mild to moderate forms
affecting 30% to 50% of adults and the severe generalized
form affecting 5% to 15% of all adults in the United States.
1

More recent data suggests that the prevalence of periodon-
titis in the United States may actually be much greater than
previously estimated.
2
Periodontitis seen in youth and
early adulthood can probably be classifed as aggressive
periodontitis, and some degree of clinical attachment loss
(CAL) in youth is well documented in population studies.
3

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 con-
nective and bone tissues caused by hyperactivated immune-
infammatory response.
4
The net result of the host response
to initiating periodontal pathogenic bacteria is destruction
of periodontal tissues and systemic interactions. Despite
great understanding of the potential therapeutic beneft of
host modulation, effective interruption of periodontal bac-
teria remains the cornerstone of effective periodontal disease
intervention. Advances in debridement devices and tech-
niques, as discussed below, can enhance a clinicians abil-
ity to successfully manage periodontal disease. Emerging
information linking oral infammation with serious, chronic
diseases of aging underscores the importance of effective
periodontal therapy. More effective approaches aimed at
helping patients achieve and then maintain a preferred level
of oral health can pay dividends to overall health.
Periodontal Disease Process
Periodontitis, viewed for years as primarily the outcome
from infection, is now seen as resulting from a complex
interplay between bacterial infection and the host response,
often modifed by behavioral factors. The host response
is now seen as a key factor in the clinical expression of
periodontitis, with only some 20% of periodontal diseases
now attributed to bacterial variance. Additionally, genetic
variance may be responsible for up to 50% of periodontal
disease expression.
5
The clinical diagnosis of periodontitis
historically has required evidence of loss of connective
tissue surrounding the teeth and bone loss detected by
radiography. For many years, clinical probing depth mea-
surement was the primary factor used to determine which
sites were in need of periodontal therapy. Current knowl-
edge of the role that infammation plays in the etiology of
many systemic diseases suggests that incorporating other
assessments into periodontal treatment decision pathways
may be important. The destruction of periodontal tissues
leads to deepening of the sulci adjacent to teeth, resulting
in the formation of periodontal pockets. Despite the aware-
ness that infammatory mediators of oral origin can affect
other body disease processes, periodontal therapy has been
aimed almost exclusively at achieving and then maintain-
ing pocket depths that the clinician considers accessible for
the patient and for professional debridement efforts.
While there is little doubt that reduction in probing
depth improves access to subgingival areas, focusing the
management of periodontal disease solely on pocket depth
may not be suffcient. Medical research underscores the
important role that infammation in the body plays in
the development and progression of many of the serious,
chronic diseases of aging. Emerging evidence continues to
suggest that the mouth can be a signifcant source of infam-
mation when periodontal disease persists.
6
The entrance of
bacteria, bacterial byproducts and infammatory mediators
released orally in response to the pathogenic periodontal
bacteria can enter the bloodstream. Infammation of peri-
odontal tissues can have adverse effects beyond loss of
periodontal attachment and bone.
7
Thus, in addition to
management of probing depths, it seems prudent for oral
infammation to take on added diagnostic and therapeutic
signifcance in the management of periodontal disease. The
following therapeutic approach is based on assessment of
patient, tooth and site risk factors. The intent is to more
effectively target therapy to improve patients oral and
overall health.
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Focusing the management of periodontal disease
solely on pocket depth may not be sufficient.
Which Patients to Treat
Environmental and genetic factors, as well as acquired risk
factors, accelerate destructive infammatory processes in
periodontitis.
8
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.
9

Realizing that risk factors for periodontal disease can make
eradication of periodontal disease more diffcult, more ag-
gressive therapy is considered for patients who have known
periodontal disease risk factors.
Table 1. Non-oral risk factors for periodontal disease
Tobacco use
Diabetes mellitus
Family history
Mental stress
Depression
Obesity
Osteoporosis
In similar fashion, adverse associations have been identi-
fed between periodontal disease and diabetes, cardiovascu-
lar disease, preterm low-birth-weight deliveries, respiratory
diseases, certain cancers, kidney diseases and other systemic
conditions.
10
It certainly seems advisable to treat more ag-
gressively those patients who have other risk factors for the
conditions that can be affected by periodontal infamma-
tion. Allowing periodontal infammation 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 ap-
proach proportionate to the level of risk.
Table 2. Adverse associations with periodontal disease
Diabetes mellitus
Cardiovascular disease
Respiratory disease
Certain cancers
Renal disease
Preterm low-birth-weight deliveries
Which Sites to Treat
Clinical and radiographic fndings are commonly used to
determine a patients periodontal status. Often treatment
resources are directed primarily to sites where probing
depth has increased (where disease progression has already
occurred). Diagnostic fndings 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.
11
Yet there is general agreement that an isolated
incidence of BOP at a site is a poor predictor of disease ac-
tivity at that site.
12
The predictive value of BOP increases
substantially when BOP is persistent. Sites that continue
to demonstrate BOP (at successive reevaluation visits) are
more likely to break down.
13
In addition to signaling im-
pending destructive activity, BOP is strongly correlated with
gingival infammation.
14
Gingival infammation is typically
expressed clinically as redness, edema and/or bleeding.
While preventing adverse changes in pocket depth has
merit, the overwhelming evidence confrming the adverse
relationship between oral infammation and systemic disease
suggests that elimination of infammation should also be
a goal of therapy. In addition to sites at which increases in
probing depth are noted, those sites with persistent bleeding
on probing or where other clinical signs of infammation are
found should be priority candidates for therapeutic attention.
Sites with increases in probing depth, persistent
bleeding on probing or where other clinical signs of
inflammation are found should be priority candidates
for therapeutic attention.
Which Treatments
Bacterial bioflm accumulations on the teeth are essential to
the initiation and progression of periodontitis.
15
Although
periodontitis begins with a microbial infection, it is the
host-mediated infammatory response that causes clinically
signifcant connective tissue and bone destruction.
16
Long-
term clinical studies have clearly demonstrated that the reg-
ular and effective removal of bacterial bioflms on the teeth
can prevent periodontitis.
17
Suppressing the host response
has also been shown to play a critical adjunctive therapeutic
role.
18
Dietary alterations intended to reduce the infamma-
tory response have also been shown to be of beneft in peri-
odontal therapy.
19
Yet mechanical disruption of the bioflm
remains the foundational approach for the resolution of
infammatory periodontal diseases. Bioflm disruption can
be accomplished by mechanical means (hand instrumenta-
tion and/or ultrasonic instrumentation), systemic and local
administration of targeted antibiotics, and laser-generated
energy.
20
The chosen methodology is most often driven by
the clinicians personal preference. However, the selected
debridement method should offer predictable results inde-
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pendent of operator skill level; be effcient to perform clini-
cally, well tolerated by patients and cost effective; and have
a low potential for adverse side effects.
Mechanical disruption of the biofilm remains
the foundational approach for the resolution of
inflammatory periodontal diseases.
Therapeutic Options
Periodontal therapy had long been focused on removal
of visible plaque and clinically detectable calculus. The
pathogens that initiate periodontal disease were thought
to be deeply embedded in the cementum of subgingival
root surfaces. For many years, the intention of mechanical
debridement was the deliberate removal of the cementum,
which was assumed to be pathogen laden. Increased dentinal
hypersensitivity
21
and pulpitis
22,23
have been reported as un-
desirable side effects of excessive cementum removal. In the
past two decades, studies have demonstrated that endotoxin
is more superfcially associated with the cementum. Thus,
deliberate cementum removal is not necessary and may not
even be prudent. While not conclusive, current research
suggests that preserving cementum can improve the degree
of periodontal regeneration.
24
In this regard, the consensus
report from the 1996 World Workshop in Periodontics states
that intentional cementum removal should not be included
in current periodontal debridement techniques for the pur-
pose of removing toxic substances from the root surface.
25

More recently, the American Academy of Periodontology
added that the goal of periodontal instrumentation is to ef-
fectively remove plaque and calculus, while causing the least
amount of root surface damage.
26

Current research suggests that preserving cementum
can improve the degree of periodontal regeneration.
When used properly, similar clinical outcomes can be
achieved with hand curettes and ultrasonic instrumenta-
tion.
26
However, the inherent operator variability due to
the design and use of a bladed instrument makes achieving
therapeutic root debridement less predictable with manual
curette use. For a curette to actively remove bioflm without
excessive removal of cementum, an adequate working edge
must be created and maintained throughout the procedure.
Additionally, that sharpened working edge has to be posi-
tioned against the root at the precise angle that permits the
working portion of the instrument to engage the root in a
way such that the movement of the instrument in a coro-
nal direction will result in sheer force suffcient to remove
endotoxin. Finally, the level of force applied during the
working stroke needs to be suffcient to dislodge endotoxin
from the surface without excessive cementum removal.
With ultrasonic instrumentation, positioning the working
portion of the instrument and applying suffcient force to
selectively dislodge endotoxin is less operator-dependent.
The cylindrical shape of most ultrasonic inserts is also more
conducive to bioflm removal (better conforms to the sur-
face) than the linear cutting edge of bladed instruments that
were really designed for effective calculus removal.
Inherent operator variability makes achieving thera-
peutic root debridement more predictable
with ultrasonic instrumentation than with
manual curette use.
Ultrasonic Scaling
There are two categories of ultrasonic instrumentation: mag-
netostrictive and piezo. These categories differ in the way they
are powered, which was thought to result in differing patterns
of tip movement. Piezo devices, powered by a crystal, were
believed to result in tip movement that is linear. Thus, only
the sides of piezo-driven tips were thought to provide active
debridement. The dimensional change in the metal stack of
a magnetostrictive-driven insert was thought to be elliptical,
with all sides of the tip capable of removing bioflm. The early
studies suggesting this fundamental difference in tip motion
were performed without load applied to the insert tips. Sub-
sequent laser vibrotomy-based studies have demonstrated
that as soon as the insert tip is loaded (placed against a tooth
surface), both piezo- and magnetostrictive-driven instrument
tips have elliptical patterns of movement.
27
Thus, anecdotal
claims of increased root trauma with magnetostrictive devices
compared to piezo devices due to the magnetostrictive tip
banging into the root in multiple directions are unfounded.
In reality, both piezo- and magnetostrictive-driven tips move
in similar fashion once under any load. Indeed, the degree of
damage to root surfaces via ultrasonic instrumentation is a
factor of tip shape, lateral force, angulation and power setting
regardless of the method of ultrasound generation. In other
words, magnetostrictive, piezo and even hand curettes are
all capable of inducing root damage. However, by using a
preferred tip, at a preferred angulation, and using a preferred
level of lateral force at a preferred power setting, the risk of
root surface damage can be eliminated for all methods.
27
Tip
angulation may be the primary determinant in causing root
damage. Forces generated with a magnetostrictive-driven
tip were lowest when the tip was parallel to the tooth surface
and increased to its maximum point as the tip was moved
ninety degrees to the tooth surface.
28
In contrast, forces from
a piezo-driven tip increased and then peaked when the tip
was moved to forty-fve degrees to the tooth surface.
29
In
other words, piezo is more technique-sensitive in terms of
minimizing root damage.
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Additionally, the degree of root substance removal via
ultrasonic devices is signifcantly infuenced by the tip
designs, increasing for wider scaler tips as compared to
narrow, probe-shaped inserts.
30
Thus, a suitable magneto-
strictive-driven insert used at proper settings is less likely
to result in root damage than a piezo-driven insert.
The degree of root substance removal via ultrasonic
devices is significantly influenced by the tip designs,
increasing for wider scaler tips as compared to
narrow, probe-shaped inserts.
Cavitation
The removal of plaque and calculus from the tooth surface
had originally been attributed mainly to the vibratory ac-
tion of the probe tip. Walmsley theorized in 1984 that while
the primary deposit removal action by ultrasonics is me-
chanical, cavitation activity causes fracture of the attached
deposits through the resultant shock waves.
31
Despite con-
ficting laboratory fndings and no reliable way to evaluate
the clinical effects of ultrasonic cavitation, the force cre-
ated via ultrasonic induced cavitation may be suffcient to
disrupt the bioflm environment, thereby facilitating the
mechanical removal of periodontopathic bacteria.
32

Surface-Specific Tips and Device Settings
Clearly, contact between the active portion of an ultrasonic
insert at a preferred power level, proper angulation to the
tooth surface and minimal force is essential for adequate
bioflm interruption. Tip selection should be based on
the type of deposit and the anatomy of the surface to be
debrided. The type of deposit encountered at a site should
determine the amplitude (power level) needed for effcient
removal. The force behind the tip movement is infuenced
by the diameter of the tip and the stroke range, with
wider-diameter tips (standard) producing greater force for
effcient removal of heavy or tenacious calculus and slim-
diameter tips producing a lower level of force appropriate
for effcient removal of light/soft deposits. The anatomy of
the treatment site should then determine the shape of tip
that will maximize contact of the active area with the root
surface for thorough deposit removal.
Tip selection should be based on the type of deposit
and the anatomy of the surface to be debrided.
A wide range of available magnetostrictive inserts
permits a preferred two-stage approach to instrumenta-
tion. The objective of the frst stage scaling is to reduce
moderate-to-heavy calculus/stain deposits. To accomplish
this most effciently, a standard-diameter insert/tip and a
higher level of power should be used. The objective of the
second stage debridement is the defnitive removal of all
the light calculus and stain deposits that remain, as well as
defnitive removal of bioflm and endotoxin. Slim inserts are
ideal for the second stage and can reach pocket areas deeper
than 4 mm and furcation areas, provided an appropriately
designed tip is used for the sites anatomy.
The use of slim insert tips also helps tactile identifca-
tion of root morphology or remaining deposits, as the tip
diameter is very similar to that of a periodontal probe. Data
obtained from probing similarly can be obtained from the
DEPOSIT AND ROOT ANATOMY INSERT SELECTION INSERT SETTINGS
Type of Deposit Root Anatomy Power Setting
Light/
Biofilm
Moderate Heavy Straight Curved Type Low Low-
Medium
Low-
High
X X X (supragingivally) X (supragingivally) Standard #3/Beavertail X
X X X X (4mm) Standard #10 X
X X X X (4mm) Standard #100 X
X X X X (4mm) Standard #1000/Triplebend X
X X X X (4mm) Slimline #10 X
X X X X Slimline Right or Left X
X X X X (4mm) Slimline #1000 X
X X X (4mm) THINSert X
X X X X SofTip (implant insert) X
X X X (w/surgical
procedure)
X (w/surgical
procedure)
DiamondCoat X
Table 3. Magnetostrictive ultrasonic insert tip selection
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slim insert during use. Slim-insert use also allows bioflm
removal without excessive cementum removal, thus reduc-
ing the likelihood of post-instrumentation dentinal hyper-
sensitivity. It is still prudent to use an explorer specifcally
designed for calculus detection (ODU 11/12) following
any scaling procedure. To complement root anatomy, right
and left inserts are used to fully access the full root circum-
ference in deep pockets, and by rotating the tip, full access
to the roof of furcations can also be achieved.
Figure 1. Insert tip designs
FSI 10 FSI 100 FSI 1000 THINSert
FSI SLI 1000 FSI SLI FSI SLI FSI SLI Implant
straight Right Left Insert


Designs with curved tips, straight tips and optimized
line angulations enable full pocket access ergonomically.
New designs with line-angle adaptation have also improved
the ability to access interproximal and subgingival areas,
offering effcient removal of deposits with a slim-tip insert
while maximizing patient comfort. A beveled edge design
at the working end of the insert tip also helps the effciency
of deposit removal, as the ultrasonic energy is specifcally
targeted to each of the four corners rather than on the full
circumference of a rounded working end.
Standard Diameter Inserts
The wider diameter and longer stroke range of standard
inserts provide a range of force (amplitude) appropriate
for the effcient reduction of moderate to heavy and/or
tenacious calculus and stain deposits. The degree of force is
further defned by the power setting of the scaling unit. The
lowest power setting at which effcacy (removal/reduction
of deposit) is achieved effciently should be utilized.
Tip designs available in standard diameter are straight
with differing number of bends and include the #10, #100,
#1000, and #3 (beavertail design). It is important to keep
in mind that the objective of the scaling stage when heavier
deposits are present is to reduce those deposits to a lesser
degree. Hence, a straight insert provides a suffcient degree
of contact to engage and reduce calcifed deposits /stain,
even in areas of more complex anatomy.
The #10 and #100 designs are similarly cylindrical in
shape, with the #10 having one bend in the shank and the
#100 having two bends in the shank. The length of either
of these inserts is suffcient to enable contact of the active
portion of the tip (terminal 4mm) to moderate-heavy sub-
gingival calculus in deeper pockets.
The #1000, or triple bend, design features a third bend
in the shank to facilitate adaptation around line angles
and interproximally, as well as a beveled active area. This
beveled edge design at the working end of the insert tip
increases the effciency of deposit removal as the ultrasonic
energy is specifcally targeted to each of the four corners
rather than on the full circumference of a rounded working
end. (Figures 2-4). With the length of the tip being reduced
by the third bend in the shank, access to deep subgingival
calculus with the #1000 is limited and better accessed by
the #10 or #100.
The #3 design, commonly recognized as the beavertail,
is indicated for the breaking of heavy ridges of supragin-
gival calculus and/or stain, most commonly on the lingual
surfaces of the mandibular anterior teeth. Unlike the other
inserts which utilize the terminal 4 mm of tip as the active
area, the active area of the beavertail is the terminal edge of
the tip, and is indicated for supragingival use only.
Figure 2. Triple bend insert tip
Note the applicability of this insert for line angles
Figure 3. THINSert tip lower left anterior quadrant
Note the applicability of this insert tip to debride multiple flat
surface areas
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Figure 4. THINSert tip lower left posterior area lingually
Slim Diameter Inserts
Slim diameter inserts are available with either straight or
curved shanks.
Indicated for the defnitive debridement of surfaces with
fat or minimal contour, straight slim inserts include the
popular #10 design as well as a newly available #1000 or tri-
ple bend design. As with the standard #10, the length of the
slim #10 facilitates access to the depth of the pocket while
the straight yet cylindrical shape conforms to relatively fat
or minimally contoured surfaces, maximizing contact and
therefore, disruption of bioflm.
The beveled tip and triple bends of the Slimline 1000
insert improve adaptation at line angles and access to in-
terproximal and subgingival surfaces, offering the clinician
an option for effcient debridement of minimally contoured
surfaces while maximizing patient comfort
For defnitive debridement of more complex root
anatomy, as found in posterior roots, curved right and left
inserts are needed to maximize access to and contact with
contoured surfaces, and by rotating the curved tip, full ac-
cess to the roof of furcations can also be achieved.
Ultra Slim Diameter Inserts
An ultra slim #10 insert with a 9 backbend (Cavitron
THINSert) is available to facilitate thorough debridement
of fat/minimally contoured surfaces where access with
the slim #10 is limited due to tight contacts or relatively
tight tissue. This insert is particularly useful for regular
maintenance care (bioflm interruption) of patients with no
signifcant hard deposits and minimal pocket depth (only
relatively fat root surface involvement).
Patient Comfort
Patient comfort with the chosen method of debridement is
essential. Tools to objectively measure patient pain percep-
tions in dentistry are lacking. Despite anecdotal claims to the
contrary, there does not seem to be any signifcant difference
in comfort levels of patients exposed to magnetostrictive or
piezo devices.
33
Periodontal debridement, especially during
the maintenance phase of therapy, typically requires relatively
short working times at various sites throughout the mouth.
For such procedures, traditional local anesthetic injections
may not be the most suitable way to manage pain. Topical
anesthetics that can allow for an adequate level of pain con-
trol without a needle injection may offer advantages. Indeed,
patients are more likely to accept treatment with effective pain
management, which increases comfort while reducing anxiety,
yet a signifcant number of patients fear injections.
34
Thus, the
appropriate use of needle-free anesthetics serves two pur-
poses pain management as well as reduced fear and anxiety
compared to the use of local anesthetics. Topical anesthetics
are convenient, but they offer short-duration anesthesia with
variable pain control
35
and must thus be selected judiciously.
A further option is the use of a locally applied noninjectable
anesthetic containing 2.5 percent lidocaine and 2.5 percent
prilocaine. This gel is syringed directly into the site of the
pocket using a blunt cannula (without injecting it into the
tissues) where site-specifc anesthesia is then obtained. This
anesthetic has been found to provide a level of anesthesia com-
parable to traditional injection anesthesia but without use of
a needle, for twenty minutes duration and without lingering
anesthesia following completion of the procedure.
36,37,38
Summary
Periodontitis is now seen as resulting from a complex interplay
between bacterial infection and host response, often modifed
by behavioral factors, with the host response playing a key
role. The overwhelming evidence confrming the adverse
relationship between oral infammation and systemic disease
suggests that elimination of infammation should be a goal of
therapy in addition to preventing adverse changes in pocket
depths and further clinical attachment loss. Mechanical dis-
ruption of the bioflm remains the foundational approach for
the resolution of infammatory periodontal diseases. Although
similar clinical outcomes can be achieved with hand curettes
and ultrasonic instrumentation, operator variability makes
achieving therapeutic root debridement more predictable with
ultrasonic instrumentation. Contact between the active por-
tion of an ultrasonic insert at a preferred power level, proper
angulation to the tooth surface and minimal force is essential
for adequate bioflm interruption. Care should be taken to se-
lect tips that are appropriate based on the type of deposit and
the anatomy of the surface to be debrided.
References
1 Burt B; Research, Science and Therapy Committee of the American
Academy of Periodontology. Position paper: epidemiology of
periodontal diseases. J Periodontol. 2005;76:140619.
2 Eke PI, Thornton-Evans GO, Wei L, Borgnakke WS, Dye BA.
Accuracy of NHANES periodontal examination protocols. J Dent
Res. 2010 Nov;89(11):120813.
3 Burt B; Research, Science and Therapy Committee of the American
Academy of Periodontology. Position paper: epidemiology of
periodontal diseases. J Periodontol. 2005;76:140619.
4 Kornman KS, Page RC, Tonetti MS. The host response to the
microbial challenge in periodontitis: assembling the players.
Periodontol. 2000. 1997;14:3353.
8 www.ineedce.com
5 Page RC, Offenbacher S, Schroeder HE, Seymour GJ, Kornman
KS. Advances in the pathogenesis of periodontitis: summary
of developments, clinical implications and future directions.
Periodontol. 2000. 1997;14:21648.
6 Williams RC. Understanding and managing periodontal diseases:
a notable past, a promising future. J Periodontol. 2008 Aug;79(8
Suppl):15529.
7 Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K.
Relationship between periodontal infections and systemic disease.
Clin Microbiol Infect. 2007 Oct;13 Suppl 4:310.
8 Schutte DW, Donley TG. Determining periodontal risk factors
in patients presenting for dental care. J Dent Hyg. 1996 Nov-
Dec;70(6):2304.
9 Friedewald VE, Kornman KS, Beck JD, Genco R, Goldfne
A, Libby P, et al. The American Journal of Cardiology and
Journal of Periodontology Editors Consensus: periodontitis and
atherosclerotic cardiovascular disease. Am J Cardiol. 2009 Jul
1;104(1):5968.
10 Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K.
Relationship between periodontal infections and systemic disease.
Clin Microbiol Infect. 2007 Oct;13 Suppl 4:310.
11 Newbrun E. Indices to measure gingival bleeding. J Periodontol.
1996;67:55561.
12 Lang NP, Joss A, Orsanic T, Gusberti FA, Siegrist BE. Bleeding on
Probing. A predictor for the progression of periodontal disease? J
Clin Periodontol. 1986;13(6)5906.
13 Schtzle M, Le H, Brgin W, Anerud A, Boysen H, Lang NP.
Clinical course of chronic periodontitis. I. Role of gingivitis. J Clin
Periodontol. 2003;30:887901.
14 Chaves ES, Wood RC, Jones AA, Newbold DA, Manwell MA,
Kornman KS. Relationship of bleeding on probing and gingival
index bleeding as clinical parameters of gingival infammation. J
Clin Periodontol. 1993;20(2):13943.
15 Schaudinn C, Gorur A, Keller D, Sedghizadeh PP, Costerton JW.
Periodontitis: an archetypical bioflm disease. J Am Dent Assoc.
2009;140(8):97886.
16 Kornman KS, Page RC, Tonetti MS. The host response to the
microbial challenge in periodontitis: assembling the players.
Periodontol. 2000. 1997;14:3353.
17 Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures
on caries and periodontal disease in adults. Results after 6 years. J
Clin Periodontol. 1981;8:23948.
18 Preshaw PM, Hefti AF, Jepsen S, Etienne D, Walker C, Bradshaw
MH. Subantimicrobial dose doxycycline as adjunctive treatment
for periodontitis. A review. J Clin Periodontol. 2004;31:697707.
19 Chapple IL. Potential mechanisms underpinning the nutritional
modulation of periodontal infammation. J Am Dent Assoc.
2009;140:178.
20 Research, Science and Therapy Committee of the American
Academy of Periodontology. Treatment of plaque-induced
gingivitis, chronic periodontitis, and other clinical conditions. J
Periodontol. 2001;72:17901800.
21 von Troil B, Needleman I, Sanz M. A systematic review of the
prevalence of root sensitivity following periodontal therapy. J Clin
Periodontol. 2002;29 Suppl 3:173-7.
22 Axelsson P. New ideas and advancing technology in prevention
and non-surgical treatment of periodontal disease. Int Dent J. 1993
Jun;43(3):223-38.
23 Wong R, Hirsch RS, Clarke NG. Endodontic effects of root planing
in humans. Endod Dent Traumatol. 1989 Aug;5(4):193-6.
24 Gonalves PF, Lima LL, Sallum EA, Casati MZ, Nociti FH Jr. Root
cementum may modulate gene expression during periodontal
regeneration: a preliminary study in humans. J Periodontol. 2008
Feb;79(2):32331.
25 Cobb CM. Non-surgical pocket therapy: mechanical. Ann
Periodontol. 1996;1:44390.
26 Drisko CL, Cochran DL, Blieden T, Bouwsma OJ, Cohen RE,
Damoulis P, et al. Position paper: sonic and ultrasonic scalers
in periodontics. Research, Science and Therapy Committee
of the American Academy of Periodontology. J Periodontol.
2000;71:17921801.
27 Lea SC, Walmsley D. Mechano-physical and biophysical properties
of power-driven scalers: driving the future of powered instrument
design and evaluation. Periodontol. 2000. 2009;51:6378.
28 Flemmig TF, Petersilka GJ, Mehl A, Hickel R, Klaiber B. Working
parameters of a magnetostrictive scaler infuencing root surface
removal in vitro. J Periodontol. 2009;69:54753.
29 Flemmig TF, Petersilka GJ, Mehl A, Hickel R, Klaiber B. The effect
of working parameters on root surface removal using a piezoelectric
ultrasonic scaler in vitro. J Clin Periodontol. 1998;25:15863.
30 Jepsen S, Ayna M, Hedderich J, Eberhard J. Signifcant infuence
of scaler tip design on root substance loss resulting from ultrasonic
scaling: a laserproflometric in vitro study. J Clin Periodontol.
2004;31(11):10036.
31 Walmsley AD, Laird WR, Williams AR. A model system to
demonstrate the role of cavitational activity in ultrasonic scaling. J
Dent Res. 1984;63(9):11625.
32 Lea SC, Walmsley D. Mechano-physical and biophysical properties
of power-driven scalers: driving the future of powered instrument
design and evaluation. Periodontol. 2000. 2009;51:6378.
33 Kocher T, Rodemerk B, Fanghnel J, Meissner G. Pain during
prophylaxis treatment elicited by two power-driven instruments.
J Clin Periodontol. 2005;32:5358.
34 Crawford S, Niessen L, Wong S, Dowling E. Quantifcation of
patient fears regarding dental injections and patient perceptions
of a local noninjectable anesthetic gel. Compendium. 2005;26(2)
Suppl 1:114.
35 Carr, MP, Horton, JE. Clinical evaluation and comparison of 2
topical anesthetics for pain cause by needle sticks and scaling and
root planing. J Periodontol. 2001;72(4):47984.
36 van Steenberghe D, Bercy P, De Boever J, Adriaens P, Geers L,
Hendrickx E, et al. Patient evaluation of a novel non-injectable
anesthetic gel: a multicenter crossover study comparing the gel to
infltration anesthesia during scaling and root planing. J Periodontol.
2004;75(11):14718.
37 Al-Melh, MA, Andersson, L, Behbehani, E. Reduction of pain
from needle stick in the oral mucosa by topical anesthetics: a
comparative study between lidocaine/prilocaine and benzocaine.
J Clin Dent. 2005;16(2):536.
38 Magnusson I, Geurs NC, Harris PA, Hefti AF, Mariotti AJ,
Mauriello SM, Soler L, Offenbacher S. Intrapocket anesthesia for
scaling and root planing in pain-sensitive patients. J Periodontol.
2003;74(5):597602.
Author Profile
Timothy Donley DDS, MSD
Dr. Timothy 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.
His course is part of the ADA Seminar Series. Dentistry To-
day recently listed him among the Leaders in Continuing
Education. He lectures and publishes frequently on topics of
interest to clinical dentists and hygienists.
Disclaimer
The author(s) of this course has/have no commercial ties with
the sponsors or the providers of the unrestricted educational
grant for this course.
Reader Feedback
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www.ineedce.com.
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Questions
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1. Mild to moderate forms of periodontitis
affect _________ of adults.
a. 10% to 30%
b. 20% to 40%
c. 30% to 50%
d. none of the above
2. Severe generalized periodontitis affects
_________ of adults.
a. 3% to 12%
b. 4% to 15%
c. 5% to 15%
d. 5% to 20%
3. The host-mediated destruction of con-
nective and bone tissues in periodontitis is
caused by a _________ response.
a. hypoactivated immune-protective
b. hyperactivated immune-protective
c. hypoactivated immune-infammatory
d. hyperactivated immune-infammatory
4. _________ remains the cornerstone of
effective periodontal disease intervention.
a. Effective intercession of periodontal bacteria
b. Effective interruption of periodontal bacteria
c. Removal of infected cementum
d. none of the above
5. Periodontitis is now seen as _________.
a. resulting from a complex interplay between
bacterial infection and host response
b. primarily the outcome from infection
c. primarily the outcome from infammation
d. a and b
6. _________ of periodontal diseases now
attributed to bacterial variance.
a. 10 percent
b. 20 percent
c. 30 percent
d. none of the above
7. The role of genetic variance in periodontal
disease is now known to be _________.
a. nonexistent
b. insignifcant
c. signifcant
d. none of the above
8. Focusing the management of periodontal
disease solely on pocket depth _________.
a. is suffcient
b. is key
c. may not be suffcient
d. none of the above
9. _______ released orally in response to the
pathogenic periodontal bacteria can enter
the bloodstream.
a. Bacteria
b. Infammatory mediators
c. Bacterial byproducts
d. all of the above
10. _________ factors accelerate destructive
infammatory processes in periodontitis.
a. Acquired risk
b. Environmental
c. Genetic
d. all of the above
11. _______ is strongly associated with
increased risk for periodontitis and disease
severity.
a. Tobacco use
b. Osteoporosis
c. Obesity
d. all of the above
12. _________ is not a non-oral risk factor for
periodontal disease.
a. Diabetes mellitus
b. Depression
c. Pulmonary embolism
d. Mental stress
13. A therapeutic approach for periodontal
disease should be developed _________
the level of risk.
a. regardless of
b. disproportionate to
c. proportionate to
d. a and c
14. There is general agreement that an
isolated incidence of bleeding on probing
at a site is _________ of disease activity at
that site.
a. an excellent predictor
b. a good predictor
c. a poor predictor
d. a detractor
15. The predictive value of BOP increases
substantially when BOP is _______.
a. transient
b. random
c. persistent
d. any of the above
16. Sites at which _________ are found
should be priority candidates for
therapeutic attention.
a. increases in probing depth
b. persistent bleeding on probing
c. clinical signs of infammation other than bleeding
on probing
d. all of the above
17. Suppressing the _________ has also
been shown to play a critical adjunctive
therapeutic role.
a. thyroid gland
b. host response
c. antigen profle
d. a and b
18. Dietary alterations intended to reduce
the infammatory response have also been
shown to be _______ in periodontal therapy.
a. of no beneft
b. of beneft
c. detrimental
d. none of the above
19. Bioflm disruption can be accomplished
by _________.
a. mechanical means
b. systemic and local administration of targeted
antibiotics
c. laser-generated energy
d. all of the above
20. The selected debridement method
should _________.
a. be effcient to perform clinically
b. be well tolerated by patients
c. have a low potential for adverse side effects
d. all of the above
21. Excessive cementum removal during
instrumentation has been reported to
result in _______.
a. dentinal hypersensitivity
b. enamel loss
c. pulpitis
d. a and c
22. According to the Academy of
Periodontology, the goal of periodontal
instrumentation is to _________.
a. effectively remove plaque
b. effectively remove calculus
c. cause the least amount of root surface damage
d. all of the above
23. Laser vibrotomy-based studies have
demonstrated that as soon as the insert tip
is loaded (placed against a tooth surface),
_________.
a. piezo driven instrument tips have elliptical patterns
of movement
b. magnetostrictive instrument tips have elliptical
patterns of movement
c. piezo driven instrument tips have vertical patterns
of movement
d. a and b
24. The risk of root surface can be eliminated
during ultrasonic instrumentation by
using a preferred _________.
a. tip
b. angulation
c. lateral force at a preferred power setting
d. all of the above
25. Tools to objectively measure patient
pain perceptions in dentistry are
_______.
a. effective
b. ineffective
c. lacking
d. none of the above
26. Slim probe-like insert tips remove
_______ wider diameter insert tips.
a. more root surface than
b. the same amount of root surface as
c. less root surface than
d. none of the above
27. Walmsley theorized that cavitation
activity causes _______ of the attached
deposits.
a. abrasion
b. fracture
c. erosion
d. a and b
28. ____ of the bioflm remains the
foundational approach for the resolution
of infammatory periodontal diseases.
a. Mechanical disruption
b. Chemical disruption
c. Genetic disruption
d. all of the above
29. The objective of the second stage of
instrumentation is the defnitive removal
of all _______.
a. heavy calculus, stain deposits, and bioflm
b. endotoxins
c. light calculus and stain deposits, bioflm and
endotoxins
d. a and b
30. It is prudent to use _________ spe-
cifcally designed for calculus detection
following any scaling procedure.
a. a slim-tip insert
b. an explorer
c. a curette
d. none of the above
Notes
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ANSWER SHEET
Instrumentation for the Treatment of Periodontal Disease
Name: Title: Specialty:
Address: E-mail:
City: State: ZIP: Country:
Telephone: Home ( ) Ofce ( ) Lic. Renewal Date:
Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course. 2) Complete all
information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score of 70% on this test will earn
you 2 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to PennWell Corp. For Questions Call 216.398.7822
Educational Objectives
1. List and describe the prevalence of periodontitis in the population
2. Describe the periodontal disease process
3. List and describe the associations between oral and systemic health
4. List and describe therapeutic options
5. List and describe the mechanism by which ultrasonic instrumentation works
6. List and describe tip selection for periodontal sites and the rationale for their selection
Course Evaluation
Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0.
1. Were the individual course objectives met? Objective #1: Yes No Objective #3: Yes No
Objective #2: Yes No Objective #4: Yes No
Objective #5: Yes No Objective #6: Yes No
2. To what extent were the course objectives accomplished overall? 5 4 3 2 1 0
3. Please rate your personal mastery of the course objectives. 5 4 3 2 1 0
4. How would you rate the objectives and educational methods? 5 4 3 2 1 0
5. How do you rate the authors grasp of the topic? 5 4 3 2 1 0
6. Please rate the instructors efectiveness. 5 4 3 2 1 0
7. Was the overall administration of the course efective? 5 4 3 2 1 0
8. Do you feel that the references were adequate? Yes No
9. Would you participate in a similar program on a diferent topic? Yes No
10. If any of the continuing education questions were unclear or ambiguous, please list them.
___________________________________________________________________
11. Was there any subject matter you found confusing? Please describe.
___________________________________________________________________
___________________________________________________________________
12. What additional continuing dental education topics would you like to see?
___________________________________________________________________
___________________________________________________________________
AGD Code 495
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