Academy of General Dentistry

Transcription

Peer-Reviewed Journal of the Academy of General Dentistry
GENERAL
DENTISTRY
January/February 2015 ~ Volume 63 Number 1
FORENSIC DENTISTRY n MICROBIOLOGY
FIXED REMOVABLE HYBRID PROSTHESIS
DIAGNOSIS AND TREATMENT PLANNING
DENTAL MATERIALS n WWW.AGD.ORG
Contents
Departments
6Editorial Top traits
7 To the editor Outdated
information?
10 Restorative Dentistry
The crown to implant ratio in
fixed prosthodontics
14 Endodontics Achieving and
maintaining apical patency in
endodontics: optimizing canal
shaping procedures
80 Answers Self-Instruction exercises
No. 343, 344, and 345
Clinical articles
16 Diagnosis and Treatment
Planning Why the general dentist
needs to know how to manage
oral lichen planus
Stephanie M. Price, DDS
Valerie A. Murrah, DMD, MS
SELF -INSTRUCTION
Continuing Dental
Education (CDE)
Opportunities
Earn 2 hours of CDE
credit by signing up
for and completing the
SELF-INSTRUCTION exercises
based on various subjects.
23 Microbiology Investigation
of antibacterial efficacy of
Acacia nilotica against salivary
mutans streptococci: a randomized
control trial
Devanand Gupta, BDS, MDS
Rajendra Kumar Gupta, PhD
28 Self-Instruction Exercise No. 361
Roger A. Solow, DDS
Please visit www.agd.org/
gdindex to peruse
our Index of Articles.
Arranged by topic,
this index provides a
comprehensive list of
articles published on a
particular topic in past
issues and includes
PubMed citation
information.
48 Anesthesia and Pain Control
Local anesthetic calculations:
avoiding trouble with pediatric
patients
Mana Saraghi, DMD
Paul A. Moore, DMD, PhD, MPH
Elliot V. Hersh, DMD, MS, PhD
54 Forensic Dentistry The role of the
dentist in identifying missing and
unidentified persons
Amber D. Riley, RDH, MS
30 Diagnosis and Treatment
Planning Clinical considerations
for selecting implant abutments
for fixed prosthodontics
General Dentistry
Index of Articles
available online.
SELF -INSTRUCTION
37 Dental Materials Surgical repair
of invasive cervical root resorption
with calcium enriched mixture
cement: a case report
Saeed Asgary, DDS, MS
Mahta Fazlyab, DDS, MS
41 Office Design Evaluation of
3 dental unit waterline
contamination testing methods
Nuala Porteous, BDS, MPH
Yuyu Sun, PhD
John Schoolfield, MS
58 Non-Surgical Endodontics
Nonsurgical endodontic treatment
of permanent maxillary incisors
with immature apex and a large
periapical lesion: a case report
Gautam P. Badole, MDS
M.M. Warhadpande, MDS
Rakesh N. Bahadure, MDS
Shital G. Badole, BDS
SELF -INSTRUCTION
61 Fixed Removable Hybrid
Prosthesis Stress analysis of
mandibular implant-retained
overdenture with independent
attachment system: effect of
restoration space and attachment
height
Behnaz Ebadian, DDS, MSc
Saeid Talebi, MSc
Niloufar Khodaeian, DDS, MSc
Mahmoud Farzin, PhD
www.agd.org
General Dentistry
January/February 2015
1
69 Oral Medicine, Oral Diagnosis,
Oral Pathology p53 expression
in oral lichenoid lesions and oral
lichen planus
A. Arreaza, MSc
H. Rivera, MSc
M. Correnti, PhD
73 Dental Materials Effect of imaging
powders on the bond strength of
resin cement
Christopher R. Jordan, DMD, MS
Clifton W. Bailey, DDS
Deborah L. Ashcraft-Olmscheid, DMD, MS
Kraig S. Vandewalle, DDS, MS
78 Implant Maintenance Crestal
approach for removing a migrated
dental implant from the maxillary
sinus: a case report
Raid Sadda, DDS, MS, MFDRCSI
e1 Cancer Screening Ameloblastic
carcinoma of the mandible
manifesting as an infected
odontogenic cyst
Adepitan A. Owosho, BChD
Anitha Potluri, DMD
Richard E. Bauer III, DMD, MD
Elizabeth A. Bilodeau, DMD, MD, MSEd
e5 Surgical Orthodontics A large
dentigerous cyst treated with
decompression and orthosurgical
traction: a case report
Rodrigo Dias Nascimento, PhD
Fernando Vagner Raldi, PhD
Michelle Bianchi de Moraes, PhD
Paula Elaine Cardoso, PhD
Deborah Holleben, DDS
Instructions for
Authors
For information on
submitting a manuscript
for publication in General
Dentistry, please visit
www.agd.org/gdauthorinfo.
2
General Dentistry
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e9 Dental Materials Impact of
toothbrushing with a dentifrice
containing calcium peroxide on
enamel color and roughness
Diala Aretha de Sousa Feitosa, DDS, MSc
Boniek Castillo Dutra Borges, PhD
Fabio Henrique de Sa Leitao Pinheiro, PhD
Rosangela Marques Duarte, PhD
Renato Evangelista de Araujo, PhD
Rodivan Braz, PhD
Maria do Carmo Moreira da Silva Santos, PhD
Marcos Antonio Japiassu Resende Montes, PhD
e12 Obturation Techniques Apical
plug technique in a calcified
immature tooth: a case report
Kumar Raghav Gujjar, MDS
Ratika Sharma, MDS
Amith H. V., MDS
Smitha Amith, MDS
Indushekar K. R., MDS
e16 Diagnosis and Treatment
Planning Central giant cell lesion:
diagnosis to rehabilitation
Ana Carolina Amorim Pellicioli, DDS
Thieni Kaefer, DDS
Marco Antonio Trevizani Martins, DDS, PhD
Vinicius Coelho Carrard, DDS, PhD
Manoela Domingues Martins, DDS, PhD
Planning Alveolar ridge splitting for
implant placement: a review of the
procedure and report of 3 cases
Prakash S. Talreja, MDS
Chandrashekhar R. Suvarna, BDS
Preeti P. Talreja, MDS
Advisory Board
For Advisory Board members’
biographies, visit www.agd.org/
gdadvisoryboard.
Dental Materials
Howard S. Glazer, DDS, FAGD
e24 Prosthodontics/Removable
Management of severe mandibular
deviation following partial
mandibular resection: a case report
Planning Atypical presentation of
salivary mucocele: diagnosis and
management
Husain Harianawala, BDS, MDS
Mohit Kheur, BDS, MDS
Supriya Kheur, BDS, MDS
Jay Matani, BDS, MDS
Kumar Nilesh, MDS
Jagadish Chandra, MDS
Dental Public Health
Larry Williams, DDS, ABGD, MAGD
Esthetic Dentistry
Wynn H. Okuda, DMD
Endodontics
Gerald N. Glickman, MS, DDS,
MBA, JD
e28 Diagnosis of Oral Pathology Rare
oral cartilaginous choristoma: a case
report and review of the literature
Marina Lara de Carli, DDS, PhD
Felipe Fornias Sperandio, DDS, PhD
Fernanda Rafaelly de Oliveira Pedreira, DDS
Alessandro Antonio Costa Pereira, DDS, PhD
Joao Adolfo Costa Hanemann, DDS, PhD
Geriatric Dentistry
Eric Zane Shapira, DDS, MAGD,
MA, MHAv
Implantology
Wesley Blakeslee, DMD, FAGD
Oral and Maxillofacial
Pathology
John Svirsky, DDS, MEd
Oral and Maxillofacial
Radiology
Dale A. Miles, BA, DDS, MS,
FRCD(C)
Coming next issue
In the March/April issue of General Dentistry
• Comparison of the effectiveness of Endo-eze, Navitip, and
Navitip FX irrigation devices in the cleansing of root canal
walls instrumented with oscillatory and rotary techniques
• Surface characteristics of resin composite materials after
finishing and polishing
• The effect of specially designed and managed occlusal
devices on patient symptoms and pain: a cohort study
Oral and Maxillofacial Surgery
Karl Koerner, DDS, FAGD
Orthodontics
Yosh Jefferson, DMD, FAGD
Pain Management
Henry A. Gremillion, DDS, MAGD
Pediatrics
Jane Soxman, DDS
Periodontics
Samuel B. Low, DDS, MS, MEd
Pharmacology
Thomas Viola, RPh, CCP
Practice Management
Mert N. Aksu, DDS, JD, MHSA, FAGD
Prosthodontics
Joseph Massad, DDS
Jack Piermatti, DMD
4
General Dentistry
www.agd.org
In the February issue
of AGD Impact
• Career transitions for
dental students and
new dentists
• Treating bruxism
General Dentistry
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General Dentistry. All rights reserved.
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Your voice for excellence
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AGD Lead Corporate Sponsor
Editor
Roger D. Winland, DDS, MS, MAGD
AGD Corporate Sponsors
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General Dentistry
5
Editorial
Top traits
A
s a dentist, you studied hard
in dental school, and you now
continue learning through
advanced certification and CE
classes, as well as by reading articles
in General Dentistry. You are a
seasoned and trusted dentist at the
top of your profession with years of
experience. But how will you stay
there? Perhaps the following traits—
which I have observed in dentists I
respect—will help guide you as you
navigate the coming years.
new things, ultimately figuring out what works best for your
patients. An anonymous sage once said, “Getting something
done is an accomplishment; getting something done right
is an achievement.”
Modesty
Positive attitude
Great dentists maintain a positive attitude and avoid slipping into
negativity. Maintaining a positive outlook, even when confronted
with difficult situations, is a start on the road to success. A negative outlook will severely diminish your opportunities.
Tenacity
Tenacity is a trait worth developing. Little is ever accomplished
with just one letter, e-mail, telephone call, request, or CE course.
There is a slogan in the safety industry that “Triumph is just an
umph added to try.”1 In my experience, the most successful dentists embody a tenacious spirit. They are undaunted by adversity
and frequently persist with their goals long after others might
have given up. It is this trait that tends to propel practitioners
into professional successes.
Honesty
Always practice honesty in your practice, as carelessness with facts
can destroy your credibility. Some patients present at our practices
after having experienced dishonesty with medical or dental providers. Many have found that promises made by so-called professionals
did not live up to their expectations. To avoid disappointing your
patients, always carefully discuss with them their diagnoses and all
available treatment options, including the costs and possible outcomes of each treatment. Dentists who run honest practices tend
to have happier patients. Happy patients return for many years,
which is always the objective in running a successful practice.
Innovation
Patients like to sense that their dentist is breaking ground with
new technology that they have personally researched or possibly originated. Are you the type of dentist who is stuck in old
ways of doing things? Do you refuse to explore new technology, even when it has proven successful? Successful dentists
have a way of finding new ways of doing things even as they
continue to maximize proven techniques. Be open to trying
6
General Dentistry
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Another good trait to develop is professional modesty. It is more
rewarding to have your patients and staff recognize your abilities
than to point them out yourself. While psychologists have longconsidered self-esteem an essential element of a healthy personality, this is not achieved by self-promotion.2 Train your staff to take
pride in their work and in every successful outcome and interaction with patients, but be careful not to constantly pat yourselves
on the back about a job well done. Doing so may detract from the
cultivation of new skills and potentially lead to missteps. Traits
of successful dentists include both professional excellence and a
healthy dose of modesty—even when everything is going well.
Style
Your style is not about your clothes, but about who you are as a
dentist in your clothes. Whether you are an introvert or an extravert by nature, try to develop a loving, caring, professional style to
complement your interactions with your staff and patients.
Loyalty
Develop downward loyalty. Great dentists protect their staff and
provide the training and attention needed to develop a good
rapport. Along the way, your staff will appreciate your straightforwardness and support that is simple and direct. A cohesive staff is
bound by this loyalty, and the power of this trait is evident to all
who enter your practice.
Will Rogers once said that “The road to success is dotted with
many tempting parking places.” As you move forward in your
experience as a dentist, you will inevitably be met with challenges.
However, continuously adapting the traits mentioned above will
help secure your success for many years to come.
Roger D. Winland, DDS, MS, MAGD
Editor
References
1. SAFTENG.net. Safety Slogans. Available at: http://www.safteng.net/index.php?option=
com_content&view=article&id=2702&Itemid=178. Accessed November 13, 2014.
2. About Education. What is Self-Esteem? Available at: http://psychology.about.com/od/
sindex/f/what-is-self-esteem.htm. Accessed November 13, 2014.
To the editor
Outdated information?
I
have just completed reading the November/December 2014
issue of General Dentistry, which I look forward to every
month as a benefit of my AGD membership over the last
10 years. Unfortunately, you have chosen to publish an article
(“Perspective of cardiologists on the continuation or discontinuation of antiplatelet therapy before dental treatment: a
questionnaire-based study,” pp. 64-68) with so many egregious
fallacies and outdated information, that under advisement from
the Editor, Dr. Roger Winland, I have put the proverbial pen
to paper. For full disclosure, I have been a licensed pharmacist
for 24 years and hold a specialty in dental pharmacology. I am
a reviewer for a number of peer-reviewed journals (including
General Dentistry), am on the Editorial Board for the Journal of
the American Dental Association, and have numerous publications in the peer reviewed literature including book chapters. I
teach, perform original research, and am on faculty at 2 universities which include the Oregon Health & Sciences University
in Portland, where I am the only non-dentist in the Faculty of
Dentistry.
While I typically applaud original research, this article is far
below the standards of General Dentistry and the conclusions
reported may not be in support of the current standard of care or
published guidelines and could in fact result in patient harm. I
cannot believe that through the usually rigorous editorial process,
this manuscript was allowed to make it to print, and from the
outset, I may even suggest that the Editor consider a possible
retraction. I have included just a few of my comments in the
highlighted sections of the attached document. I will try to be
succinct in my concerns.
References
This article has 49 references of which 42 are over 5 years
old. Four of the remaining 7 references refer to website
addresses on the internet, 1 reference (No. 9) cites an entire
textbook (Sweetman SC, ed. Martindale: The Complete Drug
Reference. 34th ed. London: Pharmaceutical Press; 2013),
and the remaining 2 articles were published in 2009 and are
based on 2008 data (again more than 5 years old). Many of
the citations refer to articles published in journals which are
not listed in the Index Medicus (such as The Journal of Indian
Society of Periodontology).
Abstract
The abstract does NOT accurately reflect the title and, therefore, purpose of the article, which immediately gave me pause.
“Perspective of cardiologists on the continuation or discontinuation
of antiplatelet therapy before dental treatment: a questionnairebased study” is very different than what the Abstract reports as,
“a survey of 50 cardiologists was conducted regarding suggested
guidelines for dentists in the management of patients who are
taking anticoagulant medication.” Antiplatelet medications
and anticoagulant medications are NOT the same drug class.
This type of disinformation will do nothing to add clarity to the
already confusing topic of medically complex patients and their
management in the dental realm. I cannot emphasize enough that
the rest of the article continues the theme of using these terms
interchangeably and worse, makes recommendations on how to
manage these patients based on VERY OUTDATED information—something that I see as a patient safety issue.
Main article
The authors miss an important opportunity to clearly define the
issue and offer a review of the recent literature in order to help
guide modern dental practice. The 4 drugs mentioned in the very
first paragraph (aspirin, clopidogrel, dipyridamole, and warfarin)
comprise an incomplete and outdated list of both anticoagulant
and antiplatelet medications, but nowhere in this article is any reference made to the more common and currently used medications:
prasugrel and ticagrelor (antiplatelet agents) and rivaroxaban, dabigatran, apixaban, vorapaxar, and edoxaban (anticoagulant agents).
Many recommendations are cited, such as the American College
of Chest Physicians in 2006, even though this does not appear as
a referenced citation, and this 2006 reference does NOT represent
the most recent guidelines supported by the American College
of Chest Physicians Evidence-Based Clinical Practice Guidelines.
These types of statements are rampant throughout the text and
in almost every case refer to outdated information: “…with
increasing concern over the thromboembolic risk, this is no longer
recommended.7 ” (Jaya Kumar A, Kumari MM, Arora N, Haritha
A. Is anti-platelet therapy interruption a real clinical issue? Its
implications in dentistry and particularly in periodontics. J Ind
Soc Periodontol. 2009;13(3):121-125.)
To further add to the confusion and misinformation, the middle
section on monitoring and blood tests has very little to do with
antiplatelet therapy (on which this study focused), and everything
to with anticoagulant treatment. It is therefore possible that oral
healthcare professionals, based on this article, will begin to use
INR measurements to gauge a patients’ antiplatelet capacity which
is NOT recommended. Furthermore, statements such as, “An
INR is advised for all patients on warfarin or heparin therapy,31”
are entirely incorrect, misleading, and NOT even supported by
the reference that is cited (No. 31). INR is not a measurement of
heparin efficacy and SHOULD NOT be ordered. The appropriate
test is a PTT. The article also states that, “before dental therapy,
patients with antiplatelet regimens should have bleeding time,
clotting time, ECG, routine investigations, blood sugar level, and
blood pressure tests.” This is definitely not the type of information we should encourage general practitioners to follow.
My intention is certainly not to rewrite this manuscript nor
point out every error of fact, but I will close with just a few additional conclusions the authors suggest:
• “If a patient is on a dual therapy of aspirin and clopidogrel, it
is recommended that the dental procedure be performed in a
hospital setting.”
www.agd.org
General Dentistry
7
• “Thomason et al reported severe bleeding following a gingivectomy
in a patient taking 150 mg aspirin qd, which was resolved by
platelet transfusion.27” This was a single case published in 1999.
• “Shalom & Wong concluded that cutaneous bleeding tests
should not be used to estimate the hemorrhagic risk in patients
on anticoagulant therapy.36 ” This was not their conclusion
and this study in plastic surgery cases from 2003 looked at
aspirin (an antiplatelet agent, NOT an anticoagulant).
• “Oral surgical procedures must be done at the beginning of
the day, as it allows more time to deal with any bleeding episode.41 ” Reference is from 2002.
• “Patients with the following medical problems taking antiplatelet medications should not be treated in primary care
without medical advice or should be referred to a hospitalbased dental clinic: liver impairment and/or alcoholism; renal
failure; hemostasis disorders; and patients currently receiving
cytotoxic medication or dual antiplatelet therapy.”
• “Medical consent is mandatory in cardiac patients taking
antiplatelet therapy.”
These few statements alone, if followed, may limit many of our
medically complex patients with oral pathologies from getting the
oral healthcare they require. My phone has not stopped ringing
with concerned dental colleagues and AGD members who are
confused by this recent publication.
I look forward to hearing from you on this matter.
Mark Donaldson, BSP, RPH, PHARMD, FASHP, FACHE
Kalispell, Montana
(with enclosures)
Response from Dr. Singh et al
At the outset, we must congratulate your journal for having such
an enlightened and knowledgeable readership. We appreciate the
points raised by our pharmacist friend as we genuinely believe
that healthy criticism is a sure shot way forward towards academic
growth. In fact, our rigorous preparation to answer the various
queries raised by the reader has improved our understanding of
the subject manifold. We would like to thank you for sharing the
concerns of the reader and for providing us with an opportunity
to respond to each one of them.
Antiplatelet and anticoagulant medications
We agree with the reader’s view that antiplatelet and anticoagulant medications are NOT the same drug class. In our
questionnaire, the questions were targeted at antiplatelet agents
only. However, the responses given by the cardiologists were not
regarding patients on antiplatelet therapy alone. They pointed
toward a growing number of patients on combined antiplatelet
and anticoagulant therapy. INR has been added when cardiologists mentioned its use in patients under anticoagulant therapy.
To maintain the transparency and authenticity of the survey,
we mentioned both the terms in our Discussion. In fact, our
Abstract begins with these terms. However, a typographical
error in the last line of the Abstract fails to mention antiplatelet
medication also. [Editor’s note: the typographical error was made
8
General Dentistry
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by the authors]. We deeply regret this error. The title does not
mention the term anticoagulant therapy, as our survey focused
on antiplatelet therapy, as reflected by our questionnaire.
Incomplete and outdated information
The reader claims that we provided an incomplete and outdated
list of antiplatelet and anticoagulant medications with no mention of more common and currently used medications.
We must EMPHASIZE that the drugs mentioned by us were
based on the responses of practicing cardiologists regarding drugs
most frequently used in Indore, India. No leading questions were
put forth, and no bias was incorporated by the authors.
Standard of care varies temporally and
geographically
We have focused on drugs most frequently used in our geographic
location. The newer drugs mentioned by our esteemed reader
were not frequently used in Indore, India at the time of submission of our article. After receiving the letter from our reader, we
extensively researched these drugs and found that many of them
are highly potent medications. However, we feel that discussion
about the merits of usage of newer drugs and their protocols is
beyond the scope of our article.
Why was INR mentioned in a study focusing
on antiplatelet therapy?
As mentioned earlier, the surveyed cardiologists mentioned the
practice of checking INR when a patient is on anticoagulants. We
have clearly stated that it is a test of coagulation. Earlier in the
same paragraph, we mentioned that there is no suitable test to
assess the increased risk of bleeding in patients taking antiplatelet
therapy; platelet function is normally assessed using the cutaneous
bleeding time test.
Only an ignorant oral health care professional will
start using INR to gauge antiplatelet capacity
The reader claims that we are recommending bleeding time,
clotting time, ECG, routine investigations, blood sugar level,
and blood pressure tests in all patients on antiplatelet regimen
before dental therapy. This however is MISCONSTRUED, as
we were merely reporting the opinions of surveyed cardiologists
when asked for medical consent.
The reader has pointed out that many “conclusions” attributed to us or cited by us are outdated and would limit many
medically complex patients with oral pathologies from getting
requisite oral health care. This could not be further from the
truth as we strongly believe in the idiom, “Discretion is the
better part of valor.”
Nowhere in the article have we recommended not to provide
care to the patient, but have only advised caution and necessary
preparedness for any untoward eventuality (however rare) that can
happen in a surgical procedure. The reader claims that dentists
might be alarmed and therefore refuse cases requiring treatment.
This is a dangerous fallacy. By this account, “Ignorance is bliss.”
There seems to be a difference of perception between the
authors and the reader owing to the difference in healthcare
standards and facilities in the developing and developed
world. Average dental clinics in India are probably not as
equipped to handle emergencies as those in the Western world.
Hence, we would always lean towards caution as opposed to
blind overconfidence.
Medical consent and physician referral
The reader has objected to our statement regarding medical
consent being mandatory for cardiac patients on antiplatelet
therapy. We steadfastly stand by our opinion based on our clinical experience that the medical referral should be mandatory for
cardiac patients on antiplatelet medication. Dental practitioners
lack the clinical acumen of judging cardiac status of patients.
Our opinion is substantiated in a 2012 article by Can et al,
who reported only 30% of the surveyed dentists had knowledge about the consequence of interrupting treatment with
clopidogrel, and only 30% were aware of the high mortality
rates associated with stent thrombosis.1 All of the respondents
were cautious and expressed willingness to consult a cardiologist before interrupting aspirin and/or clopidogrel. None of
the respondents knew the names of new generation antiplatelet
agents such as prasugrel or ticagrelor.
More importantly, the educational awareness and level of
understanding of the patients in our geographic area mandate
extra precautions to prevent any untoward sequelae and medicolegal complications. Many times, patients are noncompliant
with their regimens. We are not depriving patients of dental care
as claimed by our esteemed reader; rather, we are making their
dental management safer.
References
The reader points out that most of the references cited by us are
old and outdated. We would like to share a few facts:
• While this article is based on a study conducted nearly 3 years
ago, the article itself was in the process of publication for
almost 1.5 years.
• Most of the drugs mentioned by our respondents have been
used for a long period of time. Hence, their references are not
as recent as those of the drugs mentioned by our reader.
• Forty of the 49 references cited by us are of the current century, hence they are not archaic as claimed.
• Old data need not need be written off. In fact, we have
seen (as in the case of focal infection theory) old theories
being rejuvenated on account of newer understanding.
Hence we should not demean what is old, but look at it in
a better light.
• Many times, adverse events are not reported in the literature.
Therefore, case report references which have done so need to
be given meritorious consideration. As the idiom states, “One
swallow does not a summer make.”
• The Journal of Indian Society of Periodontology may not be
listed in the Index Medicus. However, it is listed in many other
indices, most notably PubMed.
• Standard textbooks and credible websites are an important
source of information and knowledge for clinicians. Not
all general dental practitioners read journals or articles. The
nuances of web research are mostly developed at the postgraduate level.
Clarifications and addendum
• Some respondents mentioned INR as an investigation when
the patient was on anticoagulant therapy. To avoid the confusion in the minds of readers, we have clearly mentioned that
INR and partial thromboplastin time have been used to evaluate anticoagulant levels.
• Due to a typographical error, lines cited to reference No. 34
have erroneously mentioned ‘antiplatelet’ instead of ‘anticoagulant.’ [Editor’s note: the typographical error was made by the
authors.] We would also like to clarify that a PTT is a test to
evaluate anticoagulant status in patients on heparin, and INR
is to be considered in patients on warfarin.
• In lines cited to reference No. 36, cutaneous bleeding tests
should not be used to estimate the hemorrhagic risk in patients
on antiplatelet therapy. It has been erroneously mentioned as
anticoagulant therapy.
Concluding remarks
We had no intention to confuse or alarm general dental practitioners but only to sensitize them to a controversial topic.
Each specialist or person looks at the same situation from a different perspective. Wisdom lies in accepting these differences in
perception and cultural traits with an open mind. The knowledge
domains of a dental surgeon, a cardiologist, and an eminent pharmacist shall be very different, and we have no qualms in admitting that a pharmacist will have a final word on drugs and their
merits. In the same vein, we would humbly like to profess that
prescribing a drug is a physician’s prerogative, and dental management of patients as well as seeking physician referral and medical
consent comes under the jurisdiction of dental surgeons.
We hope we have been able to clarify our position and satisfactorily answer the queries raised by our esteemed reader. We
wholeheartedly appreciate the concern and efforts on the part of
our reader. We look forward to any further correspondence in this
matter, if required.
Reference
Can MM, Biteker M, Babur G, Ozveren O, Serebruany VL. Knowledge, attitude and perception of antiplatelet therapy among dentists in Central Eastern Turkey. World J Cardiol. 2012;
4(7):226-230.
General Dentistry welcomes correspondence from its readers. You can send letters to General Dentistry Editor, AGD, 560 W. Lake St., 6th Floor, Chicago, IL 60661-6600,
or email us at [email protected]. The editors reserve the right to edit all submissions. We cannot print letters that have been submitted to other publications.
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General Dentistry
9
Restorative Dentistry
The crown to implant ratio in fixed prosthodontics
Roger A. Solow, DDS
P
rior to the advent of osseointegrated implants, a periodontal
prosthesis was the preferred treatment for a patient with
significant periodontal bone loss and altered crown to root
ratios (C/Rs). The C/R is the radiographic amount of tooth out
of alveolar bone compared to the amount within alveolar bone.1
These patients have missing, mobile, or malposed teeth with
open gingival embrasures that pose functional and esthetic problems. Drifted, over-erupted, and flared teeth are repositioned
and then restored with fixed partial prostheses. Splinting the
remaining teeth and creating a therapeutic occlusion improves
force distribution and preserves the compromised teeth.2 This
type of restoration and occlusal adjustment can be used to
decrease mobility in teeth with attachment loss. Additionally,
implant-supported restorations can predictably replace lost teeth
or teeth with a hopeless prognosis.
A dentist may encounter a normal, reduced, or amplified
restorative space when treating these areas; such changes result in
altered crown to implant ratios (C/Is). The C/I is the radiographic
amount of the crown-abutment-implant complex out of alveolar
bone compared to the amount within alveolar bone.3 Altered C/R
and C/I are not equivalent; this is important to understand when
treatment planning for implant-supported restorations. Teeth
undergo a 2-phase displacement on loading as the periodontal
ligament (PDL) is initially compressed prior to engaging the
alveolar bone.4 The PDL creates stress distribution along the root
length as well as a protective neuromuscular response. In contrast,
implants when loaded undergo a 1-phase linear deformation with
stress concentrated at the bone crest without a protective response.
The C/I affects the periodontium for all implant designs:
1-piece implant with a pre-established restorative margin, 2-piece
implant with the implant shoulder as the restorative margin, or
bone-level implant with the restorative margin on the abutment.
This column reviews the clinical considerations of C/I in fixed
prosthodontics. A normal C/I is similar to the C/R for natural
teeth (Fig. 1). The C/R of maxillary and mandibular first premolars have been measured at 0.57 and 0.61, respectively, and for
maxillary and mandibular first molars at 0.63 and 0.54, respectively.5 A 13 mm length tissue-level implant with a typical size
crown would approximate a normal C/R. Although the intent of
implant restoration is to achieve a biomimetic replacement of lost
structure, there is no reason to use the root length as the implant
length, since width is more important than length to minimize
crestal cortical bone stress.6-8
The occlusal design for posterior teeth implant-supported restorations is similar to natural teeth and should allow only vertical
force during closure or chewing excursions.9,10 Contact on closure
should be centered over the implant to maintain vertical force and
minimize shear stress. In mixed tooth and implant restorations,
implants should not contact at the same time or heavier than
teeth on firm closure. The PDL creates an intrusion displacement
10
General Dentistry
on teeth that the implants don’t have. The posterior occlusion
should be refined so that implants receive a delayed initial contact
and a lighter final contact than teeth.11 Implant canine guidance
avoids the increased stress to prosthetic components and supporting bone from group function excursive contacts.12
To prevent force overload at the buccal crestal bone, it is crucial that anterior implant-supported restorations do not contact
heavier than adjacent teeth during closure. Any loss of bone may
create gingival recession with abutment exposure or asymmetric
levels of the gingival margins. This region typically has minimal
bone thickness and is often augmented prior to or at implant
placement. The dentist should place a gloved fingernail on the
facial surface of the crown to detect heavy contact on firm or light
closure. Lateral and protrusive excursion contacts should be on the
strongest anterior tooth or implant to separate the posterior teeth.
In cases of anticipated excess force, such as patients with a history
of bruxism and attrition, multiple anterior teeth can contact in
concert during the excursion to distribute the force over a greater
surface area. A reduced C/I typically occurs when there is minimal
interocclusal space due to over-eruption of the opposing tooth,
or severe attrition with compensatory eruption of many teeth
(Fig. 2 and 3). Most posterior teeth have a crown height of 7.08.5 mm.5 A reduced restorative space could be defined as <5 mm,
where the dentist does not have a choice to use either cement or
screw retention but is restricted to using screw retention. Cemented
restorations need 5 mm space, consisting of 2 mm for material and
3 mm for minimal abutment height to resist dislodgement.
Treatment planning for a reduced C/I involves evaluating the
esthetics and functional occlusion to determine the patient’s
most appropriate procedure. Alternatives include occlusal adjustment of the opposing tooth, restoration of the opposing tooth
Fig. 1. Normal crown to implant ratio (C/I). The gold crown was placed at the
gingival margin similar to the adjacent gold crowns on natural teeth.
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Fig. 2. Reduced C/I indicating the need for a screw-retained crown. The
distance from the implant platform to the opposing tooth is 4 mm.
Fig. 3. Screw-retained gold crown with intracrevicular margins for predictable
cement clearance. Note the crown height compared to the adjacent tooth.
Fig. 4. Tissue-level implant placed subcrestal near the adjacent tooth apex.
The surgeon achieved bicortical engagement and stability but compromised
vertical position.
Fig. 5. Ten-year soft tissue reaction to excellent patient hygiene. The distal
papilla of tooth No. 5 was lost due to the absence of bone on the mesial of
tooth No. 4.
with occlusal reduction to compensate for the over-eruption,
orthodontic intrusion with temporary anchorage devices, and
segmented osteotomy with repositioning. The restorative dentist
always needs 2 measurements from the surgeon for the implant
restoration treatment plan: sulcus depth and restorative space.
Sulcus depth (gingival margin to implant shoulder) determines
the abutment collar dimension. Restorative space (gingival margin
to the opposing cusp) determines whether a screw-retained crown
or an abutment with cemented crown are indicated. The surgeon
can use a periodontal probe and communicate these measurements at the implant integration verification appointment. The
restorative dentist can then plan for a screw-retained crown with
provisional abutment or order the appropriate definitive abutment, precluding the need to maintain a large inventory of prosthetic components. An amplified C/I may result from lost bone
from periodontal destruction or trauma, failed osseous grafting,
or submerged implant placement. The surgeon should place the
implant to avoid problems in the vertical axis that compromise
oral hygiene and papilla support (Fig. 4 and 5). However, deep
placement may be needed to engage bone, or reducing gingival
height may create an esthetic problem. A deep implant platform
requires a stock mesostructure or a custom abutment to avoid a
restoration margin >1 mm subgingival with unpredictable cement
clearance. Alternatively, a screw-retained crown can be used.
A titanium stock mesostructure or titanium custom abutment
would provide better soft tissue adhesion than porcelain or gold.13
C/I problems also occur in concert with porous posterior bone
and increased forces on molar sites. This is especially true with
maxillary sinus grafting cases, where pneumatized sinuses and minimal native bone further challenge the dentist to manage occlusal
force (Fig. 6 and 7). The increased height of restorative material
above the implant platform creates a vertical cantilever that magnifies torque stresses on the crestal bone from lateral loading. Also,
the lost posterior bone resorbs preferentially from the buccal side,
creating a horizontal cantilever in the restoration. It is critical to
remove all excursive interferences so force is aligned with the long
axis of the implant. The increased restorative space and a short
implant (<10 mm), dictated by a limited amount of available bone,
synergistically increase the C/I. Amplified C/I >2.0 are well-tolerated and again show how implant-supported restorations differ
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General Dentistry
11
Fig. 6. Multiple parallel implants with stock abutment at site
No. 11 and custom abutments at sites No. 12-14. Note the
amplified restorative space of the posterior implants.
from natural teeth with compromised bone support in the periodontal prosthesis paradigm. Short implants may allow implant
placement in nongrafted atrophic ridges and avoid invasion of the
maxillary sinus, mandibular canal, or angled adjacent roots. Short
implants have been shown to be as successful as standard length
implants (>10 mm).14-16 Studies on short, single implants with
amplified C/I showed no increased marginal bone loss compared
to normal C/I.17-20 Studies on multiple short implants supporting a fixed prosthesis also found no effect of increased in C/I on
marginal bone loss.21,22 Two systematic reviews concluded that
amplified C/I resulted in less marginal bone loss than lower C/I.3,23
This result is contrary to the assumption that greater anchorage is
beneficial to stability and force distribution, and should result in
less harmful stress to crestal bone. Blanes attributed the improved
marginal bone levels to the stimulatory effect of higher but not
excessive stress to the supporting bone.23 Alveolar bone tolerance
of amplified C/I may also be due to rough or porous implant
surfaces and tapered, threaded, macroretentive design features that
contribute to high initial torque and stability.24,25
Splinting should be considered when restoring multiple
implants with amplified C/I to improve stress distribution in
crestal bone. Splinting concentrates stress in the prosthesis connectors, reducing force to the peridontium.26 Splinting has been
recommended for implants in poor quality bone to resist destructive horizontal forces.27,28 Splinting can also minimize the gingival embrasures by enlarging the interproximal contact height,
whereas normal interproximal contacts would leave large gingival
embrasures that trap food.
Splinting is not required for normal C/I multiple implantsupported restorations.29 Nonsplinted posterior teeth crowns
create a biomimetic restoration that allows normal access to
flossing. They restrict prosthetic problems—such as porcelain
fracture—that occur on a single tooth to just that tooth, whereas
multiple splinted crowns are affected by a single problem tooth.
Interproximal contact adjustment for these crowns is complicated
by the ankylotic implant support compared to the PDL resiliency
of teeth. A very tight contact may pass floss as the natural teeth
12
General Dentistry
Fig. 7. Cement-retained composite-acrylic provisional restoration No. 11 and
splinted screw-retained composite provisional restoration No. 12-14 with
amplified C/I.
deflect on pressure, whereas this same contact with implant support would not permit floss to pass. Assiduous refinement of these
contacts should be done with thin marking ribbon in the contacts
to show the exact area to be adjusted. Implant-supported crowns
require a very small space in the contact area so that floss can
pass but food won’t get trapped. Heavy interproximal contacts
can create a nonpassive cementation with increased bone strain,
which magnifies the deleterious effects of occlusal loading.26
The current literature supports the use of single and multiple
short implants to restore edentulous spaces with normal, reduced,
and amplified C/I. Short implants expand the treatment planning
options for the dental team, especially in atrophic posterior jaw
sites with an amplified C/I. This option may allow a fixed prosthodontic solution for the patient where grafting, time, or financial
concerns previously restricted treatment to a movable prosthesis.
Author information
Dr. Solow is in private practice in Mill Valley, California, and a visiting faculty member at the Pankey Institute, Key Biscayne, Florida.
References
www.agd.org
1. Grossmann Y, Sadan A. The prosthodontic concept of crown-to-root ratio: a review of
the literature. J Prosthet Dent. 2005;93(60:559-562.
2. Keough B. Occlusal considerations in periodontal prosthetics. Int J Periodontics Restorative Dent. 1992;12(5):359-371.
3. Garaicoa-Pazmino C, Suarez-Lopez del Amo F, Monje A, et al. Influence of crown/implant
ratio on marginal bone loss: a systematic review. J Periodontol. 2014;85(9):1214-1221.
4. Kim Y, Oh TJ, Misch CE, Wang HL. Occlusal considerations in implant therapy: clinical
guidelines with biomechanical rationale. Clin Oral Implants Res. 2005;16(1):26-35.
5. Kraus BS, Jordan RE, Abrams L. A Study of the Masticatory System: Dental Anatomy
and Occlusion. Baltimore, MD: The Williams and Wilkins Company; 1969.
6. Baggi L, Cappelloni I, Di Girolamo M, Maceri F, Vairo G. The influence of implant diameter
and length on stress distribution of osseointegrated implants related to crestal bone geometry: a three-dimensional finite element analysis. J Prosthet Dent. 2008; 100(6):422-431.
7. Chang SH, Lin CL, Lin YS, Hsue SS, Huang SR. Biomechanical comparison of a single
short and wide implant with monocortical or bicortical engagement in the atrophic
posterior maxilla and a long implant in the augmented sinus. Int J Oral Maxillofac Implants. 2012;27(6):e102-e111.
8. Schulte J, Flores AM, Weed M, Crown-to-implant ratios of single tooth implant-supported restorations. J Prosthet Dent. 2007;98(1):1-5.
9. Misch CE, Steignga J, Barboza E, Misch-Dietsh F, Cianciola LJ, Kazor C. Short dental implants in posterior partial edentulism: a multicenter retrospective 6-year case series
study. J Periodontol. 2006;77(8):1340-1347.
10. Merin RL. Repair of peri-implant bone loss after occlusal adjustment: a case report.
J Am Dent Assoc. 2014;145(10):1058-1062.
11. Kerstein RB. Nonsimultaneous tooth contact in combined implant and natural tooth
occlusal schemes. Pract Proced Aesthet Dent. 2001;13(9):751-755.
12. Gore E, Evlioglu G. Assessment of the effect of two occlusal concepts for implant-supported fixed prostheses by finite element analysis in patients with bruxism. J Oral Implantol. 2014;40(1):68-75.
13. Rompen E, Domken O, Degidi M, Pontes AE, Piattelli A. The effect of material characteristics, of surface topography and of implant components and connections on soft tissue integration: a literature review. Clin Oral Implants Res. 2006;17(Suppl 2):55-67.
14. Anitua E, Pinas L, Begona L, Orive G. Long-term retrospective evaluation of short implants in the posterior areas: clinical results after 10-12 years. J Clin Periodontol. 2014;
41(4):404-411.
15. Al-Hashedi AA, Taiyeb Ali TB, Yunus N. Short dental implants: an emerging concept in
implant treatment. Quintessence Int. 2014;45(6):499-514.
16. Fugazzotto PA, Beagle JR, Ganeles J, Jaffin R, Vlassis J, Kumar A. Success and failure
rates of 9 mm or shorter implants in the replacement of missing maxillary molars when
restored with individual crowns: preliminary results 0 to 84 months in function. A retrospective study. J Periodontol. 2004;75(2):327-332.
17. Birdi H, Schulte J, Kovacs A, DDS, Weed M, Chuang SK. Crown-to-implant ratios of
short-length implants. J Oral Implantol. 2010;36(6):425-433.
18. Schneider D, Witt L, Hammerle CH. Influence of the crown-to-implant length ratio on the
clinical performance of implants supporting single crown restorations: a cross-sectional
retrospective 5-year investigation. Clin Oral Implants Res. 2012;23(2):169-174.
19. Rossi F, Lang NP, Ricci E, Ferraioli L, Marchetti C, Botticelli D. Early loading of 6-mm
short implants with a moderately rough surface supporting single crowns - a prospective 5-year cohort study. Clin Oral Implants Res. 2014 [Epub ahead of print].
20. Lai HC, Si MS, Zhuang LF, Shen H, Liu YL, Wismeijer D. Long-term outcomes of short
dental implants supporting single crowns in posterior region: a clinical retrospective
study of 5-10 years. Clin Oral Implants Res. 2013;24(2):230-237.
21. Anitua E, Alkhraist MH, Pinas L, Begona L, Orive G. Implant survival and crestal
bone loss around extra-short implants supporting a fixed denture: the effect of
crown height space, crown-to-implant ratio, and offset placement of the prosthesis.
Int J Oral Maxillofac Implants. 2014;29(3):682-689.
22. Pistilli R, Felice P, Cannizzaro G, Piatelli M, et al. Posterior atrophic jaws rehabilitated
with prostheses supported by 6 mm long 4 mm wide implants or by longer implants in
augmented bone. One-year post-loading results from a pilot randomised controlled
trial. Eur J Oral Implantol. 2013;6(4):359-372.
23. Blanes RJ. To what extent does the crown-implant ratio affect the survival and complications of implant-supported reconstructions? A systematic review. Clin Oral Implants
Res. 2009;20(Suppl 4):67-72.
24. Sohn DS, Lee JM, Park IS, Jung HS, Park DY, Shin IH. Retrospective study of sintered porous-surfaced dental implants placed in the augmented sinus. Int J Periodontics Restorative Dent. 2014;34(4):565-571.
25. Steigenga J, Al-Shammari K, Misch C, Nociti FH Jr, Wang HL. Effects of implant thread
geometry on percentage of osseointegration and resistance to reverse torque in the
tibia of rabbits. J Periodontol. 2004;75(9):1233-1241.
26. Guichet DL, Yoshinobu D, Caputo AA. Effect of splinting and interproximal contact tightness on load transfer by implant restorations. J Prosthet Dent. 2002;87(5):528-535.
27. Tiossi R, Lin L, Rodrigues RC, et al. Digital image correlation analysis of the load transfer by implant-supported restorations. J Biomech. 2011;44(6):1008-1013.
28. Wang TM, Leu LJ, Wang JS, Lin LD. Effects of prosthesis materials and prosthesis splinting on peri-implant bone stress around implants in poor-quality bone: a numeric analysis. Int J Oral Maxillofac Implants. 2002;17(2):231-237.
29. Simon RL. Single implant-supported molar and premolar crowns: a ten-year retrospective clinical report. J Prosthet Dent. 2003;90(6):517-521.
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General Dentistry
13
Endodontics
Achieving and maintaining apical patency in
endodontics: optimizing canal shaping procedures
Rich Mounce, DDS
A
chieving and maintaining apical patency is a prerequisite
for predictable clinical results in endodontic treatment.
After endodontic access, cleaning and shaping of root
canal systems is made possible by negotiation of canals to their
apical terminus followed by the creation of a glide path and
nickel titanium instrumentation. Leaving untreated canal space
due to a lack of apical patency is the harbinger of iatrogenic
misadventure (canal transportation) as well as long-term endodontic failure.
The benefits of achieving and maintaining apical patency
include improved removal of organic and inorganic debris
from the root canal system. It is axiomatic that optimal debris
removal from the canal system increases postoperative comfort
relative to the alternatives (such as loss of working length,
uncleaned and unfilled canal space, and iatrogenic canal
transportation).
The minor constriction (MC) of the apical foramen is the
ideal end point of instrumentation, irrigation, and obturation
during clinical endodontic treatment. Anatomically, the MC is
the narrowest diameter of the canal before it exits to the apical
tissues. While apical anatomy can vary, and some canals do not
have a true “narrowest diameter,” there is an optimal endpoint
to which canal systems should be cleaned and obturated—most
often, the MC. Leaving the MC at its original position and
size is central to fulfilling the various objectives of endodontic
cleaning and shaping goals, which include keeping the canal
in its original position and creating a tapered funnel with
narrowing cross sectional diameters moving from orifice to
apex. For practical purposes, the MC is the anatomic landmark
delineated by a 0.0 reading on electronic “apex” locators.
Location of the MC and maintenance of apical patency
provides the clinician a reproducible landmark for all cleaning,
shaping, and obturation procedures. Should the true working
length (TWL) change in treatment for any reason (especially
electronically), the clinician should immediately troubleshoot
the source of the differential. Any loss of TWL during a clinical procedure should alert the clinician both to the need for
regaining the lost length and reconfirmation of the TWL before
moving forward. An increase in TWL should alert the clinician
to the possibility that the TWL was inaccurately determined
initially. Once apical patency is obtained and reproducible, the
canal can be predictably enlarged to prepare a glide path before
the introduction of nickel titanium instruments for bulk canal
shaping. A glide path is prepared when a No. 15 hand K file
spins freely in the canal.
Not all canals are negotiable to the MC. Severe 3-dimensional (3D) curvature, blockage, previous canal transportation,
and calcification are natural barriers to the attainment of apical
patency. An incorrectly and improperly used hand file (wrong
file type, size, and/or pre-curvature) and inadequate coronal
access, along with a lack of irrigation and viscous chelating
agents can all leave otherwise negotiable canals without proper
exploration and enlargement. Alternatively, using the correct hand file with optimal technique, access, irrigation, and
Fig. 1. Radiograph showing tooth No. 18 at severe
risk for canal blockage and nickel titanium instrument
fracture if canal negotiation is not carried out
appropriately. Note that tooth No. 19 has untreated
canal space and coronal leakage present from the
previous root canal treatment.
14
General Dentistry
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Fig. 2. Tooth No. 18 post-treatment.
Fig. 3. A clinical case treated using the concepts utilized
in this column.
Fig. 4. A clinical case treated using the concepts utilized
in this column.
sequencing improve the possibilities for canal negotiation.
In general terms, the more curved and calcified a canal, the
greater the time and attention to detail required for negotiation. Simpler anatomy is generally more forgiving, in that small
errors in clinical judgment may not lead to severe iatrogenic
issues (Fig. 1 and 2).
While a comprehensive review of all canal anatomy requiring
preoperative evaluation prior to treatment is beyond the scope
of this column, it is important to note that special care should
be taken to obtain a comprehensive radiographic assessment of
the tooth prior to making treatment-planning decisions. For
clinicians using 2-dimensional (2D) radiographic technology,
this means having multiple radiographic angles to guide the
assessment of calcification and curvature. Cone beam computed
tomography assessment is the gold standard for radiographic
anatomic evaluation. Regardless of whether the clinician is using
2D or 3D imaging, the true anatomy of the canal cannot be
fully known until the canal is being negotiated with hand files.
Aside from obvious calcification and curvature, many clinical entities, including high furcations, crowns obscuring the
furcation, rotated and tipped teeth, atypical root numbers and
canal morphology—such as C-shaped lower second molar canal
configurations and lower molars with either a third or fused
root—should inspire caution in the clinician with regard to the
complexity of the canal space being explored.
Hand files give the clinician strong clues to the complexity of
the root canal system. For example, if a hand file emerges from
a root with a 3D curve imparted onto it, the clinician literally has an impression of the canal shape. This knowledge has
ramifications for the clinician with regard to glide path size, the
means for creating the glide path, and nickel titanium sequencing, among others.
Aside from optimal visualization and magnification (surgical
microscope and/or loupes), removal of the cervical dentinal
triangle, restrictive dentin in the coronal third, and pulp chamber
debris all set the stage for hand file negotiation. It is advisable
during evacuation of the pulp chamber and coronal third to
apply a viscous EDTA gel to emulsify pulp tissue and hold it in
suspension while the aforementioned removal of pulp tissue is
taking place in the coronal third prior to apical negotiation.
Clinical technique
Clinically, a precurved No. 6 hand K file is used first to the
TWL followed by No. 8, 10, 12, and 15 files. Once a hand K
file reaches the MC, it can be safely and efficiently reciprocated
with a reciprocating handpiece that replicates the watch winding motion of the manual hand file technique while saving
time and hand fatigue. If a more stiff file is required for canal
negotiation, several marketplace options are available.
Once apical patency is obtained, the importance of frequent
recapitulation cannot be overstated. Frequent recapitulation is
critical in apical irrigation and cleansing. It involves the insertion
of a small hand file to assure the clinician that the canal is open
and negotiable. Clinically, after every insertion of a nickel titanium
file, a small hand file should be inserted to ensure the canal is open
and negotiable to the MC. As the recapitulating hand file moves
out of the canal, fresh irrigant should move apically (Fig. 3 and 4).
This column has discussed the importance of achieving and
maintaining apical patency. Emphasis has been placed on assessing the anatomy of the clinical case preoperatively and moving
sequentially to determine the position of the minor constriction
of the apical foramen.1-3 Future columns may address specific
techniques for hand file negotiation and achieving apical patency
in curved and calcified canals.
Author information
Dr. Mounce is in endodontic practice in Rapid City, South
Dakota. He has written and lectured globally on endodontics.
Disclaimer
Dr. Mounce owns MounceEndo, LLC, which markets the
rotary nickel titanium MounceFile in Controlled Memory and
Standard NiTi.
References
1. Dummer PM, McGinn JJ, Rees DG. The position and topography of the apical constriction and apical foramen. Int Endod J. 1984;17(4):192-198.
2. Meder-Cowherd L, Williamson AE, Johnson WT, Vasilescu D, Walton R, Quian F. Apical
morphology of the palatal roots of maxillary molars by using micro-computed tomography. J Endod. 2011;37(8):1162-1165.
3. Burch JG, Hulen S. The relationship of the apical foramen to the anatomic apex of the
tooth root. Oral Surg Oral Med Oral Pathol. 1972;34(2):262-268.
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General Dentistry
15
Diagnosis and Treatment Planning
Why the general dentist needs to know
how to manage oral lichen planus
Stephanie M. Price, DDS n Valerie A. Murrah, DMD, MS
Oral lichen planus (OLP) is a frequently mismanaged chronic disease
that requires care throughout a patient’s life, and therefore a condition
the general dentist must know how to manage. Patients with OLP often
suffer considerable physical discomfort and an inability to perform
proper oral hygiene, eventually resulting in poor periodontal health. In
addition, these patients are confronted with the psychological stress of
knowing that OLP is not curable. This is accompanied by a fear of other
negative health developments, particularly oral cancer. The objective of
this study was to identify major issues surrounding the management of
OLP by the general dentist.
A literature review of over 1100 articles was performed. An eclectic
compilation of the issues revealed 12 major areas of concern. This
article reviews those concerns and presents strategies for coping with
S
ince Erasmus Wilson first described
oral lichen planus (OLP) in 1869,
much has been written about the
condition.1 Oral lichen planus affects
0.5%-2% of the population, with a
predominance in women 30-70 years of
age.2-7 Clinically, OLP manifests most
frequently bilaterally, with the most
common sites being the buccal mucosa,
tongue, and gingiva.8-14 It has several
forms; the most commonly described are
reticular (containing Wickham’s striae)
and erosive (Fig. 1 and 2).9,11,14-17 While
the etiology of OLP is unknown, it is
thought to be a T-cell-mediated autoimmune response.10,18-23 The authors present
Key words: lichen planus, dental management,
malignant transformation, general dentist
compelling reasons for the general dentist
to become thoroughly knowledgeable
about this uncommon disease and to keep
current on the latest issues regarding OLP
throughout his/her professional life. The
dentist who is able to diagnose, treat,
and manage an OLP patient may not
only improve the quality of, but may also
potentially prolong, the patient’s life.
Materials and methods
Citations and abstracts of over 1100
articles were reviewed regarding all aspects
of lichen planus to identify critical issues
pertinent to the management of the OLP
patient by the general dentist.
Fig. 1. Reticular lichen planus with intersecting white net-like
lines (Wickham’s striae) with focal ulceration showing an
erosive component.
16
the myriad signs, symptoms, and complications associated with this
disease, as well as educational approaches and legal considerations. A
rationale is provided to place the responsibility for the management of
these patients under the person best positioned to coordinate care for
this condition—the general dentist. A general dentist can contribute to
the overall oral health of an OLP patient with timely diagnosis, effective
treatment, thorough patient education, and the orchestration of efforts
by a team of health care providers.
Received: June 24, 2013
Accepted: August 13, 2013
General Dentistry
Results
Twelve broad areas of concern for the
general dentist were identified in an effort
to promote a proactive approach in the
management of this disease. These are
listed in Table 1.
Discussion
Clinical presentation and
identification
The dentist may identify signs and symptoms suggestive of OLP upon meeting a
new patient or during routine follow-up
examinations. Occasionally, a new patient
may present with signs and symptoms of
OLP as his or her chief complaint. OLP can
Fig. 2. Erosive lichen planus in addition to significant plaque accumulation.
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Table 1. Twelve areas of concern for the general
dentist in the treatment of an oral lichen planus
(OLP) patient.
1. Recognition of clinical signs and symptoms
2. Optimal objective diagnosis
3. Disease management and concomitant reduction of the
patient’s pain and suffering
4. Reduction in risk of increased periodontal disease or
exacerbation of existing periodontal disease
5. Education of the patient concerning his/her disease and
management of his/her expectations
6. Appropriate referral of patient to other health care
providers for skin, nail, or genital lesions
Table 2. Partial list of
medications linked to
lichenoid reactions.39-42
Antihypertensives
Diuretics
7. Identification of correlated systemic diseases (hepatitis C
or graft versus host disease)
Methyldopa
8. Avoiding the misfortune of mistakenly treating a
patient as though he/she has OLP when he/she
has oral cancer
ACE inhibitor
β-blocking agent
9. Identification of malignant transformation early, when it
can be managed with minimal morbidity and mortality
Antimalarials
Oral hypoglycemic drugs
10.Dentist versus physician management
Phenothiazines
11.Reduction of susceptibility to litigation
Gold salts
12.Orchestrating the coordination of care
HIV antivirals
be asymptomatic; this is usually associated
with the reticular type. It may also present
with a burning sensation; this is typically
associated with the erosive type. The presentation can change within one patient over
time and these changes could be associated
with increased stress, thus making successful
symptom management challenging.9,10,14,24-29
Diagnosis
OLP can present with clinical and histologic presentations similar to many
other conditions, such as lichenoid drug
reactions (also known as lichenoid drug
eruptions), lichenoid contact mucositis,
cinnamon stomatitis, lupus erythematosus,
dysplasia, carcinoma, and graft versus
host disease—all of which require different treatments.9,10,15,30-32 Because OLP
does not have a pathognomonic appearance—except for classical Wickham’s
striae—diagnosis by biopsy is necessary.
Additionally, the practitioner must keep in
mind that multiple pathologies can exist
simultaneously in the same or in different
locations, thus complicating both diagnosis and treatment.9,33,34 Histopathological
criteria include variable keratinization,
Fig. 3. Photomicrograph of an
epithelial rete ridge showing attenuation, interface change (lyphocytic
migration into the epithelium), and
florid lymphocytic infiltrate in the
upper connective tissue (H&E,
magnification 400X).
NSAIDs
basal cell layer liquefaction, and a bandlike T-cell lymphocytic infiltrate localized
to the lamina propria proximal to the
epithelium.35,36 Other features often present are interface change characterized by
the movement of inflammatory cells into
the epithelium, Civatte (colloid) bodies,
and saw-toothed (attenuated) rete ridges
(Fig. 3).10,35-37 The findings of the clinician
and pathologist should always be correlated when making a diagnosis. A clinical
photograph should ideally be sent with the
biopsy to the lab, and the clinician should
consult the pathologist if the diagnosis
does not fit the clinical context. Specimens
should be submitted in formalin for routine microscopy and in Michel’s solution
for direct immunofluorescence (DIF). The
DIF specimen may be critical in differentiating OLP from other vesiculo-ulcerative
diseases such as benign mucous membrane
pemphigoid, lupus erythematosus, pemphigus vulgaris, chronic ulcerative stomatitis, and lichenoid reactions. Under DIF,
OLP lesions often show fluorescence at
the level of the basement membrane zone
with antibodies to fibrinogen and, less
frequently, to IgG and IgM.10,23,38
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Differential diagnoses
Lichenoid drug reactions may be more
difficult to manage since the removal
of a given medication may threaten the
patient’s overall health. In addition, these
reactions are more difficult to recognize
because manifestations may be delayed
for weeks to months, both at the start
of medication and/or after the medication has been stopped.39-42 The clinician
should take a detailed health history and
inquire about allergies and medications
commonly associated with lichenoid drug
reactions (Table 2).
A potential lichenoid drug reaction
that merits further investigation is the
use of hydrochlorothiazide in patients
who have experienced sulfa allergies.
Hydrochlorothiazide is the most commonly prescribed antihypertensive, and
treatment with this drug is commonly
associated with lichenoid mucositis.43
Patients with sulfa allergies often have
a history of a hypersensitivity response
to the sulfonamide antibiotic, sulfamethoxazole-trimethoprim.44-46 Although
there is little evidence that antimicrobial
sulfonamides cross-react with other sulfur
General Dentistry
17
Diagnosis and Treatment Planning Why the general dentist needs to know how to manage oral lichen planus
Table 3. Steroid treatment for OLP.
Fig. 4. An example of a focal lichenoid reaction to
amalgam. The lesion resolved following replacement
of the amalgam with a gold crown.
Systemic
Topical
Methylprednisolone
0.1% Triamcinolone-mild potency
Prednisone
0.05% Fluocinonide-moderate potency
0.05% Clobetasol-high potency
Topical steroids could be applied in a custom tray worn at night.
Table 4. Recommended care sequence for an OLP patient.
containing moieties, patients with sulfa
allergies may be predisposed to lichenoid
reactions from medications containing
sulfur groups such as hydrochlorothiazide
and sulfonylureas (non-antimicrobial sulfonamides).44,45,47,48 Alternatively, patients
who have a sulfa allergy may simply have
a predilection to other allergic responses
even with chemically dissimilar drugs.48
This is not surprising given the great
number of medications associated with
oral lichenoid reactions.
Unlike a lichenoid drug reaction, lichenoid contact mucositis can be differentiated
clinically by the position of the lesion next
to the offending agent (e.g., amalgam,
gold, composite, or cast alloy restorations).10,31,49-56 The dental material most
often cited as the cause of a hypersensitivity
reaction is amalgam (Fig. 4).51,52,54-56 Some
authors advocate removing restorations for
resolution of this hypersensitivity, while
other authors do not.49,51,57 Although not a
dental material, cinnamon is an even more
frequent cause of a mucositis resembling
lichen planus.32,58 There is controversy—
with both amalgam and cinnamon—over
the benefit of allergy patch testing.31,32,49
Points of contention include which mercurial or amalgam material to use for the
testing, the clinical similarity between
sensitivity and irritant responses, the length
of time that the material should be in
contact with the skin, and the relevance of
cutaneous testing to mucosal allergies.31,32
Complicating the diagnosis regarding amalgam are other factors such as the contour of
a restoration or the position of its margin.
With respect to cinnamon, discontinuation
18
1. Health history
2. Clinical exam
3. Working diagnosis
4. Biopsy (for light microscopy and DIF)
5. Definitive diagnosis
6. Patient education
7. Referral to primary care physician,
if applicable
of the use of the product or food containing cinnamon should result in resolution of
the lesions in a matter of days.
Treatment
Following the determination of the diagnosis, management can be accomplished in a
number of ways depending on the severity
of disease. The usual first line of treatment
for symptomatic OLP is topical steroids
(Table 3). Approaches to treatment could
also include an initial systemic steroid
burst, such as a methylprednisolone or a
high potency topical corticosteroid, such
as clobetasol propionate. Maintenance
treatment during symptomatic periods
could be a moderate topical steroid, such
as fluocinonide. Triamcinolone, a mild
topical steroid, is occasionally used but
often does not result in significant resolution in adults. Treatment of more severe
cases consists of systemic steroids or other
immunosuppressant agents. Topical drug
delivery via a custom tray or mouthguard—even if lesions extend beyond the
gingiva—has been shown to be efficacious,
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www.agd.org
8. Treatment (to include topical and/or
systemic steroids and increased frequency
of dental prophylaxis)
9. Re-evaluation of treatment
10. Treatment modification and additional
biopsy as needed
11. Periodic follow-up to check for malignant
transformation
particularly at nighttime, as the drug will
leak out of the tray and bathe the oral
tissues. Treatment of symptoms can be
accomplished with viscous lidocaine or
other topical anesthetics. A recommended
care sequence for an OLP patient is illustrated in Table 4.
Associated candidiasis
Since steroid treatment suppresses the
immune system, it may also promote the
development of a Candida infection that
will exacerbate the patient’s discomfort.
It is also possible that a Candida infection was already present prior to steroid
treatment for OLP.13,59 If candidiasis is suspected, clinicians should obtain a cytologic
smear, and patients with positive results
should be given appropriate antifungal
treatment, such as fluconazole, clotrimazole, or nystatin (Table 5). In addition to
alleviating additional patient symptoms, it
is helpful to have possible Candida infections cleared prior to performing a biopsy
so that only the inflammation specific to
OLP is evident in the specimen.
dentists may potentially learn more about
patients’ individual clinical presentations
and can make appropriate referrals.
Table 5. Antifungal treatment for associated candidiasis in OLP patients.
Systemic
Topical
Fluconazole 100-200 mg
Clotrimazole
10 mg troches
Nystatin
100,000-200,000 units
Topical antifungals could be administered as troches or as lozenges.
Chart. Network of providers for management of oral lichen planus.
Periodontist
Oral Surgeon
Gynecologist
or
Urologist
General
Dentist
Oral Pathologist
Primary Care
Physican
Dermatologist
Otolaryngologist
Relationship to periodontal health
One of the most significant reasons for the
general dentist to be knowledgeable about
OLP is that it can have a negative impact
on periodontal health. It is estimated that
approximately 38%-48% of OLP patients
have gingival lesions, and 7%-10% have
gingival lesions as their only clinical
manifestation.11,14,60,61 It is thought that
plaque and calculus exacerbate the clinical
presentation of OLP.11,60,62-64 All OLP types
are associated with increased bleeding
on probing, which is expected given the
inflammatory nature of the disease.11,62,64
OLP patients with symptomatic lesions
often have difficulty with oral hygiene
and have more plaque and calculus present, putting them at increased risk for
poor periodontal health.60,63 Patients with
erosive lichen planus have more clinical
attachment loss.63 Avoiding certain types
of foods, such as those that are acidic,
spicy, and/or rough textured; using a nonalcoholic chlorhexidine rinse; and placing
patients on a more frequent recall schedule
may be helpful.31,63 Trauma, heat, irritants
from smoking, and oral habits have also
been found to exacerbate the clinical
symptoms of OLP.10,31
Education
Educating OLP patients is essential to
both short- and long-term treatment
success. A 1997 survey conducted to
determine patient awareness of OLP
etiology, treatment, and malignancy
resulted in a wide variety of responses.65
The authors found a significant number
of patients reporting the treatment strategy of “learn to live” with the disease,
and only 7% of the respondents stating
that they received additional education
after the initial diagnosis.65 By providing education to their OLP patients,
dentists make them aware of potentially
exacerbating factors, help them understand the need for increased visits to the
dental office and improved home care,
and raise awareness of other associated
health concerns. According to Burkhart
et al, it is important that dentists inform
their patients about all the pertinent
information regarding this disease, and
provide them with a comprehensive treatment strategy.65 By doing so, dentists
can reduce OLP patients’ inherent stress
of uncertainty and empower them to
be part of their own health success.65 In
addition, during the educational process,
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Presentation in areas outside of
the oral cavity
Lichen planus not only presents in the
oral cavity, but also can be found in the
mucous membranes of the genitalia,
esophagus, skin, nails, and eyes.3,66-73
Approximately 19%-25% of OLP patients
have genital lesions.70 In these patients,
OLP tends to present primarily on the
gingiva.66,68,70 Most of the literature
describes women with vulvovaginal-gingival lichen planus, however there are also
a few reports of male patients, for whom
the lesions are referred to as penogingival
lichen planus.66,70 Ten percent to 20% of
OLP patients have cutaneous lesions, and
it has been found that patients with cutaneous lesions either already have or are
likely to develop OLP.3,70,74 The sequence
of presentation between OLP and lichen
planus in other locations is not predictable, and presentations may be separated
by months or years.3,69,70 Lichen planus
presenting in the fingernails, toenails,
esophagus, and eyes is uncommon; in a
study of 584 lichen planus patients, 11
showed clinical signs of nail involvement,
6 presented with esophageal involvement,
and 1 had biopsy-proven ocular lichen
planus.70 Because any given clinician does
not investigate all potential anatomic
sites of lichen planus, the condition is
frequently misdiagnosed, particularly in
the genitalia.69,70 Therefore, the general
dentist must be able to provide effective
referrals to gynecologists, urologists, and
dermatologists (Chart). If these alternate
presentations are missed during the health
history, the general dentist could discuss
the possibility of other lichen planus
lesions as part of patient education.
Associated conditions
Oral lichen planus may signal the clinician
to look for hepatitis C, as it is another
systemic condition found to be associated
with the disease.75-77 A previous worldwide
estimate found that 170 million people
have chronic hepatitis C, although its
prevalence is regionally variable.78 Many
hepatitis C patients may be asymptomatic.79 Chronic hepatitis C can lead to
hepatocellular carcinoma and to cirrhosis,
General Dentistry
19
which itself could be an independent risk
factor for oral cancer.30,80 A person with
hepatitis C is 2.8-5.4 times more likely to
have OLP than the control population.57
Therefore, it makes good sense to ensure
that one’s health history includes questions
that address hepatitis C risk factors and to
refer patients to their primary care providers as indicated.57 In the United States, risk
factors for hepatitis C include blood transfusions, intravenous drug use, or high risk
sexual practices; worldwide practitioners
should look for risk factors specific to their
region.31,78 Several authors postulate that
it is not economically advantageous for
everyone who has OLP to be screened for
hepatitis C.31,57 Regional areas that tend to
have strong associations between OLP and
hepatitis C are the Mediterranean region
of Europe (especially Spain and Italy) and
East Asia (especially Japan).10,57,75,76
Lichenoid reactions as a manifestation of
graft versus host disease may be the easiest
of systemic conditions to identify due to
their presentation after bone marrow or
stem cell transplants.81,82 Oral complications are common and associated with
donor-generated T cells attacking host
tissues.31,82-84 The reaction can be found
in more severe cases of acute graft versus
host disease (<100 days), but historically is
a frequent finding in chronic disease.84-86
Dentists should notify the patient’s transplant physician should these lesions manifest in the oral cavity so as to integrate oral
symptom management with overall disease
treatment. As with other symptomatic
lichenoid reactions, these patients can be
treated with topical corticosteroids and/or
topical anesthetics.84
Malignant transformation
Officially, OLP has been designated as
a premalignant condition by the World
Health Organization; however the rates
and mechanisms of transformation are
subject to debate.30,87-91 Researchers who
theorize that OLP is not a premalignant
condition propose that cases diagnosed
as malignant transformation of OLP
were actually instances of misdiagnosed
epithelial dysplasia.9,91,92 Published rates
of malignant transformation vary from
0%-12.5%.30,87,91 Clinicians should become
particularly suspicious of malignant transformation when there are specific sites with
a loss of homogeneity, increased size or
20
asymmetric appearance of the lesion, and
lack of response to treatment.30,60 Treatment
of patients with a diagnosis of OLP should
include a clinical examination every 3-6
months for a minimum of 5 years, ideally
with regular photographic documentation
of the lesion.30 Several studies have found
that the tongue is the preferred site for
malignant transformation, although all
areas should be observed with suspicion.30,87
One review article found that the reported
interval between a diagnosis of OLP and
oral squamous cell carcinoma ranges
from 20.8 months to 10.1 years.30 Recent
research hypothesizes that malignant transformation of OLP is related to long-term
chronic inflammation.89 In addition to
the increased rate of cellular turnover, the
thought is that the nitric oxide produced by
inflammatory cells can promote carcinogenesis.90 Some researchers have hypothesized
that steroid and/or immunosuppressive
treatment contributes to the potential for
carcinogenesis in OLP, although there is no
current evidence to support this.30,38,87
Late diagnosis of oral cancer will likely
result in a patient’s increased morbidity
and mortality. The ideal period from
diagnosis to treatment of oral cancer is
the sooner the better. A 10-year analysis
of new cases of oral squamous cell carcinoma showed that there was a significant
difference in the stage of the tumor,
and therefore prognosis, between those
referred earlier than 6 weeks and those
later.93 In 2000, the United Kingdom
placed a “2-week” rule for all suspected
cancers as a time limit for referral from
primary care to a specialist.93
Respective roles of dentists and
physicians in oral examination
Dentists are in the best position to identify
and diagnose all diseases of the oral cavity.
As specialists of the oral cavity, dental
practitioners spend more time observing
this area and thus would be more likely to
observe a soft tissue irregularity or to diagnose a chief complaint associated with an
oral mucosal lesion. While physicians are
often aware of oral diseases and understand
their implications to overall health, they
are less likely to perform oral exams than
dentists.94 In a 1995 survey conducted in
Maryland of dentists and physicians, more
physicians than dentists felt that they did
not feel adequately trained to conduct oral
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cancer exams.95 A similar 2009 survey in
Massachusetts found that dentists performed double the number of oral cancer
exams compared to physicians.94 This study
also found that 24% of dentists reported
finding suspicious lesions in >10 patients,
compared to no physicians finding such
lesions in >10 patients.94 The study further
reported that both dentists and physicians
are more confident that dentists are qualified to perform oral cancer exams when
compared to physicians.94 The hypothetical
correlation is that OLP would be found
in the same exam conducted to detect oral
cancer, and that physicians may be even
less aware of specific uncommon diseases
of the oral cavity—such as OLP—than
they are of oral cancer.
If physicians are less likely to perform
oral exams, they are consequently less
likely to manage oral lesions. In addition,
because of the association between OLP
and periodontal disease, dentists are in
the best position to manage the entire
oral health picture. Dentists are also more
likely to fabricate a custom tray for drug
delivery. This is not to suggest, however,
that physicians or other primary care providers should not conduct comprehensive
oral exams, with the goal of identifying
lesions, as it is well-recognized that some
patients visit their primary care providers more frequently than their dentist or
do not visit a dentist at all. Therefore, it
is essential that a comprehensive examination of the mouth be taught in the
medical school clinical curriculum. A
survey of 86 US medical schools found
that such training is currently brief
and incomplete.96,97 The Association of
American Medical Colleges recommends
that additional training be added to the
medical curriculum in its Medical Schools
Objective Project.98
Litigation
Litigation involving oral cancer and OLP
is not openly discussed. Consequently,
there is a dearth of information published
in the medical literature. However,
selected publications on the subject merit
the general dentist’s attention. Given that
OLP is a disease that is relatively uncommon, it is frequently misdiagnosed, resulting in a number of lawsuits for “failure to
diagnose oral cancer” as the health care
provider makes the unfortunate mistake
of treating a patient as though he/she
has OLP when he/she actually has oral
cancer.99 The top 3 allegations in oral
cancer lawsuits are failure to diagnose,
failure to biopsy, and failure to refer.100
Furthermore, patients who have had
delays in treatment resulting in poor outcomes are more likely to sue.100,101 While
there are many opportunities for delays
(such as a patient failing to return for
routine exams or a patient’s hesitation in
making an appointment with a specialist),
general dentists can minimize the amount
of time taken to obtain a definitive diagnosis and proceed to treatment. This time
element is the most relevant in avoiding a
lawsuit.93 Additionally, an increased time
to diagnosis may result in a less successful
legal defense. A review of oral cancer lawsuits determined that if the delay in diagnosis was <3 months, 86% of defendants
(practitioners) were successful, however if
the delay was >3 months, only 40% were
successful.100 In their review of litigation
involving delayed diagnosis of cancer,
Rice & Hamburger noted a rapid decline
in the ability for a defendant to succeed
in cases of >3 months delay and found
that after 6 months delay, the length of
the delay or the survival of the patient is
irrelevant in the jury’s findings.102
Summary
With the risk for development of malignancy, associated medical disorders, and
the severe symptoms often associated with
the disease, optimal management of OLP
is requisite for the accomplished practitioner. There are still unanswered questions
about OLP; however, by using a comprehensive treatment approach to clinical
symptoms and oral health maintenance
patients will experience better outcomes.
In conclusion, the general dentist is in the
best position to contribute in the most
meaningful way to the overall well-being
of the OLP patient by timely diagnosis,
effective treatment, and thorough patient
education; and by doing what a general
dentist does best—orchestrating the
coordination of care by a team of diverse
medical and dental providers.
Author information
Dr. Price is a doctoral alumna, University
of North Carolina School of Dentistry,
Chapel Hill, where Dr. Murrah is a
professor and chair, Department of
Diagnostic Sciences, and director, Oral
and Maxillofacial Pathology.
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41. Holt PJ, Navaratnam A. Lichenoid eruption due to
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46. Cribb AE, Lee BL, Trepanier LA, Spielberg SP. Adverse
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47. Dibbern DA Jr, Montanaro A. Allergies to sulfonamide
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53. Henriksson E, Mattsson U, Hakansson J. Healing of lichenoid reactions following removal of amalgam. A clinical follow-up. J Clin Periodontol. 1995;22(4):287-294.
54. Finne K, Goransson K, Winckler L. Oral lichen planus
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55. Ostman PO, Anneroth G, Skoglund A. Amalgam-associated oral lichenoid reactions. Clinical and histologic
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56. Bolewska J, Hansen HJ, Holmstrup P, Pindborg JJ,
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58. Miller RL, Gould AR, Bernstein ML. Cinnamon-induced
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59. Lundstrom IM, Anneroth GB, Holmberg K. Candida in
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60. Mignogna MD, Lo Russo L, Fedele S. Gingival involvement of oral lichen planus in a series of 700 patients. J Clin Periodontol. 2005;32(10):1029-1033.
61. Scully C, Beyli M, Ferreiro MC, et al. Update on oral
lichen planus: etiopathogenesis and management.
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62. Lopez-Jornet P, Camacho-Alonso F. Periodontal conditions in patients with oral lichen planus: a pilot study.
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63. Ramon-Fluixa C, Bagan-Sebastian J, Milian-Masanet
M, Scully C. Periodontal status in patients with oral
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64. Azizi A, Rezaee M. Comparison of periodontal status
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65. Burkhart NW, Burkes EJ, Burker EJ. Meeting the educational needs of patients with oral lichen planus. Gen
Dent. 1997;45(2):126-132; quiz 143-144.
66. Petruzzi M, De Benedittis M, Pastore L, Grassi FR, Serpico R. Peno-gingival lichen planus. J Periodontol.
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67. Panagiotopoulou N, Wong CS, Winter-Roach B. Vulvovaginal-gingival syndrome. J Obstet Gynaecol. 2010;
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68. Eisen D. The vulvovaginal-gingival syndrome of lichen
planus. The clinical characteristics of 22 patients. Arch
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69. Ramer MA, Altchek A, Deligdisch L, Phelps R, Montazem A, Buonocore PM. Lichen planus and the vulvovaginal-gingival syndrome. J Periodontol. 2003;74(9):
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70. Eisen D. The evaluation of cutaneous, genital, scalp,
nail, esophageal, and ocular involvement in patients
with oral lichen planus. Oral Surg Oral Med Oral
71. Kirsch M. Esophageal lichen planus: a forgotten diagnosis. J Clin Gastroenterol. 1995;20(2):145-146.
72. Tosti A, Peluso AM, Fanti PA, Piraccini BM. Nail lichen
planus: clinical and pathologic study of twenty-four patients. J Am Acad Dermatol. 1993;28(5 Pt 1):724-730.
73. Neumann R, Dutt CJ, Foster CS. Immunohistopathologic features and therapy of conjunctival lichen planus. Am J Ophthalmol. 1993;115(4):494-500.
74. Conklin RJ, Blasberg B. Oral lichen planus. Dermatol
Clin. 1987;5(4):663-673.
75. Lodi G, Giuliani M, Majorana A, et al. Lichen planus
and hepatitis C virus: a multicentre study of patients
with oral lesions and a systematic review. Br J Dermatol. 2004;151(6):1172-1181.
76. Petti S, Rabiei M, De Luca M, Scully C. The magnitude
of the association between hepatitis C virus infection
and oral lichen planus: meta-analysis and case control
study. Odontology. 2011;99(2):168-178.
77. Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z,
Binyou W. Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis. Arch
Dermatol. 2009;145(9):1040-1047.
78. Global surveillance and control of hepatitis C. Report
of a WHO consultation organized in collaboration
with the Viral Hepatitis Prevention Board, Antwerp,
Belgium. J Viral Hepat. 1999;6(1):35-47.
79. Merkinaite S, Lazarus JV, Gore C. Addressing HCV infection in Europe: reported, estimated and undiagnosed
cases. Cent Eur J Public Health. 2008;16(3):106-110.
80. Lekholm U, Stenman G. Induction of oral cancer by
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81. Ferrara JL, Reddy P. Pathophysiology of graft-versushost disease. Semin Hematol. 2006;43(1):3-10.
82. Vogelsang GB, Lee L, Bensen-Kennedy DM. Pathogenesis
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83. Pereira CM, de Almeida OP, Correa ME, Souza CA,
Barjas-Castro ML. Oral involvement in chronic graft
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84. Woo SB, Lee SJ, Schubert MM. Graft-vs.-host disease.
Crit Rev Oral Biol Med. 1997;8(2):201-216.
85. Arora M, Burns LJ, Davies SM, et al. Chronic graft-versus-host disease: a prospective cohort study. Biol
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86. Ratanatharathorn V, Ayash L, Lazarus HM, Fu J, Uberti
JP. Chronic graft-versus-host disease: clinical manifestation and therapy. Bone Marrow Transplant. 2001;
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87. Bombeccari GP, Guzzi G, Tettamanti M, et al. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol
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88. Mignogna MD, Lo Muzio L, Lo Russo L, Fedele S,
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PG, Kotsinas A. Oral lichen planus as a preneoplastic
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Microbiology
Investigation of antibacterial efficacy of Acacia
nilotica against salivary mutans streptococci :
a randomized control trial
Devanand Gupta, BDS, MDS n Rajendra Kumar Gupta, PhD
This double-blind, randomized control trial sought to evaluate the clinical
effects of 3 mouthrinses against salivary mutans streptococci (MS). Ninety
high-caries risk volunteers were randomly assigned to 3 groups, each
group using a selected mouthrinse BID for 30 days. Subjects in Group 1
rinsed with 10 ml of 50% Acacia nilotica, Group 2 subjects rinsed with
10 ml of 0.2% chlorhexidine (active control), and subjects in Group 3
rinsed with saline water (passive control). Unstimulated saliva samples
were collected at baseline, 30, and 60 days. MS were cultured on mitis
salivarius bacitracin agar, and colony counts were obtained. The margin
D
ental caries is one of the most prevalent infectious diseases in humans
worldwide.1 Caries is defined as a
localized, progressive demineralization of
the hard tissues of the crown and/or root
surfaces of teeth. This demineralization
is caused by acids produced by bacteria,
particularly mutans streptococci (MS),
which ferment dietary carbohydrates.
This occurs within dental plaque, a
bacteria-laden gelatinous material that
adheres to tooth surfaces and becomes
colonized by bacteria. Thus, caries
results from the interplay of 3 factors
over time: dietary carbohydrates, cariogenic bacteria within dental plaque,
and susceptible hard tooth surfaces.1 If
left untreated, caries may lead to pain,
infection, and tooth loss. During the
past few decades, changes have been
observed in the prevalence and epidemiology of dental caries.1
Mouthrinses are adjuncts to mechanical
plaque control and serve as delivery vehicles for antimicrobial agents. For decades,
chlorhexidine has been considered the
‘gold standard’ among the different antimicrobial mouthrinsees commercially
available.2 Although chlorhexidine is
effective in reducing the number of MS,
it has inherent side effects, such as staining of teeth and composite restorations,
altered taste perception, metallic taste, and
burning sensation.3 Plant compounds can
be therapeutic substitutes for synthetically
created antimicrobial agents.4
of error was fixed at 5%. ANOVA and post hoc least significant difference tests were performed. There were significant decreases in the MS
colony count in the A. nilotica and chlorhexidine groups at 30 days (85%
and 83%, respectively) and at 60 days (65% and 63%, respectively)
(P < 0.0001). The antibacterial action of A. nilotica against MS was
similar to that of chlorhexidine.
Received: November 12, 2013
Revised: April 2, 2014
Accepted: May 7, 2014
Acacia species—commonly known
as Babool (or babul), Egyptian mimosa,
Egyptian thorn, kikar, Indian gum, and
red thorn—have long been used for the
treatment of various ailments and for
other practical uses. The wood of A.
nilotica was used by ancient Egyptians
to make statues and furniture. Its use
has been reported since early Egyptian
dynasties. Dioscorides, the Greek physician considered to be the father of botany,
described the use of A. nilotica (as a
preparation extracted from the leaves and
fruit pods) in his De Materia Medica.5
He named it akakia, and it is from this
word that the modern name, acacia, is
derived. The origin of the word, acacia,
is “spiny,” which is a typical feature of
the species. The species is widely spread
in Africa, with a range extending from
Egypt to Mauritania southwards to South
Africa, and also in Asia, ranging eastwards to Pakistan and India. It has been
introduced in China, Australia (where it
is considered to be a pest plant of national
importance), Caribbean and Indian
Ocean islands, United States, Central
America, and South America. It has been
introduced as a medicinal, forage, and
fuel wood plant in many parts of world.
A. nilotica has been proven as an effective
medicine in the treatment of malaria, sore
throat (aerial part), toothache (bark), acute
diarrhea, colds, bronchitis, diarrhea, bleeding hemorrhoids, and leucoderma.6 A. nilotica twigs have been used as toothbrushes.6
www.agd.org
Considerable efforts have been made to
find an active agent against Streptococcus
mutans, as it is found to be resistant to
many antibacterial agents, such as penicillin, amoxicillin, cefuroxime, and erythromycin.7 Thus, there is a growing need to
investigate natural antimicrobial agents
that are effective and safe for patients.
A. nilotica mouthrinses have demonstrated effective antibacterial effects
against halitosis-inducing bacteria on
the tongue, and has also been used in
the treatment of gingival bleeding and
mouth ulcers.8 The antimicrobial efficacy of A. nilotica against MS has been
ascertained in previous in vitro studies.9,10
However, no in vivo studies have been
carried out to assess the antibacterial
efficacy of A. nilotica against MS in comparison with chlorhexidine. Hence, the
current study was conducted.
This double-blind, randomized control
trial was conducted on undergraduate
student volunteers in the Department of
Public Health Dentistry, Teerthankar
Mahaveer Dental College and Research
Centre, India. The protocol was approved
by the Institutional Review Board (IRB)
of Teerthankar Mahaveer University.
All subjects signed an IRB-approved
consent form. A pilot study was done on
10 patients from each of 3 test groups to
check the feasibility of the study; those
results are not included in the study.
General Dentistry
23
Microbiology Investigation of antibacterial efficacy of Acacia nilotica against salivary mutans streptococci
Table 1. Baseline background of the subjects.
A. nilotica
n = 30
Chlorhexidine
n = 30
Placebo control
n = 30
P value
15/15
10/20
12/18
0.698
Range of age (years); mean (SD)
20-24; 22.16 (2.01)
19-25; 21.42 (2.07)
20-25; 22.74 (2.28)
0.362
Number of times toothbrushing
Once–25, Twice–5
0.897
Baseline characteristics
No. of men/women
None
None
None
DMFT, mean (SD)
Additional oral hygiene aids
3.52 (3.39)
3.67 (2.43)
3.18 (2.85)
0.759
Incipient lesions, mean (SD)
5.58 (3.48)
5.42 (4.08)
5.63 (4.64)
1.098
Abbreviations: A. nilotica, Acacia nilotica ; DMFT, decayed/missing/filled teeth; SD, standard deviation.
Table 2. ANOVA results for the 3 study groups.
df
Mean square
F value
P value
21709.972
2
10854.986
0.542
1.3120
1589356.737
54
29432.532
15.825
0.0001
9.361
0.0001
Sum of squares
MS (baseline)
Between groups
Within groups
MS (Day 30)
MS (Day 60)
Between groups
468912.035
2
234456.017
Within groups
789459.474
54
14619.619
Between groups
389590.877
2
194795.438
Within groups
929856.000
54
17219.555
Abbreviations: df, degree of freedom; MS, mutans streptococci.
Preparation of extract
A water-washed section of A. nilotica
bark was subjected to coarse grating
(sieve No. 44) to produce a coarse powder
of uniform texture. A hot solid-liquid
(Kumagawa) extraction procedure was
applied to obtain the extract of A. nilotica. The powder was subjected to 50%
ethanol for 48 hours at 60°C-65°C. The
resulting separate 50% extract was then
concentrated and the ethanol solvent was
completely removed under reduced pressure by a Lyotrap dryer (LTE Scientific
Ltd.). The extract was stored at 4°C in a
tightly closed container to preserve it from
any contamination, deterioration, and/or
decomposition.
Inclusion and exclusion criteria
Volunteers who had 1 or more active
incipient lesions and/or frank carious
lesions were considered to be at high risk
for dental caries and were included in
the study. Participants having a baseline
24
plaque score >2 and a baseline DMFT
index of 2-5 were included in the study.
Volunteers who had used antibiotics or
any mouthrinse for 7 consecutive days, or
taken corticosteroids in the past 15 days
were excluded from the study. Subjects
with a history of sensitivity to any mouthrinse, and those who had used removable
prostheses or an orthodontic appliance,
were excluded from the study.
All volunteers were subjected to clinical
examination, and a sampling frame (n = 90)
was prepared of those who fulfilled the
inclusion and exclusion criteria. Subjects
were instructed to refrain from any drug
and alcohol consumption for the study
period of 60 days and to report any consumption of these products. The subjects
were divided into 3 groups (n = 30). This
sample size was chosen as the minimum size
required due to the calculations for error
used in this study: α error <5% (P < 0.05),
β error 20%, expected mean difference
3.257, and standard deviation 2.715.
General Dentistry
www.agd.org
The volunteers were randomly allocated
into 3 study groups through computergenerated numbers. Individuals were
identified by code numbers throughout
the study. The clinical trial was conducted according to American Dental
Association’s Adjunctive Dental Therapies
for the Reduction of Plaque and Gingivitis
guidelines.11 All eligible subjects participated in the study.
For the study, all subjects were asked
to rinse with 10 ml of their designated
mouthrinse BID for 30 days. Group 1
subjects were given a 50% A. nilotica
mouthrinse, Group 2 subjects were given
a 0.2% chlorhexidine mouthrinse, and
Group 3 (control) was given a saline water
mouthrinse (placebo).
Methodology
DMF scores and incipient lesion scores
were recorded at baseline. The unstimulated salivary samples were collected from
the participants and inoculated onto mitis
Table 3. Post hoc significant difference test for multiple comparisons.
95% confidence interval
Dependent variable
Group (I)
Group (J)
Standard error
P value
Lower limit
MS (baseline)
A. nilotica
Chlorhexidine
52.68
0.4220
-149.90
MS (Day 30)
MS (Day 60)
Upper limit
47.80
A. nilotica
Placebo control
52.68
0.6980
-138.12
62.17
Chlorhexidine
Placebo control
52.68
0.8970
-69.28
114.01
A. nilotica
Chlorhexidine
33.23
0.9810
-69.23
53.23
A. nilotica
Placebo control
33.23
0.0001
-212.18
-99.72
Chlorhexidine
Placebo control
33.23
0.0001
-211.18
-98.72
A. nilotica
Chlorhexidine
40.18
0.8560
-87.64
79.69
A. nilotica
Placebo control
40.18
0.0001
-224.33
-79.99
Chlorhexidine
Placebo control
40.18
0.0001
-216.85
-66.52
(I) and (J) designations according to post hoc analysis.
Abbreviations: A. nilotica, Acacia nilotica ; MS, mutans streptococci.
salivarius bacitracin (MSB) agar (M259,
HiMedia Laboratories). The MS colony
counts were obtained by a microbiologist
who was blinded to the groups. Each participant was given the same brand of toothbrush and toothpaste to minimize bias.
All 3 solutions were made in the university’s pharmacy department. Each
mouthrinse was the same color, and kept
in a coded container. Study subjects were
instructed to rinse with 10 ml of mouthrinse for 60 seconds BID, post-breakfast
and post-lunch, for 30 days. They were not
to rinse with water afterward. They were
also instructed not to consume any solid or
liquid for a half hour following mouthrinse
use. Except for the BID mouth rinsing,
the volunteers were asked to maintain their
normal oral hygiene practices. All subjects
lived in the same student housing, so they
all shared the same diet. A compliance
diary was given to each study participant;
they were asked to make an entry of each
usage and side effects experienced, if any.
Unstimulated saliva samples were collected
and inoculated on MSB agar (MS1) before
the study began (baseline). Unstimulated
saliva samples were collected from subjects
of all 3 groups at the end of 30 days and
inoculated onto MSB agar (MS2); colony
counts were obtained after 48 hours
incubation. On Day 31, the subjects were
instructed to stop using the mouthrinse and
continue with their routine oral hygiene
care. At Day 60, unstimulated saliva
samples were collected again, inoculated
onto MSB agar (MS3), and colony counts
were obtained after incubation.
Collection of saliva sample
The unstimulated saliva samples were collected during the study in the mornings
after the use of mouthrinse. The study
subjects were asked not to swallow for
60 seconds, after which time the pooled
saliva on the floor of the mouth was aspirated with a syringe. The syringes were
coded and the saliva samples were diluted
in distilled water. The sample was inoculated within 30 minutes after collection.
All the microbiological procedures were
carried out in the microbiology lab of the
university’s medical college.
Statistical analysis
SPSS version 21 (SPSS, Inc.) was used
for data analysis. Repeated ANOVA and
ANOVA followed by post hoc least significant difference (LSD) tests were used
for analysis. A P value of 0.05 was taken
to be significant.
Results
All 90 participants completed the study.
Descriptive statistics are presented in
Table 1. No statistically significant difference was found in the baseline data between
the 3 groups. Compliance with mouthrinse
use was determined to be acceptable for
both the experimental groups. Mean
www.agd.org
compliance in the A. nilotica group was
90.1% (range 87% to 95%), while that
of the chlorhexidine group was 86.3%
(range 82% to 96%). ANOVA was used
to analyze the reduction in colony counts
in the 3 groups. There was a significant
decrease in the MS colony count in both
the A. nilotica and chlorhexidine groups at
Day 30 (85% and 83%, respectively) and
at Day 60 (65% and 63%, respectively)
(P < 0.0001). The colony counts obtained
at Day 60 showed a slight increase compared to counts obtained at Day 30, but
an overall reduction to the baseline colony
count was seen (P < 0.0001). The control
group showed a slight decrease at Day 30
and a slight increase at Day 60 (3% and
7%, respectively). This variation, however,
was not statistically significant (P = 0.201).
ANOVA was carried out to assess the
intra- and intergroup variations (Table 2).
There was no significant difference in
the baseline colony count between the
3 groups (P = 1.312), while the difference
at Day 30 and Day 60 was statistically
significant (P = 0.0001). Post-hoc LSD was
performed to obtain multiple comparisons
(Table 3). The difference in the decrease
in colony counts between A. nilotica and
chlorhexidine groups was not statistically
significant (P = 0.981 and P = 0.856 at
Days 30 and 60, respectively). However,
the differences between both Group 1
and Group 2 vs Group 3 (control) were
highly significant (P < 0.0001).
General Dentistry
25
Microbiology Investigation of antibacterial efficacy of Acacia nilotica against salivary mutans streptococci
Adverse events
The most common adverse event reported
was a mild burning sensation in both the
A. nilotica and chlorhexidine groups. The
chlorhexidine group reported altered taste
and brown staining of the teeth (50% and
67%, respectively). Such side effects were
not recorded in the A. nilotica group.
Discussion
The present study was conducted to
assess the antibacterial action of a 50%
A. nilotica mouthrinse against salivary
MS in comparison with the ‘gold standard’ 0.2% chlorhexidine mouthrinse and
a placebo (saline water).
Research has been focused in recent
years on herbal medicines as alternatives to
synthetically created antimicrobial agents,
due to their wide range of biological and
medicinal activities, potentially higher
safety margins, and lower costs. Several
antibacterial agents—such as chlorhexidine, fluorides, and various antibiotics—
are commercially available that can be used
to prevent dental caries. However, some of
these have been reported to have undesirable side effects, including nausea, vomiting, tooth staining, and metallic taste.4 A.
nilotica is considered safe for human use.12
Research on A. nilotica-containing
products has demonstrated its oral health
benefits. Acacia gum has the potential to
inhibit early plaque formation, although
there is no proven long-term benefit.
For centuries, A. nilotica gum has been
used for oral hygiene in the Middle East
and North Africa.13 In a 2010 study, a
gel containing A. nilotica significantly
improved clinical gingival and plaque
index scores over a period of 6 weeks.14
In a comparison study of other herbal
remedies, Dhanya Kumar & Sidhu
indicated that an A. nilotica extract
(concentration 50%) showed the highest
antimicrobial activity against S. mutans.15
Thus, a 50% extract concentration was
chosen for this study. Following the use
of mouthrinse for 30 days, the MS colony
counts in the saliva decreased by 85%
and 83% in Groups 1 and 2, respectively.
This reduction was statistically significant. The MS colony counts at Day 60
showed a reduction in Groups 1 and 2
(65% and 63%, respectively). This suggests that the antibacterial efficacy of A.
nilotica against salivary MS parallels that
26
of chlorhexidine. In contrast, Group 3
showed a slight variation in MS colony
count. For both Groups 1 and 2, there
was a slight decrease in colony counts
at Day 30 and a slight increase at Day
60. This variation was not statistically
significant and it was possibly due to
physiological changes.
A. nilotica stem bark extracts contain
alkaloids, saponins, cardiac glycosides,
tannins, flavonoids, and anthraquinones
which might be responsible for its antibacterial properties.9 A review of the available literature revealed that some authors
have reported in vivo antibacterial activity
of herbs such as Terminalia chebula and
Triphala against salivary MS, and Aloe
vera against dental plaque, but to date, no
studies have been conducted to assess the
effect of A. nilotica on salivary MS.16-20
The results of 50% A. nilotica extract
mouthrinse on salivary MS could not be
compared with other studies, as no in vivo
studies that have tried to assess the same
effect have been reported in the literature.
However, studies have been reported
that suggest that A. nilotica possesses
other beneficial properties for general
and oral health.21
Compliance with mouthrinse use was
acceptable in both Groups 1 and 2. Mean
compliance in the A. nilotica group was
93.6% while that in the chlorhexidine
group was 91.2%. The taste of A. nilotica
mouthrinse was acceptable to all the subjects of the group. The astringent action of
A. nilotica resulted in the drying of the oral
cavity, and subjects reported that it acted
as a breath freshener. Side effect profiles
were also checked at the end of the trial.
No staining of the teeth or altered taste
perception was reported by the volunteers
in the A. nilotica group. Volunteers using
chlorhexidine reported a yellowish discolouration of the teeth and a metallic taste.
Cost effectiveness
Commercially available 0.2% chlorhexidine mouthrinse (100 ml) ranges in cost
from 55 to 100 rupees (or 0.90 to 1.63
USD). In India, this is very expensive
for people of lower economic means.
However, India’s rural population has
the option to dry and powder the bark
of an A. nilotica tree, and then mix it
with 2 parts water to 1 part powder. This
mixture can then be heated and allowed
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to simmer until the water is reduced by
75%. The extract can then be used as a
mouthrinse. This method is the prevailing oral hygiene practice in rural parts of
India. Alternatively, purified A. nilotica is
commercially available in powder form.
At 50 rupees (0.82 USD) for 500 g, the
powder is very cost efficient and can be
used instead of bark. For a family of 4,
10 mg of powder can be used to make
100 ml of mouthrinse—enough for the
entire family to use for 4 days. The cost
per 10 ml of mouthrinse use is estimated
to be approximately 1 rupee (0.02 USD).
Our data show that a mouthrinse made
from A. nilotica is just as effective in combating caries as chlorhexidine. A. nilotica
can be considered a viable substitute for
chlorhexidine, especially among populations of lower socioeconomic means.
Conclusion
As S. mutans is generally considered the
main oral pathogen responsible for dental
caries, the fact that A. nilotica inhibited
the growth of S. mutans provides some
scientific rationale for the use of this plant
for the treatment of dental caries. The
results of the present study clearly indicate
the use of A. nilotica as a viable mouthrinse among rural communities of lower
economic means, where it is easily accessible. However, as this is the first attempt
to assess the effects of A. nilotica on
salivary S. mutans, a clinical trial of longer
duration with a larger sample size is necessary in the consideration of a commercially
available A. nilotica mouthrinse.
Author information
Dr. D. Gupta is an assistant professor,
Department of Public Health Dentistry,
Institute of Dental Sciences, Bareilly, Uttar
Pradesh, India. Dr. R. Gupta is a principal,
Government Degree College, Banbasa,
Uttrakhand, India.
References
1. Bagramian RA, Garcia-Godoy F, Volpe AR. The global
increase in caries. A pending health crisis. Am J Dent.
2009;22(1):3-8.
2. Jones CG. Chlorhexidine: is it still the gold standard?
Periodontol 2000. 1997;15:55-62.
3. McCoy LC, Wehler CJ, Rich SE, Garcia RI, Miller DR,
Jones JA. Adverse events associated with chlorhexidine use: results from the Department of Veterans Affairs Dental Diabetes Study. J Am Dent Assoc. 2008;
139(2):178-183.
4. Gupta D, Bhaskar DJ, Gupta RK, et al. Effect of Terminalia chebula extract and chlorhexidine on salivary pH
and periodontal health: 2 weeks randomized control
trial. Phytotherapy Res. 2013;28(7):992-998.
5. Dioscorides. De Materia Medica. Available at: http://
penelope.uchicago.edu/~grout/encyclopaedia_
romana/aconite/materiamedica.html. Accessed October 1, 2014.
6. Gupta D, Gupta RK, Bhaskar DJ, et al. Comparative
evaluation of Terminalia chebula extract mouthwash
and chlorhexidine mouthwash on plaque and gingival
inflammation - 4-week randomised control trial. Oral
Health Prev Dent. 2014. [Epub ahead of print]
7. Jarvinen H, Tenevuo J, Huovinen P. Susceptibility of
Streptococcus mutans to chlorohexidine and six other
antimicrobial agents. Antimicrob Agents Chemother.
1993;37(5):1158-1159.
8. Dhinahar S, Lakshmi T. Role of botanicals as antimicrobial agents in management of dental infections – a
review. Int J Pharm Biosci. 2011;2(4):8690-8704.
9. Deshpande SN, Kadam DG. Phytochemical analysis
and antibacterial activity of Acacia nilotica against
Streptococcus mutans. Int J Pharm Biosci. 2013;5(1):
236-238.
10. Xavier TF, Vijayalakshmi P. Screening of antibiotic resistant inhibitors from Indian traditional medicinal plants
against Streptococcus mutans. J Plant Sci. 2007. Available at: http://www.docsdrive.com/pdfs/academicjournals/jps/2007/370-373.pdf. Accessed September 30,
2014.
11.American Dental Association Council on Scientific
Affairs. Adjunctive Dental Therapies for the Reduction of Plaque and Gingivitis. Available at: http://
www.ada.org/~/media/ADA/Science%20and%20
Research/Files/guide_adjunctive.ashx. Accessed October 2, 2014.
12. Kannan N, Sakthivel KM, Guruvayoorappan C. Protective effect of Acacia nilotica (L.) against acetaminophen-induced hepatocellular damage in Wistar rats.
Adv Pharmacol Sci. 2013. Available at: http://www.
hindawi.com/journals/aps/2013/987692/. Accessed
September 30, 2014.
13. Gazi MI. The finding of antiplaque features in Acacia
arabica type of chewing gum. J Clin Periodontol. 1991;
18(1):75-77.
14. Pradeep AR, Happy D, Garg G. Short-term clinical
effects of commercially available gel containing
Acacia arabica: a randomized controlled clinical trial.
Aust Dent J. 2010;55(1):65-69.
15. Dhanya Kumar NM, Sidhu P. The antimicrobial activity of Azardirachta Indica, Glycyrrhiza glabra, Cinnamum zeylanicum, Syzygium aromaticum, Accacia
nilotica on Streptococcus mutans and Enterococcus
faecalis: an in vitro study. Endodontology. 2011;23:
18-25.
16. Jagtap AG, Karkera SG. Potential of the aqueous
extract of Terminalia chebula as an anticaries agent.
J Ethnopharmacol. 1999;68(1-3):299-306.
17. Nayak SS, Kumar BR, Ankola AV, Hebbal M. The efficacy of Terminalia chebula rinse on Streptococcus
www.agd.org
mutans count in saliva and its effect on salivary pH.
Oral Health Prev Dent. 2010;8(1):55-58.
18. Srinagesh J, Pushpanjali K. Assessment of antibacterial
efficacy of triphala against mutans streptococci: a randomised control trial. Oral Health Prev Dent. 2011;
9(4):387-393.
19. Karim B, Bhaskar D.J., Agali C., et al. Effect of Aloe vera mouthrinse on periodontal health: triple blind randomized control trial. Oral Health Dent Manag. 2014;
13(1):14-19.
20. Gupta D, Bhaskar DJ, Gupta RK, et al. A randomized
controlled clinical trial of Ocimum sanctum and
chlorhexidine mouthwash on dental plaque and gingival inflammation. J Ayurveda Integr Med. 2014;5(2):
109-116.
21. Pradeep AR, Happy D, Garg G. Short-term clinical effects of commercially available gel containing Acacia
arabica: a randomized controlled clinical trial. Aust
Dent J. 2010;55(1):65-69.
Manufacturers
HiMedia Laboratories, Mumbai, India
91.22.6147.1919, www.himedialabs.com
LTE Scientific Ltd., Greenfield, England
44.1457.876221, www.lte-scientifc.co.uk
SPSS, Inc., Quarry Bay, Hong Kong
852.2811.9662, www.spss.com
General Dentistry
27
Exercise No. 361 Microbiology Subject Code 013
The 15 questions for this exercise are based on the article,
Investigation of antibacterial efficacy of Acacia nilotica
against salivary mutans streptococci: a randomized
control trial, on pages 23-27. This exercise was developed
by Jean Carlson, DDS, FAGD, in association with the
General Dentistry Self-Instruction committee.
Reading the article and successfully completing this exercise will enable you to:
•identify the physical properties of Acacia nilotica (AN);
•recognize the action of AN against mutans streptococci (MS); and
•understand the efficacy of chlorhexidine mouthrinses compared with
AN mouthrinses.
1. Dental caries results from the interplay
of all the following factors except one.
Which is the exception?
A.bacteria in dental plaque
B. dietary carbohydrates
C.physiologic age
D.susceptible tooth surfaces
6. In subjects using the AN mouthrinse,
the MS colony count was decreased
by _____% at 30 days.
A. 85
B. 83
C. 65
D. 63
2. Chlorhexidine has all of the following
inherent side effects except one. Which
is the exception?
A. burning sensation
B. altered taste
C. staining of teeth
D. mucosal sloughing
7. The most common adverse reaction
reported was altered taste sensation in
both the AN and chlorhexidine groups.
Brown staining was not observed in the
AN group.
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. An AN mouthrinse exhibits
antibacterial effects against halitosisinducing bacteria on the tongue. The
efficacy of AN against MS remains
unproven in in vitro studies.
the second is true.
4. Volunteers in Group 1 were given
_____% AN mouthrinse for use in
the study.
A. 40
B. 50
C. 60
D. 70
5. Study participants were instructed
to rinse their mouths with ____ ml of
solution for ____ seconds.
A.5; 30
B. 10; 30
C. 5; 60
D. 10; 60
8. In the placebo control group, a slight
variation in MS colony count was
reported. There was a slight increase
in colony count at 30 days with a slight
decrease at 60 days.
the second is true.
9. AN stem bark extracts contain all of
the following components except one.
A. free radicals
B. tannins
C. saponins
D. flavonoids
10. Mean compliance of mouthrinse use in
the AN group was ____%.
A. 91.2
B. 93.6
C. 95.2
D. 97.6
11. Mean compliance of mouthrinse use in
the chlorhexidine group was _____%.
A. 81.2
B. 83.6
C. 91.2
D. 93.6
12. The cost for 100 ml 0.2% chlorhexidine
mouthrinse ranges between ____ Indian
rupees.
A. 55-100
B. 105-150
C. 155-200
D. 205-250
13. A quantity of 500 g AN powder is
priced at _____ Indian rupees.
A. 20
B. 30
C. 40
D. 50
14. The average age of participants
in the placebo control group
was ______ years.
A. 21.16
B. 21.42
C. 22.16
D. 22.74
15. The placebo group was given _______
to use as a mouthrinse.
A. ethanol
B. saline water
C. hydrogen peroxide
D. chlorhexidine
Answer form is on the inside back cover. Answers for this exercise must be received by December 31, 2015.
28
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AGDPODCAST
The AGD Podcast series features interviews with some of the profession’s most highly
regarded speakers. To access, simply use your smartphone to scan each podcast’s QR code,
download, and enjoy!
Marketing Your Practice
with Kim McQueen
New Vistas in Periodontics
with Sam Low, DDS, MS, MEd
Insurance Coding Updates
with Charles Blair, DDS
Effective Web Marketing
with Colin Receveur
Profiting with PPO Dental
Insurance with Dana Moss
Embezzlement in the Dental
Office with David Harris
Dr. Blakeslee discusses
the latest news and
emerging trends with
prominent dental
professionals to keep
you in the know.
Wes Blakeslee,
DMD, FAGD
Clinical considerations for selecting implant
abutments for fixed prosthodontics
Roger A. Solow, DDS
There is an overwhelming number of designs and components for
dentists to choose from when treatment planning implant-supported
restorations. The selection process can be simplified by establishing
priorities on a site-by-site basis to facilitate a predictable, esthetic,
and stable final result. Clinical considerations should include prosthetic
support, periodontal stability, reparability, and oral hygiene, which often
T
reatment planning for any case that
includes implant-supported restorations may involve a complex series of
decisions about a multifactorial problem
list. The restorative dentist, who typically
finishes the case, must be able to explain to
the patient why the proposed treatment is
the optimal approach, and communicate to
the surgeon the necessary steps for achieving the desired result. One way to organize
the treatment planning is to decide on the
priorities for each site and the overall goal
of the comprehensive restoration. These
priorities are based on the clinical considerations of prosthetic support, periodontal
stability, reparability, and oral hygiene.
This article discusses how these concerns
influence treatment planning and the
selection of implant abutments for fixed
prosthodontics. Dentists must understand
the relationship between implant and abutment for optimal clinical application.
It is not possible to discuss all implant systems in a single article, and any mention of
a specific manufacturer is intended to show
a design or concept, not to make a recommendation. This article illustrates clinical
decisions based on this author’s preferences,
clinical experience, and the literature.
Anterior and posterior tooth restorations are placed in different environments.
Anterior teeth are highly visible and have
a scalloped periodontium, with the facial
and oral bone distinctly apical to the
interproximal bone level. Posterior teeth
are less visible and have flatter periodontal
architecture with less disparity between
the facial and oral bone and the interproximal bone levels. Anterior teeth have
thin bundle bone that is lost after tooth
removal, inducing significant alveolar ridge
30
occur in concert. This article addresses the principles that guide implant
abutment selection when treatment planning for fixed prosthodontics.
Received: December 16, 2013
Revised: May 28, 2014
Accepted: September 3, 2014
alteration.1 Anterior teeth experience less
masticatory and bruxing forces compared
to posterior teeth.2 When using implants
to restore anterior teeth, the main priority
of treatment is to preserve the topography of the dentogingival interface via
periodontal reconstruction and prosthetic
contours for stability and esthetics. By
contrast, the priority for implant restoration of posterior teeth is force management, in order to avoid damage to the
implant, abutment, prosthesis, or crestal
bone. However, some anterior sites are
not visible due to the marginal gingiva-lip
relationship or low lip activity, while some
posterior sites may be quite visible due to
high lip mobility, requiring tissue augmentation for acceptable esthetics.
Prosthetic support and posterior
tooth sites
Many posterior tooth restorations have
low esthetic exposure, and the priority
with implant-supported restorations is to
avoid adverse forces on the prosthesis and
the supporting periodontium.3 Placing
the implant in the center of the restorative
space is the first step toward accomplishing
these goals. Ridge augmentation may be
necessary to create the proper dimensions
for ideal implant positioning. When multiroot extraction sites are involved, immediate implant placement may be facilitated
by engaging the septal bone to provide
proper orientation.4,5 Placing an implant
into the socket of a multirooted tooth
creates a cantilevered restoration (Fig. 1).
With single crowns, off-center implant
placement forms a cantilever on 1 side of
the implant that increases stress on the
restorative material, abutment, implant,
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and crestal bone. In order to keep occlusal
forces aligned with the long axis of the
implant, the crown must be centered over
the implant platform and only contact
the opposing tooth during closure, not
mandibular excursions. The crestal bone
tolerates vertical, compressive force better
than shear forces induced by lateral torque
on the crown.6
The fracture of porcelain and implant
components can be caused by mechanical stress related to cantilevered restorations (Fig. 2). Proper implant position
in the center of the restorative space
and improved prosthetic support with
a wide diameter implant minimizes the
cantilever problem that is most noticeable
in molar sites. An average maxillary first
molar is 11 mm buccolingual and 10 mm
mesiodistal, while an average mandibular
first molar is 10.5 mm buccolingual and
11 mm mesiodistal.7 Regular diameter
Fig. 1. Implant-supported crown No. 31 with a
mesial cantilever. Abutment screw loosening was
attributed to magnified force by the cantilever.
Fig 2. Top. Fractured fragment of
implant neck due to force overload.
Bottom. Distal view of crown on
abutment with significant palatal
horizontal cantilever.
Fig. 3. Top. Soft-tissue level implant with a 6.5 mm
platform for enhanced prosthetic support, centered
in the edentulous space. Bottom. Regular diameter
implant supporting a molar crown with large
horizontal cantilever and gingival embrasures.
implant platforms typically are 3.75-5 mm,
while wide diameter implant platforms
typically are >5 mm. A mandibular molar
crown with ideal implant position and
average tooth dimension would have a
mesial horizontal cantilever of 3.25 mm
with a 4.5 diameter platform and only
2.25 mm with a 6.5 diameter platform.
Unfortunately, not all ridges are thick
enough buccolingually to accommodate
a wide diameter implant. A flared softtissue level implant with a 6.5 mm platform and a 4.8 mm body can be placed
within a 7 mm ridge (Standard Plus WN,
Straumann) (Fig. 3).
The larger platform increases the linear
prosthetic support by 2 mm (44% of a
4.5 mm implant) and normalizes the gingival embrasure by the same amount. This
abutment is torqued into the implant with
a tapered interference fit, so it is internally
connected to the implant platform edge
that forms the margin for the restoration,
eliminating the external implant-abutment
junction (IAJ) microgap.8 The wide diameter distributes force through more bone,
Fig. 4. Top. Subcrestal placement of a soft-tissue
level implant, complicating impressions and cement
clearance. Bottom. A good restoration fit was
achieved, but a nonhygienic, deep, subgingival
margin persists.
thus decreasing the crestal bone stress per
unit area.9 The implant should be placed
at the level of the gingiva or 0.5 mm
intracrevicularly for esthetics, cement
clearance, and patient hygiene. These
design features, combined with a rough
surface, minimize crestal bone loss. These
implants need to be placed in the correct
relationship with the rough-smooth border
at the crestal bone, to prevent any vertical
position errors that would require a mesostructure component or preparation of the
implant platform (Fig. 4).
Premolar teeth occupy a smaller space
than molars and encounter less force.
Providing prosthetic support is less of a
priority, as the horizontal cantilever (the
crown minus the crown margin dimension) is reduced. An average maxillary
first premolar is 9 mm buccolingual
and 7 mm mesiodistal, while an average
mandibular first premolar is 7.5 mm buccolingual and 7 mm mesiodistal.7 The
main concern with premolars is maintaining periodontal stability for esthetics and
implant longevity.
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A regular diameter soft-tissue level
implant can be used in premolar sites
similar to molars. The implant must
be placed accurately, as there is less
margin for error in the smaller sites,
and an implant malposition can result
in deficient papilla size or the need to
recontour adjacent teeth. A bone level
implant with a platform-switch abutment
is also appropriate for these sites. The
platform-switch abutment has a smaller
diameter compared to the implant platform that shifts the IAJ away from the
bone and toward the implant center.10
The bacterial-mediated inflammatory
infiltrate is displaced from the bone,
preserving higher osseous levels in comparison to symmetrical abutments, where
bone loss to the first implant thread is
typical. Platform-switch abutments have
been shown to preserve crestal bone with
bone growth onto the implant shoulder.11
Reducing the 360-degree bone loss seen
adjacent to symmetrical IAJs allows dentists to place the implants closer to natural
teeth or implants without losing the bone
General Dentistry
31
Diagnosis and Treatment Planning Clinical considerations for selecting implant abutments for fixed prosthodontics
that supports the interproximal papilla
height.12,13 The platform-switch design is
indicated for all bone level abutments.
In premolar implant sites, a stock titanium or zirconia abutment can be ordered
after the surgeon communicates the sulcus
depth (implant platform to marginal
gingiva) and the restorative space (marginal gingiva to opposing tooth occlusal
surface). These measurements are recorded
with a periodontal probe and minimize
the need for the restorative dentist to
maintain a large array of components. The
facial margin of the abutment should be
placed 0.5 mm intracrevicularly and the
oral margin should be placed at the level of
the marginal gingiva to visualize complete
crown seating (Fig. 5).14
If the interproximal margin is >1 mm
deep, compromising thorough cement
clearance, then a stock abutment with a
taller gingival collar should be customized.
This abutment should be seated and the
gingival margins marked intraorally with
a bur or ink. The abutment should be
shaped extraorally with diamond burs and
checked repeatedly by reseating it on the
implant until the margin is correct.
Alternatively, an implant level impression is obtained and the laboratory
technician creates a custom abutment
while a temporary abutment supports the
provisional restoration. This approach
involves additional time and cost, and
precludes the use of the “1 abutment at
1 time” protocol. Research has shown
that placement of the permanent abutment at the time of surgery helps to
preserve alveolar bone levels, as repetitive
detachment and attachment of titanium
abutments induces minor bone loss.15,16
The dentist must be assured of the stability of the facial periodontium to place the
permanent abutment at the time of surgery or healing abutment removal, since
gingival recession may require abutment
removal or intraoral preparation. This
technique is appropriate for thick periodontal biotypes and sites where esthetics
are not a concern.
Laser-etched 8-12 µ channels have been
shown to create an enhanced attachment
of bone and connective tissue to both
implants and abutments (Laser-Lok,
BioHorizons IPH, Inc.).17 Connective
tissue fibers inserted perpendicular to
these grooves are similar to natural teeth,
32
Fig. 5. Top. A premolar implant with a platformswitch abutment. Bottom. The flat gingiva permitted
the use of an unaltered stock abutment.
Fig. 6. Top. The dentogingival junction of the central
incisors is apical to the lip during function. Bottom. The
long contact ensured that the papilla filled the gingival
embrasure avoiding food accumulation and air passage.
instead of laying parallel as with polished
titanium. This attachment was broken and
reformed on detachment and replacement
of healing abutments with definitive abutments.18 These microgrooves are a positive
design feature to maintain crestal bone and
marginal gingiva levels.
If esthetics are not a concern because
the dentogingival junction is hidden by an
apical position beneath the lip or from an
inactive lip, restoration of the implant can
proceed as described above with bicuspid
sites. A stock abutment can be placed and
modified extraorally to create an intracrevicular margin prior to seating, impressions, and provisionalization (Fig. 6).
In most situations, anterior implantsupported restorations are placed in
highly visible areas where both white and
pink esthetics are apparent. Forces in the
anterior region are low, and the disparity
between crown dimension and prosthetic
support is small. The priority in anterior
site restoration is periodontal tissue stability and esthetics. The restorative dentist
must create a prosthetic contour—from
the orally positioned implant platform to
the incisal edge—that molds the gingiva
into the correct position and replicates
natural tooth esthetics. Platform-switch
bone level implants are recommended in
anterior esthetic sites to preserve crestal
bone and give the restorative dentist
control over the entire prosthetic contour. The restorative margin position for
tissue level implants is determined by the
surgeon and leaves little room for adjustment if the position is not correct. In ideal
Periodontal stability and anterior
tooth sites
Tomographic studies show that the buccal
plate of bone adjacent to anterior teeth
is often <1 mm thick or absent entirely,
which results in dehiscence and fenestrations.19,20 This bone is categorized as
bundle bone, a hybrid of osseous and
fibrous tissues. During root extraction,
this bone is resorbed after the periodontal
ligament ruptures.21 This loss of the socket
wall subsequently deforms the residual
alveolar ridge and complicates placement
of anterior implants. Implants placed in
the center of the resorbed ridge will be
toward the oral side of the original tooth
position. Intentional placement of the
implant further toward the oral side will
maximize buccal bone dimension. Most
anterior implant-supported restorations
require tissue augmentation to restore
the topography of the periodontium and
achieve stable esthetics.22
General Dentistry
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A
B
C
D
Fig. 7. A. One-piece implant with good mesiodistal placement and 2 mm of titanium from the restorative margin to the bone crest.
B. Provisional restoration with healthy tissue but asymmetric length with tooth No. 10. C. Gingival sculpting with retraction cord and
electrosurgery to elongate the facial length of the restoration. D. All-porcelain restoration with a facial and apical emergence profile.
circumstances, the biologic width of the
prosthetically molded and supported gingiva is allowed to mature for 3-6 months;
at that point, its contours are recorded
immediately after the provisional restoration is removed.23,24 A cement-retained
provisional on a permanent abutment
can be used for anterior restorations with
the “1 abutment at 1 time” protocol,
if the abutment properly supports the
facial tissue and a 0.5 mm intracrevicular
margin is present for cement clearance.
In this scenario, only interproximal tissue
modification would be necessary, as pressure from the provisional contour could
improve papillae shape. However, in most
anterior site cases, the need to modify the
facial contour sequentially, alter a permanent abutment margin intraorally, remove
the cement completely, or avoid cement
deterioration/re-cementation during the
maturation period make screw-retained
provisionals more practical.25,26 Screwretained provisional restorations facilitate
tissue molding for papillae and pontic sites
by maintaining constant gentle pressure,
inducing gingival blanching that dissipates
within 10 minutes.25,26
Anterior tooth restoration using an abutment and crown versus a screw-retained
crown is determined by the position and
angulation of the implant. A screw-retained
crown that attaches directly to the implant
platform requires the implant to be orally
positioned so that the screw access channel
exits through the cingulum of the crown.
When the implant is more facially positioned the abutment acts as a mesostructure to correct the position or angulation
that would result in the screw access channel exiting at, or facial to the incisal edge.
A conventional crown can be cemented on
the properly aligned abutment.
Custom abutments allow dentists to
control the cervical dimension and margin
location. They are indicated to either eliminate the access defect of screw retention or
compensate for the vertical and horizontal
implant position. A circumferential 0.5
mm intracrevicular margin creates good
esthetics with predictable cement removal.
The most coronal subgingival aspect of
a custom abutment or a screw-retained
crown has the greatest influence on the
gingival support and level.27
For predictable pink esthetics, the facial
gingival thickness should be 3 mm; at
this thickness, abutment color is not an
issue.28 A 2007 in vitro study by Jung et al
reported that titanium perceptibly altered
abutment color when gingival thickness
was 2 mm but not when it was 3 mm,
while white zirconia did not alter color for
either thickness.29 More recently, Happe
et al found that titanium induced a visible
change in gingival 1.5 mm thick while
white or dyed zirconia did not.30 A zirconia
abutment should be considered when the
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facial gingiva is less than 3 mm thick or has
a thin biotype where a periodontal probe is
visible when introduced into the sulcus. A
2009 systematic review showed that zirconia abutments met or exceeded the performance of titanium abutments in terms of
survivability and technical complications.31
One-piece implants are indicated for
anterior sites with a restricted mesiodistal
dimension. The small cervical width
of the implant would be reduced and
weakened if a screw channel was used
to attach an abutment. This system has
no IAJ or micromobility; however, the
surgeon must place the implant precisely
in 3 dimensions for an optimal restoration. The restorative dentist can customize
the coronal aspect of the implant, but
cannot substitute another abutment (in
case of over-reduction) or compensate for
problems with vertical position by using a
different abutment collar or switching to a
screw-retained crown (Fig. 7).
Reparability of cement vs
screw retention
Historically, a high incidence of abutment
screw loosening and the need to access and
retorque them favored screw retention for
fixed prostheses.32,33 According to a 2008
study by Theoharidu et al, abutment screw
loosening occurs in approximately 2.5%
of single implant restorations when proper
antirotational features and torque are
General Dentistry
33
used.34 The decision to use cement or screw
retention is based on the need to contour
periodontal tissues, interocclusal space,
subgingival implant platform location, or
anticipated need to repair a prosthesis.
Limited interocclusal space (<5 mm)
makes cement retention difficult.
Restorative material 2 mm thick would
leave an abutment height of only 3 mm
for frictional crown retention. In such
cases, screw-retained crowns are recommended, as inadequate abutment height
compromises the ability of cementretained restorations to resist dislodgement, especially in posterior tooth sites.35
Cement retention permits the same
clinical protocol as restorative dentistry on
natural teeth. Cement may act as a stressbreaker for splinted crowns and bridges,
with no occlusal access restorations to
compromise esthetics or occlusal contacts.
When necessary, crown retrieval can be
performed via occlusal access to create a
screw-retained design.
It is crucial to avoid excessive provisional
or permanent cement in the sulcus, which
could cause peri-implantitis. The following
protocol is the same for both provisional
and permanent cements. The axial wall
of the abutment is roughened with a diamond bur, or a slot undercut is placed in
the gingival third of the axial wall to resist
crown decementation due to smoothwalled abutments. Next, retraction cord is
placed in the sulcus. A slightly undersized
die, to create cement space, is fabricated
from the intaglio of the crown with a fastset polyvinyl siloxane (PVS) (Blu-Mousse,
Parkell, Inc.).36 A thin, slow-setting layer
of cement is placed inside the crown and
the crown is seated on the PVS die to
remove excess. The crown is then seated
on the abutment and removed. The cord
and any excess cement are removed and
the crown is immediately reseated. This
technique minimizes cement excess and
avoids cord entrapment under crowns.
A moderately strong provisional cement
(IRM, DENTSPLY Caulk) can retain a
relined provisional crown with a precise
fit for several months. Zinc phospate
cement is used for permanent cementation
since it is radiopaque and water soluble.
Radiotransparent, water insoluble, resin
cement should not be used for implantsupported crowns since it is the most
difficult type to detect and remove should
34
any excess polymerize past the margin.37
Residual cement removal is increasingly
difficult with deeper subgingival margins,
and this excess cement is directly related
to peri-implantitis. Screw retention avoids
this problem and is indicated for patients
with deep subgingival margins.38
Bruxers and patients who consume hard
or abrasive foods may experience a higher
incidence of repair. The anticipated need
for future repairs may be determined by
a patient’s history of repeated restoration, noncompliance with occlusal splint
therapy, or damage to high quality
provisional restorations. Large cases with
multiple, splinted, implant-supported
crowns or multiple-abutment implantsupported bridges may be more difficult
to repair. In these cases, damage to 1 area
could require accessing and disassembling
the cemented structure or the fabrication of an overcasting. Screw retention
facilitates removing the entire structure
and replacing it with a screw-retained
provisional restoration during laboratory repair. Repair may also be necessary
in the provisional phase of restoration.
Screw retention is recommended in cases
of long-term provisionalization, when
removal of the prosthesis is needed for
specialist procedures, or for patients who
risk decementation while traveling.
Multi-unit abutments are titanium components that compensate for soft tissue
thickness and implant angulation problems relative to the occlusal surfaces of a
screw-retained prosthesis. They function as
a mesostructure that allows the prosthesis
to seat at the abutment level instead of
the implant platform level, with screw
retention channels at favorable locations
through the occlusal surfaces
Oral hygiene and prosthesis
design
Oral hygiene requirements influence prosthesis design, with regard to access for routine frictional cleaning, minimizing food
entrapment in the gingival embrasure,
and creating optimal interproximal contacts. Over-contoured implant-supported
crowns inhibit access for proper hygiene,
resulting in plaque accumulation that may
lead to peri-implantitis.39 A proper gingival
embrasure form is just as important for
implant restorations as it is with orthodontic repositioning or the restoration of
General Dentistry
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Fig. 8. Top. Parallel placement of implant determined
by the surgical guide derived from a diagnostic
wax-up. Bottom. Individual gold castings on implants
No. 29 and 30, and tooth No. 31.
natural teeth for predictable maintenance.
Cantilevered restorations can create
gingival embrasures that trap food and
may compromise the ability to maintain
hygiene on the adjacent tooth (Fig. 1).40
Posterior crowns on contiguous
implants can be restored as nonsplinted
single units that have the same longevity
as splinted restorations.41,42 However,
adjusting the interproximal contacts
can be a challenge since the ankylosed
implant does not move. The resilient
periodontal ligament of a natural tooth
allows for a slight separation of the interproximal contact. The contacts must be
adjusted to allow thin floss to pass without creating an open contact that collects
food. This adjustment involves marking
the interproximal contact repeatedly by
seating the crown (with marking ribbon
between it and the adjacent tooth) and
polishing the marked area. This treatment allows patients to brush and floss
normally; however, it requires a normal
gingival embrasure dimension to create
an ideal contact area (approximately 3 x
2 mm) with the papilla, which fills the
embrasure and precludes lateral food
impaction (Fig. 8). If proper contacts
cannot be developed, the crowns should
be splinted to avoid food entrapment.
this process by analyzing the problem list
and designating priorities for each implant
site that support the total restorative plan.
Author information
Dr. Solow is in private practice in Mill
Valley, California, and a visiting faculty
member at the Pankey Institute, Key
Biscayne, Florida.
References
Fig. 9. Top. Four posterior tooth implants supporting
a cemented, splinted prosthesis. The pronounced
interproximal contacts normalize the gingival
embrasures. Bottom. Provisional restoration with
a large crown-to-implant ratio, large interproximal
contacts, and normal gingival embrasures.
Implants often are placed after traumatic
tooth loss or advanced periodontal disease
that results in significant bone loss and
a large restorative space (Fig. 9). When
these contiguous implants are restored,
they should be splinted together to bring
the restorative contours in contact with
the gingival tissue and avoid exaggerated
gingival embrasures and food entrapment.
Nonsplinted crowns would either require
perfecting large contact areas with normal
gingival embrasures or accept the normal
contact areas with open gingival embrasures that can trap food.
Summary
Treatment planning for implant-supported
restorations requires a thorough understanding of the periodontal requirements
for a stable and esthetic foundation.
Choices for the abutment and the implantabutment interface should be based on the
anatomy and the clinical considerations of
each particular site. Dentists can simplify
1. Nevins M, Camelo M, De Paoli S, et al. A study of the
fate of the buccal wall of extraction sockets of teeth
with prominent roots. Int J Periodontics Restorative
Dent. 2006;26(1):19-29.
2. Kumagi H, Suzuki T, Hamada T, Sondang P, Fujitani M,
Nikawa H. Occlusal force distribution on the dental
arch during various levels of clenching. J Oral Rehabil.
1999;26(12):932-935.
3. Crispin BJ, Watson JF. Margin placement of esthetic
veneer crown. Part II: posterior tooth visibility. J Prosthet Dent. 1981;45(4):389-391.
4. Fugazzotto PA. Implant placement at the time of mandibular molar extraction: description of technique and
preliminary results of 341 cases. J Periodontol. 2008;
79(4):737-747.
5. Fugazzotto PA. Implant placement at the time of maxillary molar extraction: treatment protocols and report
of results. J Periodontol. 2008;79(2):216-223.
6. Kim Y, Oh TJ, Misch CE, Wang HL. Occlusal considerations in implant therapy: clinical guidelines with biomechanical rationale. Clin Oral Implants Res. 2005;
16(1):26-35.
7. Kraus BS, Jordan RE, Abrams L. Dental Anatomy and
Occlusion. Baltimore, MD: Williams and Wilkins Co.;
1973:48-94.
8. Bozkaya D, Muftu S. Mechanics of the tapered interference fit in dental implants. J Biomech. 2003;36(11):
1649-1658.
9. Anitua E, Tapia R, Luzuriaga F, Orive G. Influence of
implant length, diameter, and geometry on stress distribution: a finite element analysis. Int J Periodontics
Restorative Dent. 2010;30(1):89-95.
10. Lazzara RJ, Porter SS. Platform switching: a new concept in implant dentistry for controlling postrestorative
crestal bone levels. Int J Periodontics Restorative Dent.
2006;26(1):9-17.
11. Degidi M, Perrotti V, Shibli JA, Novaes AB, Piattelli A,
Iezzi G. Equicrestal and subcrestal dental implants: a
histologic and histomorphometric evaluation of nine
retrieved human implants. J Periodontol. 2011;82(5):
708-715.
12. Vela X, Mendez V, Rodriguez X, Segala M, Tarnow DP.
Crestal bone changes on platform-switched implants
and adjacent teeth when the tooth-implant distance is
less than 1.5 mm. Int J Periodontics Restorative Dent.
2012;32(2):149-155.
13. Nevins M, Nevins ML, Gobbato L, Lee HJ, Wang CW,
Kim DM. Maintaining interimplant crestal bone height
via a combined platform-switched, Laser-Lok implant/
abutment system: a proof-of-principle canine study. Int
J Periodontics Restorative Dent. 2013;33(3):261-267.
14. Nevins M, Skurow HM. The intracrevicular restorative
margin, the biologic width, and the maintenance of
the gingival margin. Int J Periodontics Restorative
Dent. 1984;4(3):30-49.
www.agd.org
15. Degidi M, Nardi D, Piattelli A. One abutment at one
time: non-removal of an immediate abutment and its
effect on bone healing around subcrestal tapered implants. Clin Oral Implants Res. 2011;22(11):13031307.
16. Abrahamsson I, Berglundh T, Lindhe J. The mucosal
barrier following abutment dis/reconnection. An experimental study in dogs. J Clin Periodontol. 1997:
24(8):568-572.
17. Nevins M, Nevins ML, Camelo M, Boyesen JL, Kim DM.
Human histologic evidence of a connective tissue attachment to a dental implant. Int J Periodontics Restorative Dent. 2008;28(2):111-121.
18. Nevins M, Camelo M, Nevins ML, Schupbach P, Kim
DM. Reattachment of connective tissue fibers to a laser-microgrooved abutment surface. Int J Periodontics
Restorative Dent. 2012;32(4):e131-e134.
19. Braut V, Bornstein MM, Belser U, Buser D. Thickness of
the anterior facial bone wall—a retrospective radiographic study using cone beam computed tomography. Int J Periodontics Restorative Dent. 2011;31(2):
125-131.
20. Vera C, De Kok IJ, Reinhold D, et al. Evaluation of buccal alveolar bone dimension of maxillary anterior and
premolar teeth: a cone beam computed tomography
investigation. Int J Oral Maxillofac Implants. 2012;
27(6):1514-1519.
21. Cardaropoli D, Cardaropoli G. Preservation of the
postextraction alveolar ridge: a clinical and histologic
study. Int J Periodontics Restorative Dent. 2008;28(5):
469-477.
22. Buser D, Halbritter S, Hart C, et al. Early implant placement with simultaneous guided bone regeneration
following single-tooth extraction in the esthetic zone:
12-month results of a prospective study with 20 consecutive patients. J Periodontol. 2009;80(1):152-162.
23. Wilson RD, Maynard G. Intracrevicular restorative dentistry. Int J Periodontics Restorative Dent. 1981;1(4):
34-49.
24. Priest G. Developing optimal tissue profiles implantlevel provisional restorations. Dent Today. 2005;
24(11):96, 98, 100.
25. Potashnick SR. Soft tissue modeling for the esthetic
single-tooth implant restoration. J Esthet Dent. 1998;
10(3):121-131.
26. Issarayangkul C, Schoenbaum TR, McLaren EA. Prosthetic soft tissue management following two periimplant graft failures: a clinical report. J Prosthet Dent.
2013;110(3):155-160.
27.Su H, Gonzalez-Martin O, Weisgold A, Lee E. Considerations of implant abutment and contour: critical
contour and subcritical contour. Int J Periodontics
Restorative Dent. 2010;30(4):335-343.
28. Gamborena I, Blatz MB. The gray zone around dental
implants: keys to esthetic success. Am J Esthet Dent.
2011;1(1):26-46.
29. Jung RE, Sailer I, Hammerle CH, Attin T, Schmidlin P. In
vitro color changes of soft tissues caused by restorative materials. Int J Periodontics Restorative Dent.
2007;27(3):251-257.
30. Happe A, Schulte-Mattler V, Strassert C, et al. In vitro
color changes of soft tissues caused by dyed fluorescent zirconia and nondyed, nonfluorescent zirconia in
thin mucosa. Int J Periodontics Restorative Dent. 2013;
33(1):e1-e8.
31. Sailer I, Philipp A, Zembic A, Pjetursson BE, Hammerle CH, Zwahlen M. A systematic review of the performance of ceramic and metal implant abutments
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supporting fixed implant reconstructions. Clin Oral
Implants Res. 2009;20(Suppl 4):4-31.
32. Becker W, Becker BE. Replacement of maxillary and
mandibular molars with single endosseous implant
restorations: a retrospective study. J Prosthet Dent.
1995;74(1):51-55.
33. Kallus T, Bessing C. Loose gold screws frequently occur
in full-arch fixed prostheses supported by osseointegrated implants after 5 years. Int J Oral Maxillofac Implants. 1994;9(2):169-178.
34. Theoharidu A, Petridis HP, Tazannas K, Garefis P. Abutment screw loosening in single-implant restorations:
a systematic review. Int J Oral Maxillofac Implants.
2008;23(4):681-690.
35. Taylor TD, Belser U, Mericske-Stern R. Prosthodontic
considerations. Clin Oral Implants Res. 2000;
11(Suppl 1):101-107.
36. Wadhwani C, Pineyro A. Technique for controlling the
cement for an implant crown. J Prosthet Dent. 2009;
102(1):57-58.
37. Wadhwani C, Hess T, Faber T, Pineyro A, Chen CS. A
descriptive study of the radiographic density of implant restorative cements. J Prosthet Dent. 2010;
103(5):295-302.
38. Wilson TG Jr. The positive relationship between excess
cement and peri-implant disease: a prospective clinical
endoscopic study. J Periodontol. 2009;80(9):1388-1392.
39. Chaves ES, Lovell JS, Tahmasebi S. Implant-supported
crown design and the risk for peri-implantitis. Clin Adv
Periodont. 2014;4(2):118-126.
40. Chiche G. Pinault A. Considerations for fabrication of
implant-supported posterior restorations. Int J Prosthodont.1991;4(1):37-44.
41. Simon RL. Single implant-supported molar and premolar crowns: a ten-year retrospective clinical report.
J Prosthet Dent. 2003;90(6):517-521.
42. Mendonca JA, Francischone CE, Senna PM, Matos de
Oliveira AE, Sotto-Maior BS. A retrospective evaluation
of the survival rates of splinted and non-splinted short
dental implants in posterior partially edentulous jaws.
J Periodontol. 2014;85(6):787-794.
Manufacturers
BioHorizons IPH, Inc., Birmingham, AL
888.246.8338, www.biohorizons.com
DENTSPLY Caulk, Milford, DE
800.532.2855, www,caulk.com
Parkell, Inc., Edgewood, NY
800.243.7446, www.parkell.com
Straumann, Andover, MA
978.747.2500, www.straumann.com
There are more articles on
DIAGNOSIS AND TREATMENT
PLANNING in the online edition.
•Central giant cell lesion: diagnosis
to rehabilitation
•Alveolar ridge splitting for implant
placement: a review of the
procedure and report of 3 cases
•Atypical presentation of
salivary mucocele: diagnosis
and management
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General Dentistry
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Dental Materials
Surgical repair of invasive cervical root resorption
with calcium-enriched mixture cement: a case report
Saeed Asgary, DDS, MS n Mahta Fazlyab, DDS, MS
Invasive cervical resorption (ICR) occurs in the cervical area of the teeth
due to the formation of a soft tissue that progressively resorbs dentin.
The disease is asymptomatic unless the pulp is exposed. This article
presents a case involving a mandibular canine that was treated with a
calcium-enriched mixture (CEM) cement. After a full mucoperiosteal flap
was performed, the soft tissue was curetted away and the cavity filled
with CEM biomaterial. One week later, the supragingival surface of the
CEM was polished and covered with composite resin. At a 1-year followup visit, the pulp was healthy and the gingival probing depth decreased
I
rritation of the periodontal ligament
or pulp can lead to internal or external
resorption.1 Invasive cervical resorption
(ICR) refers to a type of external root
resorption, defined as a resorptive process
in the cervical area that involves the
root surface in the junctional epithelium
zone.2,3 Other terms used to describe
this process include odontoclastoma,
peripheral cervical resorption, extracanal
invasive resorption, supraosseous extracanal invasive resorption, and subepithelial
external root resorption.3,4 The term invasive describes the aggressive nature of this
lesion.3,5,6 Although early diagnosis may
be difficult, some clinical signs can indicate the presence of an ICR lesion, such as
a pinkish hue in the crown (as a result of
the thinning resorbed dentin), the translucency of enamel that makes the vascular
resorptive tissue visible, and contour
irregularities.3,7-10 The condition usually
is painless due to a predentin layer that
protects the pulp.4,7,11-14 Symptoms develop
when the resorption penetrates through
this barrier and the pulp is invaded secondarily by oral bacteria.11,13 Most lesions
seen on periapical radiographs are poorly
defined with irregular borders, with what
has been referred to as a “moth-eaten”
appearance.1,5,14 The outline of the root
canal can be seen as a radiopaque line
through the lesion.1,5,14
The etiology of ICR is poorly understood; however, it has been suggested that
a type of fibrovascular tissue and clastic
resorbing cells may be responsible.3,4,10,15
Direct contact between the dentin and
from >3 mm to 1 mm, showing attachment gain. As a biocompatible
material, CEM has proven its ability in dentinogenesis, cementogenesis,
and osteogenesis; it may prove to be a suitable biomaterial for treating
ICR cases.
Key words: calcium-enriched mixture, CEM cement, cervical
resorption, endodontic, invasive cervical root resorption
the periodontium (due to a defect in the
cementum layer) is necessary for such
an invasion.3-5,10,16 Several potential predisposing factors have been identified,
including trauma, orthodontic treatment,
dentoalveolar surgery, and periodontal
treatment; in addition, feline herpes
virus type 1 is suspected as an etiologic
cofactor.5,17 Heithersay developed a clinical classification system for such lesions:
Class 1, a small lesion near the cervical
area with shallow penetration into the
dentine; Class 2, a well-defined lesion
that has penetrated close to the coronal
pulp with little or no extension into the
radicular dentine; Class 3, a deeper invasion of dentine that not only involves the
coronal dentine but also extends into the
coronal third of the root (the majority of
patients present at this stage); and Class
4, a large resorptive process that extends
beyond the coronal third of the root.5 The
author also recommended that dentists
only treat defects categorized as Class 1,
2, or 3, as the extensive nature of Class 4
lesions makes treatment difficult.5,18,19
The basic goal of ICR treatment is the
inactivation of all resorbing tissue and the
reconstitution of the tooth structure so that
the tooth may be retained for health and
esthetics.9-11,15 In a 2004 article, Heithersay
recommended a treatment regimen that
included mechanical/chemical debridement of the resorptive lesions, followed
by restoration.6 That same article also
offered a nonsurgical technique involving
a 90% aqueous solution of trichloracetic
acid applied topically to the resorptive
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tissue, followed by curettage, and—when
necessary—endodontic treatment.6 The
defect can be restored using glass ionomer
cement, resin-modified glass ionomer, or
mineral trioxide aggregate (MTA).3,6,19-23
The material needs to be placed close to
the pulp; thus, it must be nontoxic and
biocompatible, provide a perfect seal to
prevent leakage of environmental irritants
through the cavity walls, induce dentinogenesis, demonstrate antibacterial behavior,
and cause minimal pulp inflammation.24
The selected treatment must also provide
an appropriate environment for osteogenesis and cementogenesis, which is followed
by soft tissue attachment gain.23
Recently, a new endodontic cement
composed of a calcium-enriched mixture
(CEM) was introduced.25 It has the same
clinical indications as MTA but a different
chemical formulation.25 CEM cement is
biocompatible, nontoxic, and antibacterial, while also providing a good seal.8,24,25
CEM material is hard tissue inductive,
dentinogenic, cementogenic, and osteogenic—properties that make CEM an
appropriate biomaterial for treating ICR.26
This article presents a case in which
CEM cement was used to treat a Class 3
ICR in a mandibular canine.
Case report
A man in his early thirties had the
chief complaint of a carious-like lesion
on his mandibular left canine. A brief
examination of the dental and gingival
tissues revealed that the patient had
normal hygiene and no carious lesions,
General Dentistry
37
Dental Materials Surgical repair of invasive cervical root resorption with calcium-enriched mixture cement: a case report
Fig. 1. A photograph of a periodontal
probe assessing the lesion depth of
the patient’s left mandibular canine.
Fig. 2. A radiograph of the lesion in
the affected tooth. Note the motheaten margins and lesion extending
beyond the crestal bone.
Fig. 3. Local anesthesia is injected into
the soft tissue prior to flap resection.
Fig. 5. The cavity is filled with calciumenriched mixture (CEM) cement prior
to flap replacement.
Fig. 6. A radiograph taken of the tooth
after the CEM cement restoration was
placed.
Fig. 7. Histological views of the soft tissue specimen (H&E). A. Granulation tissue
with chronic inflammatory cell infiltrate (magnification 100X). B. Same view at higher
magnification (400X). Note the dense collagen matrix and lymphocytic infiltration.
although he had some amalgam restorations on his molars and premolars. His
most recent dental visit had taken place
7 months earlier.
A cavity was visible on the buccal cervical area of the mandibular left canine; the
contour was irregular and extended apically beyond the gingival margin (Fig. 1).
An explorer revealed the tissue that filled
the defect was extremely hyperemic and
the dentin beyond the tissue on the pulpal
side appeared stiff and sound. The probing
depth on the midbuccal area was >3 mm.
Orthoradial periapical radiographs showed
a radiolucent lesion on the cervical area.
The margins had a moth-eaten pattern,
and the most apical margin had extended
38
beneath the bone crest. The root canal
could be seen through the radiolucency
(Fig. 2). The patient did not report any
sensitivity to cold or heat, and vitality
pulp testing revealed normal responses
compared to the mandibular right canine.
Given the nature of the lesion, a diagnosis
of ICR was made.
After an antibacterial mouth rinse, local
anesthesia was injected into the resorptive
soft tissue (Fig. 3), and an intrasulcular
full thickness flap was raised to disclose
the margin of the lesion. Crestal bone
had recessed to the most apical margin
of the cavity. The resorptive tissue that
replaced the dentin was curetted by using
an excavator; in addition, all granulated
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Fig. 4. A full mucoperiosteal flap is
resected and the soft tissue is curetted
away. Note the absence of pulp exposure
and the irregularity of the margins.
tissue was removed from the inner side
of the flap. The cavity was evacuated
without any exposure of the pulp space
(Fig. 4). CEM cement powder and liquid
(BioniqueDent) were mixed according
to the manufacturer’s instructions, and
placed into the cavity until it was filled
completely (Fig. 5). Another radiograph
was taken to confirm the quality of the
CEM restoration (Fig. 6). The flap was
sutured and the patient was given postoperative instructions. The patient made
a follow-up appointment to remove the
sutures 1 week postsurgery. The curetted
soft tissue was placed in a 10% formalin solution for common histological
evaluation with H&E staining (Fig. 7).
Fig. 8. An anterior view of the treated
tooth 7 days postsurgery.
Fig. 12. The tooth at a 1-year followup, with a gingival depth of 1 mm.
Fig. 9. An anterior view of the tooth
10 days post-treatment. Note the
supragingival portion of the CEM
cement is polished.
Fig. 10. The tooth 10 days posttreatment, after the surface was
covered with flowable composite resin.
Fig. 13. A radiograph of the tooth taken at the 1-year follow-up visit.
Examination of the tissue showed a
chronic infiltration with lymphocytes
dominating in a dense collagen matrix.
The CEM filling was tested clinically
at the follow-up appointment.27 The
filling remained intact, except for some
stains and debris covering the surface
(due to the porous surface of the material)
(Fig. 8). Ten days postsurgery, the patient
returned for the next treatment step. The
surface of the CEM cement was polished
to make a clean surface (Fig. 9). After
etching and placement of the bonding
resin (Margin Bond, Coltene/Whaledent,
Inc.), the supragingival portion of the
cavity was filled with composite (Synergy
Nano Formula, Coltene/Whaledent, Inc.)
(Fig. 10). Figures 11 and 12 show the
patient at 3 months and 1 year, respectively. At the 1-year follow-up, the probing
depth on the midbuccal area was 1 mm.
A radiograph taken at that follow-up visit
showed that the tooth had remained completely asymptomatic with normal periradicular and periapical tissues (Fig. 13).
During all the scheduled follow-up visits,
the patient reported no problems with this
tooth, and vitality testing confirmed the
pulp’s normal condition.
Discussion
An ICR in a mandibular canine was
exposed surgically and treated successfully
with CEM cement with no endodontic
co-intervention. In the present case, the
contributing factor to cervical resorption
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Fig. 11. The tooth at a 3-month
follow-up. Note the healthy gingival
tissues.
remains unknown. The present case was
a Heithersay Class 3 type.6 Without
treatment, the resorption would have
proceeded progressively, involving the
dental pulp or causing cervical fracture of
the tooth.6 The patient had no signs or
symptoms; the color of his tooth led him
to seek treatment.
Subgingival caries was listed in the differential diagnosis. These have a “sticky
feeling” on probing in cases of ICR. By
contrast, the remaining hard dentin on
the pulpal side made a scraping sound on
probing. In the present case, the dentin
overlying the pulp was completely sound
and stiff. According to Patel et al, the
radiolucent band across the entire neck
of the tooth on periapical radiographs
(known as the cervical burnout) needs to
be ruled out as well.3 Recently, cone beam
computed tomography (CBCT) has been
used to assess the position and the true
extent of ICR lesions.13,21 However, CBCT
is a costly and time-consuming diagnostic
tool, and it was determined that the clinical and radiographic examinations taken in
the present case revealed sufficient information about the lesion.
As mentioned previously, histological
assessment of the lesion revealed a chronic
infiltration with lymphocytes dominating in a dense collagen matrix, which is
how granulomatous tissue appears, and is
the common histological finding in ICR
cases.3 Early defects usually do not contain
acute inflammatory cells, which suggests a
General Dentistry
39
Dental Materials Surgical repair of invasive cervical root resorption with calcium-enriched mixture cement: a case report
nonbacterial etiology.3 However, it is possible that a secondary bacterial colonization
of dentinal tubules at a later stage might
induce an acute inflammatory response.
Treatment regimens for ICR include
debridement of the resorptive lesions followed by restoration.5,6,18,19 In the present
case, the granulated tissue was curetted
completely after flap reflection. The
proposed nonsurgical treatment plan by
Heithersay & Wilson, which uses 90% trichloracetic acid, was rejected in this case,
as the authors believe that there would be
a risk of incomplete tissue removal and
restoration of the cavity, due to the apical
extension of the defect.19 According to
Patel et al, treating ICR and decreasing the
chance of recurrence requires reflecting
a full-thickness periosteal flap, curetting
away the granulation tissue, and severing
the blood supply to the resorbing cells.3
The surgical technique used in the present
case eliminated the chance that trichloracetic acid (a cytotoxic material) would get
close to the vital pulp.
The drawbacks of MTA—including
its high cost, long setting time, difficult
handling properties, limited antibacterial
effects against some endodontic pathogens,
and potential for discoloration—prevent
it from being an ideal biomaterial for
treating ICR in anterior teeth.22,23 CEM
cement and MTA have similar clinical
uses; however, the water-based CEM
cement offers a shorter setting time,
increased flow, and decreased film thickness.26 In addition, CEM cement has the
ability to release indigenous calcium and
phosphorus ions to form hydroxyapatite,
which ensures an effective bioseal after
setting—a prerequisite for any biomaterial
used in proximity to pulp.24
In the present case, the cavity was
restored with CEM cement; at a follow-up
visit, the CEM cement bulk was polished
to remove the stains and leave a flat white
surface. Next, the supragingival part of
the CEM cement was covered with a
composite restoration for esthetics. CEM
cement can induce cementogenesis and
this cementum layer acts as a biologic
barrier.26 In the present case, a 2 mm
reduction in probing depth revealed the
attachment gain, offering additional proof
of CEM cement’s potential. CEM cement
had higher antimicrobial activity, and
caused less inflammation (although not
40
significantly different) when compared
to MTA.26 Advantages of this study’s
treatment plan include biocompatibility,
induction of dentinogenesis, cementogenesis, and perfect seal. CEM cement
offers a high alkalinity, which can be a
mechanism of osteoclast inactivation; it
also did not result in tooth discoloration,
a drawback of MTA.26,28
Conclusion
Given the biological properties of CEM
cement, it may be an appropriate biomaterial in cases of ICR. Further research is
recommended concerning the mechanisms
by which CEM cement stimulates regeneration and interferes with periodontal
ligament inflammation.
Author information
Dr. Asgary is a professor and dean, Iranian
Center for Endodontic Research, Research
Institute of Dental Sciences, Shahid
Beheshti University of Medical Sciences,
Tehran, Iran, where Dr. Fazlyab is an
endodontist, Dental Research Center.
References
1. Ne RF, Witherspoon DE, Gutmann JL. Tooth resorption.
Quintessence Int. 1999;30(1):9-25.
2. Vinothkumar TS, Tamilselvi R, Kandaswamy D. Reverse
sandwich restoration for the management of invasive
cervical resorption: a case report. J Endod. 2011;37(5):
706-710.
3. Patel S, Kanagasingam S, Pitt Ford T. External cervical
resorption: a review. J Endod. 2009;35(5):616-625.
4. Thonen A, Peltomaki T, Patcas R, Zehnder M. Occurrence of cervical invasive root resorption in first and
second molar teeth of orthodontic patients eight years
after bracket removal. J Endod. 2013;39(1):27-30.
5. Heithersay GS. Invasive cervical resorption: an analysis
of potential predisposing factors. Quintessence Int.
1999;30(2):83-95.
6. Heithersay GS. Invasive cervical resorption. Endod Topics. 2004;7(1):73-92.
7. Silveira LF, Silveira CF, Martos J, Piovesan EM, Cesar
Neto JB. Clinical technique for invasive cervical root
resorption. J Conserv Dent. 2011;14(4):440-444.
8. Asgary S, Ahmadyar M. One-visit endodontic retreatment of combined external/internal root resorption
using a calcium-enriched mixture. Gen Dent. 2012;
60(4):e244-e248.
9. Kim Y, Lee CY, Kim E, Roh BD. Invasive cervical resorption: treatment challenges. Restor Dent Endod. 2012;
37(4):228-231.
10. Fuss Z, Tsesis I, Lin S. Root resorption—diagnosis,
classification and treatment choices based on stimulation factors. Dent Traumatol. 2003;19(4):175-182.
11. Smidt A, Nuni E, Keinan D. Invasive cervical root resorption: treatment rationale with an interdisciplinary
approach. J Endod. 2007;33(11):1383-1387.
12. Mattar R, Pereira SA, Rodor RC, Rodrigues DB. External multiple invasive cervical resorption with
General Dentistry
www.agd.org
subsequent arrest of the resorption. Dent Traumatol.
2008; 24(5):556-559.
13. Gunst V, Mavridou A, Huybrechts B, Van Gorp G, Bergmans L, Lambrechts P. External cervical resorption: an
analysis using cone beam and microfocus computed
tomography and scanning electron microscopy. Int Endod J. 2013;46(9):877-887.
14. Trope M. Cervical root resorption. J Am Dent Assoc.
1997;128(Suppl):56S-59S.
15. Yu VS, Messer HH, Tan KB. Multiple idiopathic cervical
resorption: case report and discussion of management
options. Int Endod J. 2011;44(1):77-85.
16. Lin YP, Love RM, Friedlander LT, Shang HF, Pai MH.
Expression of Toll-like receptors 2 and 4 and the
OPG-RANKL-RANK system in inflammatory external
root resorption and external cervical resorption. Int
Endod J. 2013;46(10):971-981.
17. von Arx T, Schawalder P, Ackermann M, Bosshardt DD.
Human and feline invasive cervical resorptions: the
missing link?—Presentation of four cases. J Endod.
2009;35(6):904-913.
18. Heithersay GS, Dahlstrom SW, Marin PD. Incidence of
invasive cervical resorption in bleached root-filled
teeth. Aust Dent J. 1994;39(2):82-87.
19. Heithersay GS, Wilson DF. Tissue responses in the rat
to trichloracetic acid—an agent used in the treatment
of invasive cervical resorption. Aust Dent J. 1988;
33(6):451-461.
20. Hiremath H, Yakub SS, Metgud S, Bhagwat SV, Kulkarni
S. Invasive cervical resorption: a case report. J Endod.
2007;33(8):999-1003.
21. Estevez R, Aranguren J, Escorial A, et al. Invasive cervical resorption Class III in a maxillary central incisor:
diagnosis and follow-up by means of cone-beam computed tomography. J Endod. 2010;36(12):2012-2014.
22. Park JB, Lee JH. Use of mineral trioxide aggregrate in
the non-surgical repair of perforating invasive cervical
resorption. Med Oral Patol Oral Cir Bucal. 2008;
13(10):E678-E680.
23. Yilmaz HG, Kalender A, Cengiz E. Use of mineral trioxide aggregate in the treatment of invasive cervical resorption: a case report. J Endod. 2010;36(1):160-163.
24. Zarrabi MH, Javidi M, Jafarian AH, Joushan B. Histologic assessment of human pulp response to capping
with mineral trioxide aggregate and a novel endodontic cement. J Endod. 2010;36(11):1778-1781.
25. Asgary S, Nosrat A. Concurrent intentional replantation of maxillary molars using a novel root-end filling
biomaterial: a case report. Gen Dent. 2013;62(3):3033.
26. Asgary S, Ahmadyar M. Vital pulp therapy using calcium-enriched mixture: an evidence-based review.
J Conserv Dent. 2013;16(2):92-98.
27.Parirokh M, Torabinejad M. Mineral trioxide aggregate: a comprehensive literature review—Part III:
clinical applications, drawbacks, and mechanism of
action. J Endod. 2010;36(3):400-413.
28. Marao HF, Panzarini SR, Aranega AM, et al. Periapical
tissue reactions to calcium hydroxide and MTA after
external root resorption as a sequela of delayed tooth
replantation. Dent Traumatol. 2012;28(4):306-313.
Manufacturers
BioniqueDent, Tehran, Iran
www.bioniquedent.com (website suspended)
Coltene/Whaledent, Inc., Cuyahoga Falls, OH
330.916.8800, www.coltene.com
Office Design
Evaluation of 3 dental unit waterline
contamination testing methods
Nuala Porteous, BDS, MPH n Yuyu Sun, PhD n John Schoolfield, MS
Previous studies have found inconsistent results from testing methods
used to measure heterotrophic plate count (HPC) bacteria in dental unit
waterline (DUWL) samples. This study used 63 samples to compare
the results obtained from an in-office chairside method and 2 currently
used commercial laboratory HPC methods (Standard Methods 9215C
and 9215E). The results suggest that the Standard Method 9215E is
not suitable for application to DUWL quality monitoring, due to the
T
he water that is supplied via dental
unit waterline (DUWL) tubing to
air/water syringes, handpieces, and
ultrasonic scalers in a typical dental unit is
fed directly from the main water supply or
via a self-contained reservoir on the dental
unit itself. DUWL tubing typically is 2
mm in diameter and made of either polyvinyl chloride or polyurethane. This tubing
forms a complex network inside a dental
unit, resulting in a high ratio of tubing
surface area to water volume.1 These factors, along with the periodic pooling of
stagnant water inside the tubing, facilitate
an ideal environment for bacterial growth
and biofilm formation (up to 50µ thick)
comprised of a heterogeneous population
of organisms.2,3 Microorganisms from
the biofilm are continuously shed as the
water flows through the DUWL tubing,
resulting in microbial contamination of the
patient treatment water.4
The Centers for Disease Control and
Prevention (CDC) recommends that the
water used in dental offices should meet
the drinking water standard established
by the US Environmental Protection
Agency (EPA) of <500 colony forming
units per milliliter (CFU/ml) for routine
dental treatment output water.5,6 In order
for dental practitioners to comply with
these guidelines, DUWL monitoring
should be performed as recommended by
the dental unit manufacturers.5 Waterline
monitoring can be done in-office with
chairside kits or via commercial laboratories. The purpose of monitoring is to
measure the heterotrophic (organisms
that use a carbon source for survival) plate
count (HPC) of DUWL samples.
detection of limited numbers of heterotrophic organisms at the required
35°C incubation temperature. The results also confirm that while the
in-office chairside method is useful for DUWL quality monitoring, the
Standard Method 9215C provided the most accurate results.
Received: May 27, 2014
Currently, there is only 1 in-office,
chairside kit available: the HPC Sampler
(EMD Millipore), consisting of a removable dip paddle contained in a plastic
sampler. The dip paddle contains a 0.45µ
filter and an absorbent pad with dehydrated agar medium which absorbs 1 ml of
the liquid sample, facilitating the recovery
of stressed (that is, partially sanitized or
nutritionally starved) aerobic bacteria in
7 days. According to the manufacturer,
this method can produce accurate readings
up to 300 CFU/ml; all counts >300 CFU/
ml are considered too numerous to count
(TNTC).7 There is evidence from previous
studies to show that, although the HPC
Sampler underestimates bacterial counts
compared with other methods, it is useful
as a screening tool for regular DUWL
quality monitoring in dental offices to
ensure the water used in the treatment of
patients meets the CDC/EPA recommendation of <500 CFU/ml.8-10
Dental offices can also utilize services
offered by commercial laboratories for a
more accurate assessment of water quality.
Waterline samples are collected and mailed
using kits that are supplied to offices
by the commercial entities. Standard
laboratory methods, as published in the
“Standard Methods for the Examination
of Water and Wastewater”(hereafter
referred to as Standard Methods), are
recommended by the American Public
Health Association, American Water Works
Association, and Water Environment
Federation.11 The list includes 4 standard
methods and 5 types of media for use in
different combinations as appropriate for
testing purposes.11
www.agd.org
Standard Method 9215C (a spread plate
method on R2A medium) has long been
considered the gold standard for analysis
of DUWL quality.12 This procedure, using
a low nutrient R2A formulation (Becton,
Dickson & Company) and room temperature incubation for 7 days, was designed
for the detection of common water organisms. The disadvantages of this method
are that it is time-consuming to prepare
the R2A and it relies on a small volume of
liquid (0.1 ml), which can become quickly
absorbed if the agar dries out.11
Standard Method 9215E (SimPlate
for HPC, IDEXX Laboratories, Inc.)
is a user-friendly method that has been
included in the list of Standard Methods
in recent years.11 A proprietary enzyme
substrate is mixed with the water sample,
and as bacteria metabolize the substrate
they fluoresce after 48 hours of incubation at 35°C. The number of fluorescent
wells are counted and converted to the
most probable number (MPN), using a
table provided by the manufacturers. The
maximum MPN/ml recorded from an
undiluted sample is 73.8; for more highly
contaminated water samples, 10-fold serial
dilutions can be used.13 Since its introduction as a Standard Method, SimPlate for
HPC has become widely used in commercial laboratories, and dental offices that use
a mail-in laboratory service may be obtaining their results from this method.
A previous study by the authors found
that bacterial counts were underestimated
on the SimPlate for HPC compared to
R2A agar.14 The purpose of this experiment was to expand on those findings and
to compare bacterial counts and genera
General Dentistry
41
Office Design Evaluation of 3 dental unit waterline contamination testing methods
from all 3 currently available monitoring
methods: the spread plate R2A (Method
9215C), the SimPlate for HPC (Method
9215E), and the in-office HPC Sampler.
discarded and the Sampler was incubated at
room temperature for 7 days, at which point
CFU/ml were recorded using the comparison chart provided by the manufacturer.7
Molecular identification
A selection of HPC Samplers and R2A
plates with the largest bacterial colonies
was transported to the Department of
Microbiology at the University of Texas
Health Science Center at San Antonio
(UTHSCSA) for molecular identification, and a sequence-based approach
using the 16s ribosomal DNA regions as
targets for the molecular identification
isolates was performed.17
The experiment was designed to collect
an approximately uniform distribution of
water sample contamination based on 3
source types and 7 exposure durations yielding a total of 63 waterline samples. Sterile
collection bottles (100 ml), each containing
sodium thiosulfate to neutralize residual
chlorine (IDEXX Laboratories, Inc.) were
used to collect samples from the handpiece
lines, the air/water syringe lines, and the
source tap water in 21 randomly selected
dental operatories in a teaching institution.
Each sample was cultured on HPC
Sampler, R2A agar (Method 9215C),
and SimPlate for HPC (Method 9215E)
according to manufacturer-recommended
methods. The pH of the source tap water
and the residual free chlorine level (mg/l)
were tested before the experiment and
were found to be 7.2 and 0.5mg/l, respectively. These levels were assumed to remain
constant as previous readings in the institution had shown this to be the norm.15
Sample cultures
All laboratory procedures were conducted
by 1 laboratory technician. A 10-fold serial
dilution of each sample was made with
phosphate buffer solution.
For Method 9215C, 0.1 ml of each
sample was spread on R2A plates in triplicate, incubated at room temperature, and
the microbial CFU/ml was recorded after
7 days.11
For Method 9215E, 10 ml of each
solution were placed in the center of the
SimPlates and the manufacturer’s instructions were followed. Plates were incubated
for 48 hrs at 35°C, and the MPN/ml was
calculated.16 Following the calculation
of MPN/ml, liquid was collected (using
an inoculating loop) from randomly
selected fluorescent wells, then spread on
R2A plates and incubated at room temperature for 7 days to prepare isolates for
molecular identification.
For HPC Sampler cultures, an undiluted
10 ml sample was placed in the outer
sheath, and the dip paddle was replaced
for 30 seconds until 1 ml was absorbed.
The remainder of the DUWL sample was
42
DNA isolation
Isolates were suspended in 600 μl cell lysis
buffer (blood Maxwell LEV kit, Promega
Corporation) in a 0.5 ml microfuge tube.
The suspension was bead-beaten for
45 seconds to 1 minute to aid in cell wall
breakdown. The suspension was then pelleted for 3 minutes at maximum speed in a
microfuge according to the manufacturer’s
instructions. The supernatant was transferred to the Maxwell LEV cartridge and
then mounted on the automated Maxwell
system, resulting in 150 ng/μl of purified
bacterial DNA after a 45-minute run.
Polymerase chain reaction
Polymerase chain reactions (PCR) were
performed directly on 3 μl of the DNA
supernatant in a 50 μl reaction using a
5 prime PCR Extender system (Thermo
Fisher Scientific, Inc.), according to the
manufacturer’s instructions. 16s amplicons
were obtained using primers 27F and
1525R. Amplifications were performed in a
PTC-100 thermocycler (MJ Research, Inc.)
using the preprogrammed, 3-step protocol
as the standard program for all reactions,
consisting of 35 cycles using an annealing temperature of 55°C and 1 minute
extension time. A 5 μl aliquot of the PCR
reaction was run on a 0.7% agarose gel and
stained with ethidium bromide to confirm
amplification. The remaining PCR reaction (45 μl) was run on a gel as described
above, then purified using the Wizard SV
Gel and PCR Clean-Up System (Promega
Corporation), eluted in 30 μl sterile water
according to the manufacturer’s instructions, and incubated with proteinase K at
56°C for 15 minutes.
General Dentistry
www.agd.org
Sequencing
DNA obtained from the PCR reaction was prepared for sequencing by
cleaning with a Qiaprep Spin Miniprep
Kit (Qiagen Sciences, Inc.) according
to manufacturer’s instructions. The
purified DNA was sequenced at the
UTHSCSA Advanced Nucleic Acids
Core facility. Sequences were then
used to perform individual nucleotidenucleotide searches of the ribosomal 16s
region using the BLASTn algorithm at
the National Center for Biotechnology
Information website.18 Identifications
were calculated based on a percentage made from the alignment matches
obtained from the top 3 BLAST searches
for the 16s region to yield a variety level
identification. The 3 highest percent
identities for each isolate were analyzed
for bacterial identification.
For the 3 types of detection methods,
all possible pairwise Pearson and/or
Spearman correlation coefficients with
corresponding 95% confidence intervals
were performed to determine if any significant association was observed among
the 3 measurement methods, with log
transformations performed if appropriate. Correlations were performed for all
waterline samples and, if appropriate,
separately for each waterline sample
source type. Statistical analyses and
graphics were performed using Stata 13.0
(StataCorp LP).
Results
As expected, the R2A measures approximated an exponential distribution;
however, the SimPlate for HPC values
approximated a uniform distribution
ranging from a minimum of 0.4 MPN/ml
to the maximum 73.8 MPN/ml, followed
by 12 (19%) samples with unspecified
values >73.8 MPN/ml, as the corresponding 110 dilution plates did not provide
any results. There were also 4 samples
based on a 110 dilution that had values
ranging from 112 to 440 MPN/ml and
1 handpiece sample that could not be
assayed due to technical error. For the
purposes of graphs and correlations, an
arbitrary value of 80 MPN/ml was used
to represent all SimPlate for HPC values
>73.8 MPN/ml.
Table 1. HPC from DUWL samples
Dental
unit
Sample source
1
Handpiece
Air/water
Source water
2
4
59
1000
Handpiece
293
2.1
12
142,000
41.4
1000
Air/water
6,570
26.6
1000
Source water
8,430
29.9
1000
Handpiece
138,000
31.1
1000
Air/water
392,000
47.0
1000
Handpiece
86.7
341,000
0.4
33
55.5
1000
235,000
44.0
1000
1,470
1.9
360
Dental
unit
Sample source
12
133
15.1
39
Handpiece
411,000
55.5
1000
Air/water
244,000
80.0 b
1000
387
0.2
86
Handpiece
795,000
257.0
1000
Air/water
722,000
37.2
1000
213
1.0
151
Handpiece
233,000
73.8
1000
Air/water
362,000
62.3
1000
417
2.6
73
Handpiece
Air/water
Source water
17
80.0 b
1000
73.8
600
1000
Air/water
Source water
62.3
0
573,000
73.8
1000
327
73.8
1000
Handpiece
361,000
239.0
1000
Air/water
535,000
62.3
1000
Handpiece
Air/water
Source water
73.3
178,000
1.0
80.0
10
0.6
Handpiece
151,000
80.0
Air/water
323,000
55.5
Source water
Handpiece
Air/water
Source water
1000
b
1000
NA
1000
70,700
112.0
1000
37.2
216
Handpiece
42,300
283
80.0 b
1000
Air/water
13,100
80.0 b
1000
527
73.8
116
Handpiece
343,000
440.0
1000
Air/water
226,000
80.0 b
1000
367
13.2
36
Handpiece
91,300
55.5
1000
1000
Air/water
57,700
80.0 b
1000
Source water
51,300
73.8
1000
1000
21
24,600
33.9
1000
243,000
41.4
1000
a
b
176,000
39.2
1000
27,700
47.0
1000
Results for each of the methods can
be seen in Table 1. The HPC Sampler
detection method showed that 46 (73%)
of the dip paddle surfaces were entirely
covered with TNTC small microbial colonies. For 2 handpiece samples, no HPC
33,400
Source water
1
b
Handpiece
Source water
20
2,390
Air/water
Source water
19
20
47.0
39,900
18
39
101,000
1000
50.7
642,000
47.0
1000
68.0
Handpiece
1000
1000
80.0 b
252,000
1000
76.7
62.3
80.0 b
115,000
284,000
27.6
8,370
139,000
Handpiece
Handpiece
1,850
0
1000
80.0
80.0 b
Source water
16
CFU/ml
b
47,300
Source water
15
HPC sampler
MPN/ml
543,000
Source water
14
SimPlate
CFU/ml
Handpiece
Source water
13
R2A agar
Air/water
Air/water
Source water
11
1000
23.1
1000
Source water
10
23.9
1,130
37.2
Air/water
9
87,000
23.1
Source water
8
1000
a
102,000
Source water
7
26.6
CFU/ml
494,000
Air/water
6
61,300
MPN/ml
HPC sampler
Handpiece
Source water
5
CFU/ml
SimPlate
Air/water
Source water
3
R2A agar
1000 CFU/ml
MPN >73.8/ml
Abbreviations: CFU, colony forming units; DUWL, dental unit waterline;
HPCs, heterotrophic plate counts; MPN, most probable number; NA, not available.
counts were detected; otherwise, all
handpiece and air/water samples counts
were TNTC. For the purposes of graphs
and correlations, an arbitrary value of
1,000 CFU/ml was used to represent
TNTC results, and the 2 handpiece
www.agd.org
samples for which the HPC Sampler
failed to detect CFUs were excluded as
having implausible results. Specific HPC
counts were detected for 14 of 21 source
water samples. Due to the characteristics
of the distribution of HPC measures,
General Dentistry
43
Recovered microorganisms
As seen in Table 3, 16 genera of bacteria
were recovered. The most commonly
occurring genus was Sphingomonas,
and only 2 species—Cupriavidus metallidurans and Sphingomonas parapaucimobilis—were found on all 3 culture
media. Micrococcus luteus was the only
gram-positive species found. All other
recovered bacteria were gram-negative.
Discussion
This article describes an evaluation
of 3 currently available methods for
monitoring HPC bacteria in DUWLs.
The SimPlate for HPC (Method 9215E)
recovered the lowest numbers of microorganisms and the highest readings were
found on spread plate R2A (Method
9215C), although it must be noted that
all HPC methods enumerate only a
fraction of microorganisms in any water
44
Table 2. Correlation coefficients (95% confidence interval).
Pearson
Sample source
Spearman
R2A with SimPlate for HPC
All
0.607 (0.421, 0.744)
0.475(0.256, 0.648)
Handpiece
0.103 (-0.356, 0.522)
0.174 (-0.291, 0.572)
Air/water
-0.068 (-0.486, 0.375)
-0.268 (-0.627, 0.185)
Source water
0.481 (0.062, 0.756)
0.521 (0.115, 0.778)
All
0.650 (0.474, 0.776)
Source water
0.573 (0.188, 0.805)
Millipore with SimPlate for HPC
0.598 (0.406, 0.740)
0.624 (0.263, 0.832)
R2A with Millipore
All
0.871 (0.793, 0.921)
0.734 (0.592, 0.832)
Source water
0.795 (0.554, 0.913)
0.797 (0.557, 0.914)
Chart. R2A with SimPlate for HPC method scatterplot, displaying legend markers
indicating the range of the corresponding HPC Sampler value for each sample.
1,000,000
100,000
10,000
R2A (CFU/ml)
correlations were performed for all
samples and for source water samples
only (Table 2).
For the R2A with SimPlate for HPC,
the overall Pearson correlation coefficient of 0.607 was moderate, while
the corresponding Spearman rank correlation coefficient of 0.475 was lower.
Correlations for each source type showed
similar results for source water samples
and poorer results for handpiece and air/
water samples. To depict the pairwise
association, a scatterplot was generated
displaying the paired results for each
sample with symbols indicating the
source type (Chart).
For the HPC Sampler with SimPlate for
HPC, the overall Pearson correlation coefficient of 0.650 was significantly lower than
the overall Pearson correlation coefficient
of 0.871 for SimPlate for HPC with R2A.
Similarly, the corresponding Spearman correlation for HPC Sampler with R2A was
higher than that for SimPlate with R2A,
but the 2 Spearman correlations were not
significantly different.
When restricted to the source water
samples, the HPC Sampler with SimPlate
for HPC Pearson correlation coefficient
of 0.573 was significantly lower than
the HPC sampler with R2A coefficient
of 0.795, while the corresponding
Spearman correlations were not significantly different.
1000
100
10
HPC sampler
(CFU/ml)
>500
100-500
50-99
1-49
0 010 20304050 607080
SimPlate for HPC (MPN/ml)
Note that 2 handpiece samples for which no CFUs were detected by HPC Sampler were excluded. All samples with
R2A >1500 CFU/ml had HPC Sampler values >500 CFU/ml, while only 1 sample with R2A <1500 CFU/ml had an
HPC Sampler value >500 CFU/ml.
sample and no single method will recover
all genera.19 The overall results are not
altogether unexpected, since the media
composition and incubation parameters
were specifically designed to recover different microbial populations.
General Dentistry
www.agd.org
Statistical analysis showed moderate
correlations between Method 9215E
and the other 2 methods, while Method
9215C and HPC Samplers had high correlations. Correlations based on source
tap water samples involved fewer arbitrary
Table 3. Bacteria recovered from DUWL samples.
Acidovorax sp.a
Methylobacterium radiotolerans
Sphingomonas sanguinis
Acidovoraxcitrulli
Methylobacterium rhodesianum
Sphingomonas trueperi
Acidovoraxtemperans
Methylobacterium thiocyanatum
Sphingomonas yunnanensis
Afipia sp.
Micrococcus luteus
Sphingopyxis alaskensis
Blastomonas natatoria
Novosphingobium stygium
Sphingopyxis chilensis
Bradyrhizobium sp.
Pseudomonas koreen c
Xenophilus aerolatus
Bradyrhizobium yuanmingens
Pseudomonas libane c
Xulophilus ampelinus
Caulobacter segnis
Ralstonia sp.
a
Grown on R2A and Millipore
HPC Samplers
Cupriavidus basilensis
Sphingobium sp.
Cupriavidus metallidurans b
Sphingobium amiense
b
Methylobacterium extorquens
Sphingomonas sp.
c
Methylobacterium oryzae
Sphingomonas adhaesiva
Methylobacterium populi
Sphingomonas parapaucimobilis b
approximation values, resulting in a
decrease in Pearson correlations and an
increase in Spearman correlations.
Unlike the other 2 laboratory methods,
serial dilutions of samples were not done
prior to culturing on HPC Samplers due
to its purposeful design as an in-office,
chairside monitoring device. As stated
earlier, previous studies have shown that
HPC Samplers underestimate bacterial
counts when compared to the spread
plate R2A agar method, and some have
attributed this to its failure to grow
certain phenotypes.20,21 The results of
this study concur with those findings.
However, this study also confirms the
high sensitivity of the HPC Samplers,
as microbial counts on the majority of
the paddles were TNTC and 5 different
species of bacteria were detected. For
the 2 handpiece samples in which zero
bacterial growth was recovered on HPC
Samplers, a plausible explanation may be
variation among kits, as it was unlikely
due to laboratory error (based on the
reliability of the standard laboratory
methods employed).
The spread plate R2A agar (Method
9215C) has long been considered the gold
standard for application to DUWL monitoring with the advantage of producing a
true assessment of HPC contamination
levels. In this study, accurate counts were
obtained using serial dilutions, and 14
different genera of bacteria were detected
on R2A plates.
Grown on all 3 media
Grown on Millipore HPC
Samplers only
No symbol: grown on R2A
agar only
The inclusion of SimPlate for HPC
(Method 9215E) in the list of the
Standard Methods endorses its use for
analysis of drinking water and source water
sampes.11 It is recommended as an alternative to the pour plate method (9215A),
which uses high nutrient plate count agar
to test for general EPA compliance monitoring; studies have demonstrated good
correlation between the 2 methods.11,13,16
Both 9215A and 9215E methods require
incubation periods of 48 hours at mammalian physiological incubation temperature (35°C), favoring the growth of
bacteria from human and animal wastes.22
However, a previous study showed that
Method 9215E showed lower microbial
counts when compared to the membrane
filter method (9215D), which utilizes low
nutrient R2A agar and incubation periods
of 48 hours at 22°C-28°C.13 Lower incubation temperature (22°C-28°C), along
with a longer incubation time favor the
growth of indigenous aquatic bacteria.22
SimPlate for HPC was a method designed
for higher incubation temperatures, and
the results of this study add to the body of
existing scientific evidence showing that
Method 9215E underestimates microbial
contamination at 22°C-28°C.13,14,16
Significance of microorganisms
recovered
Culture plates that were selected for
organism identification were based on
recovered colony size, so the number of
www.agd.org
recovered organisms represents a mere
snapshot of the total bacterial population. Not surprisingly, due to the limited
number of microorganisms isolated on
SimPlate for HPC, only 2 bacterial species were identified. However, it must also
be noted that this method is not designed
for recovering particular organisms, as
stated in the Standard Methods.11
One gram-positive organism was identified on R2A: M. luteus, which is ubiquitously found in soil, dust, air, and water.
Cases of infective endocarditis due to M.
luteus have been reported in the literature.23
All other microorganisms were gramnegative, which are known to have lipopolysaccharide molecules (endotoxins) in
their cell wall that can trigger inflammatory
responses in humans. Several studies have
reported a significant association between
the presence and severity of asthma and
a raised concentration of airborne gramnegative bacteria in the indoor environment.24 A significant correlation between
endotoxin levels and high bacterial load in
DUWLs has also been reported.25
Two species of Pseudomonas isolated
on the HPC Samplers in this study have
previously been recovered from DUWLs
and reported as the causative organisms
of postoperative dental infections and
respiratory infections in immunocompromised patients.26,27
Only 2 bacterial types were common
to the 3 culture methods tested in the
study: Cupriavidus metallidurans and
Sphingomonas parapaucimobilis; these
were the only bacterial species recovered on SimPlate for HPC, verifying
the limitations of this culture method
for detection of common water organisms. C. metallidurans belongs to the
α-Proteobacteria group, known to be
the predominant survivor in chlorinated
water distribution systems.28,29
The most frequently isolated genera
in this study were Sphingomonas, also
closely aligned with the phylogenic
group α-Proteobacteria, and previously
found in DUWL samples and ultrapure
water.2,15,29,30 A review of nosocomial
infections concluded that the species S.
parapaucimobilis has emerged in recent
years as an opportunistic pathogen as it
has been associated with many cases of
bacteremia and other systemic infections
in immunocompromised patients.31
General Dentistry
45
Conclusion
The variety of potentially pathogenic
organisms recovered from waterlines in this
study reinforces the need for monitoring
DUWL quality to ensure the delivery of
high quality dental patient treatment water.
The study confirmed that Millipore
HPC Samplers are useful for routine
in-office, chairside DUWL quality monitoring when the benchmark CDC recommended level of <500 CFU/ml is used. The
study also confirmed that the spread plate
R2A agar method (9215C) provides the
most accurate analysis of DUWL quality.
The laboratory SimPlate for HPC
method (9215E) failed to detect microbial contamination of DUWL samples
to the same extent as Method 9215C,
most likely due to the specific design of
SimPlate for HPC for the recovery of
fast-growing organisms at 35°C. While
Method 9215E clearly has value for application in EPA compliance monitoring,
this study found that it is not acceptable for application in DUWL quality
monitoring, when quantification of slowgrowing water organisms at 22°C-28°C
and a correct assessment of dental patient
treatment water quality are required.
Dental offices can reliably use in-office,
chairside Millipore HPC Samplers to
screen DUWL quality, ensuring that
patient treatment water is compliant with
the EPA/CDC recommendation of <500
CFU/ml. However, for offices that rely
on commercial laboratories to provide
an accurate assessment of their DUWL
quality, it is recommended that the spread
plate R2A method (9215C) be requested,
rather than the SimPlate for HPC method
(9215E), when DUWL samples are submitted for analysis.
Author information
Dr. Porteous is an associate professor,
Department of Comprehensive Dentistry,
University of Texas Health and Science
Center at San Antonio (UTHSCSA),
where Mr. Schoolfield is a consultant biostatistician, Department of Periodontics.
Dr. Sun is an associate professor,
Department of Chemistry, University of
Massachusetts in Lowell.
Acknowledgments
Research reported in this article was supported by the National Institute of Dental
46
& Craniofacial Research of the National
Institutes of Health (NIH) under Award
Number R01 DE018707-05. The content
is solely the responsibility of the authors
and does not necessarily represent the official views of the NIH. Drs. Porteous and
Sun are co-principal investigators and Mr.
Schoolfield is a co-investigator.
The authors wish to thank Monica
Herrera, MD, research associate,
Department of Microbiology, UTHSCSA,
for her work on molecular analysis of
organisms at the time of this study.
Disclaimer
The authors have no financial, economic,
commercial, and/or professional interests
related to topics presented in this article.
References
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2000;131(10):1427-1441.
2. Szymanska J. Bacterial contamination of water in dental unit reservoirs. Ann Agric Environ Med. 2007;14(1):
137-140.
3. Cunningham AB, Lennox JE, Ross RJ, eds. Biofilm
growth and development. In: Biofilms: The Hypertextbook. Available at: http://www.biofilmbook.com. Accessed November 7, 2014.
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MJ. Localized gene expression in Pseudomonas aeruginosa biofilms. Appl Environ Microbiol. 2008;74(14):
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10. Bartoloni JA, Porteous NB, Zarzabal LA. Measuring the
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Health Association, Water Environment Federation.
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Eaton AD, Clesceri LS, eds. Standard Methods for the
Examination of Water and Wastewater. 22nd ed.
Washington, DC; 2012: 9.49-9.52.
12. De Paola LG, Mangan D, Mills SE, et al. A review of the
science regarding dental unit waterlines. J Am Dent
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13. Stillings A, Herzig D, Roll B. Comparative Assessment
of the Newly-Developed SimplateTM Method With the
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Detection of Heterotrophic Plate Count Bacteria in
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Association Conference, October 1998. Available at:
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14. Porteous N, Sun Y, Dang S, Schoolfield J. A comparison
of 2 laboratory methods to test dental unit waterline
water quality. Diag Microbiol Infect Dis. 2013;77(3):
206-208.
15. Porteous N, Luo J, Hererra M, Schoolfield J, Sun Y.
Growth and identification of bacteria in N-halamine
dental unit waterline tubing using an ultrapure water
source. Int J Microbiol. 2011;767314.
16. Jackson RW, Osborne K, Barnes G, et al. Multiregional
evaluation of the SimPlate heterotrophic plate count
method compared to the standard plate count agar
pour plate method in water. Appl Environ Microbiol.
2000;66(1):453-454.
17. Frank JA, Reich CI, Sharma S, Weisbaum JS, Wilson BA,
Olsen GJ. Critical evaluation of two primers commonly
used for amplification of bacterial 16S rRNA genes.
Appl Environ Microbiol. 2008;74(8):2461-2470.
18. National Center for Biotechnology Information. Blast:
Basic Local Alignment Search Tool. Available at: http://
blast.ncbi.nlm.nih.gov/Blast.cgi. Accessed November
10, 2014.
19. Allen MJ, Edberg SC, Reasoner DJ. Heterotrophic plate
count bacteria—what is their significance in drinking
water? Int J Food Microbiol. 2004;92(3):265-274.
20. Smith RS, Pineiro SA, Singh R, Romberg E, Labib ME,
Williams HN. Discrepancies in bacterial recovery from
dental unit water samples on R2A medium and a
commercial sampling device. Current Microbiol. 2004;
48(4):243-246.
21. Cohen ME, Harte JA, Stone ME, O’Connor KH, Coen
ML, Cullum ME. Statistical modeling of dental unit water bacterial test kit performance. J Clin Dent. 2007;
18(2):39-44.
22. Reasoner DJ. Heterotrophic plate count methodology
in the United States. Int J Food Microbiol. 2004;92(3):
307-315.
23. Miltiadous G, Elisaf M. Native valve endocarditis due
to Micrococcus luteus: a case report and review of the
literature. J Med Case Rep. 2011;5:251.
24. Rennie DC, Lawson JA, Kirychuk SP, et al. Assessment
of endotoxin levels in the home and current asthma
and wheeze in school-age children. Indoor Air. 2008;
18(6):447-453.
25. Huntington MK, Williams JF, Mackenzie CD. Endotoxin
contamination in the dental surgery. J Med Microbiol.
2007;56(Pt 9):1230-1234.
26. Martin MV. The significance of the bacterial contamination of dental unit water systems. Br Dent J. 1987;
163(5):152-154.
27. Langton Hewer SC, Smyth AR. Antibiotic strategies for
eradicating Pseudomonas aeruginosa in people with
cystic fibrosis. Cochrane Database Syst Rev. 2009;(4):
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28. von Rozycki T, Nies DH. Cupriavidus metallidurans:
evolution of a metal-resistant bacterium. Antonie van
Leeuwenhoek. 2009;96(2):115-139.
29. Williams MM, Domingo JW, Meckes MC, Kelty A, Rochon HS. Phylogenic diversity of drinking water bacteria in a distribution system simulator. J Appl Microbiol.
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Manufacturers
Becton, Dickson & Company, Franklin Lakes, NJ
888.237.2862, www.bd.com
EMD Millipore, Billerica MA
781.533.6000, www.emdmillipore.com
IDEXX Laboratories, Inc., Westbrook, ME
800.548.6733, www.idexx.com
MJ Research, Inc., St. Bruno, Quebec, Canada
450.461.6245, mj-research.com
Promega Corporation, Madison, WI
608.274.4330, www.promega.com
Qiagen Sciences, Inc., Germantown, MD
240.686.7700, www.qiagen.com
StataCorp LP, College Station, TX
800.782.8272, www.stata.com
Thermo Fisher Scientific, Inc., Waltham, MA
800.678.5599, www.thermofisher.com
www.agd.org
General Dentistry
47
Anesthesia and Pain Control
Local anesthetic calculations: avoiding trouble
with pediatric patients
Mana Saraghi, DMD n Paul A. Moore, DMD, PhD, MPH n Elliot V. Hersh, DMD, MS, PhD
Local anesthetic systemic toxicity (LAST) is a rare but avoidable
consequence of local anesthetic overdose. This article will review
the mechanism of action of local anesthetic toxicity and the signs
and symptoms of LAST. Due to physiologic and anatomic differences
between children and adults, LAST occurs more frequently in
children; particularly when 3% mepivacaine is administered. The
calculation of the maximum recommended dose based on mg/lb body
weight, Clark’s rule, and the Rule of 25 in order to prevent LAST
A
pproximately 1 million cartridges
of local anesthetic are used each
day in the United States.1 Local
anesthetic systemic toxicity (LAST) is
dose-related and although rare, occurs
more frequently in small children than
adults. LAST occurs more frequently
when the patient is administered concomitant central nervous system (CNS)
depressants, such as opioid/sedative
medications.2-9
The following case serves as a reminder
to proceed cautiously when administering
routine local anesthetic, always keeping
weight-based dosing in mind. A 50-lb,
8-year-old girl with a history of extensive
caries and dental fear—but otherwise
no medical problems, diseases, or allergies—presented for multiple extractions.
For the initial sedation, the patient
received oral promethazine, as well as
nitrous oxide-oxygen inhalational sedation. A half hour later, the sedation was
supplemented with an intramuscular dose
of meperidine. After another half hour
had elapsed, the child received injections
of 6 cartridges of 3% mepivacaine plain
(without a vasoconstrictor). Seizures and
respiratory distress followed 5 minutes
later. Resuscitation efforts followed, but
were unsuccessful, and the patient died of
anoxic encephalopathy.5
The most common cause of morbidity
and mortality due to LAST is respiratory depression or apnea.10 LAST occurs
more frequently in children when 3%
mepivacaine is administered, with the
false presumption that a local anesthetic
without a vasoconstrictor will have a
48
will also be reviewed, as well as the appropriate treatment procedures
for a local anesthetic overdose.
Received: July 17, 2013
Revised: October 30, 2013
Accepted: February 10, 2014
Key words: local anesthetic toxicity, systemic toxicity, maximum
recommended dose, Clark’s rule, lidocaine, mepivacaine
shorter duration of soft tissue anesthesia
and prevent postoperative self-inflicted
lip and cheek trauma.10,11
Local anesthesia: mechanism
of action and toxicity
Local anesthetics are essential for intraoperative dental analgesia; they work by
blocking sodium channels in neurons
so that pain signals from the periphery
cannot be transmitted to the CNS. LAST
is mediated by the same mechanism when
the maximum recommended dose (MRD)
is exceeded. This dose-related toxicity
is especially important as the sodium
channels in the cardiovascular system are
blocked along with those in the CNS.12,13
Regardless of which local anesthetic
is administered, the same progression of
effects on the CNS and cardiovascular
system occur with increasing plasma levels
of local anesthetic.12,13 Symptoms of early
toxicity consist of numbness and tingling
of the mouth and lips, metallic taste,
diplopia, tinnitus, nausea, dizziness, and
drowsiness.12,13 These reactions are usually
self-limiting and often are due to a mild
overdose or an inadvertent intravascular
injection. As the plasma concentrations
of local anesthetic increase, the inhibitory
neurons in the CNS are blocked, leaving
excitatory neurons unopposed. Clinically,
this manifests as tremors and tonic-clonic
(also known as grand mal) seizures. CNS
arousal may stimulate the cardiovascular
system, possibly resulting in hypertension, tachycardia, and increased cardiac
output.12,13 At higher plasma levels of local
anesthetic, both excitatory and inhibitory
General Dentistry
www.agd.org
neurons are blocked to such a profound
level that CNS and respiratory depression,
unconsciousness, and respiratory arrest
can occur. At even higher plasma concentrations, systemic vasodilation results in
significant hypotension and cardiovascular
depression. Local anesthetics also block
sodium channels in the myocardium,
resulting in bradycardia. Bradycardia is a
major cause of concern when bupivacaine
is used, as it can induce a use-dependent
blockade at normal heart rates.12,13 Because
of its extended duration of action, bupivacaine is rarely indicated for children. The
sequelae of depressed cardiac conduction
include atrioventricular block, ventricular
arrhythmias, cardiac arrest, and ultimately,
death. A local anesthetic overdose can
result in significant morbidity and mortality unless life support interventions
can be initiated following standard basic
and advanced cardiac life support guidelines.12,13 Concomitant opioid sedative
administration will augment respiratory
depression and decrease the seizure threshold of local anesthetics.3,5,6,12-15
LAST: a greater tendency in
pediatric patients
There are some important physiological
differences between children and adults
that play a role in the greater tendency
for LAST to be reported in the pediatric
population. Seated in the dental chair, a
child may appear deceptively large. The
reason that the child appears to be larger
is that in the dental chair—with a bib,
napkin, or blanket—only the child’s disproportionately large head is visible.4 This
6’
6’
3’
1.00
Head size
0.75
5’
3’
Height
4’
2’
1’
Figure. Diagram comparing the relative proportions in height vs head size between a 3.5-year-old child
and an adult.
Table 1. Local anesthetic calculation: amount of local anesthetic in cartridges.
2% anesthetic = 2 grams/100 ml in volume = 2000 mg/100 ml = 20 mg/ml
3% anesthetic = 3 grams/100 ml in volume = 3000 mg/100 ml = 30 mg/ml
1 cartridge of local anesthetic is 1.8 ml in volume (exception: 4% articaine has 1.7 ml)
Therefore…
2% cartridge: 20 mg/ml x 1.8 ml/cartridge = 36 mg/cartridge
3% cartridge: 30 mg/ml x 1.8 ml/cartridge = 54 mg/cartridge
makes it more critical to determine the
maximum dose and number of cartridges
based on the child’s actual weight.
The following example of a 3.5-year-old
child illustrates the point that children
often appear deceptively large and how
this may prompt the dentist to overestimate the child’s size based solely on
appearances.4 Because the head develops
quickly during early childhood, children
have disproportionately large heads; at the
age of 3.5, a child’s head is nearly 75%
of the size of his/her adult counterpart.4,5
However, the same child has only 50%
of the height, 25% of the blood volume,
and 20% of the weight compared to
his/her adult counterpart (Figure).4 The
child’s airway is also different, with narrower nasal passages, larynx, and trachea.
Meanwhile, children have relatively larger
tongues, tonsils, and adenoids than adults.
These anatomic differences—coupled with
the heightened susceptibility to CNS and
respiratory depressants—render children
more vulnerable to losing airway patency.4
Local anesthetic selection:
misconceptions about prolonged
soft tissue numbness
When treating children, it is important
to inform parents or caregivers that close
postoperative supervision is needed to
prevent the child from biting their lips,
cheeks, and tongue. While the soft tissues
are still numb, significant trauma from
lip and cheek biting can occur. There
is a misconception that using a local
anesthetic without a vasoconstrictor, such
as mepivacaine 3% plain, will provide a
shorter duration of soft tissue anesthesia
www.agd.org
than a local anesthetic with a vasoconstrictor, such as 2% lidocaine with 1:100,000
epinephrine.11,12 Mepivacaine does offer
shorter pulpal anesthesia (20-40 minutes)
as compared to lidocaine with epinephrine
(60-90 minutes), but soft tissue anesthesia is similar between the 2 anesthetics:
120-180 minutes and 120-240 minutes
for mepivacaine plain and lidocaine with
epinephrine, respectively.11 Hersh et al
found that “the onset of soft tissue numbness, peak numbness effects, and numbness duration were quite similar” when
comparing 3% mepivacaine plain and 2%
lidocaine with epinephrine.11
Using 3% mepivacaine plain instead of
2% lidocaine with epinephrine does not
provide any benefit with respect to the
prevention of postoperative lip/mouth
trauma, but the higher concentration of
local anesthetic in the 3% mepivacaine
solution makes it easier to reach or exceed
the MRD.3,4,11,16,17 A brief review of local
anesthetic calculations illustrates this
point: a 2% formulation of a drug means
that there is 2 grams of drug in 100 ml
volume. If 2 grams are in 100 ml, then
2000 mg are in 100 ml, which means
that 20 mg are in each ml. Since a dental
cartridge contains approximately 1.8 ml
volume, then there are 36 mg drug per
cartridge (Table 1). Similarly, when a drug
is in a 3% formulation, there are 30 mg
per ml, thus there are 54 mg per 1.8 ml
dental cartridge. Therefore, a cartridge
of 3% mepivacaine contains 50% more
local anesthetic than a cartridge of 2%
lidocaine; thus it would take less volume
(or fewer cartridges) of the more concentrated drug (3% mepivacaine) to reach its
respective MRD.11
Preventing local anesthetic
toxicity: calculating appropriate
weight-based dose
Respecting weight-based dosing limits
is essential, as previous cases of LAST
have resulted in significant morbidity
and mortality when dosing limits were
exceeded.3,4,12,16,17 In a 1983 retrospective study, pediatric dental patients that
received local anesthesia and opioid
sedation—either local alone or local plus
narcotic dose—exceeded their combined
MRDs by a factor of ≥3; the result was
either permanent brain damage or death.6
In a 1992 survey of local anesthetic use
General Dentistry
49
Anesthesia and Pain Control Local anesthetic calculations: avoiding trouble with pediatric patients
Table 3. Local anesthetic calculation for a 50 lb child based
on Clark’s rule.
1. Calculate the MRD from each drug for a 50 lb child.
Patient’s weight/150 lb adult x adult MRD = patient’s MRD
Table 2. Local anesthetic calculations for a 50 lb child
based on mg/lb.
Adult MRD:
2% lidocaine with 1:100,000 epinephrine: 500 mg
1. Calculate the MRD for each drug for a 50 lb child.
3% mepivacaine plain: 400 mg
2% lidocaine with 1:100,000 epinephrine = 3.2 mg/lb x 50 lb = 160 mg
Lidocaine with 1:100,000 epinephrine: 50/150 x 500 mg = 166 mg
3% mepivacaine plain = 2.6 mg/lb x 50 lb = 130 mg
Mepivacaine plain: 50/150 x 400 mg = 133 mg
2. Determine the maximum number of cartridges based on the MRD.
2. Determine the maximum number of cartridges based on the MRD.
2% lidocaine with 1:100,000 epinephrine: 160 mg ÷ 36 mg/cartridge =
4.4a cartridges
2% lidocaine with 1:100,000 epinephrine: 166 mg ÷ 36 mg/cartridge =
4.62a cartridges
3% mepivacaine plain: 130 mg ÷ 54 mg/cartridge = 2.4b cartridges
3% mepivacaine plain: 133 mg ÷ 54 mg/cartridge = 2.46b cartridges
In clinical terms, 4.5 cartridges.
Abbreviation: MRD, maximum recommended dose.
a
a
b
b
among Florida dentists who routinely
treated pediatric patients, a majority of
the respondents used an absolute number
of cartridges without accounting for the
child’s age or weight.2 A clinician can
prevent a local anesthetic overdose by
calculating the MRD and the maximum
number of cartridges by weight to appropriately administer local anesthetic in children; this dose per weight is contingent on
calculations of a weight that is consistent
with normal growth and development and
normal lean body mass.18
Based on these calculations, the MRD of
2% lidocaine with 1:100,000 epinephrine is
3.2 mg/lb; for a patient ≥150 lbs, the adult
MRD is 500 mg. The MRD of 3% mepivacaine plain is 2.6 mg/lb; for a patient
>150 lbs, the adult MRD is 400 mg.18,19
Table 2 illustrates the calculation needed to
derive the absolute maximum number of
cartridges of 2% lidocaine with epinephrine and 3% mepivacaine plain that can
be given to a child weighing 50 lb. This
number is approximately 33% of the adult
maximum number of cartridges. A vasoconstrictor (such as epinephrine) reduces
the systemic absorption of a local anesthetic, and several pharmacokinetic studies
have demonstrated that the average peak
blood levels following maxillary infiltration
injections were 3 times higher with 3%
mepivacaine plain in comparison to 2%
lidocaine with epinephrine.12,20,21
50
Table 4. Local anesthetic calculation for a 50 lb child based on the Rule of 25.
1 cartridge/25 lb weight
1 cartridge/25 lb weight x 50 lb child = 2 cartridges of any local anesthetic or combination
of local anesthetics for a 50 lb patient.
Clark’s rule is another weight-based
method for calculating the MRD.12
According to Clark’s rule, the dose of local
anesthetic should be reduced by the ratio
of the child’s weight to an adult weight
of 150 lb.5 Thus, if a child weighs 50 lb,
then he/she is 33% of the established adult
weight. Therefore, the child’s MRD for any
local would be 33% of the 150 lb adult
MRD for a given local anesthetic. As stated
before, the MRD for 2% lidocaine with
epinephrine for a 150 lb adult is 500 mg,
and the MRD for 3% mepivacaine plain is
400 mg. Therefore, the MRD for a 50 lb
patient is 33% of the adult MRD, which
calculates as 166 mg of 2% lidocaine with
epinephrine (approximately 4.5 cartridges)
or 133 mg of 3% mepivacaine plain
(approximately 2.5 cartridges.) (Table 3).12
It is important to note that the effects
of all local anesthetics, including toxicity, are mediated at the sodium channel
in a dose-dependent fashion. The effects
of various local anesthetics are additive.
Once the MRD for 1 local anesthetic is
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administered, the patient cannot receive
any other local anesthetics, including topical applications.22
Moore & Hersh describe a simplified
alternative for calculating safe maximum
doses using a conservative guideline.12
Described as the Rule of 25, this alternative calculation can be applied to all US
dental local anesthetic formulations for
healthy patients. The Rule of 25 states
that 1 cartridge of any formulation marketed in the US may be used per 25 lb of
weight. Therefore, 1 cartridge for a 25 lb
patient, 2 cartridges for a 50 lb patient,
3 cartridges for a 75 lb patient, up to a
maximum of 6 cartridges for patients
≥150 lbs (Table 4).12 The end result of the
Rule of 25 is a lower number of cartridges
administered to the child in comparison to
other weight-based calculations (Table 5).
Since the vast majority of local anesthetic
morbidity and mortality reports involve
children ≤8 years of age, the Rule of 25
may be more appropriate in this population than in calculations used for adults.12
Table 5. Summary of dosing calculations in a 50 lb child.
MRD 2% lidocaine with 1:100,000 epinephrine
Maximum cartridges with 2% lidocaine with 1:100,000 epinephrine
MRD 3% mepivacaine plain
Maximum cartridges with 3% mepivacaine plain
Adult MRD
Weight-based calculations
Clark’s rule
Rule of 25
500 mg
160 mg
166 mg
N/A
13.5
4.5
4.5
2.0
400 mg
130 mg
133 mg
N/A
7.5
2.5
2.5
2.0
When treating small children, it is advisable to determine the maximum number
of local anesthetic cartridges needed for
that appointment. Keep only this amount
of cartridges on the tray, and do not discard any used cartridges until the appointment is over. This will precisely track the
number of cartridges administered.
Aspiration and slow injection will allow
for recognition of inadvertent intravascular
injection before the entire cartridge is
injected into a vessel.22 Profound anesthesia
can often be achieved in children with less
than a full cartridge of anesthetic. Injecting
slowly—approximately 30-60 seconds per
cartridge—will minimize discomfort and
allow retention of the local anesthetic at the
target site rather than being flushed farther
away.22 Rather than giving the entire predetermined amount of local anesthetic at the
beginning of a procedure, it is preferable to
reserve 25% of the predetermined amount
of local anesthetic in case an injection fails
or if supplemental anesthesia is needed
later.5 With a reported 15%-20% failure
rate for inferior alveolar nerve blocks, it is
critical to use the proper technique in order
to reduce the need for supplemental injections.2,22 On average, a child’s mandibular
foramen is near the occlusal plane; by
adulthood, the mandibular foramen moves
posteriorly and is approximately 7 mm
above the occlusal plane.2,23 Therefore, if
the inferior alveolar nerve block is missed
in the treatment of a child but the MRD
has not been exceeded, one can attempt to
inject vertically higher.2 While lip numbness is usually considered a sign of an
adequate inferior alveolar nerve block, the
lack of gingival response to stimulation is
considered to be a more rapid and reliable
indicator of anesthesia in young children
than asking the patient about the presence
or absence of lip numbness.2,24 A possible alternative to mandibular blocks for
procedures in young children is to utilize
a buccal mandibular infiltration technique with 4% articaine plus 1:100,000
epinephrine, which appears to produce
a high success rate of mandibular pulpal
anesthesia.25,26 If the injections fail and
the predetermined maximum amount of
local anesthetic has been administered, it
is recommended to not attempt to supplement with more local anesthetic.2,22 The
best approach would be to reschedule the
treatment appointment.
Local anesthetic systemic toxicity:
warning signs and management
When providing emergency care, a dentist
needs to immediately recognize signs and
symptoms of LAST (such as tremors or
convulsions). The dental procedure should
be stopped as soon as any neurological,
respiratory, or cardiovascular signs or
symptoms of local anesthetic overdose
become apparent.5 The dentist should
monitor vital signs (such as pulse and
blood pressure), watch for coloration if
pulse oximetry is not available, and assess
breathing by looking for chest rise and
movement of air. If necessary, initiate basic
life support in the form of chest compressions and positive pressure ventilation with
oxygen until medical assistance arrives.5 In
the event of an emergency, any delay may
result in the patient’s reserves of oxygen
being consumed leading to poor oxygenation of key organs such as the brain and
heart, and irreversible damage may occur.
Three key interventions are necessary:
1) clear the airway of any obstructions
including the tongue or foreign bodies
such as gauze; 2) provide supplemental
positive pressure oxygen; and 3) if the
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patient has no pulse, apply chest compressions so that oxygenated blood can reach
the brain and heart.4
Basic life support skills are essential until
the patient can be transferred to a hospital.4
Someone on the dental team should call for
medical assistance; another should manage
seizures and respiratory depression.5 The
patient should be positioned on the left
lateral side to facilitate suction, which
should be applied to the pharynx to remove
any saliva and foreign bodies, such as dislodged stainless steel crowns, rubber dam
clamps, or pieces of gauze. An oxygen tank
should be available to provide supplemental
oxygen either by nasal cannula or nasal
hood for a patient who is able to breathe,
or by a bag-valve-mask if there is significant
respiratory depression. According to Moore,
“positive pressure oxygen ventilation is
the most important element in managing
local anesthetic overdose.”5 Although rarely
required, advanced management of seizures
may include the intravenous administration
of a benzodiazepine such as diazepam or
midazolam.5,12 Following any convulsion,
serious respiratory depression can occur,
so it is critical to continue to monitor the
patient and support the airway.5,12
Conclusions
While local anesthetics possess a wide
margin of safety in adult patients, MRDs
of these drugs can be easily exceeded in
pediatric dental patients. The prevention of LAST in young children is best
achieved by strictly adhering to weightbased MRD dosing guidelines. The more
conservative Rule of 25, which states that
no more than 1 cartridge of local anesthetic should be given for each 25 lb of
patient body weight, will impart an added
safety layer in children ≤8 years of age.
General Dentistry
51
Anesthesia and Pain Control Local anesthetic calculations: avoiding trouble with pediatric patients
Author information
Dr. Saraghi is in private practice in New
York, New York. Dr. Moore is a professor
of Dental Anesthesiology, Pharmacology,
and Public Health, University of Pittsburg
School of Dental Medicine, Philadelphia.
Dr. Hersh is a professor of Pharmacology,
Department of Oral and Maxillofacial
Surgery and Pharmacology, and the director of the Division of Pharmacology,
University of Pennsylvania School of
Dental Medicine, Philadelphia.
References
1. Personal communication with Paul Mondock, senior
vice president, Sales and Marketing, Septodont, Inc.
June 7, 2013.
2. Cheatham BD, Primosch RE, Courts FJ. A survey of local anesthetic usage in pediatric patients by Florida
dentists. ASDC J Dent Child. 1992;59(6):401-407.
3. Hersh EV, Helpin ML, Evans OB. Local anesthetic mortality: report of case. ASDC J Dent Child. 1991;58(6):
489-491.
4. Tarsitano JJ. Children, drugs, and local anesthesia.
J Am Dent Assoc. 1965;70:1153-1158.
5. Moore PA. Preventing local anesthesia toxicity. J Am
Dent Assoc. 1992;123(9):60-64.
6. Goodson JM, Moore PA. Life-threatening reactions
after pedodontic sedation: an assessment of
narcotic, local anesthetic, and antiemetic drug interaction. J Am Dent Assoc. 1983;107(2):239-245.
7. McAuliffe MS, Hartshorn EA. Anesthetic drug interactions. Quarterly update. CRNA. 1998;9(4):172-176.
8. Kohli K, Ngan P, Crout R, Linscott CC. A survey of local
and topical anesthesia use by pediatric dentists in the
United States. Pediatr Dent. 2001;23(3):265-269.
9. Zinman EJ. Letter: toxicity and mepivacaine. J Am Dent
Assoc. 92(5):858.
10. Zinman EJ. More on mepivacaine. J Calif Dent Assoc.
1976;4(4):50.
11.Hersh EV, Hermann DG, Lamp CJ, Johnson PD,
MacAfee KA. Assessing the duration of mandibular
soft tissue anesthesia. J Am Dent Assoc. 1995;126(11):
1531-1536.
12. Moore PA, Hersh EV. Local anesthetics: pharmacology
and toxicity. Dent Clin North Am. 2010;54(4):587-599.
13. Fonseca RJ. Oral and Maxillofacial Surgery. Vol 1. 1st
ed. Philadelphia: W.B. Saunders Company; 2000.
14. Malamed SF. Morbidity, mortality, and local anesthesia. Prim Dent Care. 1999;6(1):11-15.
15. Meechan J. How to avoid local toxicity. Br Dent J.
1998;184(7):334-335.
16. Berquist HC. The danger of mepivacaine 3% toxicity in
children. Can Dent Assoc J. 1975;3:13.
17. Zinman EJ. Letter: Toxicity and mepivacaine. J Am Dent
Assoc. 1976;92(5):858.
18. Novocol Pharmaceutical of Canada, Inc. Octocaine
(Lidocaine HCl 2% and Epinephrine 1:100,000 Injection) [package insert]. Available at: http://staging.test.
novocol.com/docs/product-insert/Octocaine.pdf.
Accessed October 8, 2014.
AGDPODCAST
Computer-Controlled
Anesthesia
52
General Dentistry
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19. Novocol Pharmaceutical of Canada, Inc. Isocaine
(Mepivacaine 3% Injection) [package insert]. Available
at: http://www.novocol.com/our-products/injectableanesthetics/isocaine/. Accessed October 8, 2014.
20. Goebel WM, Allen G, Randall F. The effect of commercial vasoconstrictor preparations on the circulating venous serum level of mepivacaine and lidocaine. J Oral
Med. 1980;35(4):91-96.
21. Goebel WM, Allen G, Randall F. Comparative circulatory serum levels of 2 per cent mepivacaine and 2 per
cent lignocaine. Br Dent J. 1980;148(11-12):261-264.
22. Meechan J. How to avoid local anaesthetic toxicity. Br
Dent J. 1998;184(7):334-335.
23. Berberich G, Reader A, Drum M, Nusstein J, Beck M. A
prospective, randomized, double-blind comparison of
the anesthetic efficacy of two percent lidocaine with
1:100,000 and 1:50,000 epinephrine and three percent mepivacaine in the intraoral, infraorbital nerve
block. J Endod. 2009;35(11):1498-1504.
24. Ellis RK, Berg JH, Raj PP. Subjective signs of efficacious
inferior alveolar nerve block in children. ASDC J Dent
Child. 1990;57(5):361-365.
25. Robertson D, Nusstein J, Reader A, Beck M, McCartney M. The anesthetic efficacy of articaine in buccal
infiltration of mandibular posterior teeth. J Am Dent
Assoc. 2007;138(8):1104-1112.
26. Haase A, Reader A, Nusstein J, Beck M, Drum M.
Comparing anesthetic efficacy of articaine versus lidocaine as a supplemental buccal infiltration of the
mandibular first molar after an inferior alveolar nerve
block. J Am Dent Assoc. 2008;139(9):1228-1235.
Endodontics
Exercise No. 362 Anesthesia
and Pain Control Subject Code 132
The 15 questions for this exercise are based on
the article, Local anesthetic calculations: avoiding
trouble with pediatric patients, on pages 48-52.
This exercise was developed by Riki Gottlieb, DMD,
FAGD, in association with the General Dentistry SelfInstruction committee.
1. LAST can be described using all of the
following terms except one. Which is
the exception?
A.rare consequence of LAO
B. avoidable consequence of LAO
C.allergic reaction to LAO
D.occurs more frequently in children
2. According to the article, the
most common cause of morbidity
and mortality due to LAST is
_______________________.
A.respiratory depression
B. cardiovascular stimulation
C.central nervous system (CNS) excitation
D.nerve damage
3. Symptoms of early toxicity consist of all
of the following CNS symptoms except
one. Which is the exception?
A.metallic taste
B.tinnitus
C.dry mouth
D.dizziness
4. Concomitant opioid sedative
administration will _______ respiratory
depression and ________ the seizure
threshold of local anesthetics.
A.reduce; increase
B. enhance; increase
C.reduce; decrease
D.enhance; decrease
5. All of the following are relatively larger
in children than adults except one.
A.tongue
B.tonsil
C.airway
D.adenoid
6. A local anesthetic without a
vasoconstrictor offers ______ minutes of
pulpal anesthesia.
A.20-40
B.60-80
C.100-120
D.140-160
Reading the article and successfully completing this exercise will enable you to:
•describe the signs and symptoms of local anesthesia systemic toxicity (LAST);
•understand the mechanism of action of local anesthetic toxicity (LAO); and
•learn how to calculate the maximum recommended dose (MRD) to prevent local
anesthesia toxicity.
7. Use of ______ makes it easier to reach
or exceed the MRD.
A.2% lidocaine, 1:100,000 epinephrine
B. 3% mepivacaine, no epinephrine
C.4% articaine,1:100,000 epinephrine
D.5% bupivacaine, no epinephrine
8. A 4% formulation of a drug means that
there are _____ mg/ml, and in a 1.8 ml
dental cartridge there are _____ mg/
cartridge.
A.30; 36
B. 30; 42
C.40; 54
D.40; 72
9. The MRD of 3% mepivacaine is 2.6 mg/
lb. What is the maximum number of
cartridges one can give a 45 lb child?
A.1
B.2
C.3
D.4
10. Clark’s rule is another weight-based
method for calculating the MRD.
According to Clark’s rule, the dose of
local anesthetic should be reduced by
the ratio of the child’s weight to an
adult weight of 200 lb.
A.Both statements are true.
C.The first statement is false;
the second is true.
D.Both statements are false.
11. Using Clark’s rule, what would be a
60 lb child’s MRD for the use of 2%
lidocaine with 1:100,000 epi?
A.3.5 cartridges
B. 4.5 cartridges
C.5.5 cartridges
D.6.5 cartridges
12. The effects of various local anesthetics
used in conjunction with each other
are unrelated. The effects of all local
anesthetics, including toxicity, are
mediated at the sodium channel in a
dose-dependent fashion.
A.Both statements are true.
C.The first statement is false;
the second is true.
D.Both statements are false.
13. All of the following are correct about
the Rule of 25 except one. Which is the
exception?
A.It can be applied to all US dental local
anesthetic formulations for healthy
patients.
B. The Rule of 25 states that 1 cartridge
of any formulation marketed in the US
may be used per 25 lb.
C.Using the Rule of 25 may be more
appropriate in children ≤8 years than
weight-based calculations.
D.The Rule of 25 indicates the use of
3 cartridges of local anesthetic for a
50 lb child.
14. To prevent local anesthetic overdose,
all of the following should be followed
except one. Which is the exception?
A.Determine the maximum amount of
local anesthetic at the beginning of the
appointment.
B. Keep all used local anesthetic cartridges
until the end of the appointment.
C.Inject the local anesthetic quickly, at
a rate of approximately 10-15 seconds
per cartridge.
D.Use aspiration technique to determine
intravascular injection.
15. All of the following actions are to be
performed immediately in the event of
local anesthetic overdose, except one.
A.stop dental procedure
B. administer nitrous oxide
C.position patient on left lateral side
D.begin basic life support and call 911
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General Dentistry
53
Forensic Dentistry
The role of the dentist in identifying missing
and unidentified persons
Amber D. Riley, RDH, MS
The longer a person is missing, the more profound the need for dental records becomes. In 2013, there were >84,000 missing persons and >8,000
unidentified persons registered in the National Crime Information Center
(NCIC) database. Tens of thousands of families are left without answers or
closure, always maintaining hope that their relative will be located. Law enforcement needs the cooperation of organized dentistry to procure dental
records, translate their findings, and upload them into the NCIC database
A
ny single event—be it a natural
disaster, terrorism act, or mass
transit accident—that produced
thousands of fatalities and tens of thousands of missing persons would cause
concerned citizens and outraged family
members to descend upon Capitol Hill,
demanding that law enforcement and the
government take immediate action to
answer questions and show what they are
doing to bring justice to the victims and
closure to the victims’ families. However,
even in the absence of cataclysmic events,
there are still people being reported
missing and unidentified bodies being
found every day. The statistics are staggering. According to the National Crime
Information Center’s “NCIC Missing
Person and Unidentified Person Statistics
for cross-matching with unidentified person records created by medical
examiner and coroner departments across the United States and Canada.
Received: March 24, 2014
Revised: July 24, 2014
for 2013,” there were >84,000 missing
persons (MPs) and >8,000 unidentified
persons (UPs) in the United States
and Canada that year, leaving many
families without closure for their missing
loved ones.1
In response to these daily numbers
of MPs and UPs, the US has set very
high standards for the identification of
our nation’s deceased. The scientifically
supported methods of human identification are fingerprints, dental records, and
DNA.2,3 Each method is accurate and each
requires comparison analysis.
When a person is reported missing, a
series of actions takes place. The first is
the filing of a missing person (MP) report.
This report is a detailed intake of the MP’s
information that will include not only basic
Fig 1. An example of a National Crime Information Center $.M. report.
54
Key words: missing persons, unidentified persons, HIPAA, dental records
General Dentistry
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information—such as height and weight,
eye and hair color, and where they were last
seen—but will also include information
that is not made available to the public
in order to assist in law enforcement’s
search and investigation. This information
includes the names and addresses of the
MP’s dentist and medical doctor, as well as
any referral information, such as orthodontic or endodontic specialists. This information is used in order to retrieve the MP’s
antemortem medical and dental records.
When a person is reported as missing,
it is not automatically assumed by law
enforcement that the MP is deceased;
the gathering of medical and dental data
specific to the MP is a critical part of
any investigation.2,3 A dentist (or auxiliary) who has been specially trained as
Fig 2. Postmortem dental record creation.
Fig 3. Picture of a decedent’s hand showing unusable fingerprints due to decomposition in water.
Fig 5. A decedent’s head with fourth degree
postmortem burns, still showing the preserved
dental evidence.
a dental coder by the Federal Bureau of
Investigation (FBI) translates the dental
data into the NCIC system in order to
cross-reference on a continual basis all
unidentified bodies found in the US and
Canada that have been entered into the
system.1 Possible matches are marked, and
daily reports of any “hits” are generated
and remitted to the originating agencies (such as local police departments,
county sheriffs, or highway patrol) that
initially filed the MP reports.1 These
reports are called $.M. reports (Fig. 1).
Fig 4. Facial photograph of a decedent’s head showing how despite
surrounding tissue decomposition, the dental evidence is preserved.
The reports are then reviewed by the
originating agency for their actual
relevance to the case. If dental records
need to be reviewed, it will be done by
an FBI-trained dental coder, who will
determine if the cross-match is valid
and therefore requires a follow-up by the
originating agency.
When a body is recovered and the
identity of the decedent is unknown,
a postmortem dental record will be
created as part of the autopsy (Fig. 2).
This record will contain radiographs,
photographs, and an odontogram. For a
UP, the data will be coded and uploaded
into the NCIC system for constant crossreferencing with all MP reports. It is
from these UP files that the originating
agencies investigating MPs get some of
their hits. There is a national repository
of radiographic and photographic images
that can be accessed by authorized personnel for rapid record comparison when
a strong hit from a $.M. report is received.
Every dental professional understands
how incredibly resistant to destruction
the human dentition is. From a forensic
standpoint, human teeth can withstand
blunt force trauma; fires at profoundly
high temperatures; natural decomposition; chemical erosions that destroy
other tissues; and various environmental
changes in climate, humidity, and exposure.2,3 Human skin begins to decompose
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immediately after death, and usable
friction ridges (fingerprints) may rapidly
deteriorate if the body is outdoors and
certainly if the body is in water for several
hours to a few days (Fig. 3 and 4).2,3 If
the body (including the hands) has fourth
or fifth degree burns, fingerprints will
not be retrievable, and the recovery of
usable DNA is highly compromised due
to heat-related denaturation of proteins in
the body.2,3 What will remain usable for
identification in all of these scenarios are
the decedent’s teeth (Fig. 5).
The role of the dentist in helping law
enforcement identify MPs or UPs involves
both recordkeeping and the retention of
records. The American Dental Association
recommends full dental record retention
of active and inactive patients, as well as
keeping the record of a deceased patient
for 2 years beyond their death.4 However,
this is only a recommendation. There are
many states in the US and provinces in
Canada that have no minimum standard
set for dental record retention whatsoever
(although there are some exceptions for
the records of children and the disabled).
Death investigations have been severely
compromised due to the destruction of
patients’ dental records. Loss of dental
records can be caused by overstringent
housekeeping in the dental office—especially with inactive patients—or during
changes in ownership of the practice when
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55
Forensic Dentistry The role of the dentist in identifying missing and unidentified persons
a new owner may purge old records. The
problem of dental record destruction has
become such a profound obstacle in the
endeavor to find MPs and identify UPs
that the American Society of Forensic
Odontology (ASFO) published an official
position paper on record retention directed
toward general dentistry practitioners.5
The guidelines in this paper state that if,
for good reason, a full record of a patient
cannot be retained, then the dentist should
retain—at a minimum—the most recent
bitewing, full mouth, or panoramic X-rays
for patients who have been inactivated,
as well as a patient information form that
includes the patient’s date of birth and
social security or driver’s license number.5
If a photo of the patient is available, the
dentist is advised to keep that, as well.5
If file space is at a premium, as it is in
many dental offices even though practices
are moving toward fully digitized record
keeping, the aforementioned files can be
scanned and saved onto an external drive
to free up needed physical space. Taking
this step not only maintains a record in
case it is ever requested by law enforcement, it also allows the general dentist to
organize and prioritize records for day-today practice.
To address questions that a dentist may
have about patient privacy and the legal
ramifications for releasing a dental record
without a patient’s permission, the Health
Insurance Portability and Accountability
Act (HIPAA) has a specific provision for
this very scenario. This is stated in 45 CFR
Section 164.512(g)(1), which reads in part:
A covered entity (e.g., a hospital or doctor)
may disclose protected health information
to a coroner or medical examiner for the
purpose of identifying a deceased person,
determining a cause of death, or other
duties as authorized by law.6
Dentists and their practices are indemnified from violation if they relinquish
records to a law enforcement agent. A
dentist will be given a written request
on official letterhead of the law enforcement agency that contains the name
of the patient, the case number of the
investigation, and the name and contact
information of the requesting agency
and requesting officer (Fig. 6). A dentist
should make duplicates of everything
56
Fig 6. Sample record request from the Department of the Medical Examiner, San Diego, CA.
in their patient’s record and give the
entire original record to the investigator.
Making a duplicate of the entire record is
very important since the original record
will likely be retained by the authorities,
logged as evidence, and retained with the
case material.
A warrant is not needed for a dentist to
release records to assist in an investigation.
However, if a dentist chooses not to release
dental records, a warrant will be issued,
and the requested record will be legally
confiscated in order to collect the needed
information. As such, it is advisable to
cooperate with law enforcement.
Law enforcement agencies not only need
dental records, they also need experienced
dental professionals trained by the FBI as
dental coders. A dental coder can directly
create the postmortem dental records for
the cases that enter the NCIC system from
their assigned jurisdictions.1
General Dentistry
www.agd.org
The author of this article serves as a
forensic dental autopsy technician. As
an FBI-trained dental coder, the author
is extremely aware of the importance of
dental records in identifying UPs and
MPs. No dental record is ever purged in
the author’s office, radiographs are current
and properly exposed, dental charting
(digital) is updated to include existing as
well as completed dentistry, and therapy
records are detailed to include not only
the procedure performed, but also the
materials used in the treatment. Numerous
intraoral and extraoral photographs
are collected; these images are strongly
recommended not just from a forensic
standpoint (such as unusual tori or tooth
anomalies), but also from the standpoint
of impairing any illegitimate attempts of
civil litigation against a dental practice—a
dentist should take many photos, and take
them often (Fig. 7 and 8).
of human identification. A dentist’s
responsibility to his/her patients does
not end when records are archived. For
the thousands of UPs, and the tens of
thousands of MPs, the dental profession
is obligated to retain the integrity of their
dental records.
Author information
Fig 7. A sample photograph from a patient’s file showing unique
and clinically significant intraoral anatomy (large, lobulated
maxillary torus).
Fig 8. A sample photograph from a
patient’s file showing unique dental
anatomy (accessory cusp on the buccal
of tooth No. 2).
Ms. Riley is a registered dental hygienist, San Diego, California. She is a
member of the American Academy of
Forensic Sciences, the American Society
of Forensic Odontology, the American
Dental Hygienists’ Association, the
California Dental Identification Team,
and the Disaster Mortuary Operational
Response Team.
Acknowledgments
A general dentist can contribute to the
effort of identifying the thousands of
MPs and UPs reported across the US and
Canada. The first step is to stop destroying dental records. There is always a possibility that a patient has become inactive
because they are missing or deceased.
The colder an MP case becomes, the
more important that person’s dental
record becomes, since teeth withstand the
processes of decomposition and elemental exposure long after other sources of
identification have disappeared.2,3 For
a general dentist who is selling their
practice, a provision can be added that
the new owner must retain at least the
minimal patient records—as outlined by
the ASFO—of the old practice.5
At least once (and often twice) a year,
the FBI will fund 2-day training workshops on NCIC coding for dentists and
auxiliaries.1,7 Space is extremely limited,
and positions are filled on a first-come,
first-served registration basis. After the
successful completion of this course, a
dentist may be asked by his/her local or
state bureaus to translate procured dental
records for entry into the NCIC system,
or to create postmortem records for UPs.7
The National Missing and Unidentified
Persons System (NamUs) has a website
on which anyone can view MP and UP
reports which have been entered by law
enforcement agencies.7,8 The NamUs
site is managed by the US Department
of Justice and was designed explicitly to
solicit the public’s help in solving cases.8
There is access to names, filtered search
results by state and city, and information
on how to contact the investigator managing a specific case.7,8
Unlike televised depictions of forensic
technologies that routinely locate evidence
such as usable DNA samples from objects
found at crime scenes or fingerprints
from rough textiles, complex cases in real
life are not quickly solved. The reality is
that it takes teamwork and cooperation
between law enforcement, healthcare
providers, the public, and families of the
missing to help identify and, if possible,
bring home MPs and UPs. The identification of MPs and UPs aids in investigations that will hopefully provide answers
as well as a sense of closure, and in some
cases, mete out justice to the person or
persons responsible for a victim’s demise.
Conclusion
Dentists should consider record retention
as their professional duty. The dental
profession serves as custodians of one of
the most reliable, cost-effective, expedient, and scientifically supported methods
www.agd.org
The author would like to acknowledge
Gary Bell, DDS, DABFO, Anthony
Cardoza, DDS, DABFO, Stephanie
Kavanaugh, DDS, DABFO, Craig Nelson,
MD, American Academy of Forensic
Sciences, American Board of Forensic
Odontology, and the American Society of
Forensic Odontology.
References
1. National Crime Information Center. NCIC Missing
Person and Unidentified Person Statistics for 2013.
Available at http://www.fbi.gov/about-us/cjis/ncic/
ncic-missing-person-and-unidentified-personstatistics-for-2013. Accessed November 14, 2014.
2. Senn DR, Weems RA, eds. Manual of Forensic Odontology. 5th ed. Boca Raton, FL: CRC Press; 201:78-81.
3. Senn DR, Stimson PG. Forensic Dentistry, 2nd ed. Boca
Raton, FL: CRC Press; 2010:163-183.
4. American Dental Association. Dental Records. Available at: http://raedentalmanagement.com/wp-content/
uploads/2014/03/ADA-Dental-Records.pdf. Accessed
November 14, 2014.
5. American Society of Forensic Odontology. ASFO Dental
Record Retention Position Paper. Available at: http://
asfo.org/asfo-dental-record-retention-position-paper/.
Accessed November 7, 2014.
6. U.S. Department of Health and Human Services Office
for Civil Rights. HIPAA Administrative Simplification,
Regulation Text 45 CFR Parts 160, 162, and 164.
Available at: http://www.hhs.gov/ocr/privacy/hipaa/
administrative/privacyrule/adminsimpregtext.pdf. Accessed November 7, 2014.
7. Silver WE, Souviron RR. Dental Autopsy. Boca Raton,
FL: CRC Press; 2009:125-126.
8. US Department of Justice. National Missing and Unidentified Persons System (NamUs). Available at:
http://www.namus.gov/. Accessed November 10,
2014.
General Dentistry
57
Non-Surgical Endodontics
Nonsurgical endodontic treatment of permanent
maxillary incisors with immature apex and a large
periapical lesion: a case report
Gautam P. Badole, MDS n M.M. Warhadpande, MDS n Rakesh N. Bahadure, MDS n Shital G. Badole, BDS
Immature teeth with necrotic pulp and large periapical lesions are
difficult to treat via conventional endodontic therapy. However,
they can be treated with calcium hydroxide and mineral trioxide
aggregate (MTA). This article reports the case of a nonvital tooth
with a periapical lesion and an open apex that was treated with a
single-visit MTA apical plug. A radiographic evaluation taken 6 months
S
uccessful endodontic treatment
requires cleaning and shaping to
obtain a fluid-tight seal in apical
areas.1 When teeth have incompletely
formed apices (known as blunderbuss
canals) and/or a root canal with abnormal apical constriction, it is difficult
to control the obturating material
within the canal during condensation.2,3
Apexification with calcium hydroxide
[Ca(OH)2] has been the treatment of
choice for necrotic teeth with open
apices in recent years.3,4 Ca(OH)2 can be
used alone or mixed with camphorated
monochlorophenol (CMCP), metacresyl
acetate (with or without CMCP), physiologic saline, Ringer’s solution, distilled
Key words: MTA, open apex, periapical lesion
water, or an anesthetic solution.5 The
usual time required to form a calcific
barrier is 6-24 months.5 Determining the
extent of apical closure can be difficult, as
analyzing a 3-dimensional apical closure
via a 2-dimensional radiograph can lead
to misinterpretation.6 The disadvantages
of long-term use of Ca(OH)2 include the
need for multiple appointments, possible
recontamination of the root canal, and
increased brittleness of the root dentin.7,8
A 1975 study by Roberts & Brilliant
reported the use of tricalcium phosphate as
an apical barrier.9 Mineral trioxide aggregate
(MTA) was developed as a root-end filling
material. Apexification using MTA has
several advantages, as it is not resorbed, it
Fig. 1. A preoperative radiograph
showing open apices on teeth No. 8
and 9, with a large periapical lesion
extending across teeth No. 7 and 8.
58
post-treatment showed a decrease in the periapical lesion; at 1 year,
complete healing was visible.
Received: October 21, 2013
Accepted: November 24, 2013
General Dentistry
does not weaken the root canal dentin, and
it sets in a wet environment. Satisfactory
compaction of filling material can be
achieved as MTA forms a hard and nonresorbable apical barrier.10 MTA also is used
for single-step apexification in open apex
cases, producing less inflammatory reactions
in the periapical area and favoring bone
formation. This case report used the MTA
apical plug technique for successful nonsurgical management of a tooth with a large
periapical lesion and blunderbuss canal.
Case report
A 24-year-old woman complained of mild,
intermittent pain in the maxillary anterior
region. Patient history revealed that she
Fig. 2. A radiograph taken after
placement of MTA apical plugs in
teeth No. 8 and 9.
www.agd.org
Fig. 3. A radiograph of teeth No. 7, 8,
and 9 taken postobturation.
Discussion
Fig. 4. A radiograph taken 6 months
post-treatment. Note the decrease in
size of the periapical lesion.
Fig. 5. A radiograph taken 1 year
post-treatment. Note that the periapical
lesion is completely healed.
had suffered a trauma 15 years earlier.
Clinical examination showed loss of
enamel translucency in teeth No. 7, 8, and
9. Tooth mobility within the physiologic
limit was present. Teeth No. 7 and 9
demonstrated mild pain on percussion. A
periapical radiograph revealed a large periapical lesion (5 x 5 cm) extending across
teeth No. 7 and 8. The lesion showed a
well-defined nonsclerotic border. Open
apices were found in both teeth No. 8 and
9 (Fig. 1). Soft tissue examination showed
that gingival and mucogingival tissue were
normal. None of the teeth responded to
electric and thermal pulp vitality tests.
There was no history of discharge or
swelling, and the patient’s medical history
was noncontributory.
Based on clinical and radiographic
findings, a diagnosis of chronic apical periodontitis with immature apex was made
for teeth No. 7, 8, and 9. A treatment plan
was proposed involving root canal therapy
for all 3 teeth, with an MTA apical plug
for teeth No. 8 and 9.
After rubber dam isolation, access
cavities were prepared for the 3 teeth.
Working length was established with
both radiographic and electronic apex
locators (Root ZX, J. Morita USA, Inc).
Root canals were cleaned mechanically
using H-files (DENTSPLY International)
and gentle but copious irrigation with
0.5% sodium hypochlorite and saline.
After drying the canals with paper points,
Ca(OH)2 paste was placed into the root
canal as an intracanal medicament. After
placing a sterile cotton pellet, the access
cavities were closed with cement (IRM,
DENTSPLY International).
One week later, the patient was
asymptomatic and the Ca(OH)2 was
removed. Root canals were irrigated with
0.5% sodium hypochlorite, 17% EDTA
(Pulpdent Corporation), and a final rinse
of 2% chlorhexidine gluconate. Canals
were dried with paper points, and MTA
(ProRoot MTA, DENSTPLY Tulsa) was
placed in the apical portion of teeth No.
8 and 9. Subsequent increments were
condensed with a hand plugger until
a thickness of 4-5 mm was achieved
(Fig. 2). A wet cotton pellet was placed
into the canals and the access cavity
was sealed with IRM. Using the lateral
condensation technique, tooth No. 12
was obturated with gutta percha and
root canal sealer (AH Plus, DENTSPLY
Tulsa Dental Specialties) at the same
appointment. On the following day, the
remaining canals in teeth No. 8 and 9
were obturated by applying gutta percha
with AH Plus and using the lateral condensation technique (Fig. 3). The access
cavity was sealed with resin-modified
glass ionomer cement (GC Fuji PLUS,
GC America, Inc.).
At a follow-up visit 6 months posttreatment, a radiograph revealed a marked
decrease in the size of the periapical lesion
(Fig. 4). At 1 year, the periapical radiolucency had healed completely (Fig. 5).
www.agd.org
The diagnosis of chronic apical periodontitis and immature apex was confirmed.
A large periapical radiolucency was present, suggesting periapical granuloma or
periapical/radicular cysts. Although there
are histological differences between these
conditions, they cannot be differentiated
clinically as their clinical and radiographic
appearances are identical. The borders of
the radiolucency cannot be used as diagnostic criteria.11,12
It is now accepted that a well-defined
border indicates a long-standing lesion
that is slowly increasing in size, whereas
a diffuse border is more likely to indicate
a rapidly expanding lesion.13 The size of
the radiolucency is irrelevant to the histological state of the tissue, as both small
and large lesions could be granulomas,
abscesses, or cysts. Since granulomas and
radicular cysts are difficult to diagnose
differentially, they are classified clinically by the general term chronic apical
periodontitis.11-13
When performing root canal treatment
in teeth with necrotic pulps and wide-open
apices, the main challenge is obtaining an
optimal apical seal. According to a 2005
prospective clinical study, Ca(OH)2 apexification therapy had a 100% success rate,
with a mean of approximately 12 months
to form an apical barrier.14 Disadvantages
of Ca(OH)2 apexification include failure
to control infection, recurrence of infection, and cervical fracture.15
Creating an MTA apical plug in a
single visit has been suggested for nonvital
immature permanent teeth as an alternative to long-term apexification treatment,
offering good apical seal, biocompatibility,
and pulpal and periodontal regenerating
capabilities.16 MTA has the potential to
provide an effective seal (even in the presence of blood and moisture) and form a
primary monoblock.2 A 5 mm barrier is
significantly stronger and demonstrates
less leakage than a 2 mm barrier.17
The major problem in cases of a wideopen apex is the need to limit the material
to the periapical area, thus avoiding the
extrusion of a large amount of material
into the periodontal tissue. A large volume
of the extruded material may set before it
disintegrates and is resorbed. This might
result in the persistence of the inflammatory process, which may complicate
General Dentistry
59
Non-Surgical Endodontics Nonsurgical endodontic treatment of permanent maxillary incisors
repair of the tissue. The use of a matrix is
advisable since its placement in the area
of bone destruction provides a base for a
sealing material (such as MTA). In cases of
teeth with incomplete formation of apex,
several materials have been recommended
to create a matrix. These materials include
calcium hydroxide, hydroxyapatite, resorbable collagen, and calcium sulfate.18-21
In the present case, the MTA plug
technique was used successfully for
the endodontic treatment of an open
apex with a periapical lesion. Six- and
12-month follow-up radiographs showed
complete healing for the apical lesion and
the regeneration of periradicular tissues.
Three hours after mixing, the pH of the
MTA increased from 10 to 12.5. It is
assumed that in a high pH environment,
calcium ions that are released from MTA
react with phosphates in the tissue fluid to
form hydroxyapatite, which would explain
its favorable sealing ability and biocompatibility.4,22 MTA stimulates interleukin
production and cytokine release; it also
promotes hard tissue formation.23
A 2009 cell culture study on human
alveolar osteoblasts reported the expression
of runt-related transcription factor 2 (which
is essential for osteoblast differentiation and
bone formation) in the presence of MTA
mixed with either sterile water or an anesthetic solution.24 Studies have reported that
MTA is both osteoconductive and osteoinductive; thus it favors bone formation.25-27
According to the literature, MTA showed
the highest amount of hard tissue formation
and the lowest level of periapical inflammation in open apex cases.28-29 The single-visit
MTA apical plug technique saves time
compared to Ca(OH)2 apexification, and
offers predictable apical barriers that favor
periapical tissue regeneration.
Conclusion
A single-visit MTA apical plug is an effective method to provide a good apical seal
in open apex cases. It also offers the advantages of biocompatibility, predictability, less
treatment time, and fewer appointments.
Author information
Dr. G. Badole is a lecturer, Department of
Conservative Dentistry & Endodontics,
60
VSPM’s Dental College and Research
Center, Nagpur, India, where Dr. S.
Badole is an intern. Dr. Warhadpande
is an associate professor, Government
Dental College and Hospital, Nagpur,
India, where Dr. Bahadure is a lecturer,
Department of Pedodontics.
References
1. Ng YL, Mann V, Rahbaran S, Lewsey J, Gulabivala K.
Outcome of primary root canal treatment: systematic
review of the literature—part 2. Influence of clinical
factors. Int Endod J. 2008;41(1):6-31.
2. Park JB, Lee JH. Use of mineral trioxide aggregate in
the open apex of a maxillary first premolar. J Oral Sci.
2008;50(3):355-358.
3. Raldi DP, Mello I, Habitante SM, Lage-Marques JL, Coil
J. Treatment options for teeth with open apices and
apical periodontitis. J Can Dent Assoc. 2009;75(8):
591-596.
4. Huang GT. Apexification: the beginning of its end. Int
Endod J. 2009;42(10):855-866.
5. Frank AL. Therapy for the divergent pulpless tooth by
continued apical formation. J Am Dent Assoc. 1966;
72(1):87-93.
6. Rafter M. Apexification: a review. Dent Traumatol.
2005;21(1):1-8.
7. Asgary S, Ehsani S. MTA resorption and periradicular
healing in an open-apex incisor: a case report. Saudi
Dent J. 2012;24(1):55-59.
8. Sharma R, Dhingra A, Nayar R. Delayed MTA apical
plug in immature open apex—a case report.
Endodontol. 2008;20:49-52.
9. Roberts SC Jr, Brilliant JD. Tricalcium phosphate as an
adjunct to apical closure in pulpless permanent teeth.
J Endod. 1975;1(8):263-269.
10. Trope M. Treatment of immature teeth with non-vital
pulps and apical periodontitis. Endod Topics. 2007;
14(1):51-59.
11.Ramachandran Nair PN, Pajarola G, Schroeder HE.
Types and incidence of human periapical lesions obtained with extracted teeth. Oral Surg Oral Med Oral
12. Ramachandran Nair PN. Apical periodontitis: a dynamic encounter between root canal infection and
host response. Periodontol 2000. 1997;13:121-148.
13. Abbott PV. Classification, diagnosis and clinical manifestations of apical periodontitis. Endod Topics. 2004;
8(1):36-54.
14. Dominguez Reyes A, Munoz Munoz L, Aznar Martin T.
Study of calcium hydroxide apexification in 26 young
permanent incisors. Dent Traumatol. 2005;21(3):141145.
15. Maroto M, Barbería E, Planells P, Vera V. Treatment
of a non-vital immature incisor with mineral trioxide
aggregate (MTA). Dent Traumatol. 2003;19(3):165169.
16. Torabinejad M, Watson TF, Pitt Ford TR. Sealing ability of a mineral trioxide aggregate when used as a
root end filling material. J Endod. 1993;19(12):591595.
17. Pelliccioni GA, Ciapetti G, Cenni E et al. Evaluation of
osteoblast-like cell response to Proroot MTA (mineral
General Dentistry
www.agd.org
trioxide aggregate) cement. J Mater Sci Mater Med.
2004;15(2):167-173.
18. Al-Daafas A, Al-Nazhan S. Histological evaluation of
contaminated furcal perforation in dogs teeth repaired by MTA with or without internal matrix. Oral
103(3):92-99.
19. Jantarat J, Dashper SG, Messer HH. Effect of matrix
placement on furcation perforation repair. J Endod.
1999;25(3):192-196.
20. Bargholz C. Perforation repair with mineral trioxide
aggregate: A modified matrix concept. Int Endod J.
2005;38(1):59-69.
21. Zou L, Liu J, Yin SH, Tan J, Wang FM, Li W, et al. Effect of placement of calcium sulphate when used for
repair of furcation perforation on seal produced by a
resin-based material. Int Endod J. 2007;40(2):100105.
22. Dogra S, Mukunda KS, Arun A, Rao SM. Apexification.
J Dental Sci Res. 2012;3(1):1-4.
23. Tait CM, Ricketts DN, Higgins AJ. Weakened anterior
roots-intraradicular rehabilitation. Br Dent J. 2005;
198(10):609-617.
24. Perinpanayagam H, Al-Rabeah E. Osteoblasts interact
with MTA surfaces and express Runx2. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2009;107(4):590596.
25. Cintra LT, de Moraes IG, Estrada BP, et al. Evaluation of
the tissue response to MTA and MBPC: microscopic
analysis of implants in alveolar bone of rats. J Endod.
2006;32(6):556-559.
26. Moretton TR, Brown CE Jr, Legan JJ, Kafrawy AH. Tissue reactions after subcutaneous and intraosseous
implantation of mineral trioxide aggregate and ethoxybenzoic acid cement. J Biomed Mater Res. 2000;
52(3):528-533.
27. Tani-Ishii, Hamada N, Watanabe K, Tujimoto Y, Teranaka T, Umemoto T. Expression of bone extracellular matrix proteins on osteoblast cells in the
presence of mineral trioxide. J Endod. 2007;33(7):
836-839.
28. Ham KA, Witherspoon DE, Gutmann JL, Ravindranath S, Gait TC, Opperman LA. Preliminary evaluation of BMP-2 expression and histological
characteristics during apexification with calcium
hydroxide and mineral trioxide aggregate. J Endod.
2005;31(4):275-279.
29. Felippe WT, Felippe MC, Rocha MJ. The effect of mineral trioxide aggregate on the apexification and periapical healing of teeth with incomplete root formation.
Int Endod J. 2006;39(1):2-9.
Manufacturers
DENTSPLY International, York, PA
800.877.0020, www.dentsply.com
DENTSPLY Tulsa Dental Specialties, Tulsa, OK
800.662.1202, www.tulsadentalspecialties.com
GC America, Inc., Alsip, IL
800.323.7063, www.gcamerica.com
J. Morita USA, Inc., Irvine, CA
800.831.3222, www.morita.com/usa
Pulpdent Corporation, Watertown, MA
800.343.4342, www.pulpdent.com
Fixed Removable Hybrid Prosthesis
Stress analysis of mandibular implant-retained
overdenture with independent attachment system:
effect of restoration space and attachment height
Behnaz Ebadian, DDS, MSc n Saeid Talebi, MSc n Niloufar Khodaeian, DDS, MSc n Mahmoud Farzin, PhD
In this in vitro study, 2 implants were embedded in the interforaminal
region of an acrylic model. Two kinds of retention mechanisms were
used to construct complete overdentures: ball type and direct abutment
(Locator). The ball-type retention mechanism models included 3 different collar heights (1, 2, and 3 mm) with 15 mm occlusal plane height,
and 3 different occlusal plane heights (9, 12, and 15 mm) with 1 mm
collar height. The direct abutment models included 3 different occlusal
plane heights (9, 12, and 15 mm) with 1 mm cuff height. Vertical unilateral and bilateral loads of 150 N were applied to the central fossa of
the first molar. The stress of the bone around the implant was analyzed
by finite element analysis.
The results showed that by increasing vertical restorative space, the
maximum stress values around implants were decreased in both unilateral
and bilateral loading models. The results also showed that the increase
T
he restoration of an edentulous
mandible with an overdenture supported or retained by 2 implants is
considered to be the primary prosthetic
treatment approach.1 The retention and
stability of prostheses are provided primarily by implants through attachments.2,3
Various types of attachments have been
suggested for implant-supported overdentures. Independent or dependent connection of implants through ball, O-ring,
Locator, and bar attachments are the most
common approaches.2-5 Some studies have
reported implant support via ball-type
attachments as a reliable treatment.3,6-10
The freedom of rotation within the ball
attachment allows for stress release. The
method of retaining overdentures by 1 or
2 implants using resilient attachments is a
relatively simple and inexpensive method
to reconstruct an edentulous mandible.11
Selection of the optimal attachment is
dependent upon the required retention,
jaw morphology and anatomy, oral function, and patient compliance for recall.12
The ball attachment places less stress on
implants and produces less bending movement in comparison to the bar-clip attachment.3 The Locator, which is self-aligning
and has dual retention, is another type of
independent attachment. It is available in
in maximum stress values around implants correlated with the ball
attachment collar height. The Locator attachment with a 1 mm cuff height
and 9 mm occlusal plane height demonstrated 6.147 and 3.914 MPa in
unilateral and bilateral loading conditions, respectively. While a reduction
in the collar height of a ball-type retention mechanism and an increase in
the vertical restorative space in direct abutment retention mechanisms are
both biomechanically favorable, and may result in reduced stress in periimplant bone, a ball attachment seems to be more favorable in the stress
distribution around an implant than a Locator attachment.
Received: April 11, 2013
Accepted: July 10, 2013
Key words: overdenture, stress, finite element analysis,
independent attachment, occlusal plane
various vertical heights, and its resiliency,
retention, and durability are favorable.12
The effect of a resilient or rigid attachment
system on retention and stress distribution
is a subject of controversy in the literature.12-16 Biomechanically, the advantages
of implant splinting are unclear. The
rationale of implant splinting was that it
would decrease stresses due to increased
prosthesis stability.17,18
Adequate restorative space is another
important factor in successful implantretained overdenture treatment.19 In
edentulous patients, available restorative
space is bounded by the supporting tissues
of the edentulous jaw, cheeks, lips, tongue,
and the occlusal plane. Other factors must
also be considered when defining available
restorative space, such as interocclusal distance, phonetics, and esthetics.20
The minimum vertical restorative space
required for an implant-supported overdenture is 8.5 mm for Locator attachments,
10-12 mm for ball and O-ring attachments,
and 13-14 mm for bar-clip attachments.20
The distance from the crest of the
alveolar bone to the plane of occlusion in
implant-supported prostheses is defined
as the crown height space (CHS). The
biomechanics of CHS is related to lever
arm mechanics.21 Nonaxial loading creates
www.agd.org
a lateral moment which proportionally
increases with increased CHS; this results
in stress concentration at the bone surrounding the implant neck.22 Increasing the
CHS by 1 mm results in a 20% increase in
the cervical load on a fixed-implant prosthesis. Implant splinting has been suggested
to overcome the biomechanical overload in
this situation. However, implant splinting
in fixed-implant supported prostheses has
not been proven to significantly improve
implant success rates.23
Fabricating an implant-supported
overdenture requires an adequate space
for restorative components.19 Evaluation
of space limitation after implant surgery
allows for appropriate attachment selection.
Inappropriate treatment planning before
placing a removable implant-supported
prosthesis can lead to problems such as
overcontoured or fractured prostheses. Two
height levels should be considered in any
removable prosthesis with mobility and
soft tissue support: the first is the height of
the attachment system to the crest of the
bone, and the second is the distance from
the attachment to the occlusal plane.21
In a finite element analysis (FEA) study,
Ebadian et al evaluated different vertical
restorative spaces and different bar heights
of mandibular overdentures, and showed
General Dentistry
61
Fixed Removable Hybrid Prosthesis Stress analysis of mandibular implant-retained overdenture attachments
Overdenture
Metal housing
Metal housing
Plastic cap
Plastic cap
Ball abutment
Locator abutment
Implant
Mandible
Fig. 1. Computerized mesh modeling showing jaw and overdenture with ball attachment.24
Implant
Fig. 2. Computerized mesh modeling showing Locator system.24
Fig. 3. Modeling of 3 different occlusal plane heights.24
that increasing the vertical restorative
space and decreasing the bar height led to
a decrease in the maximum stress value
around the implants when a unilateral
load was applied.24
Since the use of independent attachments in different occlusal plane heights is
not well-defined, the purpose of this study
was to evaluate the effect of different vertical restorative spaces (that is, occlusal plane
distance to gingival level) and different
ball attachment collar heights on the stress
distribution around implants by 3-dimensional (3D) finite element analysis.
In this in vitro study, the experimental
design included the fabrication of a
simulated 2-implant-retained mandibular
overdenture. For this purpose, an acrylic
model of an edentulous mandible was
fabricated with a clear acrylic resin
(Meliodent Multicryl, Heraeus Kulzer).
The configuration of the bone was duplicated from an edentulous mandibular
skeleton. Two screw-type implants, 4
x 10.5 mm with a 4.5-mm-diameter
62
abutment platform (Biohorizons Internal,
BioHorizons IPH, Inc.), were embedded
in the interforaminal region of the acrylic
model using a surveyor (Ney Surveyor,
DENTSPLY International). The implants
were vertically oriented, perpendicular to
the occlusal plane, and parallel to each
other. The crestal bone position of the
implants was on the top of the ridge.
The interimplant distance was 20 mm.
Two types of retention mechanisms were
used in this study: a ball attachment
with plastic matrix and metal housing
(BioHorizons IPH, Inc.), and a direct
abutment attachment with plastic matrix
and metal housing (Locator attachments,
4.5 mm with a 1.0 mm cuff, BioHorizons
IPH, Inc.) (Fig. 1 and 2).24
Based on the laboratory design used by
Ebadian et al, a complete overdenture was
fabricated on these attachment models.24
The plastic model, acrylic denture, implants,
Locator and ball attachments were used for
computerized reproduction. To improve
analysis, the implants were considered as flat
cylinders. The 3D geometry of the entire
system was scanned and digitized using
General Dentistry
www.agd.org
ATOS II (Triple Scan) scanning technology
(GOM mbH) and viewer software (ATOS
version 6.3.0, GOM mbH). Implants were
assumed to be completely osseointegrated,
so that a mechanically perfect interface—to
ensure the continuity of displacement and
traction vectors—was pressured between
implants and bone. Other contacts existing
between the elements were also assumed
to be perfect. The resultant dense point
cloud was transferred to CATIA modeling software (Dassault Systemes Americas
Corp.). The geometry was then meshed by
tetrahedral linear elements.
The mucosa and cortical bone were
reproduced as a 2 mm and 2.5 mm
layer, respectively. Three different collar
heights (1, 2, and 3 mm) with a 15 mm
occlusal plane height, and 3 different
occlusal plane heights (9, 12, and 15 mm)
with a 1 mm collar height were modeled
for the ball attachment system (Fig. 3).
Three different occlusal plane heights (9,
12, and 15 mm) with a 1 mm cuff height
were modeled for the Locator system.
Thus, 9 models were obtained. The value
of friction coefficient was fixed to 0.02.25
Table 1. Mechanical properties of
the prosthesis, implant, and bone
materials used in this study.13,27-30
Table 2. The number of
elements and nodes in the
ball attachment models.
Young
modulus (Pa)
Poisson
ratio
Cortical bone
1.37×1010
0.30
Trabecular bone
1.37×109
0.30
Mucosa
1.0×107
0.40
Acrylic resin
2.7×109
0.35
Titanium
1.17×1011
0.33
Gold
1.0×10
0.30
5×10
0.45
Material
Rubber
11
6
Occlusal
Collar
plane height height
(mm)
(mm)
Number
of
elements
Number
of nodes
9
1
147,640
40,898
12
1
155,058
42,095
15
1
161,329
43,240
15
2
164,140
43,828
15
3
166,287
44,355
Table 3. The number of
elements and nodes in the
Locator attachment models.
Occlusal
Cuff
plane height height
(mm)
(mm)
Number
of
elements
Number
of nodes
9
1
176,967
50,772
12
1
184,234
51,957
15
1
190,533
53,181
Table 4. Stress values generated in the bone in the ball attachment model with different occlusal plane
and collar heights by unilateral and bilateral loading.
Occlusal plane
height (mm)
Distal side force (MPa)
Mesial side force (MPa)
Maximum force (MPa)
Collar height (mm)
Unilateral
Bilateral
Unilateral
Bilateral
Unilateral
Bilateral
9
1
5.249
2.811
4.224
0.870
5.249
3.263
12
1
4.695
2.557
3.685
0.754
4.695
3.365
15
1
4.438
2.455
3.407
0.726
4.438
3.428
15
2
4.920
2.429
3.863
0.722
4.920
3.443
15
3
5.357
2.493
4.262
0.751
5.357
3.439
Table 5. Stress values generated in the bone in the Locator attachment models with different occlusal plane
heights by unilateral and bilateral loading.
Occlusal plane
height (mm)
Distal side force (MPa)
Mesial side force (MPa)
Maximum force (MPa)
Cuff height (mm)
Unilateral
Bilateral
Unilateral
Bilateral
Unilateral
Bilateral
9
1
6.147
3.914
4.143
1.063
6.147
3.914
12
1
5.702
3.450
3.823
1.008
5.702
3.450
15
1
5.378
3.103
3.606
0.855
5.378
3.422
Stress analysis was performed using FEA
software (ABAQUS version 6.11, Abaqus,
Inc.). Linear static analysis was used
in this study. Arbitrary 150 N vertical
unilateral and bilateral loads representing
the masticatory force were applied to the
central occlusal fossa of the first molar of
the prosthesis.26 Mechancial properties
for the prosthesis and all implant parts
and bone are shown in Table 1.13,27-30 The
number of elements and nodes are summarized in Tables 2 and 3.
Results
Maximum stress values on the bone in the
bilateral and unilateral loading models of
ball attachment and Locator systems are
shown in Tables 4 and 5.
www.agd.org
Maximum stresses were found in the
Locator model with 1 mm cuff height
and 9 mm occlusal plane height. The
stresses were 6.147 and 3.914 MPa in
unilateral and bilateral loading conditions, respectively.
In the ball attachment models, maximum stress values of bone were observed
mostly in the distal bone adjacent to the
General Dentistry
63
Fig. 4. Stress distribution pattern in ball attachment model when
load applied. Top. Unilateral. Bottom. Bilateral.24
ipsilateral implant when a unilateral load
was applied, and more distal to the bone
adjacent to the implants when a bilateral
load was applied (Fig. 4).
The maximum stresses in the Locator
attachment system were observed in
the distal side of the ipsilateral implant
when unilateral and bilateral loads were
applied (Fig. 5).24
Discussion
Dependent and independent attachment
systems have been used in implant-supported overdentures. Many researchers have
evaluated either ball or bar-clip attachment
systems in overdentures.8,31-34 The present
study evaluated stress distributions of an
overdenture retained by either a ball attachment or Locator system on 2 implants in
a mandibular jaw model. Various occlusal
plane heights were studied in these models.
The selection and application of different attachment systems for implant overdentures depend on many factors, such
as retention, stress, restorative space, and
maintenance.3,20 Fractures of implants,
attachments and prostheses can occur due
to biomechanical stresses. Misch showed
how stress management in implant prostheses is important in order to reduce
fracture rates.35
64
Fig. 5. Stress distribution pattern in Locator attachment model
when load is applied. Top. Unilateral. Bottom. Bilateral.24
Comparisons of ball attachment vs barclip attachments have been conducted
in other studies with varying results in
terms of retention and maintenance.36,37
Kleis et al reported a higher rate of maintenance for Locator systems in comparison to ball attachments in mandibular
2-implant overdentures.38
Cakarer et al reported no difference
between ball attachment and Locator systems regarding implant failure, replacement
of attachments, and fracture of overdentures.11 However, they found that overall,
the Locator system had more advantages
than the ball or bar-clip systems.11 Celik &
Uludag used a photoelastic model to evaluate the stress transfer of various types of
attachments in a mandibular implant overdenture.39 They reported that the Locator
system showed greater stresses as compared
to ball, bar-clip, and bar-ball attachment
systems.39 Kenney & Richards reported
less stress was transferred to implants by a
ball/O-ring attachment system than a barclip attachment.40 Tokuhisa et al compared
the transferred stresses of O-ring/ball and
bar-clip attachment systems and concluded
that, the ball/O-ring system minimized the
stress transferred to the bone surrounding
implant-supported overdentures in comparison to the bar-clip system.3
General Dentistry
www.agd.org
Maximum stresses of ball and Locator
attachments in unilateral loading models
in this study were 4.438 and 5.378 MPa,
respectively; and in bilateral loading conditions, the maximum stresses were 3.428
and 3.422 MPa, respectively. Ebadian et
al found the maximum stresses of a barclip attachment system model—with 1
mm bar height and 15 mm occlusal plane
height—were 4.753 and 3.482 MPa in
unilateral and bilateral loading conditions,
respectively.24 Comparing the result of
these 2 studies showed that the Locator
attachment transferred more stress than
the bar clip, and the ball attachment
transferred the least stress of all 3 attachment systems when a unilateral load was
applied. In bilateral loading conditions, all
3 attachments transferred almost the same
stress to the peri-implant bone.24 These
findings are in agreement with previous
studies that used unilateral loading.3,39,40
In the current study, the maximum
stress was found in bone adjacent to the
implant in unilateral loading models;
however, in bilateral loading conditions,
the maximum stress of the ball attachment was observed more distal from the
bone adjacent to the implant than the
Locator attachment. This may be due
to the more rigid behavior of a Locator
system, which restricts the movement of
the overdenture and thus increases the
stress in the bone around the implant
while decreasing the stress in the posterior
residual ridge. The maximum stress locations in these models were similar to the
study by Ebadian et al which evaluated
bar-clip attachments of mandibular overdentures.24 It is evident in Figures 4 and 5
that the stress distribution in the ball
attachment model was more uniform
than that of the Locator model, which
was concentrated around the implants.
The stress obtained from applying a
mastication load both unilaterally and
bilaterally is distributed into 2 segments:
the posterior ridge and the bone around
the implants, both of which are influenced by the retention mechanism of the
attachment system. Therefore, whenever
the attachment system is more resilient,
the stress in the bone around the implant
is subsequently lessened and a part of
the stress is transferred to the posterior
ridge; this results in better stress distribution and thus reduces the maximum
stress level. The ball attachment is more
resilient than the Locator system, thus it
causes more uniform and less maximum
stress. Resiliency in these 2 attachment
systems is closely related to the plastic
caps that are used. Therefore, because the
plastic volume in the cap of a ball attachment is greater than the plastic volume
in a Locator attachment, and because
the ball attachment has a single retention
mechanism while the Locator has dual
retention, the ball attachment is more
resilient and transfers less stress than the
Locator system.
Takeshita et al reported that the retentive forces of an attachment system affect
stresses generated in the peri-implant
bone during loading.41 This finding could
explain why more stresses are generated
in the bone by the Locator attachment in
comparison with the ball attachment. The
Locator system used in this study has a
dual retention mechanism, therefore it is
more retentive than the ball attachment.
Chen et al observed that the least retentive
attachments offer greater rotation than the
more retentive ones.10 The authors compared Locator, ERA, and O-ring systems
and reported that the O-ring system was
the least retentive system.10 Their findings
are in agreement with the present study.
A meta-analyses study on mandibular
overdentures by Cehreli et al reported no
differences in marginal bone loss around
implants in various attachment designs.42
The level of stress correlated to bone
resorption has not been clearly defined
in the literature.43 Since an FEA can only
produce theoretical conclusions, the aim
of this study was not to report absolute
values of stresses but to compare stress
values between different models.28,44 It is
very important to choose the appropriate
attachment system according to patient
characterization in terms of bone quality
and quantity, stress conditions, desired
retention and stability, available restorative
space, and patient maintenance.
By increasing the occlusal plane height
in this study from 9 to 15 mm, the
maximum stress in the bone around the
implant was decreased in the unilateral
and bilateral loading models of the ball
attachment and Locator systems, but the
maximum stress in the posterior residual
ridge was slightly increased in the bilateral loading models of ball attachments,
which tolerated the maximum stress in
these models. The study by Ebadian et
al on bar-clip attachments showed the
same results when a unilateral load was
applied—the stress with a bilateral load
slightly decreased when the occlusal plane
height was increased.24
By increasing the collar height of the
ball abutment from 1 to 3 mm, the maximum stress was increased. This was also
in agreement with the study by Ebadian
et al.24 Therefore, it can be concluded that
by increasing the first lever arm (distance
from crest of bone to attachment level),
stresses in the bone around the implants
increase. By increasing the second lever
arm (distance of occlusal plane of denture
to attachment), the stress values were
decreased in both the Locator and ballattachment systems.
According to Cehreli et al, when severe
vertical bone loss is present, vertically cantilevered occlusal loading will increase.42
However, the results of the present study
are not in agreement with that claim. This
study found that increasing the occlusal
plane height decreased the stress generated
in bone, especially with the Locator attachment system. Increasing the collar height
of abutment, or decreasing the second
lever arm could result in increased stress.
www.agd.org
So it could be concluded that in abundant
vertical space, even low height attachments
are biomechanically advantageous.
It has been recommended that a
minimum of approximately 12 mm
vertical restorative space is necessary to
consider a mandibular implant-supported
overdenture.45,46 The minimum space
required for an implant-retained overdenture with a Locator system is 8.5 mm
(vertical) x 9 mm (horizontal).47 Based
on the authors’ findings and from a biomechanical and stress-generated aspect,
in a restricted vertical space, ball attachments with minimum collar heights are
preferred to Locator attachments.
The roles of crown/implant ratio and
CHS in fixed-implant prostheses are controversial in the literature.48-50 The role of
CHS and its biomechanical effect is related
to lever mechanics.51 A CHS ≥15 mm can
be biomechanically unfavorable, resulting
in increased stress at the bone around the
implant.52 It appears that the CHS role in
fixed-implant prostheses is not completely
applicable in implant overdentures. Our
findings indicate that by increasing the
CHS (via occlusal plane height), the stress
generated in the bone was decreased. This
may be related to the different support,
movement, and leverage mechanisms of
the 2 tested prostheses.
There are some unavoidable limitations in an FEA study, mainly in biologic
simulations, which compelled the authors
to assume some simplifications. Bone is a
complex living structure without a defined
pattern; its characteristics vary among
individuals, and its actual mechanical
properties are not precisely established.
Furthermore, the use of FEA in a study
of an extremely accurate anatomy of a
bone structure may limit the results to
that particular structure. As such, certain
simplifications were adopted in this study
to generalize the results and facilitate the
study without compromising the validity of the findings. The implants were
modeled without threads, as the aim of
the study was to analyze the stresses on
implants and not the mechanical interactions within the bone.28 It has been said
that this assumption results in an underestimation of stress patterns in bone, as
reported in previous studies.53,54 In addition, the connecting screws at the implantabutment interface were not modeled,
General Dentistry
65
although some studies have shown that
modeling the screw is not necessary.28 It
was assumed that the models were homogenous and isotropic. Because this study
was comparative in nature, such assumptions would not interfere in the results,
since they were present in all models.55
Conclusion
Within the limitation of this study, it can
be concluded that by decreasing the first
lever arm (distance from crestal bone to
abutment) in unsplinted resilient attachments in a mandibular implant overdenture, the stresses generated in bone
are decreased. Also, by increasing the
second lever arm (distance from occlusal
plane to abutment), the stresses in bone
were decreased. Finally, this study found
that Locator attachments could generate
more stresses than ball attachments in
the same CHS.
Author information
Dr. Ebadian is an associate professor,
Dental Implant Research Center and
Department of Prosthodontics, School of
Dentistry, Isfahan University of Medical
Sciences, Iran, where Dr. Khodaeian
is an assistant professor. Dr. Farzin is a
professor, Department of Mechanical
Engineering, Isfahan University of
Technology, Iran. Mr. Talebi is a doctoral
student, Department of Mechanical
Engineering, Amirkabir University of
Technology, Tehran, Iran.
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Manufacturers
Abaqus, Inc., Pawtucket, RI
415.496.9436, www.abaqus.net
BioHorizons IPH, Inc., Birmingham, AL
888.246.8338, www.biohorizons.com
Dassault Systemes Americas Corp., Waltham, MA
781.810.3000, www.3ds.com
DENTSPLY International, York, PA
800.877.0020, www.dentsply.com
GOM mbH, Braunschweig, Germany
49.531.390290, www.gom.com
Heraeus Kulzer, South Bend, IN
800.435.1785, www.heraeus-dental-us.com
www.agd.org
There is an article on
PROSTHODONTICS/REMOVABLE
in the online edition.
•Management of severe
mandibular deviation following
partial
mandibular
resection:
a case
report
AGDPODCAST
Controversies in
Implant Dentistry
General Dentistry
67
Exercise No. 363 Fixed
Removable Hybrid Prosthesis Subject Code 674
The 15 questions for this exercise are based on the article, Stress
analysis of mandibular implant-retained overdenture with
independent attachment system: effect of restoration space and
attachment height, on pages 61-67. This exercise was developed by
Robert A. Busto, DMD, MBA, FAGD, in association with the General
Dentistry Self-Instruction committee.
1. All of the following are factors for
selecting the optimal mandibular
overdenture attachment except one.
A. required retention
B. patient finances
C. patient compliance
D. jaw morphology
2. The ball attachment places_______
stress on implants and produces ______
bending movement than the bar-clip
attachment.
A. less; less
B. more; less
C. less; more
D. more; more
3. What is the minimum vertical
restorative space (mm) required for
using Locator attachments on an
implant-supported overdenture?
A. 12.5
B. 10.5
C. 8.5
D. 6.5
4. The crown height space is the distance
from the ______ to the ______ in
implant-supported prostheses.
A. mandibular crest of alveolar bone;
maxillary crest of alveolar bone
B. most superior point of the implant
attachment; plane of occlusion
C. crest of the alveolar bone; most superior
point of the implant attachment
D. crest of the alveolar bone; plane of
occlusion
5. Increasing the crown height space by
1 mm results in a _____% increase in
the cervical load on a fixed implant
prosthesis.
A. 10
B. 15
C.20
D. 25
Reading the article and successfully completing the exercise will
enable you to understand the:
•theoretical force distribution on implants and surrounding bone;
•differences between ball and Locator attachments; and
•unfavorable biomechanical scenarios for implant overdenture
treatment.
6. If the vertical restorative space is 12 mm,
which implant-supported overdenture
attachment(s) is/are acceptable?
A. Locators only
B. Locators and balls
C. Locators and bar clips
D. Locators, balls, and bar clips
7. How were the implants in this study
placed in relation to the occlusal plane?
A. Angled 30 degrees
B. Angled 45 degrees
C. Angled 75 degrees
D. Angled 90 degrees
8. The implants in this study were placed
with an interimplant distance of ___ mm.
A. 14
B. 16
C. 18
D. 20
9. Which combination of implant collar
height and occlusal plane height (mm)
resulted in maximum stress?
A. 1; 9
B. 1; 15
C. 2; 9
D. 2; 15
10. Cakarer et al reported that the Locator
attachments receive greater stress
than ball attachments. Celik & Uludag
reported that Locator attachments
have a higher implant failure rate.
the second is true.
11. The Locator implant is ______ retentive
and ______ resilient than the ball
attachment.
A. equally; less
B. more; equally
C. more; less
D. less; more
12. The level of stress correlated to
bone resorption has not been clearly
defined in the literature. Finite
element analysis studies can produce
clinical conclusions to determine how
much stress an implant can take before
bone resorption.
the second is true.
13. In a restricted vertical space, this study
recommends using a _____ attachment
system with minimum collars to address
stress concerns.
A. Locator
B. ball
C. Dalbo
D. bar clip
14. Increasing the crown height space
in removable implant overdentures
decreases the stress generated in the
bone. Increasing the crown height
space in fixed implant prostheses
increases the stress in the bone.
the second is true.
15. In unsplinted implants, decreasing the
distance from the crest of the bone
to the __________ will decrease the
stresses generated in the bone.
A. abutment
B. plane of occlusion
C. apex of the implant
D. facial midline
68
General Dentistry
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Oral Medicine, Oral Diagnosis, Oral Pathology
p53 expression in oral lichenoid lesions
and oral lichen planus
A. Arreaza, MSc n H. Rivera, MSc n M. Correnti, PhD
The aim of this article was to compare the expression of p53 protein in oral lichen planus (OLP) and oral lichenoid reaction (OLR).
The study population consisted of 65 patients—31 diagnosed with
OLP and 34 with OLR.
The results showed more p53 positive cases in the OLP group than in
the OLR group. However, the difference between the 2 groups was not
statistically significant (P = 0.114). The most common immunolocalization
O
ral lichen planus (OLP) is a
chronic inflammatory condition that involves the skin and
oral mucosa.1,2 It mainly affects women
between 30 and 50 years of age, and it is
not common in children.1 The prevalence
of this condition represents 1%-4% of
the global population with no apparent
ethnic predisposition.1
OLP has a variety of clinical manifestations: papuloreticular, linear, plaque, erosive
or ulcerative, and macular or pigmented.
Reticular or plaque forms frequently occur
with single, asymptomatic lesions being the
only manifestation of the disease. However,
erythematous or ulcerative clinical presentations may also occur.1-4
OLP is caused by an immune T cell
response to an unidentified antigen in the
skin or oral mucosa of patients who have
a genetic predisposition to the disease.
The initial response is an increased production of cytokines produced by TH1
lymphocytes with gene polymorphism
in molecules such as IFN-γ and TNF-α
in oral and skin lesions. Another indicator of OLP pathogenesis is the presence
of dendritic cells (stromal plasmacytoids
and Langerhans), triggered by chemotactic agonists expressed in the vascular
endothelium.1-3
The INF-γ/TNF-α cytokine production
induces cytotoxicity against keratinocytes,
by activating natural killer cells and cytotoxic T lymphocytes, eventually resulting
in apoptosis via the Fas ligand pathway.
This is caused by adhesion molecules—
such as VCAM and ICAM-1—which
enable the activated T cells to migrate
to the oral epithelia or skin. The T cell
was observed at the basal cell layer. Due to the chance of potential future
malignancy, follow-up for all cases is recommended.
Revised: September 7, 2013
Accepted: October 2, 2013
Key words: p53, oral lichen planus, lichenoid lesions
migration to these sites leads to the expression of other molecules at the basal cell
layer, resulting in lymphocyte linkage to
the epithelium. This linkage triggers an
intense production of IFN-γ and TNF-α,
leading to matrix metalloproteinases and
p53 overexpression, ending in apoptosis.1-3
but the putative mechanism remains
unknown1,2,4,7-10 Some studies have shown
that OLR lesions may have an increased
risk of malignant transformation.1,4,6 The
annual rate of OLP malignant transformation has been estimated to be 0.2%1% worldwide.1,4
Oral lichenoid reaction
p53 expression
Oral lichenoid reaction (OLR) presents
as lesions that are clinically and histologically identical to OLP, but with an
identifiable etiologic factor.1,5,6 They may
be classified as oral lichenoid lesions as a
result of contact with dental materials—
particularly amalgam—due to both an
adverse reaction to medications or graftversus-host disease (GVHD).1-3
Clinically, OLR may be observed as
erosive lesions that occur unilaterally.
Histologically, OLR presents similarly to
OLP, with a larger proportion of diffuse
lymphocytic infiltrate, plasma cells, and
citoid bodies.1-3,5,6
Both OLP and OLR may exhibit a
band-like lymphocytic infiltrate that is
not patognomonic, which is similar to
other autoimmune diseases such as lupus
erythematous.1,5,6 The 2 conditions differ
mainly in their outcome and the treatment
modality: OLP lesions become chronic,
while OLR lesions tend to disappear as
soon as the etiologic cause is eliminated.1,5,6
The malignant potential of OLP
remains controversial. Some retrospective studies and case reports have
documented OLP transforming into oral
squamous cell carcinoma (SCC), and
there are other studies on OLR malignant transformation related to GVHD,
www.agd.org
p53 is an oncoprotein involved in the
suppression of the proliferation of DNAdamaged cells via cell cycle regulation
that results in the apoptosis of these
cells.11 Impaired function of the p53 gene
has been implicated in the development
and progression of oral epithelial dysplasia
and oral SCC.11,12 Therefore, detection of
p53 changes may help in the identification of high risk lesions or potentially
malignant OLP cases.12
Due to its established role as a genomic
“guardian,” the wild p53 protein has been
connected to a low potential for malignant transformation in OLP cells.13 In
addition, it has been recently shown that
the human TP53 gene encodes at least
9 different isoforms; while the function
of these novel isoforms is still not clearly
understood, they have been amplified
(via a quantitative real-time polymerase
reaction) in samples of SCC in the head
and neck.14 This could indicate a tumorrelated role for these isoforms. Evaluating
the oncogenic potential by using different
markers could help researchers to analyze
the ethiopathogenesis and potentially
serve as a carcinogenic prognosticator for
these conditions. This study sought to
compare the expression of p53 protein in
OLP and OLR.
General Dentistry
69
Oral Medicine, Oral Diagnosis, Oral Pathology p53 expression in oral lichenoid lesions and oral lichen planus
Table 1. Anatomical locations of oral lichen planus (OLP)
and oral lichenoid reaction (OLR) in this study.
Table 2. Incidence of histological features found in the
OLP and OLR groups.
Anatomical location
Histological feature
OLP (n = 31)
OLP (n = 31)
OLR (n = 34)
Buccal mucosa (bilateral occurrence)
14
0
Inflammatory band-like infiltrate
31
34
Buccal mucosa (unilateral occurrence)
1
9
Acanthosis
19
21
Internal lip
3
6
Basal cell degeneration
17
14
Maxillary alveolar ridge mucosa
1
5
Parakeratosis
3
15
Hard palate
3
3
Cytoid bodies
10
6
Dorsum of tongue
3
1
Orthokeratosis
9
5
Attached gingiva
2
2
Ulceration
4
7
Buccal vestibule mucosa
1
5
Epithelial atrophy
3
3
Others (retromolar area, soft palate,
floor of the mouth, ventral tongue,
mandibular ridge mucosa)
3
3
Others (amalgam remnants, basal
cell shedding, sialadenitis, vasculitis,
glandular fibrosis, ductal ectasia)
4
7
The study population consisted of 65
biopsy cases—31 diagnosed with OLP
and 34 with OLR at the Oral Pathology
Laboratory, Faculty of Dentistry, Central
University of Venezuela. These cases were
analyzed and histologically classified
according to Van der Meij et al.10
Paraffin embedded sections (3 μm)
were deparaffinized and subjected to
an antigen retrieval solution (pH = 6)
(Dako North America, Inc.) for 1 hour.
Endogenous peroxidase was blocked by
immersing the sections in methanol and
3% hydrogen peroxide for 30 minutes.
Next, a primary antibody p53 clone
in a 1:50 dilution (DO7, Dako North
America, Inc.) was applied to the sections for 30 minutes. A detection system
(EnVision, Dako North America, Inc.)
was utilized using diaminobenzidine for
10 minutes. Positive and negative controls
were performed.
The slides were observed under light
microscopy. Expression of the proteins
was studied by cell count in 4 high
magnification fields (40X). The immunoreactivity in each section was graded
according to the number of positively
stained nuclei in a field and grouped in
order from the least (-) to most (+++)
positive reaction: <1% nuclei (-), up to
30% nuclei (+), 30%-70% nuclei (++),
and >70% (+++). Separate counts were
made in the basal layer, suprabasal layers,
and inflammatory infiltrate. Counts
70
OLR (n = 34)
were made of the total cells and of the
marked cells in each field, and the mean
percentages of expression were calculated
for each case. Brown-stained cells were
considered positive, regardless of the
intensity of staining. Immunoreaction
intensity was recorded as mild, moderate,
or strong.
The Ethics Committee of the Faculty of
Dentistry, Central University of Venezuela,
approved the study. All patients signed a
written informed consent form.
The p53 immunoreactivity was correlated
in the OLP and OLR groups, while variables—including gender, age group, and
anatomical site—were analyzed separately.
A Fisher exact test was performed to assess
the correlation between variables. The
level of significance was determined to
be P < 0.05. The statistical analysis was
performed using SPSS statistical software
(version 16.0; SPSS, Inc.).
Results
The distribution of OLP and OLR
according to age was 59.5 (±11.7) years
and 57.0 (±15.1) years in the OLP and
OLR groups, respectively. Gender distribution in the OLP group was 84.6%
female and 19.3% male; the distribution
in the OLR group was 79.4% female and
20.6% male. The buccal mucosa was the
most common anatomical site in both
groups. With 1 exception, the buccal
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Table 3. Histological location
of p53 expression in the OLP
and OLR groups.
OLP
(n = 31)
OLR
(n = 34)
13
11
Basal cell/infiltrate
9
2
Inflammatory infiltrate
0
3
Basal/suprabasal
1
2
Suprabasal/basal/
infiltrate
1
0
Submucosa
0
1
Histological location
Basal cell layer
mucosa occurrence was bilateral in the
OLP group and unilateral in the OLR
group (Table 1).
According to histological analysis, all
cases of OLP and OLR showed similar
findings of an inflammatory band-like
infiltrate and acanthosis. Basal cell liquefaction was evidenced in both groups. Citoid
bodies were present in 32.2% of the OLP
cases, while parakeratosis was present in
44.1% of the OLR cases (Table 2).
In terms of immunohistochemical analysis, p53 expression was observed in 77.4%
of the OLP cases and 55.9% of the OLR
cases. However, the difference between the
2 groups was not statistically significant
(P = 0.114).
Fig. 1. A sample of oral lichen planus (OLP) with p53 expression at
the basal cell layer and an inflammatory infiltrate (immunostain,
magnification 20X).
Fig. 2. A sample of oral lichenoid reaction (OLR) with p53
expression at the basal cell layer and inflammatory infiltrate
(immunostain, magnification 20X).
Fig. 3. A sample of OLP with nuclear immunolocalization of p53 at
the basal cell layer (immunostain, magnification 40X).
Fig. 4. A sample of OLR with nuclear immunolocalization of p53
at the basal cell layer and inflammatory infiltrate (immunostain,
magnification 40X).
For both groups, nuclear p53 immunolocalization was most common at the basal
cell layer. Basal cell/infiltrate locations were
seen in 29.0% and 5.9% in the OLP and
OLR groups, respectively (Table 3). It is
noteworthy that p53 positivity was found
both alone and in combination with other
histological localizations (Fig. 1 and 2).
Immunostaining at 40X magnification
revealed that p53 was similarly expressed
in both groups. The results showed that
38.7% and 26.5% were graded (+) in
the OLP and OLR groups, respectively;
25.8% and 20.6% were graded (++) in
the OLP and OLR groups, respectively;
12.9% and 8.8% were graded (+++) in
the OLP and OLR cases, respectively.
These positively stained nuclei were
located mainly in the basal cell layer
(Fig. 3 and 4).
The intensity of the stain was mild to
moderate in the majority of cases: mild
staining was found in 25.8% and 20.6%
of the OLP and OLR groups, respectively;
moderate staining was found in 29.0%
and 20.5% of the OLP and OLR groups,
respectively. There was strong intensity
staining in 22.6% and 14.7% of the OLP
and OLR cases, respectively.
Discussion
Regarding the age group and gender distribution in the present study, women were
more affected in the fifth decade. These
www.agd.org
data were consistent with the OLP and
OLR epidemiology previously documented
in the literature.1 In terms of anatomical
location, the buccal mucosa was the most
common site in both groups, in agreement
with the literature.1-4 Bilateral occurrence
was a common feature among the OLP
cases in this study, as it is in the literature.1
White striations were observed in
both groups. The appearance of these
asymptomatic striations are considered
to be a good clinical prognostic for
malignant transformation.1-5 Lesions
symptomatic of erosion/ulcers were more
regularly observed in the OLR goup in
comparison to the OLP group; the OLP
cases presented nonpainful white plaque
General Dentistry
71
Oral Medicine, Oral Diagnosis, Oral Pathology p53 expression in oral lichenoid lesions and oral lichen planus
as a primary clinical sign. Based on similar
studies, the presence of the erosive lesions
in the OLR group indicate a potential for
malignant transformation.1,4 p53 positivity
was observed in the majority of the lesions
in both groups. While the OLP group
had a higher percentage of p53 positivity,
the difference between the 2 groups was
deemed not to be statistically significant.
The data in this study suggests an antiapoptotic potential at the basal cell layer.
Under normal conditions, the epithelia
does not show apoptotic basal cells, but in
OLP and OLR, the lymphocytic stimulation should lead to an apoptotic state in
these cells that produces an apoptotic
response as evidenced by the presence of
Civatte bodies (cytoid bodies) and the
hydropic degeneration of the epithelial
cells layer. The maintenance of a chronic
inflammatory response at this level can
result in cellular genome mutations that
lead to an alteration of this apoptotic
response. One of these mutations may
be evidenced by the expression of altered
p53 in the basal layer of the epithelium in
both diseases. This mutation can alter the
balance between the rate of epithelial cell
replication and apoptosis, resulting in the
emergence of malignancies.11
Despite the small sample size in this
study, the results—in consideration of the
widely accepted belief that the presence of
white striations is a good prognostic for
malignant transformation—indicate the
need for clinicians to follow-up on any incidence of white striations in OLP patients,
and consider a new biopsy when any clinical changes appear or when erosive symptomatic cases do not respond to therapy.1-5
Parakeratosis was a common histologic
characteristic in the OLR group (44%)
compared to the OLP group (9.6%), suggesting that an inflammatory response
generates the production of a wide
layer of parakeratin within the corneal
stratum, leading to apoptosis while maintaining the nuclei.
Several studies have mentioned the
potential of OLP to transform into
SCC.4,8,9,12 The etiology of this process
remains unknown, however protein
alterations related to apoptosis seem to be
involved.14 Other etiologic factors including viral infections and loss of heterozigocity have also been mentioned.15-17
72
The role of p53 as a prognostic marker
for SCC, as well as other malignant
disorders, has been widely documented.17
Sadafi et al reported a higher incidence
of p53 and p21 in OLP patients, suggesting a need for follow-up inspection on
these cases.18 Although previous studies
have indicated that OLR is more likely
to become malignant than OLP, the
follow-up of OLP patients should not be
dismissed readily, since these cases may
also present an oncogenic potential.18,19
The anti-p53 antibody, pAb240, recognizes an evolutive preserved epitope that is
present on the p53 protein. This antibody
uses inmmunoblots with denaturated
extracts from human and animal models.
Gonzalez-Moles et al found fewer positive
OLP cases with pAb240 compared to the
p53 DO7 clone.13 Future studies may be
necessary to verify these results.
Conclusion
In this study, the OLP group showed more
positive p53 cases compared to the OLR
group. Dentists should follow-up all OLP
and OLR cases, due to the possibility of
malignant transformation.
Author information
Dr. Arreaza is an aggregate professor,
Pharmacology Department, Faculty of
Dentistry, Central University of Venezuela,
Caracas, where Drs. Rivera and Correnti
are professors.
Disclaimer
References
1. Carrozzo M, Thorpe R. Oral lichen planus: a review.
Minerva Stomatol. 2009;58(10):519-537.
2. Farhi D, Dupin N. Pathophysiology, etiologic factors,
and clinical management of oral lichen planus, part I:
facts and controversies. Clin Dermatol. 2010;28(1):
100-108.
3. Scully C, Carrozzo M. Oral mucosal disease: lichen planus. Br J Oral Maxillofac Surg. 2008;46(1);15-21.
4. Bombeccari GP, Guzzi G, Tettamanti M, et al. Oral lichen planus and malignant transformation: a longitudinal cohort study. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2011;112(3):328-334.
5. Rad M, Hashemipoor MA, Mojtahedi A, et al. Correlation between clinical and histopathologic diagnoses of
oral lichen planus based on modified WHO diagnostic
criteria. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod. 2009;107(6):796-800.
General Dentistry
www.agd.org
6. Cortes-Ramirez DA, Rodríguez-Tojo MJ, Gainza-Cirauqui ML, Martinez-Conde R, Aguirre-Urizar JM. Overexpression of cyclooxygenase-2 as a biomarker in
different subtypes of the oral lichenoid disease. Oral
110(6):738-743.
7. Accurso BT, Warner BM, Knobloch TJ, et al. Allelic imbalance in oral lichen planus and assessment of its
classification as a premalignant condition. Oral Surg
359-366.
8. Kumagai K, Horikawa T, Gotoh A, et al. Up-regulation
of EGF receptor and its ligands, AREG, EREG, and HBEGF in oral lichen planus. Oral Surg Oral Med Oral
9. Ramos-e-Silva M, Jacques CD, Carneiro SD. Premalignant nature of oral and vulval lichen planus: facts and
controversies. Clin Dermatol. 2010;28(5):563-567.
10. Van der Meij E, Schepman K, Van der Waal I. The possible premalignant character of oral lichen planus and
oral lichenoid lesions: a prospective study. Oral Surg
164-171.
11.Agha-Hosseini F, Mirzaii-Dizgah I. p53 as a neoplastic biomarker in patients with erosive and plaque like
forms of oral lichen planus. J Contemp Dent Pract.
2013;14(1):1-3.
12. Ebrahimi M, Nylander K, Van der Waal I. Oral lichen
planus and the p53 family: what do we know? J Oral
Pathol Med. 2011;40(4):281-285.
13. Gonzales-Moles MA, Gil-Montoya JA, Ruiz-Avila I, Esteban F, Bascones-Martinez A. Differences in the expression of p53 protein in oral lichen planus based on
the use of monoclonal antibodies DO7 and pAb 240.
Oral Oncol. 2008;44(5):496-503.
14. Ebrahimi M, Boldrup L, Coates PJ, Wahlin YB, Bourdon JC, Nylander K. Expression of novel p53 isoforms
in oral lichen planus. Oral Oncol. 2008;44(2):156161.
15. Gorsky M, Epstein JB. Oral lichen planus: malignant
transformation and human papilloma virus: a review
of potential clinical implications. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod. 2011;111(4):461-464.
16. Arreaza A, Correnti M, Avila M. Deteccion del virus
Epstein-Barr en lesiones de liquen plano bucal. Acta
Odontol Vzla. 2010;48(3):1-9.
17.Georgakopoulou EA, Troupis TG, Troupis G, Gorgoulis VG. Update of the cancer-associated molecular
mechanisms in oral lichen planus, a disease with possible premalignant nature. J BUON. 2011;16(4):613616.
18. Sadafi RA, Al Jaber SZ, Hammad HM, Hamasha AA.
Oral lichen planus shows higher expressions of tumor
suppressor gene products of p53 and p21 compared
to oral mucositis. An immunohistochemical study. Arch
Oral Biol. 2010;55(6):454-461.
19. Cortes D, Agurne-Urribarri M, Gainza ML, Echevarria
MA, Aguirre JM. Enfermedad liquenoide oral: condicion premaligna emergente y controvertida. Gac Med
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Manufacturers
Dako North America, Inc., Carpinteria, CA
805.566.6655, www.dako.com
SPSS, Inc., Quarry Bay, Hong Kong
852.2811.9662, www.spss.com
Dental Materials
Effect of imaging powders on the bond strength
of resin cement
Christopher R. Jordan, DMD, MS n Clifton W. Bailey, DDS n Deborah L. Ashcraft-Olmscheid, DMD, MS n Kraig S. Vandewalle, DDS, MS
The application and incomplete removal of a computer-aided design/
computer-aided manufacture imaging powder may affect the dentin
surface prior to bonding a ceramic restoration. The purpose of this study
was to compare the effect of imaging powder residue on the shear bond
strength of a self-adhesive resin cement to dentin. Mounted human third
molars were sectioned coronally with a diamond saw to expose the dentin, which was then prepared with a diamond bur mounted in a custom
jig. The dentin surface was sprayed with 3 different imaging powders.
The 3 powder groups were then divided into 3 subgroups based on the
method of powder removal: no rinse, 1-second rinse, and 10-second rinse.
A control group was created that had no application of imaging powder.
T
he notion of computer-aided design/
computer-aided manufacture (CAD/
CAM) dentistry was first introduced
in the late 1970s by Duret.1 In 1987,
Sirona Dental Systems, Inc. released the
first version of a chairside economical
restoration of esthetic ceramics (CEREC)
technology.2 Since then, this all-ceramic
restoration treatment has been simplified
and improved, and numerous systems
have been developed and marketed.2
The most advantageous aspect of this
technology is the capability to create and
mill a restoration in the dental office,
thus reducing costs and streamlining
treatment. As of 2009, there were approximately 25,000 CEREC users worldwide.2,3 CAD/CAM is also being used to
restore endodontically treated teeth with
endocrowns and in conjunction with cone
beam volumetric tomography to plan and
restore dental implants.4,5
Very little research, however, has been
done to support specific methods and
standard processes for the restorative dentist. Additionally, manufacturers produce
a variety of materials that can be used at
different steps. The practitioner is tasked
with selecting the imaging powder and
cement that have the best performance
properties. The majority of the research
to date has been focused on the properties of the restoration itself, as well as the
marginal adaptation, retention, or durability of a particular cement.6-26 A review
of these clinical studies found that the
A self-adhesive resin cement was bonded to the surfaces and loaded to
failure in a universal testing machine after 24 hours of storage. Data was
analyzed with Kruskal-Wallis and Mann-Whitney nonparametric tests.
The bonding to dentin surfaces of the powder groups that were rinsed for
1 or 10 seconds were not significantly different from each other or the
nonpowdered control. The type of imaging powder did not significantly
affect the bond strength. The nonrinsed powdered dentin surface had a
significant reduction in bond strength compared to both the control and
the rinsed powdered surfaces.
longevity of posterior dental restorations
was dependent upon many factors related
to the chosen materials, the patient, and
the dentist. According to a 2001 study,
annual failure rates in posterior stressbearing restorations were: 0% to 7.0%
for amalgam restorations, 0% to 9.0%
for direct composites, 1.4% to 14.4% for
glass ionomers and derivatives, 0% to
11.8% for composite inlays, 0% to 7.5%
for ceramic restorations, 0% to 4.4% for
CAD/CAM ceramic restorations, and 0%
to 5.9% for cast gold inlays and onlays.20
The principle reasons for failure were secondary caries, fracture, marginal deficiencies, wear, and postoperative sensitivity.20
The type of luting agent is considered to
be one of the key factors in determining a
restoration’s longevity.26,27
A critical step in any indirect restoration is the capture of the preparation in
an impression. When using a CAD/CAM
system to mill a restoration, the impression is made by using a camera to digitally
scan the tooth (or a cast), then using a
computer program to virtually design the
restoration. The CEREC 3D AC (Sirona
Dental Systems, Inc.) system uses a camera
that projects blue wavelength light over
the area to capture all of the dimensions of
the preparation and surrounding teeth and
tissues. The blue wavelength light reportedly provides a higher resolution image
than the infrared camera used in earlier
systems, such as the CEREC 3D AU
(Sirona Dental Systems, Inc.).28
www.agd.org
In order for the CEREC camera to
capture an accurate image, the surface or
object to be scanned must be as uniform
as possible in its reflectivity. To accomplish this, a titanium dioxide powder is
typically used to coat the area. The E4D
(Planmeca E4D Technologies) is a chairside imaging and milling system that creates a digital impression from an intraoral
scan without the use of reflective powder.
The new CEREC Omnicam (Sirona
Dental Systems, Inc.) also functions
without application of imaging powder.
Other systems, such as iTero (Align
Technology, Inc.) and Lava C.O.S. (3M
ESPE), are used exclusively for digital
impressions. Whereas the iTero system
does not require powder, the Lava C.O.S.
requires a light dusting.
The improper use of imaging powder is
a possible source of error when fabricating a CEREC 3D restoration.29 The coating can be sprayed on with a delivery unit
such as PowderPro (Advanced Dental
Instruments LLC), painted on using
a liquid such as Scan Film (Dentaco
As), or sprayed on with a self-contained
propellant and powder system such
as Optispray (Sirona Dental Systems,
Inc.).30 Cameras record an over-powdered
surface as uneven, whereas one with too
little powder does not adequately reflect
light. The CEREC 3D camera must be
positioned appropriately as well. If the
camera is not properly oriented in the
path of insertion to allow capturing all
General Dentistry
73
Dental Materials Effect of imaging powders on the bond strength of resin cement
margins, without undercuts, the scan
will not capture the necessary data to
accurately allow the restoration to be
properly designed.
As an alternative to intraoral scanning,
the practitioner can make a conventional
impression and scan the impression,
thereby designing the prosthesis from an
image captured indirectly. A cast may be
fabricated using a scannable stone material—that is made specifically for indirect
optical imaging—such as Diamond Die
(Hi-Tec Dental Products)—which allows
the clinician to eliminate the intraoral
use of a powder spray and scanning.
However, the impression and cast fabrication requires an additional step, which
adds time to the procedure but may result
in a more precise scan. A study by da
Costa et al compared the marginal gap
created with a direct intraoral scan with
that of an indirect scan of a model and
found no significant difference.31 Another
study, however, found that extraoral
optical scanning methods provided the
highest precision.32
When using powder, Sirona Dental
Systems, Inc. recommends their product,
CEREC Optispray, but there are powders
on the market that contain a reflective
compound other than titanium dioxide.
Possible alternatives include an economical magnesium stearate spray (Occlude,
Pascal International, Inc.) marketed
specifically as an aid for seating castings.33
However, no research has been published
evaluating the use of Occlude as an alternative intraoral imaging powder for use
with a CEREC 3D system.
The application and incomplete removal
of an imaging powder may affect the
bonding of the restoration to the dentin
surface. CEREC manufacturers instruct
the dentist to clean the surface with air/
water spray, but do not provide detailed
directions. There is no current literature
that shows whether an air/water rinse
adequately removes the powder residue
and whether any remaining residue will
affect the cement bond. Some systems,
such as VITA CEREC Powder (Vident),
rely on the application of glycerin to coat
the surface prior to applying the powder.34
Most other self-contained systems, such as
CEREC Optispray, do not require the separate application of a coating.35 The intent
of this study was to provide guidance
74
for the use of imaging powder and resin
cements with a milled all-ceramic restoration using CEREC 3D.
RelyX Unicem (3M ESPE) is a dualcuring, self-adhesive resin luting cement
for adhesive cementation of indirect
composite, metal, or ceramic restorations.36 Self-adhesive resin cements do
not require a separate adhesive or etchant,
which can be considered a major benefit
due to their simplicity of application compared to more traditional resin cements.
Relatively little information exists about
the composition and adhesive mechanism
of these materials. The current selfadhesive cements are 2-part materials that
require hand mixing, capsule trituration,
or auto-mixing with a dispenser.37 Bond
strengths vary among self-adhesive resin
cements. Etch-and-rinse cements generally
provide the greatest retention.37,38 Selfetching cements provide an intermediate
level, while self-adhesive cements are the
least retentive.37 The vast majority of the
published literature describes one cement,
Rely-X Unicem, which was the first commercially available self-adhesive resin
cement.36,38 Rely-X Unicem has 2 components: a powder composed of glass, silica,
calcium hydroxide, pyrimidine, peroxy
compound, and initiator; and a liquid
composed of methacrylated phosphoric
ester, dimethacrylate, acetate, stabilizer,
and initiator.36,38 Studies have suggested
that Unicem shows nearly equivalent
results to other resin cements in terms
of marginal sealing and adaptation.38
However, a separate phosphoric-acid
etch of enamel margins has been shown
to improve bond strength.39 A review of
studies evaluating the physical properties
of self-adhesive resin cements suggest that
these materials may be expected to show
similar clinical performance as other dental
cements, but clinical studies are lacking, so
long-term conclusions are not possible.38
Self-adhesive resin cements have a significant reduction in dentin bond strength
when the dentin is etched with phosphoric
acid and a bonding agent is applied.37
The effect of imaging powder and its
effective removal on the bond strength of
resin cement to dentin is unknown. The
purpose of this study was to compare the
effects of imaging powder residue on the
shear bond strength of a self-adhesive resin
cement to dentin. The null hypotheses
General Dentistry
www.agd.org
to be tested were that there would be no
significant differences in the bond strength
of the self-adhesive resin cement to dentin
based on the amount of rinsing, or the
type of imaging powder.
Extracted human third molars stored
in 0.5% chloramine-T were used within
6 months following extraction. The teeth
were mounted in dental stone in plastic
pipe with the crown exposed and accessible. A diamond saw (Isomet, Buehler)
was used to remove ≥2 mm coronal tooth
structure to ensure dentin exposure and
the proper orientation of the surface
relative to the direction of shear force
applied. Each specimen was examined
under a stereomicroscope (SMZ-1B,
Nikon USA) at 10X magnification to
ensure complete exposure of the dentin
surface with no residual enamel. To simulate a prepared surface, the flat dentin
was roughened with a fine diamond bur
(No. 837, Brasseler USA) under water
spray with a jig that was used to support
the height of the handpiece head with the
surface of the tooth specimen.
The mounted specimens were then
divided into 4 groups: 3 powder groups—
VITA CEREC Powder, CEREC Optispray,
and Occlude—and 1 group that was
not powdered and served as a control.
Manufacturers’ directions were followed
in the application of the powder. For the
CEREC Powder application, the glycerin
coating was first placed with a brush and
gently air-thinned. Next, the VITA CEREC
Powder was applied using a PowderPro
system (Advanced Dental Instruments
LLC). The PowderPro system was attached
to the handpiece hose of a dental delivery
unit and the VITA CEREC Powder was
delivered through a nozzle on the handpiece with the use of a foot pedal. CEREC
Optispray and Occlude are self-contained
canister systems, and therefore did not
require an adhesive-type first coating or use
of the PowderPro system.33,35 All powders
were applied according to the manufacturers’ instructions with the applicator tip at a
standardized distance of 1 inch.
The 3 powder groups were then divided
into 3 subgroups (n = 10) based on the
method of powder removal: no rinse,
1-second rinse, and 10-second rinse. The
teeth were rinsed with distilled water
Chart 1. Shear bond strength (MPa) and standard deviation (SD) of selfadhesive resin cement (RelyX Unicem) to dentin after treatment with
3 imaging powders (VITA CEREC Powder, CEREC Optispray, and Occlude) and
subsequent rinse of different durations (no rinse, 1 second, and 10 seconds).
14
No rinse
1 second
10 seconds
Shear bond strength (MPa)
12
10
8
6
4
2
0
VITA CEREC Powder
CEREC Optispray
Occlude
Control
Chart 2. Percent fracture mode by powder and rinse groups.
Results
VITA CEREC Powder no rinse
VITA CEREC Powder 1 sec
VITA CEREC Powder 10 sec
CEREC Optispray no rinse
CEREC Optispray 1 sec
CEREC Optispray 10 sec
Occlude no rinse
Occlude 1 sec
Occlude 10 sec
No powder
0 20 40 60 80100
%
Adhesive
Cohesive cement
using a 3-way syringe tip at a standardized distance of 1 inch. A custom-made
vinyl polysiloxane jig was used to maintain the distance and angle.
The tooth specimens were then placed
in an Ultradent Jig and secured beneath
the white nonstick Delrin insert (Ultradent
Products, Inc.).The dual-curing resin
cement was mixed and applied into the
mold according to the manufacturer’s
instructions to a height of 4 mm. The
cement was cured as recommended by
the manufacturer using a Bluephase 16i
light-curing unit (Ivoclar Vivadent, Inc.).
Mixed
Cohesive dentin
Irradiance of the curing light was monitored with a radiometer (LED Radiometer,
Kerr Corporation) to verify irradiance levels
above 1200 mW/cm2. The bonding area
was limited to a 2.4 mm diameter circle
determined by the Delrin insert. Following
the application of the resin cement, all specimens were stored for 24 hours in distilled
water at 37°C. The specimens were then
loaded perpendicularly at the interface with
a customized probe (Ultradent Products,
Inc.) in a universal testing machine (Instron
Corp.) and tested with a crosshead speed of
1 mm/min until bonding failure occurred.
www.agd.org
Shear bond strength values (MPa) were
calculated from the peak load of failure
(Newtons) divided by the specimen surface
area.The mean and standard deviation
were determined for each group. Data were
analyzed with Kruskal-Wallis and MannWhitney statistical tests. Nonparametric
data analysis was used since an exploratory
graphical analysis found a non-normal
distribution of the data. A Bonferroni correction was applied because multiple comparison tests were performed (α = 0.008).
Following shear bond strength testing,
each specimen was examined using a
stereomicroscope (magnification 10X) to
determine failure mode as either: adhesive
fracture at the cement/adhesive/dentin
interface, cohesive fracture in cement,
mixed (combined adhesive and cohesive
fracture) in either the cement-bond
interface or the dentin-bond interface, or
cohesive fracture in dentin.
The nonrinsed powdered dentin surface
had a significant reduction in bond strength
compared to the control (nonpowdered) or
the rinsed powdered surfaces (P < 0.008).
The dentin surfaces that were rinsed for
1 or 10 seconds were not significantly different from the control or from each other.
There was no significant difference in the
bond strength of resin cement to dentin
based on the type of powder (P > 0.086)
(Chart 1). The nonrinsed groups failed
primarily with adhesive fractures while the
rinsed groups failed primarily with adhesive
and mixed fractures (Chart 2).
Discussion
The manufacturer’s instructions for
CEREC Optispray advise the user that
“as soon as the optical impression has
been taken, the surface should be cleaned
with air/water spray.”35 But no published
articles could be found that had studied
the amount of rinse time required to
remove imaging powders.
The first null hypothesis of this study
was rejected; there was a significant difference in bond strength of resin cement
to dentin based on rinse, though not
the duration of the rinse. The results of
this study suggest that a rinse time of
≥1 second is sufficient to remove imaging
powder residue. However, a rinse time
of 0 (the nonrinsed groups) displayed
General Dentistry
75
Dental Materials Effect of imaging powders on the bond strength of resin cement
significantly lower bond strengths. The
failure mode for the nonrinsed groups
was almost entirely adhesive fracture,
suggesting a weaker interface, while the
1- and 10-second rinse groups primarily
displayed adhesive and mixed fractures,
which was similar to the control group.
The second null hypothesis was not
rejected in this study. There was not a
significant difference in bond strength
of resin cement to dentin based on the
type of powder despite the fact that the 3
imaging powders differed greatly. While
Optispray is a self-contained propellant, CEREC Powder is applied with
a delivery unit such as the PowderPro
after the application of a glycerin coating.34,35 Occlude has not been marketed
as an imaging powder and contains
magnesium stearate instead of titanium
dioxide as found in traditional imaging
powders.33 Occlude was utilized in this
study as it has been considered an economical alternative to existing imaging
powders. This study did not attempt to
evaluate Occlude as an imaging powder
and cannot make any conclusion as to
its efficacy for that purpose. Future
research could focus on magnesium
stearate reflectivity on preparation
surfaces and margins.
Self-adhesive resin cements such as
Unicem do not require an acid-etch step
prior to bonding.36 When using etch-andrinse type resin cements, imaging powder
may be removed more thoroughly than
with self-adhesive cements. Remaining
residue was observed to result in more
adhesive-type failures. The dentin surfaces
tested were relatively flat, but roughened
with a diamond bur to simulate intraoral
tooth preparation. Clinically, less efficient
powder removal may be encountered
when rinsing 3-dimensional preparations
(with vertical surfaces and more box-like
forms). However, treating the surfaces with
flour of pumice and prophy cup prior to
cementation would likely further reduce
remnants of imaging powder.
Conclusion
The CAD/CAM imaging powders did
not affect the shear bond strength of the
self-adhesive resin cement to dentin if
the powders were rinsed with water. This
study showed that the manufacturers’
instructions, while nonspecific, were
76
adequate for removal of the 3 tested
powders. The amount of residue that
remained after rinsing with water did not
significantly affect bond strength.
Author information
Maj Jordan is a general dentist at Shaw
AFB, SC, Lt Col Bailey is the director of
Senior Resident Education and Training,
Lt Col Ashcraft-Olmscheid is the director of Prosthodontics Education, and
Col (ret) Vandewalle is the director of
Dental Research, Advanced Education
in General Dentistry Residency, US
Air Force Postgraduate Dental School,
JBSA-Lackland, Texas and Uniformed
Services University of the Health Sciences,
Bethesda, Maryland.
Disclaimer
The views expressed in this study are
those of the authors and do not reflect
the official policy of the United States Air
Force, the Department of Defense, or the
United States Government. The authors
do not have any financial interest in the
companies whose materials are discussed
in this article.
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16. Kassem AS, Atta O, El-Mowafy O. Combined effects of
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17.El-Badrawy W, Hafez RM, El Naga AI, Ahmed DR.
Nanoleakage of self-adhesive resin cements used in
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18. Bernhart J, Schulze D, Wrbas KT. Evaluation of the clinical success of CEREC 3D inlays. Int J Comput Dent.
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19. Boening KW, Wolf BH, Schmidt AE, Kastner K, Walter
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33. Pascal International, Inc. Occlude [product information].
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Manufacturers
Advanced Dental Instruments LLC, Haworth, NJ
201.384.1979
Align Technology, Inc., San Jose, CA
800.577.8767, www.itero.com
Brasseler USA, Savannah, GA
800.841.4522, www.brasselerusa.com
Buehler, Lake Bluff, IL
800.283.4537, www.buehler.com
Dentaco As, Haukeland, Norway
47.5525.4090, www.dentaco.no
Hi-Tec Dental Products, Inc., Lenoir City, TN
800.859.2006, www.hi-tecdental.com
Instron Corp., Norwood, MA
800.877.6674, www.instron.com
Ivoclar Vivadent, Inc., Amherst, NY
800.533.6825, www.ivoclarvivadent.us
Kerr Corporation, Orange, CA
800.537.7123, www.kerrdental.com
Nikon USA, Melville, NY
631.547.4200, www.nikonusa.com
Pascal International, Inc., Bellevue, WA
800.426.8051, www.pascalinternational.net
Planmeca E4D Technologies, Richardson, TX
972.234.3380, www.e4D.com
Sirona Dental Systems, Inc., Charlotte, NC
800.659.5977, www.sironausa.com
Ultradent Products, Inc., South Jordan, Utah
888.230.1420, www.ultradent.com
Vident, Brea, CA
800.828.3839, www.vident.com
3M ESPE, St. Paul, MN
800.634.2249, solutions.3m.com
www.agd.org
There is another article on
DENTAL MATERIALS
in the online edition.
•Impact of toothbrushing with
a dentifrice containing calcium
peroxide
on enamel
color and
roughness
General Dentistry
77
Implant Maintenance
Crestal approach for removing a migrated dental
implant from the maxillary sinus: a case report
Raid Sadda, DDS, MS, MFDRCSI
This article reports a rare case of a horizontally displaced dental implant
that migrated into the maxillary sinus 6 months after 3 implants were
inserted into the augmented maxillary posterior region. Migration of
dental implants into the maxillary sinus usually occurs during surgery and
can result in serious complications.
W
hile dental implants have
revolutionized the practice of
modern dentistry, they can also
be problematic, especially when placed
in the posterior maxilla. Implants in this
area have an increased risk for failure
because of low bone density and shortness
of the alveolar ridge.1 The reasons dental
implants may migrate into the maxillary
sinus are the lack of initial stability during
the surgery, poor bone quality, or—the
most common factor—local tissue infection around the implant.1 The surgeon
must be able to manage problems that
arise intraoperatively as well as those that
develop postoperatively.
Case report
A 55-year-old man was referred to a private dental office to have implants placed
in the maxillary posterior edentulous area.
Pantomograph and periapical radiographs
showed a large radiolucent lesion at the
periapical areas of the nonrestorable maxillary first and second right premolars; the
lesion extended to the maxillary sinus
(Fig. 1). A computed tomography scan
confirmed the diagnosis (Fig. 2).
After local anesthesia was administered,
the premolars were removed and the large
lesion enucleated completely from the
maxilla and maxillary sinus by separating
the maxillary sinus mucosa from the cystic
lining. The lesion was sent for histopathologic analysis and it was determined to
be a radicular dental cyst. The remaining
space was filled with a corticocancellous
bone graft which was extended to fill
part of the maxillary sinus. In addition,
a nonresorbable membrane was placed
over the bone graft. No evidence of recurrence was observed 6 months postsurgery.
78
Received: February 21, 2013
Accepted: June 24, 2013
Key words: radicular cyst, maxillary sinus augmentation,
removal of migrated dental implant
Under local anesthesia, 3 machined
implants were then placed at the site
of the first molar and 2 premolars with
initial stability. A radiograph taken 1 week
postimplantaion confirmed the stability
of the implants (Fig. 3). A radiograph
taken 5 months later revealed a horizontal
migration of the implant from the site of
the first molar into the maxillary sinus
(Fig. 4). Local anesthesia was administered
through a crestal incision, a mucoperiostal
flap was raised, and part of the crestal
bone was removed (Fig. 5). At this point,
the migrated implant was seen at the floor
of the sinus (Fig. 6). The implant was
grasped with a hemostat and removed
from the sinus. The space remaining was
irrigated; a collagen membrane was placed
over the mucosa, and a corticocancellous
bone graft was placed and covered with
a nonresorbable membrane. The wound
was closed with chromic gut sutures.
Postoperative prescription and instructions were given. The patient tolerated
the procedure well, with minimal facial
swelling and pain.
2 clinical cases involving intraosseous
apical movement of an implant several
years after placement.4
According to Pagella et al, the incidence
of metallic foreign bodies in the maxillary sinus has increased following the
development of osseointegrated implants
to treat edentulous cases.5 A 2000 article
recommended immediate removal of
failed implants that have migrated into
the maxillary sinus.6
The real reasons why dental implants
migrate from their initial placement toward
the maxillary sinus are unknown. This
migration may be a technical issue related
to poor surgical preparation, drilling, or
implant placement. Lack of bone thickness/density of an edentulous posterior
maxillary segment has been proposed as an
explanation for inadequate implant stability
and anchorage. Previously reported cases
of dental implant migration indicated that
Discussion
Implants placed in the posterior maxilla
can fail due to the low density of the bone
in that area. There are a few reports in
the literature involving dental implants
migrating into the maxillary sinus.1-6 A
1992 article by Ueda & Kaneda reported
a case of maxillary sinusitis caused by
a displaced connection screw 2 months
after implant placement.1 Quiney et al
reported a case of implant displacement
2 weeks postinsertion.2 More recently,
Haben et al reported the displacement of
a dental implant into the ethmoid sinus.3
A 2005 article by Galindo et al reported
General Dentistry
www.agd.org
Fig. 1. A preoperative radiograph showing a periapical
lesion at the maxillary second premolar and a root
lesion at the mesial of the maxillary first premolar.
Fig. 2. A computed tomography scan confirming the presence of a periapical lesion.
Fig. 3. A radiograph taken 1 week
after the insertion of 3 implants.
Fig. 4. A radiograph taken 5 months
postimplantation demonstrating the
migration of the implant into the
maxillary sinus.
migrations may have been caused by the
dentist’s surgical technique, by an alveolar
infection or lesion that resulted in bone
destruction, or by a particular bone weakness, such as osteoporosis or osteopenia.2,6
Various mechanisms have been proposed to explain the migration of an
implant into the maxillary sinus.7 These
mechanisms can include changes in intrasinal and nasal pressures, an autoimmune
reaction to the implant (resulting in periimplant bone destruction and compromised osseointegration), and resorption
produced by an incorrect distribution of
occlusal forces.7
In the present case, the implant
migrated without being subjected to
occlusal forces, as the bone depth prevented integration of the implant prior
to second stage surgery. Bone loss in the
augmented area led to implant failure.
The most common approach for removing implants that have migrated into the
maxillary sinus involves a lateral-wall
osteotomy; however, because the migrated
implant in the present case was close to the
Fig. 5. A crestal incision made to
approach the implant at the floor of
the maxillary sinus.
floor of the maxillary sinus, an alternative
crestal approach was used.8 This approach
is minimally destructive to the maxillary
sinus, while reducing the risk of injury to
the maxillary artery (which is located at
the lateral wall of the maxillary sinus).
Conclusion
Placing an implant in the posterior
maxilla—with or without sinus grafting—can offer a reasonably good
prognosis; however, the procedure is not
free of complications. An implant in a
grafted area may increase both the risk
of implant failure and migration to the
maxillary sinus. To decrease the risk of
migration and complications, the dentist
should carefully study the radiographs
before the second stage of implant surgery in order to be aware of the quality
of the bone, implant stability, and the
proper surgical technique indicated.
Author information
Dr. Sadda is a clinical associate professor,
www.agd.org
Fig. 6. The implant prior to removal by
a hemostat.
Surgery, New York University, New
York, and an attending oral surgeon, St.
Barnabas Hospital, Bronx, New York.
References
1. Ueda M, Kaneda T. Maxillary sinusitis caused by dental
implant: report of two cases. J Oral Maxillofac Surg.
1992:50(3):285-287.
2. Quiney RE, Brimble M, Hodge M. Maxillary sinusitis
from dental osseointegrated implants. J Laryngol Otol.
1990;104(4):333-334.
3. Haben CM, Balys R, Frenkiel S. Dental implant migration into the Ethmoid sinus. J Otolaryngol. 2003;32(5):
342-344.
4. Galindo P, Sanchez-Fernandez E, Avila G, Cutando A,
Fernandez JE. Migration of implants into the maxillary
sinus: two clinical cases. Int J Oral Maxillofac Implants.
2005;20(2):291-295.
5. Pagella F, Emanuelli E, Castelnuovo P. Endoscopic extraction of a metal foreign body from the maxillary sinus. Laryngoscope. 1999:109(2 Pt 1);339-342.
6. Iida S, Tanaka N, Kogo M, Matsuya T. Migration of a
dental implant into the maxillary sinus. A case report.
Int J Oral Maxillofac Surg. 2000;29(5):358-359.
7. Regev E, Smith RA, Perrott DH, Pogrel MA. Maxillary
sinus complications related to endosseous implants.
8. Akira Kitamura. Removal of a migrated dental implant
from a maxillary sinus by transnasal endoscopy. Br J
Oral Maxillofac Surg. 2007;45(5):410-411.
General Dentistry
79
Answers
Self-Instruction
Exercise No. 343
January/February 2014, p. 42
1. B
5. C
9. C
13. B
2. D
6. C
10. D
14. D
3. A
7. A
11. C
15. A
4. D
8. D
12. A
Exercise No. 344
1. B
5. C
9. B
13. B
2. C
6. A
10. A
14. A
3. B
7. C
11. B
15. D
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Exercise No. 345
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5. B
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362
363
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Cancer Screening
Ameloblastic carcinoma of the mandible
manifesting as an infected odontogenic cyst
Adepitan A. Owosho, BChD n Anitha Potluri, DMD n Richard E. Bauer III, DMD, MD n Elizabeth A. Bilodeau, DMD, MD, MSEd
Ameloblastic carcinoma (AC) is a rare malignant odontogenic tumor.
Although most ACs appear to originate de novo, some cases originate
from a pre-existing ameloblastoma. This article presents the case
of a 69-year-old man with an AC in the left body of the mandible.
Radiographically, the lesion resembled an odontogenic cyst surrounding
an impacted tooth. While ACs tend to have aggressive features that
A
n ameloblastic carcinoma (AC)
is a rare malignant odontogenic
tumor with a reported incidence of
1%-3%.1-4 In 1984, Slootweg & Muller
proposed that the term ameloblastic carcinoma should be used to designate lesions
that exhibit features of both ameloblastoma
and carcinoma in either primary and/or
metastatic lesions.5 Most ACs are presumed
to originate de novo, with some cases
involving the malignant transformation of
a pre-existing ameloblastoma.6 In 2005, the
World Health Organization classified AC
into 3 types: primary, secondary (intraosseous), and secondary (peripheral).7 A 2009
study by Yoon et al reported 6 new cases
of AC.8 At that time, there were 104 cases
in the English literature; since then, several
other cases have been reported.8-11
The age of AC manifestation ranges
from 7 to 91 years with an average age of
53, although it is most frequently found
in patients after age 60, with a 2:1 maleto-female predilection.9-11 The mandible is
involved more commonly than the maxilla, with a posterior predilection, although
a rare case involving the anterior skull base
was reported in 2005.12
AC has aggressive clinical features, such
as pain, expansion of the jaw, and perforation of the cortex. It also may metastasize;
although the regional lymph nodes are
the most common site, distant metastases
to the lungs, brain, and liver have been
reported.8,9,13-21 In most cases, radiographic
findings reveal an ill-defined radiolucency,
often with scattered sites of focal radiopaque dystrophic calcification.11,14,15,19,22
Wide local resection (resulting in a
tumor-free margin of 10-15 mm) is
thought to be the treatment of choice;
distinguish them from their benign counterparts, some are more subtle
in their presentation. Therefore, it is important that dentists rule out
malignancy in lesions that do not display obvious radiographic features.
although adjuvant radiation and/or
chemotherapy and regional lymph node
dissection have also been considered.6,23
This article presents a case involving the
diagnosis and treatment of an AC.
Case report
A 69-year-old man was referred to the
Surgery at the School of Dental
Medicine of the University of Pittsburgh,
Pennsylvania for evaluation and definitive management of an impacted left
mandibular third molar, which had been
symptomatic for 2 months. The patient
stated that he had developed pain and an
infection in the lower left mandible. He
had previously sought treatment from his
general dentist, who treated him with a
course of antibiotics.
The patient presented with periapical
radiographs taken by the referring dentist.
A panoramic radiograph was obtained
for further evaluation (Fig. 1). The radiographs revealed a full bony impaction of
tooth No. 17, which was distoangularly
positioned. There was a uniform and
mildly enlarged radiolucent follicular space
from the superior part of the crown to
the inferior and apical part of the tooth.
Expansion was noted toward the inferior
alveolar (IA) canal, pushing the IA in an
inferior direction, with associated erosion
in the superior cortex of the IA canal.
Mild sclerosis was noted at the posterior
extent of the follicular lining and inferiorly
within the radiolucency. A radiolucency
was also noted within the tooth coronally,
consistent with internal resorption. No
lamina dura or follicle lining was noted
Fig. 1. Preoperative panoramic radiograph of a 69-year-old man with an impacted left mandibular third molar
and inferior expansion of a lesion.
www.agd.org
General Dentistry
e1
Cancer Screening Ameloblastic carcinoma of the mandible manifesting as an infected odontogenic cyst
Fig. 2. A photomicrograph of the patient, showing a
tumor island with comedonecrosis. (H&E, magnification 200X).
apically. Based on these findings, an initial diagnosis of an impacted tooth with
inflammation or a secondarily infected
cystic lesion was made. The left mandibular third molar was extracted and an
excisional biopsy was performed on the
associated lesion.
The histopathologic findings revealed
odontogenic tumor islands within a
fibrous stroma, exhibiting peripheral
palisading with nuclear polarization away
from the basement membrane. The central
cells were loose and discohesive, recapitulating stellate reticulum. However, the
sections showed increased mitotic activity,
necrosis, and varying nuclear size, shape,
and staining (Fig. 2 and 3). No angiolymphatic or perineural invasion was present.
A Ki-67 stain—a proliferative immunoperoxidase marker—showed an elevated
percentage of positive cells (Fig. 4). The
histologic sections, in conjunction with
immunophenotypic studies, supported the
diagnosis of AC.
The patient returned for a follow-up
visit 1 week postsurgery; at that time,
a cone beam computed tomography
(CBCT) scan was taken. It revealed an
ill-defined radiolucency with areas of focal
radiopacities and cortical disruption, consistent with postoperative surgical margins
and the aggressive nature of the lesion
(Fig. 5). To investigate the presence of the
lesion in regional lymph nodes (as well as
e2
Fig. 3. A photomicrograph of the patient, showing
a tumor island with an increased number of mitotic
figures. (H&E, magnification 400X).
Fig. 4. A photomicrograph of the patient showed
increased positive staining, indicating a high
proliferative index. (Ki-67, magnification 400X).
Fig. 5. A postextraction CBCT scan.
distant metastases), a fluorodeoxyglucose
(FDG)-positron emission tomography
image was performed, revealing elevated
FDG uptake only in the left mandible.
There was no abnormal high uptake
anywhere else, suggesting no regional or
distant metastases.
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Wide local resection of hard and soft
tissue was planned. One month after
the initial biopsy, the patient underwent
resection of the left mandible and
reconstruction with a secondary titanium
reconstruction bar. This bar was used to
replate the mandible. Prior to surgery,
Fig. 6. An intraoperative image of the patient 1 month postsurgery, after
placement of a secondary reconstruction bar.
a stereolithic model was fabricated
and the secondary reconstruction bar
was pre-bent. Intraoperatively, 15 mm
margins were identified and 41 mm
of bone and tissue were resected from
the left mandible (Fig. 6 and 7). The
overlying periosteum and submucosa
were removed. Full thickness mucosa
and submucosa was resected at the
site of the extraction and biopsy. The
resulting orocutaneous communication
was closed primarily. A silastic block was
inserted to maintain space for future
osseous reconstruction.
The resected segment was sent to the
pathology department for definitive
histological examination. The previous diagnosis of AC was confirmed;
however, the anteromedial overlying
submucosa demonstrated 2 islands of
tumor. Due to these positive margins, a
wide local resection with a selective neck
dissection and postoperative radiation
therapy was planned. The subsequent
specimen had negative margins with no
nodal involvement.
Discussion
AC is a rare malignant odontogenic tumor,
which is treated by wide surgical resection
with consideration for the possibility of
adjuvant radiation and/or chemotherapy.
Typically, cases of AC treated using conservative therapy have a high rate of recurrence and death.9
Fig. 7. Photograph of the 41 mm of bone and soft tissue resected surgically at the
1-month follow-up visit.
The clinical symptoms of AC are
more aggressive than those of its benign
counterpart, ameloblastoma. However,
in the present case, the patient’s only
symptom was pain of approximately
2 months duration, persisting even after
treatment with antibiotics. The radiographic features of the present case were
subtle, including mild enlargement of the
follicular space, pushing of the IA canal
inferiorly, and erosion of the superior
cortex, leading to a diagnosis of either
an impacted tooth with inflammation
or a secondarily infected cystic lesion. In
retrospect, these seemingly subtle features
reflected an aggressive lesion.
Conclusion
This article presents a case of a mandibular AC with an impacted third molar
exhibiting subtle cystic radiographic features and mildly aggressive qualities. This
case indicates that even though most ACs
have aggressive features delineating them
from their benign counterparts, some can
appear subtle. Thus, care has to be taken
to rule out malignancy in lesions with
subtle radiographic features.
Author information
Dr. Owosho is the chief resident, Oral
and Maxillofacial Pathology, Department
of Diagnostic Sciences, School of Dental
Medicine, University of Pittsburgh,
Pennsylvania, where Drs. Potluri
www.agd.org
and Bilodeau are assistant professors,
and Dr. Bauer is an assistant professor with the Department of Oral and
Maxillofacial Surgery.
References
1. Ladeinde al, Ajayi OF, Ogunlewe MO, et al. Odontogenic tumors: a review of 319 cases in a Nigerian
teaching hospital. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2005;99(2):191-195.
2. Taghavi N, Mehrdad L, Rajabi M, Akbarzadeh A. A
10-year retrospective study on malignant jaw tumors
in Iran. J Craniofac Surg. 2010;21(6):1816-1819.
3. Jing W, Xuan M, Lin Y. Odontogenic tumours: a retrospective study of 1642 cases in a Chinese population.
Int J Oral Maxillofac Surg. 2007;36(1):20-25.
4. Abiko Y, Nagayasu H, Takeshima M, et al. Ameloblastic carcinoma ex ameloblastoma: report of a
case-possible involvement of CpG island hypermethylation of the p16 gene in malignant transformation.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2007;103(1):72-76.
5. Slootweg PJ, Muller H. Malignant ameloblastoma or
ameloblastic carcinoma. Oral Surg Oral Med Oral
Pathol. 1984;57(2):168-176.
6. Suomalainen A, Hietanen J, Robinson S, Peltola JS. Ameloblastic carcinoma of the mandible resembling
odontogenic cyst in a panoramic radiograph. Oral Surg
638-642.
7. Barnes L, Eveson JW, Reichart P, Sidransky D, eds.
World Health Organization Classification of Tumours:
Head and Neck Tumours. Lyon, France: IARC Press;
2005.
8. Yoon, HJ, Hong SP, Lee JI, Lee SS, Hong SD. Ameloblastic carcinoma: an analysis of 6 cases with review of
the literature. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2009;108(6):904-913.
9. Hall JM, Weathers DR, Unni KK. Ameloblastic carcinoma: an analysis of 14 cases. Oral Surg Oral Med Oral
General Dentistry
e3
Cancer Screening Ameloblastic carcinoma of the mandible manifesting as an infected odontogenic cyst
10. Carnelio S, Solomon M, Manohar V. Ameloblastic carcinoma. A case report with review of literature. Indian J
Dent Res. 2001;12(4):238-241.
11. Matsuzaki H, Katase N, Hara M, et al. Ameloblastic
carcinoma: a case report with radiological features of
computed tomography and magnetic resonance imaging and positron emission tomography. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 2011;112(1):e40e47.
12. Ozlugedik S, Ozcan M, Basturk O, et al. Ameloblastic
carcinoma arising from anterior skull base. Skull Base.
2005;15(4):269-272.
13. Akrish S, Buchner A, Shoshani Y, Vered M, Dayan D.
Ameloblastic carcinoma: report of a new case, literature review, and comparison to ameloblastoma. J Oral
Maxillofac Surg. 2007;65(4):777-783.
14. Avon SL, McComb J, Clokie C. Ameloblastic carcinoma:
case report and literature review. J Can Dent Assoc.
2003;69(9):573-576.
15. Benlyazid A, Lacroix-Triki M, Aziza R, Gomez-Brouchet
A, Guichard M, Sarini J. Ameloblastic carcinoma of the
maxilla: case report and review of the literature. Oral
104(6):e17-e24.
16. Dhir K, Sciubba J, Tufano RP. Ameloblastic carcinoma
of the maxilla. Oral Oncol. 2003;39(7):736-741.
e4
17. Jindal C, Palaskar S, Kaur H, Shankari M. Low-grade
spindle-cell ameloblastic carcinoma: report of an unusual case with immunohistochemical findings and
review of the literature. Curr Oncol. 2010;17(5):52-57.
18. Goldenberg D, Sciubba J, Koch W, Tufano RP.
Malignant odontogenic tumors: a 22-year experience.
Laryngoscope. 2004;114(10):1770-1774.
19. Bruce RA, Jackson IT. Ameloblastic carcinoma. Report of an aggressive case and review of the literature. J Craniomaxillofac Surg. 1991;19(6):267-271.
20. Simko EJ, Brannon RB, Eibling DE. Ameloblastic carcinoma of the mandible. Head Neck. 1998;20(7):654659.
21. Infante-Cossio P, Hernandez-Guisado JM, FernandezMachin P, Garcia-Perla A, Rollon-Mayordomo A, Gutierrez-Perez JL. Ameloblastic carcinoma of the maxilla:
a report of 3 cases. J Craniomaxillofac Surg. 1998;
26(3):159-162.
22. Verneuil A, Sapp P, Huang C, Abemayor E. Malignant
ameloblastoma: classification, diagnostic, and therapeutic challenges. Am J Otolaryngol. 2002;23(1):4448.
23. Zwahlen RA, Gratz KW. Maxillary ameloblastomas:
a review of the literature and of a 15-year database.
J Craniomaxillofac Surg. 2002;30(5):273-279.
General Dentistry
www.agd.org
Surgical Orthodontics
A large dentigerous cyst treated with decompression
and orthosurgical traction: a case report
Rodrigo Dias Nascimento, PhD n Fernando Vagner Raldi, PhD n Michelle Bianchi de Moraes, PhD n Paula Elaine Cardoso, PhD Deborah Holleben, DDS
This article presents the case of an 8-year-old patient who presented with
a large radiolucency associated with the maxillary left canine and a supernumerary tooth. A computed tomography scan showed the radiolucency
was in close proximity to the roots of the anterior teeth, with no areas of
root resorption, and expansion into the left maxillary sinus. The boundaries of the maxillary sinus floor were still preserved. After positive aspiration of intralesional liquid and due to the large size of the radiolucency, a
decompression technique was selected to preserve the permanent canine.
Surgery was performed to remove the supernumerary tooth, followed by
A
mong developmental odontogenic
cysts, dentigerous cysts are the most
common; 20% of the epithelial cysts
in gnathic bones are dentigerous.1 The
dentigerous cyst originates at the separation
of the follicle that lies around the crown of
an impacted tooth, binding to the crown’s
cementoenamel junction.1 Its pathogenesis
is unknown; however, it has been suggested
that it progresses through an accumulation
of fluid between the reduced enamel epithelium and the tooth crown.1
Dentigerous cysts are primarily found in
children and adolescents (most frequently
as a cystic lesion), although there is a high
incidence rate in the second and third
decades of life and a predilection for men
and Caucasians.2 Dentigerous cysts in
Fig. 1. Clinical examination revealing a vestibular
bulging in the region of the maxillary left canine.
orthodontic treatment and surgery to allow access for orthodontic traction
of the permanent canine. More than 5 years post-treatment, no recurrence was observed and the therapeutic option to position and preserve
the permanent canine was successful.
Key words: dentigerous cyst, decompression, eruption
of teeth, unerupted maxillary canine
children may expand, causing retention of
the involved dental element and deformation of the surrounding alveolar bone (with
or without bone cortical expansion or
displacement of dental roots and adjacent
anatomical structures). Due to their slow
and expansive evolution, these cysts essentially are asymptomatic; as a result, diagnoses are often due to radiographic findings.3
Facial asymmetry may result from extensive
injuries, although large dentigerous cysts
are rare, and lesions supposedly diagnosed
on the radiographic examination as large
dentigerous cysts are revealed at the histopathological examination as keratocystic
odontogenic tumors or ameloblastomas.1
Symptomatic lesions are generally the
result of periapical inflammation of an
overlying primary tooth, a periodontal
lesion that affects an adjacent tooth, or
a bone break that causes disruption in
communication with the oral cavity, nasal
cavity, or maxillary sinuses.1
It appears radiographically as a radiolucent area, unilocular with a well-defined
and usually sclerotic margin, associated
with the crown of an included tooth. In
order to differentiate a small dentigerous
cyst from an enlarged dental follicle (which
also is located above an included tooth), it
has been suggested that the typical space
around the crown of an included tooth is
approximately 3-4 mm in diameter.1
In histopathologic analysis, a dental follicle surrounding the crown of an included
tooth appears as a thin layer of reduced
enamel epithelium, thus making it difficult
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to distinguish between such a follicle and a
small dentigerous cyst.1 Furthermore, cystic
epithelium has metaplasia that is similar
to oral mucosa epithelium.3 The epithelial
lining of a dentigerous cyst consists of 2-4
layers of nonkeratinized flattened cells, with
a flat interface between the epithelium and
connective tissue.1 The capsule of fibrous
connective tissue is arranged loosely and
contains an amorphous substance consisting
of glycosaminoglycans, possibly accompanied by small islands and strands of odontogenic epithelial rests with an inactive aspect.1
For large cysts, marsupialization and
decompression often are indicated as
alternative therapies.3 These procedures
simplify the surgical procedure, assist in
the eruption of the involved tooth, and
minimize any adverse consequences.3 The
subsequent new bone formation after these
procedures results in the decrease of the
peripheral lesion size and directs the eruption of the involved tooth.3 This article
analyzes a clinical decompression technique associated with surgical orthodontic
treatment and its efficacy in treating
extensive lesions, allowing for the regeneration of bone defects and preservation of the
included dental element—resulting in its
eruption in the oral cavity.
Case report
An orthodontist referred an 8-year-old boy
with vestibular bulging in the region of the
maxillary left primary canine. The mucosa
had a normal appearance and there were
no symptoms or crackling noises (Fig. 1).
General Dentistry
e5
Surgical Orthodontics A large dentigerous cyst treated with decompression and orthosurgical traction: a case report
Fig. 2. A panoramic radiograph of the 8-year-old patient at the initial visit showing a large
radiolucency associated with the maxillary left canine and a supernumerary tooth.
Fig. 4. Aspiration of yellowish liquid after punch
biopsy.
A panoramic radiograph revealed a radiolucent image at the maxillary left permanent
canine and a supernumerary tooth, both of
which were included (Fig. 2). To determine
the limits of the lesion, a computed tomography (CT) scan was performed. The CT
scan revealed a lesion with expansive root
displacement of adjacent teeth (without
signs of resorption) while preserving the left
maxillary sinus floor (Fig. 3). Bone structure did not change. The muscles in the oral
cavity had regular tomographic aspects and
the subcutaneous tissue had no appreciable
changes, suggesting an odontogenic cyst.
Based on the clinical examination and
imaging test results, an incisional biopsy
was scheduled, preceded by a punch
biopsy. The punch biopsy collected a yellowish liquid that contained suspended
cholesterol crystals (Fig. 4). The decompression was performed and the cystic capsule fragments were collected. (Fig. 5-7).
e6
Fig. 3. A computed tomography scan (coronal slice)
revealing the lesion with expansive root displacement of adjacent teeth.
Fig. 5. Incision exposing the sealed cystic capsule.
Fig. 6. The interior of the cyst after removal of the
cystic capsule.
Fig 7. The placement of furacin gauze pads and oral
mucosa suture on the borders of the orifice.
Fig. 8. Healed orifice before placement of a shutter.
The collected material was submitted
to histopathological analysis, which confirmed the diagnosis of odontogenic cyst.
After 20 days, an acrylic shutter was
placed to maintain an open surgical
window, prevent the entrance of food,
and facilitate cleaning by the patient
(Fig. 8 and 9). At monthly follow-up
visits, shutter reduction was performed,
allowing for decompression as demonstrated by peripheral bone formation. This progressive reduction was
performed to the point that the cavity
was not deep enough to stabilize the
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Fig. 9. Acrylic shutter placed over the orifice to
provide a surgical window.
Fig. 10. Surgical removal of supernumerary tooth in
palate.
Fig. 11. Surgical exposure and orthodontic traction
of left maxillary canine.
A
B
C
Fig. 12. Histological aspects of dentigerous cyst.
Top. The fibrous cystic capsule exhibited numerous
bundles of collagen fibers associated with small
caliber vessels and small areas of bleeding (H&E,
magnification 200X). Bottom. Fibrous connective
tissue partially covered by non-keratinized stratified
squamous epithelium with 2 or 3 layers of flattened
cells and, in some cubic regions, with flat interface
between epithelium and conjunctive tissue (H&E,
Fig. 13. Results 5 years and 2 months post-treatment. A. Panoramic radiograph showing the eruption of the
left maxillary canine. B. Successful orthodontic traction of the maxillary left canine. C. Anterior photograph
showing the erupted left maxillary canine.
shutter. At that time, the surgery was
scheduled for the enucleation of the
remaining lesion.
The patient subsequently underwent
surgical removal of the supernumerary
tooth and orthodontic treatment in order
to facilitate the orthodontic traction of the
maxillary left canine (Fig. 10 and 11).
Microscopic examination of the
histological sections revealed fibrous
connective tissue covered partially by
non-keratinized stratified squamous
epithelium, with 2-3 layers of flattened
cells and—in some cubic regions—a flat
interface between the epithelium and
conjunctive tissue. The fibrous cystic
capsule in the tissues contained numerous
bundles of collagen fibers associated with
small caliber vessels and limited areas of
bleeding (Fig. 12).
Five years and two months posttreatment, no recurrence of the lesion
www.agd.org
was observed, and the preservation and
positioning of the maxillary left canine
(with the aid of orthosurgical traction)
was successful (Fig. 13).
Discussion
Dentigerous cysts are associated with mandibular third molars, permanent canines,
maxillary third molars, and second premolars; they also may be associated with
supernumerary teeth.1
General Dentistry
e7
Surgical Orthodontics A large dentigerous cyst treated with decompression and orthosurgical traction: a case report
Fenestration (a small opening of the
cyst), marsupialization (a wide opening at
the equator of the cyst), and decompression with shutters are different methods
that all work on the same principle.4 The
difference between decompression and
marsupialization has been established in
the literature. According to Tucker et al:
Decompression and marsupialization,
despite having the same function and
sharing the same basic principle of bone
regeneration, are two entirely different
techniques. Although both of them have
the purpose of relieving the pressure in
the cystic cavity and allowing new bone
formation, marsupialization is a one-stage
surgery; decompression is a procedure of
two stages.5
Marsupialization involves the opening
of a window or surgical cavity on the cyst
wall, allowing the emptying of its contents
while maintaining the continuity between
the cyst and the oral cavity. The maxillary
sinus or the nasal cavity may also need
emptying in cases of large cysts, impacted
teeth associated with cysts in pediatric
patients, or for patients with systemic diseases, such as the elderly.6
Decompression seeks the same results
as marsupialization, but requires the
placement of a device or intraoral drain
tube. The tube allows for irrigation of the
cystic cavity, helping to prevent food and
microorganisms from accumulating in
the area, which could lead to a secondary
infection. This technique provides for the
permeability of the cystic cavity, since the
union of the cyst wall epithelium with the
mucosa derives from the exteriorization of
the injury. Another advantage lies in the
fact that after the surgical procedure, the
cyst capsule tends to become thicker, which
would aid in either its complete removal or
enucleation in a second surgical step.7,8
e8
Decompression and marsupialization
both reduce lesion size and induce bone
formation, minimizing the extent of
secondary surgery by means of mitigating
pressure in the cystic cavity. It has also
been observed that histological changes
have been observed after both procedures,
as the cystic epithelium is replaced eventually by oral epithelium.4
In the present case, decompression was
the most appropriate treatment, due to
the large size of the cystic lesion in the oral
cavity. This technique made it possible
to preserve the permanent canine, which
helps to establish and maintain the form
and function of the dentition. The canine’s
presence in the dental arch is crucial for
establishing balanced dynamic occlusion,
esthetics, and facial harmony.9
In the treatment of impacted teeth,
it is possible to preserve them through
orthodontic planning; the treatment of
choice is surgical exposure of the tooth
and consequent orthodontic traction.
However, after the extraction of primary
teeth and cyst decompression, there is the
possibility of spontaneous eruption without orthodontic intervention. The potential tooth eruption also depends on the
stage of its rooting. An impacted tooth
without complete root formation and
an open apex has considerable eruption
potential.10 In cases with small or large
cystic lesions and a permanent included
tooth, orthodontic evaluation and followup are necessary.6
Conclusion
In cases involving large dentigerous cysts
and the crown of a permanent tooth—
where extraction is not indicated and the
tooth is deemed necessary for physiological occlusion—a conservative treatment
such as decompression, with or without
orthodontic traction, may be the best
treatment option.
General Dentistry
www.agd.org
Author information
Drs. Nascimento, Raldi, and de Moraes
are professors, Department of Diagnosis
and Surgery, Sao Jose dos Campos Dental
School, Sao Paulo State University,
Brazil, where Dr. Holleben is a dentist
and an intern, Oral and Maxillofacial
Surgery & Traumatology, and Dr.
Cardoso is a professor, Department of
Restorative Dentistry.
References
1. Waldron CA. Cysts and odontogenic tumors. In: Neville BW, Damm DD, Allen CM, Bouquot JE, eds. Oral
and Maxillofacial Pathology. 3rd ed. St. Louis: Elsevier
Saunders; 2009:679.
2. Bastos EG, Cruz MC, Martins GA, Mendes MC,
Marques RV. Marsupialization of mandibular dentigerous cyst in a 7-year-old child in the mixed dentition:
case report [in Portuguese]. Rev Odontol UNESP. 2011;
40(5):268-271.
3. Berden J, Koch G, Ullbro C. Case series: treatment of
large dentigerous cysts in children. Eur Arch Paediatr
Dent. 2010;11(3):140-145.
4. Martorelli S, Coelho E Jr, Marinho E, Albuquerque R,
Martorelli F, Machado de Andrade F. Keratocyst odontogenic tumor of the jaw: case report and management analysis. Int J Dent Recife. 2009;8(1):50-56.
5. Tucker WM, Pleasants JE, MacComb WS. Decompression and secondary enucleation of a mandibular cyst:
report of case. J Oral Surg. 1972;30(9):669.
6. Berti S de A, Pompermayer AB, Couto Souza PH, Tanaka OM, Westphalen VP, Westphalen FH. Spontaneous
eruption of a canine after marsupialization of an infected dentigerous cyst. Am J Orthod Dentofacial Orthop. 2010;137(5):690-693.
7.Giuliani M, Grossi BG, Lajolo C, Bisceglia M, Herb
KE. Conservative management of a large odontogenic keratocyst: report of a case and review of the literature. J Oral Maxillofac Surg. 2006;64(2):308-316.
8. Maurette PE, Jorge J, Moraes M. Conservative treatment protocol of odontogenic keratocyst: a preliminary
study. J Oral Maxillofac Surg. 2006;64(3):379-383.
9. Cappellette M, Cappellette M Jr, Fernandes LCM, de
Oliveira AP, de Oliveira WC. Caninos permanentes retidos por palatino: diagnostico e terapeutica - uma
sugesto tecnica de tratamento. Revista Dental Press
de Ortodontia e Ortopedia Facial. 2008;13(1):60-73.
10. Hyomoto M, Kawakami M, Inoue M, Kirita T. Clinical
conditions for eruption of maxillary canines and mandibular premolars associated with dentigerous cysts.
Am J Orthod Dentofacial Orthop. 2003;124(5):515520.
Dental Materials
Impact of toothbrushing with a dentifrice
containing calcium peroxide on enamel color
and roughness
Diala Aretha de Sousa Feitosa, DDS, MSc n Boniek Castillo Dutra Borges, PhD n Fabio Henrique de Sa Leitao Pinheiro, PhD Rosangela Marques Duarte, PhD n Renato Evangelista de Araujo, PhD n Rodivan Braz, PhD Maria do Carmo Moreira da Silva Santos, PhD n Marcos Antonio Japiassu Resende Montes, PhD
the Ra increased in all groups after brushing, only the dentifrice containing
calcium peroxide resulted in an increase in reflectance.
Received: July 20, 2013
Accepted: November 12, 2013
This in vitro study sought to evaluate both the bleaching potential and
changes to average surface roughness (Ra) of enamel after brushing with
a dentifrice. Fifty-four enamel specimens (4 x 4 x 2 mm) were divided
into 3 groups (n = 18) and treated with 1 of 3 dentifrices: 1 with calcium
peroxide, and 2 without. The samples were submitted to 20,000 brushing
cycles. Color and Ra were measured before and after brushing. Although
M
any patients consider an attractive smile to be synonymous
with good health.1 The increased
demand for enhanced esthetics has led
to the development of bleaching products and whitening dentifrices.2 While
bleaching peroxides cause decolorization
(whitening) of the colored materials found
within the tooth, whitening dentifrices are
used to remove extrinsic stains with specific abrasives and/or chemical agents, such
as hydrated silica, calcium pyrophosphate,
and hydrogen or calcium peroxides.2,3
The high amounts of abrasives in dentifrices may increase enamel roughness and
damage soft tissues and dental restorations,
resulting in gingival recession, cervical
Key words: dentifrice, tooth whitening, spectrophotometry, roughness
abrasion, and dentinal hypersensitivity.1 It
is expected that adding a chemical component (such as a peroxide) to a whitening
dentifrice formulation would augment the
abrasive cleaning by aiding in the removal
and/or prevention of extrinsic stains.2
Presently there is a lack of research in the
literature to confirm whether these whitening dentifrices have a greater impact on
surface roughness compared to peroxidefree dentifrices.
It has been demonstrated that calcium
peroxide can release oxygen ions slowly
and keep oxygen concentrations high.4
Bleaching is achieved, in part, from an
oxireduction reaction in which reactive
oxygen species attack the long-chained,
Table 1. Dentifrices used in this study.
Product
Chemical composition
Lot
Colgate Total
Advanced Clean
Water, sorbitol, sodium lauryl sulphate, hydrated silica,
methyl vinyl ether and maleic anhydride copolymer,
carrageenan, flavor, sodium hydroxide, sodium fluoride,
triclosan, sodium saccharin, titanium dioxide
0266BR121B
Colgate Total
Water, glycerin, hydrated silica, propylene glycol, sorbitol,
Advanced Whitening sodium lauryl, carrageenan, cellulose gum, sodium saccharin,
sodium fuoreto, triclosan, titanium dioxide, sodium hydroxide,
CI 77891 (white)
0011BR123D
Colgate Whitening
Oxygen Bubbles
0051MX113E
Water, glycerin, hydrated silica, sodium bicarbonate,
propylene glycol, sodium triphosphate, carrageenan,
tetrasodium pyrophosphate, cellulose gum, sodium saccharin,
sodium monofluorophosphate, titanium dioxide, calcium
peroxide, sodium hydroxide
www.agd.org
dark-colored chromophore molecules in
dental tissues, breaking them down into
smaller, lightly colored, and more diffusible molecules, thus this producing a
whitening effect.5 In this sense, brushing
teeth with calcium peroxide-containing
whitening dentifrices might render the
enamel prone to bleaching. This may or
may not be associated with an increase in
roughness, which varies according to the
concentration of abrasives. To the best of
the authors’ knowledge, this study is the
first to evaluate the bleaching potential
and surface roughness of enamel after
brushing with a dentifrice that contains
calcium peroxide. Two dentifrices that did
not contain calcium peroxide served as
controls. The null hypotheses tested were
that there would be no differences in the
bleaching potential among the products,
and that none of the products would alter
enamel surface roughness.
Preparation of enamel samples
This study was approved by the University
of Pernambuco Ethics Committee under
Protocol No. 194/10. Twenty-seven
caries-free human third molars were
stored for a maximum of 3 months in
an aqueous 0.2% thymol solution. As
confirmed by stereomicroscopic evaluation
(magnification 25X), none of the selected
teeth surfaces had cracks or abnormal
anatomy. Using a water-cooled diamond
saw (Isomet 1000, Buehler), a total of
54 enamel specimens (4 x 4 x 2 mm) were
General Dentistry
e9
Dental Materials Impact of toothbrushing with a dentifrice containing calcium peroxide on enamel color and roughness
Table 2. Reflectance means (SD) according to
dentifrice and time.
Table 3. Mean roughness values (SD) according
to dentifrice and time of measurement.
Dentifrice
Before brushing
After brushing
Dentifrice
Colgate Total
Advanced Clean
0.673 (0.005)
0.667 (0.006)
Colgate Total
Advanced Whitening
0.672 (0.006) Aa
Colgate Whitening
Oxygen Bubbles
0.665 (0.007) Ba
Aa
Initial color and roughness
assessment
Using a computer-assisted spectrometer
(with wavelengths ranging from 430 to
800 nm), color assessment was performed
based on light reflectance. A halogen
light (HL-2000-FSHA, Ocean Optics)
and a fiberoptic cable (QR400-7-VIS-BX,
Ocean Optics) with 6 optical fibers in a
circular arrangement were used for light
emission at a distance of 2 mm from the
enamel slabs. Reflected light was collected
by a centrally located optical fiber and
transmitted to the spectrometer, which
was connected to a computer. The wavelength-dependent light reflection intensity was calculated by using spectrometer
operating software (SpectraSuite, Ocean
Optics). Measurements were performed in
a dark room with standardized air conditioning. A white standard plate (WS-1-SS,
Ocean Optics) was used to calibrate
the measurement unit. The specimens
were attached to a holder so that the
light would always be at the same place
throughout repeated measurements (light
focus diameter = 600 µm); the holder
e10
0.11 (0.01)
0.19 (0.04) Bb
0.669 (0.005) Ba
Colgate Total
Advanced Whitening
0.11 (0.01) Aa
0.25 (0.09) Ba
0.669 (0.004) Aa
Colgate Whitening
Oxygen Bubbles
0.10 (0.01) Aa
0.25 (0.13) Ba
Different uppercase letters in rows and lowercase letters in columns
indicate statistically significant differences ( P < 0.05).
also served as an integrating sphere that
maximized the collection of diffused light
inside the sphere. Reflectance was equalized arbitrarily at a wavelength of 600 nm
(reflectance = 1:600 nm), indicating that
numerical values represented arbitrary
units rather than absolute reflectance.
Test samples were measured 4 times.
Surface roughness tests were performed
with a roughness tester (Surftest SL-201,
Mitutoyo America Corporation). Three
measurements were taken at the center of
each specimen in different directions. The
cut-off surface roughness value was 0.25
mm and the sampling length for each
measurement was 0.75 mm. The average
surface roughness (Ra) value was obtained
for each specimen.
Toothbrush test
Three dentifrices were tested in this study.
One contained calcium peroxide (Colgate
Whitening Oxygen Bubbles, ColgatePalmolive Company), while the other 2,
Colgate Total Advanced Clean (ColgatePalmolive Company) and Colgate Total
Advanced Whitening (Colgate-Palmolive
Company), were used as controls
(Table 1). After roughness and color
assessments, the specimens were brushed
using a mechanical device equipped with
10 soft bristle toothbrush heads (ColgatePalmolive Company) containing dentifrice
slurry. The machine was set to brush at a
rate of 60 reciprocal strokes per minute
and to generate a vertical load of 200 g
against the specimens. The specimens
were submerged statically during brushing
by inserting 150 ml of dentifrice slurry
(100 ml of deionized water and 50 g of
General Dentistry
After brushing
Colgate Total
Advanced Clean
Different uppercase letters in rows and lowercase letters in columns
indicate statistically significant differences ( P < 0.05).
prepared from the labial to lingual aspects.
The enamel samples were embedded
in a chemically cured resin, leaving the
exposed buccal surface to be smoothed by
a polishing machine (LaboPol-21, Struers,
Inc.). Aluminum oxide disks were used in
sequential grit sizes of 400, 600, and 1200.
A final polishing was accomplished with
a felt cloth containing a diamond paste in
a polishing machine (Ecomet 3, Buehler).
These procedures were performed to obtain
homogeneous surfaces for treatment.
Before brushing
Aa
Ba
www.agd.org
dentifrice) into the slurry bath. The total
brushing time was 10 hours, the equivalent of 20,000 cycles.6 Every 200 double
strokes was accompanied by 20 ml of
renewed slurry dispensed into the slurry
bath. The toothbrushes were replaced after
10,000 double strokes. The samples were
rinsed with deionized water and cleaned
ultrasonically for 10 minutes before
recording mean reflectance and Ra values,
as described previously.
Descriptive statistics data—including
means and standard deviation—were
calculated for each experimental group.
One-way ANOVA with repeated measurements and Tukey multicomparison tests
were used to compare the mean reflectance
and Ra values between the groups. The
significance level for all statistical tests
was set at 5%. All data were entered and
analyzed by SAS software 9.1 for Windows
(SAS Institute, Inc.).
Results
Color
The mean reflectance values are listed in
Table 2. Statistically similar values were
found between dentifrices either before
or after brushing. However, only Colgate
Whitening Oxygen Bubbles provided
increased reflectance values after brushing.
The control dentifrices saw a decrease in
enamel reflectance.
Roughness
All the Ra values are listed in Table 3. The
samples presented similar Ra values before
brushing. All tested dentifrices produced
increased Ra values, with Colgate Total
Advanced Whitening and Colgate
Whitening Oxygen Bubbles yielding the
highest Ra mean values.
Discussion
Based on the findings of this study, both
null hypotheses were rejected. Although
each dentifrice tested showed increased
enamel Ra values after brushing, the dentifrice containing calcium peroxide demonstrated some bleaching potential.
Currently, tooth color is measured
using a wide range of measurement
methods, divided into subjective (visual)
and objective (instrumental) assessments.7 Instrumental measurement
devices—such as reflectance spectrophotometers, colorimeters, and digital image
analysis systems (including quantitative
light-induced fluorescence)— are supplementary adjuncts to visual evaluation
of tooth color. The primary difference
is that spectrophotometers measure the
reflectance of light within the entire
visible spectrum, whereas colorimeters
only evaluate the reflected light through
3 wavelengths: red, green, and blue.8 In
addition, reflectance spectrophotometry
has given reproducible results when
measuring small changes in tooth color.9
Since the samples treated with the dentifrice containing calcium peroxide demonstrated statistically higher reflectance
values, it is likely that this whitening
dentifrice was the only one in the present
study capable of bleaching teeth.
As stated previously, calcium peroxide released oxygen ions slowly, thus
maintaining high levels of oxygen inside
the teeth, which is capable of breaking
long-chained, dark-colored chromophore
molecules into smaller, lightly colored,
and more diffusible molecules.4 This transition is necessary to provide the tooth
with a “brightened” appearance.5
External factors such as surface morphology can affect the amount and type
of reflection. The rough surface of the
enamel after brushing results in a diffuse
scattered reflection. All dentifrices have
varying degrees of enamel roughness. All
3 of the dentifrices used in the present
study contained abrasives that could have
promoted alterations in enamel. However,
there was no decrease in reflectance after
brushing with the dentifrice containing calcium peroxide (Colgate Oxygen
Bubbles). In this sense, it is reasonable to
assume that calcium peroxide might have
provided the enamel with a clear color
(resulting in increased light reflectance),
regardless of surface roughness. Also, the
fact that the dentifrice containing the
chemical agent calcium peroxide promoted the highest Ra values indicates that
this agent worked in association with the
abrasive found in the dentifrice. However,
further studies should investigate if saliva
could revert roughness alterations without
compromising the bleaching potential of
dentifrices containing calcium peroxide.
Conclusion
Although all 3 dentifrices changed the
surface roughness of the enamel samples in
this in vitro study, only the dentifrice containing calcium peroxide showed increased
reflectance values.
Author information
Dr. Feitosa is a doctoral candidate,
Department of Restorative Dentistry,
Pernambuco School of Dentistry,
University of Pernambuco, Camaragibe,
Brazil, where Drs. Braz, Santos,
and Montes are associate professors.
Dr. Araujo is an associate professor,
Department of Biomedical Sciences,
Federal University of Pernambuco, Recife,
Brazil. Dr. Borges is an associate professor, Department of Dentistry, Federal
University of Rio Grande do Norte,
Natal, Brazil. Dr. Pinheiro is an assistant
professor, Division of Orthodontics,
University of Manitoba, Winnipeg,
Canada. Dr. Duarte is an associate professor, Department of Restorative Dentistry,
Federal University of Paraíba, Joao
Pessoa, Brazil.
www.agd.org
Acknowledgments
This study was supported by the Brazilian
Federal Agency for the Support and
Evaluation of Graduate Education
(CAPES) and the National Institute of
Science and Technology Photonics (INCT
Fotonica CNPq), Brazil.
Disclaimer
References
1. Joiner A, Pickles MJ, Lynch S, Cox TF. The measurement
of enamel wear by four toothpastes. Int Dent J. 2008;
58(1):23-28.
2. Joiner A. Whitening toothpastes: a review of the literature. J Dent. 2010;38(Suppl 2):e7-e24.
3. Joiner A. The bleaching of teeth: a review of the literature. J Dent. 2006;34(7):412-419.
4. Huang JJ, Li YH, Sun JM, Li N. Municipal river sediment
remediation with calcium nitrate, polyaluminium chloride and calcium peroxide compound. Adv Mat Res.
2012;396-398:1899-1904.
5. Plotino G, Buono L, Grande NM, Pameijer CH, Somma
F. Nonvital tooth bleaching: a review of the literature
and clinical procedures. J Endod. 2008;34(4):394-407.
6. Belli R, Rahiotis C, Schubert EW, Baratieri LN, Petschelt
A, Lohbauer U. Wear and morphology of infiltrated
white spot lesions. J Dent. 2011;39(5):376-385.
7. Brook AH, Smith RN, Lath DJ. The clinical measurement of tooth colour and stain. Int Dent J. 2007;57(5):
324-330.
8. Karamouzos A, Papadopoulos MA, Kolokithas G, Athanasiou AE. Precision of in vivo spectrophotometric colour evaluation of natural teeth. J Oral Rehabil. 2007;
34(8):613-621.
9. Lenhard M. Assessing tooth colour change after repeated bleaching in vitro with a 10 percent carbamide
peroxide gel. J Aust Dent Soc. 1996;127(11):16181624.
Manufacturers
Buehler, Lake Bluff, IL
800.283.4537, www.buehler.com
Colgate-Palmolive Company, New York, NY
800.226.4283, colgate.com
Mitutoyo America Corporation, Elk Grove Village, IL
888.648.8869, www.mitutoyo.com
Ocean Optics, Dundein, FL
727.733.2447, oceanoptics.com
SAS Institute, Inc., Cary, NC
800.727.0025, www.sas.com
Struers, Inc., Westerville, OH
440.871.0071, www.struers.com
General Dentistry
e11
Obturation Techniques
Apical plug technique in a calcified
immature tooth: a case report
Kumar Raghav Gujjar, MDS n Ratika Sharma, MDS n Amith H.V., MDS n Smitha Amith, MDS n Indushekar K.R., MDS
Traumatic injury to an immature tooth may result in pulpal necrosis secondary to pulp canal obliteration, which makes the management of the
tooth a clinical challenge for dentists. The present case report describes
an innovative apical plug technique with mineral trioxide aggregate in a
calcified immature tooth using an ultrasonic tip and long, thin, tapered
E
pidemiological studies show that
11.6%-33.0% of boys and 3.6%19.3% of girls suffer dental trauma
of varying severity before the age of 12
years.1-3 Studies indicate that approximately 3.8%-24.0% of traumatized teeth
can develop varying degrees of pulp space
obliteration, which develops into pulpal
necrosis in 1%-16% of reported cases.4
Calcific obliteration of the pulp canal
space may happen after a severe traumatic
injury to immature permanent teeth.5
In such a scenario, the pulp becomes
necrotic, leading to the formation of a
periapical lesion around a wide-open apex.
These conditions present the following
endodontic challenges to a dentist: a partial or complete obliteration of the pulp
canal space, causing difficulty in accomplishing root canal treatment; or a periapical lesion with an open apex, potentially
preventing a hermetic apical seal with
conventional root canal treatment.6
Treatment options in such a situation
are either extraction or apicoectomy. There
is little research found in the literature on
the management of symptomatic young
permanent teeth with calcific metamorphosis. The present case report describes a
novel technique of gaining access through
the calcified root canal in a nonvital young
permanent upper central incisor followed
by apical plugging with mineral trioxide
aggregate (MTA).
Case report
A 10-year-old boy reported to the Department of Pediatric Dentistry, Seema Dental
College, Rishikesh, India, with severe
pain and swelling in the upper front
region of the jaw which had persisted for
2 days. The pain, which preceded the
e12
fissure burs. The technique was proven to be successful clinically and
radiographically at 2 years postobturation.
swelling, was continuous and severe with
resultant sleep disturbance. The swelling had appeared a day after the onset of
pain. The patient’s medical history was
noncontributory; however, his dental history revealed trauma in the upper front
region of the jaw 6 months prior via a
contact sports incident. The child had
reported to a general dentist with a broken
coronal tooth fragment and no evidence
of any displacement. Since there was no
pulp exposure, the dentist reattached the
fractured coronal tooth fragment and the
procedure was uneventful. After 6 months,
the child reported to the dentist again with
pain and swelling, and an unsuccessful
attempt was made to drain the abscess
through the root canal. The child was then
referred to the Department of Pediatric
Dentistry. The patient was febrile, and
intraoral examination showed obliteration
of the upper labial vestibule on the right
side. The permanent upper right central
incisor was extremely tender to touch and
slightly labially proclined. It showed a
yellowish discoloration in the reattached
coronal fracture fragment. The rest of the
dentition was deemed healthy.
An intraoral periapical radiograph
of the permanent upper right central
incisor region revealed the reattached
coronal fracture fragment, an attempted
endodontic access cavity preparation, loss
of lamina dura at the periapical region,
an open apex, and calcific obliteration of
the coronal pulp chamber and the cervical and middle thirds of the radicular
pulp chamber (Fig. 1). The tooth did not
respond to sensitivity tests. Clinical and
radiographic examination indicated acute
periapical abscess in the permanent upper
right central incisor.
General Dentistry
www.agd.org
A decision was made to facilitate
drainage of the abscess in the maxillary
upper right central incisor through the
root canal, followed by apical plugging
with MTA. An informed consent for
the treatment procedure was obtained
from the parents with due warning of
the risks involved, especially the risk
of perforation while gaining access
to the root canal.
Following anesthesia, access to the
apical third of the root canal was established using gentle brushing strokes
with thin, long, tapered fissure burs
(Mani, Inc.) and a long thin ultrasonic
tip (Satelec-ET20 tip, Acteon North
America) in a direction parallel to the
long axis of the tooth at the crosssectional midpoint of the root canal
to prevent perforation. A Glyde File
Prep (DENTSPLY Maillefer) was used
intermittently between instrumentation
as a chelating agent. Penetration was
continued using an endodontic explorer
to locate the orifice. A No. 8 file was
used in an attempt to negotiate the
canal. Access to the apical third of the
root canal was successfully established.
A radiograph was obtained and the estimated working length was established
as 24.5 mm. The canal was sequentially
widened by a Hedstrom file to size 30,
and the abscess was drained through the
root canal. The access cavity was sealed
with a cotton dressing. The authors
found this cautious technique useful as
it minimized the risk of perforation. The
child was prescribed a course of amoxicillin capsules 250 mg tid for 5 days, metronidazole tablets 200 mg tid for 5 days,
and ibuprofen 200 mg/paracetomol
tablets 125 mg tid for 3 days.
Fig. 1. Preoperative radiograph of the permanent
upper right central incisor.
Fig. 2. Radiograph of permanent upper
right central incisor after obturation.
The patient was assessed every 24 hours,
and the canal cleansed with endodontic
files so as to facilitate drainage. After
72 hrs, the canal of the asymptomatic
tooth was sequentially widened with
a size 60 file, and filled with Metapex
(META-BIOMED US Corporation) as an
intracanal medicament. Two weeks later,
the tooth was irrigated with saline and the
Glyde File Prep was used to remove any
remnants of Metapex and the smear layer.
After drying the canal, white MTA powder
(DENTSPLY Tulsa Dental Specialties) was
mixed with the provided water ampule per
the manufacturer’s instructions. The mix
was then placed in the canal with an amalgam carrier and packed to form an apical
plug of approximately 5 mm. A moist
cotton pellet was placed over the apical
plug and the access cavity was sealed. The
next day, the cotton pellet was removed
and the canal thoroughly dried with
absorbent points. An endodontic plugger
was used to check the consistency of the
MTA and to ensure it had completely
set. Subsequently, a backfill was performed using gutta percha (DENTSPLY
Maillefer) by cold compaction method. A
postobturation radiograph confirmed the
completion of endodontic therapy (Fig. 2).
Figure 3 shows the success of the treatment at 2 years postobturation.
Discussion
Fig. 3. Radiograph of permanent
upper right central incisor showing
evidence of healing in the periapical
region 2 years postobturation.
Fischer first indicated in 1974 that calcific
metamorphosis (CM) was a response to
trauma presenting progressive hard tissue
formation with maintenance of vital
tissue and a pulp space observed up to the
apical foramen.7 Fischer argued that such
cases require root canal treatment because
of reduced cellular content leading to
decreased ability for healing, thereby predisposing the pulpal tissue to infection.
The mechanism of hard tissue formation during CM is not yet clear, although
several hypotheses have been proposed
to explain this phenomenon. Torneck
hypothesized that the deposition of hard
tissue was either a result of stimulation of
the preexisting odontoblasts or by loss of
their regulatory mechanisms.8 Andreasen
& Andreasen described CM as a response
to a severe injury to the neurovascular
supply of the pulp, which after healing,
leads to accelerated dentin deposition,
which in turn is closely related to the
loss and reestablishment of the pulpal
neural supply.9 Ten Cate identified this
process as the deposition of tertiary or
reparative dentin in response to irritation or trauma.10 Reparative odontoblasts
are somehow able to differentiate from
dental pulp cells in the absence of any
epithelial influence.10 Subodontoblast
www.agd.org
cells under certain influences differentiate
into odontoblast-like cells and deposit
dentin-like hard tissue.10 Reparative dentin
or tertiary dentin is deposited at specific
sites in response to injury, and the rate
of deposition depends on the degree of
injury.10 With an increase in severity of
injury, there is a rapid rate of dentin deposition, possibly as much as 3.5 mm/day.10
The accelerated hard tissue formation traps
some pulpal cells and gives the histological
appearance of osteodentin with an irregular
tubular pattern. Evidence indicates that
reparative dentin is produced by odontoblast-like cells and incorporates type I and
III collagen in its matrix, which exhibits
diminished phosphophoryn content.10
Neither of the above mechanisms described
has been proven, therefore further investigation is required to provide an evidencebased understanding of this occurrence.
In the treatment of calcified canals, a
total occlusion at any level of the canal
space is a common finding.11 Smith
performed a literature review and found
that teeth with calcific metamorphosis
had a 0%-16% incidence of periapical
pathosis development.12
Teeth with CM fall into the high difficulty category of the Endodontic Case
Difficulty Assessment proposed by the
American Association of Endodontists, and
General Dentistry
e13
Obturation Techniques Apical plug technique in a calcified immature tooth: a case report
it has been suggested that achieving a predictable outcome will be challenging for
even experienced practitioners.13
The obliteration of the root canal
complicates endodontic treatment of a
symptomatic nonvital tooth. Traditionally,
the treatment in such cases involves either
extraction or apicoectomy. An early loss of
teeth, particularly in the anterior region of
the maxilla, is associated with numerous
problems. Poor esthetics, psychological
trauma, phonetic problems, and malocclusion are potential consequences. The
possibilities of prosthetic restoration during
childhood are restricted. Apicoectomy
involves a surgical retrograde approach
to access the apical portion of the tooth.
Along with the obvious risks of the surgical
procedure, there is a concomitant reduction
in the crown to root ratio, potentially causing psychological trauma if performed at an
early age, along with the inability to obtain
an appropriate apical seal if performed in
young permanent teeth. Therefore, choosing an orthograde technique in such cases
may prove to be a better option.
In the past, the treatment of choice in
an immature tooth with an open apex was
to achieve an apical closure by the apexification technique using long-term calcium
hydroxide dressings. Successful apexification depends on the formation of a hard
tissue barrier by cells that migrate from
the periradicular tissues to the apex and
differentiate under the influence of specific
cellular signals to cells capable of secreting
an organic matrix consisting of cementum
or osteodentine.14 However, the placement
of calcium hydroxide has potential disadvantages, including the variability of treatment time (3-21 months), unpredictability
of apical closure, difficulty in patient
follow-up, and delayed treatment.15,16 The
duration depends on factors such as the
diameters of the open apices, the degree
of tooth displacement by trauma, and
the method used for tooth repositioning.
During the apexification procedure, the
root canal is susceptible to reinfection
because of the temporary coronal seal.
The affected tooth is also susceptible to
fracture.17 Rosenberg et al investigated
the effect of calcium hydroxide on the
microtensile fracture strength of extracted
human permanent maxillary incisors and
reported severe decreases in the dentine
fracture strength (23.0%-43.9%).18
e14
An alternative for the multi-appointment
apexification procedure is a single-step
technique by means of an apical barrier.
Several materials, such as tricalcium
phosphate, calcium hydroxide, collagen
calcium phosphate, osteogenic protein-1,
bone growth factor, and MTA have been
proposed for use as apical barriers, and
their biocompatibility and osteogenic
potential have been demonstrated.19-21 In
1999, Torabinejad & Chivian introduced
the use of MTA as an apical plug.22 The
final setting time of MTA is approximately 3 hours; the pH directly after
mixing is 12.5.23 The main compounds
of MTA are tricalcium silicate, tricalcium
aluminate, tricalcium oxide, silicate oxide,
and other mineral oxides; bismuth oxide
is also added to increase the radiopacity
of the compound.24
MTA shows good sealing ability, good
marginal adaptation, a reasonable setting
time, and a high degree of biocompatibility.16 The 2 important contributors
for the favorable biologic response
stimulated by MTA in human periapical
tissues are bone morphogenetic protein-2
and transforming growth factor β1.25
The stimulation of interleukin production by MTA may allow for the overgrowth of cementum and facilitate the
regeneration of the periodontal ligament
and formation of bone.26 In the present
case, advanced osseous healing of the
periapical lesions was evident as early as
6 months after placement of the MTA
apical plug.
Contemporary data suggest that
MTA can be successfully used as an
apical barrier in teeth with necrotic
pulps and open apexes. Additional
investigations are needed to prove its
long-term efﬁcacy.16
This case confirmed that MTA acts
as an apical barrier and can be considered a very effective material to support
regeneration of the periapical tissue in a
young permanent tooth with an infected
root canal. Clinical and radiographic
follow-ups showed healing of the apical
area of the affected tooth. The main
advantage of the single-step procedure
for the treatment of pulpless teeth with
immature roots is the high predictability
of apical closure and the reduction of
treatment time, number of appointments,
and radiographs.
General Dentistry
www.agd.org
The inherent disadvantage of both the
traditional apexification with calcium
hydroxide and the artificial apical barrier
with MTA is that neither technique allows
for further root development in terms
of thickening of the root canal walls or
continued root formation. Recently, new
promising concepts aimed at revascularisation of the necrotic pulp of such teeth
have been advocated.27-29
Revascularization has been considered
a better option for dealing with an immature tooth with a nonvital pulp—even in
cases with severe periapical infection.28,30
This alternative method seems to have the
potential for increasing the root length and
thickness of root canal walls of nonvital
immature teeth, assisted by blood clotting
and a collagen-enhanced matrix. From this
perspective, it has been recently proposed
that apexification may not be needed in
the near future.29 Nevertheless, controlled
clinical studies to demonstrate that the
revascularization method can replace
established treatment protocols based on
calcium hydroxide or MTA are warranted.
Summary
Approximately 3.8%-24.0% of traumatized
teeth develop varying degrees of calcific
metamorphosis. Although there are different opinions on the management of pulps
exhibiting canal obliteration, studies indicate
that the incidence of pulpal necrosis in these
teeth is between 1% and 16%. Endodontic
treatment of a symptomatic nonvital young
permanent tooth with a calcified canal is a
clinical challenge to dentists who work with
pediatric patients. The authors found that
the cautious technique that was used to gain
access through the calcified canal was valuable in this case, as it minimized the risk of
perforation. This technique also confirmed
that MTA acts as an apical barrier and can
be considered a very effective material to
support regeneration of the periapical tissue
in a tooth with an infected root canal and
an open apex. Sound knowledge of tooth
morphology, coupled with meticulous
technique and patience, are the secrets of
success in this type of situation.
The meticulous orthograde technique
employed in the present case in gaining access through the calcified canal of
a young permanent tooth could be of
immense benefit to any dentist who works
with pediatric patients.
Author information
Dr. Gujjar is a senior lecturer, Pediatric
Dentistry, Faculty of Dentistry SEGi
University, Malaysia. Dr. Sharma is a
senior lecturer, Department of Public
Health Dentistry, M.N.R Dental
College, Hyderabad, India. Dr. Amith
H.V. is a reader/associate professor,
Department of Community Dentistry,
People’s College of Dental Sciences,
Bhopal, Madhya Pradesh, India, where
Dr. S. Amith is a postgraduate trainee
in Oral & Maxillofacial Pathology,
Department of Oral & Maxillofacial
Pathology. Dr. Indushekar is the director
of Postgraduate Studies, and department head, Pedodontics & Preventive
Dentistry, Sudha Rustagi College of
Dental Sciences & Research, Faridabad,
Haryana, India.
References
1. Clarkson BH, Longhurst P, Sheiham A. The prevalence
of injured anterior teeth in English school children and
adults. J Dent Child. 1973;4(1):21-24.
2. Jarvinen S. Fractured and avulsed permanent incisors
in Finnish children. A retrospective study. Acta Odontol
Scand. 1979;37(1):47-50.
3. Baghdady VS, Ghose LJ, Enke H. Traumatized anterior
teeth in Iraqi and Sudanese children—a comparative
study. J Dent Res. 1981;60(3):677-680.
4. Amir FA, Gutmann JL, Witherspoon DE. Calcific metamorphosis: a challenge in endodontic diagnosis and
treatment. Quintessence Int. 2001;32(6):447-455.
5. Heling I, Slutzky-Goldberg I, Lustmann J, Ehrlich Y,
Becker A. Bone-like tissue growth in the root canal of
immature permanent teeth after traumatic injuries.
Endod Dent Traumatol. 2000;16(6):298-303.
6. Ngeow WC, Thong YL. Gaining access through a calcified pulp chamber: a clinical challenge. Int Endod J.
1998;31(5):367-371.
7. Fischer C. Hard tissue formation of the pulp in relation
to treatment of traumatic injuries. Int Dent J. 1974;
24(3):387-396.
8. Torneck C. The clinical significance and management
of calcific pulp obliteration. Alpha Omegan. 1990;
83(4):50-54.
9. Andreasen J, Andreasen F. Textbook and Color Atlas
of Traumatic Injuries to Teeth. 3rd ed. Copenhagen:
Munksgaard; 1994.
10. Ten Cate AR. Oral Histology: Development, Structure,
and Function. 5th ed. St Louis: Mosby; 1998.
11. Gutmann J.L, Dumsha T.C, Lovdahl P.E, Hovland E.J.
Problem Solving in Endodontics: Prevention, Identification and Management. 3rd ed. St. Louis: Mosby; 1997.
12. Smith JW. Calcific metamorphosis: a treatment dilemma. Oral Surg Oral Med Oral Pathol. 1982;54(4):
441-444.
13. American Association of Endodontics. AAE Endodontic
Case Difficulty Assessment Form and Guidelines. Available at: http://www.aae.org/uploadedfiles/dental_
professionals/endodontic_case_assessment/2006case
difficultyassessmentformb_edited2010.pdf. Accessed
October 9, 2014.
14. Ripamonti U, Reddi AH. Tissue engineering, morphogenesis, and regeneration of the periodontal tissues by
bone morphogenetic proteins. Crit Rev Oral Biol Med.
1997;8(2):154-163.
15. Metzger Z, Solomonov M, Mass E. Calcium hydroxide
retention in wide root canals with flaring apices. Dent
Traumatol. 2001;17(2):86-92.
16. Giuliani V, Baccetti T, Pace R, Pagavino G. The use of
MTA in teeth with necrotic pulps and open apices.
Dent Traumatol. 2002;18(4):217-221.
17. Andreasen JO, Farik B, Munksgaard EC. Long-term calcium hydroxide as a root canal dressing may increase risk
of root fracture. Dent Traumatol. 2002;18(3):134-137.
18. Rosenberg B, Murray PE, Namerow K. The effect of
calcium hydroxide filling on dentine fracture strength.
Dent Traumatol. 2007;23(1):26-29.
19. Roberts SC Jr, Brilliant JD. Tricalcium phosphate as an
adjunct to apical closure in pulpless permanent teeth.
J Endod. 1975;1(8):263-269.
20. Michanowicz JP, Michanowicz AE. A conservative approach and procedure to fill an incompletely formed
root using calcium hydroxide as an adjunct. J Dent
Child. 1967;34(1):42-47.
www.agd.org
21. Nevins A, Finkelstein F, Laporta R, Borden BG. Induction of hard tissue into pulpless open-apex teeth using
collagen-calcium phosphate gel. J Endod. 1978;4(3):
76-81.
22. Torabinejad M, Chivian N. Clinical applications of mineral trioxide aggregate. J Endod. 1999;25(3):197-205.
23. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR.
Physical and chemical properties of a new root-end
filling material. J Endod. 1995;21(7):349-353.
24. Camilleri J, Montesin FE, Brady K, Sweeney R, Curtis
RV, Ford TR. The constitution of mineral trioxide aggregate. Dent Mater. 2005;21(4):297-303.
25. Guven G, Cehreli ZC, Ural A, Serdar MA, Basak F.
Effect of mineral trioxide aggregate cements on
transforming growth factor beta1 and bone morphogenetic protein production by human fibroblasts in
vitro. J Endod. 2007;33(4):447-450.
26. Al-Rabeah E, Perinpanayagam H, MacFarland D. Human alveolar bone cells interact with ProRoot and
tooth-colored MTA. J Endod. 2006;32(9):872-875.
27. Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: new treatment
protocol? J Endod. 2004;30(4):196-200.
28. Hargreaves KM, Geisler T, Henry M, Wang Y. Regeneration potential of the young permanent tooth: what does
the future hold? Pediatr Dent. 2008;30(3):253-260.
29. Huang GT. Apexification: the beginning of its end. Int
Endod J. 2009;42(10):855-866.
30. Huang GT. A paradigm shift in endodontic management of immature teeth: conservation of stem cells for
regeneration. J Dent. 2008;36(6):379-386.
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General Dentistry
e15
Central giant cell lesion: diagnosis to rehabilitation
Ana Carolina Amorim Pellicioli, DDS n Thieni Kaefer, DDS n Marco Antonio Trevizani Martins, DDS, PhD Vinicius Coelho Carrard, DDS, PhD n Manoela Domingues Martins, DDS, PhD
Central giant cell lesion (CGCL) is a benign bone lesion of unknown
etiology that primarily affects the mandible, with a predilection for female
children and young adults. This article describes a case of a 16-year-old
boy with a palatal swelling of approximately 18 months duration. Clinical,
radiographic, histopathological, and hematological examinations led to
a diagnosis of CGCL. Treatment involved a complete enucleation of the
lesion and the removal of several teeth. A subsequent esthetic/functional
C
entral giant cell lesion (CGCL) is a
benign bone lesion of unknown etiology.1,2 It was first described by Jeffe
in 1953.3,4 This lesion mainly affects children and young adults (<30 years of age),
with a predilection for the female gender.1-4
The mandible is the most common site
for CGCL, which accounts for <7% of all
benign lesions in gnathic bones.5
CGCL exhibits varying clinical behavior. Some lesions are asymptomatic and
demonstrate slow growth, whereas more
aggressive forms show rapid growth and
can cause pain, root resorption, tooth
mobility, perforation of the bone cortex,
and paresthesia.6,7 Histologically, CGCL
consists of a proliferation of fusiform
cells in a collagenized stroma interwoven
with multinucleated giant cells.3 Since
other conditions (such as cherubism and
brown tumor of hyperparathyroidism)
can resemble CGCL histologically and
radiographically, CGCL is diagnosed
through a combination of clinical,
histological, radiographic, and hematological examinations.3,5
rehabilitation was performed using a removable prosthesis. The patient
was submitted to rigorous clinical and radiographic follow-ups, with no
signs of recurrence over a 7-year period.
Received: October 8, 2012
Accepted: March 4, 2013
Key words: central giant cell lesion, oral rehabilitation, proliferative lesion
Treatment options range from nonsurgical options to curettage and en bloc
resection.8 The latter is the treatment of
choice for more aggressive cases, due to
the high rate of recurrence (13%-49%).9
Nonsurgical treatment options include calcitonin injections, intralesion injections of
corticosteroids, and subcutaneous injections
of α-interferon.1,10,11
This article describes the case of a
CGCL in the jaw of a 16-year-old boy and
discusses the histopathological, clinical,
radiological, and therapeutic features as
seen in the literature. Patient management
after lesion removal (including prosthetic
rehabilitation) is discussed also.
No. 12-15 (Fig. 1). A pulp vitality test was
positive for all the teeth in question.
Panoramic, occlusal, and periapical
radiographic examinations revealed a
well-defined, unilocular radiolucent
image at the periapex of teeth No. 12-15,
measuring 4 x 3 cm at its largest diameter
(Fig. 2). Computed tomography of the
patient’s face revealed an expansive lesion
in the right maxilla causing bone destruction of the nasal fossa, maxillary sinus, and
outer bone cortex (Fig. 3).
Case report
A 16-year-old boy sought treatment
for swelling in the roof of his mouth.
The swelling had started approximately
18 months earlier, and the patient reported
no pain. An intraoral examination revealed
an expansive growth in the maxilla covered
by intact mucosa (with elastic consistency
upon palpation) and mobility of teeth
Fig. 1. Photograph showing anterior view of a central
giant cell lesion (CGCL) with expansive growth in the
maxilla of a 16-year-old boy.
Fig. 2. Radiographs revealing a well-defined, unilocular radiolucent image in the right maxilla. Left. Panoramic view. Center. Occlusal view. Right. Periapical view.
e16
General Dentistry
www.agd.org
Fig. 3. Computed tomography showing an expansive lesion that is destroying adjacent bone
structures. Left. Coronal view. Right. Facial view.
Fig. 5. Photograph of teeth No. 12-15 postextraction.
The clinical and imaging examinations led to the differential diagnoses
of ameloblastoma, keratocystic odontogenic tumor, or CGCL. Calcium and
phosphorus levels were normal, which
eliminated the diagnosis of hyperparathyroidism. An incisional biopsy was
performed and the material was sent for
histopathological analysis. This analysis
revealed a proliferation of fusiform
cells with a voluminous nucleus in a
collagenized stroma interwoven with
multinucleated giant cells and sites of
hemorrhage. The histopatholological
diagnosis was CGCL (Fig. 4).
Treatment consisted of the complete
enucleation of the lesion under general
anesthesia, for which it was necessary
to remove teeth No. 12-15 (Fig. 5-7).
Initially, a temporary removable partial
denture (RPD) was made of a flexible
material; later, a permanent metallic RPD
was used for esthetic/functional rehabilitation (Fig. 8 and 9). The patient underwent
a rigorous clinical and radiographic followup period of 7 years, during which no
signs of recurrence were noted (Fig. 10).
Fig. 4. Histopathology slide revealing a proliferation of
fusiform cells in a collagenized stroma interwoven with
multinucleated giant cells (H&E, magnification 400X).
Fig. 6. Anterior radiograph of the patient after the
extraction of teeth No. 12-15.
Fig. 7. Anterior photograph showing where the teeth
were extracted.
Fig. 8. The removable partial denture (RPD) used for
patient esthetic/functional rehabilitation.
Fig. 9. Photograph of patient’s smile with the RPD.
Fig. 10. A panoramic radiograph taken 7 years post-treatment showing no signs of recurrence.
www.agd.org
General Dentistry
e17
Diagnosis and Treatment Planning Central giant cell lesion: diagnosis to rehabilitation
Discussion
The World Health Organization recently
defined CGCL as a localized benign lesion
(manifesting at times as an aggressive proliferative osteolytic lesion) that is formed
by fibrous conjunctive tissue containing
multinucleated giant cells, hemorrhage
and hemosiderin deposits, and areas of
bone formation.12 The etiopathogenesis of
CGCL is not yet well-established; however, it has been suggested that the lesion
develops due to an exacerbated repair process following trauma or hemorrhage.13,14
CGCL is a benign lesion that is divided
clinically and radiographically into
2 subtypes: aggressive and nonaggressive.4,9
The aggressive type is more common
among young patients; it exhibits fast
growth, perforation of the bone cortex, root
resorption, pain, and a tendency toward
recurrence.4,9 The nonaggressive type generally is asymptomatic, exhibiting slow growth
with no bone or root resorption and a
low incidence of recurrence.4,9 It has been
suggested that larger lesions with a greater
area of multinucleated giant cells are more
aggressive.15,16 The present case involved an
expansive lesion with slow growth (>1 year)
and well-defined edges. These symptoms
suggest the lesion was nonaggressive, which
was indicated by the lack of recurrence over
the 7-year follow-up period.
A conclusive diagnosis of CGCL
requires a combination of clinical, radiographic, and histological examinations.3
The histopathological aspects of 2 other
conditions (cherubism and brown tumor
of hyperparathyroidism) are identical to
those of CGCL.17 To discard the possibility of parathyroid abnormalities, which
require different therapeutic management,
cases of suspected CGCL should be submitted to hematological examinations so
that calcium, alkaline phosphatase, phosphorus, and parathyroid hormone levels
may be assessed.1,4 For cases involving the
mandible, it is necessary to determine
whether the lesion is singular or bilateral,
as cherubism is characterized in young
patients by osteolytic lesions on both sides
of the mandible.18
Whitaker & Waldron reported a mean
interval of 21 months between treatment
and recurrence, with rare cases of recurrence more than 2 years following initial
treatment.19 The main factors associated with recurrence are clinical lesion
e18
activity (72% of aggressive lesions recur,
whereas only 3% of nonaggressive lesions
recur), patient age, perforation of the
bone cortex, and tumor size.20-22 In the
present case, the patient showed no signs
of recurrence during a 7-year follow-up
period that involved rigorous clinical and
radiographic examinations.
A number of therapies for treating
CGCL— including the intralesion injection of corticosteroids and calcitonin—
have been studied as ways to complement
or reduce the extent of surgical resection.1
Calcitonin use is based on an immunohistochemical study that demonstrated
that the giant cells in this lesion are
osteoclasts.23 Harris presented 4 cases that
responded positively to calcitonin.24 Using
calcitonin as a complementary treatment
for the aggressive form of the lesion
reduces the chances of sequelae.1 In the
present case, the lesion was extensive and
involved several teeth; using calcitonin
prior to surgery may have reduced the size
of the tumor, thereby making the resection less extensive.
Extensive, more aggressive, or recurring lesions require ample surgical resection, which may lead to a substantial
bone defect and the loss of several teeth,
affecting both esthetics and function.9,25
Maxillary defects can be challenging
from the standpoint of rehabilitation.
Prosthetic rehabilitation after the surgical resection of such lesions in the maxilla is performed to close the bone defect,
separate the nasal passage from the oral
cavity, and reestablish the patient’s ability to chew, speak, and swallow.26 In the
present case, complete enucleation of the
lesion required removing several teeth
and making a temporary RPD, followed
by a definitive denture for esthetic/functional rehabilitation.
Conclusion
Dentists play an important role in both
the diagnosis of CGCL and its treatment,
which involves the removal of the lesion
and the reestablishment of the functions of
the stomatognathic system.
Author information
Dr. Pellicioli is a master’s candidate,
Department of Oral Pathology, Dental
School, Federal University of Rio Grande
do Sul, Porto Alegre, Brazil, where Drs.
General Dentistry
www.agd.org
Marco Martins, Carrard, and Manoela
Martins are assistant professors. Dr. Kaefer
is a master’s candidate, Department of
Oral Pathology, School of Dentistry,
Federal University of Santa Maria, Brazil.
References
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Central giant cell lesions of the jaws: a clinicopathologic study. J Oral Maxillofac Surg. 1986;44(9):708713.
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2001;9(3):189-200.
17. Motamedi MH, Eshghyar N, Jafari SM, et al. Peripheral
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18. Chavali LV, Bhimalingam RM, Sudhakar PV.
Cherubism—a case report with long term follow up.
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20. Kruse-Losler B, Diallo R, Gaertner C, Mischke KL, Joos
U, Kleinheinz J. Central giant cell granuloma of the
jaws: a clinical, radiologic, and histopathologic study
of 26 cases. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2006;101(3):346-354.
21. Minic A, Stajcic Z. Prognostic significance of cortical
perforation in the recurrence of central giant cell granulomas of the jaws. J Craniomaxillofac Surg. 1996;
24(2):104-108.
22. Bataineh AB, Al-Khateeb T, Rawashdeh MA. The surgical treatment of central giant cell granuloma of the
mandible. J Oral Maxillofac Surg. 2002;60(7):756-761.
23. Flanagan AM, Tinkler SM, Horton MA, Williams DM,
Chambers TJ. The multinucleate cells in the giant cell
granulomas of the jaw are osteoclasts. Cancer. 1988;
62(6):1139-1145.
24. Harris M. Central giant cell granulomas of the jaws
regress with calcitonin therapy. Br J Oral Maxillofac
Surg. 1993;31(2):89-94.
25. Lee H, Ercoli C, Fantuzzo JJ, Girotto JA, Coniglio JU,
Palermo M. Oral rehabilitation of a 12-year-old patient
diagnosed with a central giant cell granuloma using a
fibula graft and an implant-supported prosthesis: a
clinical report. J Prosthet Dent. 2008;99(4):257-262.
26. Segal A. Rehabilitation of a maxillary defect secondary
to recurrent giant cell granuloma. J Prosthodont.
2011;20(Suppl 2):S32-S37.
www.agd.org
General Dentistry
e19
Alveolar ridge splitting for implant placement:
a review of the procedure and report of 3 cases
Prakash S. Talreja, MDS n Chandrashekhar R. Suvarna, BDS n Preeti P. Talreja, MDS
In long-standing edentulous cases, the alveolar bone generally
demonstrates vertical and horizontal atrophy. Rehabilitating
these patients with dental implants is difficult unless treatment
is accompanied by some kind of augmentation procedures, all of
which include specific disadvantages. One such technique, alveolar
ridge splitting, is suitable only for enhancing ridge width. It has the
advantage of reducing treatment time significantly, as implants can
E
be placed simultaneously. This article offers a brief description of the
procedure along with 3 case reports.
Received: January 30, 2013
Accepted: May 7, 2013
Key words: augmentation, ridge split,
implant, piezoelectric, osteotome, chisel
vidence has shown the success
of implant-based replacement of
missing teeth.1,2 However, rehabilitating patients with implants can
be impeded by horizontal and vertical
atrophy of the alveolar ridge, especially
in long-standing edentulous cases. In
such cases, alveolar ridge augmentation
is necessary for adequate insertion of
implants. Augmentation procedures
include block grafting, guided bone
regeneration, or distraction osteogenesis,
all of which have disadvantages, such
as increased treatment cost and time,
as well as surgical morbidity related
to second donor site. In recent years,
alveolar ridge splitting has been successfully used to prepare the atrophic maxilla
and mandible for implant insertion
and augmentation.1-4
Alveolar ridge splitting is suitable
only for enhancing the width of the
edentulous ridge. It is accomplished
by making a longitudinal osteotomy
Fig. 1. (Case No. 1) Reflection of a full thickness flap
to expose the narrow ridge.
Fig. 2. (Case No. 1) Using the piezoelectric saw to
create horizontal and vertical corticotomy.
Fig. 3. (Case No. 1) Using a tapered osteotome for
ridge expansion.
Fig. 4. (Case No. 1) Implants placed in the expanded
ridge.
e20
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Fig. 5. (Case No. 1) Placement of splinted porcelain-fused-to-metal
(PFM) crowns.
Fig. 6. (Case No. 2) Implant placed in the expanded
ridge.
Fig. 7. (Case No. 2) Placement of the PFM prosthesis.
in the atrophic alveolar bone, followed
by lateral repositioning of the buccal
cortex using a greenstick fracture.1 The
space created between the buccal and
lingual/palatal cortical plate is filled
with autologous, allogenic, or alloplastic
graft material—or without any graft
material.5-8 When used in the maxilla,
this technique results in significantly
reduced treatment time compared to
other options, as implants are generally
placed simultaneously along with the
ridge split. Alveolar ridge splitting is
well-suited for the maxilla, where the
medullary bone is soft and the cortical
bone is thin, which allows for easy
expansion of the buccal cortex.9 The
technique can be carried out in the
mandible as well, although the risk of
buccal plate fracture increases, as the
thicker cortical plate makes the bone
less flexible. Hence, in the mandible, a
staged approach is recommended.10
This article presents 3 cases, each of
which involved splitting a narrow alveolar ridge. In 2 cases, implants were placed
in the maxilla simultaneously; the third
case involved delayed implant placement
in the mandible. Clinical examination
of the cases revealed severe bone resorption of the edentulous area. The reduced
dimension of the alveolar bone was confirmed through a cone beam computed
tomography scan. The procedure was
explained to the patients and written
consents were obtained.
Originally, the ridge split technique
involved creating a sagittal osteotomy of
the edentulous ridge using instruments
(such as chisels) between the 2 cortical
plates to expand the ridge and allow
implant placement.1 Subsequently, various approaches to this procedure have
been developed.5,6,11-13
The technique used in the cases presented in this article involved the use of
a piezoelectric saw, small chisel, twist
drill, and tapered osteotomes to expand
the buccal plate as carefully as possible to
avoid its fracture. Threaded, self-tapping
Osstem implants (marketed in the US as
HIOSSEN Dental Implants, HIOSSEN,
Inc.) with resorbable blast media surface
were placed in predetermined osteotomies. Implants of any diameter and
length can be placed using this technique. However, if multiple implants are
placed adjacent to each other, splinting
of the implants in the final prosthesis is
recommended.
Case No. 1
A 45-year-old woman sought to replace
her missing maxillary left canine and
first premolar with dental implants. After
local anaesthesia was administered, a
crestal incision (slightly to the palatal
side) was made, followed by 2 diverging
vertical incisions on the line angles of the
neighboring teeth. A full-thickness mucoperiosteal flap was reflected to expose
the underlying bone. The palatal flap
was raised minimally to maintain blood
supply to the bone (Fig. 1).
Using a piezoelectric saw (Mectron
s.p.a.), rectangular corticotomies were
made. The crestal horizontal corticotomy
was made 1 to 2 mm from the adjacent
teeth (Fig. 2). Next, 2 vertical corticotomies were made on the buccal cortical
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plate, extending from the edges of the initial midcrestal corticotomy. The length of
the horizontal corticotomy is dictated by
the number of implants to be placed and
the distance between the implants, while
the length of the vertical corticotomy is
usually 50% of the length of the implant
to be placed.
Next, the buccal segmented plate was
slowly dislocated in the buccal direction
by placing a small chisel in the horizontal
corticotomy and striking it carefully with
a mallet. A twist drill was used to mark
the implant’s position and depth; tapered
osteotomes were then used to expand
the buccal plate to the required depth
(Fig. 3). Care was taken to follow the
path established by the twist drill in the
bone. A gentle, slow, rotating motion was
used to increase the separation of plates
by the osteotomes.
Two Osstem implants were placed with
good primary stability in the newly created osteotomies. The cover screws were
placed next (Fig. 4) and the implants
were submerged for undisturbed healing
for a period of 6 months. The widened
space between the cortical plates was
filled with a mix of autogenous bone
and alloplastic bone grafting material
(PerioGlas, NovaBone Products, LLC).
The periosteum was released on the
inner surface of the buccal flap, and the
tissue was approximated using 3-0 black
braided silk suture (Mersilk, Ethicon,
Inc.). The patient was instructed not to
wear any dentures or to place pressure on
the healing site.
Second stage surgery was performed 6
months later. The implants were exposed,
healing abutments were placed (with tissue
approximated around them) and allowed to
heal for 2 weeks. Subsequently, an implant
level impression was obtained, and splinted
porcelain-fused-to-metal (PFM) crowns
were delivered to the patient (Fig. 5).
Case No. 2
A 35-year-old man sought to replace his
missing maxillary left lateral incisor with
a dental implant. A procedure similar to
that described in the first case was performed and the implant was placed simultaneously with the split ridge (Fig. 6).
Second stage surgery was performed 6
months later; at that time, a PFM prosthesis was delivered (Fig. 7).
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e21
Diagnosis and Treatment Planning Alveolar ridge splitting for implant placement
Fig. 8. (Case No. 3) Photograph showing the missing
mandibular teeth, after an inferior horizontal
corticotomy and ridge expansion.
Fig. 9. (Case No. 3) Implants placed in the regenerated bone between the expanded cortical plates.
Fig. 10. (Case No. 3) Final implant-supported fixed
partial denture.
Case No. 3
surgery, which involved exposing the
implants, placing healing abutments,
and positioning an apically displaced
flap to increase the width of attached
gingiva around the implant. An implantsupported PFM fixed partial denture
was delivered after a healing period of 4
weeks (Fig. 10).
success rates of 86.2%-97.5%.14 A systematic review by Aghaloo & Moy calculated
a 97.4% survival rate for the ridge splitting technique.15
In the 3 case reports presented here,
there was complete patient satisfaction in
terms of esthetics and function. In all the
cases, 6-month postprosthesis intraoral
periapical radiographs showed stable bone
levels around the implants. Long-term
follow-up, which involves recalling the
patients once every 6 months for clinical
and radiographic examination, is recommended for this technique.
Corticotomies during the ridge splitting
procedures have been performed using a
variety of instruments, including a No.
15 blade, beaver blade, razor-sharp chisel,
round bur, fissure bur, diamond disk,
reciprocal saw, and piezoelectric devices.
In the cases presented here, a series of
instruments were used to expand the bone
gently and to avoid the risk of buccal
plate fracture. Using a piezoelectric device
allows for more precise, safer corticotomies
compared to a conventional rotary bur or
reciprocating saw.16,17
As previously described, the maxilla is
well-suited for ridge splitting, as thinner
cortical plates and softer medullary bone
allows for easier expansion of the maxillary ridge. By contrast, the mandible has
denser cortical plates and less cancellous
bone, making it difficult to perform this
procedure without the risk of buccal
plate fracture. However, the posterior
mandible can be split in cases with favorable conditions, such as a long edentulous
span, cancellous bone between the dense
outer cortical plates, and a good bone
A 36-year-old woman sought to replace
her missing mandibular left premolars
and left first molar with dental implants.
Compared to the maxillary bone, the
mandibular bone has less flexibility due
to its thicker cortical plates; thus a slightly
modified technique was used to split
the ridge and avoid malfracture of the
osteotomized segment. This modification
involved extending the length of the vertical corticotomies to match the length of
the predetermined implants. In addition,
an inferior horizontal corticotomy was
made by connecting the caudal ends of
the vertical corticotomies.
Using chisels and osteotomes, the
buccal segmented plate was gently dislocated to the buccal side (Fig. 8) and the
space between the 2 plates was filled with
a mix of autogenous bone and PerioGlas.
Achieving primary stability was uncertain in this case; hence it was decided to
place the implant after a healing period
of 6 months. Mersilk was used and a
tension-free closure of the surgical site was
achieved. To avoid pressure on the surgical site, the patient was instructed not to
wear any dentures.
At the end of 6 months, the site was
re-entered under local anesthesia and
complete regeneration of new bone
between the separated buccal and
lingual plates was confirmed. Implant
osteotomies were prepared conventionally
per the manufacturer’s instructions and
2 Osstem implants were placed (Fig. 9).
A tension-free closure of the surgical
site was achieved and the patient was
recalled 3 months later for second stage
e22
Discussion
The ridge split technique is one of several
options available for ridge augmentation. The technique allows simultaneous
implant placement in most cases, thus
reducing the overall treatment time.1-4
Moreover, as it involves expansion of the
buccal plate, the correction of buccal
concavity resulting from ridge resorption
can be achieved in some cases. Morbidity
related to second donor site may be eliminated as well.
Adequate bone height is a prerequisite
for this procedure, as splitting the crest
does not increase bone volume vertically.1
Although skilled surgeons can perform
splitting and expansion for very thin
ridges, a minimum ridge width of 3 mm
with some cancellous bone is preferred.9 A
pyramidal ridge form with a wider base is
ideal for this technique as it prevents the
risk of buccal plate fracture.
Predictable results have been obtained
with this technique. In a 2006 literature
review, Chiapasco et al evaluated different augmentation procedures for rehabilitating deficient edentulous ridges and
found that ridge expansion techniques
had a reported surgical success rate of
98%-100%.14 By comparison, implants
had a survival rate of 91.0%-97.3%, with
General Dentistry
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height above the mandibular canal.9 If
the buccal plate fractures, the mobile
plate can be retained with bone fixation
screws.7 In the third case presented in
this article, a slightly different approach
was employed for ridge splitting in the
mandible, with an additional, inferior
corticotomy connecting the vertical
corticotomy. This step allowed for easier
expansion and minimized any chance of
bone fracture.
The technique of ridge splitting usually
is performed simultaneously with implant
placement, as doing so reduces the overall
treatment time.18.19 However, simultaneous implant placement can result in
complications, such as lack of initial
implant stability, fracture of the buccal
segmented bone, and compromised
implant placement in the buccolingual
and apicocoronal direction.19 When the
primary stability of the implants is compromised, an interpositional bone graft
can be placed between the expanded cortices and implants can be placed after the
healing period of the augmented site.5,11
Alternatively, complications can be
avoided by using a staged approach.10,16,19
In the third case report presented here,
there was concern about achieving
adequate primary stability; hence the
implants were placed after healing of the
augmented site was completed.
For the cases presented in this article,
the intercortical area was filled with a
mixture of autogenous bone and alloplastic bone grafting material. Although
some dentists may prefer to place particulate bone grafting materials around the
implants and in the intercortical space,
it has been reported that a bone graft
usually is unnecessary.2,7,8,12,16 A barrier
membrane was not used, as periosteum is
believed to be the best possible biologic
membrane, containing a rich supply of
osteogenic cells.18
Conclusion
Ridge splitting is a predictable, effective
technique for the horizontal augmentation
of narrow edentulous ridges. Proper case
selection and careful clinical maneuvering
during the procedure result in a successful
surgical and prosthetic outcome. Unless a
general dentist is well-trained to carry out
the ridge split procedure, referral to an oral
surgeon/periodontist is recommended.
Author information
Dr. Prakash Talreja is an assistant professor, Department of Periodontology and
Implantology, Bharati Vidyapeeth Deemed
University Dental College and Hospital,
Navi Mumbai, India. Dr. Suvarna is
in private practice in Mumbai, India.
Dr. Preeti Talreja is an associate professor, Department of Oral Medicine and
Radiology, Yerala Medical Trust Dental
College and Hospital, Navi Mumbai, India.
References
1. Simion M, Baldoni M, Zaffe D. Jawbone enlargement
using immediate implant placement associated with a
split-crest technique and guided tissue regeneration. Int
J Periodontics Restorative Dent. 1992;12(6):462-473.
2. Scipioni A, Bruschi GB, Calesini G. The edentulous
ridge expansion technique: a five-year study. Int J Periodontics Restorative Dent. 1994;14(5):451-459.
3. Engelke WG, Diederichs CG, Jacobs HG, Deckwer I.
Alveolar reconstruction with splitting osteotomy and
microfixation of implants. Int J Oral Maxillofac Implants.
1997;12(3):310-318.
4. Chiapasco M, Ferrini F, Casentini P, Accardi S, Zaniboni
M. Dental implants placed in expanded narrow edentulous ridges with the Extension Crest device: a
1-3-year multicenter follow-up study. Clin Oral Implants Res. 2006(3);17:265–272.
5. Lustmann J, Lewinstein I. Interpositional bone grafting
technique to widen narrow maxillary ridge. Int J Oral
6. Duncan JM, Westwood RM. Ridge widening for the
thin maxilla: a clinical report. Int J Oral Maxillofac Implants. 1997;12(2):224-227.
7. Basa S, Varol A, Turker N. Alternative bone expansion
technique for immediate placement of implants in the
edentulous posterior mandibular ridge: a clinical report.
www.agd.org
8. Scipioni A, Bruschi GB, Giargia M, Berglundh T, Lindhe
J. Healing at implants with and without primary bone
contact. An experimental study in dogs. Clin Oral Implants Res. 1997;8(1):39-47.
9. Misch CM. Implant site development using ridge splitting techniques. Oral Maxillofac Surg Clin North Am.
2004;16(1):65-74, vi.
10. Enislidis G, Wittwer G, Ewers R. Preliminary report on
a staged ridge splitting technique for implant placement in the mandible: a technical note. Int J Oral Maxillofac Implants. 2006;21(3):445-449.
11.Summers RB. The osteotome technique: part 4—
future site development. Compend Contin Edu Dent.
1995;16(1):1090-1099.
12. Coatoam GW, Mariotti A. The segmental ridge-split
procedure. J Periodontol. 2003;74(5):757-770.
13. Blus C, Szmukler-Moncler S. Split-crest and immediate
implant placement with ultra-sonic bone surgery: a
3-year life-table analysis with 230 treated sites. Clin
Oral Impl Res. 2006:17(6):700-707.
14. Chiapasco M, Zaniboni M, Boisco M. Augmentation
procedures for the rehabilitation of deficient edentulous ridges with oral implants. Clin Oral Implants Res.
2006;17(Suppl 2):136-159.
15. Aghaloo TL, Moy PK. Which hard tissue augmentation
techniques are the most successful in furnishing bony
support for implant placement? Int J Oral Maxillofac
Implants. 2007;22(Suppl):49-70.
16. Elian N, Jalbout Z, Ehrlich B, et al. A two-stage full-arch
ridge expansion technique: review of the literature and
clinical guidelines. Implant Dent. 2008;17(1):16-23.
17. Sohn DS. Color Atlas, Clinical Applications of Piezoelectric Bone Surgery. Seoul, South Korea: Kunja Publishing; 2008.
18. Guirado JL, Yuguero MR, Carrion del Valle MJ, Zamora
GP. A maxillary ridge-splitting technique followed by
immediate placement of implants: a case report. Implant Dent. 2005;14(1):14-20.
19. Sohn DS, Lee HJ, Heo JU, Moon JW, Park IS, Romanos
GE. Immediate and delayed lateral ridge expansion
technique in the atrophic posterior mandibular ridge.
J Oral Maxillofac Surg. 2010;68(9):2283-2290.
Manufacturers
Ethicon, Inc., Somerville, NJ
877.384.4266, www.ethicon.com
HIOSSEN, Inc., Fairless Hills, PA
888.678.0001, www.hiossen.com
Mectron s.p.a., Carasco, Italy
39.0185.351374, dental.mectron.com
NovaBone Products, LLC, Jacksonville, FL
386.462.7660, www.novabone.com
General Dentistry
e23
Prosthodontics/Removable
Management of severe mandibular deviation
following partial mandibular resection: a case report
Husain Harianawala, BDS, MDS n Mohit Kheur, BDS, MDS n Supriya Kheur, BDS, MDS n Jay Matani, BDS, MDS
Extensive mandibular resection commonly leads to a deviation of
the mandible, facial disfigurement, and difficulty with speech and
mastication. The rehabilitation of these patients is a prosthodontic
challenge. This article presents the case of a 60-year-old man
who sought prosthetic rehabilitation after a right segmental
mandibulectomy.
The prosthetic rehabilitation was planned in 2 phases. A palatal
ramp was constructed, followed by a mandibular guiding flange. After
S
urgical removal of a malignant neoplasm is the most common cause
of partial mandibular loss.1 Patients
treated for tumors of the head and neck
can suffer from morbidity and disability,
induced mainly by surgical resection,
radiation, and chemotherapy.1 The degree
of disability depends on tumor location
and size, the duration and quantity of
radiation therapy, type of reconstruction,
and the patient’s age and medical status.
Tumor resection should be as conservative
as possible, with the goal of preserving the
condyle and teeth in the vicinity, primary
reconstruction, implant placement, and, in
some cases, intermaxillary fixation.2 Recent
case reports have reported using dental
implants in the rehabilitation of completely
or partially edentulous patients who have
undergone mandibular resection.3,4
Physiotherapy should be started immediately after surgery to prevent scar formation
and trismus. Other factors that may have
an impact on the prognosis are the structure and volume of resected tissue, whether
the mandibular resection is combined with
a partial or complete glossectomy, and/
or whether a partial pharyngectomy is
required.5 Clinicians need to be aware that
these patients may also be impacted by
psychological and social difficulties postsurgery.6 Surgeons must work in conjunction with prosthodontists to formulate a
reconstruction plan that will best allow the
patient to lead a healthy, dignified life.
An interdisciplinary approach is required
to manage facial disfigurement, distorted
speech, salivation, deglutition, occlusal disharmony, and the psychosocial issues that
e24
4 months, the patient’s chewing ability, tongue movement, and facial
esthetics were improved.
Received: August 22, 2013
Revised: December 20, 2013
Accepted: January 30, 2014
Key words: hemimandibulectomy,
guiding flange prosthesis, palatal ramp, rehabilitation
can accompany a mandibular resection.6
This article describes the case of a patient
who underwent a hemimandibulectomy
and highlights the multidisciplinary
approach and prosthetic management.
Case report
A 60-year-old man reported to the M.A.
Rangoonwala College of Dental Sciences
& Research Centre hospital in Pune,
India with the chief complaint of loose
teeth in the right posterior mandibular
region. Careful examination and investigation led to the diagnosis of a squamous
cell carcinoma lesion, extending from the
mandibular first molar to the anterior
border of the ramus. Following discussions with the hospital’s Head & Neck
Cancer Team, a radical neck dissection
with a segmental hemimandibulectomy
was performed. Primary reconstruction
with a rigid fixation plate and a pectoralis major myocutaneous (PMMC)
flap was performed successfully (Fig. 1).
Periodontally compromised maxillary
teeth that would be in the line of the
oncology radiation treatment were
extracted at the time of surgery. The surgical resection was followed by a 5-week
radiation regimen consisting of 6000 rads
and 33 cycles.
Prosthetic rehabilitation began 1 month
postsurgery. The patient had a dental
midline deviation of 2.1 cm to the right
side, and was unable to occlude in maximum intercuspation despite manual guidance (Fig. 2). Diagnostic impressions were
made with a modified stock impression
Fig. 1. Radiographic presentation following surgical reconstruction.
General Dentistry
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21 mm
Fig. 2. Anterior photograph showing mandibular
deviation.
Fig. 5. Anterior photograph showing gradual correction of deviation.
tray with irreversible hydrocolloid
(Dentalign, Prime Dental Products Pvt.
Ltd.) and poured in Type III dental stone
(KAL Rock, Kalabhai Karson Pvt. Ltd.).
The patient had carious root stumps, but
declined to have them extracted following
his major surgery. Periodontal therapy
(including oral prophylaxis and root planing) was followed by restoring the carious
lesions on the remaining teeth. Given the
extensive midline deviation, the treatment
plan was divided into 2 phases: correction
of the mandibular deviation followed by
definitive prosthetic treatment for longterm comfort and function.
Phase 1
A long lever arm and a compromised
tissue bed on the resected side of the
patient’s mouth would create excessive prosthetic movement. An angular
pathway of closure would induce lateral
forces which could dislodge the denture.7 Because of these factors, a palatal
ramp was selected as the first step to
correct the deviation.8
Fig. 4. Palatal ramp in situ.
Fig. 3. Palatal ramp prosthesis on the model.
Fig. 6. Cast of partial denture design.
A heat-cured acrylic record base (DPI
RR Heat Cure, Dental Products of India)
was fabricated with a wrought wire
circumferential clasp on the anterior abutment tooth and an Adams clasp over the
first molar. The palatal ramp was fabricated by adding an autopolymerizing resin
(DPI RR Cold Cure, Dental Products of
India) to the palatal aspect of the record
base on the non-resected side and manually guiding the mandible closer to the
maximum intercuspal position within
physiologic limits. To ensure smooth gliding of the mandible, minor adjustments
were made, followed by finishing and
polishing procedures (Fig. 3).
The patient was instructed to use the
palatal ramp for at least 2 hours a day for
5 days, gradually increasing the duration
after the fifth day (Fig. 4). The patient
was recalled for the next reline only after
he was completely comfortable with the
palatal ramp prosthesis. The deviation was
corrected with 7 relines over a period of
16 weeks until the maximum intercuspal
position was achieved on the non-resected
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side of the mouth (Fig. 5). Occlusal equilibration was performed and the ramp was
adjusted for a final time. The patient was
asked to wear the prosthesis until he felt
no strain in the temporomandibular joint
and surrounding musculature.
Phase 2
The second phase of rehabilitation began
after the patient had become comfortable
with and accustomed to the palatal ramp.
To maintain the mandible in the correct
position against the maxilla, a mandibular cast partial denture was fabricated
with a buccal guiding flange on the nonresected side.
The cast partial denture was designed
so as to employ alternating buccal and
lingual retentive clasp arms on successive
posterior teeth on the non-resected side
of the mouth (Fig. 6). Reciprocating arms
were planned to have a bracing effect on
these teeth. To achieve maximum support, rest seats were planned for all posterior teeth, in addition to an interrupted
linguoplate major connector to brace all
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e25
Prosthodontics/Removable Management of severe mandibular deviation following partial mandibular resection
Fig. 7. Trial framework of partial denture to determine jaw relationship.
of the mandibular anterior teeth and a
proximal plate minor connector adjacent
to every edentulous span. The lattice-type
minor connector for the outrigger was
kept short to reduce the leverage effect
in the partial denture while providing
enough lip support for improved esthetics.
The minor connector extension (for supporting the guiding flange) was extended
from the buccal extensions of the embrasure clasps and the edentulous span. The
angulation of the minor connector on the
buccal flange was adjusted on the cast.
Both arches were prepared for the cast
partial denture. To increase the retention,
stability, and support of the mandibular
denture, the maximal extension of the
lingual flange—within physiologic
limits—was ensured on the non-resected
side. A polyether adhesive (Polyether
Tray Adhesive Refill, 3M ESPE) was
applied over the custom autopolymerized
resin tray. Next, a polyether impression
(Impregum, 3M ESPE) was made and
poured in type IV gypsum (Ultra Rock,
Kalabhai Karson Pvt. Ltd.).
A framework cobalt-chromium alloy
(IPS d.Sign, Ivoclar Vivadent, Inc.) was
fabricated. Autopolymerizing resin was
added over the minor connector overlying the outrigger to act as a custom tray.
Next, a functional impression was made
using a low-fusing compound, followed
by a secondary impression using a lightbodied condensation silicone (Speedex,
Coltene/Whaledent, Inc.). An altered
cast was poured using the Type III dental
stone. Record bases and occlusal rims were
fabricated over the minor connectors. The
jaw relation was recorded and transferred
e26
Fig. 8. Try-in of partial denture.
Fig. 9. Final partial denture in situ.
onto a semi-adjustable articulator (Hanau
Wide-Vue, Whip Mix Corporation)
(Fig. 7). Care was taken to reduce the
frontal plane rotation of the residual
mandible, which is known to occur due
to muscle imbalance that can occur after
mandibular resection. As the patient’s lips
and cheeks were pulled medially due to
scarring, the denture teeth were placed
buccal to the crest of the ridge on the
non-resected side and lingually at a higher
level on the resected side (Fig. 8).9 With a
lateral resection, bilateral occlusal contacts
serve as a stabilizing factor and mastication
is confined to the non-resected site.
During the try-in stage, the buccal extension of the cast partial frame was relined
with autopolymerizing resin to verify the
jaw relation. Heat-cured fiber-reinforced
resin (Triplex Hot, Ivoclar Vivadent, Inc.)
was used as the final denture base material.
A laboratory remount was followed by
finishing and polishing of the cast partial
denture; at which point, the prosthesis was
delivered to the patient (Fig. 9).
General Dentistry
www.agd.org
The patient was instructed to wear
the mandibular denture for 1 hour/day
for the first week, then increase its use
gradually. He reported difficulty masticating during the initial period; however,
mastication improved over time, and the
patient was satisfied with the esthetic
result of the treatment.
The patient made regular recall visits
during which the health of the abutment
teeth and the partial denture were re-evaluated. The tissue surface of the outrigger
was relined 6 months post-treatment
when increased fibrosis was seen in the
PMMC flap.
Discussion
Rehabilitation of patients who have
undergone mandibular resection is a
greater clinical challenge compared to
patients with maxillary defects. In the
present case, the mandibular deviation was very large due to the extended
radiotherapy postsurgery. Correcting
such a mandibular deviation against the
forces of the musculature and sclerosing
tissue requires a significant lateral force.
The palatal ramp prosthesis over the
maxillary arch was chosen to correct the
deviation as it provided a larger base for
stability and support of the prosthesis.
The acrylic plate also made it easy and
convenient to reline the palatal ramp
regularly until the maximum intercuspal
position was achieved.
After the deviation was corrected and
stabilized, a guiding flange prosthesis was
placed over the mandibular arch as the
final restoration. This design was selected
because it had a reduced bulk and offered
negligible interference to tongue movements compared to other types of prostheses, thus improving speech and overall
comfort. The success of this treatment
has led the authors to treat other cases
using a similar protocol.
Conclusion
Reconstructing a mandibular defect by
means of microvascular free flaps allows
the maxillofacial prosthodontist to
achieve a more effective rehabilitation.10,11
It is critical to both manage the mandibular deviation and provide psychological
counseling to the patient.6 Proper multidisciplinary treatment planning allows
dentists to place osseointegrated implants
strategically in patients with a reconstructed mandible, restoring occlusal and
masticatory function while also achieving
an acceptable esthetic result.
Author information
Drs. Harianawala and Matani are researchers and practioners, Department of
Prosthodontics, M.A. Rangoonwala College
of Dental Sciences & Research Centre,
Pune, India, where Dr. M. Kheur is a professor. Dr. S. Kheur is a professor, Dr. D. Y.
Patil Dental College, Pimpri, India.
References
1. Beumer J III, Marunick MT, Esposito SJ. Maxillofacial
Rehabilitation: Surgical and Prosthodontic Management of Cancer-Related Acquired, and Congenital Defects of the Head and Neck. 3rd ed. Hanover Park, IL:
Quintessence Publishing Co.; 2011.
2. Schneider RL, Taylor TD. Mandibular resection guidance prostheses: a literature review. J Prosthet Dent.
1986;55(1):84-86.
3. Sistos RJ, Jimenez CR, Benavides RA. Prosthetic and
surgical treatment of patient previously subjected to
hemi-mandibulectomy. Rev Odont Mex. 2013;17(1):
42-46.
4. Sravanthi Y, Rathod A, Deepa KL, Priyadarshini I. Rehabilitation of mandibulectomy patient with an overdenture: a case report. Ind J Pub Health Res Dev. 2013;
4(2):297-300.
5. Robinson JE, Rubright WC. Use of a guide plane for
maintaining the residual fragment in partial or hemimandibulectomy. J Prosthet Dent. 1964;14(5): 992999.
www.agd.org
6. Rehmani AA. The complete rehabilitation of patient
with lateral mandibular defect. J Ind Prosthodont Soc.
2002;29-32.
7. Beumer J III, Curtis TA, Marunick MT. Maxillofacial Rehabilitation: Prosthodontic and Surgical Consideration.
St. Louis: Ishiyaku Euroamerica; 1996.
8. Adisman K. Prosthetic reconstruction of a resected
mandible. J Prosthet Dent. 1962;12:384-392.
9. Kokubo Y, Fukushima S, Sato J, Seto K. Arrangement of
artificial teeth in the neutral zone after surgical reconstruction of the mandible: a clinical report. J Prosthet
Dent. 2002;88(2):125-127.
10. Shaw RJ, Sutton AF, Cawood JI, et al. Oral rehabilitation after treatment for head and neck malignancy.
Head Neck. 2005;27(6):459-470.
11. Kanan RY, Mathur BS, Tzafetta K. Single flap reconstruction for complex oro-facial defects using chimeric
free fibular flap variants. J Plast Reconstr Aesthet Surg.
2013;66(3):358-363.
Manufacturers
Coltene/Whaledent, Inc., Cuyahoga Falls, OH
330.916.8800, www.coltene.com
Dental Products of India, Mumbai, India
99.22.22079351, www.dpi.co.in
Ivoclar Vivadent, Inc., Amherst, NY
800.533.6825, www.ivoclarvivadent.us
Kalabhai Karson Pvt. Ltd., Mumbai, India
91.22.2578.1823, www.kalabhai.com
Prime Dental Products Pvt. Ltd., Maharashtra, India
91.72601.47129, www.prime-dental.com
Whip Mix Corporation, Louisville, KY
800.626.5651, whipmix.com
3M ESPE, St. Paul, MN
888.364.3577, solutions.3m.com
General Dentistry
e27
Diagnosis of Oral Pathology
Rare oral cartilaginous choristoma: a case report
and review of the literature
Marina Lara de Carli, DDS, PhD n Felipe Fornias Sperandio, DDS, PhD n Fernanda Rafaelly de Oliveira Pedreira, DDS n Alessandro
Antonio Costa Pereira, DDS, PhD n Joao Adolfo Costa Hanemann, DDS, PhD
Cartilaginous choristomas are extraosseous benign tumors. They occur in
abnormal sites that usually do not contain chondrocytes. The oral variant
of this entity is considered to be very rare, with only 38 cases currently
published in the literature. This article presents a case of an oral cartilaginous choristoma lesion. In addition to presenting clinical and histological
diagnoses, this article compares the present case to recently reported
cases. Special attention was given to analyzing cells of the oral cartilaginous choristoma, which appear as well-differentiated chondrocytes with
O
ral cartilaginous choristoma is a very
rare extraosseous chondroma that
is found usually on the tongue.1-3
Although its origins are a topic of debate
(and may include metaplastic and also
developmental derivations), a cartilaginous
choristoma shows benign behavior and
generally does not recur after a simple
excisional procedure.2,4-7 This slow-growing and asymptomatic mass may resemble
other oral benign soft tissue tumors; as a
result, a histological evaluation must eliminate the possibility of clinically similar
lesions based on the characteristic appearance of the chondroma’s cells.6,8
Case report
This case study was conducted in compliance with the Helsinki Declaration on
medical research protocols and ethics.
Permission was granted by the Alfenas
Federal University Institutional Review
Board. The patient signed an informed
consent agreement.
A 59-year-old man had an asymptomatic nodular lesion (2 years duration)
located in the dorsum of the tongue. The
patient reported that the lesion’s size had
not changed since it was first noticed.
The patient`s systemic condition was
normal and he reported that no previous
trauma had occurred in the area. The
extraoral examination was uneventful,
while the intraoral assessment revealed
a single, flaccid, round, sessile nodule
in the posterior third of the tongue
dorsum. The lesion had a yellowish color
with erythematous borders and was
e28
a pale blue cytoplasm surrounded by a light basophilic stroma and no
evidence of malignity. Following surgical excision, the lesion did not recur,
which is similar to other reported cases of oral cartilaginous choristomas.
Received: September 30, 2013
Revised: January 14, 2014
Accepted: March 6, 2014
Key words: choristoma, hyaline cartilage, biopsy, tongue
well-circumscribed, measuring 10 mm in
diameter (Fig. 1). No other lesions were
observed in the oral cavity.
An excisional biopsy of the lesion was
performed under local anesthesia and
the obtained specimen was fixed in 10%
buffered formalin and embedded in paraffin wax. Next, 5 μm-thick sections were
obtained and stained (H&E). The histopathological analysis showed that the lesion
was located in the oral submucosa and
encapsulated completely by dense fibrous
connective tissue (Fig. 2). The lesion
consisted of a benign proliferation of welldeveloped chondrocytes—exhibiting small
and highly basophilic nuclei—inserted in
a mature hyaline matrix (Fig. 3). Based on
these findings, the lesion was diagnosed as
a cartilaginous choristoma of the tongue.
The postoperative period was uneventful,
and there were no signs or symptoms of reoccurrence at a 4-month follow-up (Fig. 4).
Fig. 1. Photograph of a sessile yellowish nodule with
erythematous borders on the dorsum surface of the
patient’s tongue.
Fig. 2. Photomicrograph of the surgical specimen
showing a mature hyaline cartilage tissue separated
from the adjacent skeletal muscle and overlying
squamous epithelium by a thin capsule of fibrous
connective tissue (H&E, magnification 50X).
General Dentistry
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Discussion
The histological appearance of a cartilaginous choristoma resembles that of benign
chondromas; however, choristomas occur in
sites that usually do not contain chondrocytes.3,6,8 As a result, cartilaginous choristomas are rare soft tissue lesions that occur
mostly on the hands and feet.9 Conversely,
the very rare oral cartilaginous choristoma is
Fig. 3. Photomicrograph showing small chondrocytes
with a clear cytoplasm and round nuclei (H&E,
Fig. 4. Photograph of the patient’s tongue 4 months
post-treatment with no signs of recurrence.
Table. Comparison of 3 recent case reports of oral cartilaginous choristoma
and the present study.7,13,14
Source
Patient
Duration
(years/gender) (years)
Location
Size
(mm)
Follow-up
(months/recurrence)
Shibasaki et al (2013)
25/female
1.5
Lower lip
20
36/no recurrence
Pereira et al (2012)
64/female
>5
Dorsum, midline
left, posterior third
5
9/no recurrence
Saha et al (2011)
11/female
11
NA
Present case (2015)
59/male
2
Dorsum, midline
10
right, posterior third
NA
NA
4/no recurrence
Abbreviation: NA, not available.
usually found on the tongue (mainly in the
lateral borders).1,8
According to the literature, a number
of conditions may indicate a clinical
differential diagnosis for cartilaginous
choristoma.6,8 Sialoliths and pleomorphic
adenomas have been found; however they
are rare in this region. Neurofibromas,
schwannomas, and granular cell tumors
are more common and were considered as
differential diagnoses in the present case.
The oral cartilaginous choristoma is
generally not considered as a clinical
diagnosis due to its rarity. A granular cell
tumor is a relatively rare lesion in the
dorsal region of the tongue. It occurs in all
age groups, but most frequently in patients
40-60 years of age. This lesion is thought
to arise from Schwann cells and characteristically has a yellowish color.10 A single
asymptomatic, slow-growing nodule on the
tongue (10-20 mm) also may represent a
schwannoma or a neurofibroma—benign
tumors that originate from the nerve sheath.
A neurofibroma presents with a hamartomatous hyperplasic appearance.11,12 These
tumors should be treated with excision and
usually have low rates of reccurrence.10-12
Previously, only 37 cases of oral cartilaginous choristomas had been published
in the literature.7,8,13,14 In their 2012 literature review, Norris & Mehra reviewed 34
cases and designated the most significant
clinical aspects of this lesion.8 Based on
the literature, an oral cartilaginous choristoma occurs most frequently in the tongue
and usually does not show inclinations
based on age or gender.4 In the present
case, the choristoma was also found on
the patient’s tongue and had no significant
clinical differences compared to previously
reported cases. A literature review of 3
recent cases confirmed the lesion’s predilection for the tongue (Table).7,13,14
www.agd.org
In the present case, an excisional biopsy
was conducted. A follow-up visit 4 months
post-treatment showed no signs or symptoms of recurrence. Histologically, the
present case had no other mesenchymal
tissue except for the mature cartilage.
Previous cases in the literature (including
extraoral choristomas) reveal that these
tumors often exhibit a variety of mesenchymal tissues along with the chondrocyte
cells, such as adipose and bony tissues.1,8,15
In the present case, the tumor consisted
solely of chondrocytes.
According to the literature, immunohistochemical studies may serve as an
additional resource to characterize the
chondrocytes found in the choristoma
while also helping to distinguish between
the rare cartilaginous choristoma and other
soft oral benign lesions. Calcium-binding
proteins (such as S100) are expressed by
both choristomas and oral schwannomas.
Cytokeratins and the epithelial membrane
antigen usually are present in pleomorphic
adenomas; these markers are not found in
cartilaginous choristomas.5,6,13,16 In addition, calponin and muscle-specific actins
are not expressed by choristomas; this may
help to distinguish them from inflammatory myofibroblastic tumors.17
The present case was very easily diagnosed
as an encapsulated mass of mature chondrocytes inserted in a hyaline matrix residing
in the oral submucosa. The cellular and
nuclear morphology of the chondrocytes
was examined to eliminate the possibility
of the rare chondrosarcoma of the tongue,
a condition that may also be included in a
differential diagnosis due to its similar location, size, and nodular-shaped growth.6,18-20
Typically, no mitotic figures can be
distinguished in the analyzed field of the
choristoma and the cells should be represented (as with an intraosseous maxillary
chondroma) by well-differentiated chondrocytes surrounded by light basophilic
stroma.15 Individually, these chondrocytes
should have a pale blue cytoplasm with
no evidence of malignancy. Oddly shaped
chondrocytes (either binucleated or with
pleomorphic nuclei) usually suggest a
malignant lesion, such as a chondrosarcoma.21,22 In addition, chondrosarcoma cells
show varying mitotic activity and frequently
are arranged in lobules separated by thin
fibrous septa; in addition, occasional calcification may occur within the lesion.21,23
General Dentistry
e29
Diagnosis of Oral Pathology Rare oral cartilaginous choristoma: a case report and review of the literature
Conclusion
When diagnosing painless, slow-growing,
nodular lesions located on the tongue,
dentists should take care to distinguish
(both clinically and histologically) between
oral choristomas and malignant neoplasms.
Author information
Dr. de Carli is a postdoctoral candidate,
Department of Clinic and Surgery, School
of Dentistry, Alfenas Federal University,
Minas Gerais, Brazil, where Dr. Pedreira
is a master’s candidate, Dr. Hanemann
is a professor, and Drs. Sperandio
and Pereira are professors, Institute of
Biomedical Sciences.
References
1.Sera H, Shimoda T, Ozeki S, Honda T. A case of chondroma of the tongue. Int J Oral Maxillofac Surg. 2005;
34(1):99-100.
2.Matsushita K, Tahara M, Sato H, Nakamura E, Fujiwara
T. Cartilaginous choristoma deep in the upper midline
oral vestibule. Br J Oral Maxillofac Surg. 2004;42(5):
436-438.
3.Chou LS, Hansen LS, Daniels TE. Choristomas of the
oral cavity: a review. Oral Surg Oral Med Oral Pathol.
1991;72(5):584-593.
4.Munro JM, Singh MP. Chondroma of the tongue. Report of a case and a consideration of the histogenesis
e30
of such lesions. Arch Pathol Lab Med. 1990;114(5):
541-542.
5.Toida M, Sugiyama T, Kato Y. Cartilaginous choristoma
of the tongue. J Oral Maxillofac Surg. 2003;61(3):393396.
6.Rossi-Schneider TR, Salum FG, Cherubini K, Yurgel LS,
Figueredo MA. Cartilaginous choristoma of the
tongue. Gerodontology. 2009;26(1):78-80.
7.Shibasaki M, Iwai T, Chikumaru H, Inayama Y, Tohnai I.
Cartilaginous choristoma of the lower lip. J Craniofac
Surg. 2013;24(2):e192-e194.
8.Norris O, Mehra P. Chondroma (cartilaginous choristoma) of the tongue: report of a case. J Oral Maxillofac
Surg. 2012;70(3):643-646.
9.Chung EB, Enzinger FM. Chondroma of soft parts.
Cancer. 1978;41(4):1414-1424.
10.Speight P. Pathology and genetics of head and neck
tumours. In: Barnes L EJ, Reichart P, Sidransky D, eds.
World Health Organization Classification of Tumours.
Lyon, France: IARC Press; 2005:185-186.
11.Cohen M, Wang MB. Schwannoma of the tongue: two
case reports and review of the literature. Eur Arch Otorhinolaryngol. 2009;266(11):1823-1829.
12.Marocchio LS, Oliveira DT, Pereira MC, Soares CT,
Fleury RN. Sporadic and multiple neurofibromas in
the head and neck region: a retrospective study of
33 years. Clin Oral Investig. 2007;11(2):165-169.
13.Pereira GW, Pereira VD, Pereira Junior JA, da Silva RM.
Cartilaginous choristoma of the tongue with an immunohistochemical study. BMJ Case Rep. 2012.
14.Saha R, Tandon S, Kumar P. Chondroid choristoma: report of a rare case. J Clin Pediatr Dent. 2011;35(4):
405-407.
General Dentistry
www.agd.org
15.Scivetti M, Maiorano E, Pilolli GP, et al. Chondroma
of the tongue. Clin Exp Dermatol. 2008;33(4):460462.
16.Santos PP, Freitas VS, Pinto LP, Freitas Rde A, de Souza
LB. Clinicopathologic analysis of 7 cases of oral
schwannoma and review of the literature. Ann Diagn
Pathol. 2010;14(4):235-239.
17.Salgueiredo-Giudice F, Fornias-Sperandio F, MartinsPereira E, da Costa dal Vechio AM, de Sousa SC, dos
Santos-Pinto-Junior D. The immunohistochemical profile of oral inflammatory myofibroblastic tumors. Oral
111(6):749-756.
18.Forman G. Chondrosarcoma of the tongue. Br J Oral
Surg. 1967;4(3):218-221.
19.Al-Rawi M, Harper T, Bafakih F. Chondrosarcoma of
the tongue: a case report and a review of the literature. Laryngoscope. 2013;123(2):418-421.
20.Angiero F. Extraskeletal myxoid chondrosarcoma of the
left buccal mucosa. Anticancer Res. 2012;32(8):33453350.
21.Gallego L, Junquera L, Fresno MF, de Vicente JC.
Chondrosarcoma of the temporomandibular joint. A
case report and review of the literature. Med Oral
Patol Oral Cir Bucal. 2009;14(1):E39-E43.
22.Takahama A Jr., Alves Fde A, Prado FO, Lopes MA,
Kowalski LP. Chondrosarcoma of the maxilla: report of
two cases with different behaviours. J Craniomaxillofac Surg. 2012;40(3):e71-e74.
23.Goutzanis L, Kalfarentzos EF, Petsinis V, Papadogeorgakis N. Chondrosarcoma of the mandibular condyle
in a patient with Werner syndrome: a case report.
J Craniomaxillofac Surg. 2013;41(7):e170-e174.
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Atypical presentation of salivary mucocele:
diagnosis and management
Kumar Nilesh, MDS n Jagadish Chandra, MDS
A mucocele is a common pathological lesion involving the minor
salivary glands. It usually presents as an asymptomatic small superficial
swelling over the lower labial mucosa. However, uncommon variants
of oral mucoceles sometimes occur. Such lesions may be difficult to
diagnose due to their unusual size and atypical clinical presentation.
This article describes the case of a deeply embedded large mucocele
over the buccal mucosa. Ultrasonography was used to visualize the
O
ral mucoceles are common
lesions of the minor (accessory)
salivary glands.1 Clinically, an
oral mucocele presents as a soft, bluish
to transparent cystic swelling below the
mucosa. Mucoceles can appear at any site
where minor salivary glands are present.
However, they are most commonly seen
on lower lips, and are rarely >1.5 cm in
diameter.2 Because of the typical oral
mucocele presentation, a large mucocele
at an unusual site may cause a diagnostic
dilemma. The article presents a case of a
large buccal mucocele, and its presentation, diagnosis, and surgical removal.
Case report
A 30-year-old man presented with the
chief complaint of a painless intraoral
swelling over the left buccal mucosa. The
size and position of the lesion, and aspiration was used to help in the
eventual diagnosis. An intraoral approach was used in the complete
removal of the lesion.
Received: September 24, 2013
Accepted: January 13, 2014
patient first noticed the swelling approximately 1 year earlier. Since then, the
swelling had grown gradually to its size
at presentation. A clinical examination
of the patient’s face showed a nontender
oval swelling of approximately 1.5 cm
behind the corner of the mouth (Fig. 1).
The skin overlying the lesion was normal
and “pinchable.” Intraoral examination
revealed a dome-shaped swelling of
approximately 4 cm in diameter occupying almost the entire left buccal mucosa
(Fig. 2). The swelling was nontender,
soft, and fluctuant on palpation, with
normal overlying mucosa. The patient’s
oral hygiene was poor, and he was missing his mandibular left first molar. The
cervical lymph nodes were not palpable.
No significant medical history or history
of trauma were reported by the patient.
Fig. 1. Facial photograph showing extraoral swelling.
e32
Key words: mucocele, buccal mucosa, surgical excision
General Dentistry
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The overall clinical presentation was suggestive of a benign submucosal lesion and
the differential diagnosis was a lipoma,
fibroma, dermoid cyst, or mucocele.
Ultrasonography was advised to study
the nature, size, and extent of the lesion.
The ultrasonogram showed a hypoecogenic oval mass of 42 x 33 x 24 mm
within the buccal subcutaneous tissue
(Fig. 3). Based on this radiological assessment, a diagnosis of a fluid-filled cystic
lesion was established. Aspiration of the
cystic fluid was carried out under local
anesthesia, using an 18 gauge needle.
Four ml of a white, viscous fluid was
aspirated and sent for cytochemical evaluation. The fluid consisted of mucus and
numerous inflammatory cells. Chemical
analysis of the aspirated fluid showed
increased amylase and protein counts.
Fig. 2. Anterior photograph showing large intraoral swelling
occupying almost the entire left buccal mucosa.
2
1
Fig. 3. Ultrasonogram showing a hypoecogenic oval
mass within the buccal subcutaneous tissue.
Fig. 4. Surgical removal of lesion. Left. Line diagram showing the incision design: linear incision placed over
the buccal mucosa along the occlusal plane (1); Stensen duct on the buccal mucosa needs to be identified
and preserved (2). Right. Lesion exposed completely by submucosal blunt dissection.
1
2
1
2
Fig. 5. Histopathology. Left. Section showing mucin pooling along with mucinophages (1) surrounded by a fibrous connective tissue capsule (2) (H&E, magnification
10X). Center. Section showing lining of the lesion (1) with associated minor salivary glands (2) (H&E, magnification 10X). Right. Section at higher magnification
showing large vacuolated cells with empty cytoplasm (white arrow) and mucinophages (gray arrow) (H&E, magnification 40X).
Based on the clinical, radiological, and
cytochemical evaluations, a final diagnosis of buccal mucocele was established.
Surgical excision of the lesion by intraoral
approach was executed under local anesthesia. After attaining adequate anesthesia, a
linear incision of approximately 3 cm was
made over the buccal mucosa, keeping it
parallel to the occlusal plane. Care was taken
to indentify and preserve the opening of the
Stensen duct over the buccal mucosa (usually present on the buccal mucosa opposite
the crown of the maxillary first molar).
Submucosal blunt dissection was elected to
free the lesion from the surrounding tissue
(Fig. 4). The excised lesion was sent for histopathological evaluation. The microscopic
examination revealed a fibrous capsule with
central pooling of mucin along with mucinophages. Associated minor salivary glands
were also noted (Fig. 5). The histopathological analysis confirmed the diagnosis of
a salivary mucocele. At a 2-year follow-up,
the patient showed complete healing of the
surgical site with no recurrence.
Discussion
Etiopathogenesis and types
Mucoceles are cavities filled with mucus
and lined by epithelium or covered by
granulated tissue.1,3 Based on its etiopathogenesis, mucoceles can be classified
as extravasation or retention types. An
extravasation mucocele is caused by
trauma to the excretory duct of a minor
salivary gland. Trauma causes rupture of
the duct, resulting in extravasation and
accumulation of saliva in the surrounding
connective tissue. An extravasation cyst
consists of a central pool of extravasated
mucus surrounded by granulation tissue
(such as a pseudocyst). Unlike extravasation cysts, retention cysts result from
ductal obstruction due to sialolithiasis,
periductal scars, or invasive tumors. The
narrowing of the ductal opening does
www.agd.org
not allow an adequate salivary flow, with
subsequent ductal distention presenting as
a mucosal swelling.4
Clinical presentation
Clinically, mucoceles present as asymptomatic swellings over the oral mucosa. They are
usually small in size, with a mean diameter
of <1 cm.1 They affect both genders in all
age groups, with the peak age of incidence
between 10 and 29 years.1,2 The lower lip is
the most common site, although they can
be found in any region where there are salivary glands. However, they are more rare in
the palate, retromolar space, and the buccal
mucosa.5 In a review of 1824 cases of oral
mucoceles, Chi et al reported the incidence
to be highest on the lip (82%), followed by
floor of the mouth (6%), ventral tongue
(5%), buccal mucosa (5%), palate (1%),
and reteromolar region (<1%).6 The present
case was uncommon in view of its large size
and location on the buccal mucosa.
General Dentistry
e33
Diagnosis and Treatment Planning Atypical presentation of salivary mucocele: diagnosis and management
Investigation and diagnosis
A mucocele with its usual presentation
can be easily diagnosed based on its
clinical appearance. However, an unusual
presentation—in relation to its size and
location—may require further evaluation. Ultrasonography or other advanced
diagnostic methods (such as magnetic
resonance imaging) are extremely helpful
in visualizing the form, diameter, and
position of the lesion relative to adjacent
organs.7 Ultrasonography in the present
case showed a hypoecogenic oval mass
within the subcutaneous tissue underlying
the buccal mucosa.
Fine needle aspiration is a useful diagnostic technique for evaluating patients
with salivary gland nodules and enlargement. Differentiating between mucoceles
and vascular lesions preoperatively is
very important—if a large angioma is
mistaken for a mucocele, the excision of
the vascular lesion can result in major
bleeding.8
Management
Surgery remains the mainstay for treatment of oral mucoceles. Three possible
surgical approaches are the complete
excision of the lesion, excision along with
removal of associated salivary gland tissues, and marsupialization (for a large
lesion in close proximity to vital structures). Other techniques reported in the
literature include cryotherapy, laser (such
e34
as erbium or carbon dioxide), intralesional corticosteroids, topical γ-linolenic
acid, and intralesional sclerosing agent.9-13
Surgical excision was chosen for the
present case to allow for the complete
removal of the lesion and subsequent
histopathological evaluation to confirm
the diagnosis.
Conclusion
The presentation of a typical oral mucocele results in a simple diagnosis. When
an atypical presentation occurs, however,
it is important to evaluate and investigate
the lesion in a stepwise manner to reach
a definitive diagnosis. Oral mucocele
should be included as a differential diagnosis for any submucosal swelling over the
buccal mucosa. Recognizing these variants is important to avoid misdiagnosis.
Author information
Dr. Nilesh is a reader, School of Dental
Sciences, Krishna Institute of Medical
Sciences, Karad, India. Dr. Chandra is
a professor, Yenepoya Dental College &
Hospital, Mangalore, India.
References
1. Baurmash HD. Mucoceles and ranulas. J Oral Maxillofac Surg. 2003;61(3):369-378.
2. Ata-Ali J, Carrillo C, Bonet C, Balaguer J, Penarrocha
M, Penarrocha M. Oral mucocele: review of the literature. J Clin Exp Dent. Available at: http://www.
medicinaoral.com/odo/volumenes/v2i1/jcedv2i1p18.
pdf. Accessed October 27, 2014.
General Dentistry
www.agd.org
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