Peer-reviewed Journal of the academy of general

Comments

Transcription

Peer-reviewed Journal of the academy of general
Peer-Reviewed Journal of the Academy of General Dentistry
GENERAL
DENTISTRY
January/February 2013 ~ Volume 61 Number 1
Minimally Invasive Dentistry
Periodontics n Implant Materials
Patient Education / Motivation
Dental Materials n www.agd.org
Contents
Departments
6Editorial Possibilities and
opportunities
8 Minimally Invasive Dentistry
Minimally invasive biomimetic
endodontics: the future is here
11 Pharmacology Diet drugs Belviq
and Qsymia receive FDA approval:
what dentists need to know
14 Restorative Dentistry Implant
impression techniques including
a customized impression tray for
nonparallel implants
17 Prosthodontics Digital implant
impressions and zirconia implant
restorations
20 Ethics Call of Duty
77 Oral Diagnosis Asymptomatic
swelling in the floor of the mouth
and Asymptomatic nodule in the
posterior tongue
78 Answers Oral Diagnosis and
Self-Instruction Exercises No. 297,
298, 299
Clinical articles
23 Patient Education/Motivation
Increasing antiplaque/antigingivitis
efficacy of an essential oil mouthrinse
over time: an in vivo study
Christine A. Charles, RDH, BS
J.A. McGuire, MS
James Qaqish, BS
Pejmon Amini, DDS
Continuing Dental
Education (CDE)
Opportunities
Earn two hours of CDE
credit by signing up
for and completing the
Self-Instruction exercises
based on various subjects.
29 Patient Education/Motivation
Paste, wrap, and shimmy: a regimen
for the prevention of gum disease
Craig W. Jester, DDS
33 Tooth Whitening/Bleaching
Assessment of the release of
mercury from silver amalgam
alloys exposed to different 10%
carbamide peroxide bleaching
agents
Paloma Salomone, MDS
Renata Pla Rizzolo Bueno, MDS
Rodrigo Farcili Trinidade, MDS
Paulo Cicero Nascimento, DChem, PhD
Roselaine Terezinha Pozzobon, DDS, PhD
Self -Instruction
36 Information Technology/
Computers Overview of CEREC
CAD/CAM chairside system
Gildo Coelho Santos Jr., DDS, MSc, PhD
Maria Jacinta Moraes Coelho Santos Jr., DDS, MSc,
PhD
Amin S. Rizkalla, PhD
Dalia A. Madani, DDS, MSc, BSc
Omar El-Mowafy, BDS, PhD
41 Self-Instruction Exercise No. 321
42 Periodontics Clinical long-term
evaluation of acellular dermal matrix
in the treatment of root recession:
case report
Joao Carnio, DDS, MS
Marcel Fuganti, DDS
Self -Instruction
46 Dental Materials Marginal leakage
and microhardness evaluation
of low-shrinkage resin-based
restorative materials
Tabassom Hooshmand, DDS, PhD
Negin Tabari, DDS
Alireza Keshvad, DDS, PhD
51 Self-Instruction Exercise No. 322
www.agd.org
General Dentistry
January/February 2013
1
52 Implant materials Two case
reports involving implants and
fractured healing caps
Erdem Kilic, DDS, PhD
Kerem Kilic, DDS, PhD
Mustafa Zortuk, DDS, PhD
Alper Alkan, DDS, PhD
56 Endodontics A clinical report
of Type III dens invaginatus:
relevant aspects of a combined
therapeutic approach
Patricia de Almeida Rodrigues Silva e Souza, DDS,
MSc, PhD
Bruno Vila Nova de Almeida, DDS
Talita Tartari, DDS
Ana Claudia Braga Amoras Alves, DDS, MSc, PhD
Fabricio Mesquita Tuji, DDS, MSc, PhD
Mario Honorato Silva e Souza Jr., DDS, MSc, PhD
65 Pre-Prosthetic Surgery/Partial
Dentures Surgical resection and
prosthetic treatment of an extensive
mandibular torus
Thais Marques Simek Vega Goncalves, DDS, MSc
Jonas Alves de Oliveira, DDS, MSc
Alfonso Sanchez-Ayala, DDS, MSc
Renata Cunha Matheus Rodrigues Garcia, DDS,
MSc, PhD
Self -Instruction
69 Guest editorial Occlusion
confusion
Gene McCoy, DDS
76 Self-Instruction Exercise No. 324
Self -Instruction
60 Periodontics Obesity and
periodontitis: a link
Charlene B. Krejci, DDS, MSD
Nabil F. Bissada, DDS, MSD
64 Self-Instruction Exercise No. 323
Instructions for
Authors
For General Dentistry’s
Instructions for Authors,
please contact us at
[email protected]
2
January/February 2013
Coming Next Issue
In the March/April issue
of General Dentistry
In the February issue
of AGD Impact
• Dental findings in a child with chronic renal
failure secondary to cystinosis
• Blood contamination of used dental anesthetic
cartridges
• Prevalence and variations of the median
maxillary labial frenum in children, adolescents,
and adults in a diverse population
• Best marketing strategies for dentists
• AGD 2013 Annual Meeting preview
General Dentistry
www.agd.org
e2 Prevention/Diet/Nutrition
Five-minute nutrition workup for
children in dental practice
S.M. Hashim Nainar, BDS, MDSc
e4 Computer Designed/Fabricated
Crowns Influence of polishing
procedures on the surface
roughness of dental ceramics made
by different techniques
Osmir Batista Oliveira-Junior, DDS, MSc, PhD
Leonardo Buso, DDS, MSc, PhD
Fabio Hiroshi Fujiy, DDS, MSc
Geraldo Henrique Leao Lombardo, DDS, MSc
Fernanda Campos, DDS
Hugo Ramalho Sarmento, DDS
Rodrigo Othavio Assuncao Souza, DDS, MSc, PhD
e9 Case Presentations Vascular
leiomyoma in the oral cavity
Janaina Salomon Ghizoni, DDS, MSc, PhD
Eron Martins Baroni, DDS
Eron Jose Baroni, DDS, MSc
Marcelo Tomas de Oliveira, DDS, MSc, PhD
Luis Antonio de Assis Taveira, DDS, MSc, PhD
Jefferson Ricardo Pereira, DDS, MSc, PhD
e12 Case Presentations Peripheral
giant cell granuloma: a case report
Ruchi Banthia, MDS
Shubhra Maheshwari, MDS
Priyank Banthia, MDS
Karan Mantri, BDS, MFDS
Advisory Board
Dental Materials
Steve Carstensen, DDS, FAGD
Dental Public Health
Larry Williams, DDS, ABGD, MAGD
Esthetic Dentistry
Wynn H. Okuda, DMD
Endodontics
Stephen Cohen, DDS
Geriatric Dentistry
Lea Erickson, DDS, MSPH
Implantology
Wesley Blakeslee, DMD, FAGD
Oral and Maxillofacial
Pathology
John Svirsky, DDS, MEd
Oral and Maxillofacial
Radiology
Kavas Thunthy, BDS, MS, MEd
Oral and Maxillofacial Surgery
Karl Koerner, DDS, FAGD
Oral Medicine
Sook-Bin Woo, DMD, MMSc
Orthodontics
Yosh Jefferson, DMD, FAGD
P. Emile Rossouw, BSc, BChD,
BChD (Child-Dent), MChD (Ortho),
PhD
Pain Management
Henry A. Gremillion, DDS, MAGD
Pediatrics
Jane Soxman, DDS
Periodontics
Sebastian Ciancio, DDS
Pharmacology
Daniel E. Myers, DDS, MS
Prosthodontics
Joseph Massad, DDS
Jack Piermatti, DMD
For Advisory Board
members’ biographies,
please visit www.agd.org.
www.agd.org
General Dentistry
January/February 2013
3
Editor
Roger D. Winland, DDS, MS, MAGD
Associate Editor
Eric K. Curtis, DDS, MAGD
Director, Communications
Cathy McNamara Fitzgerald
Executive Editor
Elizabeth Newman
Managing Editor
Tiffany Nicole Slade
Associate Editor, Publications
Sheila Saldeen
Specialist, Communications
Cassandra Bannon
Manager, Production/Design
Timothy J. Henney
Graphic Designer
Phillip Montwill
Associate Designer
Jason Thomas
Advertising
M.J. Mrvica Associates
2 West Taunton Ave.
Berlin, NJ 08009
856.768.9360
[email protected]
Reprints
Rhonda Brown
Foster Printing Company
866.879.9144, ext. 194
Fax: 219.561.2017
[email protected]
General Dentistry
211 E. Chicago Ave., Ste. 900
Chicago, IL 60611-1999
888.AGD.DENT (888.243.3368)
www.agd.org
Email: [email protected]
Fax: 312.335.3442
Back Issues and Change of Address
Members, call 888.AGD.DENT (toll-free) and
ask for a Member Services representative.
Nonmembers, call Derria Murphy (ext. 4097).
Mailing Lists
For information about ordering AGD mailing lists,
call Derria Murphy (ext. 4097).
All materials subject to copying and appearing
in General Dentistry may be photocopied for the
noncommercial purposes of scientific or educational advancement. Reproduction of any portion
of General Dentistry for commercial purposes is
strictly prohibited unless the publisher’s written
permission is obtained.
Disclaimer
The AGD does not necessarily endorse opinions
or statements contained in essays or editorials
published in General Dentistry. The publication
of advertisements in General Dentistry does not
indicate endorsement for products and services.
AGD approval for continuing education courses
or course sponsors will be clearly stated.
AGD Lead Corporate Sponsor
January/February 2013
General Dentistry (ISSN 0363-6771) is published
seven times for 2013 by the AGD, 211 E. Chicago
Ave., Suite 900, Chicago, IL 60611-1999. AGD
members receive General Dentistry as part
of membership.
The nonmember individual subscription rate for
General Dentistry is $100 for the print version,
$100 for the online version, and $175 for print
and online versions; the nonmember institution
rate is $300 (add $20 for Canada and $50 for
outside the U.S. and Canada). Single copies of
General Dentistry are available to nonmember
individuals for $15 and nonmember institutions
for $18 (add $3 for orders outside the U.S.).
© Copyright 2013 by the Academy of
General Dentistry. All rights reserved.
Your voice for excellence
through education and advocacy
Subscriptions
Derria Murphy
Academy of General Dentistry
888.AGD.DENT (888.243.3368),
ext. 4097
[email protected]
4
This online edition contains hyperlinks or references
to other sites on the World Wide Web. These links
are provided for your convenience only. As soon as
you use these links, you leave this publication. The
linked sites are not under the control of the Academy
of General Dentistry (AGD); therefore, the AGD is
not responsible for the contents or for any form of
transmission received from any linked website or
reference linked to or from this publication. The
AGD disclaims all warranties, expressed or implied,
and accepts no responsibility for the quality, nature,
accuracy, reliability, or validity of any content on any
linked website. Links from this publication to any
other website do not mean that the AGD approves,
endorses, or recommends that website.
General Dentistry
www.agd.org
AGD Corporate Sponsors
Editorial
Possibilities and opportunities
O
ld age has its perks and its distractions. Some people have
a tendency to call you Sir or
Ma’am, and many even open doors
for you. You may have more aches
and pains, your hair thins, and new
wrinkles constantly appear. Wisdom,
patience, and knowledge should
be accumulating as you age. You
become more forgiving and learn to
appreciate each day as a gift. Just as
our bodies are changing, so is the
world around us; we must be ready
to change with the times—or lose out on opportunities.
As Rita Coolidge said, “Too often the opportunity knocks,
but by the time we disengage our mental chains, push back the
bolt, unhook the locks, and shut off the burglar alarms, it’s too
late.” If we see change as a threat, we have a tendency to become
defensive, irrational, and prone to discouragement. We go home
drained and discouraged because our energies are spent fighting
our fear of change and its perceived negative impact. As a result,
hundreds of opportunities are lost because our focus is blurred;
we become blind to positive prospects.
Change is a natural part of the world. Snakes take change and
growth in stride, shedding their skin as they outgrow it. Dentists
also need to shed the habits that have outlived their usefulness or
inhibit the pursuit of new possibilities.
Loosening our grip on the known and reaching for something
in which we believe but of which we are not entirely sure is necessary for survival. Taking risks is central to everything worthwhile
in life. Without taking risks, no one would find true love, develop
political power, or gain celebrity and prestige. Everything we as
humans desire in life involves taking a risk.
It’s a test to let go and enjoy the possibilities each day will bring.
I understand how chancy it is for dentists to leap outside the box
of status quo. Fortunately, you too can experience how exciting
it can be to expose yourself to the unknown—not recklessly, but
6
January/February 2013
General Dentistry
www.agd.org
with calculated enthusiasm—and enjoy all available possibilities.
Just think—some of the things that you currently enjoy were once
things you were fearful of trying simply because you didn’t want
to appear clumsy, inept, or uneducated. Test your limits to prove
what you can do, even in a world that seems crazy. Try something
new three times—once to get over the fear of doing it, twice to
learn how to do it, and a third time to figure out whether or not
you like it.
Will fear go away? Probably not. There will be a recurring fear
of failure or embarrassment. The fears of rejection, uncertainty,
and disappointment will rear their ugly heads, and the fear of difficulty will threaten. The desire for safety will continually tempt
you to stop where you are and fall back into the status quo. But don’t let these things stop you.
Win or lose, risk-takers learn to focus on the process as well
as the results. We learn to rise above what doesn’t work and find
another way to be successful. We see possibilities and opportunities that propel us past the status quo and mediocrity, and experience the challenges of sacrifice and the satisfaction of solutions.
The world is full of wonders, riches, powers, and puzzles, and
what it holds can make us horrified, sorrowful, amazed, confused,
and joyful. Boredom is the unconscious friend of those who fail
to experience the world’s wonders. Don’t become so caught up in
your own world that you fail to take advantage of opportunities
available to you. Allow security to remain a stranger and risk to
become your friend.
As American science fiction writer Ray Bradbury once said,
“Living at risk is jumping off the cliff and building your wings
on the way down.”
Roger D. Winland, DDS, MS, MAGD
Editor
Minimally Invasive Dentistry
Minimally invasive biomimetic endodontics:
the future is here
Mark Malterud, DDS, MAGD
A
s mentioned in an earlier column, minimally invasive
biomimetic dentistry (MIBD) can reach all aspects of dentistry from preventive care all the way to complex implant
restoratives.1 Most dentists never think of endodontics as fitting
solidly into the area of MIBD, but with straight-line access being
taught with rotary endodontics, crown down techniques, and
conventional hand instrumentation of canals, their eyes have
been opened to the amount of tooth structure that is necessary to remove in order to achieve the best straight-line access.
Considering the complexity of root canal morphology, none of the
above-mentioned techniques seemed to resolve how to best clean,
disinfect, and, hopefully, sterilize the canals; therefore, many
adjunctive techniques were added, along with chemical intervention and solution activation. Reciprocating handpieces and sonic
devices were introduced with the idea of saving precious tooth
structure, but these methods didn’t seem to satisfy the problem
with extra canals, anastomoses, multiple apical foramina, and
lateral canals. Recent articles have been written in peer-reviewed
literature describing a new way to effectively remove canal debris
from all of these areas with minimal additional instrumentation,
utilizing a stripped radial firing Er:YAG laser tip (Fotona D.D.).2-5
This new technology, photon-induced photoacoustic streaming
(PIPS), was presented by its developers, DiVito and Colonna, at
the World Congress of Minimally Invasive Dentistry meeting
in San Francisco, in August, 2009. PIPS technology creates a
turbulent 3-dimensional flow of irrigants in the canals. These
extremely short bursts of laser energy are directed down into the
canals, and the action pumps the tissue debris out of the canals
and cleans, disinfects, and sterilizes each main canal to the apex
and out into the lateral canals, dentin tubules, and anastomoses. This movement is achieved without the need to place the
stripped radial firing laser tip (PIPS tip) into the canal, as with
conventional hand and ultrasonic systems; rather, the PIPS tip
stays in the coronal aspect of the access preparation only. This
allows the clinician to better debride and decontaminate the
root canal system without the need to overshape and enlarge
the preparation needed for adequate access to the apical onethird. A canal system prepared this way will allow the use of a
hydrophilic resin filler system to obturate all the prepared canals,
accessory canals, apical foramina, and anastomoses.
In endodontic therapy, dentists who work on root canals have
been working nearly blind in a deep, dark hole that has all kinds
of nooks and crannies, using only tactile senses to be effective.
Studies on root canal success rates range all over the board,
depending on if they are multicentered, single site, or single
operator, and the parameters describing success vary greatly with
all of these studies.6-9 These success rates might only relate to
patient comfort or how the tissues have appeared to heal with
8
January/February 2013
General Dentistry
www.agd.org
2-dimensional X-rays, and not indicative of the full removal of
debris. Three-dimensional viewing, using cone-beam computerized tomography (CBCT), of the endodontically treated teeth,
shows more pathology than has been previously believed. Often,
accessory canals, lateral canals, and apices have been missed, and,
consequently, organisms capable of reinfection are left behind.
Hopefully these organisms have been entombed in the treated
teeth and will eventually die, but in many cases all that is needed
is an opportunity, such as a “dip” in the patient’s immune system,
or loss of a coronal seal, for reinfection to occur. Recent articles in
peer-reviewed journals presented protocols using the PIPS technology that demonstrated how this technology virtually sterilizes
the root canal system.2-5,10 This new process, along with careful
obturation, may cause the success rates exhibited in these studies
to climb to even higher levels in future studies.
Since the root forms and canal systems are so varied in size,
shape, and patterns, the ability to effectively instrument with conventional systems is nearly impossible. Fig. 1 shows the variation
of these canal forms, and the inherent difficulty of trying to reach
a file into any one of these lateral canals, the multiple apical openings, and the cross-bridging between the canals. The only way
around these canal patterns with conventional root canal treatments (RCTs) is to remove more tooth structure, which thereby
weakens the tooth. However, with PIPS technology protocols,
the canal systems are cleaned out with the turbulence created by
the Er:YAG laser PIPS tip (Fig. 2). Consequently, the canals are
left with very bondable surfaces, as shown by scanning electron
microscopal (SEM) analysis (Fig. 3 and 4). Fig. 4 not only shows
how clean the tooth canal surface is after the PIPS protocols but
also offers a view into a lateral canal.
Fig. 1. Intricacies of
the canal system on
a maxillary molar
using a differential stain
technique.
Fig. 2. PIPS tip in laser handpiece showing the
stripped and radial firing tip.
Fig. 3. After laser-activated irrigation using PIPS, an
SEM analysis reveals extremely clean collagen fibril
networks of bondable surfaces.
Fig. 4. Well-cleaned lateral canal after laseractivated irrigation using PIPS.
Fig. 5. SEM of surface biofilm infected with
Enterococcus faecalis.
Fig. 7. SEM surface photo of an E. faecalis-infected
tooth, after laser-activated irrigation using PIPS
protocol, showing extremely clean dentinal tubules.
Fig. 8. Clarified root after PIPS and placement of
flowable sealer demonstrating the minimally invasive
3-dimensional obturation of the intricate apical
morphology.
Bacteria in dentinal tubules
Fig. 6. Left: SEM photo showing E. faecalis
infecting dentinal tubules. Right: Confocal image
of same sample shown on the left, demonstrating
penetration of live (green) E. faecalis deep into the
dentinal tubules.
Confocal microscopal studies have validated the effectiveness of
the PIPS technique in killing bacteria deep into the dentin tubules
and canal systems.10 Extracted teeth, with their canals opened to
the outside, were stored in a culture medium of Enterococcus faecalis, which resulted in severely infected surfaces (Fig. 5). A confocal
micrograph of the dentinal tubules shows the deep penetration of
bacteria (Fig. 6). After the tooth has been put through the entire
PIPS protocol, there is nothing notable left on the canal surfaces
(Fig. 7). With virtually no biofilm and bioburden left in the intricate canal systems, the tooth can be filled thoroughly with hydrophilic root canal resin filling materials. The canal surface prepared
in this way allows for these free-flowing materials to reach deep into
the open dentinal tubules and out into lateral canals and apices,
sealing the canal system thoroughly. When a tooth has been treated
using the PIPS protocol and subsequently filled with hydrophilic
resin filling material, a close-up view through the clarified tooth of
the fill of the canal systems shows the ability of these procedures to
reach deep into areas that cannot be reached by a file. Fig. 8 shows
the apex of one of these teeth and illustrates the ability of the PIPS
process to open up and fill canals, apices, and lateral canals that
used to be either extremely difficult or very time consuming to fill.
Looking at the overall procedures involved in the use of conventional or rotary endodontics, one of the tenets of success has
been the ability to get straight-line access of the canals to keep
the flex of the rotary instruments to a minimum. These processes
remove a significant amount of coronal structure that leaves the
tooth weaker and more prone to fracture.11-13
Many new irrigation systems and chemical lavage techniques
have been brought to market to help remove the materials from
these areas that are not addressed with many of the systems. All of
these new processes can be incorporated into the simple process
of utilizing a modified Er:YAG laser and the PIPS technique.
The actual process of utilizing the PIPS procedure is as follows. First, an anesthetic is delivered to create profound anesthesia to the tooth requiring root canal treatment. The area is
carefully isolated with a rubber dam to prevent not only leakage
of intraoral fluids into the canal, but also to keep fluids from
entering the mouth once they are being activated with the PIPS
laser energy. The patient is fitted with laser radiation safety
glasses for the prevention of any inadvertent use of the laser
and, more importantly, to protect the patient from any splatter
of the PIPS-activated solutions.
www.agd.org
General Dentistry
January/February 2013
9
The tooth is opened to the pulp chamber wide enough to allow
access to all the canals with the PIPS tip and also to allow files
to be placed to the apex to determine the working length and to
locate constrictions. Once the working length is established for all
of the canals, the canals can be opened with filing to accommodate a size 20 file at the working length. The PIPS protocol is then
initiated to remove debris and sterilize the canals. This procedure
is done with low energy levels so that it is virtually subablative.
Consequently, the PIPS energy cleans out the canal systems using
the acoustic shock and the turbulence created within the canals
with these fluids. The first solution to be utilized in the PIPS
protocol is sodium hypochlorite (NaOCl). This solution is placed
in the pulp chamber and the PIPS tip is activated in the chamber
aiming at the canals. High volume suction is utilized to keep the
NaOCl and canal debris spatter from reaching areas outside the
rubber dam owing to the turbulence of the acoustic shock. Extra
NaOCl is syringed into the pulp chamber to replenish the solution that is pulsed out of the access by the PIPS technique. The
pulsed energy is utilized for a very specific number of cycles and
times using the recommended PIPS protocol.
The NaOCl is evacuated from the canals, the chamber is rinsed
with water, and the PIPS tip is activated to remove the leftover
NaOCl and canal debris. Once the canal is cleaned out, a chelating agent, EDTA in a fluid form, is placed into the canals and
pulp chamber and the PIPS tip is activated again to open up the
dentinal tubules to give access to more of the canal anatomy. Once
the EDTA has been pulsed, the canal system is rinsed with water
and the PIPS tip is activated to remove any remaining EDTA
materials so that the tooth can be bonded effectively.
The canal is dried, but not desiccated, with extra-fine paper
points, a good quality hydrophilic resin cement root canal filler is
placed into the canals, and a gutta-percha point is placed so that
the resin can be displaced apically and laterally to help in obturation of the lateral and apical canals as well as the anastomoses
within the canal systems.
The PIPS procedure described in this article minimally opens up
the coronal aspect of the tooth, then cleans and allows the thorough
obturation of the canal system to prevent future issues. This fits well
into the MIDB philosophy. MIBD can be included in all areas
of dentistry, including endodontics, as shown in this article. The
PIPS procedure isn’t the only way to endodontically subscribe to
the MIBD philosophy, but this process creates a situation in which
very little hard tooth structure is removed and the soft tooth structure is selectively removed along with any pathologic materials that
are in the canal system. Lasers are becoming more involved daily in
our lives and Er:YAG lasers have a wide range of uses beyond the
endodontic procedures described within this article. Future MIBD
articles will, over time, include information on the use of lasers as a
minimally invasive technique in hard- and soft-tissue applications.
10
January/February 2013
General Dentistry
Author information
Dr. Malterud is in general practice in St. Paul, Minnesota. He
has lectured and published about minimally invasive dentistry for
more than 17 years.
Acknowledgments
The author wishes to thank Drs. DiVito and Colonna for their
help in collating information and the pictures used in this article.
References
1. Malterud MI. Minimally invasive dentistry—a biomimetic approach. Gen Dent.
2012;60(3):186-187.
2. Peters OA, Bardsley S, Fong J, Pandher G, Divito E. Disinfection of root canals with photon-initiated photoacoustic streaming. J Endo. 2011;37(7):1008-1012.
3. DiVito E, Peters OA, Olivi G. Effectiveness of the erbium:YAG laser and new design
radial and stripped tips in removing the smear layer after root canal instrumentation.
Lasers Med Sci. 2012;27(2):273-280.
4. DiVito E, Crippa R, Iaria G, Kaitsas V, Benedicenti S, Olivi G. Lasers in endodontics.
Roots. 2012;1:38-44.
5. DiVito E, Colonna MP, Olivi G. The photoacoustic efficacy of an Er:YAG laser with radial
and stripped tips on root canal dentin walls: an SEM evaluation. J Laser Dent.
2001;19(1):156-161.
6.Ricucci D, Russo J, Rutberg M, Burleson JA, Spangberg LS. A prospective cohort study
of endodontic treatments of 1,369 root canals: results after 5 years. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2011;112(6):825-842.
7. Bernstein SD, Horowitz AJ, Man M, et al; Practitioners Engaged in Applied Research
and Learning (PEARL) Network Group. Outcomes of endodontic therapy in general
practice: a study by the Practitioners Engaged in Applied Research and Learning
Network. J Am Dent Assoc. 2012;143(5):478-487.
8.Lazarski MP, Walker WA 3rd, Flores CM, Schindler WG, Hargreaves KM. Epidemiological
evaluation of the outcomes of nonsurgical root canal treatment in a large cohort of
insured dental patients. J Endod. 2001;27(12):791-796.
9. Ng YL, Mann V, Rahbaran S, Lewsey J, Gulabivala K. Outcome of primary root canal
treatment: systematic review of the literature – part 1. Effects of study characteristics
on probability of success. Int Endod J. 2007;40(12):921-939.
10. Jaramillo DE, Aprecio RM, Angelov N, DiVito E, McClammy TV. Efficacy of photon induced photoacoustic streaming (PIPS) on root canals infected with Enterococcus faecalis: a pilot study. Endod Pract. Available at: http://www.endopracticeus.com/web/
continuing-education/ce-articles/334-efficacy-of-photon-induced-photoacousticstreaming-pips-on-root-canals-infected-with-enterococcus-faecalis-a-pilot-study.html.
Accessed Nov. 12, 2012.
11.Topcuoglu HS, Arslan H, Keles A, Koseoglu M. Fracture resistance of roots filled with
three different obturation techniques. Med Oral Patol Oral Cir Bucal. 2012;17(3):e528e532. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3476110/. Accessed
November 12, 2012.
12.Wu MK, Shemesh H, Wesselink PR. Limitations of previously published systematic reviews evaluating the outcome of endodontic treatment. Int Endod J. 2009;42(8):656666.
13.Taha NA, Palamara JE, Messer HH. Fracture strength and fracture patterns of root filled
teeth restored with direct resin restorations. J Dent. 2011;39(8):527-535.
Manufacturer
Fotona D.D., Slovenia
386.1.500.91.00, www.fotona.com
www.agd.org
Pharmacology
Diet drugs Belviq and Qsymia receive FDA approval:
what dentists need to know
Richard L. Wynn, PhD
T
he diet drug lorcaserin, known as Belviq (Arena
Pharmaceuticals, Inc.) was approved in June 2012, and the
diet drug known as Qsymia (active drugs phentermine and
topiramate; Vivus Inc.) was approved in mid-July 2012. They
were both approved for chronic weight management, as an adjunct
to a reduced-calorie diet and increased physical activity, in patients
with either an initial body mass index (BMI) of ≥30 kg/m2, or an
initial BMI of ≥27 kg/m2 and at least one weight-related comorbid
condition (such as sleep apnea, hypertension, dyslipidemia, or type
2 diabetes). Both of these drugs work through the central nervous
system to suppress appetite, by either activating serotonin receptors (Belviq) or enhancing norepinephrine levels (Qsymia).
Previous diet drugs such as fen-phen, the common name for a
combination of phentermine (Loramin; still available) and fenfluramine (Pondimin; removed from the US market), as well as
Redux (dexfenfluramine; also removed from the US market), were
associated with cardiac valvular defects and potential hypertension, and were a source of concern for both medical doctors and
dentists. According to the American Heart Association recommendations, dental patients who had formerly used fen-phen
“would require prophylactic antibiotic before invasive dental
procedures, including oral prophylaxis.”1 This column reviews the
reported adverse reactions caused by Belviq and Qsymia, and if
there should be any concerns for dentists and their patients.
Lorcaserin (Belviq)
Lorcaserin (Belviq) works through activation of the 5-hydroxytryptamine (5-HT, or serotonin) receptor subtype 2C (5-HT2C),
which decreases food intake through the proopiomelanocortin
system of neurons.2 Lorcaserin is a small molecular agonist of the
serotonin 2C receptor that is designed to promote weight loss.
Other serotonin receptors have been associated with appetite,
such as the 5-HT2A and 5-HT2B receptors.3 Previously, fenfluramine, a component of fen-phen, was shown to activate the
5-HT2B receptors, which resulted in serotonin-associated valvulopathy.4 Fenfluramine has since been removed from the market.
Lorcaserin selectively activates central 5-HT2C receptors with a
selectivity of 15× that of fenfluramine for 5-HT2A receptors and
100× that of fenfluramine for the 5-HT2B receptors.2 According
to a report in the New England Journal of Medicine in 2010
by Smith et al, a 12-week clinical trial involving obese patients
showed that lorcaserin was associated with dose-dependent weight
loss without any apparent effects on heart valves.2
The trial by Smith et al randomly assigned 3,182 obese or
overweight adults into 2 groups: one to receive lorcaserin at a
dose of 10 mg and the other to receive a placebo, twice daily for
52 weeks.2 All subjects underwent diet and exercise counseling.
At week 52, patients in the placebo group continued to receive
placebo, but patients in the lorcaserin group were randomly
reassigned to receive either placebo or lorcaserin. Primary outcomes were weight loss at 1 year and maintenance of weight
loss at 2 years.
In the Smith et al study, the results at 1 year showed that
47.5% of patients in the lorcaserin group and 20.4% of patients
in the placebo group had lost 5% or more of their body weight.2
Among the patients who received lorcaserin during year 1 and
who had lost 5% or more of their baseline weight at 1 year, the
loss was maintained in more patients who continued to receive
lorcaserin during year 2 (67.9%) than in patients who received
placebo during year 2 (50.3%).2
Echocardiography was used to identify patients in whom
valvulopathy developed. Among the 2,472 patients evaluated
at the 1-year and 1,127 evaluated at the 2-year follow-up, the
rate of valvulopathy was not increased with the use of lorcaserin.
Valvulopathy had developed in 2.7% of patients in the lorcaserin
group and 2.3% of patients in the placebo group at year 1. At
year 2, the rate of valvulopathy was 2.6% in patients receiving
lorcaserin and 2.7% in the placebo group.2
Changes in valvular insufficiency scores for the mitral and aortic
valves did not differ significantly among the study groups during
the trial. No severe mitral or aortic insufficiency was reported.2
In the study by Smith et al, reported adverse drug reactions in
3% or more of subjects included headache, dizziness, nausea, or
dry mouth.2 The study showed no elevations in blood pressure,
nor any increases in heart rate in study subjects.2
Smith et al concluded that lorcaserin used in conjunction with
behavioral modification was associated with significant weight
loss and improved maintenance of weight loss.2 Lorcaserin caused
no significant increase in the incidence of valvulopathy. This
observation supports the finding that valvulopathy is not associated with activation of the 5-HT2C receptor.
Dental considerations
At this time there is no information to warrant any precautions in
using local anesthetic with vasoconstrictor and no effects or complications have been reported to require any special precautions in
dental treatment. Lorcaserin has no reported addictive liabilities
and is not classified as a controlled substance.2
Qsymia
Qsymia is the brand name for a combination of phentermine
and topiramate in a controlled-release pill taken once a day.
Phentermine is a stimulant and topiramate is available as an
anti-seizure drug under the brand name of Topamax. Qsymia is
supplied in three different dose combinations of phentermine/
topiramate: 3.75 mg/23 mg, 7.5 mg/46 mg, and 15 mg/92 mg.
www.agd.org
General Dentistry
January/February 2013
11
This is the second time that phentermine has been combined
with another drug. The first was in the drug fen-phen where
it was combined with fenfluramine.3 This drug was removed
from the market due to fenfluramine-associated serious heart
valve problems.4
Phentermine is a sympathomimetic amine with pharmacologic
properties similar to the amphetamines. The mechanism of action
in reducing appetite appears to be secondary to central nervous
system effects, including stimulation of the hypothalamus to
release norepinephrine.5 The mechanism of action of topiramate
on chronic weight management is not known. Labeling states that
topiramate causes appetite suppression through a combination
of γ-aminobutyric acid (GABA) receptor activity, modulation
of voltage-gated channels, inhibition of excitatory glutamate
receptors, and inhibition of carbonic anhydrase.5 Phentermine
alone has been on the market since the 1960s and is presently
available as a generic drug and under the US brand names of
Adipex-P (Teva Pharmaceuticals USA, Inc.) and Suprenza (Alpex
Pharma SA) and the Canadian brand name Ionamin (Celltech
Pharmaceuticals Inc.).6
Qsymia adverse reactions
Qsymia was approved with a designation of a Risk Evaluation
and Mitigation Strategy (REMS). This means that both prescribers and patients must be educated about the increased risk
of birth defects associated with first-trimester exposure to the
drug, along with the need to avoid pregnancy while taking it.
Also, the drug will only be dispensed through specially certified
pharmacies.5 Fetal exposure to topiramate has been linked to an
increased risk for cleft lip with or without cleft palate.5 Women
who might become pregnant are being advised to use effective
birth control while on the drug, and monthly pregnancy tests
are also being recommended, along with a negative pregnancy
test before starting the medication. Qsymia is listed under
FDA Pregnancy Category X, indicating that studies in animals
or humans have identified fetal abnormalities associated with
the drug.5 Adverse reactions of Qsymia leading to treatment
discontinuation included blurred vision, headache, irritability,
dizziness, paresthesia, insomnia, depression, or anxiety. Some
postmarketing reports included elevation of blood pressure.5
Adverse reactions of interest to dentists
According to its labeling, Qsymia can cause an increase in
resting heart rate.5 A higher percentage of Qsymia-treated
overweight and obese adults experienced heart rate increases
from baseline of more than 5, 10, 15, and 20 beats per minute
compared to placebo-treated overweight and obese adults. The
clinical significance of a heart rate elevation with Qsymia treatment is presently unclear. Regular measurement of resting heart
rate is recommended for all patients taking Qsymia, and patients
should inform health care providers of any palpitations or a rapid
heartbeat while at rest. Qsymia does not affect cardiac electrophysiology and does not affect QTc interval. Although Qsymia
does not seem to be a risk factor in cardiac arrhythmias, it is not
recommended for people with recent or unstable heart disease
or stroke. Adverse reactions that were reported more frequently
than placebo during first year of treatment (n = 1580) were
12
January/February 2013
General Dentistry
paresthesia (experienced by ≤20% of patients), dysgeusia (specifically metallic taste, experienced by ≤9 % of patients), and dry
mouth (experienced by ≤19% of patients).5 The paresthesia was
characterized as tingling in hands, feet, or face, and occurred
in 4%, 14%, and 20% of patients treated with Qsymia from
lowest to highest doses, respectively.5 Metallic taste occurred in
1%, 7%, and 9% of patients treated with Qsymia from lowest to
highest doses, respectively.5 Concomitant use of benzodiazepines
with phentermine or topiramate may potentiate CNS depression.5 Qsymia is controlled by Schedule IV of the Controlled
Substances Act. The phentermine component has a known
potential for abuse. It is related chemically and pharmacologically to the amphetamines. Amphetamines have been widely
abused and the possibility of abuse of phentermine should be
kept in mind when using Qsymia for weight control.5
Fen-Phen
The combination drug fen-phen contained fenfluramine and
phentermine. In 1997, fenfluramine was voluntarily withdrawn
from the market. The action was based on findings from physicians
who evaluated with echocardiograms patients taking fenfluramine.
The findings indicated that approximately 30% of patients had
abnormal echocardiograms, even though they had no symptoms.3,4
Under normal conditions, <1% of patients would be expected
to show signs of heart valve disease. The findings suggested that
fenfluramine was the likely cause of the heart valve problems. The
type of valve damage had only been seen before in persons who
were exposed to large amounts of serotonin. Fenfluramine increases
the availability of serotonin. The phentermine component was not
implicated in the cardiac problem, and therefore was allowed by the
FDA to be kept on the market as a single agent.
Phentermine as single agent
As mentioned above, phentermine is also presently available as a
single agent under the US brand names Adipex-P and Suprenza
and the Canadian brand name Ionomin. It is also generically
available. The following information on phentermine can be
found on the LexiComp dental drug database.6 Phentermine can
be used as a short-term (a few weeks) adjunct therapy in obese
patients with an initial body mass index (BMI) ≥30 kg/m2 or ≥27
kg/m2 in the presence of other risk factors (including diabetes,
hyperlipidemia, and controlled hypertension); therapy should be
used in conjunction with a comprehensive weight-management
program. Phentermine is a sympathomimetic amine with pharmacologic properties similar to the amphetamines. The mechanism of action in reducing appetite appears to be secondary to the
CNS effects, including stimulation of the hypothalamus to release
norepinephrine. When taking phentermine, vasoconstrictors
should be used with caution. Amphetamines enhance the sympathomimetic response of epinephrine and norepinephrine, leading
to potential hypertension and cardiotoxicity.6
Adverse reactions of interest to dentists
The key adverse events related to dental treatment in conjunction with phentermine are xerostomia (normal salivary
flow resumes upon discontinuation) and unpleasant taste.
Hypertension may present in ≤10% of patients.6
www.agd.org
The proopiomelanocortin system in
appetite regulation
Lorcaserin (Belviq) works through activation of the 5-hydroxytryptamine (5-HT, or serotonin) receptor subtype 2C (5-HT2C),
which decreases food intake through the proopiomelanocortin
system of neurons.2 Proopiomelanocortin is a polypeptide within
the pituitary gland that acts as the precursor for the production
of a group of peptide hormones known as the melanocortins.7
The melanocortins exert their effects by binding to and activating
the melanocortin receptors. There are at least 5 of these receptors,
including MC1R, MC2R, MC3R, MC4R, and MC5R.7 The
functions of these receptors are modulated by the family of melanocortin peptides. The melanocortin system is involved in a diverse
number of physiological functions, including pigmentation, energy
homeostasis, inflammation, temperature control, and sexual function.8 The MC4R receptor located in the brain appears to be the
key melanocortin receptor involved in regulating food intake.9 The
5-HT2C receptor, when stimulated, promotes a decrease in food
intake via activation of MC4R.10 Lorcaserin appears to suppress
appetite by acting at the 5-HT2C receptor to activate MC4R.2
Author information
Dr. Wynn is a professor of pharmacology, Department of Oral
Craniofacial Biological Sciences, Dental School, University of
Maryland at Baltimore.
References
1. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines
from the American Heart Association: a guideline from the American Heart Association
Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research
Interdisciplinary Working Group. Circulation. 2007;116(15):1736-1754.
2.Smith SR, Weissman NJ, Anderson CM, et al. Multicenter, placebo-controlled trial of
lorcaserin for weight management. N Engl J Med. 2010;363(3):245-256.
3.Cardiac valvulopathy associated with exposure to fenfluramine or dexfenfluramine:
U.S. Department of Health and Human Services interim public health recommendations, November 1997. MMWR Morb Mortal Wkly Rep. 1997;46(45):1061-1066.
4.Connolly HM, Crary JL, McGoon MD, et al. Valvular heart disease associated with fenfluramine-phentermine [published correction appears in N Eng J Med. 1997;337(24):
1783]. N Eng J Med. 1997;337(9):581-588.
5. Vivus, Inc., Mountain View CA; Qsymia [prescribing information]. 2012. Available at:
http://www.qsymia.com/pdf/full-prescribing-information.pdf. Accessed Aug. 16, 2012.
6.Wynn RL, Meiller TF, Crossley HL, eds. Drug Information Handbook for Dentistry. 18th
ed. Hudson, OH: Lexi-Comp, Inc; 2012:1027.
7. Xu Y, Jones JE, Kohno D, et al. 5-HT2CRs expressed by pro-opiomelanocortin neurons
regulate energy homeostasis. Neuron. 2008;60(4):582-589.
8. Heisler LK, Cowley MA, Tecott LH, et al. Activation of central melanocortin pathways by
fenfluramine. Science. 2002;297(5581):609-611.
9.Lam DD, Przydzial MJ, Ridley SH, at al. Serotonin 5-HT2C receptor agonist promotes
hypophagia via downstream activation of melanocortin 4 receptors. Endocrinology.
2008;149(3):1323-1328.
10.Rothman RB, Baumann MH. Therapeutic and adverse actions of serotonin transporter
substrates. Pharmacol Ther. 2002;95(1):73-88.
Manufacturers
Alpex Pharma SA, Luzano, Switzerland
091.935.51.10, www.alpex.com
Arena Pharmaceuticals, Inc., San Diego, CA
858.453.7200, www.arenapharma.com
Celltech Pharmaceuticals Inc., Rochester, NY
585.475.9000, www.celltechgroup.com
Teva Pharmaceuticals USA, Inc., Wales, PA
888.838.2872, www.tevagenerics.com
UCB-USA, Rochester, NY
800.234.5535, www.ucb-usa.com
Vivus Inc., Mountain View, CA
650.834.5200, www.vivus.com
www.agd.org
General Dentistry
January/February 2013
13
Restorative Dentistry
Implant impression techniques
including a customized impression
tray for nonparallel implants
Bruce W. Small, DMD, MAGD
Author’s note: This month’s Restorative Dentistry column will be my last as a regularly scheduled columnist in General Dentistry. I have enjoyed
sharing information that I sincerely hope has helped some of you over the 15 years that I have been writing this column. It is time to make room for
someone else who hopefully will have the same passion for our profession and love of sharing knowledge about excellence in restorative dentistry that
I have. Thank you, Academy of General Dentistry, for the honor of allowing me to write this column, and I look forward to continuing to support our
organization in every way I can.
S
ince the middle 1980s when Branemark introduced his
“osseointegrated” implant technique to dentistry, more and
more implants have been placed by dentists worldwide.1
Many different types of fixtures, of various shapes and surface
treatments, as well as of different connection types, have been
introduced over the last 30 years. This month’s column will briefly
review both open- and closed-tray impression techniques as well
as construction of an impression tray for a multiple-implant case
with nonparallel-placed implants.
Open tray vs. closed tray
Open tray and closed tray are the 2 basic methods of taking an
impression of an osseointegrated implant. A new, third method
has also been introduced (optical or digital impressions), which
will be mentioned later.
The open technique uses a tray with a hole or holes for the
impression copings to go through that are loosened and removed
with the tray. This is also called the pick-up type of impression, as
we are picking up the impression copings. The closed method is
similar to a crown and bridge impression, utilizing a tray without
any opening for the impression copings. A stock or customized tray
is placed over the implant and adjacent teeth or tissue and removed.
Following removal, the coping is placed back into the impression
and a laboratory analog is added prior to pouring the model.
For clinical cases with 3 or fewer implants, the majority of
research shows very little difference in the accuracy of open or
closed tray techniques.2 When 4 or more implants are being
impressed at the same time, the open tray or pick-up technique
results in greater accuracy.3 In addition, some authors recommend
connecting the impression copings with an autopolymerizing
resin prior to taking the impression.4,5
Fig. 1. Implant verification jig, ready for placement.
Fig. 2. Anterior retracted view of patient seeking restorative dentistry.
14
January/February 2013
General Dentistry
Fig. 3. Maxillary occlusal view of patient prior to extractions.
www.agd.org
Fig. 4. Maxillary occlusal view of implant locations
and angles.
Fig. 7. Baseplate wax placed on
maxillary model.
Fig. 5. Maxillary study model of patient.
Fig. 8. Slots cut into tray to allow passive placement
of tray.
By connecting the impression copings, the potential for any
unwanted movement is reduced, including leaving 1 of the copings in the mouth. If there is any doubt about the accuracy of the
impression, an implant verification jig (Fig. 1) can be constructed
on the master model and placed in to check the fit through clinical inspection and radiographs.
Recently, Lee & Gallucci and Ono et al compared digital or
optical impression methods and concluded that they were within
an “acceptable accuracy range.”6,7 Lee & Gallucci discovered that
60% of study participants preferred the digital impression technique compared to 7% who preferred conventional methods.6
Customized tray construction
Fig. 6. Black marker arrows indicating implant
locations.
Fig. 9. Occlusal view of completed customized tray.
Fig. 10. Maxillary occlusal view of 4 impression copings showing
nonparallel alignment.
A female patient was referred to our office for an implant restorative consultation (Fig. 2 and 3). It was decided to construct two
implant-supported bridges on both the right and left maxillary
arches following the removal of hopeless teeth No. 5, 11, and 15.
The patient was referred to an oral surgeon, who removed
the teeth and, following an appropriate healing time, placed 4
implants. Unfortunately, the 4 implants were not placed parallel
to each other, making a closed-tray impression impossible (Fig. 4).
Due to the position of the implants, the lack of a mucobuccal fold,
and the presence of a few remaining teeth, it was decided to make a
customized tray to be used for an open tray (pick-up) impression.
The model was prepared and the differences in angles of the
implants were evaluated (Fig. 5). The 2 on the left side were
within 10° of each other; therefore, the goal was to have 1 slot
for the 2 copings on the left and 2 slots for the 2 copings on the
right. The tray would be seated over the left side first, then rotated
to the right between the 2 copings present.
A black-tip marker was used on the side of the model to
indicate the implant locations (Fig. 6), then a layer of baseplate
wax was adapted to the model (Fig. 7). A light-cured custom
tray material was draped over the model and cured in the laboratory. Both slots on the left side and the 2 slots on the right
side were cut using a carbide acrylic bur (Fig. 8 and 9). The
tray was placed and path of insertion checked (Fig. 10 and 11).
A small amount of periphery wax was placed around the
impression retaining screws to keep impression material out of
the holes (Fig. 12).
www.agd.org
General Dentistry
January/February 2013
15
Fig. 11. Placement of customized tray.
Fig. 12. Blue periphery wax placed on impression
retaining screws.
Fig. 14. Syringe loaded with a polyether impression material.
A few small holes were drilled in the palate area of the tray for
relief of the impression material. The tray was coated with an
adhesive (Fig. 13) and loaded with a polyether impression material (Fig. 14). The tray was carefully placed over the impression
copings, teeth, and edentulous areas, and held until set. The
impression retaining screws and the tray were removed (Fig. 15).
Summary
The use of implants in restorative dentistry has changed the way
many dentists treat patients. Today’s state-of-the-art implants have
become the first choice for replacing teeth. Determining which type
of impression technique is optimal, and learning how to take an
accurate impression increases the success of any implant procedure.
The case report discussed described an open-tray impression technique for nonparallel implants. This concept can be
expanded to accommodate additional fixtures if necessary and
makes taking of impressions easier for the operator and more
tolerable for the patient.
Fig. 15. Finished impression ready for lab analogs
and pouring.
of New Jersey. He also is on the Board of Advisors and a visiting
faculty member, Pankey Institute, Key Biscayne, Florida.
References
1. Branemark PI. Osseointegration and its experimental background. J Prosthet Dent.
1983;50(3):399-410.
2.Lee H, So JS, Hochstedler JL, Ercoli C. The accuracy of implant impressions: a systematic
review. J Prosthet Dent. 2008;100(4):285-291.
3. Vigolo P, Fonzi F, Majzoub Z, Cordioli G. An evaluation of impression techniques for
multiple internal connection implant prostheses. J Prosthet Dent. 2004;92(5):470-476.
4.Tarib NA, Seong TW, Chuen KM, Kun MS, Ahmad M, Kamarudin KH. Evaluation of
splinting implant impression techniques: two dimensional analyses. Eur J Prosthodont
Restor Dent. 2012;20(1):35-39.
5.Al Quran FA, Rashdan BA, Zomar AA, Weiner S. Passive fit and accuracy of three dental
implant impression techniques. Quintessence Int. 2012;43(2):119-125.
6.Lee SJ, Gallucci GO. Digital vs. conventional implant impressions: efficiency outcomes
[published online ahead of print February 22, 2012]. Clin Oral Implants Res. 2012. doi:
10.1111/j.1600-0501.2012.02430.x.
7.Ono S, Yamaguchi S, Kusumoto N, Nakano T, Sohmura T, Yatani H. Optical impression
method to measure three-dimensional position and orientation of dental implants
using an optical tracker [published online ahead of print June 19, 2012]. Clin Oral
Implants Res. 2012. doi: 10.1111/j.1600-0501.2012.02519.x.
Author information
Dr. Small is in private practice in Lawrenceville, New Jersey, and is
an adjunct professor at the University of Medicine and Dentistry
16
January/February 2013
General Dentistry
Fig. 13. Adhesive painted onto inside of tray.
www.agd.org
Prosthodontics
Digital implant impressions and
zirconia implant restorations
Samuel M. Strong, DDS, DICOI
D
igital scans for natural tooth-borne dentistry have been utilized for over a decade by restorative clinicians. Although the
market penetration of these digitized impressions has been
relatively small, their usage has steadily increased in recent years.
These digital images of teeth prepared for crowns and fixed bridges
have either been incorporated with in-office milling machines
to fabricate the final restoration in 1 appointment or emailed to
dental laboratories. In the latter cases, the digital scans of teeth
preparations can be converted into working models or these
computerized images can be used by themselves, without models,
for prosthesis fabrication. This digital scanning technology is now
also applied to impressions for dental implant restorations. For
this application, a specialized impression coping is placed into the
dental implant for the digital image to be captured.
The clinician can choose between fabrication of a cementretained or a screw-retained implant crown from the digital image
and model format. In recent years, the potential for entrapment
of cement subgingivally around implant crowns has received considerable interest. Minimal submersion below the gingival crest is
advocated for the cement-retained implant crown, particularly in
the non-cosmetic posterior areas of the maxilla or mandible.
Screw-retained implant crown selection can avoid the problems
associated with peri-implantitis, bone loss, and possible implant
failure due to cement trapped below the gingival crest around
implants. In addition, the use of a monolithic zirconia-milled
material can provide appropriate fracture resistance for posterior
site implant restorations.
Fig. 1. Panoramic radiograph post-orthodontic therapy with
spacing in the No. 12, 13, 20, and 28 sites.
Case study
A 17-year-old male with congenitally missing teeth had recently
completed a long-term orthodontic treatment. The orthodontist
was unable to close all spaces, leaving site No. 12, 13, 20, and 28
vacant as receptive areas for implant placement (Fig. 1). The patient
was referred to an oral surgeon for evaluation of the surgical phase
for implant placement. A surgical template was fabricated to aid the
surgeon in placement of the implants. This appliance was also used
as a space maintainer during the implant integration period to prevent teeth adjacent to the implants from moving or collapsing into
the edentulous spaces (Fig. 2). Implants (Nobel Replace Internal
Tri-channel connection 5.0 mm × 10 mm implants, Nobel Biocare
USA, LLC) were placed in the No. 20 and 28 sites by the surgeon.
Due to the deficit of available bone and maxillary sinus size, a
large bone graft was required in the No. 12 and 13 areas prior to
placement of an implant. Therefore, the mandibular implants were
integrated and restored prior to the maxillary implant.
Four months after placement, the mandibular implants
were torque tested at 35 Ncm with a torque wrench (Nobel
Biocare USA, LLC) to confirm their readiness for restoration.
An implant-level digital scan impression was procured for the
No. 28 site. A standard polyvinyl siloxane (PVS) impression was
made of the No. 21 site as a comparison for ease of use. A scan
body (Glidewell Laboratories) was connected into the No. 28
site after removal of the healing abutment (Fig. 3). The retaining
screw for the scan body was tightened by hand and a radiograph
made of the connection.
Fig. 2. Surgical template used for guidance in placing
the mandibular implants and as a space maintainer
during the implant integration period.
www.agd.org
General Dentistry
Fig. 3. A digital scan body was seated
into the No. 28 implant site in order
to make a digital impression using the
iTero digital scan system.
January/February 2013
17
Fig. 4. Virtual computer design of No. 28 crown showing occlusal, buccal, and
lingual contours.
Fig. 6. Occlusal view of the No. 28 Bruxzir
screw-retained implant crown. The screw access hole
has been sealed with Teflon tape over the retaining
screw and light cured composite.
Fig. 7. Buccal view of the No. 28 Bruxzir screwretained implant crown.
An iTero digital camera (Align Technology, Inc.) was used to
create a digital image of the scan body, adjacent quadrant teeth,
and opposing teeth. A digital occlusal bite registration was also
procured with the scanning camera (Fig. 4). Upon completion
of the in-office digital scanning, the image was sent to an iTero
facility, where the image was refined and then sent to a dental
laboratory (Glidewell Laboratories).
Our prescription called for the lab to fabricate a screw-retained
monolithic zirconia crown (Bruxzir, Glidewell Laboratories) for
No. 28. The lab technician designed the implant crown with
computer software integrating the iTero digital image. The emergence profile, interproximal contacts, and occlusal surface design
were completed on a virtual model by computer (3Shape Dental
System, 3SHAPE A/S) (Fig. 4 and 5). The final No. 28 implant
crown was then milled, polished, and completed with exterior
stain and glaze. The No. 20 implant crown was completed in
a different lab using a conventional stone model from the PVS
impression and bite registration (Green Dental Laboratory). This
crown was also completed as a monolithic zirconia restoration.
At the patient’s request, both implant crowns were fabricated in
a brighter shade than the adjacent teeth in preparation for an inoffice whitening procedure to be done at a later date (Fig. 6).
18
January/February 2013
General Dentistry
Fig. 5. Virtual computer design of No. 28 crown in occlusion.
Fig. 8. Occlusal view of No. 20 Bruxzir
screw-retained implant crown.
At the delivery appointment, No. 20 and 28 implant crowns
were seated into their respective implants and secured with
retaining screws (Fig. 6-8). Periapical radiographs confirmed
the complete connection of the crowns to the implant platforms (Fig. 9). Occlusion was checked with articulating paper
(AccuFilm, Parkell, Inc.) and shim stock. An implant-protected
occlusion was established to allow only the natural teeth to
occlude initially on light mandibular closure. The patient also
confirmed that his natural occlusal balance was maintained and
felt comfortable.
The retaining screws were torqued to the manufacturer’s recommended 35 Ncm (Nobel Biocare USA, LLC). A Teflon (polytetrafluoroethylene, PTFE) tape strip was placed into each occlusal
access opening in the screw-retained crowns over the retaining
screw head. Light-cured composite was then placed over the
PTFE tape sealing the occlusal opening (Fig. 6).
Following sinus-lift grafting and consolidation in the No. 12-13
area, a single implant was placed into the No. 12 site (Nobel
Replace Internal Tri-channel connection 4.3 mm × 10 mm
implants, Nobel Biocare USA, LLC). The edentulous area was
deemed insufficient to restore with 2 standard sized implants and
crowns. This condition was thoroughly discussed with the patient
www.agd.org
Fig. 9. Periapical radiograph of No. 28 Bruxzir crown shows
complete seating into the Nobel Replace implant.
Fig. 10. The No. 12 screw-retained Bruxzir crown with access hole
sealed using Teflon tape and light cured composite.
and his parents. The decision was made to restore the No. 12 site
and close the entire area between the implant crown and the No.
14 natural tooth, realizing that the mesial-distal dimensions of
the implant crown would be larger than a typical bicuspid restoration. By choosing to restore with a retrievable, screw-retained
crown, the interproximal areas could be modified if necessary due
to hygienic or esthetic concerns.
Three months after placement of the No. 12 implant, a scan
body was placed into the implant and a digital scan procured with
the iTero digital camera. The resulting digital image and model
were sent to Glidewell Laboratories for fabrication of a screwretained Bruxzir crown (Fig. 7). The implant crown emergence
profile, interproximal contacts, and occlusal surface were designed
on the computer and approved for milling of the monolithic zirconia material (Fig. 8). Upon return of the completed restoration
to the dental office, the connection into the No. 12 implant was
performed. The retaining screw was torqued to 35 Ncm, correct
occlusion confirmed, and the screw access opening sealed with
Teflon tape and light-cured composite (Fig. 10).
Digital impressions provide yet another method for accurately
transferring the implant position to a working master cast or
virtual image. The lab technician can then design all aspects of
the final restoration prior to milling. This process, combined
with the use of monolithic zirconia crown material, provides
strength, esthetics, retrievability, and elimination of concerns
about cement retention adjacent to the implant crown.
Author information
Dr. Strong lectures and publishes about restorative and implant
dentistry, and is in private general practice in Little Rock, Arkansas.
Manufacturers
Align Technology, Inc., San Jose, California
408.470.1000, www.aligntech.com
Glidewell Laboratories, Newport Beach, California
800.854.7256, www.glidewelldental.com
Green Dental Laboratory, Heber Springs, AR
800.247.1365, www.greendentallab.com
Nobel Biocare USA, LLC, Yorba Linda, California
800.322.5001, www.nobelbiocare.com
Parkell, Inc., Edgewood, NY
800.243.7446, www.parkell.com
3SHAPE A/S, Copenhagen, Denmark
45.7027.2620, www.3shape.com
www.agd.org
General Dentistry
January/February 2013
19
Ethics
Call of duty
Toni M. Roucka, DDS, MA n Cesar D. Gonzalez, DDS, MS
D
entists often encounter ethical dilemmas that are not necessarily treatment related. We, as health care professionals,
are in a unique position to have a significant impact on
people’s lives; both clinically and personally. Put yourself in Dr.
Miller’s shoes and imagine what you would do in this situation.
Enjoy the case.
Dr. Miller worked at Community Clinic for 8 years. A practice
that serves primarily low income patients, Community Clinic
provided Dr. Miller with difficult but rewarding work. The
dental needs of the population there were overwhelming, but she
felt it was a way to give back to the community. The neighborhood in which the clinic resides had a high crime rate. During
her tenure there, it wasn’t unusual to hear of a shooting or other
incidents occurring nearby. The staff at the clinic, being very
dedicated to their work, took it in stride. For their safety, however, clinic management encouraged staff to walk to and from
the building in the company of others, especially in the evening.
One beautiful fall afternoon was unusually slow at the office.
Dr. Miller and her colleague, Dr. Gira, were on duty and scheduled to work until 5 pm. At 4:30, a 15-year-old male, Joseph, and
his mother walked in. Joseph’s mother, Theresa, stated that Joseph
was playing basketball when he was hit in the mouth and his
front tooth was knocked out. The dental receptionist processed
the new patient paperwork and Joseph and his mother were
swiftly escorted into Dr. Miller’s operatory.
Upon hearing the nature of the emergency, Dr. Miller was
quick to respond. The clinical exam showed that the maxillary
right permanent central incisor was missing and the socket was
beginning to heal over. The maxillary anterior frenum was torn
but also healing. Joseph’s right cheekbone was bruised and his
right eye was black. It was obvious that this injury did not occur
that day. The radiographic examination showed no signs of maxillary fracture nor the presence of a root tip in the socket. The
tooth was cleanly avulsed.
When questioned about the details of the injury, Theresa and
Joseph were very vague with their answers and Dr. Miller suspected they were not being truthful in describing what happened.
Theresa finally admitted that the injury occurred two days prior.
When asked why they didn’t come in right away, Theresa said she
didn’t have time and that Joseph was not in any pain when it happened. In fact, the only reason they came in that day was to “get
a new tooth.” They did not have the avulsed tooth with them as
they said they could not find it. Joseph would not look Dr. Miller
in the eye when answering questions regarding the injury. Joseph
was a tall, tough-looking teenager, but he sat slouched in the
dental chair looking over strangely at his mother with each answer
he gave. Dr. Miller asked Theresa to step out of the room so that
she could speak with Joseph alone, thinking he might be more
20
January/February 2013
General Dentistry
comfortable talking about the injury without his mother there.
However, both Theresa and Joseph became very anxious over this
request and Theresa refused to leave.
Dr. Miller felt uneasy and believed that Theresa and Joseph were
trying to hide something. She also had the feeling that Joseph
may have been intentionally punched in the face and that the
injury was no accident; his black eye was pretty severe. Dr. Miller’s
instinct told her it could possibly be a case of child abuse.
Unsure of exactly how to handle the situation in that moment,
Dr. Miller explained the process of making a provisional partial
denture for Joseph as an initial treatment option until more
definitive treatment could be done. Theresa and Joseph agreed,
impressions and a bite registration were taken, and they were
dismissed for the day. They were scheduled for the partial
delivery in 2 weeks.
After Joseph and Theresa left the office, Dr. Miller’s feelings
of uneasiness persisted. Should she just dismiss her suspicions
of child abuse or should she call the Department of Child
Protective Services (DCPS) and make a report? She weighed
her options (Table).
Relevant facts
As health care providers, dentists not only have the ethical obligation but are also required by law to report suspected cases of child
abuse to the proper authorities. Dental professionals are known as
mandated reporters. The American Dental Association Principles
of Ethics and Code of Professional Conduct (ADA Code) dictates
this obligation, as do laws in all 50 states under the Child Abuse
Protection Act of 1974.1,2
Making the call is difficult­—both diagnostically, as the signs
of physical abuse may be hidden, and emotionally, as the dentist
must get involved in a patient’s personal life. Abuse comes in all
shapes and sizes, so frequently it is not easy to recognize the signs.
There are implications to reporting suspected cases of abuse and
neglect for the child and the family involved, as well as for the
reporting party. Sorting through these issues and making the right
call in any given circumstance is the challenge.
Craniofacial, head, oral and neck injuries are common in cases
of child abuse.2,3,4 In one study of 260 documented cases of
child abuse, more than 65% involved such injuries.3 By nature,
dentists are in a unique position to recognize abuse and report it.
However, less than 1% of reported cases of child abuse are generated by dentists.3 The reasons for this could be:
• the fear of making a false assumption;
• the fear of losing patients;
• the fear of reprisals; or
• being unaware of the obligation to report.2
For fiscal year 2010 in the United States, nearly 700,000 children were confirmed victims of child abuse or neglect.5(p.22) In the
same year, over 1500 died as a result of their injuries.5(p.58)
www.agd.org
Table. Options available to Dr. Miller.
Option 1
Option 2
Option 3
Dismiss her suspicions of child abuse. Make
the partial denture for Joseph and make no further
mention of the injuries.
Report Joseph’s injuries
immediately to DCPS as a possible
case of child abuse.
Wait until Joseph comes back for the partial delivery
to make a decision on referral to DCPS. Reassess the
situation at his next visit.
Rationale
Rationale
Rationale
Joseph was a physically mature teenager and probably
able to take care of himself. His injuries, though severe,
could have been caused by the basketball game as they
stated. Reporting suspected abuse without reasonable
grounds for suspicion could result in embarrassment to
Joseph and his family and consume a tremendous amount
of their time. Dr. Miller also feared for her own safety if
she angered Joseph or his family members unnecessarily.
They might seek some type of revenge.
As a dentist, Dr. Miller is a
mandated abuse/neglect reporter.
Therefore she has to put her
patient’s best interest ahead of
her own and make that difficult
call to DCPS. It is better to err
on the side of safety and the
patient’s welfare in such cases.
Joseph and his mother may be more forthright with
information at the next visit and Dr. Miller may be able
to make a better assessment of the situation. She does
not want to jump to conclusions about abuse just yet.
The partial denture should be ready in 2 weeks and that
is not too long a time to wait to make a more accurate
determination of the events. She could call DCPS at that
time if she deems it appropriate. However, the lack of
intra-oral and extra-oral photographs could jeopardize the
reporting process.
In the current case, the victim may not be considered “typical.” It is not unusual for male teenagers to experience facial
injuries from participation in sports or even from having altercations with peers. Joseph, despite his physical size and appearance, is only 15 years old and therefore still a minor; as such, he
is entitled to protection from abuse and neglect under the terms
mentioned above. It would have been very easy for Dr. Miller
to accept that Joseph received a basketball injury and leave it at
that. However, it was through thorough history-taking as well
as keen observation and diagnostic skills that she was able to
detect a potential problem.
Each state has its own statutory definition of child abuse, as
well as child abuse and neglect reporting statutes. Almost every
state statute also has a penalty for failure to report suspected
cases. While these statutes may differ slightly in detail, they are
similar in content.3
Child abuse is considered an act of commission and is defined
as non-accidental injuries or trauma inflicted on a minor child
by a parent or other caregiver. Child neglect, as defined in state
statutes, refers to acts of omission. Neglect is a failure to provide
adequate care, support, nutrition, or medical or surgical care.2,3
In this case, Dr. Miller suspects Joseph of having been abused
based on the nature of his injuries and the suspicious manner in
which he and his mother were behaving during the course of the
dental appointment.
It is important to mention the fact that each state statute
provides protection to mandated reporters from civil and
criminal liability arising from good faith reports; therefore,
it is always best for a dentist, as a mandated reporter, to err
on the side of child protection. One only needs to suspect
that abuse or neglect has occurred in order to report it. The
reporter will then be protected from legal retribution from the
accused should they initiate legal action against them. The
investigative aspect of the case is then conducted by the agency
receiving the report.2,3,6
Relevant values at play
When the ADA Code addresses this topic, it does so
under the principle of Beneficence.1 Under this principle,
dentists have the ethical duty to always put the patient’s
welfare first. It states:
The public and the profession are best served by dentists who
are familiar with identifying the signs of abuse and neglect and
knowledgeable about the appropriate intervention resources
for all populations.
A dentist’s ethical obligation to identify and report the signs of
abuse and neglect is, at a minimum, to be consistent with a dentist’s
legal obligation in the jurisdiction where the dentist practices.
Dentists, therefore, are ethically obliged to identify and report suspected cases of abuse and neglect to the same extent as they are legally
obliged to do so in the jurisdiction where they practice. Dentists have
a concurrent ethical obligation to respect an adult patient’s right to
self-determination and confidentiality and to promote the welfare
of all patients. Care should be exercised to respect the wishes of an
adult patient who asks that a suspected case of abuse and/or neglect
not be reported, where such a report is not mandated by law. With
the patient’s permission, other possible solutions may be sought.
Dentists should be aware that jurisdictional laws vary in their
definitions of abuse and neglect, in their reporting requirements
and the extent to which immunity is granted to good faith reporters. The variances may raise potential legal and other risks that
should be considered, while keeping in mind the duty to put the
welfare of the patient first. Therefore a dentist’s ethical obligation
to identify and report suspected cases of abuse and neglect can vary
from one jurisdiction to another. Dentists are ethically obligated to
keep current their knowledge of both identifying abuse and neglect
and reporting it in the jurisdiction(s) where they practice.
It is good for us to be reminded of this ethical obligation
mandated by our profession. Its strong language and articulate
wording leave nothing to the imagination; dentists must report
suspected cases of abuse and neglect notwithstanding.
www.agd.org
General Dentistry
January/February 2013
21
The principle of veracity, or truthfulness, also applies to this
case. Dr. Miller had to be honest with herself when examining
the evidence. Although she did not want to believe this was
actually a case of abuse, all the facts seemed to be pointing in
that direction. Joseph and Theresa seemed to not honor veracity
here, as Dr. Miller felt they were not being truthful in answering her questions.
Lastly, nonmaleficence, or doing no harm, comes into play.
This can be looked at in multiple dimensions. The most
obvious aspect of nonmaleficence in this case is the potential
harm to Joseph in the future if Dr. Miller chose not to report
the suspected abuse and Joseph was indeed an abuse victim.
The physical and psychological effects of abuse and neglect on
children are horrifying. Also, if this is indeed a case of abuse,
who is the abuser? Further harm could come to Joseph or other
family members if the abuser is angered by the child abuse
investigation. On the other hand, an unwarranted report of
child abuse could possibly ruin a good person’s reputation if this
information becomes known publically. Dr. Miller may fear for
her own safety as well after making the report. The abuser could
possibly seek revenge on her if he/she discovers that she initiated
the report. Fear of retribution is one of the main reasons abuse
goes unreported.2,3,6
Discussion and postscript
The above scenario is based on a real case. Dr. Miller’s ethical
and legal obligation to report any suspected case of child abuse or
neglect supersedes any fear of retribution to herself or to Joseph’s
family that she may have. Waiting 2 weeks to reassess is too
long. A lot could happen during that time in an abusive home.
Dr. Miller did indeed decide to call DCPS that day. The DCPS
initiated an investigation into Joseph’s case and the report of
abuse was substantiated. Joseph was indeed being abused by his
stepfather, Jake. Often, Joseph and Jake did not see eye to eye
and Jake responded by “punishing” Joseph; he punched him in
the face causing the injuries observed by Dr. Miller. It turns out
that this was not the first time something like this happened.
Theresa felt helpless and was afraid to say or do anything to
further upset Jake, so the abuse had continued. Joseph was taken
to a safe place, got his provisional partial denture, but was never
seen at Community Clinic again.
This case illustrates the fact that dentists need to be aware of the
signs and symptoms of abuse and neglect and their ethical and
legal obligations to report it. Child abuse can happen in many different ways—physical, sexual, and emotional, as well as by neglect.
The following are common possible indicators of child abuse:
displaced or avulsed teeth, bruising of the hard or soft palate, oral
lesions of sexually transmitted diseases, pregnancy, black eyes,
22
January/February 2013
General Dentistry
broken bones, bruises at different stages of healing, head injuries,
cigarette or immersion burns, human bite marks, being dressed
inappropriately for the weather, failure to make eye contact, displaying a fear of being touched, or exhibiting severe anxiety.4.7,8
Every dentist has a professional duty to become familiar with
the statutes of his/her state and its reporting agencies. Making
the call is never easy, but it only takes the suspicion of abuse
or neglect to trigger the reporting process. Since mandated
reporters are protected from litigation when making a good
faith referral, one should always err on the side of child protection when making the decision whether or not to call the
reporting agency. Dentists must be willing to do their part to
help stop the violence and perhaps save a life. Dr. Miller made
the right call.
Author information
Dr. Roucka is a fellow of the American College of Dentists, a
Navy veteran, and president-elect of the American Society for
Dental Ethics. She is also an assistant professor and program
director, General Dentistry, Marquette University School of
Dentistry, Milwaukee, Wisconsin, where Dr. Gonzalez is a
board-certified pediatric dentist, and associate professor and
director, Undergraduate Program in Pediatric Dentistry.
References
1.ADA. American Dental Association Principles of Ethics and Code of Professional Conduct. Revised 2012:7-8. Available at: http://www.ada.org/sections/about/pdfs/code_
of_ethics_2012.pdf. Accessed September 5, 2012.
2.Graskemper. JP. Professional Responsibility in Dentistry: A Practical Guide to Law and
Ethics. 1st ed. Hoboken, NJ: Wiley-Blackwell. 2011:47-49.
3. Mouden LD, Bross DC. Legal issues affecting dentistry’s role in preventing child abuse
and neglect. J Am Dent Assoc. 1995;126(8):1173-1180.
4.American Academy of Pediatrics Committee on Child Abuse and Neglect, American
Academy of Pediatric Dentistry, American Academy of Pediatric Dentistry Council on
Clinical Affairs. Guideline on Oral and Dental Aspects of Child Abuse and Neglect.
Reaffirmed 2011. Available at: http://archive.acf.hhs.gov/programs/cb/pubs/cm10/
cm10.pdf. Accessed November 9, 2012.
5.U.S. Department of Health and Human Services, Administration for Children and Families, Administration on Children, Youth and Families, Children’s Bureau. (2010). Child
Maltreatment 2010. Available at: http://www.acf.hhs.gov/programs/cb/pubs/cm10/
cm10.pdf. Accessed December 4, 2012.
6.Ozar DT, Sokol DJ. Dental Ethics at Chairside. 2nd ed. Washington, DC: Georgetown
University Press; 2002:115, 237-238.
7.Child Welfare Information Gateway, U.S. Department of Health and Human Services,
Fact Sheet: Recognizing Child Abuse and Neglect: Signs and Symptoms. 2007:3-4.
Available at: http://www.childwelfare.gov/pubs/factsheets/signs.pdf. Accessed December 4, 2012.
8.Cage R, Salus MK. Office on Child Abuse and Neglect, Children’s Bureau. Child Welfare
Information Gateway, U.S. Department of Health and Human Services. The Role of First
Responders in Child Maltreatment Cases: Disaster and Nondisaster Situations.
2010:12-18. Available at: http://www.childwelfare.gov/pubs/usermanuals/first_
responders/firstresponders.pdf. Accessed December 4, 2012.
www.agd.org
Patient Education/Motivation
Increasing antiplaque/antigingivitis efficacy of an
essential oil mouthrinse over time: an in vivo study
Christine A. Charles, RDH, BS n J.A. McGuire, MS n James Qaqish, BS n Pejmon Amini, DDS
Financial Disclosure: Two of the authors are employed by Johnson & Johnson Healthcare Products Division of McNeil-PPC Inc., Skillman, New Jersey,
makers of Listerine Antiseptic Mouthwash, an essential oils-containing mouthrinse. The remaining two authors are employed by BioSci Research America
Inc., an independent clinical research organization in Las Vegas, Nevada.
This randomized, observer-blind, parallel, controlled study determined
the efficacy of an essential oils-containing (EO) antiseptic mouthrinse (in
conjunction with toothbrushing) in reducing and/or controlling existing
plaque or gingivitis over 6 months. Toothbrushing, combined with placebo rinsing, served as the control (C). Following ethics board approval
(Biosci Research Canada, Ltd. Institutional Review Board), 139 healthy
adults with mild to moderate plaque and gingivitis were randomized
into EO or C groups. All subjects received oral/written instructions,
monthly monitoring, and assigned unsupervised rinses. Efficacy variables
were whole-mouth mean modified gingival index (MGI), Turesky modification of the Quigley Hein plaque index (PI), bleeding index (BI) at 6,
12, and 24 weeks, and data analysis through an analysis of covariance
(ANCOVA) model. The EO group provided greater and increasing MGI,
A
dequate control of plaque biofilm is
essential to prevention and control
of periodontal diseases, dental
caries, and the patient’s oral health. Given
the prevalence of these diseases globally—
with caries in 60%-90% of children,
gingivitis in up to 80% of the populations
in developed countries, and periodontitis
in 50% of global populations—it would
seem that mechanical oral hygiene procedures alone are not practiced sufficiently
by a majority of the population.1-3 This
lack of sufficient oral hygiene provides
a rationale for implementing additional
means of improving oral hygiene.
Mechanical oral hygiene techniques,
such as toothbrushing, generally focus
only on the teeth, which comprise about
25% of the oral surfaces.4 Antiseptic
mouthrinses, by virtue of their liquid
nature, reach nearly 100% of oral surfaces.4 Plaque bacteria are prevalent on
the oral mucosal tissues that comprise the
majority of the oral surface, which provide
reservoirs for bacteria to recolonize on the
tooth surfaces.4,5 Daily rinsing with an
effective antimicrobial mouthwash may
help to reduce the total microbial burden
in the oral cavity, thereby contributing to
better oral hygiene.
PI, and BI reductions than did C group over all examination periods.
Compared to the C group, at 6, 12, and 24 weeks, MGI reductions for
the EO group were 4.7%, 9.1%, and 20.4%, and PI reductions were
7.6%, 12.6%, and 26.3%, respectively. BI scores decreased over time
and were significant compared to those for the C group (P < 0.001).
Additionally, the percentages of sites improved versus baseline MGI
over time for EO were 14.1%, 26.4%, and 43.3%, respectively. This
study demonstrated that an EO-containing mouthrinse can provide an
increasing benefit over a period of 6 months with twice daily use. This
study also confirmed that an antiseptic EO rinse can provide a clinically
significant benefit in reducing existing plaque and gingivitis.
Received: April 25, 2012
Accepted: July 26, 2012
Efficacy in plaque and gingivitis reduction resulting from use of antimicrobial
mouthrinses—that is, mouthrinses containing chemotherapeutic agents such as
chlorhexidine, cetylpyridinium chloride,
and essential oils (EO)­­—has been demonstrated in both short-term experimental
gingivitis models that do not utilize
mechanical oral hygiene and in 6-month
clinical trials utilizing the ADA Council
on Scientific Affairs’ Acceptance Program
Guidelines: Chemotherapeutic Products
for Control of Gingivitis (2008).6-17
In two 6-month trials where a regimen
of toothbrushing and daily flossing (BF)
was compared to a regimen of toothbrushing, daily flossing, and rinsing (BFR) with
an EO-containing mouthrinse, the BFR
group demonstrated a statistically and clinically significant advantage in both plaque
reduction (up to 51.9%) and gingivitis
reduction (up to 21%) compared to the
BF group (P < 0.001).18,19 Both plaque
and gingivitis were also reduced—by up to
56.3% and 29.9%, respectively—compared
to a brushing alone group at 6 months
(P < 0.001). BF provided an advantage to
brushing alone by up to 11.2% (P < 0.001).
In most of the referenced 6-month trials,
a dental prophylaxis was included in the
www.agd.org
clinical study design at the initiation of the
study and a greater benefit was provided at
6 months than at 3 months.
Since it has been shown that regular
professional care and a regimen of brushing, flossing, and rinsing with an antimicrobial EO rinse can provide a clinically
meaningful improvement in oral health,
the objective of this study was to evaluate only the effect of daily usage of an
antimicrobial EO-containing mouth rinse
(Listerine, Johnson & Johnson) on reducing existing dental plaque and gingivitis
over the course of 6 months without an
initial prophylaxis, and to determine if
there would be an increasing benefit over
this period of time, including an earlier
evaluation at 6 weeks.20
Materials and methods
A randomized, controlled, observerblind, parallel-group, 6-month clinical
trial was conducted in accordance with
ADA Acceptance Program Guidelines on
Chemotherapeutic Products for Control
of Gingivitis and standard operating procedures that comply with the International
Conference on Harmonisation’s Good
Clinical Practice (ICH GCP) guidelines.16
The clinical protocol, including informed
General Dentistry
January/February 2013
23
Patient Education/Motivation Increasing antiplaque/antigingivitis efficacy of an essential oil mouthrinse over time
Chart 1. Study flow diagram.
Enrollment
Assessed for eligibility (n = 162)
Excluded (n = 23)
Selected (n = 139)
Randomization
Allocated to
C intervention
(n = 70)
• Received
allocated
intervention
(n = 70)
Allocated
to EO
intervention
(n = 69)
• Received
allocated
intervention
(n = 69)
Follow-Up
Adverse Event
(n = 1)
Discontinued
intervention
(personal
reasons)
(n = 3)
Lost to followup (n = 2)
Discontinued
intervention
(personal
reasons)
(n = 1)
Analysis
Completed
(n = 66)
ITT (n = 67) a
Evaluable
(n = 63)
Completed
(n = 66)
ITT (n = 66)
Evaluable
(n = 65)
a
There were 67 subjects in the ITT group at 6 weeks,
but only 66 completed the study at 6 months.
24
January/February 2013
consent, was reviewed and approved by an
institutional review board, and the study
was conducted at BioSci Research America
in Las Vegas, Nevada. All subjects read and
signed an informed consent form prior to
the start of this study.
Subjects refrained from oral hygiene
for at least 8 hours, but no more than
18 hours, prior to the baseline examination. The oral examination included hard
and soft tissue assessment and scoring
of gingival, bleeding, and plaque clinical
indices by a trained and calibrated dental
examiner who demonstrated repeatability
(R ≥ 0.90) in the indices utilized. Gingivitis
was assessed using the MGI at 4 sites (the
buccal and lingual marginal gingivae and
interdental papillae) of all scorable teeth
and scored on a 5-point scale where 0 =
normal (absence of inflammation); 1 =
mild inflammation (slight change in color,
little change in texture) of any portion of
the gingival unit; 2 = mild inflammation
of the entire gingival unit; 3 = moderate
inflammation (moderate glazing, redness,
edema, and/or hypertrophy) of the gingival
unit; and 4 = severe inflammation (marked
redness and edema/hypertrophy, spontaneous bleeding, or ulceration) of the gingival
unit.21 BI was assessed using a periodontal
probe with a 0.5 mm diameter tip inserted
into the gingival crevice and swept from
distal to mesial, around the tooth at an
angle of approximately 60° while in contact
with the sulcular epithelium.22,23 Each
of the four gingival sites (distobuccal,
midbuccal, midlingual, and mesiolingual)
around each tooth was assessed. After
approximately 30 seconds, bleeding at each
gingival unit was recorded according to
the following scale: 0 = absence of bleeding after 30 seconds, 1 = bleeding after
30 seconds, and 2 = immediate bleeding.
Following disclosing, the plaque area
was scored using the PI on 6 surfaces
(Soparkar modification), mesial, middle,
and distal surfaces on the facial and
lingual aspects of all scorable teeth and
scored on the following scale: 0 = no
plaque; 1 = separate flecks or discontinuous band of plaque at the gingival
(cervical) margin; 2 = thin (up to 1 mm),
continuous band of plaque at the gingival margin; 3 = band of plaque wider
than 1 mm, but less than one-third of
surface; 4 = plaque covering one-third or
more, but less than two-thirds of surface;
General Dentistry
www.agd.org
and 5 = plaque covering two-thirds or
more of surface.24,25
All subjects were required to have a
whole-mouth mean MGI > 1.75 and
PI > 1.95 at baseline to qualify for the
study. A total of 139 healthy volunteers
with mild to moderate levels of plaque and
gingivitis were enrolled in the study.
Following the baseline examinations,
all qualified subjects were randomized
into 2 groups and instructed to brush
twice daily with an ADA-accepted toothbrush (Oral-B 35, Proctor & Gamble)
and a fluoride dentifrice (Colgate MFP,
Colgate-Palmolive Company).
Subjects were instructed to rinse morning
and evening with their assigned mouthrinse, either a hydroalcohol negative control
rinse (C) or an EO-containing mouthrinse.
Oral and written instructions were
provided to subjects. Daily rinsing was
unsupervised, with the exception of the
initial visit. All subjects were instructed
to brush thoroughly twice daily and were
provided with a toothbrush and dentifrice
as needed. All subjects were instructed
to rinse for 30 seconds with 20 ml of the
EO or C rinse full strength, morning and
night, to standardize twice daily usage
consistent with marketed product label
directions. All subjects were provided 1oz
plastic dosage cups with the 20 ml level
marked. They were allowed their usual
dietary habits, but instructed to refrain
from using any oral care products other
than what was provided to them for the
duration of the study. Use of dental floss
or other interdental devices was allowed
as needed to remove food debris. Subjects
returned at monthly intervals for compliance evaluation, replenishment of test
materials, and adverse event monitoring.
A dentist, trained and calibrated in
the clinical indices, performed all study
examinations. Care was taken to minimize
bias and guarantee the blindness of the
study by using rinses that were the same
color and identical bottles that were individually labeled by subject number. The
dental examiner and recorder were totally
separated from distribution and handling
of rinses. Prior to the 6-, 12-, and 24-week
examinations, subjects refrained from use
of all test products for at least 8 hours
prior to the examination so as not to
introduce any telltale rinse odor to the
examiner. In addition, product dispensing
personnel did not participate in the examination of subjects.
Table 1. Demographic characteristics of subjects in study.
Statistical methods
Results
Population
A total of 139 subjects were randomized
into 2 treatment arms, 70 to the C group
and 69 to the EO group. Seven subjects
discontinued the study, with 66 ITT
subjects in the C group and 66 in the EO
group completing the study (Chart 1).
Subjects ranged in age from 18 to 61
years old with a mean of 30.9 years.
There were 61 (43.9%) male and 78
(56.1%) female subjects. Approximately
half were white (49.6%) and the majority
had never smoked (79.9%). Treatment
groups were balanced with respect to all
baseline characteristics (Table 1).
Control (n = 70)
EO rinse (n = 69 )
Total (N = 139)
30.6 ± 11.07
31.3 ± 9.30
30.9 ± 10.20
Age (years)
Mean ± SD
Gender, n (%)
Male
32(45.7%)
29(42.0%)
61(43.9%)
Female
38(54.3%)
40(58.0%)
78(56.1%)
Race, n (%)
White
38(54.3%)
31(44.9%)
69(49.6%)
Black
11(15.7%)
19(27.5%)
30(21.6%)
Asian
5(7.1%)
5(7.2%)
10(7.2%)
Other
16(22.9%)
14(20.3%)
30(21.6%)
Ex-smoker
6(8.6%)
5(7.2%)
11(7.9%)
Never smoked
54(77.1%)
57(82.6%)
111(79.9%)
Smoker
10(14.3%)
7(10.1%)
17(12.2%)
Smoker, n (%)
Note: There were no significant differences between groups for any variables ( P < 0.38).
Chart 2. Whole mouth mean scores over 6 months: ITT subjects.
3.0
Whole-mouth mean scores
The primary efficacy variables were
whole-mouth mean MGI and mean PI at
6 months (24 weeks). Secondary variables
were whole-mouth mean MGI and PI at
6 weeks and 12 weeks and mean BI at 6,
12, and 24 weeks.
Statistical comparisons for primary
and secondary variables were based on
the ANCOVA model with treatment as a
factor and the corresponding baseline value
as a covariate. For each variable, treatment groups were compared at the 0.05
level, two-sided. The primary analysis for
each variable was based on intent-to-treat
(ITT) subjects, defined as all randomized
subjects who used at least 1 dose of study
mouthrinse and had data for mean MGI
or mean PI at post-baseline. Secondary
analyses were based on data from evaluable
subjects, defined as ITT subjects with no
major protocol violations. Summary statistics were provided by treatment group.
The planned sample size of 100 (50 per
treatment group) completed subjects was
based on data from previous studies. Using
the 6-month data from these studies, the
standard deviations were conservatively
estimated to be 0.27 for mean MGI and
0.50 for mean PI. Based on these estimates,
a sample size of 50 per treatment group
provides 90% power to detect a difference
in treatment means of 0.29 for mean MGI
and 90% power to detect a difference of
0.36 for mean PI. These differences represented 15% reductions from the estimated
placebo mean in the previous studies.
Brushing + EO
Brushing + Placebo
2.5
2.0
1.5
1.0
0.5
0
0 61224 0 61224
0 61224 0 61224
WeeksWeeks
Plaque index
Modified gingival index
Safety
The safety analysis was based on all
randomized subjects. One subject withdrew from the study due to an issue not
related to the study. There were only 2
subjects with at least 1 adverse event in
each group representing 2.9% of the
groups. The adverse events were considered unrelated to study treatment. The
mouthrinse treatments were well tolerated by the subjects.
www.agd.org
Efficacy
Chart 2 presents whole-mouth mean
scores for PI and MGI for ITT subjects.
Results for evaluable subjects were consistent with those for ITT subjects, therefore
only ITT data is presented. This figure
provides mean scores at each examination
period for the 2 primary variables in the
study, plaque and gingivitis.
Plaque Index: PI scores were statistically significantly lower for the EO group
General Dentistry
January/February 2013
25
Patient Education/Motivation Increasing antiplaque/antigingivitis efficacy of an essential oil mouthrinse over time
Chart 3. Percentage of subjects with an MGI score of 0 or 1 at each site scored in the maxillary facial regions after 6 months.
Percentage of subjects healthy at that site
100
EO GroupControl Group ( C )
90
80
70
60
50
40
30
20
10
0
2pap3pap4pap5pap6 pap7pap 8MID9pap10pap11pap12pap13pap14pap15
Tooth Number
Chart 4. Percentage of subjects with an MGI score of 0 or 1 at each site scored in the mandibular facial regions after 6 months.
Percentage of subjects healthy at that site
100
90
Brushing Alone
80
70
60
50
40
30
20
10
0
31pap30pap29pap28pap27 pap26pap 25MID24pap23 pap22pap21pap20pap19pap18
Tooth Number
than for the C group at 6, 12, and 24
weeks (P < 0.001) with percent reductions
for EO versus C of 7.6%, 12.6%, and
26.3%, respectively.
A site-based analysis of the plaque data
provides 20.4%, 32.1%, and 51.4% of
sites improved (or lower plaque score)
compared to baseline for the EO group
at 6, 12, and 24 weeks respectively. In
comparison, the C group demonstrated
10.8%, 14.5%, and 11.5% improvement
from baseline scores at 6, 12, and 24
weeks, respectively, showing a relatively
consistent result over time.
Gingivitis Index: Whole-mouth MGI
scores were statistically significantly lower
for the EO group than for the C group
26
Brushing + Rinsing
January/February 2013
(P < 0.001) with increasing reductions
of 4.7%, 9.1%, and 20.4% at 6, 12, and
24 weeks, respectively. Using a site-based
approach, the percent of sites improved
for MGI was 14.1%, 26.2%, and 43.5%
for the EO group and 8.6%, 12.6%, and
12.5% for the C group at 6, 12, and 24
weeks, respectively.
The percentage of subjects experiencing
any improvement in gingivitis (based on
reduction in mean MGI score) from baseline was 75.8%, 90.9%, and 98.5% in the
EO group and 17.9%, 53%, and 30.3%
in the C group at 6, 12, and 24 weeks,
respectively. At 6 months, nearly 100%
of subjects had an improved gingivitis
score in the EO rinse group compared to
General Dentistry
www.agd.org
30.3% in the C group. To further illustrate this improvement in gingival health,
Charts 3 and 4 provide the percentage of
subjects with an MGI score of 0 or 1 at
each site scored in the maxillary and mandibular facial regions after 6 months. This
site-by-site view helps to demonstrate the
additive effect that an EO antimicrobial
rinse can provide beyond toothbrushing in achieving a greater incidence of
healthy sites (sites where ≥ half of the
subjects achieved a 0 or 1 MGI score). It is
interesting to note that the marginal sites
(noninterproximal sites for the EO rinse
showed better results (Charts 3 and 4).
The combination of better mechanical removal and antimicrobial rinsing
provided a greater incidence of “healthy”
sites as shown by the picket fence image of
the site-based results beginning on the left
with the buccal of tooth No. 2 followed
by the papilla then buccal of tooth No. 3
followed by the papilla and so on ending
with buccal of tooth No. 15.
Bleeding Index: Table 2 summarizes
the BI results by providing mean scores
and transitions of scores. The EO group
showed statistically significantly lower
bleeding index than the control group
at 6, 12, and 24 weeks (P < 0.001).
Using the site-based analysis transition of scores (Table 2), the EO group
demonstrated 4.5%, 7.3%, and 9% sites
improved, while the C group experienced
2.9%, 4.3%, and 5.6% sites improved
at 6, 12, and 24 weeks, respectively. In
the C group, approximately 5% of sites
worsened at 6 months as compared to
only 2% in the EO group. The majority
of sites remained unchanged for bleeding
status over the course of the study.
Discussion
The goal of oral hygiene care is to achieve
plaque control and healthy gingiva.
The results from this study add to the
published data, confirming the benefit
of regular and consistent daily use of an
essential oils-containing antimicrobial
mouthrinse in reducing existing plaque
and gingivitis and in demonstrating
an increasing advantage with regular
and consistent twice-daily use over the
course of 6 months.26 Considering there
was no dental prophylaxis at the initiation of this study, it is interesting to
note the continued reduction in plaque
scores over time.
Adding an antimicrobial rinse to
daily brushing provides an additional
means of controlling the plaque biofilm,
since the average time spent brushing is
approximately 46 seconds, only 2%-10%
of patients floss regularly and effectively,
and most cannot or will not floss on a
daily basis.27,28 A recent systematic review
concluded: “There is some evidence from
12 studies that flossing in addition to
toothbrushing reduces gingivitis compared to toothbrushing alone. There is
weak, very unreliable evidence from 10
studies that flossing plus toothbrushing
may be associated with a small reduction
in plaque at 1 and 3 months.”29
Table 2. Whole-mouth bleeding index and site-based transition of scores.
Whole-Mouth Bleeding Index
Control
EO
Baseline Mean
0.10
0.11
6 Week adjusted mean (S.E.)
0.11 (0.003)
0.08a (0.003)
12 Week adjusted mean (S.E.)
0.10 (0.003)
0.06a (0.003)
24 Week adjusted mean (S.E.)
0.10 (0.004)
0.04a (0.004)
6 Weeks
n
%
n
%
188
2.9
281
4.5
Sites unchanged
5975
93.7
5886
93.5
Sites worsened
213
3.3
131
2.1
Sites improved
12 Weeks
n
%
n
%
277
4.3
459
7.3
Sites unchanged
5744
90.1
5695
90.4
Sites worsened
257
4.0
144
2.3
Sites improved
24 Weeks
n
%
n
%
354
5.6
566
9.0
Sites unchanged
5599
87.8
5608
89.0
Sites worsened
325
5.1
124
2.0
Sites improved
a
P < 0.001 compared to control
Even with regular brushing and flossing, bacteria may be left behind in hardto-reach areas. Antimicrobial mouthrinses
reduce the bacterial count and stop bacterial activity in the dental plaque that can
lead to gingivitis, which is quite prevalent
in most adults.30,31
Rinsing with an antimicrobial rinse
reduces the overall oral microbial load by
up to 99.9% immediately after rinsing, as
shown by an analysis of salivary samples
for total microorganisms that measures
ATP bioluminescence or colony forming
units (CFU/ml) indicating presence of
bacteria.32 Fine et al reported that 1) the
in vivo antimicrobial effectiveness of an
EO-containing mouthrinse 12 hours after
a single use and after 14-day use can have
long-lasting effects in reducing anaerobic
bacteria overall as well as Gram-negative
anaerobes and volatile sulfur compound
(VSC)-producing bacteria, 2) that significant reduction of these bacteria plays
a key role in explaining the EO rinse’s
effectiveness in reducing supragingival
plaque and gingivitis, and 3) consistent
twice daily rinsing with an antimicrobial
rinse such as an EO rinse that penetrates
www.agd.org
the plaque biofilm provides a mechanism
for reducing the total microbial load and
plaque scores, contributing to the reduction in gingivitis.33 In another study, Fine
et al demonstrated the effect of rinsing
with an EO mouthwash on the properties
of developing plaque by measuring limulus
lysate activity and concluded that “EO has
a dramatic effect on plaque toxic activity as measured by a decrease in limulus
lysate assay, as well as on its biomass.”34
This reduction in plaque toxic activity and
biomass may contribute to the reduction
in gingivitis demonstrated in this and multiple clinical trials of the EO rinse.12,13
In the studies incorporating brushing, daily flossing, and rinsing with an
EO rinse, a similar sitewide analysis (as
shown in Charts 2 and 3) of the proximal or papillary sites demonstrated that
up to 50% of the maxillary sites were
considered “healthy” (at least half of
the subjects scored 0 or 1 at those sites)
compared to none for the toothbrushing
plus flossing group or toothbrushing-only
group.18-19 Reviewing the site-to-site data,
it was found that although adding flossing to toothbrushing provided a benefit,
General Dentistry
January/February 2013
27
Patient Education/Motivation Increasing antiplaque/antigingivitis efficacy of an essential oil mouthrinse over time
adding the EO rinse to a routine of brushing and flossing contributed substantially
more to reducing inflammation and
returning the gingiva to a healthy state.35
Applying the criteria of at least a 15%
difference in gingivitis scores versus negative
control described in the ADA Guidelines
(15% for a single study and 20% when
combining 2 studies) suggests that there is a
clinically relevant reduction in gingivitis in
this study (20.4% reduction at 6 months)
as a result of adding an EO rinse to daily
toothbrushing as compared to toothbrushing and placebo rinse. Furthermore, on a
subject-by-subject basis, at 6 months 39.4%
of the subjects in the EO group experienced
at least a 20% improvement in wholemouth MGI scores compared to baseline,
while none of the subjects in the C group
experienced that level of improvement.
Conclusion
Using an EO-containing mouthrinse
provides a clinically meaningful and statistically significant reduction in existing plaque
and gingivitis, and provides an increasing
incremental benefit to toothbrushing
through twice daily use for 6 months.
This study confirmed the beneficial effect
twice-daily regular use of an EO-containing
mouthrinse on existing plaque and gingivitis, with gingivitis reductions within the
range of previously reported results.
Author information
Ms. Charles is director, Scientific and
Professional Affairs, Global Consumer
Healthcare Research and Development,
Johnson & Johnson Consumer and
Personal Products Worldwide, a division of
Johnson & Johnson Consumer Companies
Inc., Skillman, New Jersey, where Mr.
McGuire is director, Global Biometrics
and Clinical Data Systems. Mr. Qaqish
is manager, Clinical Operations, BioSci
Research America, Inc., Las Vegas, where
Dr. Amini is dental examiner.
References
1.Edelstein BL. The dental caries pandemic and disparities problem. BMC Oral Health. 2006;6(suppl 1):S2.
2.Albandar JM, Rams TE. Global epidemiology of periodontal diseases: an overview. Periodontol 2000. 2002;
29:7-10.
28
January/February 2013
3. Petersen PE, Bourgeois D, Ogawa H, Estupinan-Day S,
Ndiaye C. The global burden of oral diseases and risks
to oral health. Bull World Health Organ. 2005;83(9):
661-669.
4. Kerr WJ, Kelly J, Geddes DA. The areas of various surfaces in the human mouth from nine years to adulthood. J Dent Res. 1991;70(12):1528-1530.
5. Danser MM, Timmerman MF, van Winkelhoff AJ, van
der Velden U. The effect of periodontal treatment on
periodontal bacteria on the oral mucous membranes.
J Periodontol. 1996;67(5):478-485.
6.Amini P, Araujo MW, Wu MM, Charles CA, Sharma NC.
Comparative antiplaque and antigingivitis efficacy of 3
antiseptic mouthrinses: a two week randomized clinical trial. Braz Oral Res. 2009;23(3):319-325.
7.Charles CA, McGuire JA, Sharma NC, Qaqish J. Comparative efficacy of two daily use mouthrinses: randomized clinical trial using an experimental gingivitis
model. Braz Oral Res. 2011;25(4):338-344.
8. Mankodi S, Ross NM, Mostler K. Clinical efficacy of
Listerine in inhibiting and reducing plaque and experimental gingivitis. J Clin Periodontol. 1987;14(5):285288.
9.Witt JJ, Walters P, Bsoul S, Gibb R, Dunavent J, Putt M.
Comparative clinical trial of two antigingivitis mouthrinses. Am J Dent. 2005;18(spec no):15A-17A.
10.Lorenz K, Bruhn G, Heumann C, Netuschil L, Brecx M,
Hoffmann T. Effect of two new chlorhexidine mouthrinses on the development of dental plaque, gingivitis,
and discolouration. A randomized, investigator-blind,
placebo-controlled, 3-week experimental gingivitis
study. J Clin Periodontol. 2006;33(8):561-567.
11. Brecx M, Netuschil L, Reichert B, Schreil G. Efficacy of
Listerine, Meridol and chlorhexidine mouthrinses on
plaque, gingivitis and plaque bacteria vitality. J Clin
Periodontol. 1990;17(5):292-297.
12. Van Leeuwen MP, Slot DE, Van der Weijden GA. Essential oils compared to chlorhexidine with respect to
plaque and parameters of gingival inflammation: a
systematic review. J Periodontol. 2011;82(2):174-194.
13.Gunsolley JC. A meta-analysis of 6-month studies of
antiplaque and antigingivitis agents. J Am Dent Assoc.
2006;137(12):1649-1657.
14.Stoeken JE, Paraskevas S, van der Weijden GA. The
long-term effect of a mouthrinse containing essential
oils on dental plaque and gingivitis: a systematic review. J Periodontol. 2007;78(7):1218-1228.
15. Haps S, Slot DE, Berchier CE, Van der Weijden GA. The
effect of cetylpyridinium chloride-containing mouth
rinses as adjuncts to toothbrushing on plaque and parameters of gingival inflammation: a systematic review. Int J Dent Hyg. 2008;6(4):290-303.
16. Herrera D. Cetylpyridinium chloride-containing mouth
rinses and plaque control. Evid Based Dent. 2009;
10(2):44.
17.American Dental Association Council on Scientific
Affairs. Acceptance Program Guidelines: Chemotherapeutic Products for Control of Gingivitis. Available
at: http://www.ada.org/sections/scienceAndResearch/pdfs/guide_chemo_ging.pdf. July 2008.
Accessed October 10, 2012.
18.Sharma NC, Charles CH, Lynch MC, et al. Adjunctive
benefit of an essential oil-containing mouthrinse in
reducing plaque and gingivitis in patients who brush
General Dentistry
www.agd.org
and floss regularly: a 6-month study. J Am Dent Assoc.
2004;135(4):496-504.
19.Simmons K, Charles C, McGuire J, Hee A, Qaqish J,
Amini P. Efficacy of BRUSH, FLOSS, & RINSE™ regimen versus mechanical oral-hygiene [abstract].
2010 J Dent Res. 89 (spec iss A): Abstract 168.
20. Johnson & Johnson. Original Listerine Antiseptic [product
information]. Available at: http://www.listerine.com/
products/product-original. Accessed October 30, 2012.
21.Lobene RR, Weatherford T, Ross NM, Lamm RA, Menaker L. A modified gingival index for use in clinical trials.
Clin Prev Dent. 1986;8(1):3-6.
22.Saxton CA, van der Ouderaa FJ. The effect of a dentifrice containing zinc citrate and triclosan on developing gingivitis. J Periodontol Res. 1989;24(1):75-80.
23.Ainamo J, Bay I. Problems and proposals for recording
gingivitis and plaque. Int Dent J. 1975;25(4):229-235.
24.Lobene R, Soparkar M, Newman B. Use of dental floss.
Effect on plaque and gingivitis. Clin Prev Dent. 1982;
4(1):5-8.
25.Turesky S, Gilmore ND, Glickman I. Reduced plaque
formation by the chloromethyl analogue of victamine
C. J Periodontol. 1970;41(1):41-43.
26.Lamster IB, Alfano MC, Seiger MC, Gordon JM. The
effect of Listerine antiseptic on reduction of existing
plaque and gingivitis. Clin Prev Dent. 1983;5:12-16.
27. Beals D, Ngo T, Feng Y, Cook D, Grau DG, Weber DA.
Development and laboratory evaluation of a new
toothbrush with a novel brush head design.
Am J Dent. 2000;13(Spec No):5A-14A.
28. Bader HI. Floss or die: implications for dental
professionals. Dent Today. 1998;17(7):76-78, 80-82.
29. Matthews D. Weak, unreliable evidence suggests flossing plus toothbrushing may be associated with a small
reduction in plaque. Evid Based Dent. 2012;13(1):5-6.
30. Brushing your teeth. American Dental Association Web
site. http://www.ada.org/3072.aspx?currentTaqb=1.
Accessed October 10, 2012.
31.Oliver RC, Brown LJ, Loe H. Periodontal diseases in the
United States population. J Periodontol. 1998;69(2):
269-278.
32.Ricci-Nittel D, Charles C, Morris A, McGuire JA, Ghaim
J. In vivo evaluation of antimicrobial activity of an essential-oil mouthrinse. J Dent Res. Issue 2011 #90A abstract 1626.
33. Fine DH, Furgang D, Sinatra K, Charles C, McGuire A,
Kumar LD. In vivo antimicrobial effectiveness of an essential oil-containing mouthrinse 12 h after a single
use and 14 days’ use. J Clin Periodontol. 2005;32(4):
335-340.
34. Fine DH, Letizia J, Mandel ID. The effect of rinsing with
Listerine antiseptic on the properties of developing
dental plaque. J Clin Periodontol. 1985;12(8):660-666.
35.Lisante TA, Wu M, Araujo MW, Ghaim J. Novel analysis
of gingivitis scoring in clinical trials. J Dent Res. 2012;
(91)(spec iss A):40.
Manufacturers
Colgate-Palmolive Company, New York, NY
800.2COLGATE, www.colgate.com
Johnson & Johnson, Skillman, NJ
800.690.1826, www.jnj.com
Proctor & Gamble, Cincinnati, OH
513.983.1100, www.pg.com
Patient Education/Motivation
Paste, wrap, and shimmy: a regimen for the
prevention of gum disease
Craig W. Jester, DDS
The body of evidence showing a possible correlation between gum
infection and systemic diseases is well documented and growing. At the
same time, the prevalence of gum infection is increasing in the general
populace. Gum infection and disease are routinely seen in patients who
adhere to regular dental hygiene regimens and see their dentists on a
regular basis. One of the reasons typical daily dental care does not eradicate gum disease (gingivitis) is that the usual home care regimens do not
attack a major underlying cause of gingivitis: the layer of biofilm in the
sulcus surrounding the tooth’s root. This biofilm harbors and protects the
bacteria that cause gum disease and root decay. Research has shown that
there are no “magic bullets” in the form of rinses, pills, or special tools
that effectively destroy the bacteria and its protective calyx. Therefore,
daily dental regimens must be changed until the absence of gum infection
and inflammation becomes the standard of care.
M
any dental patients exhibit both
root decay and gingivitis. These
distinct problems frequently occur
in tandem. In even the most fastidious
people—those who brush and floss twice
or more daily—localized areas of gum
infection and inflammation can be found.
How can this be when these patients are
committed to doing what their dentist
advises? The reason is that in their cleaning
efforts, they miss the area under the cuff
of soft tissue—the sulcus or periodontal
pocket—that surrounds the base of every
tooth (Fig.1).1 Even in healthy mouths,
there is a 1-3 mm space between the gum
and tooth that acts as an undisturbed, protected culture tube for bacteria.2 Typical
daily dental regimens don’t eradicate the
layer of biofilm that forms in the sulcus
surrounding the tooth’s root.3 This biofilm
acts as a protective structure (calyx) that
harbors and protects the bacteria that
cause gum disease and root decay. Here,
according to Schacter, “the bacterial biofilm is in direct contact with host tissues
along an ulcerated epithelial interface,”
and releases its metabolic byproducts
to infect the gum and decay the roots
(Fig. 1).4 The most highly organized form
of the biofilm occurs after 3 to 12 weeks
and is capable of causing the most harmful
gum infections.5 Reduced salivary flow
(dry mouth) and lowered host resistance
The Paste, Wrap, and Shimmy method is presented in a way that can be
understood by all patients. It can be reproduced and used as a teaching
supplement by the dental team. The method is conceptually simple and
inexpensive, but not intuitive or easy. It must be coached and reinforced;
however, if implemented, it can be very effective. The author’s office has
increased the length of new patient and recurring hygiene visits so that
the method can be properly taught through repetitive practice and visual
presentations. Prevention is not insurance-driven, so dentists most often
provide it as a free service. The rewards are significant, however, and on
initial exposure to this method, patients routinely ask: “Why haven’t I been
shown this before?” They will also have an expectation that the learning
process will be repeated at each visit until they are free of infection.
Received: February 9, 2012
Accepted: June 20, 2012
also contribute to these infections in the
elderly, but all ages are affected. Paquette
et al predicted that 75% of the adult
population has at least mild gingivitis.6
The author of this article estimates that the
number is closer to 95%.
Conventional flossing and brushing
do not thoroughly disrupt the organized
plaque from the tooth surface (the biofilm
attaches to the tooth, not the gum). Many
people regularly floss without ever going
deeply under this cuff of tissue. They
believe their flossing procedure to be incorrect if it causes their gums to bleed; so
frequently, the bacteria thrive undisturbed.
The biofilm forms an effective protective barrier, a mucopolysaccharide film,
which resists rinsing, water jets, ultrasonic
brushes, and even harsh antibacterials.7-11
How can patients effectively clean under
this cuff of tissue and disrupt the biofilm
on the roots without damaging their gums?
moisten the brush) and loaded with an
ADA-approved toothpaste, which can be
found at the ADA MouthHealthy Seal
Products website (www.mouthhealthy.org/
ada-seal-products).15,16
This pumice must be carried onto the
root with very short, choppy movements,
tooth by tooth, using the ends of the
bristles to move the paste and clean the
root surfaces from the cheek side and then
the tongue side, with the patient lightly
biting the back of the brush to sink the
bristles under the tissue. The goal is to
Materials and methods
Commercial toothpastes contain an
abrasive, which is useful in breaking
up the biofilm.12-14 However, for this
pumice to be effective, the toothpaste
needs to access the tooth surface under
the gumline and be carried onto the
root. To do this, the patient should
begin by using a soft, rounded bristle
brush that is dry (saliva will quickly
www.agd.org
Fig. 1. Biofilm in the periodontal pocket. (Illustration
courtesy of Dr. Fay Goldstep.)
General Dentistry
January/February 2013
29
Patient Education/Motivation Paste, wrap, and shimmy: a regimen for the prevention of gum disease
Fig. 2. Deep-angled brushing.
Fig. 3. Flossing under the gum tissue.
work around the arch, pushing the pumice
down the tooth and under the tissue cuff
to clean the root surface (Fig. 2).17 The
brushing can be effectively done with a
mechanical or ultrasonic brush as well,
but care should be given to hold the brush
longer in each area to allow it time to work
along the gum line.
After spitting out excess saliva, the
patient moves to the second, and more
important, part of the routine: flossing
the toothpaste under the tissue cuff and
onto the roots (Fig. 3). Since the brush
bristles will only reach a third of the
depth into a healthy sulcus, more root
surface can be pumiced with the floss
than with the brush. Have the patient
apply toothpaste to his/her finger and
rub the toothpaste along the base of their
teeth on the cheek side, a quarter of the
mouth (quadrant) at a time. Reloading of
the paste for each quadrant will be necessary, due to the dilution of the toothpaste
by the saliva (Fig. 4). Then, wrap 18-24
inches of floss around the last 3 fingers
of each hand (with the index fingers and
thumbs free), leaving 0.5 in between the
opposing fingers (Fig. 5). If the index fingers are further apart than 0.5 in, the floss
cannot be properly controlled. Moving
their index fingers inside the mouth, the
patient should slide the floss through the
contact point between the first 2 teeth,
wrap the floss around 1 of the teeth and
30
January/February 2013
Fig. 4. Sulcular flossing with toothpaste.
shimmy the toothpaste up and down, 2
to 3 times on the first root, then move to
the next tooth—over the mound of gum
between the 2 teeth (papillae)—and clean
the adjacent root in the same way. The
mantra is paste, wrap, and shimmy.
In between each set of tooth contacts,
the patient should push forward when
wrapping around 1 root and pull back
in order to wrap around the next tooth.
The patient should pumice 2 roots in
each interdental space, and then release
1 end of the floss and pull it through
General Dentistry
www.agd.org
rather than popping up through the
contact and doing any damage to crowns,
inlays, or fillings. The patient should
work his/her way down the quadrant.
Thoroughness is the key.
All commercial toothpastes have 3
important ingredients: a pumice, a
bactericidal, and fluoride.15,16 Of these,
the abrasive is the most important. The
most common pumices are hydrated
silica (H2SiO3). The antibacterials are
usually some form of sodium, and the
fluorides can be either stannous or sodium
Table. Key techniques of the Paste, Wrap, and Shimmy method.
The benefits are not just dental.
There are correlations between gum
infection and systemic illness, stroke,
heart disease, diabetes, high blood
pressure, and even cancer.
Carry the floss and paste down the root
surface until you feel mild resistance in
the soft tissue.
Going any deeper is of no value and may
cut the gums.
Wrap and shimmy up and down the root
surface to break up the biofilm.
It is the root being cleaned, not the gums.
Once a day is enough.
Regrowth of the bacteria and the resultant
biofilm takes 24 hours. Regular brushing is
still recommended.
Fig 5. Flossing technique that uses 0.5 in of floss for
proper control.
fluoride. The pumice physically disrupts
the biofilm’s mucopolysaccharide covering, increasing both the bactericide’s and
fluoride’s effectiveness. The patient should
expect a little tingling as these elements
are carried down the root into the sulcus,
and there may be some bleeding in the
most inflamed areas due to ulcerations in
the lining of the sulcus. Both the tingling
sensation and bleeding resolve quickly.
The patient should expect an overall
decrease in bleeding after 2 to 3 weeks of
Timing of practice is important.
This routine is best done in early morning
or right after the evening meal. Bedtime is
the least effective.
It is messy, especially at first.
While there may be initial bleeding as your
gums adjust to the new cleaning, it usually
subsides after 2 to 3 weeks.
This is a lifetime habit.
Learn and practice this procedure for 40
days to develop a lifelong habit.
Remember…
Thoroughness is the key.
this daily treatment.17 Areas of bulky or
bulbous tissue should shrink as well. If
some of the more difficult areas continue
to bleed, the patient should spend more
time on these isolated areas at each cleaning, and usually these areas will cease
to bleed. Breath odor issues should also
improve. In periodontal pockets greater
than 4 mm, you may not touch bottom
with the floss, and these pockets may
require professional help. Scaling and
root planing in the dental office is still the
standard of initial care.18
Be aware that many toothpastes are so
heavily laden with flavorings and astringents that when first contact is made with
the tongue and taste buds, the mouth may
feel clean before any removal of bacteria
from the teeth. Key techniques for patients
to effectively remove bacteria using the
Paste, Wrap, and Shimmy method can be
found in the table.
Conclusion
In 5 years of teaching this technique, the
author and his staff have had some very
satisfying results. The staff schedules an
extra 15 minutes at every new patient’s
first appointment to teach the regimen,
and additional hygiene time is allotted
at every recall appointment to reinforce
it. The techniques are demonstrated in
the patient’s mouth, and the staff uses
www.agd.org
intraoral images and presentations for
reinforcement. Approximately 20% of
the people accept it and use the technique
after their first exposure to the regimen.
Another 20% never master it due to lack
of interest. For the 60% who make some
attempt at brushing and flossing in this
manner, we see very steady improvement.
In teaching events around the country,
the author finds that many dentists practice this technique themselves in some
form—but don’t believe their patients will
put forth the effort to master it. However,
when first introduced to it, almost every
patient asks, “Why hasn’t anyone shown
me this before?”
It is a fair question, and it deserves
an answer. In 1972, Dr. Robert Barkley
wrote a popular book of the period,
Successful Preventive Dental Practices.19
He did not have intraoral cameras or
PowerPoint presentations to help him
teach his patients, nor did he have a complete understanding of biofilms. But he
did have a passion to educate his patients
to become independently healthy. He
proclaimed a need for the dental team to
become educators, or watch the profession
“dilute...toward mediocrity.” Our patients
deserve this self-help and health-centered
dental approach. To paraphrase a popular
marketing theme, “Paste, Wrap, and
Shimmy...you can do it; we can help.”
General Dentistry
January/February 2013
31
Patient Education/Motivation Paste, wrap, and shimmy: a regimen for the prevention of gum disease
Author information
Since 1980, Dr. Jester has taught AGDcertified continuing education programs for
the United States Dental Institute. He maintains a broad spectrum preventive dental
practice in West Chester, Pennsylvania.
Disclaimer
The author has no financial, economic,
commercial, and/or professional interests
related to topics presented in this article.
References
1. Kho P, Smales FC, Hardie JM. The effect of supragingival plaque control on the subgingival microflora. J Clin
Periodontol. 1985;12(8):676-686.
2. Page RC. The pathobiology of periodontal diseases
may affect systemic diseases: inversion of a paradigm.
Ann Periodontol. 1998;3(1):108-120.
3.Center for Biofilm Engineering. Biofilm Basics. Available at: http://www.biofilm.montana.edu/biofilmbasics.html. Accessed November 7, 2012.
4.Schacter B. Slimy business—the biotechnology of biofilms. Nat Biotechnol. 2003;21(4):361-365.
5. Nield-Gehrig JS. Dental Plaque Biofilms. In: Nield-Gehrig JS, Willmann DE, eds. Foundations of Periodontics
32
January/February 2013
for the Dental Hygienist. Philadelphia, PA: Lippincott,
Williams & Wilkins; 2003:67-73.
6. Paquette DW, Nichols T, Williams RC. Oral inflammation, CVD, and systemic disease. Connections. 2005;
1(1):1-8.
7.Greenstein G; Research, Science and Therapy Committee of the American Academy of Periodontology. Position paper: The role of supra- and subgingival irrigation
on the treatment of periodontal diseases. J Periodontol.
2005;76(11):2015-2017. Available at: http://www.
drnolf.com/hygiene%20perio%20self%20study%20
course/irrigation.pdf. Accessed November 7, 2012.
8.Allen DR, Battista GW, Petrone DM, et al. The clinical efficacy of Colgate Total Plus Whitening Toothpaste containing a special grade of silica and Colgate Total Fresh
Stripe Toothpaste in the control of plaque and gingivitis:
a six-month clinical study. J Clin Dent. 2002;13(2):59-64.
9. van der Ouderaa FJ, Cummins D. Delivery systems for
agents in supra- and sub-gingival plaque control.
J Dent Res.1989;68(Spec Iss):1617-1624.
10. van der Weijden, FA. Timmerman MF, Piscaer M, Ijzerman Y, Warren PR, van der Velden U. A comparison of
the efficacy of a novel electric toothbrush and a manual toothbrush in the treatment of gingivitis.
Am J Dent. 1998;11(Spec No):S23-S28.
11. Jannesson L, Renvert S, Kjellsdotter P, Gaffar A, Nabi
N, Birkhed D. Effect of a triclosan-containing toothpaste supplemented with 10% xylitol on mutans
streptococci in saliva and dental plaque. A 6-month
clinical study. Caries Res. 2002;36(1):36-39.
General Dentistry
www.agd.org
12.Wang C, Lippert F, Lucas R, Creeth J, Smith A. Abrasive
particle and toothbrush filament effects on dental tissue wear. Paper presented at: 87th General Session
and Exhibition of the International, American and Canadian Associations for Dental Research (IADR/AADR/
CADR); April 4, 2009; Miami, FL.
13.Creeth JE, Platts AT, Jones SP. The effect of abrasive
silica level in a toothpaste on tooth cleaning and abrasivity in vitro. Paper presented at: 81st General Session
of the International Association for Dental Research;
June 26, 2003; Goteborg, Sweden.
14. De la Rosa M, Zacarias Guerra J, Johnston DA, Radike
AW. Plaque growth and removal with daily toothbrushing. J Periodontol. 1979;50(12):661-664.
15. Material Safety Data Sheets: MSDS Identifiers - 8 Dentifrices. Mason, OH: The Proctor and Gamble Company, Health Care Research Center; May 7, 2008.
16. Material Safety Data Sheets: MSDS Identifiers - 5 Dentrifices. New York, NY: Colgate Palmolive Company;
May 7, 2008.
17.Gaffar A, Afflitto J, Nabi N, Herles S, Kruger I, Olsen S.
Recent advances in plaque, gingivitis, tartar and caries
prevention technology. Int Dent J. 1994;44(1 suppl 1):
63-70.
18. Drisko CH. Nonsurgical periodontal therapy. Periodontol 2000. 2001;25:77-88.
19. Barkley RF. Successful Preventive Dental Practices.
Macomb, IL: Preventive Dentistry Press; 1972: 7-8.
Tooth Whitening/Bleaching
Assessment of the release of mercury from
silver amalgam alloys exposed to different
10% carbamide peroxide bleaching agents
Paloma Salomone, MDS n Renata Pla Rizzolo Bueno, MDS n Rodrigo Farcili Trinidade, MDS n Paulo Cicero Nascimento, DChem, PhD Roselaine Terezinha Pozzobon, DDS, PhD
This in vitro study assessed the amount of mercury (Hg) released from
a silver amalgam alloy following the application of different 10%
carbamide peroxide bleaching agents. A total of 30 specimens (2 mm
thick x 4 mm in diameter) were stored in deionized water at 37°C for
7 days. Next, the control group ( n = 10) remained in the deionized
water for 15 days, while the remaining samples were exposed to 1 of
2 bleaching agents ( n = 10) for 8 hours daily (total exposure = 120
hours); for the remaining 16 hours, specimens in the test groups were
I
n recent years, there have been great
technological advances in restorative
and adhesive materials and new restorative techniques, such as dental bleaching.
Bleaching is intended to restore the natural
aspect of teeth whose color has been
altered for various reasons. Dentists must
not only know the techniques for dental
bleaching, they also must understand how
bleaching agents interact with different
restorative materials that could be present
in patients’ teeth.
One common dental bleaching technique is performed by patients under the
dentist’s supervision. This supervised home
technique uses carbamide peroxide gel at
concentrations ranging from 10% (used
most frequently) to 22%.1-3 The basic
mechanism of action for bleaching agents
involves an oxidation reaction that acts on
the pigments, fractionating them and producing simultaneous, uniform bleaching
on the entire exposed tooth structure.3-5
Resin composites and silver amalgam are
common restorative options for posterior
teeth. Silver amalgam is a metal alloy consisting of copper, zinc, silver, tin, and mercury (Hg); it is used to form a plastic mass
that allows for insertion, condensation,
and finishing. Silver amalgam is commonly
used for restorations in posterior teeth due
to its wear strength and sealing properties
at the tooth/restoration interface.
Over the last few years, the indications
for fabricating silver amalgam restorations
have been limited; however, patients with
stored in deionized water at 37°C under relative humidity. After this
period, the quantity of Hg in the deionized water was assessed (using
atomic absorption spectrophotometry) and compared to the amount
of Hg at baseline. The results indicate that exposing amalgam alloys to
bleaching agents released greater amounts of Hg compared to exposing
samples to ionized water.
Received: July 13, 2011
Accepted: September 20, 2011
these restorations might wish to improve
the esthetics of their smile through bleaching techniques. In these cases, the bleaching agent will contact the amalgam. This
study sought to determine if and how 10%
carbamide peroxide bleaching agents cause
a silver amalgam alloy to release Hg.
Materials and methods
A silver amalgam alloy with a high copper
content (Permite-C, SDI (North America)
Inc.), was used to fabricate 30 specimens
(2 mm thick x 4 mm diameter). All specimens were immersed in deionized water
at 37°C for 7 days. Specimens then were
divided into 3 groups for the 15-day test
period. Specimens in Group 1 (control
group) (n = 10) remained in deionized
water, while specimens in Groups 2 and
3 (n = 10) were exposed for 8 hours daily
(following the manufacturer’s recommendations) to one of two 10% carbamide peroxide bleaching gels (Table 1).
Group 2 was exposed to Opalescence PF
(Ultradent Products, Inc.), which contains
10% carbamide peroxide, 0.5% potassium
nitrate and 0.11% (1,100 ppm) fluoride
ion. Group 3 was exposed to a generic
10% carbamide peroxide compound
(Dermapelle Handling Pharmacy). For
the other 16 hours each day, samples in
Groups 2 and 3 were kept in deionized
water at 37°C under relative humidity.
After 15 days, ions released in the
deionized water were assessed using
atomic absorption spectrophotometry.
The nominal amounts of Hg released were
tabulated in spreadsheets and analyzed
using a descriptive statistical program
(SPSS version 18.0, IBM Corporation).
Normality of distribution was verified by
the Shapiro-Wilk test, and homoscedasticity was verified by the Levene test. The
values for Hg released underwent base-10
log transformation to perform the parametric tests; at that point, ANOVA and
Tukey post hoc tests (P < 0.05) were used
to compare data in Groups 1-3.
Table 1. Composition of bleaching agents used.
Bleaching agent
Composition
Manufacturer
Opalescence PF
10% carbamide peroxide, 0.5% potassium
nitrate, 0.11% (1,100 ppm) fluoride ion
Ultradent Products, Inc.
10% carbamide
peroxide compound
10% carbamide peroxide, stabilizers, and
thickeners
Dermapelle Handling
Pharmacy
www.agd.org
General Dentistry
January/February 2013
33
Tooth Whitening/Bleaching Assessment of the release of Hg from silver amalgam alloys exposed to bleaching
Table 2. Quantity of released Hg (in mg/L) by the different
experimental groups.
Group
Mean Hg released (SD)
Mean Hg log10 released (SD)
1
22.80 (31.69)
0.93 (0.65) b
2
162.09 (168.89)
1.81 (0.73) a
3
292.00 (321.25)
2.08 (0.71) a
Different superscript letters indicate statistically significant differences between
Group 1 and Groups 2 and 3 ( P < 0.05).
Chart. Mean amount of Hg released in each group.
2.5
Log of Hg in mg/L
2.0
1.5
1.0
0.5
0
Group 1 (control)Group 2Group 3
Results
Table 2 shows the mean values and SDs
obtained after performing the statistical
analysis. There is a statistically significant
difference between the release of Hg in
Groups 2 and 3 and the amount released
by the control group (Group 1).
Statistics d and r were used to calculate
the effect sizes for each of the three groups.
Effect sizes complement other, more inferential statistics, such as P values. A great
effect is the same as a statistically significant
difference between groups. A medium effect
means that although there is a difference, it
is not statistically significant. Statistics for
Group 3 resulted in d = -1.28 and r = -0.54,
which is considered a great effect; while
statistics for Group 2 resulted in d = 0.37
and r = 0.18, considered a medium effect.
Although Group 3 specimens produced
higher mean values of Hg compared to
Group 2 specimens, this difference was
34
January/February 2013
not considered statistically significant.
Differences were considered to be statistically significant only when specimens in
Groups 2 or 3 were compared with those in
Group 1. The chart shows the amount of
Hg released by each group.
Discussion
Silver amalgam is a restorative material
consisting primarily of Hg, silver, copper,
and tin. This material is not technically
considered to be sensitive; however, it
undergoes a continuous corrosion process,
which gives it a self-sealing quality.
In the experimental design used in
the present study, the use of silver amalgam alloy capsules with a high copper
content enabled the standardization of
the quantity of Hg present in each test
specimen. The alloy’s high copper content
offered improved mechanical and physical
properties, including a reduction in the
General Dentistry
www.agd.org
formation of the gamma 2 phase, reduced
corrosion, and increased strength.6 For the
present study, 10% carbamide peroxide
was chosen as the test material, as this
concentration is used most frequently in
supervised home bleaching techniques and
mentioned most frequently in studies that
assess the effect of bleaching agents on
restorative materials.2,7-12
Exposure to metal ions (especially
Hg) is a potential danger to health and
could cause serious toxic effects, damaging the brain, kidneys, and lungs and
leading to such conditions as acrodynia,
Minamata disease, and Hunter-Russell
syndrome.13 According to the World
Health Organization, the maximum recommended intake of Hg is 40 mg/kg of
body weight per day, while the provisional
tolerable weekly intake (PTWI) limit is
estimated to be 300 μg of total Hg and
200 μg of methylmercury, which corresponds to 5 μg/kg of total Hg or 3.3 μg/kg
of methylmercury for a person weighing
60 kg.14 In turn, these values produce an
acceptable daily intake (ADI) of 0.5 μg/kg
of methylmercury and 0.7 μg/kg of total
Hg.14 The literature has reported adverse
effects on the central nervous system of
adults following a daily Hg intake of
3-7 μg/kg, resulting in levels of Hg in the
blood ranging from 200 to 500 μg/L.12
Exposure to Hg can also occur from
breathing contaminated air, using and/or
improperly disposing of fluorescent lamps,
coal combustion in power plants, and
intake of food containing residues of Hg.
In addition, silver amalgam restorations
might release Hg after dental bleaching.
Previous studies have assessed how
exposure to bleaching agents affects
surface changes in silver amalgam restorations. In a 2004 study, Schemehorn
et al applied a 6% concentration of a
hydrogen peroxide bleaching agent to
silver amalgam for 20 minutes a day for
28 consecutive days; scanning electronic
microscopy (SEM) performed at the end
of this period found no surface changes.9
Similarly, Duschner et al applied peroxides for 70 hours but found no surface
changes or altered microhardness.8
However, a 2003 study by Campos et al
exposed silver amalgam to 10% and 15%
carbamide peroxide bleaching agents (6
hours a day for 21 days) and reported a
loss of microhardness.7
More recently, a 2007 in vitro study by
Al-Salehi et al analyzed the release of Hg
ions from silver amalgam after treating
specimens with hydrogen peroxide at concentrations of 1%, 3%, 10%, and 30%.15
In the first 24 hours of treatment, the
authors collected samples to determine the
release of metal ions and measured surface
roughness before and after bleaching. As in
the present study, metal alloy corrosion was
higher and Hg release increased as concentrations of hydrogen peroxide increased.15
The release of metal ions and Hg from
amalgam restorations varies, depending
on the time and in proportion to the
size of the restoration surface.16,17 The
amount of Hg released daily from an
amalgam restoration can vary. Rotstein et
al assessed amalgam samples bleached with
10% carbamide peroxide 48 hours after
the completion of bleaching treatment
and found concentrations of Hg ranging
from 0.6 to 4.24 μg/mm2.12 Mackert &
Berglund reviewed 6 different in vivo
studies and found that the amount of Hg
released from dental amalgam restorations
ranged from 0.014 to 0.016 μg/mm2.18
A similar study by Hummert et al found
that exposing amalgam restorations to
dental bleaching released 0.014-0.020 μg/
mm2 of Hg, compared to 0.001 μg/mm2
when amalgam was exposed to a saline
solution.19 These results are in keeping
with the values found in the present study,
where the amount of Hg released increased
significantly (P < 0.05) when amalgam was
exposed to 10% carbamide peroxide. The
mean values for the three groups are listed
in Table 2.
Based on the literature and the present
study, solutions of 10% carbamide peroxide increase the amount of Hg released
from silver amalgam.10-12 Because Hg is
released naturally in the oral cavity when
saliva is present, frequent and prolonged
exposure to bleaching agents might
increase the risk of poisoning by Hg
exposure while also causing changes in
physical, mechanical, and structural properties of restorations, thus reducing their
longevity. When performing bleaching
treatments on patients with silver amalgam restorations, dentists must avoid
unnecessarily exposing these restorations
to 10% carbamide peroxide bleaching
agents. It is recommended that bleaching
treatments are performed by the dentist in
the office or that silver amalgam restorations are replaced before patients perform
any at-home bleaching treatments.
Conclusion
Silver amalgam specimens treated with
10% carbamide peroxide bleaching
agents produced a statistically significant
increase in the quantity of Hg released
after 15 days compared with the control
group. Additional studies are needed
to assess the impact of this increase.
However, the authors recommend
avoiding the indiscriminate exposure
of silver amalgam restorations to carbamide peroxide bleaching agents.
Author information
Drs. Salomone and Bueno, and Mr.
Trinidade are at the Federal University of
Santa Maria, Rio Grande do Sul, Brazil,
where Dr. Nascimento is in the Department
of Chemistry and Dr. Pozzobon is in the
Department of Restorative Dentistry.
References
1. Haywood VB, Heymann HO. Nightguard vital bleaching: how safe is it? Quintessence Int. 1991;22(7):515523.
2. Haywood VB. History, safety, and effectiveness of current bleaching techniques and applications of the
nightguard vital bleaching technique. Quintessence
Int. 1992;23(7):471-488.
3. Haywood VB. Commonly asked questions about
nightguard vital bleaching. J Indiana Dent Assoc.
1993;72(5):28-33.
4. Hahn LJ, Kloiber R, Vimy MJ, Takahashi Y, Lorscheider
FL. Dental ”silver“ tooth fillings: a source of mercury
exposure reveled by whole-body image scan and tissue analysis. FASEB J. 1989;3(14):2641-2646.
5. Haywood VB. Nightguard vital bleaching: information
and consent form. Esthet Dent Update. 1995;6:129132.
6.Anusavice KJ. Phillips’ Science of Dental Materials.
11th ed. Philadelphia, PA: Elsevier; 2003.
7.Campos I, Briso AL, Pimenta LA, Ambrosano G. Effects
of bleaching with carbamide peroxide gels on microhardness of restorative materials. J Esthet Restor Dent.
2003;15(3):175-182.
www.agd.org
8. Duschner H, Gotz H, White DJ, Kozak KM, Zoladz JR.
Effects of hydrogen peroxide bleaching strip gels on
dental restorative materials in vitro: surface microhardness and surface morphology. J Clin Dent. 2004;
15(4):105-111.
9.Schemehorn B, Gonzalez-Cabezas C, Joiner A. A SEM
evaluation of a 6% hydrogen peroxide tooth whitening gel on dental materials in vitro. J Dent. 2004;
32(suppl 1):35-39.
10.Rotstein I, Ayron Y, Shemesh H, Dogan H, Mor C, Steinberg D. Factors affecting mercury release from dental
amalgam exposed to carbamide peroxide bleaching
agent. Am J Dent. 2004;17(5):347-350.
11.Steinberg D, Blank O, Rotstein I. Influence of dental
biofilm on release of mercury from amalgam exposed
to carbamide peroxide. J Biomed Mater Res B Appl
Biomater. 2003;15:67(1):627-631.
12.Rotstein I, Dogan H, Avron Y, Shemesh H, Steinberg D.
Mercury release from dental amalgam after treatment
with 10% carbamide peroxide in vitro. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2000;89(2):216219.
13. Jones DW. Exposure or absorption and the crucial
question of limits for mercury. J Can Dent Assoc. 1999;
65(1):42-46.
14.World Health Organization. Guidance for Identifying
Populations at Risk From Mercury Exposure. 2008.
Available at: http://www.who.int/foodsafety/publications/chem/mercuryexposure.pdf. Accessed November
14, 2012.
15.Al-Salehi SK, Hatton PV, McLeod CW, Cox AG. The effect of hydrogen peroxide concentration on metal ion
release from dental amalgam. J Dent. 2007;35(2):172176.
16. Berglund A, Pohl L, Olsson S, Bergman M. Determination of the rate of release of intra-oral mercury vapor
from amalgam. J Dent Res. 1988;67(9):1235-1242.
17.Certosimo A, Robertello F, Dishman M. Bogacki R,
Wexel M. The effect of bleaching agents on mercury
release from spherical dental amalgam. Gen Dent.
2003;51(4):356-359.
18. Mackert JR Jr, Berglund A. Mercury from dental amalgam fillings: absorbed dose and potential for adverse
health effects. Crit Rev Oral Biol Med. 1997;8(4):410436.
19 Hummert TW, Osborne JW, Norling BK, Cardenas HL.
Mercury in solution following exposure of various
amalgams to carbamide peroxide. Am J Dent. 1993;
6(6):305-309.
Manufacturers
Dermapelle Handling Pharmacy, Santa Maria,
Rio Grande do Sul, Brazil
55.55.2103.3300, www.dermapelle.com.br
IBM Corporation, Armonk, NY
800.523.6825, www.ibm.com
SDI (North America) Inc., Bensenville, IL
800.228.5166, www.sdi.com.au
Ultradent Products, Inc., South Jordan, UT
888.230.1420, www.ultradent.com
General Dentistry
January/February 2013
35
Information Technology/Computers
Overview of CEREC CAD/CAM chairside system
Gildo Coelho Santos Jr., DDS, MSc, PhD n Maria Jacinta Moraes Coelho Santos Jr., DDS, MSc, PhD n Amin S. Rizkalla, PhD Dalia A. Madani, DDS, MSc, BSc n Omar El-Mowafy, BDS, PhD
This article describes CAD/CAM technology used in dentistry and
different restorative materials used in conjunction with adhesive
cementation with particular attention given to the evolution of
the CEREC system, as well as various ceramics developed for this
T
he demand for esthetic restorations has
increased dramatically over the past
two decades. The search for new methods has been driven in part by patients
who have increasingly high expectations in
esthetic dentistry and concerns about the
intraoral biocompatibility of metals.1 While
metal-ceramic systems are a high-strength
mode of treatment with positive long-term
success rates, they also are associated with
certain disadvantages, including esthetic
concerns and the potential for allergic
reactions (gold allergies are rare, but have
been documented in the literature).2 Several
studies have investigated the prevalence of
metal contact allergy among various populations.3-7 Metal contact allergy was reported
to be 0.8%-9.5% for gold, 1.6% for silver,
9% for cobalt, 8.2% for tin, 8% for palladium, 8% for chromium, and 14.3%-29%
for nickel.3-7
Ceramics have become a popular restorative material due to their high esthetic
quality, wear resistance, durability,
color stability, and biocompatibility.8-12
Disadvantages of ceramics include the
high cost of fabrication, low fracture
resistance, difficulty in repairing, excessive wear of opposing teeth, the need for
a more aggressive preparation design,
technique sensitivity, and less-than-ideal
marginal adaptation.8,13-16
Advancements in dental materials,
computer technology, and equipment have
made it possible to fabricate an indirect
esthetic restoration in one appointment
while the patient is waiting. The computeraided design/computer-aided manufacture
(CAD/CAM) CEREC (computer-assisted
CERamic REConstruction) system is used
for electronically designing and milling
restorations. Using this system, the dentist
can manufacture a restoration without the
need for laboratory assistance, impressions,
36
January/February 2013
system. Advantages and limitations of materials and technique are
also discussed.
Received: November 21, 2011
Accepted: April 11, 2012
or temporary restorations.17 The restoration
can be designed in less than five minutes
and milled in 10-12 minutes, resulting
in significant time savings for both the
patient and dental practice.18 The CEREC
system (Sirona Dental Systems, Inc.) was
the first operational CAD/CAM system
to be used in the dental offices.19 The first
chairside inlay was fabricated with the
CEREC I in 1985.20 In 1988, onlay and
veneer capabilities were added to the unit.
Full and partial crowns and copings were
made possible in 1994 with the introduction of the CEREC 2. In 2000, the
CEREC 3 (Sirona Dental Systems, Inc.)
was introduced; by 2003, the CEREC
units had 3-dimensional capability. New
software was added in 2005 that enabled
automatic virtual occlusal adjustment.20
Several studies criticized the marginal fit
of CEREC restorations.21,22 However, with
the latest improvements in the CEREC
unit and software, it is possible to produce
a more clinically acceptable marginal fit of
the milled restorations.23-24
The design and manufacturing process
involves optically scanning and digitizing
dies created from the master impression of
the prepared teeth/cores, so that the dimensions of the margins may be duplicated
precisely. The scanned 3-dimensional
images of the dies are then used to design
the substructure, prompted by computer
software. The CAD unit is linked to a
robotic CAM center that creates a restoration according to the design specifications.1
Advantages of the CEREC
technology
The clinical success and longevity of
CEREC restorations have been documented
in the literature.25 Restoration size, tooth
vitality, and tooth location do not significantly affect the prognosis. A 2003 study by
General Dentistry
www.agd.org
Posselt & Kerschbaum reported a survival
probability of 95.5% over nine years.25
The CAD/CAM ceramic blocks are fabricated under optimum conditions, creating
a restoration with higher intrinsic strength
without the variation in materials found
in laboratory-fabricated restorations.26 The
computer-controlled fabrication diminishes the potential for inaccuracies due
to human error and makes it possible to
generate a restoration within a clinically
acceptable fit of 50 µm, as established by
the American Dental Association.27
Because only one appointment is
needed to complete the restoration, the
patient is subjected to only one administration of local anesthetic. In addition,
there is no need to fabricate a temporary
restoration which is at risk of loss, breakage, or leakage and may produce sensitivity and/or contaminate the dentinal
tubules.28 Temporary restorations may be
hard to clean and maintain during the
temporization period, which can lead to
gingival irritation; in addition, pulpal
stress may occur when the temporary
restoration is removed, due to excessive
cleaning, drying, or trauma.29
By manufacturing and completing the
restoration in a single appointment, the
office can improve efficiency by decreasing second-chair setup costs, reducing the
number of instruments that require sterilization, and eliminating the cost of disposable supplies required for conventional
restorations (including impression materials, wax, stone, temporary resin material,
and temporary cement).29 In addition, the
clinician has complete control over the
final result and esthetics of the restoration
since the software delivers a restoration that
should require only staining or glazing.29 A
well-trained, dedicated staff is mandatory
for a successful restoration. However, staff
members can make the restoration after the
dentist has prepared the tooth. This saves
time, which adds to the financial viability
of the CEREC technology.
CEREC restorations are associated with
minimal reported postoperative sensitivity,
due to rubber dam isolation in the clinical
trials that ensures a clean, isolated tooth
surface for adhesion bonding.30 Inserting
the restoration at the same appointment
as the preparation prevents possible tooth
contamination during the temporization
phase; in addition, using factory-manufactured composite and ceramic blocks
minimizes the polymerization shrinkage by
limiting it to the resin-cement interface.30
Finally, no laboratory fee is involved with
CAD/CAM restorations.
Limitations of CEREC technology
One factor that could limit the use of
CEREC technology is the cost of the
equipment, especially for dentists in solo
practices. In addition, the color of the
finished restoration may not be ideal since
the restoration is milled from a monochromatic block. However, multicolor blocks
have been developed to overcome this
limitation; in addition, dentists can place
superficial stains to mimic any shade variability in the patient’s teeth.
It takes significant time for a dentist
to become proficient enough in the use
of this system to achieve financial success.28 A 2007 study reported that dental
students introduced to CEREC 3 in their
last semester were able to produce clinically acceptable inlays with a high shortterm (2 years) success rate.31
It is difficult to digitally capture subgingival-placed margins for severely broken teeth;
in such cases, gingival retraction is needed.
CAD/CAM technology in the dental
office is limited to single units only, and a
CEREC restoration takes longer to polish
compared with a laboratory-manufactured
restoration. However, with experience,
the dentist may become faster and more
efficient in performing these tasks.28
Concerns of the CEREC materials
Strength
The blocks used with the CEREC equipment are fabricated under ideal manufacturing conditions in a reproducible manner
that eliminates human error, which
results in a dense, defect-free, high-quality
material. Conventionally fabricated restorations are made by hand, which may
lead to human error that could affect
the restoration’s mechanical and esthetic
properties.32 A 2000 study by Tinschert
et al concluded that industrially prepared
ceramics are more structurally reliable
than conventional laboratory-fabricated
ceramics, although CAD/CAM milling
procedures may induce surface and subsurface flaws that may adversely affect the
strength of this ceramic.33 However, the
strength can be restored by polishing the
material with rubber wheels and diamond
paste. Further enhancement of strength (to
approximately 160 MPa) can be acquired
by a combination of polishing and glazing.32 In a 2004 study, Attia and Kern
concluded that the fracture resistance of
teeth restored with CEREC-manufactured
crowns was equal to that of unprepared
natural teeth, but was significantly higher
than that in teeth restored with conventional low-fusing ceramic crowns.16
Esthetics
As noted earlier, the esthetics of CEREC
materials are a concern due to the monochromatic nature of the blocks. However,
a porcelain restoration can be stained
and glazed after milling; in addition, the
blocks are available in a variety of shades
to match the adjacent natural dentition. A
clinical study by Herrguth et al compared
the esthetics of CEREC-manufactured
crowns to crowns fabricated using the layering technique, and concluded that both
restorations were esthetically acceptable
to all patients with no statistically significant difference in the esthetic ratings
between the two crowns.34
A series of studies evaluated 66 ceramic
inlays (Vitablocs Mark II, Vident)
and reported that the color mismatch
increased after 10 years from 16% to
38%.35-37 According to Fasbinder et al,
the increased color mismatch was due
to the tooth changing color rather than
a color shift in the milled restoration.38
More recently, Fasbinder et al reported
a significantly better color match for
CEREC-manufactured composite inlays
(Paradigm, 3M ESPE) compared with
Vitablocs Mark II ceramic inlays at 3
years, as the composite resin appeared to
reflect the surrounding tooth color to a
better degree than the ceramic inlays.39
www.agd.org
CEREC-manufactured restorations
can provide an esthetically acceptable
restoration when polished, and an esthetically optimum one when stained and
glazed. The decreased color match over
time can be attributed to a change in
tooth shade and translucency, rather than
a change in the color of the CERECmanufactured restoration.40
Postoperative sensitivity
Early clinical studies reported significant
levels of postoperative sensitivity among
CEREC restorations. In a study of 301
inlays, Magnuson et al reported that 9%
experienced immediate post-operative
sensitivity.41 Most cases involving postoperative sensitivity resolved within
1 month.41 A 3-year clinical study by
Fasbinder et al reported that 13% of 92
Vitablocs Mark II onlays were slightly
sensitive after 1 week, and 4% of the
92 onlays were slightly sensitive after
2 weeks.42 All postoperative sensitivity
was resolved after 1 month, and no other
postoperative sensitivity was reported
during the 3-year period of observation.
Most cases of postoperative sensitivity
can be attributed to occlusal interference, since the restorations are inserted
in a single appointment. Fasbinder
advised equilibrating the occlusal
contacts after the effects of the local
anesthetic have dissipated.40
More recent studies have reported less
postoperative sensitivity, which could
be attributed to the significant improvement of the adhesive materials. Molin &
Karlsson examined 20 CEREC-generated
Vitablocs Mark I inlays (Vident) over five
years and reported no postoperative sensitivity throughout the observation period.43
The absence of significant postoperative sensitivity in such restorations can
be attributed to several factors. First,
the optical imaging of the preparation
requires careful isolation, which ensures
optimum fluid control and which maximizes the predictability of cementation.40
The fact that CEREC-manufactured
restorations eliminate the need for
temporization contributes to the lack of
postoperative sensitivity, preventing contamination of the dentin tubules during
the temporization period that can occur
with a lost, fractured, or leaking temporary restoration.39
General Dentistry
January/February 2013
37
Information Technology/Computers Overview of CEREC CAD/CAM chairside system
Margin adaptation
In 2003, Nakamura et al studied how
abutment occlusal conversion angle and
the computer luting space setting affected
the internal fit and marginal adaptation of
the ceramic CEREC 3-milled restoration.44
The authors found that setting the computer luting space at 30-50 µm produced
a marginal gap of 53-67 µm that was not
influenced by the abutment angle of occlusal conversion.44 Other researchers measured margins of approximately 50 µm,
suggesting that the marginal fit of CAD/
CAM-generated restorations is adequate
for clinical use.27,45 Denissen et al reported
a margin gap of 85 μm for CEREC
3-manufactured onlays, a gap that was not
significantly different from laboratoryfabricated onlays.23 These recorded gaps are
well within the reported maximum clinically accepted gap of 120 μm.46
A well-fitting margin is expected to
maximize the longevity of a restoration. Almost all clinical studies of
CEREC-manufactured restorations
reported ditching due to wear of the
composite resin cement at the margin.40
However, this ditching was not associated with margin discoloration or
recurrent decay. A 1992 clinical study of
CEREC-manufactured inlays cemented
with microfilled or hybrid resin-based
composite luting agent reported a linear
wear rate in the first year that decreased
after 3 years by approximately 50%.47
The authors reported that the vertical loss
of cement at the margin stopped when
it reached 50% of the margin width
and that no microleakage or secondary
decay was reported at the margin.47 More
recently, Heymann et al reported that
the wear of the adhesive luting agent at
the occlusal margin of inlays increased
over the first 3 years, and decreased
over the next 3 years.19 No margin
chipping or staining was identified in
the enamel or porcelain inlays as the
adhesive cement started to wear.19 In an
in vitro comparative study with hot-press
technique and CEREC-manufactured
restorations, Keshvad et al reported that
leucite-reinforced glass-ceramic inlay
restorations fabricated using CAD/CAM
technology and the hot-pressed technique
provided clinically acceptable marginal
and internal fit with comparable fracture
loads after luting.48
38
January/February 2013
Enamel wear
Enamel wear is always a concern when
ceramics are used as a restorative material.
Several factors may influence how ceramics
affect enamel tooth structure. It is possible
to minimize enamel wear by using finegrained ceramics and polishing or glazing
the ceramic surface.32 Several studies have
demonstrated that the wear of enamel
against polished or glazed ceramic restorations was essentially the same as that for
enamel against enamel.49-52
Longevity
Several studies have examined the success
and longevity of CEREC-manufactured
restorations. In the first such clinical trial,
Mormann et al evaluated 94 Vitablocs
Mark I inlays between September 1985
and August 1987 and reported only 2
fractured inlays during that time.53 In
2002, Otto & De Nisco studied 200
Vitabloc Mark II inlays over 10 years of
clinical service and reported a 90.4%
survival rate.54 In 8 cases, failure was
caused by ceramic fracture; in 3 cases, by
tooth fracture.54 In a 2004 in vivo study,
Bindl & Mormann compared 18 anterior
Vitablocs Mark II crowns to 18 anterior
ceramic core crowns over 2 to 5 years.55
The ceramic core crown survival rate was
91.7%, compared to 94.4% for Vitablocs
Mark II, without a statistically significant
difference.55
A 2003 study by Posselt & Kerschbaum
evaluated 2,328 ceramic inlays and onlays
in 794 patients and reported a survival
rate of 95.5% at 9 years.25 The majority of
failures were caused by inlay fracture, tooth
fracture, tooth extraction, and replacement
for occlusal reconstruction.25 A series of
articles evaluated 1,011 inlays and onlays
placed in 299 patients between 1987 and
1990 for up to 18 years. The authors determined a survival probability of 95% after
5 years, 91.6% after 7 years, and 90.0%
at 10 years; a survival rate comparable to
conventional ceramic restorations.24,56-58
The low failure rate of CERECmanufactured restorations documents the
reliability and the clinical predictability of
such restorations.
Ceramics used for chairside CEREC
Feldspathic porcelain-based ceramic
Vitablocs Mark II is a fine-grained feldspathic ceramic that produces fine crystal
General Dentistry
www.agd.org
(average size = 4 μm). The pore-free ceramic
is easier to polish and demonstrates
low enamel wear and high strength.59,60
According to the manufacturer, the feldspar
particles are uniformly embedded in the
glass matrix, avoiding a detrimental “sanding (abrading) effect” on the antagonist.60
When polished, the strength of this ceramic
material is approximately 130 MPa and it
could reach 160 MPa or higher if glazed.
This strength is approximately twice that of
conventional feldspathic ceramics and also
is higher than several pressable ceramics.60,61
Empress CAD blocks
IPS Empress CAD (Ivoclar Vivadent) is a
leucite glass-ceramic of the SiO2 -Al 2O3 K 2O materials system with leucite crystals
ranging from 5 to 10 µm in size.59,62
The leucite (KAlSi 2O6) crystals increase
the material’s strength and slow down
or deflect crack propagation, while the
crystalline phase absorbs fracture energy.
According to Giordano, this leucite-reinforced ceramic material has properties of
strength and surface characterization similar to those found in Vitablocs Mark II.32
IPS e.max CAD blocks
IPS e.max CAD (Ivoclar Vivadent) is a
lithium disilicate glass-ceramic for CAD/
CAM applications.63 The blocks are produced by massive casting of transparent
glass ingots. A continuous manufacturing
process based on glass technology (that
is, pressure-casting) is utilized to prevent
the formation of defects (pores, accumulation of pigments, and so forth) in the
bulk of the ingot. Partial crystallization
ensures that the blocks can be processed
in a crystalline intermediate phase, which
enables fast machining with CAD/CAM
systems. The partial crystallization
process leads to a formation of lithium
metasilicate (Li 2SiO3) crystals, which
are responsible for the material’s optimal
processing properties, edge stability, and
relatively high strength.63
After the milling procedure, the
restorations are tempered and lithium
disilicate (Li 2Si 2O5) crystals are formed,
which impart the ceramic object with
the desired high strength.63 A 2010 study
by Guess et al tested monolithic CAD/
CAM lithium disilicate and hand-layerveneered zirconia all-ceramic crowns
and found that using IPS e.max CAD
resulted in fatigue-resistant crowns, while
hand layer-veneered zirconia crowns
revealed early veneer failures.64
Paradigm MZ100
Paradigm MZ100 (3M ESPE) is a bisphenol A-diglycidyldimethacrylate/triethylene
glycol dimethacrylate resin-based composite with filler composed of nanocrystalline
zirconia in an amorphous silica matrix.65
Paradigm MZ100 block material contains
85% ultrafine zirconia-silica ceramic particles by weight, which reinforce a highly
crosslinked polymeric matrix (with a mean
particle size of 0.6 µm). It has superior
physical properties compared to conventional resin due to controlled manufacturing conditions, which leads to a dense
and pore-free material that is completely
cured throughout. An in vitro study by
Kassem et al found that crowns made with
Paradigm MZ100 were highly resistant to
failure from mechanical fatigue and produced significantly higher mean microleakage scores compared to ceramic crowns.66
More recently, the same authors conducted
an in vitro study in which Paradigm
MZ100 and fine particle feldspar ceramic
blocks crowns were submitted to thermocycling (500 cycles) and load-cycling
(1,000,000 cycles ranging from 60-600
N). The results indicated that Paradigm
MZ-100 crowns were more resistant to
fracture after combined load and thermal
fatigue; in addition, microleakage scores
were similar for both types of crowns.67
Summary
In this review, the authors presented
current evidence suggesting that CERECmanufactured restorations have an acceptable marginal adaptation and clinical
longevity along with reduced chair time
and improved esthetics. Evidence from
many clinical studies suggests that clinicians may choose this system on the basis of
patients’ esthetic needs. The evidence provided here should enable clinicians to enter
into informed consent decisions with their
patients who desire all-ceramic restorations.
Author information
Dr. G. Santos is an associate professor and chair, Division of Restorative
Dentistry, Schulich School of Medicine &
Dentistry, Western University, Ontario,
Canada, where Dr. M. Santos is an
assistant professor, and Dr. Rizkalla is
an associate professor and chair, Division
of Biomaterials Science. Dr. Madani is
in private practice in Toronto, Canada.
Dr. El-Mowafy is a professor and chair,
Department of Operative Dentistry,
University of Toronto, Canada.
Disclaimer
The authors have no financial, economic,
commercial, and/or professional interests
related to topics presented in this article.
References
1. Barnfather KD, Brunton PA. Restoration of the upper
dental arch using Lava all-ceramic crown and bridgework. Br Dent J. 2007;202(12):731-735.
2.Laeijendecker R, van Joost T. Oral manifestations of
gold allergy. J Am Acad Dermatol. 1994;30(2 Pt 1):
205-209.
3. Marks JG, Belsito DV, DeLeo VA, et al. North American
Contact Dermatitis Group patch-test results, 19961998. Arch Dermatol. 2000;136(2):272-273.
4.Silva R, Pereira F, Bordalo O, et al. Contact allergy to
gold sodium thiosulfate. A comparative study. Contact
Dermatitis. 1997;37(2):78-81.
5. Kranke B, Binder M, Derhaschnig J, et al. Patch testing
with the “Austrian standard series”—epidemiologic
test values and results [in German]. Wien Klin
Wochenschr. 1995;107(11):323-330.
6. Fowler JF Jr. Allergic contact dermatitis to metals.
Am J Contact Dermat. 1990;1:212-223.
7.Sertoli A, Francalanci S, Acciai MC, et al. Epidemiological survey of contact dermatitis in Italy (1984-1993)
by GIRDCA (Gruppo Italiano Ricerca Dermatiti da Contatto e Ambientali). Am J Contact Dermat. 1999;10(1):
18-30.
8.Rosenstiel SF, F. Martin F, Fujimoto J. Contemporary
Fixed Prosthodontics. 2nd ed. St. Louis, MO: Mosby;
2001.
9.Schillingburg HT. Fundamentals of Fixed Prosthodontics. Chicago, IL: Quintessence Publishing Co; 1997.
10.Siervo S, Pampalone A, Siervo P, Siervo R. Where is the
gap? Machinable ceramic systems and conventional
laboratory restorations at a glance. Quintessence Int.
1994;25(11):773-779.
11.Anusavice KJ. Phillips’ Science of Dental Materials.
11th ed. St. Louis, MO: Saunders; 2003.
12.Sjogren G, Sletten G, Dahl JE. Cytotoxicity of dental
alloys, metals, and ceramics assessed by millipore filter,
agar overlay, and MTT tests. J Prosth Dent. 2000;
84(2):229-236.
13.Eliades G, Eliades T, Barntley WA, Watts DC. Dental Materials In Vivo: Aging and Related Phenomena. 1st ed.
Chicago, IL: Quintessence Publishing Co; 2003.
14.Wiley MG. Effects of porcelain on occluding surfaces
of restored teeth. J Prosth Dent. 1989;61(2):133-137.
15. Blatz MB. Long-term clinical success of all-ceramic
posterior restorations. Quintessence Int. 2002;33(6):
415-426.
16.Attia A, Kern M. Fracture strength of all-ceramic
crowns luted using two bonding methods. J Prosth
Dent. 2004;91(3):247-252.
17.Leinfelder KF, Isenberg BP, Essig ME. A new method
for generating ceramic restorations: a CAD/CAM system. J Am Dent Assoc. 1989;118(6):703-707.
www.agd.org
18.Trost L, Stines S, Burt L. Making informed decisions
about incorporating a CAD/CAM system into dental
practice. J Am Dent Assoc. 2006;137(suppl):32S-36S.
19. Heymann HO, Bayne SC, Sturdevant JR, Wilder AD Jr,
Roberson TM. The clinical performance of CAD-CAMgenerated ceramic inlays: a four-year study. J Am Dent
Assoc. 1996;127(8):1171-1181.
20. Mormann WH. The evolution of the CEREC system.
J Am Dent Assoc. 2006;137(suppl):7S-13S.
21. Hickel R, Dasch W, Janda R, et al. New direct restorative materials. FDI commission project. Int Dent J.
1998;48(1):3-16.
22. Bayne SC, Heymann HO. CAD/CAM in dentistry: present and future applications. Quintessence Int. 1996;
27(6):431-437.
23. Denissen H, Dozic A, van der Zel J, van Waas M. Marginal fit and short-term clinical performance of porcelain-veneered CICERO, CEREC, and Procera onlays.
J Prosthet Dent. 2000;84(5):506-513.
24.Reiss B, Walther W. Clinical long-term results and
10-year Kaplan-Meier analysis of Cerec restorations.
Int J Comput Dent. 2000;3(1):9-23.
25. Posselt A, Kerschbaum T. Longevity of 2328 chairside
Cerec inlays and onlays. Int J Comput Dent. 2003;6(3):
231-248.
26. Mormann WH, Bindl A. The new creativity in ceramic
restorations: dental CAD-CIM. Quintessence Int.
1996;27(12):821-828.
27.Estafan D, Dussetschleger F, Agosta C, et al. Scanning
electron microscope evaluation of CEREC II and
CEREC III inlays. Gen Dent. 2003;51(5):450-454.
28.Christensen GJ. Computerized restorative dentistry.
State of the art. J Am Dent Assoc. 2001;132(9):13011303.
29.Trost L, Stines S, Burt L. Making informed decisions
about incorporating a CAD/CAM system into dental
practice. J Am Dent Assoc. 2006;137(suppl):32S-36S.
30. Fasbinder DJ, Dennison JB, Heys DR, Lampe K. The clinical performance of CAD/CAM-generated composite
inlays. J Am Dent Assoc. 2005;136(12):1714-1723.
31.Wrbas KT, Hein N, Schirrmeister JF, Altenburger MJ,
Hellwig E. Two-year clinical evaluation of Cerec 3D
ceramic inlays inserted by undergraduate dental students. Quintessence Int. 2007;38(7):575-581.
32.Giordano R. Materials for chairside CAD/CAM-produced restorations. J Am Dent Assoc. 2006;137(suppl):
14S-21S.
33.Tinschert J, Zwez D, Marx R, Anusavice KJ. Structural
reliability of alumina-, feldspar-, leucite-, mica- and zirconia-based ceramics. J Dent. 2000; 28(7):529-535.
34. Herrguth M, Wichmann M, Reich S. The aesthetics of
all-ceramic veneered and monolithic CAD/CAM
crowns. J Oral Rehabil. 2005;32(10):747-752.
35.Sjogren G, Bergman M, Molin M, Bessing C. A clinical
examination of ceramic (Cerec) inlays. Acta Odontol
Scand. 1992;50(3):171-178.
36.Sjogren G, Molin M, van Dijken JW. A 5-year clinical
evaluation of ceramic inlays (Cerec) cemented with a
dual-cured or chemically cured resin composite luting
agent. Acta Odontol Scand. 1998;56(5):263-267.
37.Sjogren G, Molin M, van Dijken JW. A 10-year prospective evaluation of CAD/CAM-manufactured (Cerec)
ceramic inlays cemented with a chemically cured or
dual-cured resin composite. Int J Prosthodont. 2004;
17(2):241-246.
38. Fasbinder DJ, Lampe K, Dennison JB, Peters MC, Nematollahi K. Three year clinical performance of CAD/CAM
generated ceramic onlays (abstract 1883). J Dent Res.
2001;80 (special issue):271.
General Dentistry
January/February 2013
39
Information Technology/Computers Overview of CEREC CAD/CAM chairside system
39. Fasbinder DJ, Dennison JB, Heys DR, et al. The clinical
performance of CAD/CAM-generated composite inlays. J Am Dent Assoc. 2005;136(12):1714-1723.
40. Fasbinder DJ. Clinical performance of chairside CAD/
CAM restorations. J Am Dent Assoc. 2006;37(suppl):
22S-31S.
41. Magnuson D, Oden A, Krystek I. Clinical evaluation of
CEREC restorations. In: Mormann WH, ed. International Symposium on Computer Restorations: State of the
Art of the Cerec Method. Chicago: Quintessence;
1991:339.
42. Fasbinder DJ, Dennison JB, Heys DR, Lampe K. Clinical
performance of CAD/CAM generated ceramic onlays.
J Am Dent Assoc. 2005;136(12):1714-1723.
43. Molin MK, Karlsson SL. A randomized 5-year clinical
evaluation of 3 ceramic inlay systems. Int J Prosthodont. 2000;13(3):194-200.
44. Nakamura T, Dei N, Kojima T, et al. Marginal and internal fit of Cerec 3 CAD/CAM all-ceramic crowns.
Int J Prosthodont. 2003;16(3):244-248.
45. Reich S, Wichmann M, Nkenke E, Proeschel P. Clinical fit of all-ceramic three-unit fixed partial dentures,
generated with three different CAD/CAM systems.
Eur J Oral Sci. 2005;113(2):174-179.
46. McLean JW, von Fraunhofer JA. The estimation of cement film thickness by an in vivo technique. Br Dent J.
1971;131(3):107-111.
47. Isenberg BP, Essig ME, Leinfelder KF. Three-year clinical
evaluation of CAD/CAM restorations. J Esthet Dent.
1992;4(5):173-176.
48. Keshvad A, Hooshmand T, Asefzadeh F, Khalilinejad F,
Alihemmati M, Van Noort R. Marginal gap, internal fit,
and fracture load of leucite-reinforced ceramic inlays
fabricated by CEREC inLab and hot-pressed techniques. J Prosthodont. 2011;20(7):535-540.
49. Krejci I, Lutz F, Reimer M. Wear of CAD/CAM ceramic
inlays: restorations, opposing cusps, and luting cements. Quintessence Int. 1994;25(3):199-207.
50. McLaren EA, Giordano RA, Pober R, Abozenada B. Material testing and layering techniques of a new
40
January/February 2013
two-phase all glass veneering porcelain. Quintessence
Dent Technol. 2003;26:69-81.
51. McLaren EA, Giordano RA II. Zirconia-based ceramics:
material properties, esthetics, and layering techniques
of a new veneering porcelain, VM9. Quintessence
Dent Technol. 2005;28:1-12.
52. Abozenada B, Pober R, Giordano R. In vitro wear of
restorative dental materials. J Dent Res. 2002;81(special issue) (Abstract 1693).
53. Mormann WH, Gotsch T, Krejci I, Lutz F, Barbakow F.
Clinical status of 94 CEREC ceramic inlays after 3 years
in situ. In: Mormann WH, ed. International Symposium
on Computer Restorations: State of the Art of the
Cerec Method. Chicago, IL: Quintessence; 1991: 355.
54. Otto T, De Nisco S. Computer-aided direct ceramic restorations: a 10-year prospective clinical study of
Cerec CAD/CAM inlays and onlays. Int J Prosthodont.
2002; 15(2):122-128.
55. Bindl A, Mormann WH. Survival rate of mono-ceramic
and ceramic-core CAD/CAM-generated anterior
crowns over 2-5 years. Eur J Oral Sci. 2004;112(2):
197-204.
56. Reiss B. Clinical results of Cerec inlays in a dental
practice over a period of 18 years. Int J Comput Dent.
2006;9(1):11-22.
57. Reiss B, Walther W. Survival analysis and clinical
evaluation of CEREC restorations in a private practice. In: Mormann WH, ed. International Symposium
on Computer Restorations: State of the Art of the
Cerec Method. Chicago: Quintessence; 1991:215.
58. El-Mowafy O, Brochu JF. Longevity and clinical performance of IPS-Empress ceramic restorations—a literature review. J Can Dent Assoc. 2002;68(4):233-237.
59. Fasbinder DJ. Restorative material options for CAD/
CAM restorations. Compend Contin Educ Dent.
2002;23(10):911-916, 918, 920; quiz 924.
60. Vitablocs Mark II for CEREC. Materials Science and
Clinical Studies. Available at: http://vident.com/
wp-content/uploads/2009/01/cerecmarkii.pdf.
Accessed October 2012.
General Dentistry
www.agd.org
61. Giordano R, Kanchanatawewat K, Asvanund P, Nathanson D. Flexural strength of ceramics for Celay
restorations. J Dent Res. 1996;75(special issue):125.
62. IPS Empress CAD Scientific Documentation [product
insert]. Lichtenstein: Ivoclar Vivadent AG; 2011.
63. IPS e.max CAD Scientific Documentation [product insert]. Lichtenstein: Ivoclar Vivadent AG; 2011.
64. Guess PC, Zavanelli RA, Silva NR, Bonfante EA,
Coelho PG, Thompson VP. Monolithic CAD/CAM
lithium disilicate versus veneered Y-TZP crowns:
comparison of failure modes and reliability after fatigue. Int J Prosthodont. 2010;23(5):434-442.
65. Rusin RP. Properties and applications of a new composite block for CAD/CAM. Compend Contin Educ
Dent. 2001;22(suppl 6):35-41.
66. Kassem AS, Atta O, El-Mowafy O. Fatigue resistance
and microleakage of CAD/CAM ceramic and composite molar crowns. J Prosthodont. 2011;21(1):28-32.
67. Kassem AS, Atta O, El-Mowafy O. Combined effects
of thermocycling and load-cycling on microleakage
of computer-aided design/computer-assisted manufacture molar crowns. Int J Prosthodont. 2011;24(4):
376-378.
Manufacturers
Ivoclar Vivadent Inc., Amherst, NY
800.533.6825, www.ivoclarvivadent.us
Siemens, Washington, DC
800.743.6367, www.usa.siemens.com
Sirona Dental Systems, Inc., Long Island City, NY
718.937.5765, www.sirona.com
Vident, Brea, CA
800.828.3839, www.vident.com
3M ESPE, St. Paul, MN
888.364.3577, solutions.3m.com
Exercise No. 321 Information
Technology/Computers Subject Code 561
The 15 questions for this exercise are based on the article
Overview of CEREC CAD/CAM chairside system, on pages
36-40. This exercise was developed by Daniel S. Geare, DMD,
in association with the General Dentistry Self-Instruction
committee.
1. The disadvantages of metal-ceramic
restorations include all of the following
except one. Which is the exception?
A. Metal allergy
B.Esthetics
C.Corrosion
D. Low shear strength
2. Prevalence for contact allergy in nickelcontaining crowns is reported to be as
high as _____%.
A0.88
B.8
C.9
D.29
3. Popular characteristics of ceramic crowns
include all of the following except one.
Which is the exception?
A. Greater esthetics
B. Increased durability
C. Reduced pulpal trauma
D. Greater wear resistance
4. The maximum clinically acceptable
margin gap for all crowns is _____ μm.
A.65
B.80
C.120
D.135
5. The CAD/CAM CEREC system eliminates
the need for all of the following except
one. Which is the exception?
A.Impressions
B.Provisionalization
C. Lab assistance
D. Preparation design
Reading the article and successfully completing this exercise will
enable you to understand:
•the advantages and limits of CEREC technology;
•the clinical qualities of CAD/CAM restorations; and
•the types of porcelain and composite used in CAD/CAM technology.
6. Criticism of the CEREC system was
focused on
A. marginal fit.
B. color stability.
C. occlusal design.
D. fracture resistance.
7. The CEREC crowns have been shown
to have better esthetics than standard
porcelain crowns. There is a reduction
in color matching due to the change in
tooth shade over time.
A. Both statements are true.
B. The first statement is true;
the second is false.
C. The first statement is false;
the second is true.
D. Both statements are false.
8. The CAD/CAM restorations have a
marginal fit of approximately _____ μm.
A.15
B.25
C.50
D.90
9. Limits of the CAD/CAM system include
all of the following except one. Which is
the exception?
A. Need to use gingival retraction
B. Single units only
C. Polishing time
D. Unpredictable shades
10. CAD/CAM-prepared restorations
are more structurally reliable than
laboratory-made restorations. This is
because CAD/CAM restorations eliminate
subsurface flaws in the ceramic.
A. Both statements are true.
B. The first statement is true;
the second is false.
C. The first statement is false;
the second is true.
D. Both statements are false.
11. According to Attia & Kern, fracture
resistance of teeth restored with
CEREC-manufactured crowns
was _____________ unprepared
natural teeth.
A. equivalent to
B. less than
C. more than
D. unrelated to
12. Postoperative sensitivity with CEREC
restorations is primarily attributed to
A. occlusal interference.
B. marginal leakage.
C. excessive preparation depth.
D. poor tooth isolation on cementation.
13. Failure of ceramic inlays and onlays is
caused by all of the following except one.
Which is the exception?
A. Poor preparation design
B. Tooth fracture
C. Tooth extraction
D. Inlay fracture
14. All of the following statements are true
except one. Which is the exception?
A. Feldspathic porcelain uses leucite
particles embedded in a glass matrix.
B. Empress porcelain resists cracks due to
leucite crystals.
C. IPS e.max porcelain resists fracture
by high-pressure fusing of porcelain
powder.
D. Paradigm MZ100 crosslinks zirconia
with a silica matrix.
15. Disadvantages of CAD/CAM include
all of the following except one. Which
is the exception?
A. Time for training
B. Cost of equipment
C. Time to polish restorations
D. Capturing the digital impressions
Answer form is on page 80. Answers for this exercise must be received by December 31, 2013.
www.agd.org
General Dentistry
January/February 2013
41
Periodontics
Clinical long-term evaluation of acellular dermal
matrix in the treatment of root recession: case report
Joao Carnio, DDS, MS n Marcel Fuganti, DDS
Several clinical studies have documented success when using an
acellular dermal matrix (ADM) to treat mucogingival defects; however,
information concerning its long-term stability is limited. This article
presents a case involving a patient with root recession treated with
an ADM. Probing depth, marginal tissue recession, and the amount
O
ne of the key goals of periodontal
surgery is obtaining predictable and
esthetic root coverage, while increasing the area of attached gingiva. Various surgical techniques that have been employed
to achieve this goal include pedicle flaps,
epithelialized free palatal grafts, subepithelial connective tissue grafts (CTGs), and
guided tissue regeneration.1 Among these,
the subepithelial CTG is considered the
gold standard technique for root coverage
procedures.2,3 However, this graft requires
autogenous palatal donor tissue, which
causes an additional surgical patatal wound
that could increase the risk of complications, and it is directly related to greater
postoperative discomfort to the patient.4
The literature has reported on the success
of an acellular dermal matrix (ADM) for
periodontal purposes.5 This material is an
allograft, obtained from an aseptic process
in which skin cells are removed, eliminating
the source of infection, disease transmission, and immunological reaction.6 ADM
has been used extensively to replace autogenous donor tissues in cases of primary and
secondary burn reconstruction.7 Its structure serves as an architectural support for
fibroblast migration and revascularization
to periodontal tissues, reducing operative
time, avoiding possible palatal complications, and improving the patient’s postoperative recovery. According to Harris,
these advantages have increased acceptance
among both patients and periodontists.8
According to the literature, the use of
Alloderm (LifeCell Corporation) provides
predictable root coverage, with mean root
coverage ranging from 86% to 95.8%;
however, this information about Alloderm
was obtained from studies and cases with
short follow-up periods (≤6 months ).9-11
42
January/February 2013
of keratinized and attached tissues were evaluated for 10 years
post-treatment; the results showed long-term stability during the
observation period.
Received: August 18, 2011
Accepted: November 11, 2011
This case report sought to evaluate
the long-term stability of a root coverage
procedure that utilized an ADM. The
preoperative and postoperative amount of
root coverage and the increase in keratinized and attached tissues were compared.
Materials and methods
A 36-year-old nonsmoking woman in
good general health had a chief complaint
of root hypersensitivity to cold. Clinical
examination showed the presence of
incipient marginal tissue recession in the
region of teeth No. 28 and 29, as well as a
minimal apico-coronal dimension of keratinized tissue, and abrasion of the cervical
root region due to traumatic toothbrushing
(Fig. 1 and 2, Table). The patient agreed to
receive the ADM for a palatal wound that
caused great postoperative discomfort.
Professional plaque control was performed prior to the surgical procedure and
the patient was instructed in proper oral
hygiene habits. Presurgical measurements
Fig. 1. Teeth No. 28 and 29, showing an incipient
Class I recession.
General Dentistry
www.agd.org
included probing depth, marginal tissue
recession, and the amount of keratinized
and attached tissues (Table). After topical application of Schiller’s solution, all
clinical measurements were made with a
University of North Carolina periodontal
probe (to the nearest millimeter) on the
straight buccal aspect of the teeth.
After local anesthesia was administered, a pouch was created by extending
a sulcar incision from the distal surface
of tooth No. 30 to the mesial surface
of tooth No. 27, giving the flap enough
mobility to avoid vertical releasing
incisions (Fig. 3).12 To facilitate the
postoperative healing process, a bleeding
area was created in the interproximal
lingual papillae. A partial thickness flap
was made and the roots were scaled and
planed to achieve a flattened surface
and make the site more suitable for
receiving the graft (Fig. 4). The ADM
was trimmed to 8 mm x 15 mm and
prepared according to the manufacturer’s
Fig. 2. Teeth No. 28 and 29 following application of
Schiller’s solution. Note the presence of a moderate
amount of keratinized tissue.
Table. Clinical periodontal measurements (mm) taken
on the straight buccal aspect of teeth No. 28 and 29
pretreatment and post-treatment.
Time point
Baseline
29
5-Year
28
28
Pocket depth
1.0
1.0
1.0
1.0
1.0
1.0
Keratinized tissue
1.0
2.0
2.0
3.0
3.0
3.0
Attached gingiva
0.0
1.0
1.0
2.0
2.0
2.0
Gingival recession
2.0
1.0
0.0
0.0
0.0
0.0
Fig. 4. The receptor site after scaling and root planing.
instructions (LifeCell Corporation).13
The graft was placed so that it extended
approximately 3 mm over the surrounding bone. The material was oriented
so that the white basement membrane
side (Fig. 5) was placed adjacent to the
bone and tooth, and the red connective
tissue side (Fig. 6) was placed toward the
flap. The orientation used was opposite
from what the manufacturer suggested
for a free gingival graft; however, this
orientation is normally utilized when
the ADM is subepithelialized.
The graft was stabilized in the cementoenamel junction using No. 6-0 absorbable
suspensory sutures (Fig. 7) and the flap
was positioned coronally using No. 4-0 silk
interrupted single sutures. Approximately
1 mm of the ADM was intentionally
exposed to the oral environment (Fig. 8).
Postoperative recommendations included
500 mg of amoxicillin (taken 3 times daily
for 7 days), 600 mg of ibuprofen (twice
daily for 4 days, as needed), and 0.12%
chlorhexidine mouthwash (twice daily for
4 weeks, beginning after the second week
of healing). The patient was instructed
29
10-Year
Tooth
28
29
Fig. 3. A partial thickness flap from the distal
surface of tooth No. 30 to the mesial surface of
tooth No. 27.
Fig. 5. The basement membrane.
Fig. 6. The connective tissue.
Fig. 7. The graft following stabilization with No. 6-0
absorbable suspensory sutures.
Fig. 8. The graft positioned coronally with simple
suture.
to refrain from mechanical oral hygiene
practices for 6 weeks after surgery (professional tooth cleaning was performed every
week during that period), when the patient
could resume home brushing and flossing.
slight increase in the corono-apical direction (with variations of approximately
1 mm), but remained stable over the
3-month healing period and throughout
the 10-year observation period (Table).
Clinically, the connective tissue thickness increased significantly, although it
was not measured initially (Fig. 13-15).
The exposed area of the ADM remained
clinically visible for 2 weeks postsurgery, and was integrated into the tissues
completely after 4 weeks (Fig. 8). It
is important to note that the patient
did not return for periodontal support
Results
Healing occurred uneventfully during the
first 12 weeks of observation (Fig. 9-12).
Probing depth remained unchanged,
marginal tissue recession was eliminated
and stability was maintained throughout
the observation period. Keratinized tissue
and attached gingiva demonstrated a
www.agd.org
General Dentistry
January/February 2013
43
Periodontics Clinical long-term evaluation of acellular dermal matrix in the treatment of root recession
Fig. 9. The patient 2 weeks postsurgery.
Note that the “white” aspect of the
exposed ADM was still present.
Fig. 10. The patient 4 weeks postsurgery, with the ADM incorporated
into the tissues.
Fig. 11. The patient 8 weeks postsurgery, with complete root coverage.
Fig. 12. The patient 12 weeks
postsurgery.
Fig. 13. The patient 5 years postsurgery.
Fig. 14. The grafted site 10 years postsurgery.
Notice the increase in mucosal thickness as
compared to Fig. 1.
Fig. 15. A Schiller’s solution was applied to identify
the mucogingival junction.
therapy after the initial 12-week maintenance care program; however, the
surgical site always showed a high level
of plaque control during recall visits.
by other host cells. Fibroblasts and
capillaries invade these spaces and tend
to proliferate into the new tissue. New
collagen fibers replace the existing graft
fibers, which are reabsorbed gradually.7
Although histological studies concerning
the incorporation of ADMs are limited,
animal and human studies have reported
the graft integrating with the tissues in
a single highly vascularized structure
(without the presence of inflammatory
cells) over a period of 10-12 weeks.15-17
The use of ADM in periodontal
procedures is currently for root coverage.18-21 In comparative studies with
subepithelial CTGs, ADM showed a
minor increase of keratinized tissue.5,15
Because the graft tissue assumes the
characteristics of the donor site, keratinization occurs through an induction
mechanism.22 Although ADM derives
from keratinized human skin, it is
conceivable that the vitality of the graft
may be essential to induce the keratinization of the overlaid flap.23 Unlike the
subepithelial CTG, where the portion
that remains exposed tends to differentiate itself, ADM must be covered
completely to increase blood flow.22,24
Because an ADM is a non-vital
allograft, its restructuring process
depends on the proliferation of epithelial cells, blood vessels, and collagen
fibers along its entire length. In turn,
the CTG has some vessels and cells;
as a result, healing and vascularization
occurs through anastomoses between
the recipient bed and the graft.25,26
The process of increasing keratinized
tissue with the use of an ADM is still
unclear. Some authors suggest that this
keratinization process will depend on
the type and amount of cells that will
colonize the graft.22,23 Since only the
cells of the periodontal ligament and
gingival tissue are capable of inducing
the formation of keratinized epithelium,
keratinization by the ADM depends
on the quantity of these cells in the
tissue. Thus, the type of tissue and the
amount of keratinization on the flap
covering the graft will determine the
final amount of keratinization.14,19
In the present case, the main purpose
of the allograft was to provide root
coverage; however, it also was expected
to increase the amounts of keratinized
tissue and attached gingiva. During
Discussion
ADM was developed as a dermal replacement for burn patients.7 It is an allograft,
derived from human skin, in which
the epidermis and all of the cells of the
dermis have been removed through a
freeze-drying process, which prevents
specific inflammatory reactions due to
the graft. ADM is a biomaterial containing components of types IV and VII
collagen, elastin, and laminin, and can
be inserted without the risk of rejection
from the host’s immune system.6,7
Histologically, ADM resembles normal
dermis, without the skin’s cellular and
vascular components. Compared to
human gingival tissue, ADM has an
abundance of elastin, which is present in
the oral mucosa, but not in the gingival
tissue.14 ADM acts as a scaffold (matrix)
for the formation of normal tissue
architecture and also as a mold for tissue
regeneration.6 When an ADM is transplanted, it creates a space that is occupied
44
January/February 2013
General Dentistry
www.agd.org
the observation period, marginal tissue
recession was eliminated and the probing
depth remained unchanged. The amount
of keratinized tissue and attached gingiva
were considered to be satisfactory, as
both increased slightly. The notion that
the increase in keratinized tissue is due
to the amount of ADM left exposed is
questionable, since the graft must be,
by indication, completely covered by
the flap. It is in contrast to the use of
subepithelial CTG, where in order to
enhance the apico-coronal amount of
keratinized tissue, one should leave a
portion of the graft exposed to the oral
environment.24,27,28 The final results
are within acceptable limits since the
literature has shown that approximately
2 mm of keratinized tissue with 1
mm of attached gingiva is enough to
maintain a clinically healthy site.29
Clinical examination revealed an
increase in the buccolingual dimension
of the entire mucosal/gingival complex
on the buccal aspect of teeth No. 28 and
29. Although soft tissue thickness was not
evaluated objectively in the present case,
an increase was evident based on pretreatment and post-treatment evaluations.
The data in this case report showed
that an ADM was effective as a means of
achieving root coverage, producing an
increase in the apico-coronal dimension
and thickness of keratinized tissue that
remained stable for a period of 10 years.
Conclusion
Local results presented in the present case
demonstrate that an ADM graft heals
within expected parameters, completely
integrates into the tissues within a period
of 8 to 12 weeks, and remains stable for
a long period of observation. The results
indicate that ADM is a viable alternative for eliminating recession without
needing palatal donor tissue. However,
when interpreting the results, it should be
noted that only one case was examined;
as a result, whereas these data should
be viewed as proof of the principle,
additional research—utilizing a larger
population—should be conducted to
confirm the long-term stability of ADMs.
Author information
Dr. Carnio is associate professor,
Department of Periodontics, University of
Florida College of Dentistry. Dr. Fuganti
is in private practice in Londrina-Parana,
Brazil.
References
1.Wennstrom JL. Mucogingival therapy. Ann Periodontol.
1996;1(1):671-701.
2.Langer B, Calagna LJ. The subepithelial connective tissue graft. A new approach to the enhancement of anterior cosmetics. Int J Periodontics Restorative Dent.
1982;2(2):22-33.
3.Langer B, Langer L. Subepithelial connective tissue
graft technique for root coverage. J Periodontol 1985;
56(12):715-720.
4.Reiser GM, Bruno JF, Mahan PE, Larkin LH. The subepithelial connective tissue graft palatal donor site: anatomic considerations for surgeons. Int J Periodontics
Restorative Dent. 1996;16(2):130-137.
5. Harris RJ. A comparative study of root coverage obtained with an acellular dermal matrix versus a connective tissue graft: results of 107 recession defects in
50 consecutively treated patients. Int J Periodontics
Restorative Dent. 2000;20(1):51-59.
6.Livesey SA, Herndon DN, Hollyoak MA, Atkinson YH,
Nag A. Transplanted acellular allograft dermal matrix.
Potential as a template for the reconstruction of viable
dermis. Transplantation. 1995;60(1):1-9.
7.Achauer BM, VanderKam VM, Celikoz B, Jacobson
DG. Augmentation of facial soft-tissue defects with
Alloderm dermal graft. Ann Plast Surg. 1998;41(5):
503-507.
8. Harris RJ. A short-term and long-term comparison of
root coverage with an acellular dermal matrix and a
subepithelial graft. J Periodontol. 2004;75(5):734743.
9. Harris RJ. Root coverage with a connective tissue
with partial thickness double pedicle graft and an
acellular dermal matrix graft: a clinical and histological evaluation of a case report. J Periodontol. 1998;
69(11):1305-1311.
10.Aichelmann-Reidy ME, Yukna RA, Evans GH, Nasr HF,
Mayer ET. Clinical evaluation of acellular allograft
dermis for the treatment of human gingival recession.
J Periodontol. 2001;72(8):998-1005.
11. Novaes AB Jr, Grisi DC, Molina GO, Souza SL, Taba
Júnior M, Grisi MFM. Comparative 6-month clinical
study of a subepithelial connective tissue graft an acellular dermal matrix graft for the treatment of gingival
recession. J Periodontol. 2001;72(11): 1477-1484.
12.Raetzke PB. Covering localized areas of root exposure employing the “envelope” technique.
J Periodontol. 1985;56(7):397-402.
13.LifeCell Corporation. Alloderm Regenerative Tissue
Matrix [instructions for use]. Available at: http://www.
lifecell.com/downloads/LC_Allodem114_IFU_B_
T4.pdf. Accessed July 3, 2012.
14.Cummings LC, Kaldahl WB, Allen EP. Histologic evaluation of autogenous connective tissue and acellular
dermal matrix grafts in humans. J Periodontol. 2005;
76(2):178-186.
www.agd.org
15. Paolantonio M, Dolci M, Esposito P, et al. Subpedicle
acellular dermal matrix graft and autogenous connective tissue graft in the treatment of gingival recessions:
a comparative 1-year clinical study. J Periodontol.
2002;73(11):1299-1307.
16.Luczyszyn SM, Grisi MF, Novaes AB Jr, Palioto DB,
Souza SL, Taba M Jr. Histologic analysis of the acellular
dermal matrix graft incorporation process: a pilot
study in dogs. Int J Periodontics Restorative Dent.
2007;27(4):341-347.
17.Scarano A, Barros RR, Iezzi G, Piattelli A, Novaes AB Jr.
Acellular dermal matrix graft for gingival augmentation: a preliminary clinical, histologic, and ultrastructural evaluation. J Periodontol. 2009;80(2):253-259.
18.Shulman J. Clinical evaluation of an acellular dermal
allograft for increasing the zone of attached gingiva.
Pract Periodontics Aesthet Dent. 1996;8(2):201-208.
19.Wei PC, Laurell L, Geivelis M, Lingen MW, Maddalozzo D. Acellular dermal matrix allografts to achieve
increased attached gingiva. Part 1. A clinical study.
J Periodontol. 2000;71(8):1297-1305.
20. Fowler EB, Breault LG. Ridge augmentation with a
folded acellular dermal matrix allograft: a case report.
J Contemp Dent Pract. 2001;2(3):31-40.
21. Novaes AB Jr, Papalexiou V, Luczyszyn SM, Muglia VA,
Souza SL, Taba Junior M. Immediate implant in extraction socket with acellular dermal matrix graft and bioactive graft: a case report. Implant Dent. 2002;
11(4):343-348.
22. Karring T, Lang NP, Loe H. The role of gingival connective tissue in determining epithelial differentiation. J Periodontal Res. 1975;10(1):1-11.
23.Allen EP. AlloDerm: an effective alternative to palatal
donor tissue for treatment of gingival recession. Dent
Today. 2006;25(1):48-52.
24. Han JS, John V, Blanchard SB, Kowolik MJ, Eckert GJ.
Changes in gingival dimensions following connective
tissue grafts for root coverage: comparison of two procedures. J Periodontol. 2008;79(8):1346-1354.
25. Barros RR, Novaes AB, Grisi MF, Souza SL, Taba MJ,
Palioto DB. A 6-month comparative clinical study of a
conventional and a new surgical approach for root
coverage with acellular dermal matrix. J Periodontol.
2004;75(10):1350-1356.
26.Oliver RC, Loe H, Karring T. Microscopic evaluation of
the healing and revascularization of free gingival
grafts. J Periodontal Res. 1968;3(2):84-95.
27. Maurer S, Hayes C, Leone C. Width of keratinized tissue
after gingivoplasty of healed subepithelial connective
tissue grafts. J Periodontol. 2000;71(11):1729-1736.
28.Carnio J, Camargo PM. Clinical and histological longterm evaluation of a subepithelial connective tissue
graft used as treatment for a mucogingival defect: report of a case. Clin Adv Periodont. 2012;2:1-8 .
29.Lang NP, Loe H. The relationship between the width
of keratinized gingiva and gingival health.
J Periodontol. 1972;43(10):623-627.
Manufacturer
LifeCell Corporation, Branchburg, NJ
800.367.5737, www.lifecell.com
General Dentistry
January/February 2013
45
Dental Materials
Marginal leakage and microhardness evaluation of
low-shrinkage resin-based restorative materials
Tabassom Hooshmand, DDS, PhD n Negin Tabari, DDS n Alireza Keshvad, DDS, PhD
This study sought to compare the marginal leakage and microhardness
of low-shrinkage resin-based dental restorative materials containing ormocer- and silorane-based composites to that of conventional
methacrylate-based systems. A total of 50 noncarious extracted human
teeth were collected after debridement and standard Class V cavities
were prepared. Teeth were randomly assigned to five groups (n = 10)
and restored with 5 types of resin-based restorative material composites:
hybrid, microhybrid, nanohybrid, ormocer-based, and silorane-based.
After thermocycling, all teeth were placed in a silver nitrate solution, sectioned longitudinally in a buccolingual direction, and observed under a
stereomicroscope to determine the degree of dye penetration. Data were
analyzed using a non-parametric Kruskal-Wallis test ( P < 0.05). For the
microhardness test, five specimens were made for each restorative material, using Teflon molds with disk-shaped specimen wells. Specimens
C
oncerns related to mercury in dental
amalgams, along with the desire for
improved esthetics in dental restorations, have increased interest in resin
composites as alternative dental restorative material. Inherent disadvantages of
resin composites include polymerization
shrinkage and inadequate wear resistance,
which contribute to such clinical challenges as marginal leakage, postoperative sensitivity, secondary caries, wear
leading to loss of anatomy and occlusal
relationships, and degradation leading
to fracture.1,2 The contraction stress
associated with polymerization shrinkage can also lead to cuspal displacement
and cracks in healthy tooth structure.3
Recently, attempts have been made to
reduce polymerization shrinkage by modifying the monomer matrix. Organically
modified ceramics (known as ormocers)
are a new category of resin-based restorations that combine inorganic (ceramic)
and organic materials. Multifunctional
urethane- and thioether(meth)-acrylate
alkoxysilanes have been developed as solgel precursors for the synthesis of copolymer ormocer composites. The alkoxysilane
groups allow the formation of an inorganic
Si-O-Si network to form via hydrolysis and
polycondensation reactions, whereas the
(meth)acrylate groups make photochemically-induced organic polymerization
46
January/February 2013
were photocured and placed in distilled water (at 37°C) for 24 hours.
Vickers Hardness Number (VHN) measurements were performed using
a microhardness tester. Data were analyzed by one-way ANOVA and
Bonferroni post hoc tests. In terms of microhardness, there was no
statistically significant difference among the resin-based restorative
materials ( P > 0.05). The degree of microleakage at the gingival margins
was lowest for the silorane composite, followed by microhybrid and
nanohybrid. The silorane composite was significantly lower than that of
the ormocer and hybrid composites ( P < 0.05). Based on the results of
this study, it was concluded that the silorane-based composite material
could provide a marginal seal comparable to that provided by microhybrid or nanohybrid resin composites.
Received: December 1, 2011
Accepted: March 14, 2012
possible. After the filler particles are incorporated, the ormocers can be manipulated
by the dentist the same as a hybrid composite.4-6 Several studies have demonstrated
ormocers displaying similar performance
to bisphenol A-glycidyl-methacrylate
(bis-GMA)-based composites.2,7,8
Cationic ring opening monomer systems
have been incorporated for the purpose of
creating a highly reactive, biocompatible
composite that offers little shrinkage and
withstands the aggressive environment
of the oral situation.3 This silorane-based
composite material is a hybrid monomer
system that contains both siloxane and
oxirane structural moieties.9 Previous
studies have shown that silorane-based
composites demonstrate reduced polymerization stress and shrinkage compared with
methacrylate-based restorative systems.3,9,10
The performance of a dental restorative
material in the oral cavity can be predicted
by its surface behavior. Surface hardness is
directly related to the material’s ability to
withstand polishing, scratching, and the
stress from opposing dental structures or
materials.11 The literature has little information regarding marginal leakage and
surface hardness of ormocers compared
to that of silorane-based composites.
This study sought to assess and compare
in vitro marginal leakage and microhardness of low-shrinkage resin-based
General Dentistry
www.agd.org
restorative materials containing ormocerand silorane-based composites with
conventional methacrylate-based systems.
Materials and methods
Microleakage evaluation
Twenty-five non-carious extracted human
premolars or molars were collected (after
debridement) and stored for 7 days in
0.5% chloramine solvent. At that point,
the teeth were stored in distilled water at
room temperature. Using a high-speed
diamond flat end fissured bur (that used
water as a coolant), 50 standard Class V
cavities were prepared (one on the buccal
and one on the lingual surface of each
tooth); the preparations included an occlusal margin in enamel and a gingival margin
in dentin. The bur was replaced after every
fifth preparation. Each preparation was
approximately 3 mm x 3 mm x 2 mm.
The teeth were distributed randomly into
5 groups (n = 10).
Group 1 samples received a microhybrid resin composite (Tetric Ceram,
Ivoclar Vivadent Inc.), with 2 layers of
bonding agent (Excite, Ivoclar Vivadent
Inc.) applied to the whole cavity surface.
Each layer was left for 10 seconds and
air-dried for 5 seconds before the last
layer was photocured (at 800 mW/cm2)
for 20 seconds with a halogen curing unit
(Coltolux 75, Coltene/Whaledent Inc.).
Table 1. Resin-based restorative materials and adhesive
systems used.
Group (n = 10)
Restorative material (composite)
Adhesive system
1
Tetric Ceram1 (microhybrid)
Excite1
2
Tetric Evo Ceram1 (nanohybrid)
Excite1
3
Ceram X Mono2 (ormocer)
Prime & Bond, NT2
4
Spectrum TPH (hybrid)
Prime & Bond, NT2
5
Filtek Silorane3 (silorane)
Bond 23
2
Figure. Longitudinal section showing silver nitrate
penetration.
Ivoclar Vivadent Inc., 2DENTSPLY Caulk, 33M ESPE
1
Group 2 samples received a nanohybrid resin composite (Tetric EvoCeram,
Ivoclar Vivadent Inc.) and were prepared
similar to the samples in Group 1.
Group 3 samples were treated with an
ormocer (Ceram X Mono, DENTSPLY
Caulk). A layer of bonding agent (Prime
& Bond NT, DENTSPLY Caulk) was
applied, left for 20 seconds, air-dried for 5
seconds, and photocured for 20 seconds.
Group 4 samples utilized a hybridresin composite (Spectrum TPH,
DENTSPLY Caulk), using the same
process as Group 3 samples.
Group 5 samples received a siloranebased composite (Filtek Silorane, 3M
ESPE), to which a layer of self-etching
primer (Primer 1, 3M ESPE) was applied,
left for 15 seconds, air-dried, and then light
cured for 10 seconds. At that point, a bonding agent (Bond 2, 3M ESPE) was applied,
air-dried, and photocured for 10 seconds.
With the exception of Group 5, that
used a self-etching primer, all groups
were etched using 37% phosphoric
acid, on the enamel and dentin surfaces
(enamel = 20 seconds, dentin = 15
seconds). The cavities were rinsed thoroughly with water for 20 seconds and
blotted dry, leaving the dentinal surfaces
slightly moist. At that point, the bonding
procedures were applied. All of the resinbased materials evaluated in this study
were used in combination with their
matching adhesive systems, according
to the recommendation of the respective manufacturers. All preparations,
etching and bonding procedures were
conducted by the same operator. The
description of composite materials and
bonding agents used are listed in Table 1.
All restorative materials were placed
using a bulk technique and photocured for 40 seconds (at 800 mW/cm2)
using Coltolux 75. The restorations
were then finished and polished with
fine-grit finishing diamond burs.
The specimens were stored in distilled
water (at 37°C) for 7 days and subjected
to thermocycling (at 3,000 cycles) in
water baths (5°C-55°C), immersed for 20
seconds and transferred for 20 seconds.
After thermocycling, the root ends were
sealed with resin composite and the
entire surface of each tooth (except for
2 mm around the circumference of the
restoration margins) was coated with a
clear nonfluorescent nail polish to ensure
a perfect seal. At that point, the specimens were immersed for 6 hours into a
unimolar silver nitrate solution, rinsed
thoroughly, and stored for 12 hours in a
photochemical developer. Specimens were
exposed to a fluorescent light for 6 hours
(to reduce silver ions to metallic silver)
and embedded in a transparent self-cure
acrylic resin (Meliodent Rapid Repair,
Heraeus Kulzer). Using a slow speed diamond saw (Isomet, Buehler) with watercooling, each specimen was cut vertically
in a buccolingual direction through the
center of the restoration (Figure).
Marginal leakage was determined
with a stereomicroscope (SLX 12,
Olympus). A micrometer scale was
placed diagonally across each image
(1024 x 768 pixels) for calibration
and metric assessment of distances.
Microhardness evaluation
For specimen preparation, a clear glass
slab on top of a dark background was
www.agd.org
used as a supporting surface and to
decrease the reflectivity of the underlying surface toward each specimen. A
polytetrafluoroethylene (PTFE) mold (5
mm diameter x 2 mm height) was placed
on the glass slab. A total of 25 specimens
were made from the 5 resin-based restorative materials groups (n = 5). Initially,
the molds were slightly overfilled with
material, covered with a plastic matrix
strip, and pressed flat with a microscopic
glass slide to extrude excess material.
The resin-based restorative materials were
photocured continuously with a quartz
tungsten halogen curing light (Coltolux
75) at 800 mW/cm2 for 40 seconds. The
light tip was in close contact with the
microscopic slide. The top surfaces of
all specimens were wet-ground slightly,
using a 1200 grit size silicon carbide paper
to remove uncured resin. All specimens
were stored for 24 hours in light-proof
containers with distilled water (37°C).
The microhardness was measured using
a microhardness tester (Micromet 2100,
Buehler), with a marker for Vickers units.
Microhardness indentations were made
on the top and bottom surfaces of each
specimen. Three readings with a 50 g load
for 15 seconds were taken on the top and
bottom surfaces of each specimen and
the average was converted into a VHN.
Hardness ratios were computed within
each group by dividing the mean bottom
hardness by the mean top hardness.
Statistical analysis
To compare the microleakage levels of
different composites, a nonparametric
Kruskal-Wallis test and a Dunn’s multiple range test were used to analyze the
General Dentistry
January/February 2013
47
Dental Materials Marginal leakage and microhardness evaluation of low-shrinkage resin-based restorative materials
Table 2. Microleakage mean rank scores using
Kruskal-Wallis statistical analysis.
Buccal surfaces
Group
1 (microhybrid)
Lingual (palatal) surfaces
Table 3. The mean top and bottom surface VHNs (SD)
and hardness ratios.
Occlusal
(ceramic)
Gingival
(dentin)
Occlusal
(ceramic)
Gingival
(dentin)
12.50
6.50
9.50
7.50
1 (microhybrid)
47.38 (5.19)
44.73 (6.2)
95.07
2 (nanohybrid)
50.50 (4.38)
42.66 (6.73)
85.63
Group
Top surface
Bottom surface Hardness ratio (%)
2 (nanohybrid)
12.50
11.42
12.25
9.38
3 (ormocer)
14.75
20.33
9.50
18.38
3 (ormocer)
57.34 (5.22)
40.61 (3.81)
71.28
48.16 (4.64)
38.04 (4.28)
79.29
46.32 (9.6)
40.98 (3.52)
92.71
4 (hybrid)
12.50
19.67
11.70
17.30
4 (hybrid)
5 (silorane)
14.58
8.08
13.85
4.50
5 (silorane)
statistical differences among groups. A
Wilcoxon signed rank test was used to
assess the correlation between the microleakage at buccal and lingual (palatal)
surfaces for the resin-based materials.
To compare the microhardness level
of each composite, the data were analyzed using one-way ANOVA, as the
raw data was characterized by a normal
distribution based on the one-sample
Kolmogorov-Smirnov test.
The statistical operations were
performed using computer software (SPSS
for Windows 11.5, IBM Corporation).
The selected level of statistical significance
was P < 0.05.
Results
Table 2 lists the mean microleakage scores
for the various materials tested in this study.
For buccal and lingual (palatal) surfaces, samples in Groups 1, 2, and 5
demonstrated the smallest amount of
microleakage at the gingival margins, with
no significant difference between the three
groups (P > 0.05); Groups 3 and 4 demonstrated the most microleakage, with no statistically significant difference (P > 0.05).
Among the resin-based restorative materials tested, statistical analysis showed no
significant difference in the microleakage
at the occlusal margins of the buccal or
lingual (palatal) surfaces (P > 0.05). There
was no correlation between buccal surface
microleakage and palatal (lingual) surface
microleakage for any of the restorative
materials used in this study (P > 0.05).
Samples in Groups 1 and 5 demonstrated
the highest hardness ratios; however, there
were no statistically significant differences
48
January/February 2013
among the restorative materials in terms
of hardness ratio or microhardness of
upper and lower surfaces (P > 0.05).
Table 3 lists the mean microhardness
values for all groups.
Discussion
Marginal seal is important for the success
and longevity of a dental restoration. Dye
penetration is the most common method
for evaluating the sealing ability of dental
materials in vitro.12 To investigate the
effectiveness of resin-based materials in
a high C-factor preparation, the present
study used a Class V preparation with
enamel and dentinal margins.
Silver nitrate—which has been considered suitable for measuring both
microleakage and nanoleakage—was used
to evaluate microleakage.13 The silver ion
is small (diameter = 0.059 nm) compared
to a typical bacterium (0.5-1.0 µm). The
ion’s small size, and its high reactivity to
stain after binding to exposed collagen
fibrils, makes silver nitrate the most
appropriate agent for detecting nanoporosities within the hybrid layer.14,15
Dental materials are subjected to thermal changes and induced thermal stresses
in the mouth, as the different coefficients
of thermal expansion in materials and
dental structure generate stresses at the
interface.16 A thermocycling protocol
was used in the present study to simulate
these thermal changes and stresses.
The bonding of resin-based composites
to dentin has been known to be a great
challenge.17 However, bonding of resinbased restorative materials to enamel is
adequate.17 In the present study, neither
General Dentistry
www.agd.org
the resin-based restorative materials nor
the conventional methacrylate-based
composites provided complete marginal
seal in Class V cavities. In terms of
microleakage, no statistically significant
difference was detected between occlusal
(enamel) margins at the buccal or palatal
surfaces, a finding in keeping with previous studies.18-20 However, varying degrees
of microleakage were reported along
the gingival margins in the dentin.
In this study, Tetric Ceram and Filtek
Silorane demonstrated the smallest amount
of microleakage at the gingival margins,
followed by Tetric EvoCeram, with no statistically significant difference between the
three composites. These findings are similar
to a 2005 study in which a silorane-based
composite and a methacrylate-based composite displayed comparable gingival microleakage.10 Other studies have shown that
silorane-based composites show reduced
polymerization shrinkage and stress, as
well as significantly improved marginal
adaptation compared with conventional
methacrylate-based composites.3,9,21,22
The ring-opening chemistry of silorane
produces polymerization shrinkage values
<1%.3 However, the difference in terms
of microleakage between Filtek Silorane
and the free-radical polymerization of the
methacrylate-based resin composites used
in this study (Tetric Ceram and Tetric
EvoCeram) may indicate modest decreases
in the deleterious effects of shrinkage
stress.10 It should be noted that polymerization shrinkage stress depends on a number
of factors, including the volumetric shrinkage and elastic modulus of the restorative
material, curing speed, the configuration
of the cavity, and the surrounding tooth
tissue.23 Depending on the configuration,
plastic flow may improve during the early
phases of polymerization by using less
rigid materials and a slower polymerization reaction, reducing polymerization
contraction stress with less damage at the
adhesive interface.24 Additional studies
are needed to evaluate the effect of these
variables on the marginal adaptation of
new low-shrinkage resin composites.
In addition to their potential for reduced
shrinkage, ormocer materials have lower
cytotoxicity and lower water solubility compared to conventional resin composites.23,25
In addition, ormocers demonstrate marginal sealing equal to and even better than
methacrylate-based resin composites.7,20,26,27
Conversely, in the present study, ormocer demonstrated a significantly higher
degree of microleakage at the gingival
margins than the other methacrylate-based
resin composites and the siloranebased composite used in this study.
In a 2001 study, Chen et al found that an
ormocer demonstrated a high contraction
stress and lower elastic modulus than the
other composites tested, due to the fact that
ormocers have a more rigid resin matrix.28
Ormocers have a resin system with inorganic/organic copolymers, producing a
high molecular weight that may result in
higher residual rigid contraction stress.
In the present study, the ormocer-based
Ceram X and Spectrum TPH hybrid
composites produced the highest mean
microleakage values, with no significant
difference between them. One might
argue that the adhesive system could
affect the marginal leakage of resin-based
restorative materials. It should be noted
that a 2002 study by Bedran de Castro et
al reported that an ormocer material (different from Ceram X used in the present
study) demonstrated significantly higher
values of microleakage than Spectrum
TPH when either a self-etching primer
or one-bottle adhesive system (Prime
& Bond NT) was used compared with
the Spectrum TPH (hybrid) group that
used Prime & Bond NT adhesive.29
Ceram X is an ormocer-based, nanoceramic composite that contains glass
fillers (1.1-1.5 μm) but differs from conventional hybrid composites in that it uses
methacrylate-modified silicon dioxide-containing nanofiller (10 nm) in place of the
microfiller (agglomerates of silicon dioxide
particles) typically used in hybrid composites; in addition, most of the conventional
resin matrix is replaced by a matrix containing highly dispersed methacrylate-modified
polysiloxane particles (2-3 nm). According
to the manufacturer’s information, these
nanoceramic particles are inorganic/organic
hybrid particles. Nanoceramic particles and
nanofillers both have methacrylate groups
available for polymerization.30 Additional
studies are needed to determine the factors that affect the marginal seal of this
nanoceramic ormocer-based composite at
the gingival margins of Class V cavities.
Surface hardness indicates the mechanical properties of a material. There is a
positive correlation between the hardness of dental resin composites and
the inorganic filler content.31 Increased
filler levels increase hardness. This phenomenon results from an interaction of
multiple factors (including particle size
and distribution) with the resin matrix
and the fillers.6 Hardness also depends on
the polymerization of the resin matrix.
An increased conversion rate of carbon
double bonds would in turn improve
physical properties and VHNs.6,32
The results of the present study showed
no statistically significant differences among
the resin-based restorative materials in terms
of upper and lower surface microhardness or
hardness ratio. These findings are consistent
with previous studies that showed no significant difference between ormocers and conventional methacrylate-based composites.33
By contrast, previous studies have reported
significantly higher VHNs for ormocerbased composites compared to microhybrid
composites.6,34 In a 2010 study, Hahnel et
al aged Filtek Silorane, Ceram X, and other
methacrylate-based composites artificially
for one year, reporting that the Filtek
Silorane demonstrated the lowest microleakage values.35 It should be noted that the
results of the present study cannot be compared automatically with previous studies, as
the materials, curing lights, exposure times,
indentation loadings, and storage conditions differ. In addition, the complex oral
environment means that the results of this
in vitro study cannot necessarily be extrapolated to the clinical situation. Additional
long-term clinical studies assessing the
performance of new low-shrinkage resinbased restorative materials are required.
www.agd.org
Summary
Within the limitations of this in vitro
study, none of the resin-based restorative
materials evaluated was able to impede
microleakage in Class V cavities. Siloranebased composite material could provide
an effective marginal seal similar to that
of microhybrid or nanohybrid resin composites. Ormocer-based composite and
conventional hybrid composites demonstrated significantly greater microleakage
at the gingival margins. The microhardness of silorane-based composite was comparable to that of the ormocer and other
methacrylate-based composite materials.
Author information
Dr. Hooshmand is an associate professor,
Department of Dental Materials, School of
Dentistry/Research Center for Science and
Technology in Medicine, Tehran University
of Medical Sciences, Iran. Dr. Tabari is a
postgraduate dental student, Department
of Operative Dentistry, School of Dentistry,
Babol University of Medical Sciences,
Iran. Dr. Keshvad is an assistant professor,
Department of Prosthodontics, School of
Dentistry, Shahed University, Tehran, Iran.
Acknowledgments
This study was supported by the Research
Center for Science and Technology in
Medicine, Tehran University of Medical
Sciences. The authors also wish to thank
Dr. M.J. Kharazifard for his invaluable
assistance in the statistical analysis.
Disclaimer
The authors have no financial, economic,
commercial, and/or professional interests
related to topics presented in this article.
References
1.Roulet JF. The problems associated with substituting
composite resins for amalgam: a status report on posterior composites. J Dent. 1988;16(3):101-113.
2. Bottenberg P, Alaerts M, Keulemans F. A prospective
randomized clinical trial of one bis-GMA-based and
two ormocer-based composite restorative systems in
class II cavities: three-year results. J Dent. 2007;35(2):
163-171.
3.Weinmann W, Thalacker C, Guggenberger R. Siloranes
in dental composites. Dent Mater. 2005;21(1):68-74.
4. Hickel R, Dasch W, Janda R, Tyas M, Anusavice K. New
direct restorative materials. FDI commission report. Int
Dent J. 1998;48(1):3-16.
5.Wolter H, Storch W, Ott H. New inorganic/organic copolymers (ORMOCERs) for dental applications. Mater
Res Soc Symp Proc. 1994;346:143-149.
General Dentistry
January/February 2013
49
Dental Materials Marginal leakage and microhardness evaluation of low-shrinkage resin-based restorative materials
6. Manhart J, Kunzelmann K, Chen HY, et al. Mechanical
properties of new composite restorative materials.
J Biomed Mater Res (Appl Biomater). 2000;53(4):353361.
7. Mahmoud SH, El-Embaby AE, AbdAllah AM, Hamama HH. Two-year clinical evaluation of ormocer,
nanohybrid and nanofill composite restorative systems in posterior teeth. J Adhes Dent. 2008;10(4):
315-322.
8.Ilie N, Hickel R. Investigations on mechanical behaviour of dental composites. Clin Oral Investig. 2009;
13(4):427-438.
9.Eick JD, Kotha SP, Chappelow CC, et al. Properties of
silorane-based dental resins and composites containing a stress-reducing monomer. Dent Mater. 2007;
23(8):1011-1017.
10. Palin WM, Fleming GJ, Nathwani H, Burke FJ, Randall RC. In vitro cuspal deflection and microleakage
of maxillary premolars restored with novel lowshrink dental composites. Dent Mater. 2005;21(4):
324-335.
11. Polydorou O, Monting JS, Hellwig E, Auschill TM. Effect
of in-office tooth bleaching on the microhardness of
six dental esthetic restorative materials. Dent Mater.
2007;23(2):153-158.
12.Raskin A, D’Hoore W, Gonthier S, DeGrange M, Dejou
J. Reliability of in vitro microleakage tests: a literature
review. J Adhes Dent. 2001;3(4):295-308.
13. Mair LH. Staining of in vivo subsurface degradation in
dental composite with silver nitrate. J Dent Res. 1991;
70(3):215-220.
14.Li H, Burrow MF, Tyas MJ. The effect of thermocycling
regimens on the nanoleakage of dentin bonding systems. Dent Mater. 2002;18(3):189-196.
15.Awliya WY, El-Sahn AM. Leakage pathway of Class V
cavities restored with different flowable resin composite restorations. Oper Dent. 2008;33(1):31-36.
16. Hilton TJ. Can modern restorative procedures and materials reliably seal cavities? In vitro investigations.
Part 2. Am J Dent. 2002;15(4):279-289.
17.Swift EJ Jr, Perdigao J, Heymann HO. Bonding to enamel and dentin: a brief history and state of the art,
1995. Quintessence Int. 1995;26(2):95-110.
50
January/February 2013
18.Santini A, Plasschaert AJ, Mitchell S. Effect of composite resin placement techniques on the microleakage of
two self-etching dentin-bonding agents. Am J Dent.
2001;14(3):132-136.
19. Nakabayashi N, Ashizawa M, Nakamura M. Identification of a resin-dentin hybrid layer in vital human dentin created in vivo: durable bonding to vital dentin.
Quintessence Int. 1992;23(2):135-141.
20.Gerdolle DA, Mortier E, Droz D. Microleakage and polymerization shrinkage of various polymer restorative
materials. J Dent for Child (Chic). 2008;75(2):125133.
21.Yamazaki PC, Bedran-Russo AK, Pereira PN, et al. Microleakage evaluation of a new low-shrinkage composite restorative material. Oper Dent. 2006;31(6):
670-676.
22. Bagis YH, Baltacioglu IH, Kahyaogullari S. Comparing
microleakage and the layering methods of siloranebased resin composite in wide Class II MOD cavities.
Oper Dent. 2009;34(5):578-585.
23.Leprince J, Palin WM, Mullier T, Devaux J, Vreven J, Leloup G. Investigating filler morphology and mechanical
properties of new low-shrinkage resin composite
types. J Oral Rehabil. 2010;37(5):364-376.
24. Helvatjoglu-Antoniades M, Kalinderis K, Pedulu L, Papadogiannis Y. The effect of pulse activation on microleakage of a ‘packable’ composite resin and two
‘ormocers’. J Oral Rehabil. 2004;31(11):1068-1074.
25.Yap AU, Chung SM, Chow WS, Tsai KT, Lim CT. Fracture
resistance of compomer and composite restoratives.
Oper Dent. 2004;29(1):29-34.
26.Efes BG, Dorter C, Gomec Y. Clinical evaluation of an
ormocer, a nanofill composite and a hybrid composite
at 2 years. Am J Dent. 2006;19(4):236-240.
27.Yazici AR, Celik C, Ozgunaltay G. Microleakage of different resin composite types. Quintessence Int. 2004;
35(10):790-794.
28.Chen HY, Manhart J, Hickel R, Kunzelmann KH. Polymerization contraction stress in light-cured packable
composite resins. Dent Mater. 2001;17(3):253-259.
29. Bedran de Castro AK, Pimenta LA, Amaral CM, Ambrosano GM. Evaluation of microleakage in cervical margins of various posterior restorative systems. J Esthet
Restor Dent. 2002;14(2):107-114.
General Dentistry
www.agd.org
30.Schirrmeister JF, Huber K, Hellwig E, Hahn P. Two-year
evaluation of a new nano-ceramic restorative material.
Clin Oral Investig. 2006;10(3):181-186.
31. Boyer DB, Chalkley Y, Chan KC. Correlation between
strength of bonding to enamel and mechanical properties of dental composites. J Biomed Mater Res.
1982;16(6):775-783.
32. Ferracane JL, Greener EH. The effect of resin formulation on the degree of conversion and mechanical
properties of dental restorative resins. J Biomed Mater
Res. 1986;20(1):121-131.
33.Say EC, Civelek A, Nobecourt A, Ersoy M, Guleryuz.
Wear and microhardness of different resin composite
materials. Oper Dent. 2003;28(5):628-634.
34.Tagtekin DA, Yanikoglu FC, Bozkurt FO, Kologlu B, Sur
H. Selected characteristics of an Ormocer and a conventional hybrid resin composite. Dent Mater. 2004;
20(5):487-497.
35. Hahnel S, Henrich A, Bürgers R, Handel G, Rosentritt
M. Investigation of mechanical properties of modern
dental composites after artificial aging for one year.
Oper Dent. 2010;35(4):412-419.
Manufacturers
Buehler, Lake Bluff, IL
800.283.4537, www.buehler.com
Coltene/Whaledent Inc., Cuyahoga Falls, OH
330.916.8800, www.coltene.com
DENTSPLY Caulk, Milford, DE
800.532.2855, www.caulk.com
Heraeus Kulzer, South Bend, IN
800.435.1785, www.heraeus-dental-us.com
IBM Corporation, Armonk, NY
800.426.4968, www.ibm.com
Ivoclar Vivadent Inc., Amherst, NY
800.533.6825, www.ivoclarvivadent.com/en
Olympus, Center Valley, PA
888.553.4448, www.olympusamerica.com
3M ESPE, St. Paul, MN
888.364.3577, solutions.3m.com
Exercise No. 322 Dental
Materials Subject Code 017
The 15 questions for this exercise are based on the article,
Marginal leakage and microhardness evaluation of lowshrinkage resin-based restorative materials, on pages
46-50. This exercise was developed by Steven E. Holbrook,
DMD, MAGD, in association with the General Dentistry
Self-Instruction committee.
Reading the article and successfully completing this exercise will enable you to:
•recognize the components of low-shrinkage resin-based restorative materials;
•recognize the factors that contribute to their microhardness;
•identify the advantages of reducing polymerization shrinkage in them; and
•understand how they compare to conventional materials.
1. Which restorative material used in
this study incorporates a modified
monomer matrix in an attempt to reduce
polymerization shrinkage?
A.Compomers
B.Ormocers
C.Hybrids
D.Siloranes
6. When compared to conventional resin
composites, ormocers exhibit all of the
following properties except one.
Which is the exception?
A. Lower shrinkage
B. Less cytotoxicity
C.Less rigid resin matrix
D.Lower water solubility
2. Which of the following is an inherent
disadvantage of a composite restoration?
A.Inadequate esthetics
B.Inadequate wear resistance
C.Inadequate biocompatibility
D.Inadequate marginal seal
7. Surface hardness is relevant to all of the
following with regard to a restorative
material except its ability to
A. be polished.
B. withstand scratching.
C. withstand occlusal stress.
D. resist polymerization shrinkage.
3. The surface hardness was measured
utilizing
A. Knoop hardness values.
B. plastic deformation variables.
C. Vickers hardness numbers.
D. Kruskal-Wallis testing.
4. A restorative material’s ability to
undergo plastic flow during the
early phases of polymerization
causes a/an _______________ in
polymerization contraction stress
and _______________ microleakage.
A. reduction; less
B. increase; more
C. increase; less
D. reduction; more
5. Polymerization shrinkage stress is
dependent upon all of the following
except one. Which is the exception?
A.Elastic modulus
B.Curing speed
C. Volumetric shrinkage
D. Bonding agent
8. Spectrum TPH and what other restorative
material exhibited the greatest amount
of microleakage at the gingival margins?
A.Microhybrid
B.Nanohybrid
C.Ormocer
D.Silorane
9. Which restorative material contains
methacrylate-modified silicon dioxide
containing nanofiller and a matrix of
highly dispersed methacrylate-modified
polysiloxane particles?
A.Hybrid
B.Nanohybrid
C.Microhybrid
D.Ormocer
10. Which of the following materials
exhibited the highest hardness ratio?
A.Microhybrid
B.Ormocer
C.Silorane
D.Hybrid
11. Silorane-based composite material
provided a marginal seal comparable to
that of microhybrid or nanohybrid resin
composites. Silorane-based composite
material exhibited a microhardness
significantly higher than that of microhybrid
or nanohybrid resin composites.
A. Both statements are true.
B.The first statement is true;
the second is false.
C.The first statement is false;
the second is true.
D. Both statements are false.
12. Which material exhibited the lowest
hardness ratio?
A.Microhybrid
B.Ormocer
C.Silorane
D.Hybrid
13. The contraction stress associated with
polymerization shrinkage can lead to
cracks in healthy tooth structure. No
statistically significant difference in the
hardness ratio was found among the
restorative materials.
A. Both statements are true.
B.The first statement is true;
the second is false.
C.The first statement is false;
the second is true.
D. Both statements are false.
14. The resin-based restorative materials
evaluated were used in combination with
_______________ adhesive system.
A. a self-etching primer and
B. total etch and a two-step
C. a one-bottle
D. manufacturer’s recommended
15. There is a positive correlation between
surface hardness of a resin composite
restoration and the
A. inorganic filler content.
B. modulus of elasticity.
C. contraction stress.
D. plastic flow.
Answer form is on page 80. Answers for this exercise must be received by December 31, 2013.
www.agd.org
General Dentistry
January/February 2013
51
Implant Materials
Two case reports involving implants and
fractured healing caps
Erdem Kilic, DDS, PhD n Kerem Kilic, DDS, PhD n Mustafa Zortuk, DDS, PhD n Alper Alkan, DDS, PhD
The widespread use of endosseous osseointegrated implants to replace
missing natural teeth increases the chances of implant complications and
failures, despite the high initial success rate reported in the literature.
Implant and healing cap fracture are possible rare complications that can
cause significant problems for both clinicians and patients. This article
D
ental implants are a functional
esthetic solution to partial and
total edentulism with an initial
success rate of 90%-95%.1 However,
complications can occur in specific situations that affect osseointegrated dental
implants. Dentists must be aware of
treatment limitations and avoid risky
situations that can lead to implantsupported prosthesis failure due to
biomechanical complications, such as
implant fracture or loosening or fracture
of the prosthetic or abutment screws.2,3
Although implants rarely fracture (with
an incidence between 0.16% and 1.5%),
this complication can present a major
problem for patients and clinicians.4,5
This article reports on 2 cases: the first,
an implant fracture in a locator attachment-retained overdenture, and the second,
a healing cap fracture that was retrieved
successfully using an implant repair kit. To
the authors’ knowledge, these are the first
examples of such cases in the literature.
Case No. 1
A 60-year-old edentulous man was referred
for implant treatment. His medical history
was unremarkable. Eight implants, all
12 mm long × 3.3 mm in diameter (ITI
Dental Implant System, Straumann) were
inserted in the region of the lateral incisors
and first premolars for maxillary and mandibular arches (Fig. 1). All of the implants
achieved good initial stability. After a
3-month preloading healing period with
no complications, clinical osseointegration
was achieved, and the patient was sent
back to the referring prosthodontist for
dentures. The patient was treated using an
implant-supported overdenture prosthesis,
retained with 4 locator attachments by 4
implants for each arch.
The patient underwent maintenance
therapy on an irregular basis (approximately once per year). A radiograph
taken 1 year after the completion of
treatment revealed mild resorption
around the implant in the right lateral
Fig. 1. Postoperative panoramic radiograph of dental implants 3 months after
implant placement.
52
January/February 2013
reports on 2 unique cases of implant and healing cap fracture, their
possible causes, and how the cases were managed.
Received: September 14, 2011
Accepted: January 1, 2012
General Dentistry
Fig. 2. The fractured
part of the implant with
locator attachment.
www.agd.org
and first premolar region; no clinical
symptoms were evident at that time.
Two years after implant placement, the
patient came to the office complaining
of discomfort in the right lateral maxilla
and loosening of the locator attachment.
Clinical examination revealed excessive
horizontal movement of the locator attachment and swelling in the adjacent mucosa.
Using very light force, the locator attachment was removed along with the upper
third of the implant (Fig. 2); however, the
acrylic resin prosthesis was undamaged.
Radiographs taken at that time revealed
broken edges on the apical part of the
osseointegrated implant and noticeable
bone loss, coronal to the broken edge of the
implant (Fig. 3). The patient had a strong
muscle pattern and stated that he slept
with the dentures in place; however, he
also described a history of tooth grinding.
After clinical and radiographic
examinations, 2 treatment options were
considered. The dentist could leave the
Fig. 3. A periapical radiograph showing the
remaining part of the dental implant. Bone loss can
be seen around the implant.
Fig. 4. The fractured healing cap and an unfractured
healing cap.
Fig. 5. A radiograph taken 2 months post-surgery showing the remaining part of
the fractured healing cap (white arrow).
Fig. 6. A model is used to demonstrate cutting a
fractured screw into splinters.
Fig. 7. A periapical radiograph taken
after removal of the fractured screw.
remaining portion of the implant in place
and modify the existing denture with
3 locator attachments, or remove the
remaining portion of the implant and
replace the entire implant with a new
one. For economic reasons (and because
the patient refused new surgery for the
implant placement), the remaining portion of the fractured implant was left in
place and the existing denture was modified with 3 locators. Two years later, he
reported being satisfied with his modified
implant-supported overdenture prosthesis
both esthetically and functionally.
caps were placed after surgery with no
problems.
Ten days later, a mandibular heatprocessed acrylic resin removable partial denture (RPD) was adjusted and
seated as a temporary prosthesis prior
to implant osseointegration. At that
point, the patient entered a program of
monthly maintenance therapy. Clinical
and radiographic examination of the
right molar region showed that a healing cap had fractured (according to the
patient, while eating) 2 months after
implant placement (Fig. 4). There was
no damage to the RPD. The apical part
of the screw remained threaded into
the implant (Fig. 5). The implant was
osseointegrated and showed no sign of
peri-implantitis. After consulting with
the patient, it was decided to remove the
fractured screw and restore the implant.
An implant service set (consisting of
drills and a drill guide) (Straumann) was
used (per manufacturer’s instructions) to
Case No. 2
A 62-year-old partially edentulous man was
referred for implant treatment. His medical
history was negative for diseases, injuries, or
other treatments. After evaluating clinical
and radiographic data, 13 implants (ITI
Dental Implant System) were inserted in
the edentulous parts of the maxilla and
mandible during 1-stage surgery. Healing
www.agd.org
Fig. 8. Panoromic radiograph taken 3 years post-surgery.
remove the apical part of the fractured
healing cap that was stuck in the implant.
One drill (1.6 mm in diameter) was used
counterclockwise (at a speed of at least
600 rpm) along with the respective drill
guide. The drill guide was stabilized on
the implant and the drill was inserted
into the guide (Fig. 6). Drilling was performed under continuous cooling until
the shank of the drill reached the guide.
It is important to perform intermittent
drilling and to eject the metal chips continuously. The fractured screw fragment
was not unscrewed, but cut into splinters
and removed successfully. The inner aspect
of the implant body was rinsed with
saline solution and evaluated thoroughly.
The entire procedure was completed in
approximately 15 minutes. No damage to
the implant’s threads was detected (Fig. 7),
and a new healing cap was inserted into
the implant. After nearly 3 years with the
fixed implant-supported prosthesis, no
problems have been reported (Fig. 8).
General Dentistry
January/February 2013
53
Implant Materials Two case reports involving implants and fractured healing caps
Discussion
Despite high success rates, osseointegrated
dental implant therapy is not free from
complications. Problems may include
implant fracture, which may lead to
unpleasant clinical outcomes for both the
patient and clinician.6 As it happens, most
authors report a very low incidence of
fracture: Mericske-Stern et al found only
1 case in a study of 66 implants, while a
1992 study by Tolman & Laney observed
3 fractures in 1,778 implants.7,8 A 1993
report by Jemt & Lekholm reported a
single fracture out of 259 implants, while
Zarb & Schmittt found no fractures
in a series of 274 implants.9,10 During a
5-year follow-up study, Balshi reported
8 fractured implants in 4,045 implants
(0.2%).11 The cases presented in this
article included an implant fracture with
a locator attachment and a healing cap
fracture. To the authors’ knowledge, these
are the first documented instances of such
cases in the literature.
Although implant fractures are infrequent, it is important to adopt measures
that will prevent them. In this context,
dentists should be aware of the possible
existence of parafunctional activity,
implant location, diameter, and the type
of prosthesis involved.3 According to
Balshi, the causes of implant fracture
can be divided into 3 categories: defects
in implant design or material, a nonpassive fit of the prosthetic framework,
and physiological or biomechanical
overload.11 Both overload and a nonpassive fit can cause the prosthetic screw
to fracture or loosen before implant
fracture. These minor complications are
warning signs that should be addressed
to prevent future invasive, costly, and
time-consuming procedures.11 According
to Eckert et al, implant fractures commonly involve commercial pure titanium
3.75 mm diameter threaded implants,
and are typically preceded by the loosening of prosthetics or abutment screws.12
Many studies have reported an association between bruxism and implant failure;
a 2000 study by Wannfors et al reported a
significant relationship between bruxism
and implant failure after the implants had
been functional for 1 year.13 Likewise,
Glauser et al found a higher percentage of implant loss in bruxism patients
(41%) compared to nonbruxism patients
54
January/February 2013
(12%) after 1 year.14 A 2001 study by
Bragger et al reported technical implant
problems in 60% of patients with bruxism over 5 years, compared to approximately 20% of nonbruxism patients.15
In the first case, the implant fracture was
attributed to a combination of bruxism,
occlusal overload, metal fatigue, and small
implant diameter. Signs of parafunctional
habits included hypertrophic masticatory muscles and wear of the occlusal
and incisal surfaces. Occlusal overload
due to parafunctional habits resulted
in metal fatigue, which led to implant
fracture; in addition, the patient stated
that he slept with his dentures in place.
In the edentulous mandible, overdentures supported by a few implants appear
to be very successful, while maxillary overdentures are less predictable.16-18 Recently,
a review of clinical implant studies found
that maxillary overdentures produced the
highest failure rate (21.3%) for any type
of prosthesis.17 The lower success rates
were attributed primarily to the quality
of bone in the edentulous maxilla because
a looser arrangement of trabecular bone
with a thin (or absent) cortical plate
generally is considered to be less capable
of stabilizing and supporting implants.17
A prospective clinical study by
Bergendal & Engquist found that ballretained overdentures resulted in greater
implant loss in the maxillary arch (38.8%)
than bar-retained overdentures (20.6%).19
When planning the overdenture, the
choice of retention mechanism can be critical for promoting an equitable load transfer within the maxilla. If a bar between
implants is loaded, the load is distributed
to the bone surrounding the neighboring
implants. In the case of solitary attachments (ball attachments), the load is
distributed to the bone that surrounds
that one implant. Complications with ball
attachments occurred in subjects where the
implants were not perfectly parallel to each
other.20 The maxillary alveolar bone position means that it is much more difficult
to ensure parallel implants in the maxillary arch than in the mandibular arch.21
In the first case, the patient was treated
with an implant-supported overdenture prosthesis, retained with 4 locator
attachments in 4 implants for each arch.
The implant in the right lateral maxilla
fractured. Based on this case and previous
General Dentistry
www.agd.org
literature, a bar-retained overdenture may
be more appropriate within the maxillary
arch than a ball-retained overdenture.
Treatment options for implant fractures
include removing the implant, modifying
the existing prosthesis, and modifying
the fractured implant. When implant
retrieval can compromise the integrity
of adjacent vital structures (due to the
proximity to the inferior alveolar canal or
adjacent teeth), the least invasive option
involves leaving the fractured portion
of the implant in place.3 This approach
was taken in the first case and the existing denture was modified with 3 locator
attachments, both for economic reasons
and because the patient did not want to
undergo another surgical procedure.
The following precautions were taken
to avoid fracturing another implant: The
locator attachments (Straumann) were
tightened (per manufacturer’s recommendations), and the patient was given
psychological support to overcome the
bruxism habit, asked to come back every
6 months for regular follow-up, and cautioned not to wear the prosthesis at night.
In the second case, the healing cap
fracture was attributed to a combination
of parafunctional habits, as evidenced by
hypertrophic masticatory muscles, premature contact between the RPD and the
healing cap (due to screw loosening), and
the development of metal fatigue (as a result
of repeated use of the healing cap). Once a
screw fracture has occurred, the fractured
screw segment inside the implant must
be removed; otherwise, the implant may
remain osseointegrated, but will be unable
to retain the prosthesis.22 The fractured part
of the healing cap was retrieved successfully
using an implant repair kit developed for
the ITI Dental Implant System, although
it may be used for other implant systems.
However, the results from this repair
system depend on the individual case. In
some situations, failure might result from
a reduced interocclusal distance, a restless
patient, or a dentist’s inadequate skills.
Roughening the fragment initially and
using drill guides for axial drilling helped
to reduce the risk of damaging the internal
aspect of the implant body. The drill guide
should be positioned with great care.
Screwing out the perforated fragment was
advantageous because the implant threads
remained intact; if the threads had been
damaged, they would have needed to
be recut with the tapping instrument.23
In this case, the fractured healing cap
screw was removed successfully and no
damage to the threads was detected.
To avoid healing cap fractures in the
future, it would be appropriate to add
a soft lining material to the temporary
removable prosthesis. In addition, after
the fixed implant-supported prosthesis was
cemented, the patient was given an occlusal splint to protect the teeth, implants,
and restorations from occlusal overload.
A routine patient recall system is very
important for avoiding complications (such
as screw or abutment loosening), which
may constitute an early warning sign of
implant or healing cap fracture.21 Regular
recall appointments might prevent further
screw or implant fractures because problems could be diagnosed and treated earlier.12 For this reason, it is essential not only
to retrieve the fractured component, but
also to determine the reason for the failure
and to modify the prosthesis, if necessary.
Conclusion
In this article, the authors presented 2
examples of complications related to
implant treatment that have not been
reported previously. These complications
can be minimized by taking into account
certain aspects of treatment such as correct
presurgical planning, the use of adequate
surgical techniques, postsurgical follow-up,
respecting the osseointegration period,
appropriate design of the superstructure
and correct distribution of occlusal loads.
In addition, outcomes of implant treatment would be improved if implant manufacturers offered their own implant service
sets for solving these type of complications.
Author information
Dr. E. Kilic is an assistant professor,
Department of Oral and Maxillofacial
Surgery, Erciyes University, Melikgazi,
Kayseri, Turkey, where Dr. K. Kilic is
an assistant professor, Department of
Prosthodontics, Dr. Zortuk is an associate
professor, Department of Prosthodontics,
and Dr. Alkan is a professor, Department
of Oral and Maxillofacial Surgery.
Disclaimer
The authors have no financial, economic,
commercial, and/or professional interests
related to topics presented in this article.
References
1.Tagger-Green N, Horwitz J, Machtei EE, Peled M.
Implant fracture: a complication of treatment with
dental implants—review of the literature [article in
Hebrew]. Refuat Hapeh Vehasinayim. 2002;19(4):
19-24, 68.
2.Tagger-Green N, Machtei EE, Horwitz J, Peled M. Fracture of dental implants: literature review and report of
a case. Implant Dent. 2002;11(2):137-143.
3. Mendonca G, Mendonca DB, Fernandes-Neto AJ,
Neves FD. Management of fractured dental implants: a
case report. Implant Dent. 2009;18(1):10-16.
4.Sanchez-Perez A, Moya-Villaescusa MJ, Jornet-Garcia
A, Gomez S. Etiology, risk factors and management of
implant fractures. Med Oral Patol Oral Cir Bucal. 2010;
15(3):e504-e508.
5.Gargallo Albiol J, Satorres-Nieto M, Puyuelo Capablo
JL, Sanchez Garces MA, Pi Urgell J, Gay Escoda C. Endosseous dental implant fractures: an analysis of 21
cases. Med Oral Patol Oral Cir Bucal. 2008;13(2):
e124-e128.
6. Piattelli A, Piattelli M, Scarano A, Montesani L. Light
and scanning electron microscopic report of four fractured implants. Int J Oral Maxillofac Implants. 1998;
13(4):561-564.
7. Mericske-Stern R, Steinlin Schaffner T, Marti P, Geering
AH. Peri-implant mucosal aspects of ITI implants supporting overdentures. A five-year longitudinal study.
Clin Oral Implants Res. 1994;5(1):9-18.
8.Tolman DE, Laney WR. Tissue-integrated prosthesis
complications. Int J Oral Maxillofac Implants. 1992;
7(4):477-484.
9. Jemt T, Lekholm U. Oral implant treatment in posterior partially edentulous jaws: a 5-year follow-up
report. Int J Oral Maxillofac Implants. 1993;8(6):
635-640.
10. Zarb GA, Schmitt A. The longitudinal clinical effectiveness of osseointegrated dental implants: the Toronto
study. Part III: problems and complications encountered. J Prosthet Dent. 1990;64(2):185-194.
www.agd.org
11. Balshi TJ. An analysis and management of fractured
implants: a clinical report. Int J Oral Maxillofac Implants. 1996;11(5):660-666.
12.Eckert SE, Meraw SJ, Cal E, Ow RK. Analysis of incidence and associated factors with fractured implants:
a retrospective study. Int J Oral Maxillofac Implants.
2000;15(5):662-667.
13.Wannfors K, Johansson B, Hallman M, Strandkvist T. A
prospective randomized study of 1- and 2-stage sinus
inlay bone grafts: 1-year follow-up. Int J Oral Maxillofac Implants. 2000;15(5):625-632.
14.Glauser R, Ree A, Lundgren A, Gottlow J, Hammerle
CH, Scharer P. Immediate occlusal loading of Branemark implants applied in various jawbone regions: a
prospective, 1-year clinical study. Clin Implant Dent
Relat Res. 2001;3(4):204-213.
15. Bragger U, Aeschlimann S, Burgin W, Hammerle CH,
Lang NP. Biological and technical complications and
failures with fixed partial dentures (FPD) on implants
and teeth after four to five years of function. Clin Oral
Implants Res. 2001;12(1):26-34.
16. Fanuscu MI, Caputo AA. Influence of attachment systems on load transfer of an implant-assisted maxillary
overdenture. J Prosthodont. 2004;13(4):214-220.
17.Goodacre CJ, Kan JY, Rungcharassaeng K. Clinical
complications of osseointegrated implants. J Prosthet
Dent. 1999;81(5):537-552.
18.Engquist B, Bergendal T, Kallus T, Linden U. A retrospective multicenter evaluation of osseointegrated implants supporting overdentures. Int J Oral Maxillofac
Implants. 1988;3(2):129-134.
19. Bergendal T, Engquist B. Implant-supported overdentures: a longitudinal prospective study. Int J Oral Maxillofac Implants. 1998;13(2):253-262.
20. Quirynen M, Naert I, van Steenberghe D. Fixture design and overload influence marginal bone loss and
fixture success in the Branemark system. Clin Oral Implants Res. 1992;3(3):104-111.
21. Meijer HJ, Kuiper JH, Starmans FJ, Bosman F. Stress
distribution around dental implants: influence of superstructure, length of implants, and height of mandible. J Prosthet Dent. 1992;68(1):96-102.
22.Luterbacher S, Fourmousis I, Lang NP, Bragger U. Fractured prosthetic abutments in osseointegrated implants: a technical complication to cope with. Clin Oral
Implants Res. 2000;11(2):163-170.
23. Nergiz I, Schmage P, Shahin R. Removal of a fractured
implant abutment screw: a clinical report. J Prosthet
Dent. 2004;91(6):513-517.
Manufacturer
Straumann, Andover, MA
978.747.2500, www.straumann.com
General Dentistry
January/February 2013
55
Endodontics
A clinical report of Type III dens invaginatus:
relevant aspects of a combined therapeutic
approach
Patricia de Almeida Rodrigues Silva e Souza, DDS, MSc, PhD n Bruno Vila Nova de Almeida, DDS n Talita Tartari, DDS
Ana Claudia Braga Amoras Alves, DDS, MSc, PhD n Fabricio Mesquita Tuji, DDS, MSc, PhD
Mario Honorato Silva e Souza Jr., DDS, MSc, PhD
Dens invaginatus is a developmental abnormality that alters dental morphology; as a result, treating this condition is a challenge for endodontic
practices. This article describes how a combination of nonsurgical and
surgical therapies was utilized to treat a maxillary central incisor with
Type III dens invaginatus and vital pulp. The treatment plan included
using computed tomography (CT) for a detailed analysis of the dental
anatomy and periapical area, endodontic and surgical procedures, and a
4-year follow-up period that included periodic clinical and radiographic
D
ens invaginatus is a developmental
abnormality that results from the
invagination of the enamel organ
into the dental papilla prior to calcification
of the tissue.1 The etiology of this abnormality is unknown at present; however,
several factors (including trauma, infection, and genetics) have been suggested as
likely causes.1,2 Dens invaginatus involves
a rare malformation in the primary or permanent dentition.3 An affected tooth can
be normal in appearance or its shape and
size may be altered. Dens invaginatus may
be assumed when the crown of the tooth is
wide and includes a prominent cusp with a
palatogingival groove.4,5
The most common classification of
this abnormality was proposed in 1957
by Oehlers, who subdivided the condition into three types according to the
invagination depth and its connection to
the periapical tissue or periodontal ligament.6 In Type I cases, the invagination
extends to the cementoenamel junction.
In Type II, the invagination extends
beyond the cementoenamel junction
and invades the root, but is confined
within the root in a manner similar to a
blind sac (although it may connect to the
pulp). In Type III cases, the invagination
extends to the inner root of the tooth to
the apical area and has its own foramen
in either the apical or lateral region;
in addition, the invagination often is
connected to the pulp.
56
January/February 2013
examinations. The follow-up examinations revealed a regression of the
apical lesion and no other signs or symptoms. Based on the present
case report, the authors concluded that this combination of surgical and
nonsurgical approaches was effective and that CT is a valuable auxiliary
tool for the study of dental anatomy.
Received: December 7, 2011
Accepted: March 14, 2012
In addition to the anatomical characteristics of dens invaginatus, the clinical
area of interest may compromise the pulp
tissue, resulting in inflammation, internal
resorption, a loss of vitality, and subsequent involvement of the periapical region
that can lead to periapical diseases.7
The treatment of choice for dens
invaginatus depends on the degree of
malformation and the clinical symptoms.
Intervention can include prophylactic treatment, conservative restorative treatment,
endodontic treatment alone, endodontic
treatment in combination with surgery, and
extraction.1,7-19 If construction of a periapical barrier or root-end filling is needed for
an open apex, mineral trioxide aggregate
(MTA) should be used because of its antibacterial and sealing properties, as well as
its pulp and periapical biocompatibility.20-22
The use of computed tomography (CT)
has been shown to aid both in evaluating
root canal morphology during endodontic
presurgical planning and in determining the
extent of bone lesions.11-13,18,23 This article
presents a case report involving Type III
dens invaginatus and its treatment through
a combination of endodontic and surgical
approaches. CT was used as an auxiliary tool
to study the internal anatomy of the tooth.
Case report
An 11-year-old boy sought treatment,
complaining of a fistula with secretions in
the vestibular region of the maxillary right
General Dentistry
www.agd.org
central incisor. The crown was enlarged
in the vestibule-lingual direction and was
characterized by a prominent cingulum.
There was no change in the crown’s color.
Palpation and percussion tests produced
responses within the normal limits; in
addition, there was a positive response to
the cold test.
It was reported that periodontal treatment had been performed previously in the
region—including open-field scraping and
regression of the fistula—and symptoms disappeared for approximately 1 year. During a
radiographic examination (Fig. 1), an image
consistent with Type III dens invaginatus
was noted; in addition, the extensive radiolucent image suggested periapical lesions.
Because of the positive response to the
cold test, the presence of pulp vitality was
considered. To obtain better anatomic
details and guide subsequent operatory procedures, a CT scan was taken
using a 64-channel multislice scanner,
Lightspeed VCT (GE Global Research)
(Fig. 2). The radiographic and CT
images revealed the presence of the main
canal located at a distobuccal area, the
C-shaped invagination, and the rudimental canal; in addition, it was possible to
define the size of the periapical lesion.
Guided by the radiographic and CT
images, a rubber dam was placed and
access was made through the mesiolingual
aspect of the tooth to reach the invagination and rudimental canal. Therefore,
Fig. 1. Initial radiograph of tooth No. 11 reveals dens invagination
(green arrows), the main canal (yellow arrows), and the rudimental
canal (blue arrows).
Fig. 3. A view of buccal bone loss
detected during endodontic surgery.
Fig. 2. A multislice CT image (paraxial section) taken
prior to the start of treatment reveals the main
canal (yellow arrow), invagination (green arrow),
the rudimental canal (blue arrow), and a periapical
lesion (red arrows).
Fig. 4. CT image (paraxial section)
taken 4 years post-treatment,
revealing invagination (green arrow)
and a rudimental canal (blue arrow).
the endodontic treatment was initiated
using biomechanical preparation with a
double-flared technique, using first and
second series stainless steel K-type files
(DENTSPLY Maillefer) and abundant
irrigation with 2.5% sodium hypochlorite. Upon completing the biomechanical
preparation, a paste made of calcium
hydroxide and 2% chlorhexidine digluconate was used as an intracanal medication. The paste was replaced once a month
for the next 3 months.
Fig. 5. CT image (axial section) taken 4 years post-treatment,
revealing invagination (green arrow) and the rudimental canal
(blue arrow).
Based on the extent of the lesion and the
lack of fistula regression after 3 months, it
was decided to perform endodontic surgery with a transoperative root obturation.
After anesthesia, incision and dilatation
procedures were performed; at that time,
the presence of cervical bone resorption
was observed to the level of the middle
third vestibular region of the tooth
(Fig. 3). During the osteotomy, the collected bone was placed in a container with
saline solution. Later, the bone was mixed
www.agd.org
with lyophilized bone substitute (Bio-Oss,
Geistlich Pharma North America Inc.) to
fill the surgical site.
The periapical lesion was removed using
a Lucas curette. Next, master cones were
prepared for invagination and rudimental
canal obturation. An epoxy resin sealer
containing calcium hydroxide (AH 26,
DENTSPLY Maillefer) was used to fill
the area, while Microseal (SybronEndo)
was used as the obturation system. To
make space for the root-end filling, 3 mm
General Dentistry
January/February 2013
57
Endodontics A clinical report of Type III dens invaginatus: relevant aspects of a combined therapeutic approach
of the obturation was removed apically
and white mineral trioxide aggregate
(MTA) cement was applied.
After the MTA cement set initially,
the region was irrigated extensively with
saline. The bone area was filled with
the lyophilized Bio-Oss and previously
collected bone. In addition, a biological
membrane of bovine origin (Bio-Gide,
Geistlich Pharma North America Inc.)
was placed on the vestibular face of the
tooth. The flap was repositioned and
secured with a 4.0 suture.
During a 4-year follow-up, which
included periodic examinations, the pulp
continued to provide positive responses
to pulp sensibility testing. The responses
indicated that the pulp in the main root
canal had survived. To evaluate the longterm success of the treatment, a conebeam volumetric tomography scanner
(i-CAT, Imaging Sciences International)
was used to take a CT scan at the final
examination (Fig. 4 and 5).
Discussion
Endodontic treatment of dens invaginatus
is highly complex, especially in Type III
cases, as the invagination extends to the
apical region of the tooth and is associated
with the presence of a lesion.6 It has been
described in the literature as an isolated
canal; however, the literature also has
reported several cases of dens invaginatus
with involvement of vital pulp tissue.5,1013,24,25
In these studies, only the invagination received endodontic treatment, while
the main canal remained intact, as seen in
the present case.
Some studies have reported successfully
preparing cases of Type III dens invaginatus by using manual files, nickel titanium
(NiTi) rotary instruments, and ultrasonic
files.5,8,10,25,26 However, the use of rotary
instruments is not recommended because
of the enamel line inside the invagination
and because invaginations usually have
an irregular shape and rotary instruments
would increase the risk of fracture.12
Manual files were chosen for safety reasons.
The CT images revealed the anatomical
details of the invagination, including the
extent and location of the palatine apical
lesion. This information was critical to executing the treatment plan, as these images
provided data that could not be found
using conventional radiography.10,11,16
58
January/February 2013
In the present case, surgical supplementation was considered due to the
persistence of the fistula, which indicated
that the invagination was not decontaminated. It is possible that irregularities in
the invagination may have prevented
the necessary direct contact between the
therapeutic agent (calcium hydroxide) and
microorganisms. The bone resorption at
the vestibular root also may have contaminated the periapical tissues, contributing
to the fistula’s inability to regress.
Previous studies have reported that the
sealing capacity of thermoplastic methods
makes them an ideal choice for filling
the root canal system.27,28 The Microseal
system, which combines a gutta-percha
master cone with thermoplastic guttapercha, was used in the present case.29
MTA often is used as a root-end filling
material because of its ability to induce
the formation of mineralized tissue in
the root apex region; in addition, it offers
antimicrobial qualities, sealing ability,
and adequate biocompatibility.19-21 These
proven clinical and histological properties
led the authors to use MTA as the rootend filling material in the present case.
Summary
Based on the clinical and radiographic
features observed during this case, it is
reasonable to assume that a combination
of surgical and endodontic treatments is
a valid option for successful treatment of
Type III dens invaginatus. It also should
be emphasized that CT scanning plays
an important role in the study of dental
anatomy and adjacent areas, and it may
contribute to the treatment of complex
dental anatomical abnormalities.
The use of CT images to understand
the complexity of the dens invagination
anatomic details as well as to assist in the
surgical supplementation were critical to
the success of this treatment.
Author information
Dr. P. Souza is a professor, Department
of Endodontics, Federal University of
Para, Brazil, where Dr. Alves is a professor, Department of Periodontics; Dr. Tuji
is a professor, Department of Radiology;
Dr. M. Souza, Jr. is a professor and
chairman of the master’s program in
dentistry; and Drs. Almeida and Tartari
are postgraduate students.
General Dentistry
www.agd.org
References
1. Hulsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosis, and treatment considerations. Int Endod J. 1997;30(2):79-90.
2. Hamasha AA, Alomari QD. Prevalence of dens invaginatus in Jordanian adults. Int Endod J. 2004;37(5):
307-310.
3. Bimstein E, Shteyer A. Dilated type of dens invaginatus
in the permanent dentition: report of a case and review of the literature. ASDC J Dent Child. 1976;43(6):
410-413.
4.Tsurumachi T, Hayashi M, Takeichi O. Non-surgical root
canal treatment of dens invaginatus type 2 in a maxillary lateral incisor. Int Endod J. 2002;35(3):310-314.
5.Tsurumachi T. Endodontic treatment of an invaginated
maxillary lateral incisor with a periradicular lesion and
a healthy pulp. Int Endod J. 2004;37(10):717-723.
6.Oehlers FA. Dens invaginatus (dilated composite
odontome). I. Variations of the invagination process
and anterior crown forms. Oral Surg Oral Med Oral
Pathol. 1957;10(11):1204-1218.
7.Cole GM, Taintor JF, James GA. Endodontic therapy of
a dilated dens invaginatus. J Endod. 1978;4(3):88-90.
8. Jung M. Endodontic treatment of dens invaginatus
type III with three root canals and open apical foramen. Int Endod J. 2004;37(3):205-213.
9. Bishop K, Alani A. Dens invaginatus. Part 2: clinical,
radiographic features and management options. Int
Endod J. 2008;41(12):1137-1154.
10. de Sousa SM, Bramante CM. Dens invaginatus: treatment choices. Endod Dent Traumatol. 1998;14(4):152158.
11. John V. Non-surgical management of infected type III
dens invaginatus with vital surrounding pulp using
contemporary endodontic techniques. Aust Endod J.
2008;34(1):4-11.
12. Patel S. The use of cone beam computed tomography
in the conservative management of dens invaginatus:
a case report. Int Endod J. 2010;43(8):707-713.
13. Keles A, Cakici F. Endodontic treatment of a maxillary
lateral incisor with vital pulp, periradicular lesion and
type III dens invaginatus: a case report. Int Endod J.
2010;43(7):608-614.
14. Nallapati S. Clinical management of a maxillary lateral
incisor with vital pulp and type 3 dens invaginatus: a
case report. J Endod. 2004;30(10):726-731.
15.Chaniotis AM, Tzanetakis GN, Kontakiotis EG, Tosios
KI. Combined endodontic and surgical management of
a mandibular lateral incisor with a rare type of dens
invaginatus. J Endod. 2008;34(10):1255-1260.
16.Ozcakir Tomruk C, Tanalp J, Yurdaguven H, Ersev H.
Endodontic and surgical management of a maxillary
lateral incisor with type III dens invaginatus: a
12-month follow-up. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2008;106(3):e84-e87.
17.Reddy YP, Karpagavinayagam K, Subbarao CV. Management of dens invaginatus diagnosed by spiral computed tomography: a case report. J Endod.
2008;34(9):1138-1142.
18.Subay R, Kayatas M. Dens invaginatus in an immature
maxillary lateral incisor: a case report of complex endodontic treatment. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2006;102(2):e37-e41.
19.Stamfelj I, Kansky AA, Gaspersic D. Unusual variant of
type 3 dens invaginatus in a maxillary canine: a rare
case report. J Endod. 2007;33(1):64-68.
20.Torabinejad M, Hong C, McDonald F, Pitt Ford TR.
Physical and chemical properties of a new root-end
filling material. J Endod. 1995;21(7):349-353.
21. Torabinejad M, Smith PW, Kettering JD, Pitt Ford TR.
Comparative investigation of marginal adaptation of
mineral trioxide aggregate and other commonly used
root-end filling materials. J Endod. 1995;21(6):295299.
22. D’Arcangelo C, D’Amario M. Use of MTA for orthograde obturation of nonvital teeth with open apices;
report of two cases. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2007;104(4):e98-e101.
23.Estrela C, Bueno MR, Leles CR, Azevedo B, Azevedo
JR. Accuracy of cone beam computed tomography and
panoramic and periapical radiography for detection of
apical periodontitis. J Endod. 2008;34(3):273-279.
24. Khabbaz MG, Konstantaki MN, Sykaras SN. Dens invaginatus in a mandibular lateral incisor. Int Endod J.
1995;28(6):303-305.
25.Wells DW, Meyer RD. Vital root canal treatment of a
dens in dente. J Endod. 1993;19(12):616-617.
26.Goncalves A, Goncalves M, Oliveira DP, Goncalves N.
Dens invaginatus type III: report of a case and 10-year
radiographic follow-up. Int Endod J. 2002;35(10):873879.
27.Alani A, Bishop K. The use of MTA in the modern management of teeth affected by dens invaginatus. Int
Dent J. 2009;59(6):343-348.
28. Davalou S, Gutmann JL, Nunn MH. Assessment of apical and coronal root canal seals using contemporary
endodontic obturation and restorative materials and
techniques. Int Endod J. 1999;32(5):388-396.
29. Korzen BH. Endodontic obturation using the MicroSeal
technique. Oral Health. 1997;87(10):67-70,73.
Manufacturers
DENTSPLY Maillefer, Tulsa, OK
800.924.7393, www.maillefer.com
DENTSPLY Tulsa Dental Specialties, Tulsa, OK
800.662.1202, www.dentalspecialties.com
Geistlich Pharma North America Inc., Princeton, NJ
855.799.5500, www.geistlichonline.com
GE Global Research, Niskayuna, NY
262.544.3011, ge.geglobalresearch.com
Imaging Sciences International, Hatfield, PA
800.205.3570, www.i-cat.com
SybronEndo, Orange, CA
800.346.3636, www.sybronendo.com
www.agd.org
General Dentistry
January/February 2013
59
Periodontics
Obesity and periodontitis: a link
Charlene B. Krejci, DDS, MSD n Nabil F. Bissada, DDS, MSD
Obesity and periodontitis are both diseases that represent significant
health problems. Obesity currently impacts approximately one-third of
the US population and periodontitis affects an estimated 50% of the
same population, ages 30 and over. It has been suggested that the possible relationship between obesity and periodontitis lies in the diseases’
O
besity, defined as a body mass
index (BMI) ≥ 30.0 kg/m2, is a
major public health problem and,
according to the latest National Health
and Nutrition Examination Survey
(NHANES) data from 2007-2008, has
a documented prevalence in the United
States of 32.2% among adult men and
35.5% among adult women.1,2 Obesity is
a systemic disease that has been identified
as a risk factor for the development of
hypertension, type 2 diabetes, cardiovascular disease, dyslipidemia, certain forms
of cancer, respiratory problems, and, most;
recently, periodontitis.3
Periodontitis, by definition, is a chronic
inflammatory disease of bacterial origin
that affects the surrounding and supporting structures of the teeth and remains
one of the most ubiquitous diseases of
mankind, affecting an estimated 50%
of the US population over the age of
30.4,5 It is believed that the destructive
process of periodontitis begins with the
accumulation of subgingival plaque
biofilms and the subsequent release of
toxic products from the pathogenic
plaque bacteria. The host’s response to
these bacteria and their toxic products
triggers an inflammatory response that
can cause gingival ulcerations, tissue
destruction, alveolar bone loss, and tooth
loss. This results in the local production of
cytokines and other biological mediators
along with an increase in the concentration of systemic inflammatory markers.
Emerging scientific evidence indicates a
possible link between periodontitis and
a number of systemic diseases, including
cardiovascular disease (CVD), adverse
pregnancy outcomes, diabetes mellitus, respiratory disease, osteoporosis,
rheumatoid arthritis, certain forms of
cancer, and obesity.6-12
60
January/February 2013
underlying inflammatory processes. The aim of this paper is to present
those inflammatory pathways and to review the literature that has
examined the association between obesity and periodontitis.
Received: January 14, 2012
Accepted: April 25, 2012
The inflammatory pathways
It is well documented that adipose
tissue is not simply a repository for fat
cells, but is a metabolically active organ
that secretes more than 50 bioactive
substances, including pro-inflammatory
cytokines such as tumor necrosis factoralpha (TNF-α) and interleukin-6 (IL-6),
both of which are the main inducers of
acute phase hepatic protein production
including that of C-reactive protein
(CRP).13,14 Obese individuals have been
reported to have elevated levels of circulating TNF-α and IL-6 as compared to
normal-weight controls; TNF-α, IL-6,
and CRP are closely related to obesity and
insulin resistance.15,16 Leptin, a 16-kDa
non-glycosylated polypeptide that acts
as both a cytokine and a hormone, is
also produced by adipose tissue and is
involved in a multitude of biological
processes including energy metabolism,
endocrine functions, reproduction, and
bone metabolism.17 Leptin functions as
a circulating appetite suppressant that
regulates adipose tissue mass through
a negative feedback system.18 Elevated
leptin levels result in decreased food
intake, increased energy expenditure, and
a negative energy balance whereas leptin
deficiency results in hyperphagia and
severe obesity.18 However, obese individuals generally exhibit unusually high levels
of circulating leptin, which suggests a
resistance to leptin in much the same way
individuals with type 2 diabetes are resistant to insulin.19 In addition to leptin’s
role as an appetite regulator, several studies have clearly demonstrated that it plays
a significant role in the inflammatory
process and there is a consensus of opinion that regards leptin as a pivotal proinflammatory agent. An increase in leptin
production occurs during infections
General Dentistry
www.agd.org
and inflammatory processes and is
therefore implicated in the pathogenesis
of chronic inflammatory diseases.20-23
Periodontitis, as noted above, is a
chronic inflammatory disease whose bacterial origin and resultant endotoxin production can trigger host responses at both the
local and systemic levels.24 Inflammatory
mediators, including interleukins (IL-1β,
IL-6, IL-8, IL-17, and IL-23) and TNF-α,
as well as bone-related factors, have
been identified in periodontal tissues at
both the mRNA and protein levels.25 In
periodontitis, the proinflammatory actions
of TNF-α contribute to bone loss and the
loss of periodontal attachment; the proinflammatory actions of IL-17 contribute
to the production of other proinflammatory mediators including IL-6 and IL-8
and has also been implicated in alveolar
bone destruction.26-28 Beck et al reported
an up to tenfold increase in local and
systemic inflammatory cytokines including
TNF-α and IL-6 in some subjects with
periodontitis.29 These same cytokines can
then trigger an increase in the production of acute phase proteins such as CRP,
which results in an upregulation of the
inflammatory response similar to that seen
in obesity. In a study by Gomes-Filho et
al, levels of CRP were higher in patients
with periodontitis as compared to patients
without the disease.30 Similarly, higher
levels of serum leptin have been associated with increased periodontal destruction.31-33 It is increasingly clear from the
periodontal literature that it is the host
response, rather than the bacteria, that
drives the inflammatory processes both
locally and systemically.34-36 Failure to
contain the local inflammatory response,
along with research documenting the
presence of inflammatory mechanisms in
most of the chronic diseases of aging, has
led researchers to explore the commonality
of the inflammatory pathways and to suggest a possible bidirectional link between
periodontal disease and multiple chronic
diseases—including obesity.
The literature
The relationship between obesity and
periodontitis was first reported by Perlstein
& Bissada in 1977 when histopathologic
changes were observed in the periodontium of obese rats subjected to ligatureinduced periodontitis.37 In response
to plaque accumulation, periodontal
inflammation and alveolar bone resorption were found to be greater in the obese
rats as compared to nonobese controls.
In humans, an association between
obesity and periodontitis was first
reported in an epidemiological study
conducted by Saito et al in Japan using
241 healthy individuals to which the
community periodontal index of treatment needs (CPITN) was applied.38 After
adjusting for confounding variables, they
found that the relative risk for periodontitis was 3.4 in persons with a BMI of
25-29.9 kg/m2 and 8.6 in those with a
BMI ≥ 30 kg/m2.38 An additional study by
Saito et al utilizing 643 Japanese individuals who had at least 1 tooth per sextant
with a probe depth of ≥4 mm showed that
high upper-body obesity and high total
body fat were associated with a higher risk
of periodontitis as compared to normal
weight individuals.39 A longitudinal study
recently published by Morita et al involving 2,787 Japanese men and 803 Japanese
women, whose BMI and the incidence of
periodontal disease as defined by a probing depth >4 mm, were evaluated over a
5-year period.40 The study reported that
the men and women in the BMI groups of
25-29.9 kg/m2 and ≥30 kg/m2 were statistically more likely to develop periodontitis
than those whose BMI was <22 kg/m2.40
Moreover, these findings demonstrated a
dose-response relationship between BMI
and the development of periodontal disease in the population studied.
In a large cross-sectional study utilizing
data from the Study of Health in Pomerania
(SHIP), the impact of obesity on inflammation in both dentate and edentulous subjects was evaluated through anthropometric
measurements including BMI and waistto-hip ratio (WHR), along with diagnostic
periodontal parameters and systemic markers of inflammation.41 The results indicated
that obesity was associated with both the
extent and severity of periodontal disease
along with markers of systemic inflammation. These associations were characterized
by a strict dose-effect relationship between
WHRs and periodontal attachment loss,
and between serum CRP and fibrinogen
levels or white blood cell (WBC) count.
When adjusted for age, sex, smoking,
diabetes, education, physical activity, and
last dental appointment, it was found that
serum CRP, fibrinogen, and WBC count
were significantly correlated to WHR (P <
0.001), as well as to the BMI, in dentate
and edentulous subjects.41
An analysis of the NHANES III data
involving 13,665 individuals having one
or more sites with clinical attachment loss
(CAL) of ≥3 mm and probe depths of
≥4 mm was completed by Genco et al, and
a positive correlation was found between
BMI and the severity of periodontal
attachment loss.42 Al-Zahrani et al and
Wood et al analyzed the same data from
different perspectives and found that fat
in general, as well as specific fat distribution patterns, could be correlated with
periodontal disease.43,44 Recently, Kim et al
conducted a cross-sectional study of Korean
adults using the Fourth Korean National
Health and Nutrition Examination Survey
(KNHANES) and found a significant
association between abdominal obesity as
measured by waist circumference and periodontitis; correlations between BMI and
periodontitis were not as strong, however,
thus lending credence to the possibility that
it may be the location of body fat, not the
overall amount, that has a greater association with periodontitis.45
Another analysis of the NHANES III
data that was undertaken by Al-Zahrani
et al in 2005 found that individuals who
maintained normal weight, exercised
regularly, and followed a diet utilizing the
US Department of Agriculture Center for
Nutrition Policy and Promotions’ Food
Guide Pyramid and Dietary Guidelines
for Americans were 40% less likely to
have periodontitis.46
In a recent study by Lakkis et al, 30 obese
individuals with at least 20 teeth who were
also affected by chronic periodontitis as
defined by a mean periodontal attachment
loss of ≥2 mm were evaluated with respect
www.agd.org
to bariatric surgery, weight loss, and periodontal disease.47 All patients underwent
nonsurgical periodontal therapy involving
oral hygiene instructions, scaling, and root
planing. Of the 30 patients, 15 underwent
bariatric surgery and lost at least 40% of
their excess weight while the remaining 15
patients served as controls. At the end of
the study period, a statistically significant
improvement was noted in the periodontal
status of those who underwent bariatric
surgery and lost weight over those who did
not. This represents the first interventional
pilot study that clinically demonstrates the
bidirectorial interaction between these two
disease conditions.47
An extensive review of the periodontal
literature was undertaken by Chaffee &
Weston to systematically compile studies
that examined the relationship between
obesity and periodontitis.12 The result of
their literature search was a quantitative
summary of the association between these
two disease states. Of the 554 citations
found in the literature, 70 studies representing 57 independent populations met
the inclusion criteria, nearly all of which
were cross-sectional in design. Of the 70
studies included, 41 suggested a postive
association. Findings suggested a higher
mean BMI among periodontal patients,
a greater mean attachment loss among
obese individuals, and a trend toward
increasing odds of periodontal disease
with increasing BMI. As noted by the
authors, however, cross-sectional studies
represent only a moment in time and—
while able to show an association between
obesity and periodontitis—cannot therefore show evidence of causality.12
Conclusion
In an overview of periodontics and
obesity, whether one condition stands
as a risk factor for another or whether
one disease causes another has yet to be
elucidated. What has emerged from the
literature, however, is that an association between obesity and periodontitis
exists and that association most likely
lies in the commonality of their inflammatory pathways. According to Genco,
the relentless release of pro-inflammatory
cytokines into the systemic circulation
from adipose tissue in obese individuals
provides a systemic inflammatory overload.48 These cytokines may directly
General Dentistry
January/February 2013
61
Periodontics Obesity and periodontitis: a link
Chart. Systemic inflammatory overload is secondary to obesity and periodontitis.
Systemic Inflammatory
Overload
Specific Bacteria
Periodontitis
Host Response
TNF-αTNF-α
IL-1B
IL-6IL-6
IL-8
IL-17CRP
IL-23
CRP
Serum Leptin
Serum Leptin
Obesity
injure the periodontal tissues or reduce
the vascular blood flow to the periodontal
tissues, as first suggested by Perlstein &
Bissada, thus promoting the development
of periodontitis.37 Periodontitis, itself an
inflammatory disease, induces its own set
of cytokines both locally and systemically
in response to bacterial pathogens and
endotoxins and thus adds to the level of
circulating proinflammatory mediators
(Chart). As such, periodontitis increases
the systemic level of inflammation and
thus may contribute to systemic inflammatory diseases and a bidirectional link.47
Long-term prospective studies are needed
to further elucidate specific cause and
effect relationships between obesity and
periodontitis as well as to the wider body
of other chronic inflammatory diseases.
In the interim, health care professionals
need to be cognizant of the complexity
of obesity and its relationship to multiple
health care issues while at the same time
giving credence to the role of periodontitis
to overall health. This necessitates the full
cooperation and collaboration of all health
care professionals, in whatever capacity, to
educate patients regarding the ramifications of obesity and periodontitis and
to encourage counseling, treatment, and
intervention strategies as needed.
Author information
Dr. Krejci has a private practice limited
to periodontics with services in dental
implants. She is also an associate
clinical professor, Department of
62
January/February 2013
Periodontics, Case Western Reserve
University School of Dental Medicine,
Cleveland, OH, where Dr. Bissada
is a professor and chairman.
References
1.NHLBI Obesity Education Initiative Expert Panel on the
Identification, Evaluation, and Treatment of Obesity in
Adults (US). Clinical guidelines on the identification,
evaluation, and treatment of overweight and obesity
in adults: The evidence report. Bethesda, MD: National
Heart, Lung, and Blood Institute; 1998. Available at:
http://www.ncbi.nlm.nih.gov/books/NBK2003/. Accessed October 24, 2012.
2. Flegal KM, Carroll MD, Ogden CL, Curtain LR. Prevalence and trends in obesity among US adults, 19992008. JAMA. 2010;303(3):235-241.
3. Pischon N, Heng N, Bernimoulin JP, Kleber BM, Willich
SN, Pischon T. Obesity, inflammation, and periodontal
disease. J Dent Res. 2007;86(5):400-409.
4.The American Academy of Periodontology. Glossary of
Periodontal Terms. 4th ed. Chicago, IL: The American
Academy of Periodontology; 2001:38.
5.Albander JM. Underestimation of periodontitis in
NHANES surveys. J Periodontol. 2011;82(3):337-341.
6.Scannapieco FA. Position paper of The American Academy of Periodontology: periodontal disease as a potential risk factor for systemic diseases. J Periodontol.
1998;69(7):841-850.
7. Van Dyke TE. Inflammation and periodontal diseases:
a reappraisal. J Periodontol. 2008;79(suppl 8):15011502.
8. Beck JD, Offenbacher S. Systemic effects of periodontitis: epidemiology of periodontal disease and cardiovascular disease. J Periodontal. 2005;76(suppl 11):
2089-2100.
9. Joshipura K, Zevallos JC, Ritchie CS. Strength of evidence relating periodontal disease and atherosclerotic
disease. Compend Contin Educ Dent. 2009;30(7):430439.
10.Offenbacher S, Katz V, Fertik G, et al. Periodontal infection as a possible risk factor for preterm low birth
weight. J Periodontol. 1996;67(suppl 10):1103-1113.
General Dentistry
www.agd.org
11.Yao SG, Fine JB. Periodontitis and cancer…a link? A
review of the recent literature. Compend Contin Educ
Dent. 2010;31(6):436-442; quiz 443-444.
12.Chaffee BW, Weston SJ. Association between chronic
periodontal disease and obesity: a systematic review
and meta-analysis. J Periodontol. 2010;81(12):17081724.
13.Ritchie CS. Obesity and periodontal disease. Periodontol 2000. 2007;44:154-163.
14.Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V.
Inflammation, obesity, stress and coronary heart disease: is interleukin-6 the link? Atherosclerosis. 2000;
148(2):209-214.
15. Ziccardi P, Nappo F, Giugliano G, et al. Reduction of
inflammatory cytokine concentrations and improvement of endothelial functions in obese women after
weight loss over one year. Circulation. 2002;105(7):
804-809.
16. Kern PA, Ranganathan S, Li C, Wood L, Ranganathan
G. Adipose tissue tumor necrosis factor and interleukin-6 expression in human obesity and insulin resistance. Am J Physiol Endocrinol Metab. 2001;280(5):
e745-e751.
17. Zhang Y, Proenca R, Maffei M, Barone M, Leopold L,
Friedman JM. Positional cloning of the mouse obese
gene and its human homologue. Nature. 1994;
372(6505):425-432.
18. Friedman JM. Leptin, leptin receptors, and the control
of body weight. Nutr Rev. 1998;56(2, pt 2):s38-s46;
discussion s54-s75.
19. Margetic S, Gazzola C, Pegg GG, Hill RA. Leptin: a review of its peripheral actions and interactions. Int J
Obes Relat Metab Disord. 2002;26(11):1407-1433.
20.Lago R, Gómez R, Lago F, Gómez-Reino J, Gualillo O.
Leptin beyond body weight regulation–current concepts concerning its role in immune function and inflammation. Cell Immunol. 2008;252(1-2):139-145.
21.Otero M, Lago R, Lago F, et al. Leptin, from fat to inflammation: old questions and new insights. FEBS
Lett. 2005;579(2):295-301.
22. Bokarewa M, Bokarew D, Hultgren O, Tarkowski A.
Leptin consumption in the inflamed joints of patients
with rheumatoid arthritis. Ann Rheum Dis. 2003;
62(10):952-956.
23.Otero M, Lago R, Gomez R, et al. Changes in plasma
levels of fat-derived hormones adiponectin, leptin, resistin and visfatin in patients with rheumatoid arthritis.
Ann Rheum Dis. 2006;65(9):1198-1201.
24.Tatakis DN, Kumar PS. Etiology and pathogenesis of
periodontal diseases. Dent Clin North Am. 2005;49(3):
491-516, v.
25.Ribeiro, VF, de Mendonca AC, Santos VR, Bastos MF,
Figueiredo LC, Duarte PM. Cytokines and bone-related
factors in systemically healthy patients with chronic
periodontitis and patients with type 2 diabetes and
chronic periodontitis. J Periodontol. 2011;82(8):11871196.
26.Garlet GP, Martins W Jr, Fonseca BA, Ferreira BR, Silva
JS. Matrix metalloproteinases, their physiological inhibitors and osteoclast factors are differentially regulated by the cytokine profile in human periodontal
disease. J Clin Periodontol. 2004;31(8):671-679.
27. Boyce BF, Li P, Yao Z, et al. TNF-alpha and pathologic
bone resorption. Keio J Med. 2005;54(3):127-131.
28.Sato K, Suematsu A, Okamoto K, et al. Th17 functions
as an osteoclastogenic helper T cell subset that links T
cell activation and bone destruction. J Exp Med. 2006;
203(12):2673-2682.
29. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher
S. Periodontal disease and cardiovascular disease.
J Periodontol. 1996;67(suppl 10):1123-1137.
30.Gomes-Filho IS, Freitas Coelho JM, da Cruz SS, et al.
Chronic periodontitis and C-reactive protein levels.
J Periodontol. 2011;82(7):969-978.
31. Karthikeyan BV, Pradeep AR. Gingival crevicular fluid
and serum leptin: their relationship to periodontal
health and disease. J Clin Periodontol. 2007;34(6):
467-472.
32. Karthikeyan BV, Pradeep AR. Leptin levels in gingival
crevicular fluid in periodontal health and disease.
J Periodontol Res. 2007;42(4):300-304.
33.Shimada Y, Komatsu Y, Ikezawa-Suzuki I, Tai H, Sugita N, Yoshie H. The effect of periodontal treatment
on serum leptin, interleukin-6, and C-reactive protein. J Periodontol. 2010;81(8):1118-1123.
34.Offenbacher S. Periodontal diseases: pathogenesis.
Ann Periodontol. 1996;1(1):821-878.
35. Page RC, Kornman KS. The pathogenesis of human
periodontitis: an introduction. Periodontol 2000. 1997;
14:9-11.
36.Taubman MA, Kawai T, Han X. The new concept of
periodontal disease pathogenesis requires new and
novel therapeutic strategies. J Clin Periodontol. 2007;
34(5):367-369.
37. Perlstein MI, Bissada NF. Influence of obesity and hypertension on the severity of periodontitis in rats. Oral
Surg Oral Med Oral Pathol. 1977;43(5):707-719.
38.Saito T, Shimazaki Y, Sakamoto M. Obesity and periodontitis. N Engl J Med. 1998;339(7):482-483.
39.Saito T, Shimazaki Y, Koga T, Tsuzuki M, Oshima A. Relationship between upper body obesity and periodontitis. J Dent Res. 2001;80(7):1631-1636.
40. Morita I, Okamoto Y, Yoshii S, et al. Five-year incidence
of periodontal disease is related to body mass index.
J Dent Res. 2011;90(2):199-202.
41. Meisel P, Wilke P, Biffar R, Holtfreter B, Wallaschofski
H, Kocher T. Total tooth loss and systemic correlates of
inflammation: role of obesity. Obesity (Silver Spring).
2012;20(3):644-650.
42.Genco RJ, Grossi SG, Ho A, Nishimura F, Murayama Y.
A proposed model linking inflammation to obesity,
diabetes, and periodontal infections. J Periodontol.
2005;76(suppl 11):2075-2084.
43.Al-Zahrani MS, Bissada NF, Borawskit EA. Obesity and
periodontal disease in young, middle-aged, and older
adults. J Periodontol. 2003;74(5):610-615.
44.Wood N, Johnson RB, Streckfus CF. Comparison of
body composition and periodontal disease using nutritional assessment techniques: Third National Health
and Nutrition Survey (NHANES III). J Clin Periodontol.
2003;30(4):321-327.
45. Kim EJ, Jin BH, Bae KH. Periodontitis and obesity: a
study of the Fourth Korean National Health and Nutrition Examination Survey. J Periodontol. 2011;82(4):
533-542.
46.Al-Zahrani MS, Borawski EA, Bissada NF. Periodontitis
and three health-enhancing behaviors: maintaining
normal weight, engaging in recommended level of exercise, and consuming a high-quality diet. J Periodontol. 2005;76(8):1362-1366.
47.Lakkis D, Bissada NF, Saber A, et al. Response to periodontal therapy in subjects who had weight loss following bariatric surgery and obese counterparts: a
pilot study. J Periodontol. 2012;83(6):684-689.
48.Genco RJ. The three-way street. In: Oral and Whole
Body Health. New York, NY: Scientific American, Inc.;
2006:18-22.
www.agd.org
General Dentistry
January/February 2013
63
Exercise No. 323 Periodontics Subject Code 490
The 15 questions for this exercise are based on the article,
Obesity and periodontitis: a link, on pages 60-63. This
exercise was developed by Gustav Gates, DDS, MAGD,
in association with the General Dentistry Self-Instruction
committee.
1. A person who has a body mass index
(BMI) of _____ is considered obese.
A.15
B.22
C.29
D.36
2. In the United States _____% of adult
men and _____% of adult women are
considered obese.
A. 15.8; 16.9
B. 18.2; 21.3
C. 28.6; 29.4
D. 32.2; 35.5
3. Obesity is a systemic disease which
has been identified as a risk factor for
development of all the following except
one. Which is the exception?
A.Hypertension
B.Type 1 diabetes
C.Cardiovascular disease
D.Dyslipidemia
4. Elevated leptin levels in healthy
individuals have been shown to
A. increase food intake.
B. create positive energy balance.
C. increase energy expenditure.
D. cause hyperphagia.
5. Obese individuals generally exhibit
unusually high levels of circulating leptin.
This suggests a resistance to leptin in
much the same way individuals with type
2 diabetes are resistant to insulin.
A. Both statements are true.
B.The first statement is true;
the second is false
C.The first statement is false;
the second is true.
D. Both statements are false.
Reading the article and successfully completing this exercise will enable you to:
•understand the current information regarding the link between obesity
and periodontitis;
•understand the role of inflammatory pathways connecting periodontitis to obesity; and
•review the current literature on obesity and periodontitis.
6. Adipose tissue has been shown to be a
metabolically active organ. It has been
shown to do all of the following except
one. Which is the exception?
A. Be a repository for fat cells
B.Secrete over 50 bioactive substances
C.Secrete C-reactive protein (CRP)
D.Secrete proinflammatory cytokines
7. Leptin is produced by the adipose tissue.
It is involved in all of the following
except one. Which is the exception?
A.Reproduction
B.Energy metabolism
C.Exocrine function
D. Bone metabolism
8. In periodontitis, the proinflammatory
actions of TNF-α contribute to the
loss of attachment. One inflammatory
mediator that has been implicated in
alveolar bone loss is IL-17.
A. Both statements are true.
B. The first statement is true;
the second is false.
C. The first statement is false;
the second is true.
D. Both statements are false.
9. It has become increasingly clear from
the periodontal literature that bacteria
drive the inflammatory process. Levels
of CRP are lower in patients with
periodontal disease.
A. Both statements are true.
B.The first statement is true;
the second is false
C.The first statement is false;
the second is true.
D. Both statements are false.
10. The relationship between obesity
and periodontitis was first reported
by _____ in 1977.
A.Offenbacher & Beck
B.Carroll & Flegal
C. Perlstein & Bissada
D.Carroll & Beck
11. An analysis of the data from the United
States NHANES III survey found that
an individual was 40% less likely
to have periodontitis if they did all
of the following except one. Which
is the exception?
A. Maintained normal weight
B.Exercised regularly
C. Followed the Food Guide Pyramid
D.Took 3000 IU of vitamin C daily
12. A study of patients who underwent
bariatric surgery and lost _____% of
their excess weight had a statistically
significant improvement in periodontal
status.
A.10
B.20
C.30
D.40
13. Chaffee & Weston found 70 studies
that examined the relationship
between obesity and periodontitis.
Of the 70 studies, _____ suggest a
positive association between the two.
A.24
B.35
C.41
D.56
14. Analysis of the Fourth Korean
National Health and Nutrition Survey
found a significant association
between _____ and periodontitis.
A. location of body fat
B. age of patient
C. dental visits per year
D. socioeconomic status
15. By definition, periodontitis is an acute
inflammatory disease of bacterial origin.
It affects <30% of the United States
population 30 years of age and over.
A. Both statements are true.
B.The first statement is true;
the second is false
C.The first statement is false;
the second is true.
D. Both statements are false.
Answer form is on page 80. Answers for this exercise must be received by December 31, 2013.
64
January/February 2013
General Dentistry
www.agd.org
Pre-Prosthetic Surgery
Surgical resection and prosthetic treatment
of an extensive mandibular torus
Thais Marques Simek Vega Goncalves, DDS, MSc n Jonas Alves de Oliveira, DDS, MSc n Alfonso Sanchez-Ayala, DDS, MSc Renata Cunha Matheus Rodrigues Garcia, DDS, MSc, PhD
The aim of this case report was to describe the surgical removal of an
extensive mandibular torus and the conventional prosthetic treatment that
was performed. During surgery, the torus was exposed by an intrasulcular
lingual incision from molar to contralateral molar side and displacement
of the mucoperiosteal flap. The bone volume was carefully removed in
3 separate blocks by sculpting a groove in the superior lesion area and
chiseling. After a 30-day postoperative period, a prosthetic treatment was
A
torus is a local bone hyperostosis
formed at the longitudinal ridge of
the half palatine (palatine torus) or
on the mylohyoid line on the lingual surface of the mandibular body (mandibular
torus).1,2 This benign bone projection presents very slow and progressive growth, due
to the asymptomatic nature of the lesion,
and is usually incidentally diagnosed
during a routine clinical examination.3-5
Clinically, a mandibular torus commonly emerges in the premolar region
above the mylohyoid attachment; however,
it can be distally extended to the third
molar area and mesially toward the lateral
incisor.1,3,6 A normal but thin mucosa
covers this bone projection, and ulcerations
can occur if the region is traumatized,
especially in the case of extensive lesions.1-4
Imaging examinations (for example, X-ray
or CT) of mandibular tori reveal that a
circumscribed radiodense region often
encroaches upon the roots of premolars
and molars, impairing the observation of
tooth details.1,4 Histological aspects show
cortical and cancellous bone, which form
as a result of lamellar periosteal outgrowth
of the mandible; presence of the spongy
layer is very rare and is present only in
large tori.1,4 Mandibular tori are classified
according to size as either small (<2 mm),
medium (2-4 mm), or large (>4 mm).7,8
Tori are usually (61%) nodular in shape;
87% of tori emerge unilaterally or bilaterally, in single or multiple forms.3,6,9 The
prevalence of mandibular tori is 2.1%;
however, only 1% of palatine tori can be
seen in patients at a mean age of 49.10
Although the prevalence of mandibular
performed using a conventional distal extension removable partial denture.
The patient’s esthetic and functional expectations were achieved. The
surgical procedure and prosthetic treatment performed in the treatment
of the mandibular torus in this clinical case is a viable treatment that produces few complications and re-establishes normal masticatory function.
Received: July 22, 2011
Accepted: October 3, 2011
tori does not differ between males and
females, some ethnic groups, such as
Eskimos, Japanese, and North Americans,
demonstrate a higher prevalence index,
suggesting a multifactorial etiology.3,6 There
is evidence that there are environmental
influences on torus development, such as
nutritional disturbances, dietary habits
(including the use of calcium supplements
and diets rich in vitamin D), side effects of
continuous phenytoin use, and masticatory
hyperfunction.6-8,11-14 Eggen & Natvig,
using logistic regression, proposed another
theory that 30% of torus etiology is
genetically determined (due to a dominant
autosomal gene on the X chromosome).7
Mandibular and palatine tori must be
surgically removed when they present
with superficial mucosal ulceration and
food retention, and when they interfere
with esthetics, speech, or prosthetic
rehabilitation.1-3,5,9,15-17 Other aspects
that must be considered regarding
torus surgical excision include whether
the area is associated with infectious
processes, such as osteomyelitis, or neoplastic processes, such as carcinomas.4
In an effort to inform dentists of the
possible complications of torus removal,
this article presents a clinical report
on the surgical removal of an extensive
mandibular torus and the prosthetic
treatment performed afterward.
Case description
The patient, a healthy 45-year-old man
with leukoderma, was referred to the
Piracicaba Dental School, State University
of Campinas (FOP-UNICAMP) for
www.agd.org
general and prosthetic treatment. The
subject was completely dentate in the
maxilla and partially dentate in the
mandible, so he was classified as Kennedy
Class II, modification 1 (Fig. 1 and 2).
At the clinical examination, a highly
extensive mandibular nodular torus (>4
mm on each side) was detected bilaterally in the premolar and molar area.
The lesion was not painful; however,
the patient reported discomfort due to
its volume, which altered speech. The
patient also reported difficulties with oral
hygiene, due to areas of food retention,
and consequent halitosis. Teeth adjacent
to the torus were vital without alterations
in sensitivity and had healthy marginal
periodontium. The torus lesion was
covered by attached gingival tissue with
normal color, continuity, and volume.
Periapical and occlusal radiographs of
the patient’s remaining teeth were taken.
The resulting images confirmed the health
of the teeth next to the lesion as well as
an increase of bone volume in the lingual
area, beginning in the canine apical region
and extending bilaterally to the molars,
in correspondence with the torus.
After the imaging procedures, complete maxillary and mandibular arch
impressions were made using irreversible hydrocolloid impression material
(Jeltrate, Dentsply International)
and stock trays (Tecnodent Industria
e Comercia). Diagnostic casts were
processed using Type III dental stone
(Herodent, Vigodent S/A Industria
e Comercio) and were manually
articulated in the maximum intercuspal
General Dentistry
January/February 2013
65
Pre-Prosthetic Surgery Surgical resection and prosthetic treatment of an extensive mandibular torus
Fig. 1. Complete dentition in the maxilla.
Fig. 2. Extensive bilateral mandibular nodular torus located in the
premolar and molar areas.
Fig. 3. Lesion after the displacement of the
mucoperiosteal flap.
Fig. 4. Aspect of the area immediately after torus
removal.
Fig. 5. Aspect of the area 30 days after the
procedure.
position and fixed using a dental
sticky wax (Asfer Industria Quimica).
Afterward, the pair of casts was mounted
on a semi-adjustable articulator (Gnatus
8600, Gnatus) with the help of the
facial bow of the articulator device. A
removable partial mandibular prosthesis
was the chosen treatment in the present
case; its advantages include the possibility of replacing a greater number of
missing teeth, ease of cleaning, and low
cost.18 Implant therapy was not recommended due to the low quality of the
bone in the torus area, which could have
resulted in a weak osteogenic capacity of the torus bone.3,16 Moreover, the
high density and slight vascularization
of the bone in the torus region could
produce excess heat and tension during
implant placement, which could influence implant longevity.3 Due to the
dimensions of the torus, the proposed
treatment was surgical removal of the
lesion, including an excisional biopsy,
followed by the insertion of a removable partial mandibular denture.
The surgical procedure was performed
in the surgical center of FOP-UNICAMP
under local infiltration anesthesia. The
first step was an intrasulcular lingual
incision from molar to contralateral
molar side and displacement of the
mucoperiosteal flap, exposing the
entire lesion (Fig. 3). Bone volume was
removed by making a groove in the
superior lesion area with a 702 bur (KG
Sorensen). The entire lesion was cleaved
into three separate blocks. Once the
torus had been removed, the area was
smoothed with a large round bur (KG
Sorensen) under saline rinsing, and the
surgical site was irrigated to clean bone
debris (Fig. 4). The surgical procedure
was concluded with local suturing.
During the postoperative period, the
patient was given aftercare instructions
regarding medication (analgesic), diet (soft
and liquid food), and hygienic care (tooth
brushing and cleaning of the surgical area).
Ten days after the surgical procedure,
the sutures were removed, and a 30-day
healing period was allowed (Fig. 5).
The oral cavity was then prepared for
the prosthesis. Occlusal rest seats were
performed on the mesial marginal ridge
of the left second premolar, the distal
marginal ridge of the right second premolar, and the mesial marginal ridge of
the right second molar. Guide planes and
additional retentions were not necessary.
A definitive impression was obtained
using Jeltrate, and a custom tray was
fabricated using autopolymerizing acrylic
resin (Classico, Artigos Odontologicos
Classico Ltda.). The final master cast
was prepared using Type IV dental stone
66
January/February 2013
General Dentistry
www.agd.org
Fig. 6. Removable partial denture in position.
(Vel-Mix, Kerr Corporation), and a
chromium-cobalt metal framework was
processed. The design of the framework
involved two circumferential clasps on
the right second premolar and second
molar, and a back action clasp on the left
second premolar. A mandibular single
bar was used as a major connector.
After the framework was processed,
it was fitted in the patient’s mouth. The
mandibular and maxillary master casts presented a stable relationship, so they were
manually articulated in the maximum
intercuspal position and fixed. Afterward,
the final casts were mounted in a Gnatus
8600. Artificial teeth (Biotone, Dentsply
International) were arranged in a wax rim
(Polidental Ltda.) on the acrylic resin base
for trial evaluation. Heat-polymerized
acrylic resin (Classico) was processed and
the denture was completed. The denture
was inserted into the patient’s mouth and
occlusal adjustments were made using
60 μ straight strip articulating paper
(Bausch Articulating Papers, Inc.) to
mark the occlusal contacts (Fig. 6). The
patient was given instructions regarding regular cleaning and maintenance.
Recall evaluations were performed at
7, 15, and 21 days in order to adapt the
prosthesis to the patient’s mouth. After
this period, the patient experienced no
complications associated with the oral
rehabilitation. The patient’s esthetic and
functional expectations were satisfied.
Discussion
The present case report describes the
excision of an extensive mandibular torus
from an otherwise healthy patient. The
most common treatment of a mandibular
torus is long-term clinical monitoring,
as most are small and do not cause oral
damage.3,5,17 However, because the patient
in the present case revealed discomfort
during speech and the hygiene process,
and given that the size of the lesion could
affect the insertion of any prosthetic
device, resulting in prosthesis instability
and chronic tissue irritation, it was decided
to perform the surgical procedure.17
Currently, several options exist for rehabilitation of such clinical cases, including
removable prostheses, more complex
treatments such as implant-supported
dental prostheses, and combinations of
these therapies.18
However, some subjects may not have
access to implant treatment or may not
be physically capable of receiving it.
Moreover, despite the fact that studies
have revealed that the torus bone can be
indicated as autogenous graft material
for implants, the large amount of dense
cortical bone in the torus area is likely to
affect implant placement due to the weak
osteogenic capacity of torus bone.3,16
Although the technique presented here
is simple, there can be complications with
surgical excision of the torus. Generally,
these can occur when the mucoperiosteum is lifted, leading to sectioning of the
Wharton or submaxillary duct, or lacerations of the floor of the mouth or other
anatomical structures that could require
subsequent surgical repair.1 The surgical
procedure must be performed carefully in
order to avoid damaging the inferior alveolar or lingual nerves, which can result
in paresthesia. Postsurgical precautions
must also be taken to prevent infections
that could worsen the patient’s prognosis
or require additional procedures.1,17 In
some severe cases, the use of general anesthesia is necessary and could represent
an operative risk.3 However, a thorough
knowledge of anatomical structures in the
oral region and the proper use of instruments will prevent most complications.1
A mandibular torus is typically encountered during a routine examination, and
while complications are rare, they can
occur as a result of the clinician’s iatrogenic surgical maneuvers. For this reason,
clinical dentists must be acquainted
with and able to treat this common
lesion in a predictable, optimized way.
www.agd.org
Summary
Mandibular torus removal must be
considered when traumatic ulcers
resulting from mastication are noted,
when the lesion volume interferes
with normal speech or tongue functions, or when prosthodontic considerations are required. In the present
case report, conventional excision
of the lesion was performed without
surgical complications and a good
prognosis was made after rehabilitation with a removable partial denture.
Acknowledgments
The authors gratefully acknowledge the
support of Prof. Dr. Marcio de Moraes
and graduate student Sergio Monteiro
Lima Jr. for their assistance with the
surgical procedure, and wish to thank
Barbara Prestes Del Cistia for her assistance with the prosthetic treatment.
Author information
Drs. Goncalves, de Oliveira, and
Sanchez-Ayala are postgraduate students, Department of Prosthodontics
and Periodontology, Piracicaba
Dental School, State University of
Campinas, Piracicaba, Sao Paulo,
Brazil, where Dr. Garcia is a professor.
References
1. Pynn BR, Kurys-Kos NS, Walker DA, Mayhall JT. Tori
mandibularis: a case report and review of the literature. J Can Dent Assoc. 1995;61(12):1057-1058;
1063-1066.
2. Manganaro AM, Faulk-Eggleston J, Schanzer RB, Dagostino M. Osteitis in a torus mandibularis secondary
to trauma. Gen Dent. 1997;45(1):74-77.
3.Garcia-Garcia AS, Matinez-Gonzales JM, Gomez-Font
R, Soto-Rivadeneira A, Oviedo-Roldan L. Current status of the torus palatinus and mandibularis. Med Oral
Patol Oral Cir Bucal. 2010;15(2):e353-e360.
4.Seah YH. Torus palatines and torus mandibularis: A
review of the literature. Aust Dent J. 1995;40(5):318321.
5. Ponzoni D, Guarino JM, Perez AP, Souza RM, Paro RF.
Remocao cirurgica de toro palatino para confeccao de
protese total convencional—indicacoes de diferentes
incisoes [in Portuguese]. RFO. 2008;13:66-70.
6.Al-Bayaty HF, Murti PR, Matthews R, Gupta PC. An epidemiological study of tori among 667 dental outpatients in Trinidad & Tobago, West Indies. Int Dent J.
2001;51(4):300-304.
7.Eggen S, Natvig B. Variation in torus mandibularis
prevalence in Norway. A statistical analysis using logistic regression. Community Dent Oral Epidemiol. 1991;
19(1):32-35.
8.Eggen S, Natvig B. Concurrence of torus mandibularis
and torus palatines. Scan J Dent Res. 1994;102(1):
60-63.
General Dentistry
January/February 2013
67
Pre-Prosthetic Surgery Surgical resection and prosthetic treatment of an extensive mandibular torus
9. Sonnier KE, Horning GM, Cohen ME. Palatal tubercles,
palatal tori, and mandibular tori: prevalence and anatomical features in a U.S. population. J Periodontol.
1999;70(3):329-336.
10. Henrique PR, Bazaga Junior M, Araujo VC, Junqueira
JLC, Furuse C. Prevalencia de alteracao da mucosa bucal em individuos adultos da populacao de Uberaba,
Minas Gerais [in Portuguese]. RGO. 2009;57:261-267.
11. Bruce I, Ndanu TA, Addo ME. Epidemiological aspects
of oral tori in a Ghanaian community. Int Dent J. 2004;
54(2):78-82.
12. Clifford T, Lamey PJ, Fartash L. Mandibular tori, migraine and temporomandibular disorders. Br Dent J.
1996;180(10):382-383.
13. Sasaki H, Ikedo D, Kataoka M, Kido J, Kitamura S, Nagata T. Pronounced palatal and mandibular tori observed in a patient with chronic phenytoin therapy: a
case report. J Periodontol. 1999;70(4):445-448.
14. MacInnis EL, Hardie J, Baig M, al-Sanea RA. Gigantiform torus palatinus: review of the literature and report of a case. Int Dent J. 1998;48(1):40-43.
15. Haugen LK. Palatine and mandibular tori. A morphologic study in the current Norwegian population. Acta
Odontol Scand. 1992;50(2):65-77.
16. Rouas A, Midy D. About a mandibular hyperostosis: the
torus mandibularis. Surg Radiol Ant. 1997;19(1):41-43.
17. Castro Reino O, Perez Galera J, Perez Cosio Martin J,
Urbon Caballero J. Rev de Actual Odontoestomatol
Esp. [in Portuguese]. 1990;50:47-50;53-56.
68
January/February 2013
18. Grossmann Y, Levin L, Sadan A. A retrospective case
series of implants used to restore partially edentulous
patients with implant-supported removable partial
dentures: 31-month mean follow-up results. Quintessence Int. 2008;39(8):665-671.
Manufacturers
Asfer Industria Quimica, Sao Caetano do Sul, SP, Brazil
55.11.2786.5487, Website unavailable
Artigos Odontologicos Classico Ltda., Sao Paulo, SP, Brazil
55.11.3022.2588, www.classico.com.br
Bausch Articulating Papers, Inc., Nashua, NH
888.622.8724, www.bauschdental.com
Dentsply International, York, PA
800.877.0020, www.dentsply.com
Gnatus, Ribeirao Preto, SP, Brazil
55.16.2102.5000, gnatus.com.br
Kerr Corporation, Orange, CA
877.685.1484, www.kerrdental.com
KG Sorensen, Cotia, SP, Brazil
55.11.4777.1061, www.kgsorensen.com.br
Polidental Ltda., Cotia, SP, Brazil
55.11.4613.6133, www.polidental.com.br
Tecnodent Industria e Comercia, Sao Paulo, SP, Brazil
55.11.5641.2695, www.tecnodent.com.br
Vigodent S/A Industria e Comercio, Rio de Janeiro, RJ, Brazil
55.21.3866.5600, www.vigodent.com.br
General Dentistry
www.agd.org
Guest Editorial
Occlusion confusion
Gene McCoy, DDS
The subject of occlusion is fraught with controversy and confusion. As a
result, there is no consensus on occlusal morpholology, normal function
of the mandible, or occlusion’s relationship to temporomandibular joint
(TMJ) disorders. The purpose of this paper is to explain the reasons
for the controversy and to provide suggested guidelines, based on
M
ost dentists agree that a good
understanding of occlusion is
essential to ensuring optimal
dental health; however, that seems to be
the only point of consensus for this important, controversial subject. As Gordon
Christensen stated in a letter (November
6, 2008), “Unfortunately, occlusion in its
broad definition is not a popular subject in
continuing education courses or in actual
practice. Although occlusion principles
permeate almost all of dentistry, the area
is confounded by confusing theories,
non-practical techniques, contradictory
‘beliefs,’ and practitioners unaware of the
basic concepts of occlusion. As a result,
most dental patients go without the benefits of dental therapy based on several
misleading occlusal assumptions.” These
“misleading occlusal assumptions” inspire
an important question: What is the precise
role that occlusion plays in the etiology of
temporomandibular joint (TMJ) disorders?
How many times have you heard
someone blame a restorative failure on
the occlusion? It might be worth asking
what that means, since the word occlusion has three different interpretations.
The original definition referred to the act
or process of occluding (from the Latin
occludere, which means to “shut up” or
“close up”).1 As a result, dental occlusion
was originally defined as the relation of
the teeth when the jaws are closed.1 In
1959, the definition was expanded to
mean “the contact of the teeth of both
jaws during those excursive movements
of the mandible essential to the function
of mastication.”2 This new definition was
published even though early studies suggested that teeth rarely touch during mastication (and when they do touch, they do
so only lightly) and that excursive movements of the mandible are not essential to
engineering principles, for the restorative dentist to follow in order to
minimize and prevent TMJ-related problems.
Received: February 14, 2012
Accepted: June 20, 2012
mastication.3,4 The dental profession had
witnessed patients grinding their teeth in
lateral excursions, saw that it was doing
damage, and sought to find the horizontal
vector with the least resistance or interference. Although it may have been assumed
that these horizontal excursions were an
integral part of normal function, they
were actually examples of parafunction.
People do not normally eat in horizontal
excursions unless forced to do so by a flattened dentition. Still another interpretation of occlusion was Jablonski’s definition
that, instead of simply describing the way
teeth touch each other, developed into
a 60-word description of all the components of the stomatognathic system.5
Current texts on occlusion do not merely
describe the simple touching of maxillary
and mandibular teeth, but rather present
a detailed analysis of the whole stomatognathic system.3-9 Occlusion (that is, the
way teeth touch each other during closure)
and the stomatognathic system are entirely
different things and should be described
separately to remove any ambiguity.
The function of the
stomatognathic system
When defining occlusion, the confusion
stems from the fact that there are two
entirely different viewpoints as to how
the stomatognathic system should function. With the vertical function paradigm
model, the mandible functions vertically.
People speak vertically, swallow vertically,
and eat vertically. The vector of mastication is a vertical teardrop with a lateral
movement of 5-6 mm during the first
phase of chewing; as the teeth approach
each other, the lateral displacement is
reduced to 3-4 mm from the starting
position. During closure, the mandible
is guided into position by the occlusal
www.agd.org
incline planes of the teeth. It is not a consistent and reproducible movement, but
a function of head position. As the head
tilts forward, the mandible goes forward;
after each vertical function, the mandible
returns to a state of physiological rest.6
During opening and closing, there
is condylar centricity where the axis is
maintained; upon complete closure, the
condyles are seated in the anterior-superior portion of the glenoid fossae. There
are seldom any border movements and
most mandibular movements take place
within a reasonably limited 3-dimensional
space. The model in this paradigm is
free from parafunction.
While there is no disagreement that
speaking and swallowing occur vertically,
the horizontal paradigm is based on the
premise that the mandible functions laterally rather than vertically. This paradigm
was first developed in the early 20th
century when a number of dentists became
preoccupied with the mandible’s ability
to rotate around axes in three planes. It
was the objective of the gnathologists who
studied these jaw movements to produce
a proper occlusal form that would be
dictated by mandibular movements—in
other words, one that would accommodate
free passage for the opposing dentition by
eliminating interferences in laterotrusive
movements from centric. This goal was
defined as optimal functional occlusion.7
This definition conflicts with the definition of functional occlusion, which refers to
the touching of maxillary and mandibular
teeth during mastication and deglutition.
Both activities are vertical, not horizontal.
In other words, function in lateral excursions is actually parafunction.
The anterior teeth are a major interference for anterior excursions; to eliminate
that obstacle, it would be necessary to
General Dentistry
January/February 2013
69
Guest Editorial Occlusion confusion
shorten the incisors considerably. The
gnathologists’ solution was to declare that
the purpose of the anterior teeth being
longer was to disengage the posterior
teeth during these parafunctional excursions for their protection, a principle
referred to as anterior guidance, which is
half of the concept of protected articulation.8 Nothing was said about the trauma
that the anterior teeth would receive
during this exercise.
In the author’s opinion, the vertical paradigm, free from parafunction, is the model
to emulate. If parafunction occurs, treatment should focus on management and
prevention rather than accommodation.
Morphology of the dentition
Three key benchmarks are used to evaluate
the overall status of the stomatognathic
system: the muscles of mastication,
the condyle, and the dentition. When
the system is healthy and functioning
efficiently, the muscles of mastication
are relaxed and the condyles are seated
properly in the anterior superior part of
the fossae. However, there is no consensus
regarding the morphology of the dentition,
how the maxillary and mandible should
contact each other in closure, and more
importantly, the dentition’s involvement in
temporomandibular disorders (TMDs).
There are design principles that appear
to govern the structure-function relationship in organisms; that is, there is an
interface between mechanical engineering
and biology which indicates that biological materials and structures are designed
for specific functions.9 Teeth are a perfect
example of a structure-function relationship. The fossae are intended to hold food
for cutting, while the sharp cusps have
two purposes: to cut the food and to
direct mastication forces vertically down
the long axis upon closure.
The space between the incline planes
allows for resistance-free repositioning of
the mandible/condyle during swallowing
and anterior posterior postural changes. It
would appear that the original design or
morphology of our teeth is best suited to
serve our stomatognathic system; unfortunately, not everyone emulates this standard.
For instance, when constructing removable
dentures, seven different designs are available for the posterior teeth, with occlusion
ranging from 33°- 0° (flat plane).10
70
January/February 2013
Two developments programmed the
dental community for the concept of flat
plane occlusion: the gnathologists’ horizontal function paradigm—research which
suggested that 33° of occlusion would be
harmful to the alveolar bone—and the
perception that people were designed to
eat with a flattened dentition.8,11-13 In
research conducted by Ortman, Kydd,
Regli & Kydd, and Swoope & Kydd,
investigators placed strain gauges in dentures and had patients eat various types
of foods with different morphologies of
0°-33°occlusion.8,11-13 All four studies followed the same protocols. In these studies,
the strain gauges measured highest with
33° occlusion and lowest with 0° occlusion. The various authors concluded that
the increased strain of 33° occlusion would
be harmful to the alveolar bone.8,11-13 As it
happened, the fact that the strain gauges
registered high with this occlusion meant
that the denture was working efficiently,
directing valuable vertical stimulation to
the alveolar ridge. The 0° occlusion diminished alveolar stimulation, dislodging the
dentures laterally as the flattened teeth
forced the patient to eat laterally.
It has been suggested that our evolutionary blueprint has programmed people for
0° of occlusion and that all living humans
were designed to eat with a flattened
dentition. Neiburger, a dentist and anthropologist, warned the dental community
in 1977 that deviation from this model
may cause serious problems for patients
and encouraged dentists to assist patients
toward a flattened dentition, labeling this
process as normal.14 It may be considered normal because it is common, but
common isn’t necessarily good. It is poor
speculation to declare that humans are
predestined to have a flattened dentition
when it is commonly known that many
seniors maintain naturally sharp teeth.
Dental compression syndrome
McCollum & Stuart described a subtle
pathology of function between the opposing teeth and movements of the mandible,
declaring that the lack of understanding
regarding this pathology has prevented
dentistry from rendering substantial
health services to its patients.15 That subtle
pathology is called dental compression
syndrome (DCS) (also known as parafunction or bruxism). DCS is defined as a total
General Dentistry
www.agd.org
parafunctional activity that includes the
grinding, gnashing, or clenching of teeth
during the day and/or night. Capable of
forces in excess of 500 psi, DCS can inflict
compressive, tensile, shearing, and flexural
forces on the dentition while simultaneously imposing unwanted force on the
alveolar bone and the TMJ.
The goals in restorative dentistry are to
treat the cases successfully and to keep the
patient’s stomatognathic system healthy and
comfortable until the next restorative case.
In the author’s opinion, DCS is the biggest
threat to those goals. DCS is a subconscious activity. Since many affected patients
are unaware of the activity, the dentist must
recognize the visual signs to address the
problem. Obvious signs include a flattened
dentition and hypertrophied masticatory
muscles; in addition, there are certain
deformations caused by clenching and
grinding that affect the dentition, bone,
and restorative materials and which many
dentists misdiagnose or don’t understand.16
These deformations are not germane to
each patient affected, as there are far too
many variables, including the power and
frequency of the compression, the genetic
resistance of the alveolar bone, the patient’s
gender, and his or her biologic strength.
DCS can be identified by four distinct
types of deformations: a wedge-shaped
noncarious lesion (NCL) found at the gingiva (Fig. 1); the inverted cupola, another
NCL found at the tips of functional cusps
(Fig. 2); exostosis (Fig. 3); and deformed
restorative materials (Fig. 4).
Gingival noncarious lesions
Gingival NCLs are wedge-shaped and
usually occur at the dentinoenamel junction (DEJ) (Fig. 5). This unique loss of
tooth substance has been the subject of
controversy among dentists for almost
100 years.17 The mystery is reduced if one
understands the science of biomechanics—
that is, the mechanical behavior of living
materials and structure. Gingival NCLs
that are multi-shaped examples of fatigue
due to compression and tension are shown
in Fig. 6-9.18
Fatigue refers to changes in the properties of a material due to repeated applications of stress or strain; in this case,
compression failure from DCS. Gordon
described fatigue as one of the most
insidious reasons why a structure loses
Fig. 1. An example of a gingival NCL.
Fig. 2. An example of inverted cupolas
due to compression or static or cyclic
loading.
Fig. 5. An anterior view of NCLs at the gingiva.
its strength.19 If an object rebounds to its
original shape after repeated compressions
(such as a tennis ball), it is said to be elastic
in nature; however, if an object exhibits
residual defects after repeated compression, it is said to be plastic in nature.
Biological structures such as teeth and bone
are termed viscoelastic and are subject to
deformation. Engineers refer to this type of
fatigue as corrosion fatigue.20 Dentists don’t
recognize corrosion fatigue because this is
an engineering problem and the mechanisms of engineering are not emphasized in
dental school, which often overlooks high
math to focus more on chemistry.
It would behoove us to examine the
design aspects of the dentition from an
engineering point of view. In 1975, stress
generated in a premolar as a result of occlusal forces was studied by using the finite
element method, a mathematical technique
Fig. 3. An example of exostosis.
Fig. 6. Cross-section of tooth No. 6 demonstrating
an angular NCL.
Fig. 4. Stress-related Luder lines.
Fig. 7. NCL in the palatal root of tooth
No. 3.
Fig. 8. Multiple NCLs revealed in a postmortem
examination.
Fig. 9. Facial NCLs demonstrated in mandibular
anterior incisors.
well-suited to analyzing stress in teeth and
dental restorations because it can closely
simulate the geometrics, loads, and material
in homogeneities in the system being studied.20 The analysis revealed that the DEJ
was susceptible to cleavage or failure planes
(Fig. 10).20 In this figure, a failure plane is
apt to occur on the lingual face running
through the DEJ well down into the root—
the classic geometry of a gingival notch.
A year later, another team of engineers
performed a similar study.21 They used
the finite element method to demonstrate
stress distribution and concluded that
www.agd.org
General Dentistry
January/February 2013
71
Guest Editorial Occlusion confusion
Fig. 10. Magnitude and direction of principal
stresses at selected locations. (Reprinted with
permission from John Wiley & Sons.)
Fig. 12. Multiple NCLs in tandem on
teeth No. 3, 4, and 6.
Fig. 13. NCLs in tandem on the facial
aspect of tooth No. 20. Note contact
on tooth No. 12 forcing tooth No. 20
toward the lingual.
the tensile forces in the gingival area are
powerful enough to pull apart the enamel
prisms.21 The authors concluded that
these high stresses are likely responsible
for the pain experienced by patients with
cervically placed restorations. This study
was conducted during the prebonding
era, when dentists would mechanically
lock in a restoration.
In a 1972 study, Hood demonstrated
the unusual flexibility of teeth by using
photoelasticity, placing teeth in a loading
frame and applying pressure (Fig. 11).22
The frozen stress technique demonstrated
an actual shortening of the tooth occlusal
72
January/February 2013
Fig. 11. Compression of a tooth in a loading frame
to demonstrate flexibility of teeth. (Reprinted with
permission from the New Zealand Dental Journal.)
Fig. 14. An example of
inverted cupolas at the
tips of functional cusps.
gingivally with an increase in its buccolingual diameter. The compression failure of
an object occurs at its most vulnerable site,
and teeth are most susceptible to failure
in the gingival area. If the alveolar bone
recedes, the failure site will also be lowered. Fig. 12 and 13 demonstrate defects
that appear in tandem as the supporting
bone atrophies, changing the fulcrum
point. The only occlusal contact in Fig.
13 occurs on the incline plane, forcing the
premolar to flex toward the lingual when
the patient clenches. In orthopedics, these
sites of destructive stress are termed vertical compression or wedge fractures.23
General Dentistry
www.agd.org
The inverted cupola
The inverted cupola is the most common
compression NCL. Inverted cupolas are
perfectly rounded depressions (sometimes
referred to as occlusal dimples) that are found
at the tips of functional cusps (Fig. 14).
Nothing of significance has been written
about occlusal dimples except that they are
associated with compression. Although the
inverted cupola contrasts dramatically in
geometric design with the wedge-shaped
NCL, there are two striking similarities
between them: both are site-specific (in
that they are found at sites of high stress on
teeth) and both exhibit a glassy sheen.24
As early as 1932, Kornfeld observed this
glassy sheen—hard, smooth, and glasslike
in appearance—on both wedge-shaped
NCLs and inverted cupolas.25 The author
suggests that this glassy sheen is due to the
exit of positive ions produced by the compression of apatite crystals in the dentition
vand the alveolar bone, which is a result of
the piezoelectric effect.25 The piezoelectric
effect occurs when a mechanical stress is
applied to a substance (such as dentin)
that squeezes or stretches the substance,
producing an electric charge. Conversely,
a mechanical deformation is produced
when an electric field is applied. Electricity
consists of both negative and positive ions
and it is possible that positive ions are
being emitted through these focal points
of high stress, carrying minute particles
of tooth structure. This emission would
explain not only the glassy sheen, but the
loss of tooth structure as well. It is not
unusual to find these glassy concavities on
the first molars only. These molars appear
first during the transition from primary
to secondary dentition and receive the full
force of bruxism that is common during
this transitional period. Compression
forces on the six-year molars are reduced as
the remaining dentition emerges.
It should be noted that the stress that
results from the various loading forces
(such as compression, tension, flexion, and
shearing) leads to tooth degradation and
its effects on bone and materials.
Deformation of bone
Articles on bony protrusions (that is,
torus palatinus and torus mandibularis)
appeared in the literature as early as 1814
(Fig. 15-18).26 Although there is no consensus as to the etiology of bony protrusions,
Fig. 15. Piezoelectric induced exostosis
in the left mandibular quadrant.
Fig. 16. Exostosis in center and lateral
aspects of palate.
Fig. 17. Massive exostosis in the palate
due to compression.
Fig. 18. Multiple bony exostosis
on buccal alveolar bone due to
compression.
Fig. 19. Luder (stress) lines in an old
amalgam.
Fig. 20. Luder lines in an occlusal alloy
on tooth No. 30.
Fig. 21. Luder-like stress lines
demonstrated in the occlusal surface
of a partial denture. (Photo courtesy of
Dr. Gregori Kurtzman.)
Fig. 22. Luder-like lines on the buccal
of a removable partial denture. (Photo
courtesy of Dr. Gregori Kurtzman.)
many associate their occurrence with
TMDs and masticatory hyperfunction.27,28
The negative ions generated from the compression of apatite crystals are responsible
for the aggregates of new bone growth.
Deformations of restorative
materials
Fatigue manifests easily in prostheses and
restorative materials such as amalgam and
acrylic. The wavy patterns (referred to
by engineers as Luder lines or molecular
slipbands) result from molecules in the
alloy rearranging themselves following
compressive strain. Fig. 19-22 demonstrate
Luder lines in restorative materials. The
deformations in the oral environment
are important diagnostic tools, but their
appearance does not mean that the patient
is currently affected with DCS, as it may
have occurred during a prior stressful
period in his or her life.29
Guidelines
There are two objectives when restoring a
segment of a patient’s dentition: to design
the new restoration correctly from an
engineering point of view, and to ensure
that the new restoration is in harmony
with a healthy stomatognathic system. To
that end, the new restoration should be
designed to satisfy good engineering principles, with the occlusal contact at the tip
of the functional cusp and touchless incline
planes. As noted earlier, the stomatognathic
system should be evaluated for signs of
DCS and the remaining dentition should
be evaluated to determine whether an
equilibration might be indicated.
Management of DCS begins by recognizing the deformations of the dentition,
bone, and restorative materials in the oral
environment. In the author’s experience,
many patients with 0° occlusion have
claimed to be quite comfortable because
the damage had occurred in the past; to
equilibrate their teeth would be disastrous. If the patient’s occlusion is uncomfortable, it should be determined whether
equilibration is indicated.
In the author’s opinion, it is not necessary to use complicated instrumentation
to accomplish equilibration. Instead,
simply apply occlusal indicator wax on
www.agd.org
the occlusal surfaces of one arch, ask the
patient to squeeze once, and analyze the
areas of displaced wax. Ideal contacts
are small and confined to the tips of the
cusps and the central fossae. If the incline
planes are touching, they should be
reduced. If there is heavy contact in the
central fossae, the opposing functional
cusps should be sharpened. Lateral excursions should be checked for interferences.
The teeth are never shortened. The equilibration reduces the stress on the teeth and
allows greater freedom for the mandible;
however, it doesn’t mean the patient won’t
clench in moments of stress.
There is an exception to the rule that
the original morphology of our teeth is
superior to that of a flattened dentition.
This isn’t meant to imply that all flat
teeth should be equilibrated (sharpened).
However, there should be a general understanding that preserving the original morphology of the dentition is superior to and
more efficient than a flattened dentition.
The stomatognathic system best serves
the patient when it functions vertically
and is free from clenching and grinding.
General Dentistry
January/February 2013
73
Guest Editorial Occlusion confusion
If clenching occurs during waking hours,
patients must monitor themselves and
make a conscious effort to keep their teeth
apart (that is, keep the mandible at rest).
If clenching and/or grinding occur while
sleeping, the dentist must provide a comfortable guard.
The main reason for what the author
refers to as occlusion confusion is that
dentists have been accommodating the
horizontal component of DCS instead
of trying to prevent it. According to the
Journal of Prosthetic Dentistry, anterior
guidance (also known as mutually protected occlusion or mutually protected
articulation) is defined as an occlusal
scheme in which the posterior teeth
prevent excessive contact of the anterior
teeth in maximum intercuspation, and
the anterior teeth disengage the posterior
teeth in all mandibular excursions.10 The
general understanding of anterior guidance is that there is some sort of mutual
protection at work, although nothing
could be further from the truth.
Is it possible that clenching the posterior teeth can prevent excessive contact
on the anterior teeth? Not necessarily. A
posterior tooth will be subject to more
stress upon clenching than an anterior
tooth simply because there is more surface
contact upon closure; that is, stress is a
result of lb/contact unit2 (stress = force/
area). However, if the occlusal contact
upon closure is equal for both molars and
the lingual of the maxillary anterior teeth,
the stress will be equal as well.
The author is aware of exceptions to the
rule, but generally people do not grind
their teeth during waking hours; rather,
they clench. Since grinding in protrusion
occurs only while sleeping, a comfortable
nightguard would be appropriate. The
idea of mutual protection is flawed in that
it does not address the damage that the
anterior teeth incur during parafunction.
If this concept were credible, there would
be little use for guards.
If patients are actively compressing their
teeth while sleeping, then a guard is mandatory. It is normal for many patients to
grind and clench while sleeping. The guard
is not intended to stop such activities, but
rather to provide an acrylic spacer that will
absorb the compressive forces. The author’s
preference is for the smaller anterior
hard guards as they significantly reduce
74
January/February 2013
compression force. However, others recommend the larger guard that also covers the
molars. They point out that the purpose
of the larger guard is to support the TMJ,
while this author believes that such guards
only add more stress to the TMJ. Soft
guards may encourage clenching and
guards should only be worn while sleeping.
Excessive use of a guard during waking hours
can cause micromovement of the teeth.
Rehabilitation and reconstruction
A small percentage of dentists (estimated
by the author to be less than 1%) limit
their practices to patients who are severely
compromised with problems related to
occlusion. The mastication muscles are the
benchmark for the neuromuscular concept
of rehabilitation. The goal of neuromuscular rehabilitation is to establish a physiologic terminal contact position (that is,
the myocentric bite), using transcutaneous
electric nerve stimulation (TENS). The
incline planes of the teeth are then refined
to ensure physiologic mandibular function. The masticatory system is stabilized
by using a removable anatomical orthotic
appliance that incorporates canine rise.
The gnathological approach is based
on the position of the condyles in the
glenoid fossae. During the reconstruction/rehabilitation of the stomatognathic
system, the gnathologist seeks an optimum orthopedically stable joint position
called centric relation, which refers to the
condyles when they are in the anteriorsuperior position in the glenoid fossae,
resting against the posterior slopes of the
articular eminences, with the articular
discs properly interposed. This position
is considered to be the mandible’s most
stable musculoskeletal position. Another
goal of the gnathologist is stable holding contacts on all teeth to support the
condyles in this centric relation, a position
known as centric occlusion. The ultimate
objective gnathological approach is to
establish long-term occlusal stability: the
ability for the dentition to accept heavy
forces with minimal damage and function
efficiently at the same time.5
There are so many conflicting ideas,
theories, and practical concepts related to
the subject of restorations that a majority of dentists are unsure as to the right
approach. One unfortunate effect of this
confusion is that there is no consensus
General Dentistry
www.agd.org
as to the best design for teeth. It is
important that teeth retain their original
morphology so they can work harmoniously and not distract the mandible
from normal function.30 Regrettably,
the role of the dentition in the function
and dysfunction of the system has been
obfuscated to the point that many believe
there is no relationship at all. In 1995,
Ramfjord & Ash reported that “a trend
of thinking has developed that virtually
denies any relationship between occlusal
factors and disorders of the masticatory
system.”31 Unfortunately, this attitude
remains prevalent today.
An important step that could clarify
some of the confusion would be to stop
using the word occlusion in such a broad
sense. Being more specific will simplify
the thought or question. A 2008 article
by Turp et al suggests that ideal occlusion
is rarely found in real life, that the idea is
open to personal interpretation, and that
it is presumptuous to state nature’s intention for idealism.32 The author completely
disagrees. We don’t need a clairvoyant to
define ideal occlusion; we merely need
a bioengineer with some knowledge of
physiology. We also need to be specific
about what is meant by the question.
If we are concerned about the stomatognathic system, an ideal system—be it
Class I, II, or III—would be one free
from parafunction. The teeth in this
system, be they crooked or straight, are
naturally sharp, fit loosely with their
antagonists, and confine occlusal contact
to the tip of the cusp upon closure.
It is recognized that problems involving
the TMJ can be the result of trauma, developmental deformities, or a disease process;
however, in the author’s opinion, the vast
majority of TMJ problems are the result of
repetitive motion trauma from DCS. In the
author’s 40-plus years of clinical practice,
there has yet to be a single case of TMD
that did not demonstrate one or more signs
of parafunction. It would be appropriate
to determine how parafunction relates to
TMDs and determine whether the occlusal
contacts are a contributing factor.
Summary
The confusion regarding the subject of
occlusion has been a major distraction
from dentistry’s focus on the far more
important issue of parafunction. This
problem is unique in that it is part engineering and part psychological. For optimal results, dentists need to perform these
three steps:
1. Design new restorations to satisfy
accepted engineering principles (such
as occlusal contact at the tip of the
functional cusp and touch-free incline
planes).
2. Evaluate the stomatognathic system
itself for signs of DCS. If the patient
has any parafunctional habits, the
dentist must work with the patient to
manage them properly.
3. Evaluate the remaining dentition to
determine whether an equilibration is
indicated.
Every five years, the Japanese sponsor
an international consensus meeting on
implantology. Respected authorities are
invited to express their views on important issues, and a panel of judges determines a consensus for each issue for that
point in time. Isn’t it about time we had
one on occlusion? In the meantime, the
author suggests that dentists keep teeth
sharp and keep them apart.
Author information
Dr. McCoy is in private practice limited
to the treatment of DCS in San Francisco,
California. He teaches occlusion at the
Peking University School of Stomatology
in Beijing, China, and is a visiting lecturer
at Tsurumi University in Yokohama,
Japan, and Jordan University of Science
and Technology in Irbid, Jordan.
References
1. Dorland W, ed. Dorland’s Pocket Medical Dictionary.
Philadelphia: W.B. Saunders;1898.
2.Dorland’s Pocket Medical Dictionary. 20th ed. Philadelphia: W.B. Saunders;1959.
3. Jankelson B, Hoffman GM, Hendron JA Jr. The physiology of the stomatognathic system. J Am Dent Assoc.
1952;46(4):375-386.
4.Rugh JD, Smith BR. A Textbook of Occlusion. Chicago:
Quintessence Publishing Co.;1988:143.
5. Jablonski S. Illustrated Dictionary of Dentistry. Philadelphia: W.B. Saunders; 1982.
6.Okeson JP. Management of Temporomandibular Disorders and Occlusion, 3rd ed. St. Louis: CV Mosby;1993:
51.
7.Okeson JP. Management of Temporomandibular Disorders and Occlusion, 3rd ed. St. Louis: CV Mosby;1993:
125.
8.Ortman HR. Complete denture occlusion. In: Winkler S,
ed. Essentials of Complete Denture. 2nd ed. St. Louis:
Mosby-Year Book; 1988.
9. McCoy G. The truth about occlusion. Paper presented
at: 2007 Yankee Dental Congress; San Francisco.
10. Glossary of Prosthodontic Terms, 8th ed. J Prosthet
Dent. 2005;94(1):54.
11. Kydd WL. Complete denture base deformation with
varied occlusal tooth form. J Prosthet Dent. 1956;6:
714-718.
12.Regli CP, Kydd WL. A preliminary study of the lateral
deformation of metal base dentures in relation to
plastic base dentures. J Prosthet Dent. 1953;3:326330.
13.Swoope CC, Kydd WL. The effect of cusp form and
occlusal surface area on denture base deformations.
J Prosthet Dent. 1966;16:34-43.
14. Neiburger EJ. Flat-plane occlusion in the development
of man. J Prosthet Dent. 1977;38(4):459-469.
15. McCollum BB, Stuart CE. A Research Report. Ventura,
CA: Scientific Press; 1955.
16. Dzakovich JJ, Oslak RR. In vitro reproduction of noncarious cervical lesions. J Prosthet Dent. 2008;100(1):
1-10.
17. Ferrier WI. Clinical observations on erosions and their
restorations. J Calif State Dent Assoc. 1931;7:187196.
www.agd.org
18 McCoy G. The etiology of gingival erosion. J Oral Implantol. 1982;10(3):361-362.
19.Gordon JE. Structures: or Why Things Don’t Fall Down.
New York: Da Capo Press; 1978:333-334.
20.Selna LG, Shillingburg HT Jr, Kerr PA. Finite element
analysis of dental structures—axisymmetric and plane
stress idealizations. J Biomed Mater Res. 1975;9(2):
237-252.
21.Yettram AL, Wright KW, Pickard HM. Finite element
stress analysis of the crowns of normal and restored
teeth. J Dent Res. 1976;55(6):1004-1011.
22. Hood JA. Experimental studies on tooth deformation:
stress distribution in class V restorations. N Z Dent J.
1972;68(312):116-131.
23.Old JL, Calvert M. Vertebral compression fractures in
the elderly. Am Fam Physician. 2004;69(1):111-116.
24. McCoy G. Examining the role of occlusion in the function and dysfunction of the human masticatory system. Nippon Dental Rev. 1997;659:163-183.
25. Kornfeld B. Preliminary report of clinical observation of
cervical erosions. Dental Items Interest. 1932;54:905909.
26. McCoy G. Dental compression syndrome and TMD:
examining the relationship. Dent Today. 2007;26(7):
118-123.
27.Seah YH. Torus palatinus and torus mandibularis: a
review of the literature. Aust Dent J. 1995;40(5):318321.
28. Pynn BR, Kurys-Kos NS, Walker DA, Mayhall JT. Tori
mandibularis: a case report and review of the literature. J Can Dent Assoc. 1995;61(12):1057-1066.
29.Sirirungrojying S, Kerdpon D. Relationship between
oral tori and temporomandibular disorders. Int Dent J.
1999;49(2):101-104.
30. McCoy G. Dental compression syndrome: a new look
at an old disease. J Oral Implantol. 1999;25(1):35-49.
31.Ramfjord S, Ash MM. Occlusion. 4th ed. Philadelphia:
W.B. Saunders Co.;1995:114.
32.Turp JC, Greene CS, Strub JR. Dental occlusion: a critical reflection on past, present and future concepts.
J Oral Rehabil. 2008;35(6):446-453.
General Dentistry
January/February 2013
75
Exercise No. 324 TM
Disorders (Occlusion) Subject Code 182
The 15 questions for this exercise are based on the article,
Occlusion Confusion, on pages 69-75. This exercise
was developed by Thomas C. Johnson, DMD, MAGD,
in association with the General Dentistry Self-Instruction
Committee.
1. Which of the following statements is true
regarding occlusion?
A. Most practitioners are aware of the
basic concepts of occlusion.
B. Most dental patients receive dental
therapy based on occlusal principles.
C.Occlusal principles permeate almost all
of dentistry.
D.Commonly taught occlusal techniques
are practical in daily practice.
2. A valid definition of occlusion is a
description of all the components of the
stomatognathic system. The preferred
definition of occlusion is the contact
of the teeth of both jaws during those
excursive movements of the mandible
essential to the function of mastication.
A. Both statements are true.
B.The first statement is true;
the second is false.
C.The first statement is false;
the second is true.
D. Both statements are false.
3. Which is true regarding the vertical
function paradigm?
A.There is 5-6 mm lateral parafunction
(bruxing).
B.On closure, the mandible is guided by
the glenoid fossae.
C.The condyles seat in the anteriorsuperior portion of the fossae.
D.The chewing movement is consistent
and reproducible.
4. Which is true according to the horizontal
function paradigm?
A.It seeks to accommodate free passage
for opposing dentition.
B.Laterotrusive contacts are prevented,
not eliminated.
C.Lateral excursions are parafunctional
movements.
D.Anterior guidance involves shortening
the anterior teeth.
Reading the article and successfully completing this exercise will enable you to:
•discuss the 3 factors contributing to occlusion confusion;
•learn the signs of parafunction/dysfunction; and
•understand the management of parafunction and an ideal occlusal scheme.
5. According to gnathology, proper occlusal
form is dictated by anterior guidance.
Functional occlusion is defined as the
touching of upper and lower teeth during
mastication and deglutition.
A. Both statements are true.
B.The first statement is true;
the second is false.
C.The first statement is false;
the second is true.
D. Both statements are false.
6. Which type of denture morphology has
been shown to transfer higher vertical
stimulation to the alveolar ridge?
A. 20° occlusion
B.Upper 10° occlusion
C. 33° occlusion
D. 0° (flat plane) occlusion
7. The signs of DCS include all of the
following except one. Which is the
exception?
A. Deformation of restorative materials
B.Atrophy of the alveolar bone
supporting teeth
C. Hypertrophy of the muscles of
mastication
D. Flattening of the dentition
10. Which is the most common compression
NCL?
A.Luders’ lines
B.Wedge-shaped gingival lesion
C.Cracked fillings
D.Inverted cupola
11.The inverted cupola is most commonly
found on permanent second molars. This
is due to the higher incidence of occlusal
prematurities on these teeth.
A. Both statements are true.
B.The first statement is true;
the second is false.
C.The first statement is false;
the second is true.
D. Both statements are false.
12. When planning an occlusal equilibration,
the author’s initial analysis involves use of
A. mounted models and trial equilibration.
B. occlusal indicator wax.
C. multiple colors of Mylar articulating strips.
D. Mylar articulating strips and 8-µm
shim stock.
13. The author’s approach to the treatment of
parafunction advocates which of the following?
A.LVI neuromuscular
B. Pankey centric relation equals centric
occlusion scheme
C.Okeson orthopedically stable joint
position
D. Prevention of DCS
8. The characteristics of the wedge-shaped
noncarious lesions (NCLs) include all of
the following except one. Which is the
exception?
A. Position will change as bone support
is lost
B.Site-specific with a dull matte
appearance
C. Variously shaped and located
depending on the vectors of forces
D.Explained by biomechanical stress studies
14. The vast majority of temporomandibular
joint dysfunction problems are a result of
A. repetitive motion trauma from DCS.
B. arthritic disease processes.
C. developmental deformities.
D.trauma.
9. Evidence supporting parafunction as a
cause of wedge-shaped NCLs include
all of the following except one. Which is
the exception?
A. Photodensitometry studies
B.Stress analysis
C. Piezoelectric effect
D.Compression fatigue
15. Teeth in an ideal occlusion have all of
the following characteristics except one.
Which is the exception?
A. Mutually protected scheme
B. Fit loosely with their antagonists
C.Are naturally sharp
D.Occlusal contact confined to the tip
of the cusp
Answer form is on page 80. Answers for this exercise must be received by December 31, 2013.
76
January/February 2013
General Dentistry
www.agd.org
Oral Diagnosis
Nikolaos G. Nikitakis, MD, DDS, PhD n John K. Brooks, DDS
Asymptomatic swelling in the floor of the mouth
A 63-year-old male was referred to a specialized
oral medicine clinic for assessment of an asymptomatic swelling in the floor of the mouth. The
swelling was noticed for at least 6 months and
had progressively enlarged; no other symptoms
were reported. The patient reported a history
of hypertension (controlled by atenolol) and
was a nonsmoker. Clinical examination showed
a dome-shaped swelling that was firm to
palpation, approximately 2 cm in maximum
dimension, covered by normal mucosa of bluish
color in the right floor of the mouth (Fig. 1).
Imaging studies, including ultrasonography and
computed tomography, confirmed the presence
of a hypodense lesion, 1.9 cm in diameter,
without involvement of the submandibular
gland or its duct, and without evidence of a
salivary stone (Fig. 2). The lesion was surgically
removed and submitted for histopathological
examination (Fig. 3).
Fig. 1. Dome-shaped swelling of bluish color in the
right floor of the mouth.
Fig. 2. CT scan showing a hypodense
lesion (arrows) in the right floor of the
mouth.
Which of the following is the most probable
diagnosis?
A.Sialolithiasis
B.Salivary duct cyst (ranula)
C.Cystadenoma
D.Chronic sialadenitis
E.Lipoma
Diagnosis is on page 78.
Fig. 3. Photomicrograph showing a cystic space
lined by thin epithelium and surrounded by a fibrous
wall with salivary gland elements in the periphery
(H & E stain, magnification 40X).
Asymptomatic nodule in the posterior tongue
A 42-year-old female visited a
specialized oral medicine clinic for
evaluation of an asymptomatic
swelling in the right tongue of
unknown duration. The patient
was a smoker (approximately
1 pack per day); her medical history was noncontributory. Clinical
examination revealed a nodule
of soft consistency covered by
intact pinkish-yellowish mucosa
with distinct surface capillaries in
the right posterior lateral border
of the tongue (Fig. 1). The rest
of the oral mucosa was within
normal limits. An excisional biopsy
was performed and histopathological examination showed dense
lymphoid tissue with germinal
center formation surrounding an
epithelial-lined cavity (Fig. 2).
Which of the following is the
most likely diagnosis?
A.Reactive lymphadenitis
B.Lipoma
C.Oral lymphoepithelial cyst
D.Lymphoepithelial carcinoma
E. Branchial cleft cyst
Fig. 1. Nodule (arrows) covered by
intact pinkish-yellowish mucosa with
distinct surface capillaries in the right
posterior lateral border of the tongue.
Fig. 2. Photomicrograph showing a
cleft-like cavity lined by epithelium
and surrounded by dense lymphoid
tissue with germinal center formation
(H & E stain, magnification 200X).
Diagnosis is on page 78.
Author information: Dr. Nikitakis is an assistant professor, Department of Oral Pathology and Oral Medicine, School of Dentistry of the National
and Kapodistrian University of Athens, Greece. Dr. Brooks is a clinical professor, Department of Oncology and Diagnostic Sciences, Dental School of the
University of Maryland, Baltimore.
www.agd.org
General Dentistry
January/February 2013
77
Answers
Oral Diagnosis
Asymptomatic swelling in the floor of the mouth
Diagnosis:
B. Salivary duct cyst (ranula)
Unlike mucoceles, which are caused by mucin extravasation,
salivary duct cysts represent true cysts arising in minor or major
salivary glands, most commonly within the parotid. When a
salivary duct cyst occurs in the floor of the mouth, it is frequently
called a ranula, although some authors prefer to reserve the use
of this term only for lesions caused by mucin spillage, usually
derived from the body of the adjacent sublingual gland, the submandibular duct, or from minor salivary glands situated in the
floor of the mouth.
Salivary duct cysts develop in adults and are usually asymptomatic. The floor of the mouth is a common location for the
development of salivary duct cysts, which appear clinically similar
to ranulas attributed to spillage of mucin, i.e., dome-shaped
nodular swellings of soft, fluctuant, or, less often, firm consistency
and bluish or pinkish color. If they acquire a large size, they may
cause elevation of the tongue. The plunging ranula is a subtype
and manifests as a soft swelling in the neck owing to extension of
the spilled mucin below the mylohyoid muscle.
Histopathological examination of a salivary duct cyst shows a
dilated cystic space lined by thin squamous, cuboidal, or columnar epithelium, and surrounded by a fibrous wall. In contrast,
ranulas typically lack an epithelial lining and present as an accumulation of mucin surrounded by a granulation tissue wall.
Imaging studies may provide useful information regarding
the exact size and location of a ranula, its association with the
adjacent major salivary glands, and the potential presence of a
sialolith or a mass obstructing a salivary duct. This information
is useful during the surgical intervention, which, based on the
clinical, imaging, and intraoperative findings, may entail marsupialization, dissection, and removal of the lesion alone and/or
removal of the offending major salivary gland. The likelihood of
recurrence varies according to the surgical procedure and appears
higher for lesions managed by marsupialization.
Bibliography
1.Takeda Y, Yamamoto H. Salivary duct cyst: its frequency in a certain Japanese population group (Tohoku districts), with special reference to adenomatous proliferation of
the epithelial lining. J Oral Sci. 2001;43(1):9-13.
2. Zhao YF, Jia Y, Chen XM, Zhang WF. Clinical review of 580 ranulas. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2004;98(3):281-287.
3.Salivary gland pathology. In: Neville BW, Damm DD, Allen CW, Bouquot JE. Oral and
Maxillofacial Pathology. 3rd ed. St. Louis: Saunders/Elsevier; 2009:456-459.
78
January/February 2013
General Dentistry
Asymptomatic nodule in the posterior tongue
Diagnosis:
C. Oral lymphoepithelial cyst
The oral lymphoepithelial cyst is an uncommon developmental
soft tissue cyst of the oral mucosa. It can affect patients of any age,
more often young adults, and does not show gender predilection.
As implied by its name, the oral lymphoepithelial cyst is composed of an epithelium-lined cystic cavity surrounded by abundant
lymphoid tissue. It develops in areas harboring oral lymphoid
tissue, such as the floor of the mouth (accounting for about half of
the cases), ventral surface and posterolateral border of the tongue
(up to 40% of cases), and around the Waldeyer ring. Various theories of pathogenesis have been proposed, such as the entrapment of
epithelial elements within oral lymphoid tissue aggregates during
embryogenesis or the obstruction of normal epithelial invaginations into the underlying oral lymphoid tissue. Subsequent epithelial proliferation results in the formation of a cystic mass.
The branchial cleft cyst can be considered to be the counterpart
of the oral lymphoepithelial cyst in a lateral cervical location. In
addition, lymphoepithelial cysts of the parotid glands have been
seen with increased frequency among HIV-positive patients.
The oral lymphoepithelial cyst usually presents as a <1cm submucosal nodule of soft or rubbery consistency covered by intact
mucosa of whitish, yellowish, or pinkish color. It is asymptomatic unless secondarily traumatized. Microscopic examination
reveals a cystic cavity, sometimes filled with keratin, lined by
stratified squamous epithelium that is often parakeratinized.
The cyst wall is occupied by dense lymphoid tissue with frequent
germinal center formations.
Conservative surgical removal is considered to be the treatment
of choice and recurrences are not expected.
Bibliography
1. Developmental defects of the oral and maxillofacial region. In: Neville BW, Damm DD,
Allen CW, Bouquot JE. Oral and Maxillofacial Pathology. 3rd ed. St. Louis: Saunders/
Elsevier; 2009:36-38.
2.Regezi JA, Sciubba JJ, Jordan RCK. Oral Pathology: Clinical Pathologic Correlations. 5th
ed. St. Louis: Saunders; 2008:219.
3.Yang X, Ow A, Zhang CP, et al. Clinical analysis of 120 cases of intraoral lymphoepithelial cyst. Oral Surg Oral Med Oral Pathol Oral Radiol. 2012;113(4):448-452.v
www.agd.org
Self-Instruction
Exercise No. 297
Exercise No. 298
January/February 2012, p. 25
1. B
5. C
9. B
13. A
2. C
6. D
10. C
14. B
3. A
7. A
11. B
15. D
January/February 2012, p. 44
4. D
8. B
12. B
1. A
5. A
9. B
13. A
Message to
Subscribers
2. B
6. B
10. D
14. C
3. C
7. D
11. A
15. D
4. B
8. A
12. C
Exercise No. 299
January/February 2012, p. 56
1. B
5. D
9. C
13. B
2. C
6. C
10. A
14. B
3. A
7. A
11. A
15. D
4. B
8. B
12. B
Name
Periodically, we allow carefully selected
organizations to send promotional
literature to our members.
AGD/ID#
Address
If you prefer not to receive such
information, please let us know by
returning this coupon to:
CityState/Province
Academy of General Dentistry
Membership Services
211 E. Chicago Ave., Ste. 900
Chicago, IL 60611-1999
ZIP/Postal Code
Telephone
DateJF13
Advertisers Index
If you would like more information about the companies who advertised
in this issue of General Dentistry, please contact:
Page Company
Page Company
Cover 2
Blue Sky Bio
www.blueskybio.com
Cover 3
Glidewell Laboratories
800.521.0126
www.glidewelldental.com
Cover 4
Hands On Training
Institute
7
Ivoclar Vivadent
800.533.6825
www.ivoclarvivadent.com
5Sunstar
800.528.8537
www.sunstar.com
888.806.4442
www.handsontraining.com
We try to present an accurate index. Occasionally, this is not possible because
of a last-minute change.
www.agd.org
General Dentistry
January/February 2013
79
Answer Sheet
AGD/ADA ID: ___________________________________________________________
First name: ___________________________________________ Middle initial: _______ Last name: _________________________________________________________
Address 1: _______________________________________________________________________________________________________________________________
Address 2: _______________________________________________________________________________________________________________________________
City: _______________________________________________________ State/Province: ______________________ ZIP/Postal code: ______________________________
Payment  Currently enrolled in Self-Instruction  Enrolling today
I am paying by:  Check (Payable to AGD)  Credit Card (Complete payment information)
Select the number of exercises you wish
to purchase:
Credit Card Number: ___________________________________________________ Expiration Date: _______________
Signature: ______________________________________________________________________________________
ANSWERS Select the best answer by completely filling in one box for each response.
Correct Incorrect A Incorrect A
A
Exercise No.
321
Exercise No.
Exercise No.
322
AGD Member
Non-member
1 Exercise.................  $30.................  $50
2 Exercises...............  $50.................  $75
3 Exercises...............  $60.................  $90
6 Exercises...............  $100...............  $150
Best Value!
12 Exercises.............  $150...............  $225
Exercise No.
323
Each exercise is worth 2 CE credits.
324
A B C D
A B C D
A B C D
11
11
A B C D
A B C D
A B C D
22
22
A B C D
A B C D
A B C D
33
33
A B C D
A B C D
A B C D
44
44
A B C D
A B C D
A B C D
55
55
A B C D
A B C D
A B C D
66
66
A B C D
A B C D
A B C D
77
77
A B C D
A B C D
A B C D
88
88
A B C D
A B C D
A B C D
99
99
A B C D
A B C D
A B C D
1010
1010
A B C D
A B C D
A B C D
1111
1111
A B C D
A B C D
A B C D
1212
1212
A B C D
A B C D
A B C D
1313
1313
A B C D
A B C D
A B C D
1414
1414
A B C D
A B C D
A B C D
1515
1515
A B C D
This form can be submitted via mail or fax.
A B C D
A B C D
A B C D
A B C D
A B C D
A B C D
A B C D
A B C D
Self-Instruction312.440.4261
Academy of General Dentistry
211 E. Chicago Ave., Suite 900
Chicago, IL 60611-1999
Answers can also be submitted online.
www.agd.org
A B C D
A B C D
A B C D
A B C D
A B C D
For more information, contact Cassandra
Bannon at 888.AGD.DENT (888.243.3368),
ext. 4353, or at [email protected]
Please allow 2 weeks for credit to be awarded.
A B C D
Evaluation Please respond to the statements below, using the following scale: 1 Poor; 2 Below average; 3 Average; 4 Above average; 5 Excellent
Exercise No.
Exercise No.
321
Practicality of the content.................................................................
Benefit to your clinical practice........................................................
Quality of illustrations........................................................................
Clarity of objectives.............................................................................
Clarity of exercise questions.............................................................
Relevance of exercise questions.......................................................
Did this exercise achieve its objectives?......................................... Did this article present new information?..................................... How much time did it take you to complete this exercise?........ Exercise No.
322
Exercise No.
323
324
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
1
2
3
4
5
YesNo
YesNo
_________ mins
YesNo
YesNo
__________ mins
Yes No
Yes No
_________ mins
Deadline for submission of answers to Exercises 321-324 is December 31, 2013.
YesNo
YesNo
_________ mins
Prevention/Diet/Nutrition
Five-minute nutrition workup for children
in dental practice
S.M. Hashim Nainar, BDS, MDSc
Overweight and obesity are significant health concerns for children in the
United States; however, dentists can provide a nutrition workup for their
patients as part of the effort to address this issue. A child’s weight status
can be assessed after measuring the child’s height and weight without
the need to compute body mass index. At that point, 5 nutrition- and
health-related items can be discussed with patients and parents. Both
I
n a 2011 article, Lamster & Eaves
proposed a dental practice model for
the 21st century that would reconceptualize and expand the scope of practice
to include primary health care activities,
such as screening for diabetes mellitus and
obesity interventions.1 According to the
literature, chairside testing of blood glucose to determine the presence of diabetes
mellitus has been well-received both by
patients and by practitioners; in addition,
weight screening strategies for children
and adults in the dental office also have
been described in the literature.2-4
Screening children for overweight/
obesity presents unique challenges
compared to screening adults. As with
adults, the body mass index (BMI) must
be computed; however, age and genderspecific BMI percentile data also must be
consulted to determine a child’s weight
status.3,4 These additional steps may
explain why only 52% of U.S. pediatricians and 45% of family physicians bother
to routinely assess BMI in children.5,6
The importance of screening children
for overweight/obesity is underscored
by data from the National Health and
Nutrition Examination Survey (NHANES)
2009-2010, which reported that 33% of
U.S. school-age children (aged 6-19 years)
are overweight; of those, 18% are reported
to be obese.7 Increased body weight in
children leads to such comorbidities as
type 2 diabetes mellitus, nonalcoholic fatty
liver disease, and cardiovascular disease.8
According to Singh et al, overweight/
obese children also are more likely to
become overweight adults.9 Of the lifelong implications of unhealthy weight in
childhood, Olshansky et al reports, “the
e2
January/February 2013
can be accomplished in just a few minutes. Evidence-based nutrition
guidance can be integrated into contemporary nutrition counseling for
caries prevention in a seamless manner without negative connotations
regarding a patient’s weight.
Received: March 14, 2012
Accepted: May 7, 2012
youth of today may, on average, live less
healthy and possibly even shorter lives
than their parents.”10 This proposition
provides an even greater motivation for
dentists to incorporate obesity counseling
into practice as part of their “desire to have
an impact on patients’ general health.”11
According to a 2010 survey by Curran
et al, dentists “are in an ideal position to
recognize patients at risk of developing
weight problems” as they already offer
nutrition counseling to children to prevent
dental caries.12 A 2009 article by Tavares
& Chomitz described an intervention
program for dental practices designed to
help children maintain a healthy weight.3
The protocol for their pilot study was
based upon motivational interviewing
and was directed toward all 139 of the
children involved, regardless of their
weight status. The intervention included
measuring the child’s height and weight,
assessing BMI, and providing “recommendations for healthy behavior modifications.”3 Dental hygienists who provided
the intervention were able to complete all
of their duties for each preventive dental
visit (including the intervention) within
an average of 40 minutes. Caregivers
responded positively to the intervention
with 96% making better food choices
for their children, 81% reporting less
television/video time, 72% reporting
more exercise, and 67% reporting that
their child ate breakfast more often.3
According to a recent survey of U.S.
dentists and their attitudes toward obesity
prevention/intervention, more than 50%
of the respondents expressed concern
about appearing judgmental or offending
patients and their parents.12 The survey
General Dentistry
www.agd.org
also found that 51% of the respondents
were interested in offering obesity-related
services, although some reported a lack
of knowledge regarding the topic.12
The current authors sought to provide
a pragmatic and concise evidence-based
nutrition workup—based in part on the
recommendation of Tavares’ & Chomitz’s
recommended behavioral strategies
for healthy weight in children—that
could be utilized in the dental office.3
Assessment of weight status
in children
After the child’s height and weight have
been measured, his or her weight status
can be assessed using recently published
gender-specific screening tables based
on growth charts from the Centers for
Disease Control and Prevention.13 These
simplified overweight/obesity screening
tables eliminate the need to compute
individual BMI or determine BMI percentiles and simply indicate whether the
child has normal weight or is overweight/
obese.13 Based on the assessment, parents
and patients can then be informed as to
whether the child has healthy weight.
Counseling children for
healthy weight
In addition to nutrition counseling for the
prevention of dental caries, the following
five counseling items can be provided to all
children, regardless of their weight status.14
Do not skip breakfast
Data from NHANES (1999-2006)
has shown that 20% of children ages
9-13 and 32% of those ages 14-18
skipped breakfast.15 Those who skipped
breakfast had higher BMI scores and
a greater prevalence of obesity.15
Limit/avoid sugar-sweetened
beverage consumption
A systematic four-decade literature
review (1966-2005) found an association between increased consumption of
sugar-sweetened beverages (particularly
soda) and weight gain and obesity
among children and adolescents.16
Be physically active for at
least 1 hour per day
Data from NHANES (2003-2004 and
2005-2006) concerning children ages 6-17
reported that “weight status was inversely
related to activity.”17 The American
Academy of Pediatrics advises that children
and adolescents “be physically active for at
least 60 minutes per day,” preferably participating in activity that is “unstructured and
fun” to ensure good compliance.18
Limit screen time to less than
2 hours per day
Data from NHANES (1988-1994) regarding 8- to 16-year-old children has shown
that obesity was lowest among those who
watched television for 1 hour or less per
day and was highest among those children
who watched television for 4 hours or
more per day.19 The American Academy of
Pediatrics recommends that children limit
screen time to less than 2 hours per day
with an “electronic media-free environment in children’s rooms.”20
Get adequate sleep
While the amount of sleep per day considered to be sufficient differs for each
child, data from the U.S. Panel Survey of
Income Dynamics Child Development
Supplements indicate 12-14 hours
for children ages 1-3, 11-13 hours for
children ages 3-5, 10-11 hours for children ages 5-10, and 8.5-9.5 hours for
adolescents.21 Insufficient sleep has been
associated with increased weight.21
These 5 counseling items can provide
positive guidance for children with
unhealthy weight while reinforcing good
habits in children with normal weight.
Conclusion
The nutrition workup described can be
integrated into contemporary dental
practice to promote healthy living. The
5 counseling items allow dentists to
address the issue of overweight/obesity
without concern for overtly targeting
the child’s weight. This perception is
important as Curran et al reported that
U.S. dentists have expressed concern that
causing offense or appearing judgmental
of the patient or the parent is the most
common barrier to providing obesityrelated interventions.12
Assessing weight status in children and
providing the select counseling described
in the present nutrition workup can
presumably be accomplished in a few
minutes. Tavares & Chomitz found that
as part of a regular preventive dental visit,
the healthy weight intervention detailed
in their 2009 article (including computation of individual BMI, determination of
BMI percentile score, and motivational
interviewing on select nutrition topics)
could be accomplished in less than 40
minutes.3 Therefore, it should be possible to integrate the nutrition workup
described in the present study into dental
checkups in a timely and efficient manner.
Author information
Dr. Nainar is an associate professor of
pediatric dentistry, University of Toronto,
Ontario, Canada.
References
1.Lamster IB, Eaves K. A model for dental practice in the
21st century. Am J Public Health. 2011;101(10):18251830.
2. Barasch A, Safford MM, Qvist V, Palmore R, Gesko D,
Gilbert GH; for The Dental Practice-Based Research
Network Collaborative Group. Random blood glucose
testing in dental practice: a community-based feasibility study from The Dental Practice-Based Research Network. J Am Dent Assoc. 2012;143(3):262-269.
3.Tavares M, Chomitz V. A healthy weight intervention
for children in a dental setting: a pilot study. J Am
Dent Assoc. 2009;140(3):313-316.
4. Hague AL, Touger-Decker R. Weighing in on weight
screening in the dental office: practical approaches.
J Am Dent Assoc. 2008;139(7):934-938.
5. Klein JD, Sesselberg TS, Johnson MS, et al. Adoption of
body mass index guidelines for screening and counseling in pediatric practice. Pediatrics. 2010; 125(2):265272.
www.agd.org
6.Sesselberg TS, Klein JD, O’Connor KG, Johnson MS.
Screening and counseling for childhood obesity: results from a national survey. J Am Board Fam Med.
2010;23(3):334-342.
7.Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence
of obesity and trends in body mass index among U.S.
children and adolescents, 1999-2010. JAMA. 2012;
307(5):483-490.
8.Orsi CM, Hale DE, Lynch JL. Pediatric obesity epidemiology. Curr Opin Endocrinol Diabetes Obes. 2011;
18(1):14-22.
9.Singh AS, Mulder C, Twisk JWR, van Mechelen W, Chinapaw MJ. Tracking of childhood overweight into
adulthood: a systematic review of the literature. Obes
Rev. 2008;9(5):474-488.
10.Olshansky SJ, Passaro DJ, Hershow RC, et al. A potential decline in life expectancy in the United States in
the 21st century. N Engl J Med. 2005; 352(11):11381145.
11.Glick M. A concern that cannot weight. J Am Dent Assoc. 2005; 136(5):572, 574.
12.Curran AE, Caplan DJ, Lee JY, et al. Dentists’ attitudes
about their role in addressing obesity in patients: a
national survey. J Am Dent Assoc. 2010;141(11):13071316.
13. Nainar SM. Identification of overweight in children in
the United States: a simplified approach. Obesity (Silver Spring). 2012;20(4):819-829.
14. Marshall TA. Chairside diet assessment of caries risk.
J Am Dent Assoc. 2009;140(6):670-674.
15. Deshmukh-Taskar PR, Nicklas TA, O’Neill CE, Keast
DR, Radcliffe JD, Cho S. The relationship of breakfast skipping and type of breakfast consumption
with nutrient intake and weight status in children
and adolescents: the National Health and Nutrition
Examination Survey 1999-2006. J Am Diet Assoc.
2010;110(6):869-878.
16. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review.
Am J Clin Nutr. 2006;84(2):274-288.
17.Chung AE, Skinner AC, Steiner MJ, Perrin EM. Physical
activity and BMI in a nationally representative sample
of children and adolescents. Clin Pediatr (Phila). 2012;
51(2):122-129.
18.Council on Sports Medicine and Fitness; Council on
School Health. Active healthy living: prevention of
childhood obesity through increased physical activity.
Pediatrics. 2006;117(5):1834-1842.
19.Crespo CJ, Smit E, Troiano RP, Bartlett SJ, Macera
CA, Andersen RE. Television watching, energy intake,
and obesity in U.S. children: results from the Third
National Health and Nutrition Examination Survey,
1988-1994. Arch Pediatr Adolesc Med. 2001;155(3):
360-365.
20.Strasburger VC; Council on Communications and Media, American Academy of Pediatrics. Media education.
Pediatrics. 2010;126(5):1012-1017.
21. Bell JF, Zimmerman FJ. Shortened nighttime sleep
duration in early life and subsequent childhood obesity.
Arch Pediatr Adolesc Med. 2010;164(9):840-845.
General Dentistry
January/February 2013
e3
Computer Designed/Fabricated Crowns
Influence of polishing procedures on
the surface roughness of dental ceramics
made by different techniques
Osmir Batista Oliveira-Junior, DDS, MSc, PhD n Leonardo Buso, DDS, MSc, PhD n Fabio Hiroshi Fujiy, DDS, MSc Geraldo Henrique Leao Lombardo, DDS, MSc n Fernanda Campos, DDS n Hugo Ramalho Sarmento, DDS Rodrigo Othavio Assuncao Souza, DDS, MSc, PhD
The aim of this study was to evaluate the influence of 2 different surface
polishing procedures—glazing (GZ) and manual polishing (MP)—on the
roughness of ceramics processed by computer-aided design/computeraided manufacturing (CAD/CAM) and conventional systems (stratification
technique). Eighty ceramic discs (diameter: 8 mm, thickness: 1 mm) were
prepared and divided among 8 groups (n = 10) according to the type
of ceramic disc and polishing method: 4 GZ and 4 MP. Specimens were
glazed according to each manufacturer’s recommendations. Two silicone
polishing points were used on the ceramic surface for manual polishing.
Roughness was measured using a surface roughness tester. The roughness
measurements were made along a distance of 2 mm on the sample surface and the speed of reading was 0.1 mm/s. Three measurements were
taken for each sample. The data (µm) were statistically analyzed using
T
he increased development of ceramic
materials and number of patients
searching for esthetic oral rehabilitation, combined with some of the
limitations of metallic restorations such as
toxicity, allergenic potential, and esthetics,
have made ceramics one of the most commonly employed materials in restorative
dentistry.1-4 Many in vitro and in vivo
studies have been performed to improve
porcelain restorations to satisfy the cosmetic, mechanical, and physical requirements of a restorative material.5
CAD/CAM systems have been used
in dentistry since their development by
Duret in the 1970s.6 Revolutionizing
dentistry, several ceramic systems were
developed based on computation science
to enhance laboratory steps and clinical
results of ceramic restorations. Using
prefabricated high-quality, homogenous
ceramic blocks, these CAD/CAM systems are different from the conventional
feldspathic ceramic powder, and they
result in a combination of biocompatibility, absence of metal, natural esthetics,
durability, and a low rate of fractures.7,8
Among them, the CEREC system
(CEramic REConstruction) is one of the
most popular in the world.9
e4
January/February 2013
analysis of variance (ANOVA) and Tukey’s test (a = 0.05). Qualitative
analysis was performed using scanning electron microscopy (SEM). The
mean (± SD) roughness values obtained for GZ were: 1.1 ± 0.40 µm;
1.0 ± 0.31 µm; 1.6 ± 0.31 µm; and 2.2 ± 0.73 µm. For MP, the mean
values were: 0.66 ± 0.13 µm; 0.43 ± 0.14 µm; 1.6 ± 0.55 µm; and 2.0
± 0.63 µm. The mean roughness values were significantly affected by the
ceramic type (P = 0.0001) and polishing technique (P = 0.0047). The SEM
images confirmed the roughness data. The manually polished glass CAD/
CAM ceramics promoted lower surface roughness than did the glazed
feldspathic dental ceramics.
Received: August 30, 2011
Revised: December 31, 2011
Accepted: January 25, 2012
Regardless of the technique used, glazed
ceramic restorations need some adjustments in several clinical situations, mainly
with the occlusal and interproximal areas,
even when a new glazing procedure will
not be performed again.10,11 These adjustments have the potential of increasing
the ceramic’s roughness and, thus, the
potential of wearing down the antagonist
teeth and promoting excessive dental
biofilm.12-14 Several studies have demonstrated that dental biofilm is formed in
larger amounts and more quickly on rough
surfaces.13 Moreover, the microbial colonization on oral surfaces and on restorative
materials is considered an important factor
that contributes to the development of
caries and periodontal disease.15 In ceramic
adjustments, the roughness must be minimized using intraoral polishing techniques
to achieve an acceptable smoothness.3
According to Al-Wahadni & Martin,
glazed ceramic accumulates the least
amount of dental biofilm and also allows it
to be easily removed.5 On the other hand,
according to Scotti et al, ceramic surfaces
that are polished mechanically with a silicon rubber wheel accumulate less biofilm
than glazed ceramic.16 According to Bottino
et al, efficient manual mechanical polishing
General Dentistry
www.agd.org
should use diamond burs on ceramic surfaces, followed by the use of abrasive rubber
tips and felt discs with diamond paste.3
However, mechanical polishing can be
influenced by the ceramic microstructure
and production techniques; therefore,
glazing procedures have traditionally been
recommended.17 In the case of clinical
ceramic adjustments, additional clinical
steps are necessary.
Thus, the aim of this study was to evaluate the influence of 2 different surface
polishing procedures—glazing (GZ) and
manual polishing (MP)—on the roughness of ceramics processed by CAD/CAM
and stratification technique. The hypothesis was that the roughness is influenced by
both the surface polishing procedure and
by the ceramic type.
Materials and methods
The brand names, types, and manufacturers of the materials used in this study are
presented in Table 1.
Fabrication of the samples
Twenty discs (diameter: 8 mm, thickness:
1 mm) were prepared for each ceramic type.
To fabricate the CAD/CAM samples—
ProCAD (Ivoclar Vivadent AG) and Vita
Mark II (VITA Zahnfabrik)—the CEREC
inLab system (Sirona Dental Systems, Inc.)
and CEREC 3D program (version 2.9x,
Sirona Dental Systems, Inc.) were used.
Each disc image (8 mm x 1 mm) was sent
to the computer-aided manufacturing unit
and 40 discs where milled. A new set of
cylindrical milling burs (diameter: 1.6 mm;
1.2 mm/step), was used for each group.
To fabricate the conventional ceramic
samples—VM7 (VITA Zahnfabrik) and
IPS e.max Ceram (Ivoclar Vivadent AG), a
metallic device (diameter: 8 mm, thickness:
1 mm) was used to standardize the sample
size. The dentin ceramic powder and liquid
were mixed, homogenized, and inserted
into the metallic device. After removal
from the assembly, the ceramics were fired
in their respective ovens: For the VM7, a
Vacumat 40 (VITA Zahnfabrik) was used,
and for the IPS e.max Ceram, a Programat
P500 (Ivoclar Vivadent AG) was used. Due
to shrinkage, a second layer was applied
and the specimens were submitted to a final
firing. The firing cycles of the dental ceramics and glazes are presented in Table 2.
Polishing procedures
One surface of each ceramic disc was
then leveled and polished in a polishing
machine (PSK-2V, ERIOS Equipamentos)
using silicon-carbide papers in sequence
(600-, 800- and 1200-grit sandpaper, 3M
ESPE) under water-cooling.
The ceramic discs were then divided
into 8 groups (n = 10) according to type
of ceramic disc (4 levels: Vita Mark II,
ProCAD, IPS e.max Ceram, and VM7) and
polishing procedures (2 levels: GZ and MP).
The glazing procedures were carried out
according to each manufacturer’s recommendations. For manual polishing, 2-step
silicone rubber wheel points were used on
the ceramic surface (Exa-Cerapol, Edenta
AG) for 10 seconds each step, with a mean
speed of 400 rpm and manual pressure. All
procedures were performed by the same
operator, in order to standardize the pressure during the polishing procedures.
Roughness test
A portable surface roughness tester
(Hommel tester T200, Hommel-Etamic
GmbH) was used to measure the mean
roughness of the polished surfaces. The
roughness measurements were made on
three different areas (central line and
Table 1. Brand names, types, and manufacturers of materials used.
Brand name
Type
Manufacturer
ProCAD
Glass ceramic block
Ivoclar Vivadent AG, Schaan, Liechtenstein
Vita Mark II
Glass ceramic block
VITA Zanhfabrik, Bad Sackingen, Germany
VM7
Low-fusing feldspathic ceramic
VITA Zanhfabrik, Bad Sackingen, Germany
IPS e.max Ceram
Low-fusing feldspathic ceramic
Ivoclar Vivadent AG, Schaan, Leichtenstein
Vita Akzent 25
Glaze
VITA Zanhfabrik, Bad Sackingen, Germany
IPS e.max Ceram Glaze Glaze
Ivoclar Vivadent AG, Schaan, Leichtenstein
Exa-Cerapol
(gray and pink)
Edenta AG, Zurich, Switzerland
Silicone ceramic polisher points
Table 2. Firing procedures of the dental ceramics and glazes.
Starting
Temperature
(°C)
Ceramics/Glazes
Drying
Time
(min)
Final
Temperature
(°C)
Temperature
rate of increase
(°C/min)
Holding time
(min)
VM7
500
6
910
55
1
Akzent 25
500
4
900
80
1
IPS e.max Ceram
403
4
750
50
1
IPS e.max Ceram Glaze
403
6
725
60
1
above and below the central line) on each
sample surface in order to take a surface
profile (peaks and inverted valleys) and
determine the arithmetic average values
of the departures from profile from the
center line (Ra values).
The test was performed by the same
operator on each polished surface and was
performed three times for each sample
(scanned length: 2 mm, speed of reading:
0.1 mm/s).
Morphology analysis
Morphology and chemical analysis was
performed on a sandblasted surface of a
sample from each of the 8 groups using
a scanning electron microscope (JEOLJSM-5400, JEOL Ltd.) equipped with
an energy dispersive X-ray and the INCA
Energy program (Oxford Instruments).
These samples were initially fixed on an
aluminum support with double-sided
carbon adhesive tape and after were sputter-coated with a gold-palladium alloy in a
sputter coater (Polaron SC7620, Quorum
www.agd.org
Technologies Ltd.) (time: 130 s; current:
10-15 mA; vacuum: 130 mTorr; sputter
coating rate: 3.5 nm/min, approximate
layer of Pd-Au of 80 Å) for SEM analysis
with 5000X and 1500X magnifications.
Statistical analysis
Statistical analysis was performed using
Statistix for Windows (version 8.0,
Analytical Software). The mean roughness
(µm) of each group was analyzed using
two-way ANOVA and Tukey’s test, with
the variables of ceramic type and polishing
method. P values < 0.05 were considered
statistically significant in all tests.
Results
The results of two-way ANOVA for the
experimental conditions are presented
in Table 3. The mean of the roughness
values were significantly affected by the
ceramic types (P = 0.0001 < 0.05: CAD/
CAM: 0.8 µm; conventional feldspathic:
1.85 µm) and polishing technique
(P = 0.0047 < 0.05: GZ: 1.47 µm; MP: 1.18
General Dentistry
January/February 2013
e5
Computer Designed/Fabricated Crowns Influence of polishing procedures on the surface roughness of dental ceramics
Table 3. Results of two-way ANOVA for the polishing and ceramic
conditions and the interaction terms according to roughness data
(1P < 0.05).
Degrees of
freedom
Effect
Polishing
1
Sums of
squares
1.7642
Mean
squares
1.76418
F ratio
8.53
Probability
value
0.00471
Ceramic
3
24.8573
8.28578
40.05
0.00011
Polishing1Ceramic
3
1.0671
0.35571
1.72
0.1706
Residue
72
14.8953
Total
79
42.5840
0.20688
Table 4. Mean (± SD) roughness values (µm) for
polishing and ceramic conditions (Tukey’s test,
α = 0.05).1
Polishing Technique
Ceramics
0.66 ± 0.13
ProCAD
0.43 ± 0.14
E.max Ceram
1.63 ± 0.5a,b
1.6 ± 0.31a,b
2 ± 0.63
2.2 ± 0.7a
VM7
Roughness values (µm)
e.max Ceram
ProCad
Mark II
VM7
1.0
0.5
e6
ManualGlaze
Polishing technique
January/February 2013
a
1.18 (± 0.78)
1.1 ± 0.4b,c
1 ± 0.3b,c,d
1.47 (± 0.66)
to the glazed ceramics (Figure). However,
small pores could be found in the glazed
samples when analyzed with higher magnifications, suggesting that this procedure
can promote higher roughness values
when compared to polished surfaces.
Discussion
1.5
µm). The interaction between the ceramic
types and polishing technique factors was
not statistically significant (P = 0.1706).
Mean (± SD) roughness values and the
homogeneous groups are presented in
Table 4. The results of Tukey’s multiple
comparison test demonstrated that, when
the factor of polishing technique was
analyzed for each ceramic, the roughness
values after manual polishing were statistically lower when compared to glazing.
Moreover, when the factor ceramic type
was analyzed, the conventional ceramics
(VM7 and IPS e.max Ceram) presented
higher roughness values when compared
to the CAD/CAM ceramics (ProCad and
Vita Mark II) (Table 4 and Chart).
d
Means followed by the same letter(s) represents that the groups are
similar statistically.
Chart. Means (±SD) of roughness values according to the
experimental conditions: ceramic and polishing technique.
0
c,d
1
Confidence interval (α = 0.05)
2.0
Glaze
Vita Mark II
Mean (± SD)
1
2.5
Manual
The Vita Mark II and ProCad presented
better roughness values, mainly after
manual polishing (0.66 µm and 0.43 µm,
respectively). The VM7 ceramic showed
significantly worse roughness values after
both glazing (2.2 ± 0.73) and manual
polishing (2.0 ± 0.63) than did the other
ceramics. However, these values were statistically similar to E-max Ceram, according to the Tukey’s test (Table 4).
SEM analyses
The SEM analyses of the ceramic surfaces
revealed that the specimens submitted
to manual polishing with silicone points
(regardless of the ceramic used) presented
similar morphology than when compared
General Dentistry
www.agd.org
Several studies have compared glazing
to manual polishing techniques.3,18-20 A
smooth surface is especially desirable in
order to reduce the rate of plaque biofilm
accumulation, decrease wear of the opposing dentition, and provide a shiny appearance.12,13,18 Moreover, smooth ceramic
surfaces may improve the overall strength
of the ceramic restoration.21
Surface roughness refers to the irregularities on a specific surface. In the current
study, Ra values were obtained using a
surface roughness tester and measured in
micrometers (µm), as with other studies.3,20,21-24 However, other methods were
used in previous studies to measure surface
roughness, including a profilometer,
atomic force microscopy, and confocal
laser microscopy.12,18,19,25-32
In the current study, CAD/CAM
ceramics (Mark II and ProCad) presented
the lowest roughness values, regardless of
the polishing technique used. This can
be explained by the material’s characteristics, such as the homogeneity and high
quality of the components in the ceramic
material. These results confirm findings
previously reported by Sarikaya & Guler,
who compared the roughness of conventional and machinable ceramics polished
Author information
Figure. Representative SEM micrograph (1500X) on the polished surfaces of the ProCad groups. Left: glazed
surface. Right: manual polished surface.
by different techniques.30 According to
that study, ceramics manufactured by the
same processing method showed similar roughness values after polishing or
manual glazing.30 This can be explained
by the similarities in the chemical composition (Table 1) of the materials that
use the same processing technique, which
causes them to behave similarly with the
polishing methods employed.
In this study, the roughness values for
glazed specimens were statistically higher
when compared to the manually machine
polished specimens (Table 4). Studies
have shown that polishing methods can
result in a final ceramic surface that has
a similar or better roughness than glazefired ceramic surfaces.3,18,19,25,28-30 Other
studies presented opposing data.20,21,23,31
However, roughness values occasionally
do not represent the actual topography of
the ceramic surface because the profilometer measures only some areas and not the
whole surface. For this reason, a qualitative analysis using SEM technology has
been recommended to analyze the surface
roughness of ceramic materials.3
When the SEM data was analyzed, the
images corresponded with the roughness
values found with the Hommel tester.
Similar results were found by other studies.25,28 On the other hand, Bottino et al
used SEM analysis to show that manual
polishing was unable to produce surface
values similar to those of glazed surfaces.3
The current study used rubber tips for
polishing the ceramic surfaces. Several
studies have shown that the use of Sof-Lex
discs (3M ESPE) has better results than
polishing with rubber tips.12,22,24 However,
Sof-Lex discs are difficult to use on molar
occlusal surfaces, which limits their use.22
Thus, mechanical polishing of ceramic
restorations using rubber wheels can be
clinically indicated, especially in areas with
limited access such as with the occlusal
surface of posterior teeth.
Based on the results obtained in this
study, mechanical polishing can be used
after adjustments made to CAD/CAM or
conventional ceramic surfaces, promoting
lower roughness values compared to those
provided by glazing. However, other CAD/
CAM systems might respond differently
to the testing scenario. Further studies
should be developed in order to define the
most appropriate mechanical polishing for
dental ceramics. Additionally, it is important to conduct long-term in vitro and
clinical studies to confirm the current data.
Conclusion
The aim of this study was to evaluate the
influence of 2 different surface polishing
procedures on the roughness of ceramics
processed by CAD/CAM and stratification
technique. The hypothesis the authors
proposed in the introduction was that the
roughness is influenced by both the surface
polishing procedure and by the ceramic
type. This hypothesis was accepted. Within
the limitations of the present study, glass
CAD/CAM ceramics associated with
manual polishing promoted lower surface
roughness values when compared to glazed
feldspathic ceramics.
www.agd.org
Dr. Oliveira-Junior is an adjunct professor,
Department of Restorative Dentistry, Sao
Paulo State University, Araraquara Dental
School (UNESP), Araraquara, Brazil.
Drs. Buso, Fujiy, and Lombardo have
private clinical practices. Dr. Campos is a
postgraduate student in Prosthodontics,
Sao Jose dos Campos Dental School,
Sao Paulo State University, Sao Jose
dos Campos, Brazil. Dr. Sarmento is a
postgraduate student in Prosthodontics,
Federal University of Pelotas (UFPel),
Rio Grande do Sul, Brazil. Dr. Souza
is an adjunct professor, Department
of Restorative Dentistry, Division of
Prosthodontics, Federal University of
Paraiba (UFPB), Joao Pessoa, Brazil.
References
1. Kelly JR, Rose TC. Nonprecious alloys for use in fixed
prosthodontics: a literature review. J Prosthet Dent.
1983;49(3):363-370.
2. Baran GR. Selection criteria for base metal alloys for
use with porcelains. Dent Clin North Am. 1985;29(4):
779-787.
3. Bottino MC, Valandro LF, Kantorski KZ, Bressiani JC,
Bottino MA. Polishing methods of an alumina-reinforced feldspar ceramic. Braz Dent J. 2006;17(4):285289.
4. Zahran M, El-Mowafy O, Tam L, Watson PA, Finer Y.
Fracture strength and fatigue resistance of all-ceramic
molar crowns manufactured with CAD/CAM technology. J Prosthodont. 2008;17(5):370-377.
5.Al-Wahadni A, Martin DM. Glazing and finishing dental porcelain: a literature review. J Can Dent Assoc.
1998;64(8):580-583.
6. Heymann HO, Bayne SC, Sturdevant JR, Wilder AD Jr,
Roberson TM. The clinical performance of CAD-CAMgenerated ceramic inlays. A four-year study. J Am Dent
Assoc. 1996;127(8):1171-1181.
7. Kurbad A, Reichel K. Multicolored ceramic blocks as an
esthetic solution for anterior restorations. Int J Comput
Dent. 2006;9(1):69-82.
8. Bindl A, Mormann WH. Survival rate of mono-ceramic
and ceramic-core CAD/CAM-generated anterior
crowns over 2-5 years. Eur J Oral Sci. 2004;112(2):
197-204.
9. Mormann WH. The evolution of the CEREC system.
J Am Dent Assoc. 2006;137(suppl):7S-13S.
10.Sasahara RM, Ribeiro Fda C, Cesar PF, Yoshimura HN.
Influence of the finishing technique on surface roughness of dental porcelains with different microstructures. Oper Dent. 2006;31(5):577-583.
11.Albakry M, Guazzato M, Swain MV. Effect of sandblasting, grinding, polishing and glazing on the
flexural strength of two pressable all-ceramic dental
materials. J Dent. 2004;32(2): 91-99.
12.Aykent F, Yondem I, Ozyesil AG, Gunal SK, Avunduk
MC, Ozkan S. Effect of different finishing techniques for
restorative materials on surface roughness and bacterial
adhesion. J Prosthet Dent. 2010;103(4):221-227.
13. Kawai K, Urano M, Ebisu S. Effect of surface roughness
of porcelain on adhesion of bacteria and their synthesizing glucans. J Prosthet Dent. 2000;83(6):664-667.
General Dentistry
January/February 2013
e7
Computer Designed/Fabricated Crowns Influence of polishing procedures on the surface roughness of dental ceramics
14.Raimondo RL Jr, Richardson JT, Wiedner B. Polished
versus autoglazed dental porcelain. J Prosthet Dent.
1990;64(5):553-557.
15.Scotti R, Zanini Kantorski K, Scotti N, Monaco C,
Valandro LF, Bottino MA. Early biofilm colonization
on polished- and glazed-zirconium ceramic surface.
Preliminary results. Minerva Stomatol. 2006;55(9):
493-502.
16.Scotti R, Kantorski KZ, Monaco C, Valandro LF, Ciocca L, Bottino MA. SEM evaluation of in situ early bacterial colonization on a Y-TZP ceramic: a pilot study.
Int J Prosthodont. 2007;20(4):419-422.
17.Cattell MJ, Chadwick TC, Knowles JC, Clarke RL. The
development and testing of glaze materials for application to the fit surface of dental ceramic restorations.
Dent Mater. 2009;25(4):431-441.
18.Sarac D, Sarac YS, Yuzbasioglu E, Bal S. The effects of
porcelain polishing systems on the color and surface
texture of feldspathic porcelain. J Prosthet Dent. 2006;
96(2):122-128.
19.Tholt de Vasconcellos B, Miranda-Junior WG, Prioli R,
Thompson J, Oda M. Surface roughness in ceramics
with different finishing techniques using atomic force
microscope and profilometer. Oper Dent. 2006;31(4):
442-449.
20. Brentel AS, Kantorski KZ, Valandro LF, Fucio SB, Puppin-Rontani RM, Bottino MA. Confocal laser microscopic analysis of biofilm on newer feldspar ceramic.
Oper Dent. 2011;36(1):43-51.
21.Chu FC, Frankel N, Smales RJ. Surface roughness and
flexural strength of self-glazed, polished, and
reglazed In-Ceram/Vitadur Alpha porcelain laminates. Int J Prosthodont. 2000;13(1):66-71.
22. Martínez-Gomis J, Bizar J, Anglada JM, Samso J, Peraire M. Comparative evaluation of four finishing
e8
January/February 2013
systems on one ceramic surface. Int J Prosthodont.
2003;16(1): 74-77.
23.Al-Wahadni A. An in vitro investigation into the surface
roughness of 2 glazed, unglazed, and refinished ceramic materials. Quintessence Int. 2006;37(4):311-317.
24. Flury S, Lussi A, Zimmerli B. Performance of different
polishing techniques for direct CAD/CAM ceramic
restorations. Oper Dent. 2010;35(4):470-481.
25.Wright MD, Masri R, Driscoll CF, Romberg E, Thompson GA, Runyan DA. Comparison of three systems for
the polishing of an ultra-low fusing dental porcelain.
J Prosthet Dent. 2004;92(5):486-490.
26. Kou W, Molin M, Sjogren G. Surface roughness of five
different dental ceramic core materials after grinding
and polishing. J Oral Rehabil. 2006;33(2):117-124.
27.Sarac D, Turk T, Elekdag-Turk S, Sarac YS. Comparison
of 3 polishing techniques for 2 all-ceramic materials.
Int J Prosthodont. 2007;20(5):465-468.
28.Wang F, Chen JH, Wang H. Surface roughness of a
novel dental porcelain following different polishing
procedures. Int J Prosthodont. 2009;22(2):178-180.
29.Yuzugullu B, Celik C, Erkut S, Ozcelik TB. The effects
of extraoral porcelain polishing sequences on surface
roughness and color of feldspathic porcelain. Int J
Prosthodont. 2009;22(5):472-475.
30.Sarikaya I, Guler AU. Effects of different polishing
techniques on the surface roughness of dental porcelains. J Appl Oral Sci. 2010;18(1):10-16.
31.Yilmaz K, Ozkan P. Profilometer evaluation of the
effect of various polishing methods on the surface
roughness in dental ceramics of different structures
subjected to repeated firings. Quintessence Int.
2010; 41(7):e125-e131.
32.Al-Shammery HA, Bubb NL, Youngson CC, Fasbinder
DJ, Wood DJ. The use of confocal microscopy to
General Dentistry
www.agd.org
assess surface roughness of two milled CAD-CAM
ceramics following two polishing techniques. Dent
Mater. 2007; 23(6):736-741.
Manufacturers
Analytical Software, Tallahassee, FL
850.893.9371, www.statistix.com
Edenta AG, Zurich, Switzerland
41.7174.453.53, www.edenta.com
ERIOS Equipamentos, Sao Paulo, Brazil
11.2274.9466, www.eriosequipamentos.com.br
Hommel-Etamic GmbH, Villingen Schwenningen, Germany
49.7720.602.0, www.hommel-etamic.com
Ivoclar Vivadent AG, Schann, Liechtenstein
00423.235.35.35, www.ivoclarvivadent.com/en
JEOL Ltd., Welwyn Garden City, England
44.1707.377117, www.jeol.com
Oxford Instruments, Oxfordshire, England
01865.393200, www.oxford-instruments.com
Quorum Technologies Ltd., Newhaven, England
44.1273.510535, www.quorumtech.com
Sirona Dental Systems, Inc., Long Island City, NY
718.937.5765, www.sirona.com
VITA Zahnfabrik, Bad Sackingen, Germany
49.0.7761.56.20, www.vita-zahnfabrik.com
3M ESPE, St. Paul, MN
888.364.3577, solutions.3M.com
Case Presentations
Vascular leiomyoma in the oral cavity
Janaina Salomon Ghizoni, DDS, MSc, PhD n Eron Martins Baroni, DDS n Eron Jose Baroni, DDS, MSc Marcelo Tomas de Oliveira, DDS, MSc, PhD n Luis Antonio de Assis Taveira, DDS, MSc, PhD n Jefferson Ricardo Pereira, DDS, MSc, PhD
The aim of this study was to examine a case report of vascular
leiomyoma located in the oral mucosa of the oral cavity. Vascular
leiomyoma is a benign tumor arising from smooth muscle. One factor
that makes vascular leiomyomas in the oral cavity rare is that there
is little smooth muscle in the mouth. The most common histological
subtype in the oral cavity is the vascular subtype. The greatest difficulty
in histological diagnosis of this entity is the similarity in morphology
V
ascular leiomyoma is a benign tumor
arising from smooth muscle that
is commonly found in the uterus
(95%), skin (3%), and gastrointestinal
tract (1.5%), and occurs rarely in the head
and neck (less than 1% of cases).1
According to Silveira et al, clinical
features of vascular leiomyomas found in
the mouth include the following: small
nodules with a smooth submucosa; rarely,
epithelium overlying an ulcer (although in
some cases, there is histological evidence
of ulceration); slow growth; variable size
(although rarely larger than 5 cm); color
variation due to vascularization and depth
in the tissues; asymptomatic; and in a
few cases, there were reports of pain.2
Histologically, the neoplasm is characterized by bundles of smooth muscle
fibers arranged in a standard interlaced,
sometimes storiform, pattern intermingled
with connective tissue in variable quantity.
With regard to its morphology, the World
Health Organization calls for subdivision
into three variants: solid, vascular (vascular
leiomyoma), and epithelioid. The most
common histological subtype in the oral
cavity is the vascular subtype. Vascular
leiomyoma has a frequency of 74% and is
characterized by a well-defined proliferation of mesenchymal cells with tapered
eosinophilic cytoplasm and elongated
nuclei basophils showing conical endings.3
The literature, with regard to clinical
and pathological findings, has demonstrated that there are few differences in
behavior between immuno-enzymes and
subcellular entities. The greatest difficulty
in histological diagnosis of this entity is
the similarity in morphology with other
malignancies, particularly those of neural
with other malignancies, particularly of neural or fibroblastic lineage.
Wide surgical resection is the only treatment reported in the literature
with good results. The recurrence rate is very low if complete resection
is achieved. The study of rare or unusual lesions is very important for
the clinical diagnosis of vascular leiomyoma.
Received: November 17, 2012
Accepted: March 16, 2012
or fibroblastic lineage. Special stains with
proven diagnostic value are often not
successful in demonstrating myofibrils.
This has led authors to use other techniques to elucidate the diagnosis, such
as transmission electron microscopy and
immunohistochemistry.4 Other authors
believe leiomyomas arise from the remnants of embryonic tissue found in such
areas as the lingual duct or taste buds.5
Some authors believe that men and
women are affected in equal proportion;
however, there is considerable controversy
on this point because other researchers
have reported a 2:1 predilection for
females, while others have shown that
men outnumber women at a ratio of 2:1.6
There are also discrepancies in the
literature as to the site of predilection for
oral cancer; authors such as WertheimerHatch et al have reported that the vascular
leiomyoma is most commonly located on
the tongue, followed by the palate, cheek
mucosa, and lower lip.7 However, Savage et
al reviewed the literature and argued that
the sites most affected are the lips, followed
by the palate, tongue, and cheek mucosa.8
Additionally, Baden et al found vascular
leiomyomas more commonly on the lips,
followed by the tongue, cheek, and palate.9
The differential diagnosis of vascular
leiomyoma of the oral cavity should be
done with other tumors that occur in this
region and is based mainly on histopathological examination. For diagnosis, a lesion
that serves as a comparison to leiomyoma
in the oral cavity is the fibroma, which
is the most frequent oral fibrous lesion
and is considered by some authors to be
a non-neoplastic benign lesion (that is an
increase of focal reactive oral mucosa).7,8
www.agd.org
Distinguishing between leiomyoma
and leiomyosarcoma of low-grade malignancy can be tricky. The morphological
differentiation is based on the degree of
cellular pleomorphism, necrosis, hyperchromatism, and nuclear atypia, especially
in the presence of mitosis.10 Of note, 5
or more mitoses per field should also be
observed.11 The spindle cell lesions have
morphological differences, which can be
explained by their histogenesis from the
mesenchymal stem cells during embryogenesis. Like fibroblasts, leiomyocytes are
spindle cells, and making the distinction
between these cells can be difficult.11
Neoplasms of neural origin, such as
neurilemmomas, neurofibromas and
granular cell tumors, and lesions usually confined to reports of occurrence in
the literature, must be researched and
included in the differential diagnosis
because of their histopathology.12
Some symptoms are due to local
growth; difficulty swallowing, toothache, loose teeth, or pain in the temporomandibular joint have also been
reported.13 Shortness of breath can also
be caused by large tumors. Pain at the
site is suspected to be attributable to
ischemia and tumor vessel contraction
due to nerve irritation by the tumor.13
Treatment of these tumors is based
on local resection with no reports of
recurrence after total excision. In 2001,
Bloom et al reported a case of recurrence after spontaneous extrusion of the
tumor, but the patient was retreated and
no recurrence occurred after surgical
excision.14 This event demonstrates the
potential recurrence after an incomplete
removal and the need for complete
General Dentistry
January/February 2013
e9
Case Presentations Vascular leiomyoma in the oral cavity
Fig. 1. Photograph of a patient with complaints about her left
unilateral facial asymmetry.
Fig. 4. Complete resection of the lesion is achieved.
excision to ensure a definitive treatment.
The patient was free of disease 1 year
after complete surgical excision.14
The first case of leiomyoma in the oral
cavity was reported by Blanc et al in
1984, but from 1984 to 1996, only 139
cases of leiomyoma of the oral cavity were
reported in the literature.15 The aim of
this study was to examine a 2005 case of
vascular leiomyoma located in the oral
mucosa of the oral cavity.
Case report
In 2005, a 25-year-old female was sent to
the oral and maxillofacial department of
St. Joseph Hospital in Criciuma, Santa
Catarina, Brazil, with unilateral facial
asymmetry on the left side (Fig. 1). The
intra-oral lesion showed submucosal consistent palpation with a color similar to
the mucosa, of approximately 4 to 5 cm
in diameter, that was located in the oral
mucosa on the left. A clinical hypothesis
of dentoalveolar abscess was made.
e10
January/February 2013
Fig. 2. Superficial incision on the
affected area. Displacement of the soft
tissues of the oral mucosa.
Fig. 5. Macroscopic view of the lesion.
An ultrasound of the patient’s face
was performed and an oval lesion was
observed in the subcutaneous tissue
of the left hemiface. The lesion was
hypoechoic relative to fat with welldefined borders. In ultrasonography, it
was observed that the lesion measured
5.4 cm at its greatest diameter (anteroposterior) and 4.0 cm at its largest
diameter side. It was not possible to
measure the craniocaudal length due
to overlap with the zygomatic arch.
It was given a possible diagnosis of
parotid pleomorphic adenoma originating from the accessory salivary gland.
The patient underwent surgery that
included an excisional biopsy under
general anesthesia with orotracheal intubation. A superficial incision was made
on the affected area, and after displacing the soft tissues of the oral mucosa,
as well as the nerves and vessels, the
lesion was dissected and removed. An
internal suture with absorbable thread
General Dentistry
Fig. 3. View of lesion dissection.
www.agd.org
Fig. 6. Macroscopic view inside the
lesion.
and external suture with silk thread were
made. The lesion material was then sent
for pathological examination (Fig. 2-4).
Macroscopically, it was observed to
be a 6.5 x 4 mm, 76 g nodule with an
elastic-firm consistency and smooth
surface with whitish parenchyma with
fibrous bands and areas of a myxoid
aspect (Fig. 5 and 6). Microscopically, it
was diagnosed as leiomyoma with myxoid
areas and no malignancy (Fig. 7 and 8).
After complete resection was achieved,
follow-up examinations were done at 2, 5,
and 12 months (Fig. 9-11). A recurrence
could not be detected.
Discussion
One factor that makes vascular leiomyomas in the oral cavity rare is that there is
little smooth muscle in the mouth. The
formation of fibroids is possibly due to the
fact that the oral cavity is rich in blood
vessels and, therefore, it has been proposed
that the endothelium, the smooth muscle
Fig. 7. Microscopic view of the lesion diagnosed as
vascular leiomyoma.
Fig. 8. Proliferation of mesenchymal cells with
tapered eosinophilic cytoplasm and elongated nuclei
basophils showing conical endings.
of the University of Southern Santa
Catarina, Tubarao, Santa Catarina,
Brazil, where Dr. Oliveira is a member
of the Department of Clinical Practice,
Dr. E. J. Baroni is in the Department
of Dental Surgery, and Drs. E. M.
Baroni and Ghizoni are members of
the Department of Oral Pathology.
Dr. Taveira is a member of the
Department of Oral Pathology, Bauru
Dental School of the University of
Sao Paulo, Bauru, Sao Paulo, Brazil.
References
Fig. 9. Two-month follow up after surgery.
Fig. 11. Twelve-month follow-up after surgery with
no recurrence.
medial layer of those blood vessels, and
smooth muscles of the excretory duct
of the salivary glands, are the source of
vascular leiomyoma of the oral cavity.3
This lesion type accounts for 5% of
all fibrous proliferation that undergoes
biopsy. It is usually observed in young
patients and is more frequent in the first
3 decades of life, presenting as asymptomatic lesions or papillary, lobulated,
or pedunculated tumors measuring
less than 1 cm in diameter and mainly
affecting the lower gum and the apex
and lateral border of the tongue.11 The
literature also suggests that there is a
slight predilection for females to present
with these lesions.6
Fig. 10. Five-month follow-up after surgery.
The diagnosis of fibroids is relatively
difficult to establish due to the similarity
of these lesions with other spindle cell
tumors. The differential diagnosis should
include other mesenchymal tumors (such
as neurofibroma, lipoma, etc) and salivary
gland neoplasms (such as mucocele, pleomorphic adenoma, etc).6
The neoplastic nature of leiomyomas
has been questioned by some authors who
discuss the possibility that vascular leiomyomas represent a final stage in the progressive maturation of a hemangioma and
are therefore hamartomatous lesions.2
Wide surgical resection is the only
treatment reported in the literature with
good results. The recurrence rate is very
low if complete resection is achieved.13
The study of rare or unusual lesions is
very important for the clinical diagnosis
of vascular leiomyoma in the oral cavity.
These studies allow clinicians to collect
new information about the biological
behavior and prognosis of these lesions.
For more meaningful clinical use, future
studies and case reports should be done.
Author information
Dr. Pereira is a member of the Department of Prosthodontics, Dental School
www.agd.org
1.Ardekian L, Samet N, Talmi YP, Roth Y, Bendet E, Kronenberg J. Vascular leiomyoma of the nasal septum.
Otolaryngol Head Neck Surg. 1996;114(6):798-800.
2.Silveira VAS, Amadei SU, Machado ASP, et al. Oral vascular leiomioma: report of two cases, review of literature and immunohistochemistry study [in Portuguese].
J Bras Patol Med Lab. 2007;43(3):211-217.
3.Gaitan Cepeda LA, Quezada Rivera D, Tenorio Rocha F,
Leyva Huerta ER, Mendez Sanchez ER. Vascular leiomyoma of the oral cavity. Clinical, histopathological
and immunohistochemical characteristics. Presentation
of five cases and review of the literature. Med Oral
Patol Oral Cir Bucal. 2008;13(8):e483-e488.
4. Jaeger MMM, Jaeger RG, Araujo VC. Morphologic subcelular and immunoenzimatic study of oral vascular leiomyoma [in Portuguese]. An Bras Dermatol. 1991;66(2):61-64.
5. Praal FR, Ioannides CA, van Beek GJ, van de Molengraft
F. Oral leiomyomas. J Maxillofac Surg. 1982;10(4):
229-235.
6.Gonzalez Sanchez MA, Colorado Bonnin M, Berini
Aytes L, Gay Escoda C. Leiomyoma of the hard palate:
a case report. Med Oral Patol Oral Cir Bucal. 2007;
12(3):e221-e224.
7.Wertheimer-Hatch L, Hatch GF 3rd, HatchB S KF, et al.
Tumors of the oral cavity and pharynx. World J Surg.
2000;24(4):395-400.
8.Savage NW, Adkins KF, Young WG, Chapman PJ. Oral
vascular leiomyoma: review of the literature and report of two cases. Aust Dent J. 1983;28(6):346-351.
9. Baden E, Doyle JL, Lederman DA. Leiomyoma of the
oral cavity: a light microscopic and immunohistochemical study with review of the literature from 1884 to
1992. Eur J Cancer B Oral Oncol. 1994;30B(1):1-7.
10. Fletcher CD, Kilpatrick SE, Mentzel T. The difficulty in
predicting behavior of smooth-muscle tumors in deep
soft tissue. Am J Surg Pathol. 1995;19(1):116-117.
11. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral
and maxillofacial pathology. 2nd ed. Philadelphia, PA:
W.B. Saunders Co.; 2002.
12. Brooks JK, Nikitakis NG, Goodman NJ, Levy BA. Clinicopathologic characterization of oral angioleiomyomas. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2002;94(2):221-227.
13.Luaces Rey R, Lorenzo Franco F, Gomez Oliveira G, Patino Seijas B, Guitian D, Lopez-Cedrun Cembramos JL.
Oral leiomyoma in retromolar trigone. A case report.
Med Oral Patol Oral Cir Bucal. 2007;12(1):e53-e59.
14. Bloom DC, Finley JC Jr, Broberg TG, Cueva RA. Leiomyoma of the nasal septum. Rhinology. 2001;39(4):233-235.
15. Blanc B, Gamerre M, Adrai J, Merger C. The elderly primipara [in French]. Rev Fr Gynecol Obstet. 1984;79(2):
109-114.
General Dentistry
January/February 2013
e11
Case Presentations
Peripheral giant cell granuloma: a case report
Ruchi Banthia, MDS n Shubhra Maheshwari, MDS n Priyank Banthia, MDS n Karan Mantri, BDS, MFDS
Peripheral giant cell granuloma is a rare exophytic lesion that develops
on the gingiva and alveolar ridge. Although the precise etiology of
this lesion is unknown, it could represent a local reaction to trauma or
irritation. Management requires a surgical excision of the lesion and
elaborate recall due to possible recurrence. This report describes the
P
eripheral giant cell granuloma
(PGCG) (also known as giant cell
epulis) is the most common giant cell
lesion in the oral cavity.1 Generally, it is an
asymptomatic hyperplastic lesion of the
attached gingiva or alveolar mucosa that
is believed to originate from the gingival
connective tissue or the periosteum of the
alveolar ridge.2 It manifests as a soft tissue,
extra-osseous, purplish-red nodule consisting of multi-nucleated giant cells with
a background of mononuclear stromal
cells and extravasated red blood cells. This
lesion may not represent a true neoplasm
but rather could be a reactive lesion. It is
believed that this lesion is stimulated by
local irritation or trauma; however, its precise etiopathogenesis is still unclear.1
This article describes the clinical and
histopathological findings of a PGCG in a
female patient.
Case report
A 35-year-old woman presented with
the chief complaint that her gums in the
maxillary left anterior region had progressively increased in size over the last three
months. Besides causing esthetic concerns,
Fig. 1. A preoperative view of the
lesion.
e12
January/February 2013
clinical and histopathological features and management of a peripheral
giant cell granuloma as it appeared in the maxillary anterior region of a
35-year-old female patient.
Received: August 31, 2011
Accepted: February 6, 2012
this enlargement had led to pain and difficulty with mastication. The systemic history of the patient was noncontributory.
The patient did not report any history of
trauma or irritation related to this region.
Extraoral examination showed incompetent lip seal and mild swelling in the
left labial region. Intraoral examination
revealed an enlarged (5 mm x 10 mm),
pedunculated, reddish-purple lesion in
the area of tooth No. 23 (maxillary left
canine) extending from the gingival
margin to the vestibule. A focal surface
ulceration was seen on the lesion (Fig. 1).
The lesion itself was tender and bled
easily upon slight manipulation; in addition, it displayed a soft consistency upon
palpation. The tooth was vital and nonmobile. A periapical radiograph showed a
generalized widening of the periodontal
ligament space and mild crestal bone loss
on the maxillary lateral incisor (Fig. 2).
The patient’s oral hygiene was found
to be satisfactory; a small amount of
calculus was seen.
A provisional diagnosis of irritational
fibroma was made and an excisional
biopsy was planned after thorough
hematological investigations (all of
which were within normal range) were
conducted. After informed consent
was obtained from the patient, the
lesion was excised under local anaesthesia and sent for histopathological
examination (Fig. 3).
Microscopic examination of an H&Estained section showed proliferative
orthokeratinized and parakeratinized
stratified squamous epithelium. In some
places, epithelium showed short broad
or flat rete ridges. Underlying connective tissue stroma was dense fibrocellular
tissue interspersed with fibroblasts; in
addition, many multinucleated giant
cells were seen scattered throughout
the stroma (Fig. 4 and 5). Stroma also
showed irregular trabeculae of vital bone.
The tissue was adequately vascular with
small to large dilated single endothelially
lined blood vessels with intravasated red
blood cells. Hemorrhagic areas were also
seen. Dense, diffuse, chronic inflammatory infiltrate (consisting primarily of
lymphocytes and plasma cells) was also
visible (Fig. 6). Based on these findings,
PGCG was diagnosed.
Fig. 2. A periapical radiograph of the area, revealing
mild crestal bone loss.
Fig. 3. An excisional biopsy of the lesion.
General Dentistry
www.agd.org
Fig. 4. Histopathological view of the epithelium
showing short broad or flat rete ridges. Underlying
connective tissue stroma is dense (H&E stain;
original magnification 10X).
Fig. 5. A histopathological view of the lesion,
revealing multinucleated cells throughout the
stroma. (H&E stain; original magnification 40X).
At a follow-up visit 7 days after surgery,
the patient demonstrated a satisfactory
healing response. A 6-week follow-up
showed no recurrence of lesion (Fig. 7).
The patient was previously informed that
excising the lesion could result in root
exposure, which would require additional
corrective periodontal plastic surgical procedure; the patient declined the procedure
for personal reasons.
hypophosphatemic rickets (that is, subclinical hyperparathyroidism) are also at an
increased risk of developing PGCG.8-10
A 1995 review by Stratakis et al concluded that women had a slightly higher
prevalence of PGCG, and patients between
fourth and sixth decades were more prone
to the development of PGCG.9 Lesions
have been found more frequently in the
mandible than in the maxilla, and usually
between the first permanent molar and the
incisors; however, even though the lesion
in this case appeared between the first
permanent molar and the incisors, it was
found in the maxilla.2,5
Florid granulation tissue is one of the
primary histopathological features of
PGCG. The lesions also are characterized by the presence of a non-capsulated,
highly cellular mass with abundant
multinucleated giant cells, inflammatory
cells, interstitial hemorrhage, hemosiderin
deposits, and mature bone or osteoid. A
varying number of chronic inflammatory
cells and neutrophils usually are present in
underlying ulcerated areas; however, the
abundance of multinucleated giant cells are
the main feature that differentiates PGCG
from other reactive lesions.2,11-14 All of these
features were observed during the histopathological examination of this lesion.
Radiographic evaluation is prudent
to determine the extent and origin of a
lesion. Superficial resorption or cupping
of alveolar bone is seen frequently in
radiographs. A widened periodontal ligament space may represent extrusion of the
lesion around the root.10 In the present
Discussion
PGCG is an exophytic lesion that begins in
the gingiva and alveolar ridge; it is believed
to originate from the gingival connective
tissue or the periosteum of the alveolar
ridge.2-4 PGCG is not a neoplasm but rather
a reactive lesion caused by local irritation.
Though the etiology of PGCG is unclear,
many hypotheses have been proposed.
Some studies have suggested that a history
of trauma is responsible for the development of PGCG.5-7 According to Shields,
the proliferation of giant cells associated
with the resorption of primary teeth
may be involved in the development of
PGCG, which explains how these lesions
occur in children but does not explain
how they appear in edentulous patients.2,4
Other factors that have been implicated
as predisposing factors in giant cell lesions
include hormonal disturbances, primary
and secondary hyperparathyroidism (that
is, secondary to chronic renal disease),
irritation due to dental restorations or
ill-fitting dentures, tooth extractions,
orthodontic therapy, plaque, and calculus.2,3,7 In addition, children with X-linked
www.agd.org
Fig. 6. Histopathological view showing the dense,
diffuse, chronic inflammatory infiltrate (consisting
primarily of lymphocytes and plasma cells) (H&E
stain; original magnification 10X).
Fig. 7. An anterior view of the patient’s
mouth 6 weeks postoperatively.
case, mild crestal bone loss in the maxillary
lateral incisor and generalized widening of
periodontal ligament spaces were observed.
Giant cells are multinucleated cells.
The origin of giant cells is still not clear,
but these cells may represent a reaction to
unknown stimuli.2 Some authors believe
that multinucleated giant cells originate
from osteoclasts while others believe they
derive from macrophages.13,14
There is a growing body of opinion that
giant cells are derived from bone marrow
mononuclear cells and reach the site via
bloodstream.15 They represent a reactionary response to unknown stimuli from
stroma.16 These concepts on the origins
of giant cells are based on the results of
various studies using cell culture and
transplantation in which giant cells have
been found to be short-lived and disappear
early in the culture in contrast to active
proliferation of stromal cells.15
A 1995 study by Lim & Gibbins confirmed that the multinucleated giant cells
reacted strongly to a monoclonal antibody
General Dentistry
January/February 2013
e13
Case Presentations Peripheral giant cell granuloma: a case report
(MB1), which reacts with lymphocytes
and a proportion of T cells and monocytes.17 The MB1 antibody is expressed by
osteoclasts in fetal bone. Although PGCG
lesions appear to be extremely vascular, the
re-expression of the blood vessels in the
lesion (for the widely used endothelial cell
marker factor VIII-related antigen) failed
to demonstrate the presence of blood
vessels anywhere but on the periphery of
the lesion. A 1998 study by Pammer et
al showed an increased expression of two
apoptotic proteins (bak and bax) in osteoclasts such as giant cells, which supports
the theory that giant cells are reactive and
not neoplastic.18
A 1990 study by Bonetti et al showed
that giant cells did not react to antibodies
with myelomonocytic and macrophage
markers (including lysozyme, Mac 387,
and HAM 56), while they showed strong
immunoreactivity with antibodies directed
to osteoclast surface markers.19 More
recently, Liu et al concluded that receptor activator NF-kb ligand (RANKL),
osteoprotegerin (OPG), and RANK may
be involved in osteoclastogenesis.20 Willing
et al concluded in their 2001 study that
monocyte chemoattractant protein-1
(MCP-1), osteoclast differentiation
factor (ODF), and macrophage-colony
stimulating factor (M-CSF) are monocyte
chemoattractants that are essential for
osteoclast differentiation.21 These molecules
stimulate blood monocyte immigration
into tissue and enhance their fusion into
osteoclast-like multinucleated giant cells.
Disintegrin and metalloproteinase may
play a role in the multinucleation of mononuclear precursor cells into osteoclasts and
macrophage-derived giant cells.22 Woven
bone and lamellar bone are found routinely in PGCG, which can be attributed
to proliferative osteoblasts or osteoprogenitor cells developing in response to intense
irritation of the periosteum. Mineralized
tissue has also been reported.3,9
Most lesions respond well to surgical
excision and the elimination of local
irritating factors, with a recurrence rate of
e14
January/February 2013
approximately 10% that can be attributed
mainly to failure to eliminate all local factors.9 In the present case, a residual recession of 3 mm was found near the maxillary
left canine and lateral incisor, which could
be treated by root coverage procedures.
PGCG can be differentially diagnosed
from pyogenic granuloma, parulis, peripheral ossifying fibroma, and hemangioma on
the basis of histopathological examination.
Conclusion
Although PGCGs are benign, they can be
locally aggressive. In case of isolated gingival enlargement, histopathological investigation is compulsory to confirm clinical
diagnosis. Surgical excision and planned
recall are the keys to proper management.
Author information
Dr. R. Banthia is a professor, Department
of Periodontics, Modern Dental College
& Research Centre, Indore, Madhya
Pradesh, India. Dr. Maheshwari is at
Total Dental Care, Hastings, East Sussex,
United Kingdom, where Dr. Mantri is an
associate dentist. Dr. P. Banthia is professor and head, Department of Periodontics,
Inderprastha Dental College, Ghaziabad,
Ultar Pradesh, India.
References
1.Subarnbhesaj A. Peripheral giant cell granuloma: a
case report and review literature. Kerala Dent J. 2005;
8(2):125-130.
2.Sahingur ES, Cohen RE, Aguirre A. Esthetic management of peripheral giant cell granuloma. J Periodontol.
2004;75(3):487-492.
3. Dayan D, Buchner, Spirer S. Bone formation in peripheral giant cell granuloma. J Periodontol. 1990;61(7):
444-446.
4.Shields JA. Peripheral giant cell granuloma: a review.
J Irish Dent Assoc. 1994;40(2):39-41.
5. Katsikeris N, Kakarantza-Angelopoulou E, Angelopoulos AP. Peripheral giant cell granuloma. Clinicopathologic study of 224 new cases and review of 956
reported cases. Int J Oral Maxillofac Surg. 1988;17(2):
94-99.
6.Shadman N, Ebrahimi SF, Jafari S, Eslami M. Peripheral
giant cell granuloma: a review of 123 cases. Dent Res
J (Isfahan). 2009;6(1):47-50.
7.Etoz OA, Demirbas AE, Bulbul M, Ebru A. The peripheral giant cell granuloma in edentulous patients: report
of three unique cases. Eur J Dent. 2010;4(3):329-333.
General Dentistry
www.agd.org
8. Flaitz CM. Peripheral giant cell granuloma: a potentially aggressive lesion in children. Pediatr Dent. 2000;
22(3):232-233.
9.Stratakis CA, Mitsiades NS, Sun D, Chrousos GP,
O’Connell A. Recurring oral giant cell lesion in a child
with X-linked hypophosphatemic rickets: clinical manifestation of occult parathyroidism? J Pediatr. 1995;
127(3):444-446.
10. Pandolphi PJ, Felefli S, Flaitz CM, Johnson JV. An aggressive peripheral giant cell granuloma in a child.
J Clin Pediatr Dent. 1999;23(4):353-355.
11. Falaschini S, Ciavarella D, Mazzanti R, et al. Peripheral
giant cell granuloma: immunohistochemical analysis of
different markers. Study of three cases. Av Odontoestomatol. 2007;23(4):189-196.
12.Adlakha VK, Chandna P, Rehani U, Rana V, Malik P.
Peripheral giant cell granuloma. J Indian Soc Pedod
Prev Dent. 2010;28(4):293-296.
13. Flanagan AM, Nui B, Tinkler SM, Horton MA, Williams
DM, Chambers TJ. The multinucleate cells in giant cell
granulomas of the jaw are osteoclasts. Cancer. 1988;
62(6):1139-1145.
14.Regezi JA, Zarbo RJ, Lloyd RV. Muramidase, alpha-1
antitrypsin, alpha-1 antichymotrypsin, and S-100 protein immunoreactivity in giant cell lesions. Cancer.
1987;59(1):64-68.
15. el-Mofty SK, Osdoby P. Growth behaviour and lineage
of isolated and cultured cells derived from giant cell
granuloma of the mandible. J Oral Pathol. 1985;14(7):
539-552.
16.Cohen MA, Grossman ES, Thompson SH. Features of
central giant cell granuloma of the jaws xenografted
in nude mice. Oral Surg Oral Med Oral Pathol. 1988;
66(2):209-217.
17.Lim L, Gibbins JR. Immunohistochemical and structural
evidence of a modified microvasculature in the giant
cell granuloma of the jaws. Oral Surg Oral Med Oral
Pathol. 1995;79(2):190-198.
18. Pammer J, Weninger W, Hulla H, Mazal P, Horvat R.
Expression of regulatory apoptotic proteins in peripheral giant cell granulomas and lesion containing osteoclast-like giant cells. J Oral Pathol Med. 1998;27(6):
267-271.
19. Bonetti F, Pelosi G, Martignoni G, et al. Peripheral giant cell granuloma: evidence for osteoclastic diferrentiation. Oral Surg Oral Med Oral Pathol. 1990;70(4):
471-475.
20.Liu B, Yu SF, Li TJ. Multinucleated giant cells in various
forms of giant cell containing lesions of the jaws express features of osteoclasts. J Oral Pathol Med. 2003;
32(6):367-375.
21.Willing M, Engels C, Jesse N, Werner M, Delling G, Kaiser E. The nature of giant cell tumor of bone. J Cancer
Res Clin Oncol. 2001;127(6):467-474.
22.Abe E, Mocharla H, Yamate T, Taguchi Y. Monolages
SC. Meltrin-alpha, a fusion protein involved in multinucleated giant cell and osteoclast formation. Calcif
Tissue Int. 1999;64(6):508-515.

Similar documents