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editorial
Rethinking the Dental Model
Reversing current downward trends in income may entail a change in the way we practice dentistry.
I
n May, I attended a conference in Albany held
in conjunction with a NYSDA-sponsored meeting
of the president elects of the Association’s components. The title of the conference was “The Changing
Dental Care Landscape.” The moderator was Marko
Vujicic, Ph.D., managing vice president of the ADA
Health Policy Institute. The ADA recently completed a study, headed by Dr. Vujicic, concerning the
future of dental practice in the United States. What
the study uncovered is eye-opening.
The current downturn in dental spending didn’t
just happen. It began around 2002. At the beginning
of the recession, dental spending flattened out; it has
yet to recover to pre-recession levels. As a consequence, incomes of dentists have declined. A disturbing aspect of this is that these income figures show
no sign of improving, as has happened in the past.
Driving this downturn has been a decrease in
dental usage by people 19 to 64 years of age. Conversely,
children’s dental use has actually increased, as has that
of the elderly. The increase in pediatric dental services
is due to a rise in Medicaid eligibility. On the opposite
side of the spectrum, children from more affluent
families haven’t curtailed dental visits, but they also
haven’t increased them significantly.
Why the downturn in the middle-age group? It
basically comes down to needs vs. wants. Since den4
JUNE/JULY 2014 • The New York State Dental Journal
tistry is more discretionary-income driven, it
appears that this age group prefers to spend money
on other things. Its members also tend to be healthier. And they don’t see the need for regular dental
care if they are not experiencing symptoms of a
problem. Moreover, people in the middle tend to
have more constraints on their time. They don’t, or
perceive they don’t, have time to go to the dentist.
Add to this the fact that there has been a
decrease in the amount of dental insurance coverage available to this group, either privately or as
part of their compensation packages at work.
Poorer individuals do not have the income needed
to pay for dental services, and only a few states offer
adult Medicaid coverage.
People in the middle have also seen sluggish
growth in their personal incomes, leading to more
and more adults saying they need dental services
but can’t afford them. This in turn has led to an
increase in emergency room dental visits. Over the
past 10 years, the number of visits to an emergency
room for dental problems has doubled, an increase
driven by people 21 to 35 years old. Unfortunately,
their ER visits rarely attack the problem that caused
the visit in the first place. Treatment is usually palliative, aimed at getting the patient out of pain, not
at correcting the problem.
NYSDA
Directory
OFFICERS
John J. Liang, President 2813 Genesee St., Utica, NY 13501
David J. Miller, President Elect
467 Newbridge Rd., East Meadow, NY 11554
Richard F. Andolina, Vice President
74 Main St., Hornell, NY 14843
Mark J. Weinberger, Treasurer
78 Southbury Rd., Clifton Park, NY 12065
Robert M. Peskin, Speaker of the House
601 Franklin Ave., #225, Garden City, NY 11530
Mark J. Feldman, Executive Director 20 Corporate Woods Blvd., Albany, NY 12211
Steven Gounardes, ADA Trustee
351 87th St., Brooklyn, NY 11209
BOARD OF TRUSTEES
All of this change in spending has hurt dentists
financially. Practice revenues are down on
average for both generalists and specialists.
Looking ahead, we see a shift in emphasis
on value. What value will we give our patients
with the treatments we render? Will patients
perceive this value? What are the appropriate
quality values in dentistry? It seems it will take
some time to determine exactly what this
means and how we can control the outcome.
But control it we must, or we will be bulldozed
into irrelevance.
There is a movement in medicine away
from the solo practitioner, or silo, mentality toward
the team approach. Dentistry is still a cottage
industry. Most of its practitioners work alone
or in partnership arrangements. Even though
the corporate model is beginning to grow,
most dental offices don’t operate that way.
Meanwhile, physicians are moving into larger
groups with more specialists as part of the
group. Dr. Vujicic recommended that dentistry
follow this trend. He sees larger group practices
in the future, with all specialists represented in
them. And, he predicts, as with medicine, participants will be rewarded by positive outcomes
and not just by rendering treatment.
Joel M. Friedman, Immediate Past President
525 E. 68th St., New York, NY 10065
NY – Edward J. Miller Jr
121 E. 60th St., #7A, New York, NY 10022
2 – James Sconzo
1666 Marine Pkwy, Brooklyn, NY 11234
3 – Lawrence J. Busino
2 Executive Park Dr., Albany, NY 12203
4 – Frederick W. Wetzel
1556 Union St., Schenectady, NY 12309
5 – William H. Karp
Bldg. 6, 4500 Pewter Lane, Manlius, NY 13104
6 - Scott J. Farrell
39 Leroy St., Binghamton, NY 13905
7 - Robert J. Buhite II
564 E. Ridge Rd., #201, Rochester, NY 14621
8 – Brendan Dowd
6932 Williams Rd., #1900, Niagara Falls, NY 14304
9 – Anthony Cuomo
667 Stoneleigh Ave., #301, Carmel, NY 10512
N – Michael S. Shreck
1300 Union Turnpike, #201, New Hyde Park, NY 11040
Q – Joseph R. Caruso
40-29 Utopia Pky., Auburndale, NY 11358
S – Paul R. Leary
80 Maple Ave., #206, Smithtown, NY 11787
B – Richard P. Herman
2 Lockwood Lane, New Windsor, NY 12553
COUNCIL CHAIRPERSONS
Council on Awards
Steven Gounardes
351 87th St., Brooklyn, NY 11209
Dental Benefit Programs
Viren Jhaveri
43-70 Kissena Blvd., #LEL, Flushing, NY 11355
Dental Education & Licensure
Anthony Ficara
880 Western Ave., Albany, NY 12203
Dental Health Planning & Hospital Dentistry
Carl H. Tegtmeier
359 E. Main St., #2C, Mt. Kisco, NY 10549
Dental Practice
Paul Abicocco
2877 Hylan Blvd., Staten Island, NY 10306
Ethics
Richard B. Serchuk
5 Valentines Lane, Old Brookville, NY 11545
Governmental Affairs
Lauro Medrano
5802 6th Ave., Brooklyn, NY 11220
Membership & Communications
Jay Skolnick
39 W. Main St., Webster, NY 14580
Peer Review & Quality Assurance
Egidio Farone
115 E. 61st St., #15S, New York, NY 10065
Professional Liability Insurance
David Delaney
476 Albany-Shaker Rd., Loudonville, NY 12211
OFFICE
Suite 602, 20 Corporate Woods Blvd., Albany, NY 12211
(518) 465-0044 (800) 255-2100
Mark J. Feldman
Lance Plunkett
Beth M. Wanek
Michael J. Herrmann
Judith L. Shub
Joshua Poupore
Laura B. Leon
Mary Grates Stoll
Executive Director
General Counsel
Associate Executive Director
Assistant Executive Director Finance-Administration
Assistant Executive Director Health Affairs
Assistant Executive Director Marketing and Communication
Assistant Executive Director
Managing Editor
The New York State Dental Journal • JUNE/JULY 2014
5
All is not lost, though. There will be plenty of opportunities out
there for dentists who can adapt to future changes. Dr. Vujicic
likened this to how Wayne Gretzky played hockey. Gretzky was
such an accomplished player because he always anticipated where
the puck would be, not where it was at the time. The same will be
true in dentistry. We can’t continue to chase yesterday’s challenges. We must anticipate what the future challenges will be and
address them now. Toward that end, the ADA has established its
Center for Professional Success, a go-to resource to assist dentists
in their practices and professional lives.
Dentists need to rethink how they dispense care. They must
put the value of the service at the forefront and think about the
best way to deliver that value. It may be something as simple as
revisiting the “see your dentist twice a year” dogma we have all
accepted during our professional lives. We must adjust the treatment to fit the patient’s needs. Some patients may need more
frequent visits, while others need to be seen less often. Patients
must be able to see the value in what we provide and not just the
price tag associated with it.
Dentists must leverage the value agenda. They need to consolidate their services and measure their practices. Analytics is the
big thing in sports today. Every team measures all sorts of data.
Dentists need to do the same. After all, if you don’t know what you
are doing, and how you are doing it, you can’t respond to change.
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JUNE/JULY 2014 • The New York State Dental Journal
We need to interact more with our medical colleagues. Physicians
know close to nothing about the oral cavity. We can help correct
this situation. Screening for chronic diseases in the dental office
through sialography is becoming an important part of dental
practice. This can be a win/win for the dentist and the physician.
The patient gets screened in the dental office and gets referred to
the physician for any disease discovered.
Physicians need to understand the important relationship
between the oral cavity and a patient’s overall health. We know
this, but they don’t. We must educate them. Many diseases have
oral components. Sometimes the first indication of a systemic
problem appears in the mouth. With good communication with
our physician colleagues, we build trust and, through that trust,
are able to treat our patients more completely.
We must be more proactive in our approach to the future.
The dental landscape is changing, and the challenges that lie
ahead are formidable. This is a seminal moment for dentistry.
How we react to the changes coming will determine if we are in
control or if we will be controlled. I definitely want to be on the
side of control. How about you?
D.D.S.
THE NEW YORK STATE DENTAL JOUR­NAL
CONTRIBUTORS EDITOR
Kevin J. Hanley, D.D.S.
MANAGING EDITOR
Mary Grates Stoll
ADVERTISING MANAGER
Jeanne Deguire
ART DIRECTORS
Kathryn Sikule / Ed Stevens
EDITORIAL REVIEW BOARD
Frank C. Barnashuk, D.D.S.
David A. Behrman, D.M.D.
Michael R. Breault, D.D.S.
Ralph H. Epstein, D.D.S.
Daniel H. Flanders, D.D.S.
Joel M. Friedman, D.D.S.
Chester J. Gary, D.D.S., J.D.
G. Kirk Gleason, D.D.S.
John T. Grbic, D.M.D., M.S., MMSc.
Brian T. Kennedy, D.D.S.
Stanley M. Kerpel, D.D.S.
Elliott M. Moskowitz, D.D.S., M.Sd
Francis J. Murphy, D.D.S.
Eugene A. Pantera Jr., D.D.S.
Root Amputation
A New Look into an Old Procedure
Rania Livada, D.D.S., M.S., is assistant professor in the Department of
Periodontology, College of Dentistry, University of Tennessee Health Science
Center, Memphis, TN.
Norman Fine, D.M.D., M.S., is in private practice limited to periodontics and
implants in Greenville, SC.
Jacob Shiloah, D.M.D., is professor in the Department of Periodontology, College
of Dentistry, University of Tennessee Health Science Center, Memphis, TN.
Management of the Dental Patient on
Anticoagulant Medication
A Review
Manoj Agarwal, M.D.S., is assistant professor, Department of Conservative Dentistry
and Endodontics, Government Dental College and Hospital, Jaipur, Rajasthan, India.
Sankalp Mittal, M.D.S., is assistant professor, Department of Oral and Maxillofacial
Surgery, Government Dental College and Hospital, Jaipur, Rajasthan, India.
Sharmistha Vijay, M.D.S., is associate professor, Department of Periodontology and
Implantology, Government Dental College and Hospital, Jaipur, Rajasthan, India.
Pooja Yadav, M.D.S., is assistant professor, Department of Prosthodontics,
Mahatma Gandhi Dental College and Hospital, Jaipur, Rajasthan, India.
Vasim Raja Panwar, B.D.S., is a research fellow.
Neha Gupta, M.D.S., is assistant professor, Department of Prosthodontics,
Government Dental College and Hospital, Jaipur, Rajasthan, India.
Robert M. Peskin, D.D.S.
John L. Santopolo, D.D.S.
Georgios Romanos, D.D.S.,
D.M.D., Ph.D., Prof.Dr.med.dent
Robert E. Schifferle, D.D.S., MMSc., Ph.D.
PRINTER
Fort Orange Press, Albany
NYSDJ (ISSN 0028-7571) is published six times a year,
in January, March, April, June/July, August/ September
and November, by the New York State Dental Association, 20 Corporate Woods Boulevard, Suite 602, Albany,
NY 12211. In February, May, October and December,
subscribers receive the NYSDA News. Periodicals postage paid at Albany, NY. Subscription rates $25 per year
to the members of the New York State Dental Association; rates for nonmembers: $75 per year or $12 per issue, U.S. and Canada; $135 per year foreign or $22 per
issue. Postmaster: Please send change of address to the
New York State Dental Association, Suite 602, 20 Corporate Woods Boulevard, Albany, NY 12211. Editorial
and advertising offices are at Suite 602, 20 Corporate
Woods Boulevard, Albany, NY 12211. Telephone (518)
465-0044. Fax (518) 465-3219. E-mail info@nysdental.
org. Website www.nysdental.org. Microform and article
copies are available through National Archive Publishing Co., 300 N. Zeebe Rd., Ann Arbor, MI 48106-1346.
2
Angiofibrolipoma of the Retromolar Pad Region
Case Report with a Review of Literature
Farzaneh Agha-Hosseini, D.D.S., M.Sc., is professor in the Department of Oral
Medicine, Dentistry School, Tehran University of Medical Sciences, Tehran, Iran.
Elham Moslemi, D.D.S., M.Sc., is professor in the Department of Oral
Medicine, Dentistry School, Tehran University of Medical Sciences, Tehran, Iran.
The Residual Radicular Cyst
Jessica Lee, D.D.S., is an oral and maxillofacial surgery resident at NYU
Langone Medical Center, Bellevue Hospital Center, New York, NY. She is a former research assistant in the Salivary Gland Center, Columbia University College
of Dental Medicine, New York, NY.
John Costandi, D.M.D., is an oral and maxillofacial surgery resident at New
York-Presbyterian Hospital (Columbia campus), New York, NY.
Louis Mandel, D.D.S., is director of the Salivary Gland Center and associate
dean and clinical professor, oral and maxillofacial surgery, Columbia University
College of Dental Medicine, New York, NY.
Treatment of a Mandibular Cyst Before Implant Placement
Case Report
Miles Yacker, D.D.S., is clinical associate professor and course director of
implant dentistry: Biological Basis and Implant Surgery Seminar in the Ashman
Department of Periodontology and Implant Dentistry, New York University
College of Dentistry, New York, NY, and in private practice in Lawrence, NY.
JUNE/JULY 2014 • The New York State Dental Journal
John Ricci, Ph.D., is associate research scientist in the
Department of Biomaterials and Biomimetics, New York
University College of Dentistry, New York, NY.
Ioana Chesnoiu Matei, D.D.S., M.S., is a resident in postgraduate periodontics, Ashman Department of Periodontology
and Implant Dentistry, New York University College of
Dentistry, New York, NY.
Bin Hu, M.D., is associate research scientist in the
Department of Biomaterials and Biomimetics, New York
University College of Dentistry, New York, NY.
Sachin Mamidwar, M.B.B.S., M.S., is general manager of
Orthogen, LLC, Springfield, NJ.
Dr. Agarwal
Dr. Mittal
Dr. Vijay
Dr. Yadav
Dr. Panwar
Dr. Gupta
Dr. Agha-Hosseini
Dr. Mandel
Dr. Yacker
Dr. Ricci
Dr. Matei
Dr. Hu
Dr. Mamidwar
Dr. Maloney
Dr. Raymond
Dr. Hershkowitz
Dr. Bakhtiar
Dr. Asna-Ashari
Oral and Dental Manifestations of Celiac Disease
William James Maloney, D.D.S., is a clinical associate professor in the Department of Cariology and Comprehensive Care at
New York University College of Dentistry, New York, NY.
George Raymond, D.D.S., is a clinical instructor in the
Department of Cariology and Comprehensive Care, New
York University College of Dentistry, New York, NY.
David Hershkowitz, D.D.S., is clinical assistant professor and
associate chair, Department of Cariology and Comprehensive
Care, New York University College of Dentistry, New York, NY.
Glenn Rochlen, D.D.S., is clinical assistant professor,
Department of Cariology and Comprehensive Care, and
group practice director, New York University College of
Dentistry, New York, NY.
The Plasma-Rich in Growth Factor as a
Suitable Matrix in Regenerative Endodontics
A Case Series
Hengameh Bakhtiar, D.D.S., M.Sc., is assistant professor
in the Department of Endodontics, Tehran Dental Branch,
Islamic Azad University, Tehran, Iran.
Mehdi Vatanpour, D.D.S., M.Sc., is assistant professor in
the Department of Endodontics, Tehran Dental Branch,
Islamic Azad University, Tehran, Iran.
Arezoo Rayani, D.D.S., is a general dentist in Tehran, Iran.
Fina Navi, D.D.S., M.Sc., is assistant professor in the
Department of Endodontics, Tehran Dental Branch, Islamic
Azad University, Tehran, Iran.
Ehsan Asna-Ashari, D.D.S., M.Sc., is assistant professor in
the Department of Endodontics, Tehran Dental Branch,
Islamic Azad University, Tehran, Iran.
Anahid Ahmadi, D.D.S., is a general dentist in Tehran, Iran.
Hamid Jafarzadeh, D.D.S., M.Sc., is associate professor in
the Dental Research Center, Department of Endodontics,
Faculty of Dentistry, Mashhad University of Medical Sciences,
Mashhad, Iran.
Dr. Jafarzadeh
The New York State Dental Journal • JUNE/JULY 2014
3
Medicaid Covers Smoking Cessation
Counseling by Dentists and Hygienists
Judith L. Shub, Ph.D.
Coverage for smoking cessation counseling (SCC) became effective on April 1 in the fee-for-service
Medicaid program and on July 1 for the Medicaid managed care program.
The New York State Department of Health (DOH) has prioritized
tobacco cessation as a public health initiative. The department
now includes coverage for smoking cessation counseling (SCC)
for Medicaid patients by dental practitioners. This policy is consistent with public health recommendations from numerous
sources, including the American Dental Association. The associated Medicaid policies are included in the May 2014 DOH Medicaid Update, available on the DOH website, www.health.ny.gov.
Dental practitioners will be able to provide and receive Medicaid
reimbursement for SCC services as defined in their scope of practice.
There have been changes to New York State law defining the scope
of practice of dentistry since 1992, including inclusion of the term
“maintaining dental health” in the scope of practice and continuing
education requirements on the topic of the adverse health effects of
tobacco use. Based on these changes, the State Board for Dentistry
has determined that prescribing smoking cessation products is currently within the scope of practice of dentistry. The DOH’s expansion of Medicaid benefits does not supersede or alter any regulations
issued by the New York State Department of Education governing
scope of practice for dentists or dental hygienists.
Medicaid Coverage for SCC
Coverage for SCC in Medicaid became effective April 1 in the fee-forservice Medicaid program and on July 1 for the Medicaid managed
care program. Dental practitioners will be allowed to provide two SCC
sessions to a Medicaid beneficiary within any 12 continuous months.
NYSDA advises dentists who provide treatment to Medicaid recipients
enrolled in managed care to review their contracts to determine how
this change affects their reimbursement and whether any changes
need to be made to their participating provider contracts.
According to DOH, reimbursement to office-based dental
practitioners will be at the rate of $10 per visit. To be eligible for
reimbursement, claims must meet the following criteria:
l SCC must be provided face-to-face by either a dentist or a
dental hygienist who is supervised by a dentist.
l SCC must be billed by either an office-based dental practitioner or by an Article 28 clinic that employs a dentist.
l Dental practitioners can only provide individual SCC servic-
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JUNE/JULY 2014 • The New York State Dental Journal
es. There is no reimbursement for SCC provided to groups of
patients in one session.
l SCC must be greater than three minutes in duration.
l Dental claims for SCC must include the CDT procedure code
D1320 (tobacco counseling for the control and prevention
of oral disease).
l Article 28 clinics that bill based on ambulatory patient group
models must include the ICD-9 CM Diagnosis code 305.1
(tobacco use disorder).
l In a dental office or an Article 28 clinic, SCC should only
take place during a dental visit as an adjunct when providing
a dental service. It cannot be billed as a stand-alone service.
l A dental practitioner will be allowed to provide two smoking cessation counseling sessions to a Medicaid beneficiary
within any 12 continuous months.
l SCC complements existing Medicaid-covered benefits for
prescription and non-prescription smoking cessation products, including nasal sprays, inhalers, Zyban (bupropion),
Chantix (varenicline), over-the-counter nicotine patches
and gum. (Bear in mind that dental hygienists cannot prescribe medication to patients.)
To receive reimbursement for SCC services, the following information must be documented in the patient’s dental record:
1. At least four of the “5 A’s” as described below.
2. If patient is willing to quit, an offer of medication as needed,
a target date for quitting and a follow-up date—with documentation in the record that the follow-up occurred.
3. If patient is unwilling to quit, the patient’s expressed roadblocks.
4. Referrals to the New York State Smoker’s Quitline and/or
community services to address roadblocks and for additional
cessation resources and counselling, if needed.
Smoking Cessation Guidelines
DOH’s criteria for Medicaid reimbursement for SCC are based on
two guidelines: the “5 A’s of treating tobacco dependence” and the
“5 R’s.” DOH cites the Clinical Practice Guideline “Treating Tobacco
Use and Dependence: 2008 Update” that demonstrated that efficacious treatments for tobacco users exist and recommends that prac-
titioners follow the “5 A’s” of treating tobacco dependence. They are:
1. Ask the patient about tobacco use at every visit and document the response.
2. Advise the patient to quit in a clear and personalized manner.
3. Assess the patient’s willingness to make a quit attempt at this
time.
4. Assist the patient to set a quit date and make a quit plan. Offer medication as needed.
5. Arrange to follow up with the patient within the first week,
either in person or by phone, and take appropriate action to
assist him or her.
For patients who are not ready to make a quit attempt, clinicians should use a brief intervention designed to promote the motivation to quit. Specific content areas that should be addressed
can be captured by the “5 R’s.” They are:
1. Relevance. Encourage the patient to state why quitting is
relevant to him or her, being as specific as possible.
2. Risks. Ask the patient to identify potential negative consequences of his or her tobacco use, including acute, environmental and long-term risks.
3. Rewards. Ask the patient to identify potential benefits, such
as improved health, saving money, setting a good example for
children and better physical performance.
4. Roadblocks. Ask the patient to identify barriers (e.g., fear
of withdrawal or weight gain) and provide treatment and resources to address them.
5. Repetition. The motivational intervention should be repeated every time the patient is seen.
Submitting Medicaid Claims for SCC
Medicaid coverage for smoking cessation counseling is clearly a
well-intended adjunct to DOH’s efforts to reduce tobacco use in
New York State in which dentists can play an important part. The
decision to provide SCC and submit claims for Medicaid reimbursement requires serious consideration by any dentist. To help
ensure that reimbursement will be made, it is advisable to:
l Perform all specific requirements enumerated in Medicaid policy.
l Document the time interval, details of the counseling and/
or intervention, patient response, follow-up, etc., and adherence to the specific Medicaid requirements.
And, again, dentists who provide treatment to Medicaid recipients enrolled in managed care should review their contracts,
confirm with the managed care company how this change will be
implemented in writing, and determine whether any change is
needed to their participating provider contracts. p
Dr. Shub is NYSDA Assistant Executive Director for Health Affairs.
The New York State Dental Journal • JUNE/JULY 2014
19
A Conversation with
NYSDA President
John J. Liang, D.M.D.
Photos by Jeffrey Walters /JF
Can you tell us something about yourself?
Where did you grow up?
I was born in Hong Kong BCC in 1951. I am Chinese by descent. My parents and two older sisters were all born on mainland
China. My father was Ping Tchang Liang, M.D. My mother Theresa Chiao-ming Liang. I have two sisters—Hilda and Maria. We
were all born about four years apart. My father graduated in 1942
from medical school at Aurora University in Shanghai, a private
Catholic university established by the French and run by Jesuit
priests. The Jesuits were an extremely strict order and set firm
curfews for their students. My father had to sneak out to date my
mom. Nonetheless, my parents were extremely devout Catholics
throughout their entire life. One of their proudest moments had
to have been their visit to the Vatican.
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JUNE/JULY 2014 • The New York State Dental Journal
When did you come to the United States?
My parents and sisters survived the atrocities of the Japanese invasion and Communist takeover of China. In 1950, my father
smuggled our family out of the country through the underground, escaping to Hong Kong. These were extremely dangerous
times. My parents lost many close friends to both the Japanese
and the Communists. My mother was pregnant with me at the
time, and that’s how I was born in Hong Kong, just a ferry ride
away from mainland China.
In Hong Kong, my father worked for the British Merchant
Marine as a ship’s surgeon and was away for months at a time.
My mother cared for the family while he was away. All the while,
my father still felt the Communists remained a real threat. It was
a near impossible feat but in 1959, after years of waiting to qualify
for a visa, and with a loan from Catholic missions, my father succeeded in bringing our family to the United States. This explains
why my father felt indebted to and remained in close touch with
Catholic missions through his entire life.
My father, in his mid-30s in 1959 when he arrived in the
United States, determined to succeed. My family lived in New
Jersey for a brief time before settling in Pittsburgh, PA. My father
interned at Shadyside Hospital in Pittsburgh, passed his medi-
John and family. Daughter, Kirsten with her son, Connor; Kirsten’s husband, Brian Getchell with
their daughter, Harper; son, Kyle.
cal boards and went on to specialize in pathology at St. Joseph’s
Hospital, also in Pittsburgh. He was employed at Allegheny Valley
Hospital in Natrona Heights, PA, as a pathologist. That’s where
he was fondly given his nickname “Ping.” And it was during his
tenure there that he proudly became an American citizen.
His becoming a citizen was an indication of how much my
parents valued freedom. And it provided an opportunity for all
of their children to become educated. My parents’ sacrifices and
high regard for education were not wasted. My sister Hilda earned
her M.S. in chemistry. She and her husband, Stephen Hui, a retired Ph.D., in biophysics, have relocated to Kennwick, WA, after
years of living in Buffalo. My sister Maria received her M.D. from
the University of Pittsburgh and went on to specialize in neurology. She and her husband, Mario Ludmer, a retired neurosurgeon,
live in North Palm Beach, FL
My niece, Jennifer, is a neurologist in Monterey, CA, and my
nephew, Peter, has his Ph.D. in computer science and is living in
Kennewick.
And I have my parents to thank for being where I am today!
Who was most influential in your becoming a dentist?
My high school years were spent growing up in a suburb of
Pittsburgh called Natrona Heights. My neighbor across the
street, Robert Maple, was a semi-retired dentist. He was a
graduate of the School of Dental Medicine at the University
of Pittsburgh. He provided me with the most fantastic dental
John and love of his life, Sharon Tarallo.
care, personally driving me to and from his small second-story
office, showing me how he made his dentures with vulcanite,
how he triturated his amalgam, and how he used a dental dam
for every procedure (this was in the 1960s). I never knew how
meticulous and great a dentist he was until I went to dental
school myself years later. He even tried to teach me how to
swing a golf club!
Dr. Maple was an important part of my growing up, but my
sister Maria was the one who really encouraged me to apply to
dental school when the doors of medical school would just not
open for me. I have no regrets.
How did you end up in Central New York?
I graduated from the University of Pittsburgh School of Dental
Medicine in 1980 and was commissioned as a reserve officer in
the Air Force. I was stationed at Griffiss Air Force Base in Rome, in
upstate New York. I separated from the Air Force in 1985, having
decided to go into private practice. That’s how I ended up in Central New York. I met my wife (since divorced) in the Air Force.
Kirsten, my stepdaughter, was 4 years old at the time. In December 1986, son, Kyle, was born—a proud moment in my life. I loved
and raised Kirsten as my own. She is now a child life specialist at
Boston Children’s Hospital and a graduate of Wheelock College
in Boston, where she earned her Master’s degree. She and husband, Brian Getchell, are the proud parents of 2-year-old Connor
and 1-year-old Harper.
The New York State Dental Journal • JUNE/JULY 2014 21
Next to his family, John Liang’s proudest possessions are his cars, including this reconditioned 1990 BMW, a rare 12-cylinder
model that belonged to his mother.
Kyle graduated from Cortland College with a B.S. in athletic
training. He earned his M.S. from Canisius College in Buffalo
and is now employed as an athletic trainer at SUNY Cobleskill.
We understand you share your home with several dogs.
True?
My significant other and love of my life, Sharon Tarallo, and I
share many things in common. But we both have a strong affection for living things. Before I met Sharon, I had one dog, Biddy,
a Westie. Sharon has adopted and rescued many dogs and cats.
She has a 7-year-old Australian Shepherd and a cat named Beso
(Spanish for “kiss”). Together we saw and fell in love with two
eight-week-old sibling rescues from a local foster agency, Dillon and Cassie. The pups were inseparable, so we adopted both
of them. The animals get along wonderfully and are extremely
affectionate.
What is the last movie you saw?
“Captain Phillips” with Tom Hanks. He is truly an accomplished
actor. The movie did not have a dull moment, even though I knew
the outcome from the start. One of my favorite TV shows has to
be “NCIS.” We also enjoy watching “The Voice.”
What do you do to relax/unwind?
My general dental practice and taking care of four dogs and a cat
doesn’t leave me much time for myself. My hobbies include pho-
22
JUNE/JULY 2014 • The New York State Dental Journal
Days off at home, John enjoys time in kitchen with his significant
other, Sharon Tarallo.
tography, woodworking, home improvements, tinkering with my
cars and gardening/landscaping. I also enjoy cooking. My mother taught me a lot of the basics of Chinese cooking, but I also
learned by watching the chefs at an upscale Chinese restaurant
where I worked as a waiter all through dental school. If I really
want to zone out, I park my brain in neutral, get on my big 60”
Ferris zero-turn commercial mower and zip around my five acres
of lawn on a bright sunny day!
What is your idea of a perfect day?
I would take my entire family, including the grandchildren, to
Watkins Glen for the day. We would drive my 2006 Z06 Corvette
and my 1990 750iL with a V12 around the famed Watkins Glen
racetrack. Then we would stop by the Glenora Winery and have
a wonderful lunch out on the deck overlooking the vineyard and
Seneca Lake. Of course, the adults would go wine tasting after.
My children Kyle and Kirsten actually gave me such a day as a
Father’s Day gift about two years ago.
Did you ever imagine you would be president of the New
York State Dental Association?
No! The thought never even remotely came to mind in all the
years of participating in organized dentistry. It’s like the opportunity presented itself all of a sudden and before I knew it, I was
going through the chairs for NYSDA. It is a great honor. I only
wish my mother and father could be alive to witness this time in
Devoted to animals, especially those in need of rescue, John and Sharon share their home with
four dogs and a cat.
my life. Sadly, I lost both my parents, my father to acute leukemia
and my mother to squamous cell carcinoma.
John is aided in his Utica general dental practice by, from left, Patty Cotronea, Sue Krebs,
Becky Irizarry.
THE PARTICULARS
Employment
What are your goals for the coming year?
I look forward to working with my fellow officers, trustees, members of the House and councils, the NYSDA executive director and
staff, and grassroots members to continue advancing the wonderful initiatives that have been created by my predecessors, such as
recruitment and retention, communications and technology, and
fiscal responsibility.
I think the dental profession is hardly immune to economic
pressures and political influences. My suspicions were confirmed
at the ADA Presidents-Elect Conference in Chicago, and again
at this year’s NYSDA Presidents-Elect Conference in Albany. The
featured speaker, Marko Vujicic, managing vice president of the
ADA Health Policy Institute, spoke to this very issue. The ADA
has performed environmental scans and published white papers
on the changing dental profession. These changes have already
been in effect for some time now. We need to take a hard look at
where our profession is headed so that NYSDA and the tripartite
can develop strategic plans to help our profession and members
continue to succeed in the future. p
General Dentist
Utica, NY
Attending Dentist/Dental Hygiene Advisory Board
SUNY Canton Dental Hygiene Program, Rome, NY
Education
BS Chemistry, University of Pittsburgh,
Pittsburgh, PA
MS Forensic Chemistry, University of Pittsburgh,
Pittsburgh, PA
DMD, University of Pittsburgh School of Dental Medicine,
Pittsburgh, PA
Professional Offices/Titles
Captain, USAF Dental Officer, 1980-85
USAF Reserve IMA Dental Officer, 1985-87
Past President, Fifth District Dental Society
Fellow, American College of Dentists
Fellow, International College of Dentists
Fellow, Pierre Fauchard Academy
Third Degree Knight, Knights of Columbus
The New York State Dental Journal • JUNE/JULY 2014 23
Periodontology
Root Amputation
A New Look into an Old Procedure
Rania Livada, D.D.S., M.S.; Norman Fine, D.M.D., M.S.; Jacob Shiloah, D.M.D.
ABSTRACT
A treatment option for managing furcation invasions
is root amputation. Long-term survival of resected
molars requires a complete harmony of sequential
endodontic, periodontic, restorative and maintenance procedures. The main objective of this article
is to provide a concise historical perspective of this
procedure and to review available literature regarding its efficacy and limitations. It also illustrates a
current modification of the procedure using guided
bone regeneration (GBR) and socket preservation to
eliminate some of the potential disadvantages of the
traditional root amputation procedure.
Root amputation—once a common surgical procedure aimed at
eliminating furcation invasion in multirooted teeth—was first described by Farrar1 in 1884. It was reintroduced into periodontics
by Messinger and Orban in 1954.2 (Similar cases were described
in Germany by Gottlieb and Orban in 1933.3) Since then, the
procedure has been modified, and its clinical outcomes evaluated
longitudinally by several researchers.
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JUNE/JULY 2014 • The New York State Dental Journal
The main objective of this article is to provide a historical perspective of root amputation, review available literature regarding
its efficacy and illustrate a current modification of the procedure
that combines recent advances in bone regeneration and ridge
augmentation.
Root Amputation Technique
The indications for root amputation were clearly set forth by
Basaraba4 and Staffileno.5 They include Class III furcation involvement; deep Class II furcation; cases of isolated severe bone
loss involving one of the roots; vertical root fracture; subgingival root caries; and endodontic indications, such as a persisting
periapical pathologic lesion, root resorption or iatrogenic root
perforation. Minsk and Polson in 20066 added another indication that includes teeth with high strategic value. This may
include teeth with a preexisting fixed prosthesis (as the case presented below) or in cases where anatomic considerations preclude implant placement.
A long-term successful outcome of root amputation depends
upon four variables, including meticulous endodontic, periodontic and restorative procedures, and a highly motivated patient.
A prerequisite for root amputation is proper endodontic therapy prior to periodontal surgery in order to determine the feasibility of complete canal obturation. Bühler7 attributed the high
failure rate (32.1%) of root resections to endodontic reasons. It
is well documented that multirooted teeth do not respond as favorably as single rooted teeth to endodontic therapy following
nonsurgical retreatment8 or surgical intervention.9 The complex
pulp anatomy of molar teeth presents a greater challenge to eliminating root canal infection, especially when accessory canals are
present. The incidence of these canals has been reported to range
from 42% to 52% in the mesio-buccal root of maxillary molars.10
However, in questionable cases of root proximity or possible
root fusion or ankylosis, it is recommended that periodontal surgery be completed prior to endodontic intervention in order to
ensure its feasibility. In these cases, vital root amputation could
be executed without adverse clinical and histological effects, if
the exposed pulp is properly managed.11,12 Definitive endodontic
therapy should be completed within two weeks11 to six months,13
since tooth vitality is significantly reduced six months following a
vital root amputation.13
A successful root amputation requires complete removal of
any ledges or undercuts from the remaining furcation area, after
extraction of the resected root. Backman14 reported four cases of
improper or incomplete root resections. In these cases, the roof of
the furcation persisted and the sites continued to lose bony sup-
port due to an environment that favored biofilm accumulation
and retention. To prevent such undue sequelae, it is highly recommended that completeness of the surgical procedure be verified
radiographically. Newell15 examined 70 root-resected teeth, of
which 30% were determined to be inadequate due to remaining
ledges or residual roots. Majzoub and Kon16 reported that 86% of
resected maxillary first molars exhibited violation of the biologic
width. Additionally, only 6% of the examined resected molars had
a topography that was easily amenable to periodontal maintenance.16
Restoring the remaining tooth properly imposes many clinical
challenges. The tooth may require a new fixed prosthesis, which,
in turn, may require additional retention with fabrication of a
post and core, a procedure that might weaken the root. In order
to promote a healthy environment, the new restoration should
not violate the biologic width or hinder proper plaque control.
Special considerations must be given to the occlusal loads that the
tooth has to endure in order to promote longevity. Biomechanical
elements and root fractures17,18 have been cited as main causes of
failure of root amputation. To minimize this risk, the “occlusal
table” should be narrow bucco-lingually and free of any occlusal
interference.19
The New York State Dental Journal • JUNE/JULY 2014
25
Because of these factors and the complex nature of this procedure, a suitable candidate must be highly motivated, free of parafunctional habits such as bruxism or risk factors such as smoking.
As with any periodontal patient, periodic supportive maintenance
treatment is required to prevent recurrence of the disease process.
Figure 1A. Preoperative view of #14 illustrating 8
mm probing depth (UNC-15 probe), attachment loss
and bleeding on probing.
Figure 2A. Radiograph taken during surgery to
verify complete amputation of mesio-buccal root
of #14. Patient was informed about open margin
on distal of existing crown. Patient declined further
treatment due to financial reasons.
Figure 1B. Preoperative radiographic appearance of #14 area. Note
radiolucency along mesial root. Tooth
had been treated endodontically twice
without alleviating symptoms during
function.
Figure 2B. Closer view of surgical site
following extraction of MB root and fracture
of thin buccal plate. Note complete removal
of furcation roof.
Figure 3. Guided bone regeneration procedure: placement of allograft bone overfilling socket
and coverage by barrier membrane prior to replacement of full thickness flap.
26
JUNE/JULY 2014 • The New York State Dental Journal
Long-term survival of root amputation requires a complete harmony
of sequential endodontic, periodontic, restorative and maintenance
procedures. A shortfall of any step may lead to failure. Review of the
literature on its long-term effectiveness has yielded mixed results.
Bergenholtz20 was first to report on survival of resected molars 11
years postoperatively, with an overall success rate of 85%. Similar
success rates were reported by Carnevale and his co-workers 21 in
a retrospective study of resected mandibular molars. These general
findings are supported by short-22 and long-term studies.18
In contrast to these positive results, several studies have reported adverse outcomes and poor long-term survival of resected
molars. Langer and his coworkers,17 in a retrospective study of
100 resected teeth, reported a high rate of failure of 38% over a
10-year observation period. The main cause of failure in the maxilla was progression of periodontal disease, while mandibular molars succumbed most frequently to root fractures. They concluded
that while the initial outcome of resected molars was favorable,
it had no lasting effects, and that most failures in their study occurred 5 to 10 years postoperatively.17
In a more recent 10-year retrospective study, Blomlöf and
co-workers23 evaluated the survival rates of resected molars in 80
patients. The initial survival rate at five years was 89%. This greatly decreased to 68% at 10 years, with smokers demonstrating a
greater failure rate than nonsmokers. Dannewitz and his coworkers24 reported a lower success rate of 57.9% for root amputation
following an approximately nine-year observation period.
The high failure rate of amputated molars is not surprising considering the complex therapeutic procedures that require the outermost clinical skills and expertise. Furthermore, after extraction of
the root(s), resorption of the alveolar bone occurs, resulting in a
diminished ridge height and width.25 This may lead to permanent
deformity of the alveolar ridge and to food impaction under the
fixed prosthesis, which complicates optimal oral hygiene. It may also
compromise the site for future implant placement, and often causes
esthetic problems in patients with an extended buccal corridor.
In light of this negative data and the rise in popularity of
dental implants, the procedure has lost its acceptance among
many clinicians, while dental implants have been shown to be
more predictable with a much higher long-term success rate.26
In order to minimize the aforementioned limitations of the
root resection procedure, a modified technique has been used in
our clinic with promising results. The principle of guided bone
regeneration (GBR) has been employed following the extraction of the resected root(s). Using bone grafts and barrier membranes, the rapidly growing epithelial cells are excluded, allowing
the wound to be populated by osteogenic cells.27 The literature
supports grafting freshly extracted sockets with bone grafts.28-29
When freeze-dried bone allograft (FDBA) was used in conjunction with a collagen membrane barrier, the width of the alveolar
ridge decreased by only 1.2 mm, compared to a 2.7 mm loss in
untreated, controlled sockets. In addition to width loss, the average loss of bone height in the control group was 1 mm, while the
grafted sites gained height.28 Similar positive results have been
reported with other types of allografts and xenografts.29
The following case illustrates a current technique used in our
clinic in conjunction with root amputation.
Case History
A 70-year-old male patient was referred in March 2010 to the
graduate periodontal clinic at the University of Tennessee, College
of Dentistry, in Memphis due to sharp pain during function on
his maxillary left first molar (#14). The patient said the tooth had
been treated endodontically twice (in 2006 and 2009) without alleviation of the symptoms. A thorough oral examination revealed
the existence of an isolated probing depth of 8 mm and attachment
loss on the mesio-palatal root aspect of #14, along with a mesial
Class II furcation involvement (Figure 1A). A radiographic survey
of the area revealed radiolucency along its mesio-buccal (MB) root
(Figure 1B). A fracture of the MB root was highly suspected. The
patient declined the extraction option of the offending tooth and
replacement with a single dental implant because of his previous
negative experience of replacing #15 with an implant. Root amputation of the MB root became a consented viable option.
The occlusion was adjusted to eliminate centric and lateral occlusal contacts on the mesial portion of #14. The area was anesthetized, and buccal and palatal full thickness flaps were reflected
from #13 to #14. Removal of the inflamed granulation tissue revealed the presence of a vertical fracture along the MB root and a
Class II furcation invasion. The root was amputated using a long
diamond bur and high-speed handpiece. Special care was taken to
smooth the remaining tooth to remove any ledges or tooth fragments. This was verified clinically and radiographically (Figure 2A).
However, during the extraction process of the offending root,
the thin buccal bony wall of the socket was fractured (Figure 2B).
Using GBR principles (Figure 3), the area was grafted with a mineralized cancellous particulate allograft (Oragraft, LifeNet Health, Virginia
Beach, VA) and covered with an absorbable collagen membrane (CollaTape, Zimmer Dental, Carlsbad, CA). Flaps were repositioned and sutured with vicryl (Ethicon Inc., Johnson & Johnson, New Brunswick, NJ) and
chromic gut sutures (Ethicon Inc., Johnson & Johnson, New Brunswick, NJ).
The area healed uneventfully, and the patient did not report any
undue consequences. He was placed on a four-month periodontal
maintenance recall program. Photographic and radiographic survey of
the surgical site at 12 and 27 months (Figures 4 & 5) revealed a healing
socket and a preserved bony ridge, along with shallow probing depths.
Summary
This is the first report in periodontic literature that combines the
principles of guided bone regeneration in conjunction with an “old
procedure” of root amputation. However, a publication by Oh30 in
Figure 4. 27-month postoperative buccal and palatal view of #14 illustrating minimal ridge
deformity, shallow pocket (Michigan O probe) and healthy gingival contours.
Figure 5. Radiographic appearance of area taken 27 months postoperatively.
The New York State Dental Journal • JUNE/JULY 2014
27
2012 in the International Endodontic Journal describes a similar approach to managing periodontic-endodontic lesions with positive
results. Further research is needed to verify its long-term efficacy. p
Queries about this article can be sent to Dr. Livada at [email protected].
REFERENCES
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Farrar JM. Radical and heroic treatment of alveolar abscess by amputation of roots of teeth.
Dental Cosmos 1884; 26:79-81.
Messinger TF, Orban B. Elimination of periodontal pockets by root amputation. J Periodontol 1954;25:213–215.
Gottlieb B, Orban B. Zahnfleisch Entzundung und Zahn Lockerung (“Gingival Inflammation and Loosening of the Teeth”). Berlin, Germany, 1933.
Basaraba N. Root amputation and tooth hemisection. Dent Clin North Am 1969; 13:121 -132.
Staffileno H Jr. Surgical management of the furca invasion. Dent Clin North Am 1969; 13:103–119.
Minsk L, Polson AM. The role of root resection in the age of dental implants. Compend
Contin Educ Dent 2006 Jul; 27(7):384-8.
Bühler H. Evaluation of root resected teeth. Results after 10 years. J Clin Periodontol 1988;
59:805–810.
Imura N, Pinheiro ET, Gomes BP, Zaia AA, Ferraz CC, Souza-Filho FJ. The outcome of
endodontic treatment: a retrospective study of 2000 cases performed by a specialist. J Endodontics 2007; 33:1278–82.
Wang Q, Cheung GS, Ng RP. Survival of surgical endodontic treatment performed in a
dental teaching hospital: a cohort study. International Endodontic J 2004;37:764–75.
Pattanshetti N, Gaidhane M, Al Kandari AM. Root and canal morphology of the mesiobuccal and distal roots of permanent first molars in a Kuwait population—a clinical study.
International Endodontic J 2008;41:755–62.
Smukler H, Tagger M. Microscopic study of the pulps of human teeth following vital root
resection. Oral Surg Oral Med Oral Pathol 1977; 44:96-105.
Haskell EW, Stanley HR. A review of vital root resection. Int J Periodontics Restorative Dent
1982; 2:28-49.
Filipowicz F, Umstodd P, England M. Vital root resection in maxillary molar teeth: a longitudinal study. J Endodontics 1984;10:264-268.
Backman K. The incomplete root resection-case presentations. Int J Periodont Rest Dent
1982;2:61-71.
Newell DH. The role of the prosthodontist in restoring root resected molars: a study of 70
molar root resections. J Prosthet Dent 1991;65:7-15.
Majzoub Z, Kon S. Tooth morphology following root resection procedures in maxillary first
molars. J Perio 1992;63:290-296.
Langer B, Stein SD, Wagenberg B. An evaluation of root resections. A ten-year study. J Periodontol 1981;52:719–723.
Svärdström G, Wennström J L. Periodontal treatment decisions for molars: an analysis of
influencing factors and long term outcome. J Periodontology 2000;71:579–585.
Langer B. Root resection revisited. Int J Periodontics Restorative Dent 1996;16:200-201.
Bergenholtz A. Radectomy of multirooted teeth. J Amer Dental Assoc 1982;85:870–875.
Carnevale G, Di Febo G, Tonelli MP, Mann C, Fuzzi M. A retrospective analysis of the
periodontal-prosthetic treatment of molars with interradicular lesions. Int J Periodont Rest
Dent 1991;11:188–205.
Hamp SE, Nyman S, Lindhe J. Periodontal treatment of multirooted teeth. Results after 5
years. J Clin Periodontol 1975;2:126–135.
Blomlöf L, Jansson L, Appelgren R, Ehnevid H, Lindskog S. Prognosis and mortality of rootresected molars. Int J Periodont Rest Dent 1997;17:191–201.
Dannewitz, B, Krieger JK, Husing J, Eickholz P. Loss of molars in periodontally treated patients: a retrospective analysis five years or more after active periodontal treatment. J Clinical Periodontology 2006;33:53–61.
Schropp L, Wenzel A, Kostopoulos L, Karring T. Bone healing and soft tissue contour
changes following single-tooth extraction: a clinical and radiographic 12-month prospective study. Int J Periodontics Restorative Dent 2003;23(4):313-23.
Simonis P, Dufour T, Tenenbaum H. Long-term implant survival and success: a 10-16-year
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Dahlin C, Linde A, Gottlow J, et al. Healing of bone defects by guided tissue regeneration.
Plast Reconstr Surg 1988; 81:672-676.
Iasella JM, Greenwell H, Miller RL, Hill M, Drisko C, Bohra AA, et al. Ridge preservation with
freeze-dried bone allograft and a collagen membrane compared to extraction alone for implant
site development: a clinical and histologic study in humans. J Periodontol 2003; 74(7):990–999.
Artzi Z, Tal H, Dayan D. Porous bovine bone mineral in healing of human extraction sockets.
Part 1: Histomorphometric evaluations at 9 months. J Periodontol 2000; 71(6):1015–23.27.
Oh S. Mesiobuccal root resection in endodontic-periodontal combined lesions. International Endodontic J 2012;45:660-669.
care of high-risk patient
Management of the Dental Patient on
Anticoagulant Medication
A Review
Manoj Agarwal, M.D.S.; Sankalp Mittal, M.D.S.; Sharmistha Vijay, M.D.S.; Pooja Yadav, M.D.S.;
Vasim Raja Panwar, B.D.S.; Neha Gupta, M.D.S.
ABSTRACT
Patients taking anticoagulant medication pose a challenge for the clinician. Dentists are often required to
manage bleeding as part of routine oral surgery or
dental procedures, and altered hemostasis can lead
to complications. Nevertheless, use of these medications is generally important for the patient’s health
and any alteration in the anticoagulant regimen may
have untoward sequelae. In addition, several medica-
sidered when a patient is on anticoagulant therapy. Generally,
controlling bleeding is less of a problem than the management of
thrombi and vascular occlusion from decreased coagulotherapy.1
Hemostasis depends upon several critical factors. An adequate number of platelets and proper platelet function are essential. The integrity of the vasculature also plays an important role
in hemostasis. Vascular integrity can be compromised by vitamin
C deficiency, viral and bacterial infections, or as a result of the
aging process or through various disease states. Adequate levels of
clotting factors and proper functioning of the fibrinolytic pathway are also essential.2
tions can affect the clotting mechanism, potentially
compromising hemostasis. This article will review a
variety of anticoagulant medications and the medical
conditions that necessitate their use.
Anticoagulation therapy is prescribed for patients when there is
a high risk of intravascular clot formation. It may be indicated
following embolic stroke, myocardial infarction (MI), atrial fibrillation, placement of a prosthetic heart valve, pulmonary emboli, deep vein thrombosis and any other condition that carries
a high risk of intra-arterial or intravenous clotting. Questions
commonly arise as to what dental procedures may safely be con-
Patient Evaluation and Management
History Taking
A complete medical history should be taken to gather preliminary
information about the patient’s general medical condition and
should include more detailed questioning about specific medications known or reported to interfere with hemostasis. The specific
drug, dose, route of administration and duration of use should be
recorded for each medication.
Laboratory Tests
The coagulation cascade involves the intrinsic, extrinsic and common pathways, which have been found to be highly intercon-
The New York State Dental Journal • JUNE/JULY 2014
29
nected. The intrinsic pathway requires the clotting factors VII, IX,
X, XI and XII. The extrinsic pathway is initiated by the release of
tissue factor II. The common point in both pathways is the activation of factor X to factor Xa. Factor Xa activates prothrombin
(factor II) to thrombin (factor IIa). Thrombin, in turn, converts
fibrinogen to fibrin. Dentists should be able to order and interpret
appropriate laboratory tests when minor oral surgery is required
for anticoagulated patients. The most frequently used tests are
the prothrombin time (PT) and international normalized ratio
(INR).2,3
The PT measures the effectiveness of the extrinsic and common pathways. The normal value is approximately 10 to 15 seconds. Because of the variability in PT reported by different laboratories, it is no longer considered adequate to use PT to monitor
the level of anticoagulation.2
In order to reduce variability, INR was introduced in 1983 by
the World Health Organization Committee on Biological Standards to assess patients receiving anticoagulation therapy more
accurately.4 INR is the patient PT divided by the standard PT of
the laboratory, raised to the power of the international sensitivity
index value (ISI): INR = Patient PT/mean normal PT
It is a more reliable and sensitive value for determining the
level of anticoagulation, because it depends upon the patient’s
blood and the sensitivity of the thromboplastin reagent and the
assigned ISI value. Therefore, PT may not be the laboratory value
of importance when evaluating the level of anticoagulation.4
A patient with a normal coagulation profile would have an
INR of 1.0. It is recommended that a patient undergoing invasive
treatment have a PT within 1.5- to 2.0-times the normal value.
This corresponds to an INR of 1.5 to 2.5 when the ISI is 1.0.5
In patients with anticoagulant therapy, an INR between 2.0
and 3.0 is recommended for most indications. Thus, an INR of
2.5 (range 2.0 to 3.0) minimizes the risk of either hemorrhage or
thromboembolism.5 Conditions such as post-myocardial infarction and deep venous thrombosis (DVT) could cause serious morbidity or death through thromboembolism. Additionally, patients
with atrial fibrillation are anticoagulated because of the greater
likelihood of blood clot formation due to turbulent blood flow
through the heart. In individuals with prosthetic heart valves and
certain hypercoagulable states, the INR should be approximately
3.5. If the dentist encounters a patient with an INR greater than
4.0, the patient should be referred to the physician for evaluation.
An INR greater than 4.0 is usually considered nontherapeutic,
and the patient is at risk for serious bleeding complications.2,6
Anticoagulant and Antiplatelet Medications
The goal of anticoagulation medication is to prevent clot formation or expansion. Warfarin is the most commonly used anticoagulation drug. Platelets provide the initial hemostatic plug at the
site of vascular injury, are involved in pathological processes and
30
JUNE/JULY 2014 • The New York State Dental Journal
are an important contributor to arterial thrombosis leading to MI
and ischemic stroke.7 The most common antiplatelet drugs are
acetylsalicylic acid, clopidogrel and dipyridamole.
Warfarin
In 1940, Karl Paul Link, a veterinarian from the University of
Wisconsin, studied this sweet clover, isolated the active compound and named it WARFARIN, which stands for Wisconsin
Alumina Research Foundation. “ARIN” was added to link it to
coumarin, because warfarin is a 4-hydroxycoumarin derivative. It
is a vitamin K analogue that is rapidly and completely absorbed
one hour after ingestion and has a half-life of 36 hours.
Warfarin is also known as coumarin. It was approved for use
in humans in 1950 as oral anticoagulant therapy. It is an antagonist of vitamin K, an element necessary for the synthesis of
clotting factors II, VII, IX and X, as well as the naturally occurring endogenous anticoagulant proteins C and S. Antagonism of
vitamin K or a deficiency of this vitamin reduces the rate at which
these factors and proteins are produced, thereby creating a state
of anticoagulation.
Warfarin has two functions: anticoagulant activity and antithrombotic effect. Therapeutic doses of warfarin reduce the
production of functional vitamin K-dependent clotting factors by
approximately 30% to 50% and cause a 10% to 40% decrease in
the biologic activity of the clotting factors. As a result, the coagulation system becomes functionally deficient.5
Acetylsalicylic Acid (ASA)
ASA is an non-steroidal anti-inflammatory drug (NSAID) used
to prevent thromboembolic diseases.8 The antithrombotic action
of ASA depends upon the irreversible inhibition of arachidonic
cyclo-oxygenase activity in platelets. The recommended dose of
ASA is 75 mg to 150 mg daily for the long-term prevention of
serious vascular events in high-risk patients.9,10
Clopidogrel
Clopidogrel has more antiplatelet activity than ASA and is used to
prevent MI and peripheral arterial insufficiency. The antiplatelet
effect of clopidogrel is irreversible and lasts for the life of the
platelet (7-10 days).10,11
Dipyridamole
Dipyridamole inhibits adenosine uptake in erythrocytes and endothelial cells. This increases plasma adenosine levels, leading to
more adenosine being available for binding to the adenosine receptor on the platelet. The antiplatelet activity of dipyridamole is
less than that of ASA; its action is reversible and ceases about 24
hours after the drug is discontinued.10.12
NSAIDs, other than aspirin—for example, ibuprofen, diclofenac—have a reversible effect on platelet aggregation and platelet
thromboembolic events associated with stroke or MI. Cessation of low-dose aspirin therapy prior to oral surgery has been
controversial; dentists have been concerned about potential
bleeding complications. However, patients who are receiving
aspirin therapy are at risk for emboli and MI if the medication
is stopped. Studies have shown that patients undergoing minor
oral surgery, including implant surgery and third molar extraction, experienced minimal bleeding complications when on
low-dose aspirin therapy. These complications were controlled
with local measures. The results indicated that low-dose aspirin therapy may be continued even if a patient requires minor
oral surgery.
Balancing Bleeding Risks and Thromboembolic Risks
However, many primary care dental procedures are unlikely to
Patients seen in the dental office may have been instructed by
cause bleeding that cannot be managed with local measures. These
their physician to take one low-dose aspirin daily to prevent
include minimally invasive procedures such as peri14
odontal probing, scaling above the gumline, polishing
Figure 1. Management of Patient on Oral Anticoagulant (by Edward Hui)
and orthodontic procedures. Invasive procedures, such
as local infiltration, scaling below the gums, root planPatient under anticoagulant therapy
ing, biopsies, tooth extractions, minor periodontal surgery, cavity filling, endodontic procedures (root canals)
and prosthodontic procedures (crowns, bridges and
Check INR
implants), are also unlikely to cause significant bleeding. Significant bleeding is more likely to occur with
INR 1.5-2.0
INR >2.0
Full medical
more invasive procedures, such as extraction of imhistory
pacted teeth and use of periodontal flaps.15-19 Patients
including
reason of
with liver disease, kidney disease, hypertension and
anticoagulant
1. Simple extraction
1. Multiple
gingival disease also have an increased risk of bleeding.
2. Superficial scaling in
extractions
The skill and experience of the dental practitioner and
absence of marked
2. Scaling with
inflammation
marked
availability of hemostatic measures must also be coninflammation
sidered when deciding whether to stop anticoagulants
Precautions
3. Surgical
according to
or antiplatelet agents.20
extractions
relevant
4. Other minor
A frequently cited study of thromboembolic risks
history, e.g.
oral surgeries
in dentistry is Wahl’s literature review, in which seantibiotic
cover
rious embolic complications, including death, were
three-times more likely to occur in patients whose anDiscussion with physician in charge of
ticoagulant therapy was interrupted than were bleedanticoagulation
ing complications in patients whose anticoagulant
therapy was continued (and whose anticoagulation
levels were within or below therapeutic levels).21
function, which is restored once the drug is cleared from circulation. NSAIDs are not used clinically for their antiplatelet activity.13
When deciding the appropriate management of a dental patient prescribed warfarin, three questions must be answered: 1.
Why is the patient on warfarin? 2. Is it necessary to modify the
warfarin regimen? 3. How should the regimen be modified?14
Edward Hui’s recommendations for appropriate management
of a patient prescribed oral anticoagulation therapy is shown in
Figure 1. The reason for anticoagulation therapy may indicate the
need for other precautions.14
No modification of
anticoagulant dosage
1.
2.
Stop warfarin
2-3 days prior
to dental/
surgical
treatment.
Recheck INR
for appropriate
level.
1.
2.
3.
Stop warfarin
2-3 days prior
to dental/
surgical
treatment.
Continue
anticoagulant
with intravenous
heparin with
close monitoring
of activated
partial.
In-patient
monitoring.
Maintaining Hemostasis
With the recommendation not to alter anticoagulant
therapy for patients requiring routine dentoalveolar
surgery, dentists must adhere to meticulous surgical
technique, have the skills to ensure proper wound
closure and be familiar with adjunctive hemostatic
techniques.
Oral procedures must be done at the beginning
of the day, because this allows more time to deal with
immediate re-bleeding problems.22
The New York State Dental Journal • JUNE/JULY 2014
31
Local anesthetic containing a vasoconstrictor should be administered by infiltration or by intraligamentary injection wherever
practical.22,23 Regional nerve blocks should be avoided when
possible. However, if there is no alternative, local anesthetic can
be administered cautiously using an aspirating syringe.24
An extraction socket should be gently packed with a resorbable gelatin sponge and then sutured carefully. The gelatin sponge acts as a mechanical matrix to facilitate clotting.
Resorbable oxidized cellulose is used similarly to the gelatin
sponge. It should be noted that any type of packing material
can be a nidus for infection, and caution in the use of these
products should be the rule when operating in an infected
area. Hemostatic collagen provides a mechanical matrix. When
in contact with blood, the collagen causes an aggregation of
platelets. This material is also resorbable within 14 to 56 days.
Other products that can be used include bone wax, thrombinsoaked gauze and fibrin sealants.22,23
Tranexamic acid 4.8% solution is a topical antifibrinolytic
that is commonly used to prevent excessive hemorrhage during
surgery. The patient is instructed to rinse with 10 mL of the solution for two minutes, four times a day for seven days.22,23
Resorbable sutures are preferable, as they attract less plaque.
If non-resorbable sutures are used, they should be removed after
four to seven days. Following closure, pressure should be applied
to the socket using a gauze pad that the patient bites down on for
15 to 30 minutes. Efforts should be made to make the procedure
as atraumatic as possible. And any bleeding needs to be managed
using local measures.22
The following instructions should be given to patients for
managing the clot in the postoperative period: 24
l Look after the initial clot by resting while the local anesthetic
wears off and clot fully forms (2-3 hours).
l Avoid rinsing the mouth for 24 hours.
l Do not suck hard or disturb the socket with the tongue and
any foreign object.
l Avoid hot liquids and hard foods for the rest of the day.
l Avoid chewing on affected side until it is clear that a stable
clot has formed.
l If bleeding continues or restarts, apply pressure over the
socket using a sterile gauze pad for 20 minutes. If bleeding
does not stop, the dentist should be contacted.
The optimal INR value for dental surgical procedures is
2.5, because it minimizes the risk of either hemorrhage or
thromboembolism. Nevertheless, minor dental surgical procedures can safely be done with the INR between 2.0 and 4.0,
being aware that local hemostatic measures may be needed to
control bleeding. Patients who have an INR greater than 4.0
should not undergo dental surgical procedures, and they must
be referred to the clinician responsible for maintaining their
anticoagulation.
32
JUNE/JULY 2014 • The New York State Dental Journal
Conclusion
Most of the recent literature regarding anticoagulants and dental
surgery is in agreement that, with good local hemostatic measures, routine oral surgical procedures can be undertaken without
the need for alteration of the INR, when it is within the therapeutic range. The management plan is individualized according to
the levels of surgical trauma and anticoagulation. Any change of
anticoagulation therapy should be made in collaboration with the
prescribing physician. p
Queries about this article can be sent to Dr. Agarwal at [email protected].
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
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19.
20.
21.
22.
23.
24.
Aldous JA, Olson CJ. Managing patients on warfarin therapy: a case report. Spec Care Dentist 2001,May-Jun;21(3):109-12.
Rada RE, Management of the dental patient on anticoagulant medication. Dentistry Today
Aug 2006.
Meehan S, Schmidt MC, Mitchell PF. The international normalized ratio as a measure of
anticoagulation: significance for the management of the dental outpatient. Spec Care Dentist 1997;17:94-96.
Hirsh J, Poller L. The international normalized ratio. A guide to understanding and correcting its problems. Arch Intern Med 1994;154:282-288.
Hirsh J, Dalen J, Anderson DR, Poller L, Bussey H, Ansell J, Deykin D. Oral anticoagulants:
mechanism of action, clinical effectiveness, and optimal therapeutic range. Chest 2001,
Jan;119( 1 Suppl):8S-21S. Troulis MJ, Head TW, Leclerc JR. Dental extractions in patients on an oral anticoagulant: a
survey of practices in North America. J Oral Maxillofac Surg 1998, Aug;56(8):914-917.
Merritt JC, Bhatt DL. The efficacy and safety of preoperative antiplatelet therapy. J Thrombolysis 2002, Apr;13(2):97-103.
Dogne JM, de Leval X, Benoit P, et al. Recent advances in antiplatelet agents. Curr Med
Chem 2002, March;9(5),577-589.
Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomized trials of
antiplatelet therapy for prevention of death, MI and stroke in high risk patients. BMJ 2002,
Jan 12;324:71-86.
Pototski M, Amenabar JM. Dental management of patients receiving anticoagulation or
antiplatelet treatment. J Oral Science 2007, Dec;49(4):253-258.
CAPRIE Steering Committee. A randomized, blinded, trial of clopidogrel versus aspirin in
patients at risk of ischemic events (CAPRIE). Lancet 1996;348,1329-1339.
Lenz TL, Hilleman DE. Aggrenox: a fixed dose combination of aspirin and dipyridamole.
Ann Pharmacother 2000;34:1283-1290.
Schafer AI. Effects of nonsteroidal anti-inflammatory drugs on platelet function and systemic hemostasis. J Clin Pharmacol 1995;35:209-19.
Edward Hui. Management of dental patients on warfarin. Hong Kong Dental J 2005;2:49-51.
Sandor G. Do patients taking oral anticoagulants need to discontinue their medication
before surgical procedures? J Can Dental Assoc 2004;70:482-3.
Nematullah A, Alabousi A, Blanas N, et al. Dental surgery for patients on anticoagulant therapy
with warfarin: a systematic review and meta-analysis. J Can Dent Assoc 2009; 75: 41a-i.
Gupta A, et al. Bleeding disorders of importance in dental care and related patient management. Can Dent Assoc 2007;73:77-83.
Hermann WW, Konzelman JL Jr, Sutley SH. Current perspectives on dental patients receiving anticoagulant therapy. J Am Dental Assoc 1997;128:327-35.
Bacci C, Maglione M, Favero L, et al. Management of dental extraction in patients undergoing anticoagulant treatment. Results from a large, multicentre, prospective, case-control
study. Thromb Haemost 2010;104:972-5.
Perry DJ, et al. Guidelines for the management of patients on oral anticoagulants requiring
dental surgery. Br Dent J 2007; 203:389-93.
Wahl MJ. Myths of dental surgery in patients receiving anticoagulant therapy. J Am Dent
Assoc 2000;131:77-81.
Scully C, Wolff A. Oral surgery in patients on anticoagulant therapy. Oral Surg Oral Med
Oral Pathol Oral Radiol Endod 2002;94,57-64.
Lockhart PB, Gibson J, Pond SH, Leitch J. Dental management considerations for the patient with an acquired coagulopathy. Part 1: coagulopathies from systemic disease. Br Dent
J 2003;195,439-445.
Scully C, Cawson RA. Medical problems in dentistry. 4th ed. Wright Butterworth-Heinemann: Oxford, 1998;49-100.
oral medicine
Angiofibrolipoma of the Retromolar Pad Region
Case Report with a Review of Literature
Farzaneh Agha-Hosseini, D.D.S., M.Sc.; Elham Moslemi, D.D.S, M.Sc.
ABSTRACT
Angiofibrolipoma is a rare histopathological variant
of lipoma, characterized by mature adipocytes, blood
vessels and dense collagenous tissue. It is seldom seen
in the oral and maxillofacial region. Diagnosis of
angiofibrolipoma is only possible based on its histopathological features.1 This report presents the case
of a 63-year-old male patient with the complaint of
a polyp-like mass, felt from the left retromolar pad
region. The mass was found as a small prominent lesion that had grown gradually for 1.5 years. Our differential diagnosis was irritation fibroma and fibrous
pyogenic granuloma. This report also includes a comprehensive reference to previously reported data, as
found through PubMed and Google Search, which revealed this type of case rarely has been documented.
Lipomas present benign mesenchymal tumors composed of mature adipocytes. They are well separated from surrounding tissues by a thin fibrous capsule.1-3 Although lipomas are among
the most common mesenchymal neoplasms, the head and neck
regions are affected in 15% to 20% of cases, and only 1% to 4%
of these tumors are located in the oral cavity.3-5 The most affected
anatomical sites in the oral cavity are the buccal mucosa, lips and
tongue. The floor of the mouth, palate, retromolar pad and salivary glands are involved less frequently.3
Lipomas are lesions of the middle-aged, seen mostly in patients older than 40 years.1 They seldom present before the third
decade of life; and they have a slight gender predilection towards
males.6 However, some studies have shown a female preponderance, while others did not find any gender preference.7
Clinically, oral lipomas are slow-growing tumors in the form
of well-circumscribed, mobile, painless, sub-mucosal, sometimes
fluctuant, yellowish-colored nodules, depending upon the thickness of the overlying mucosa.1,6,5
There are two alternative classifications for lipomas, which
is important for differential diagnosis. WHO’s classification consists of classic lipoma, angiolipoma, chondroid lipoma, myolipoma and spindle cell/pleomorphic lipoma, according to their
characteristic clinical and histopathological features.8,9 In the alternative classification, histological variants of lipomas include fibrolipomas, angiolipomas, angiofibrolipomas, angiomyolipomas
and infiltrating angiolipomas.10,11
The first description of an oral lesion was provided in 1848
by Roux in a review of masses, which were referred to as a “yellow
epulis.” The pathogenesis of lipoma is uncertain, but it appears to
The New York State Dental Journal • JUNE/JULY 2014
33
Angiofibrolipomas of the oral cavity are not frequently reported.
To the best of our knowledge, the review of the English literature
performed through PubMed and Google between 1961 and 2011
revealed a total of two cases of intraoral angiofibrolipomas (tonsil
and buccal mucosa) and one case in the ear canal. Demographic
characteristics of previous case reports of intraoral lipomas are
shown in Table 1.
In this paper, we report one case of angiofibrolipoma in the
left retromolar pad region of a 63-year-old man. We believe this
is the first reported case of angiofibrolipoma located in this area
in a male patient.
Additionally, we have searched for previous case reports and
carried out an analysis of the data on the different histological
types of intraoral lipomas, which we present in this paper.
Figure 1. Clinical appearance of polyp-like mass of angiofibrolipoma on left retro-molar pad.
be more common in obese people. However, the metabolism of
lipoma is completely independent of normal body fat. If the caloric intake is reduced, normal body fat may be lost, but lipomas
do not decrease in size. Although its etiology is unknown, possible
causes can include trauma, infection, and chronic irritation and
hormone alterations.4
34
JUNE/JULY 2014 • The New York State Dental Journal
Case Report
A 63-year-old male was referred to the Department of Oral Medicine, School of Dentistry, Tehran University of Medical Science,
Iran, with the complaint of a polyp-like mass, felt from the left
retromolar pad. From the past history, it was discovered that the
mass appeared 1.5 years previously as a small prominent area on
the retromolar pad and grew gradually.
Intraoral examination revealed a polypoid mass, about 1 cm
in diameter, located on the left retromolar pad. The color of the
covering mucosa was the same as the normal surrounding mu-
TABLE 1
Demographic Characteristics of Previous Case Reports of Intraoral Lipomas
Author
Brucoli
Kaur
Oliveira dos santos
Taira
Venkateswarlu
Rafieiyan
Martínez-Mata
Ono
Caldeira
Nayak
Amirth Raj
Jaiswal
Gupta
Brikic
Thakur
Majunatha
Rehani
Altug
Colella
Annibali
Ayberk Alug
Adoga
Scariot
Imai
Brooks
Kacker
Coimbra
Chidzonga
Tosoios
Weitzner
Ghandour
Dale
Yonemochi
Metgud
Vera JL
Tan
Epivatianos
Kaku
Agoff
Piattelli
Dutt
Aphshari
Dattilo
Khoo
Anavi
Lombadi
Begin
Christopoulos
Krausen
Vazirani
Tripp
McDaniel
Campos
Shapiro
Orlean
M: male
Num Year
1
2011
3
2011
1
1
1
1
1
1
2
1
1
1
1
1
1
3
1
1
1
1
1
1
1
1
3
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
1
2
1
2011
2011
2011
2011
2011
2011
2011
2011
2011
2011
2011
2010
2010
2010
2010
2009
2009
2009
2009
2008
2008
2008
2008
2007
2006
2006
2006
2005
2005
2005
2005
2004
2004
2004
2003
2003
2001
2000
1999
1997
1996
1995
1995
1994
1993
1989
1986
1985
1985
1984
1980
1969
1961
Age
43
54
52
55
58
65
6
60
12
52
38,60
63
72
65
2.5
59
?
Mean:66.6
42
22
75
58
22
35
71
72
?
78
29
58
55
4
72
?
69
17
74
55
73
75
61
?
42
?
?
23
70
68
42
58
?
?
?
33
44
?
?
Gender
M
M
M
M
M
F
M
M
M
M
M,M
M
M
F
M
M
F
M
F
M
M
F
M
F
M
M
?
M
F
F
M
M
M
?
M
M
M
M
M
M
F
?
F
?
?
M
M
F
F
M
?
?
?
F
?
?
?
Location
Right buccal mucosa
Labial mucosa
Buccal mucosa
Buccal mucosa
Right jugal mucosa above alveolar ridge and fromen mentonian
Extending superiorly from mandibular gingivobuccal fold to gingiva
Buccal mucosa
Tongue
Buccal mucosa
Tongue
Buccal mucosa, hard palate
Right palatal
Floor of mouth
Buccal mucosa
Buccal mucosa
Buccal mucosa
Buccal mucosa
2 Buccal mucosa,1 palate
Buccal mucosa
Buccal mucosa
Tongue
Floor of mouth
Buccal mucosa
Buccal mucosa
Buccal mucosa
Bilateral margins of tongue
2 Buccal mucosa,1 mandibular labial/buccal vestibule
Tongue
Laterally to opening of right duct of Wharton
Tongue
Buccal mucosa
Buccal mucosa
Floor of mouth
Soft palate
Buccal mucosa
Tongue
Floor of mouth
Floor of mouth
Buccal mucosa
Bilateral margins of tongue
Right gingivobuccal sulcus
?
?
?
?
Buccal/labial mucosa
Floor of mouth
Ttongue
Left palatine tonsil
Hard palate
Tonsil
?
Buccal vestibule
Anterior floor of mouth
Buccal mucosa
?
Labial mucosa
Histological Type
Fibrolipoma
Lipoma
Lipoma
Fibrolipoma
Lipoma
Lipoma
Angiomyxolipoma
Myxoidlipoma
Spindle cell lipoma
Lipoma
Lipoma
Lipoma
Fibrolipoma
Angiofibrolipoma
Angiolipoma
Fibrolipoma
Fibrolipoma
Angiolipoma
Lipoma
Lipoma
Angiolipoma
Lipoma
Lipoma
Spindle cell lipoma
Lipoma
Lipoma
Spindle cell lipoma
Lipoma
Spindle cell lipoma
Angiolipoma
Lipoma
Lipoma
Angiolipoma
Lipoma
Lipoma
Lipoma
Myxoidlipoma
Spindle cell lipoma
Spindle cell lipoma
Spindle cell lipoma
Spindle cell lipoma
Lipoma
Lipoma
Spindle cell lipoma
Lipoma
Spindle cell lipoma
Lipoma
Spindle cell lipoma
Fibrolipoma
Lipoma
Spindle cell lipoma
Angiolipoma
Lipoma
Llipoma
F: female ?:Data were not accessible
The New York State Dental Journal • JUNE/JULY 2014
35
Figure 2. Histopathological features of angiofibrolipoma (hematoxylin-eosin staining) show
matured adipose tissue intermixed with dilated vascular elements and collagen-rich fibrous
tissue.
cosa, with no signs of ulceration or infection. The mass was welldemarcated from the surrounding area, mobile but non-pedunculated, soft in consistency, elastic and non-tender (Figure 1).
Extraoral examination revealed no asymmetry or lymphadenopathy. Panoramic view did not show the presence of any pathological change of the jaw structure.
Our differential diagnosis was irritation fibroma and fibrous
pyogenic granuloma. An excisional biopsy was performed. Microscopic examination demonstrated numerous vascular channels,
surrounded by collagen-rich fibrous tissue and mature adipocytes.
The histopathological diagnosis of the lesion was angiofibrolipoma (Figure 2).
Discussion
Intraoral lipomas are relatively rare tumors, although they occur
with higher frequencies in other areas, especially the back, abdomen and shoulder of adults.12 Lipomas of the oral cavity are diagnosed more frequently in adult patients at a mean age of 50.2 to
62 years.3 These data are consistent with the 63-year-old subject of
the study presented here. In contrast to the male predominance of
lipomas involving other regions of the body, in the case of lipomas
of the oral cavity, studies have demonstrated a relatively balanced
gender distribution, or a slight bias toward women.8 However, in
this case, the report concerns a male patient. An important characteristic of oral lipomas is their small size, with a diameter of 1 cm
to 3 cm.1 In this case, the mass was 1 cm in diameter.
Lipomas are similar to normal fat tissue. But their metabolism is quite different, because these lipids are not available for
normal metabolism.12 The etiology of lipoma is still unknown.
It varies from the differentiation of multi-potent mesenchymal
cells in fat tissue, cartilage and bone, to metaplasia of a pre-existing lipoma. Mesenchymal cells are modified by systemic and
36
JUNE/JULY 2014 • The New York State Dental Journal
local influences that range from local trauma to prolonged ischemia.6 Further indistinct etiology of osseous/chondroid change
in lipoma has been discussed; and most researchers have mentioned that their origin is from different types of undifferentiated mesenchymal cells.
Piattelli et al. described two hypotheses for the origin of chondroblasts and osteoblasts. One hypothesis is that the neoplastic
transformation occurs in multi-potential, undifferentiated mesenchymal cells that later differentiate into lipoblasts, chondroblasts,
or osteoblasts and fibroblasts. The other hypothesis is that only the
adipose cells have a neoplastic transformation, and the cartilage
and bone are produced by differentiation of undifferentiated mesenchymal cells of stroma in chondroblasts or osteoblasts.13
Various pathogenic mechanisms, such as an origin from lipoblastic
embryonic cell nests, metaplasia of muscle cells and fatty degeneration, have been proposed as putative causative factors for simple
lipoma. Other factors, such as trauma, infection, chronic infection
and hormonal imbalance, are also thought to have a role.14 Additionally, it is believed that diabetes mellitus induced by hypercholesterolemia and obesity, radiation, and a familial or genetic link,
such as abnormality of chromosomes,12 may be involved in lipoma
development.1 Few lipomas show rearrangement of 12q, 13q or 6p
chromosomes.15 They usually have chromosomal aberrations, such
as translocations involving 12q13-15, locus interstitial deletions of
13q, and rearrangements involving 8q11-13 locus.7
However, in the literature, trauma is also mentioned as one
of the etiological factors. There are two different opinions about
the occurrence of so-called “traumatic lipomas.” The first is that
after trauma, adipose tissue prolapsed through fascia results in
a direct impaction. The second opinion is that after soft-tissue
trauma and hematoma formation, cytokines mediate differentiation and proliferation of pre-adipocytes, resulting in lipoma
formation.16 While most lesions are developmental anomalies,
those that occur in the maxillofacial region usually arise late in
life and are presumed to be neoplasms of adipocytes, occasionally associated with trauma. Oral lipomas located on the buccal
mucosa may not represent true tumors but, rather, herniation of
the buccal fat pad through the buccinator muscle. Such cases may
occur subsequent to local trauma in young children or the surgical removal of third molars in older patients.17
Among the rarest seen histopathological variants of lipoma
is angiofibrolipoma. This neoplasm is composed of fibroblasts,
capillaries and adipose tissue that is not encapsulated, but is well
separated from neighboring tissues.1 In the literature, there are
few reports of angiofibrolipoma associated with the oral and maxillofacial region. Brick et al.1 reported a case of angiofibrolipoma
of the buccal mucosa in a 59-year-old female. However, our case
was reported in a male in the same age group, and the lesion was
located on the retromolar pad region. A report by Jacob et al.
described a case of ear canal angiofibrolipoma.11 Also, Krause et
al. reported a tonsillar angiofibrolipoma.18 Saddik et al. reported
a case of lip sarcoma of the base of the tongue and tonsillar fossa
in a patient who underwent several resections of the mass, which
was once diagnosed as angiofibrolipoma.19 We believe this is the
first reported case of angiofibrolipoma located on the retromolar
pad region in a male patient. Histopathological analysis of the biopsy specimen taken from the retromolar pad revealed numerous
vascular channels surrounded by collagen-rich fibrous tissue and
mature adipocytes, which was diagnosed as angiofibrolipoma.
The clinical differential diagnosis may include ranula, dermoid cyst or thyroglossal duct cyst, regardless of its location and
ectopic thyroid tissue, pleomorphic adenoma and mucoepidermoid carcinoma, angiolipoma, fibrolipoma, granular cell tumor,
neurofibroma, traumatic fibroma and malignant lymphoma. The
definitive diagnosis is made by means of microscopic examination, which shows adult fat tissue cells embedded in a stroma of
connective tissue and surrounded by a fibrous capsule.6,7,20
Surgical excision of lipomas is the preferred treatment modality,
and if adequately resected, recurrence is rare. Therefore, complete resection should be emphasized during the first surgical operation. Recurrence is more likely in deep lipomas, which have a recurrence rate
of 30% to 50%, probably because of the difficulty of complete surgical removal.1,7,14 Well-encapsulated lipomas easily shell out with no
possibility of recurrence or damage to the surrounding structures.7
The surgical approach is dependent upon the site of the tumor and
the proposed cosmetic result. Lesions outside of the oral cavity may
show greater recurrence rates after surgical excision.5
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
Fletcher CDM, Unni K, Mertens F. World Health Organization classification of tumors:
pathology and genetics tumors of soft tissue and bone. IARC Press, Lyon. 2002;9:9-46.
Liggettt AD, Frazier KS, Styer EL. Angiolipomatous tumors in dogs and a cat. Vet Pathol
2002;39:286-289.
Jacob A, Kneile J, Welling DB. Angiofibrolipoma of the ear canal. Laryngoscope 2005;115(8):1461-2.
Jaiswal R, Aurora JK, Singh A, Singh G. Lipoma of buccal mucosa: a case report. JIDA
2011;5(11):1162-1163.
Kuyama K, Fifta SF, Komiya M, Sun Y, Akimoto Y, Yamamoto H. Rare lipomatous tumors
with osseous and/or chondroid differentiation in the oral cavity: report of two cases and
review of the literature. Int J Dent 2009;1-6.
Demir Y, Aktepe F. Unusually large intraoral submucosal lipoma. Kocatepe Tip Dergisi
2002;3:63-67.
Gupta SH, Pathak S. Fibrolipoma of buccal mucosa: case report. JIDA 2011;5(6):237-238.
Aust MC, Spies M, Kall S, Jokuzies A, Gohritz A, Vogt P. Post-traumatic lipoma: fact or fiction? Skin Med 2007;6:266-270.
Venkateswalu M, Geetha P, Srikanth M. A rare case of intraoral lipoma in a six-year-old
child: a case report. Int J Sci 2011;3:43-46.
Krausen C, Becker K, Hamann KF. Angiofibrolipoma of the tonsil. Laryngol Rhinol Otol
(Stuttg) 1986;65(6):355-6.
Saddic M, Oldring DJ, Mourad WA. Liposarcoma of the base of tongue and tonsillar fossa:
a possibly underdiagnosed neoplasm. Arc Pathol Lab Med 1996;120(3):292-5.
Santos L, Rocha M, Carvallo N, Porangaba E, Oliverira A, Neves D. Intraoral lipoma: an
atypical case. Braz J Otorhinolaryngol 2011;77(5):676.
Conclusion
This paper reports the case of a left retromolar pad angiofibrolipoma in a 63-year-old male. In referencing the literature to date,
this type of case has been rarely documented. p
The authors thank Dr. K. Drudgar and Dr. M. Mirza-Mohammad in the
Department of Oral Medicine and their colleagues in oral pathology in the
Dentistry School, Tehran University of Medical Sciences, Tehran, Iran, for
their assistance in the preparation of this report. Queries about this article can
be sent to Dr. Agha-Hosseini at [email protected].
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
Brick A, Ozcamur C, Koseoglu B, Olgac V. Angiofibrolipoma of the buccal mucosa: a case
report. J Oral Science 2010;52(1):173-176.
Manjunatha BS, Deepak Pateel GS, Shah V. Oral fibrolipoma rare histologic entity: report of
3 cases and review of literature. J Dent Tehran University of Medical Sciences, Tehran, Iran
2010;7(4):226-231.
Rodrigues J, Weege N, et al. Lipoma of the oral cavity: clinical and histopathologic study of
41 cases in Brazilian population. Eur Arch Otorhinolaryngol 2010;267;459-465.
Kaur RP, Kler SH, Bhullar A. Intraoral lipoma: report of 3 cases. Dent Res J (Isfahan)
2011;8(1):48-51.
Rafieiyan N, Hamian M, Anbari F, Abdolsamadi HR. Lipoma of the tongue: a case report.
DJH 2011;2(1).
Sekar B, Augustine D, Murali S. Lipoma, a rare intraoral tumor—case report with review of
literature. J Oral & Maxillofacial Pathology 2011;2(2):174-177.
Annibali S, Cristalli MP, La Monaca G, Giannone N. Lipoma in the soft tissue of the floor
of the mouth: a case report. J Open Otorhinolaryngology 2009;3:11-13.
Altug HA, Sahin S, Sencimen M, Dogan N. Non-infiltrating angiolipoma of the cheek: a
case report and review of the literature. J Oral Science 2009;51(1):137-139.
The New York State Dental Journal • JUNE/JULY 2014
37
oral surgery
The Residual Radicular Cyst
Jessica Lee, D.D.S.; John Costandi, D.M.D.; Louis Mandel, D.D.S.
ABSTRACT
The existence of a true residual radicular cyst has been
called into question. When observed, it probably represents, with rare exceptions, a resolving radicular cyst—a
“work in progress.”
The epithelial debris of Malassez represents the remnants of the
sheath of Hertwig. The debris resides in the tooth’s periodontal
ligament. With tooth devitalization, the apically located epithelial
debris becomes incorporated into the developing periapical granuloma. Bacteria, present in the necrotic pulp, act as the antigenic
stimulus for the formation of the granuloma. In turn, cytokines,
proteins secreted by the cells present in the granuloma, stimulate
proliferation of the dormant periodontal epithelial debris.1-4
Eventually, the central mass of the proliferating epithelium becomes deprived of its vascular nutrition and degenerates to form a
cyst cavity. With shedding of epithelial cells and lytic products into
the cavity, an increase in osmotic pressure occurs.2,5 The resulting
fluid intake increases the cyst lumen’s hydrostatic pressure and leads
to bone resorbtion as the cyst expands.1 Alternatively, it has also
been suggested that proliferating epithelium will surround any apical
abscess initiated by an infected necrotic pulp. Because of its innate
nature, the epithelium will proliferate to cover the exposed connective tissue surfaces and form an epithelially lined cyst cavity.2
38
JUNE/JULY 2014 • The New York State Dental Journal
The seminal microscopic review by Bhaskar6 of 2,308 periapical lesions indicated that 48% were granulomas, while 42% of the lesions
were radicular cysts. Subsequent studies reported that a varying incidence of 6% to 55% of the periapical lesions were cysts.2,7-9 With the
known, very high success rates following endodontic therapy, it is apparent that routine endodontic care will eradicate these cysts.5,6,8,10,11
Many periapical lesions are left behind following dental extractions.
And because many are radicular cysts, their presence should frequently be recognized postoperatively years later. Nevertheless, the
residual radicular cyst (RRC) has proven to be a rarity. Therefore,
it would seem that resolution of a periapical radicular cyst can also
occur following removal of the causative tooth.10-12
The relatively rare RRC is best defined as an odontogenic cyst
that persists after the associated tooth has been extracted.13 It
is generally believed that the majority of them represent slowly
resolving radicular cysts.10,12 Although most RRC resolve with removal of the irritant (the tooth), a small percentage persist for
unknown reasons.12 Inflammation from some form of irritation
may be the key factor in the continued presence or growth of the
RRC. Failure to eliminate the irritant, or its reactivation, can serve
to maintain the epithelial lining or even activate its further prolifFrom the Department of Oral and Maxillofacial Surgery, Columbia University
College of Dental Medicine, New York, NY
eration.10 However, it can be expected that the RRC will resolve if
the associated inflammatory process also recedes.12
Clinically, the RRC is recognized as a well-defined, asymptomatic, circumscribed radiolucency in an edentulous area. It is
reported to occur more commonly in the anterior maxilla, usually in males whose ages range from 30 to 60 years.1,8,14 Radiologically, the RRC has a well-defined periphery of cortical bone.
Its size and lucency will decrease with the passage of time.12,14
Histologically, there is a thinning of the cyst’s differentiated
epithelial lining and a decrease in the cyst wall’s inflammatory
cells. These cells reflect the granuloma that pre-existed the original radicular cyst.10,12,14 A mature avascular connective tissue
wall surrounds the cyst.10
Case Report
A 44-year-old African-American male was seen in Columbia University College of Dental Medicine for a routine dental examination. When the radiologic examination revealed a well-defined
lucency in the area of the missing maxillary right lateral incisor
(Figure 1), the patient was referred to the oral and maxillofacial
surgery service.
A history indicated that the patient was in excellent health.
He denied all systemic diseases; and he stated he was using no
medications. A non-vital maxillary right lateral incisor had been
extracted approximately 10 months previous to his present visit.
Healing had been uneventful; and no subjective discomfort or
swelling has developed. Because he is aware that he has other
carious teeth, he now seeks further care.
Extraorally, no anterior facial swelling was apparent. Intraorally, a normally healed mucosa overlying the edentulous maxillary right lateral incisor area was observed (Figure 2). The adjoining mucobuccal fold was not swollen, and palpation of the entire
region around the edentulous area elicited no discomfort. Carious involvements of the adjacent vital canine and central incisor
were present.
A radiograph of the involved area revealed that a well-defined
circular lucency, measuring approximately 1 cm in diameter, occupied the alveolar process in the right maxillary lateral incisor
region. No connection of the lucency to the adjacent canine or
central incisor was noted. The lucency was delineated by a layer
of cortical bone.
A decision was made to intervene surgically. A mucoperiosteal flap was mobilized exposing an intact buccal alveolar plate. A
surgical bur was used to expose an encapsulated soft tissue mass,
which was readily enucleated from its bony crypt (Figure 3). After debridement, the flap was reflected and coapted with sutures.
Healing was rapid. Two weeks later, the patient was referred for
restorative dental care.
The histologic diagnosis made by the oral pathologist was
RRC. A lumen surrounded by a stratified squamous epithelial lin-
Figure 1. Periapical film
demonstrating well-defined
radiolucency in area of
missing right maxillary lateral
incisor.
Figure 2. Clinical appearance of area of missing right maxillary lateral incisor.
Figure 3. Surgical view of bony crypt after removal of residual radicular cyst.
Figure 4. Microscopic appearance of residual radicular cyst. Cyst lumen (C)
surrounded by well-defined epithelial wall (E) based on non-inflamed connective tissue (T) (H and E stain, x 100 magnification).
The New York State Dental Journal • JUNE/JULY 2014
39
ing based on a relatively non-flamed connective tissue wall was
identified (Figure 4). Rushton bodies were noted.
Discussion
There are only rare and sporadic reports of the RRC. Because our
case fits the criteria for the diagnosis of the RRC, the authors wish
to call the profession’s attention to the uncommon existence of
this cyst. It can be presumed that in our patient the previously extracted devitalized lateral incisor was associated with a radicular
cyst. Resolution of the cyst could be expected because the irritant
(the tooth) was removed. Probably the resolution was ongoing,
and the process had not yet been completed in the 10-month
time frame between extraction of the lateral incisor and the patient’s visit to our clinic. It is also possible that although most
RRCs resolve with time, a small percentage is static in behavior
and persists unchanged in configuration.12
Another reason for the presence of the RRC is failure of the
pre-existing inflammation to resolve following extraction or endodontic care. Additionally, the reinstitution of a new inflammatory irritant that serves to stimulate further epithelial proliferation
may occur. Inhibition of resolution from inflammatory stimulation does not seem to be the problem in our reported case because
histologically, inflammation was not deemed to be significant
(Figure 4). Rather, we believe that resolution of the pre-existing
radicular cyst was proceeding as a “work in progress.” We intervened surgically before the process had a chance to be completed.
The absence of an inflammatory infiltrate in the cyst wall and a
well-defined periphery of cortical bone suggest such a conclusion.
Rushton bodies, identified during the histologic examination, occur in about 8% of RRCs.15 These bodies are thought to
represent eosinophilic straight, rounded or curved irregular structures with an epithelial lining.15 They probably develop when
secretory products of odontogenic epithelium are deposited on
particulate matter, such as cell debris or cholesterol crystals, in
the cyst wall.15
Conclusion
The existence of the RRC as a separate pathologic entity has
been questioned. It is best interpreted as an intermediate healing stage of a radicular cyst following removal of the cyst’s etiologic cause. The rare exceptions that persist probably result from
failure to eradicate the inflammatory condition that may exist
in the cyst’s wall or if a new inflammatory state is initiated by
an exogenous cause. p
Queries about this article can be sent to Dr. Mandel at [email protected].
REFERENCES
1. Murmura G, Traini T, Di Iorio D, Varvara G, Orsini G, Caputi S. Residual and inflammatory radicular cysts. Clinical and pathological aspects of 2 cases. Minerva Stomatol
2004;53:693-701.
2. Nair PNR, Sundquist G, Sjogren U. Experimental evidence supports the abscess theory
of development of radicular cysts. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2008;106:294-303.
3. Muglali M, Komerik N, Bulut E, Yarim GF, Celebi N, Sumer M. Cytokine and chemokine
levels in radicular and residual cyst fluids. J Oral Pathol Med 2008;37:185-9.
4. Nonaka CFW, Maia AP, Ferreira do Nascimento GJ, Freitas R, deSouza LB, Galvao HC. Immunoexpression of vascular endothelial growth factor in periapical granulomas, radicular
cysts, and residual radicular cysts. Oral Surg Oral Med Oral Pathol Oral Radiol Endod
2008;106:896-902.
Bernstein B. The residual radicular dental cyst. NY State Dent J 1976;42:548-50.
5. 6. Bhaskar S. Periapical lesions−types, incidence and clinical features. Oral Surg Oral Med
Oral Pathol 1966;21:657-71.
Lalonde ER, Luebke RG. The frequency and distribution of periapical cysts and granulomas.
7. Oral Surg Oral Med Oral Pathol 1968;25:861-8.
Stockdale CR, Chandler NP. The nature of the periapical lesion—a review of 1108 cases. J
8. Dent 1988;16:123-9.
Nair PNR. New perspectives on radicular cysts: do they heal? Internat Endod J 1998;31:155-60.
9. 10. Oehlers FAC. Periapical lesions and residual dental cysts. Br J Oral Surg 1970; 8:103-13.
11. Walton RE. The residual radicular cyst: Does it exist? (editorial). Oral Surg Oral Med Oral
Pathol 1996;82:471.
12. High AS, Hirschmann PN. Age changes in residual radicular cysts. J Oral Pathol
1986;15:524-8.
13. Weine FS, Silverglade LB. Residual cysts masquerading as periapical lesions: three case reports. J Am Dent Assoc 1983;106:833-6.
14. High AS, Hirschmann PN. Symptomatic residual radicular cysts. J Oral Pathol 1988;17:70-2.
15. Jacob S. Rushton bodies or hyaline bodies in radicular cysts: A morphologic curiosity. Indian
J Pathol Microbiol 2010;53:846-7.
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JUNE/JULY 2014 • The New York State Dental Journal
oral surgery
Treatment of a Mandibular Cyst
Before Implant Placement
Case Report
Miles Yacker, D.D.S.; John Ricci, PH.D.; Ioana Chesnoiu Matei, D.D.S.,M.S.; Bin Hu, M.D.;
Sachin Mamidwar, M.B.B.S, M.S.
ABSTRACT
The aim of this case study is to present a clinical approach to treatment of a mandibular intrabony cyst
employing guided bone regeneration principles and
protection of the mandibular nerve prior to implant
placement. A treatment approach employing a combination of grafting materials and membranes was used
to treat the cyst and protect the mandibular nerve
prior to implant placement. Micro CT, as well as histology and histomorphometrics, was used to evaluate
treatment outcomes. Histological inspection showed
bone regeneration at the grafting site. Histomorphometric analysis of the biopsy core rendered a total
bone percent area of 58.87% and 41.13% soft tissue.
Out of the total bone percent area, 90.45% was revealed as vital bone and 9.55% was graft remnant.
The grafted area is supporting an implant-supported
prosthesis in full function.
Human bone has the capacity to heal itself through regeneration
following different pathologies, such as fractures and resections.
Odontogenic cysts are a common occurrence in the dental surgi-
cal field. The standard care of treatment, as described by Partsch,
for such pathologies is surgical enucleation of the cyst, followed
by suturing (Partsch 1910). There has been some debate about the
size of the cysts that can be treated through cystectomy. Partsch
said the limit should be 2 cm, otherwise complications would
arise. However, literature studies reported positive results when
different size cystectomy defects were treated in the conventional
way without any adjuvant grafting material.1-3 In 1965, Schulte
introduced a collagen sponge into the cystectomy defects, based
on the notion that the blood clot cannot stabilize in a large defect.
Since then, numerous materials have been investigated as
possible treatments for large bone defects. Autografts, allografts,
xenografts and alloplasts have been widely investigated. The “gold
standard” of treatments has been autografts; however, cystic defects are large and autologus bone is scarce.
Calcium sulfate (CS) has often been used in combination
with other graft materials, such as allografts. Mixing CS with particulates of different bone graft materials helps to bind the particulates together and prevents the composite graft from migrating out of the site.4-8 Also, this mixture aids in the handling and
insertion of particle-based grafts. It was reported by Sottosanti
et al. that the combination of CS and allograft results in better bone formation compared to allograft alone. In this study, a
combination of CS and demineralized freeze-dried bone allograft
(DFDBA) was used in the treatment of periodontal defects.9 The
researchers found that CS binds the graft particles and accelerates
the mineralization process, thus enhancing bone regeneration.10
The New York State Dental Journal • JUNE/JULY 2014
41
Figure 1. Intraoral view after elevating full thickness flap.
Figure 2. Collagen membrane just before placement in bone
defect.
Figure 3. Placement of collagen membrane at base of bony
defect.
Figure 4. Bone defect after graft placement.
Figure 5. View of surgical area after suturing.
Figure 6. View of grafted area after 11 months of healing.
Methods and Materials
A patient presented in private practice for implant treatment. Following medical and dental history, the patient reported removal
of an intrabony cyst. This cyst was treated by a previous clinician with extraction of two posterior teeth and a marsupialization procedure. The biopsy report obtained from the previously
treating clinician stated: “Large intrabony destructive lesion left
mandible which involves multiple teeth and extends significantly
inferior. Clinical diagnosis: R/O neoplasia vs. possible inflammatory cystic lesion. Final diagnosis: Consistent with inflamed cyst
of mandible.”
After waiting 14 months from the previous marsupialization procedure, cone beam computed tomography and re-entry to
Figure 7. Bone core taken for micro CT and histology
analysis.
42
lower left mandibular quadrant confirmed recurrence of a large
boney cyst. A full thickness flap was raised, and the site was completely curetted and debrided of all granulation tissue. Upon removal of tissue, all remaining mandibular walls were intact, with
a large defect resulting within the confines of these boney walls
(Figure 1). The defect was in close approximation to the ceiling of
the mandibular canal.
In order to protect the mandibular canal, a Helios collagen
membrane was placed over the mandibular canal (Figures 2,3).
A mixture of calcium sulfate (DentoGen, Orthogen LLC, Springfield, NJ)
and allograft Puros small particle, 250 micron to 1,000 micron,
(Zimmer Dental, Carlsbad, CA) in a ratio of 40% to 60% CS:P was applied. Collatape was placed over the entrance to the cystic cavity
Figure 8. Implant placement employing surgical guide.
JUNE/JULY 2014 • The New York State Dental Journal
Figure 9. Radiograph of implant placement day of surgery.
(Figure 4) while the soft tissues were repositioned using a resorbable vicryl suture (Ethicon, Inc., Somerville, NJ) (Figure5).
The sutures were removed seven days later. The graft was left
for 11 months to heal until implant placement (Figure 6). Only
after drilling past the crestal bone cortex was a trephine drill used
to obtain a core, thus eliminating any pre-existing bone and only
obtaining bone in the grafted site (Figure 7). The core of the osteotomy was submitted for micro CT analysis, as well as histological
and histomorphometric analysis (Figures 10-13).
Histological Protocol
Retrieved bone core was fixed in 10% phosphate buffered formalin
and then transferred to different gradients of alcohol concentrations
(70% ethanol for 24 hours, 95% ethanol for 24 hours, 100% ethanol [x2] for 48 hours). After dehydration, the sample was infiltrated
and embedded in polymethyl methacrylate (PMMA). Sectioning was
performed with a low-speed saw (Isomet, Buehler, Lake Bluff, IL). The
sample was glued on a Plexiglas slide and ground down and polished
to a thickness of approximately 100 m. The stain used was Stevenel’s Blue and Van Gieson’s Picro-Fuchsin. A slide scanner (ScanScope
GL, Aperio, Vista, CA) was used to image the slide and histomorphometrical analysis, using Leica QWin software. It was conducted to
quantify the amount of total vital bone present in the core. Since
the human allograft can stain similar to vital bone, the presence of
stained cells was a positive indicator for vital bone.
Results
The patient’s healing occurred without complications. The grafted
area presented keratinized soft tissue, without signs of inflammation or infection. Following flap elevation, inspection and probing revealed robust bone formation, with a suitable ridge that allowed for proper placement of an implant based on a surgical
guide (Figures 8,9).
Histological inspection showed bone regeneration at the
grafting site (Figure 10). Histomorphometric analysis of the
biopsy core rendered a total bone percent area of 58.87% and
41.13% soft tissue. Out of the total bone percent area, 90.45%
was revealed as vital bone and 9.55% as graft remnant.
Discussion
Treatment modalities to surgically remove cysts include enucleation, marsupialization, curettage, removal of the content with
curettage, or, occasionally, surgical resection (1,11-13). After removal of the cyst, guided bone regeneration principles facilitate
osteoblasts and other osteogenic factors to occupy and play a critical role in the healing and regenerative phases in a boney defect.
Although some clinicians may wait less time to allow for healing
before implant placement, it was decided, based on the size of the
intrabony defect, to wait 11 months.
During osteotomy preparation for implant placement, a dense
bone was encountered in the grafted area. This clinical impression
Figure 10. Light histology of bone core showing mostly vital
bone with small amounts of graft. (SVG stain)
Figure 11. 3-D reconstruction of bone core from planar
images. Bar = 1.0 mm.
Figure 12. Planar micro CT of bone core showing dense and
cancellous regions of bone. Bar =.0 mm
Figure 13. Planar micro CT of bone core showing dense
regions and cancellous bone. Bar = 1.0 mm.
The New York State Dental Journal • JUNE/JULY 2014
43
was supported by the histology and histomorphometric analysis,
which showed 58.87% total bone present in the core, of which
90.45% is newly generated bone. The patient received a fixed screwretained implant-supported prosthesis that is both functional and
comfortable. The placement of a Helios membrane was for two
purposes: 1. to help protect the mandibular canal; and 2. to establish a base on which to place the bone graft inferiorly. By employing both an allograft and calcium sulfate, a scaffold was established
that aided in osteoconduction and aided in the osteogenic cascade
during the healing phase. One proposed mechanism of calcium
sulfate biochemistry is that it can break down into calcium and
sulfate ions, thereby leaving free calcium ions to bind with phosphate, which will allow for bone deposition and remodeling.
In addition, calcium sulfate lowers the PH and helps nearby
bone release bone morphogenic proteins like BMP2.14 Clinically,
implants have successfully osseointegrated in the grafted area and
are supporting a screw-retained prosthesis (Figure 9).
Conclusion
Following curettage, the combination of an allograft and calcium sulfate employing principles of guided bone regeneration
resulted in new bone fill and functional regeneration for a patient who presented with a large boney defect replacing two posterior teeth. p
Queries about this article can be sent to Dr. Yacker at [email protected].
REFERENCES
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
44
JUNE/JULY 2014 • The New York State Dental Journal
Iatrou I, Theologie LN, Leventis M. Intraosseous cystic lesions of the jaws in children:
a retrospective analysis of 47 consecutive cases. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, Endodontics 2009;107(4):485-492.
van Doorn ME. Enucleation and primary closure of jaw cysts. International J Oral
Surgery 1972;1(1):17-25.
Ihan HN, Miljavec M. Spontaneous bone healing of the large bone defects in the
mandible. International J Oral & Maxillofacial Surgery 2008;37(12):1111-1116.
Becker W, Clokie C, Sennerby L, Urist M, Becker B. Histologic findings after implantation and evaluation of different grafting materials and titanium micro screws into
extraction sockets: case reports. J Periodontology 1998;69(4):414.
Becker W, Urist M, Becker BE, Jackson W, Parry DA, Bartold M, Vincenzzi G, De Georges D,
Niederwanger M. Clinical and histologic observations of sites implanted with intraoral autologous bone grafts or allografts. 15 human case reports. J Periodontol 1996;67(10):1025-33.
Gitelis S, Piasecki P, Turner T, Haggard W, Charters J, Urban R. Use of a calcium sulfatebased bone graft substitute for benign bone lesions. Orthopedics 2001;24(2):162.
Dellavia C, Tartaglia G, Sforza C. Histomorphometric analysis of human maxillary sinus lift with a new bone substitute biocomposite: a preliminary report. Clinical Implant
Dentistry & Related Research 2009;11:e59-e68.
Aichelmann-Reidy M, Heath C, Reynolds M. Clinical evaluation of calcium sulfate in
combination with demineralized freeze-dried bone allograft for the treatment of human intraosseous defects. J Periodontol 2004;75(3):340-347.
Sottosanti J. Calcium sulfate-aided bone regeneration: a case report. Periodontal Clinical Investigations: official publication of Northeastern Society of Periodontists 1995;17(2):10.
Sottosanti J. Calcium sulfate: a biodegradable and biocompatible barrier for guided tissue
regeneration. Compendium 1992;13(3):226-8, 230, 232-4.
Sapp P, Eversole L, Wysocki G. Contemporary Oral and Maxillofacial Pathology. 2nd ed. St.
Louis, MO;Mosby;2004.p46-69.
Shear M. Cysts of the oral regions. 3rd ed. Oxford, UK:Wright; 1992.
Marx RE, Stern D. Oral and Maxillofacial Pathology: A Rational for Diagnosis and
Treatment. Chicago, IL;Quintessence;2003. p573-614.
Levine JP, Bradley J, Turk AE, Ricci JL, Benedict JJ, Steiner G, Lonraker MT, McCarthy JG.
Bone morphogenic protein promotes vascularization and osteoinduction in performed
hydroxyapatite in the rabbit. Ann Plast Surg 39(2):158-168,1997.
disease detection
Oral and Dental Manifestations of Celiac Disease
William James Maloney, D.D.S.; George Raymond, D.D.S.; David Hershkowitz, D.D.S.;
Glenn Rochlen, D.D.S.
ABSTRACT
Celiac disease is an autoimmune disease characterized
by the malabsorption of nutrients because the villi of
the small intestines are unable to process these nutrients. It is brought on by gluten food products. A pattern of enamel defects and oral aphthae are common
findings in celiac disease, thus making the dentist an
integral part of the diagnostic team.
The dentist plays a vital role in the diagnosis of celiac disease (CD),
as it manifests itself dentally with bilateral enamel defects that follow
the chronological pattern of tooth development. Also, oral aphthae
are commonly seen in patients with CD. The dentist has the ability
to assimilate the information gathered from the dental examination,
the patient’s medical history and the intraoral examination and formulate a tentative diagnosis of CD. The dentist would then refer the
patient to the proper medical specialist for appropriate diagnostic tests
and counseling. This would be a valuable service, as the diagnosis of
CD can be difficult and is often misdiagnosed, leading to much suffering and worry on the part of the individual with undiagnosed disease.
Celiac Disease
CD is a chronic systemic autoimmune disease that occurs in genetically susceptible individuals. It was first recognized in 1887.1
Its prevalence is between 1% and 2% of the population in some
nations.2 There are a number of gastrointestinal manifestations
of this disorder, such as diarrhea, weight loss, abdominal pain
and irritability.3 A thorough list of the systemic manifestations of
the disorder is presented in Table 1. Some individuals with CD do
not have diarrhea or weight loss but, rather, have iron deficiencies
or alterations in blood chemistry.2
CD damages the villi of the small intestine. The villi act to
absorb vitamins, minerals and various other nutrients. In CD,
they are damaged, resulting in the malabsorption of nutrients
required for health and growth.4 CD is difficult to diagnose because it resembles several other conditions that can cause malabsorption. The immune system of an individual with CD may be
identifying gluten as a foreign substance and producing elevated
levels of antibodies to rid the body of it.4 Most individuals with
CD have celiac disease-associated antibodies and specific pairs of
allelic variants in two HLA genes—HLA-DQA1 and HLA-DQB1.3
There have been various case reports in the medical literature
demonstrating a link between CD and Addison’s disease. O’Leary
et al.5 have shown, in a series of patients with Addison’s disease,
that there is a higher co-morbidity with CD than in any previously studied endocrine condition. It is strongly suggested that
individuals with Addison’s disease be tested for CD.
The diagnosis of CD is achieved by two specific and sequential criteria.2 First, prior to treatment, there needs to be shown
The New York State Dental Journal • JUNE/JULY 2014
45
typical biopsy changes in the proximal small intestine. Second,
there needs to be a definite clinical and/or pathological response
to certain foods in the diet. Foods that may contain gluten include breads, biscuits, cakes, pastries, pizza, pasta, sausage meats,
and certain soups, gravies, breakfast cereals and sauces.5 Glutenfree foods include unprocessed fruit, vegetables, milk, eggs, rice,
fish and meat.6
In the future, new forms of treatment for CD may include
the use of substrates that regulate intestinal permeability to prevent gluten entry across the epithelium, different forms of immunotherapy, the development of gluten-free grains by genetic
modification and use of gluten-degrading enzymes.7
CD in Individuals of Irish Descent
Population-based screening studies have demonstrated a higher
prevalence of CD in Ireland than elsewhere in the world.8 This
prevalence rate is slightly less than 1% of the population. Mylotte
et al.9 demonstrated a high prevalence of CD in workers in Galway in 1973.
The genetic stock of the Irish people is thought to have been
established approximately 5,000 years ago,8,10 before the arrival of
the Celts. It is thought that the ethnic and genetic mix is homog-
46
JUNE/JULY 2014 • The New York State Dental Journal
enous and distinct relative to much of mainland Europe.8 From
prehistoric times to recent history—the great potato famine of
the 19th century—oats were the only cereal and source of gluten
consumed by most of the population of Ireland.8 Today, the Irish
diet differs little from the rest of western civilization. Cronin8,10
states that until only very recently, the Irish diet has been almost
gluten-free. He postulates that there is a suggestion that the possession of CD genes in areas of low-gluten consumption must
confer a survival advantage and thus explains the high prevalence
of CD in the modern-day Irish, who have only recently been exposed to such a wide variety of food with a high gluten content.
Dental Significance of CD
Numerous authors have stated there is an increased prevalence of
dental issues in patients with CD.11-14 These oral manifestations
are dental enamel defects5,11,15-31 and recurrent oral aphthae.15,32-36
Macroscopic mucosal changes have been found in as many as 40%
of patients with CD.30,47 It has been postulated that these dental
issues may provide a clue that could aid in the diagnosis of CD,
which has historically proven hard to identify.11,14
The enamel defects seem to be linked to the time course of
odontogenesis. Aine28 stated that in children with CD, the central
TABLE 1
Systemic Manifestations of Celiac Disease2-4,20
Mood changes
Bloating
Joint pain
Skin rash
Reduced fat padding in feet
Amenorrhea
Iron-deficiency anemia
Dehydration
Weight loss
Muscle cramping in hands and legs
Difficulty gaining weight in children
Acidosis
Back pain
Dry skin
Night blindness
Bone disease
Hyperparathyroidism
Weakness
Edema
Electrolyte depletion
Diarrhea
Weakness
Abdominal discomfort
Abdominal distention
Lactose intolerance
Other autoimmune disorders
Recurrent fetal loss
Short stature
Delayed puberty
Osteoporosis/osteopenia
Epilepsy
Attention-deficit disorder
Migraines
TABLE 2
Oral and Dental Manifestations of Celiac Disease1-5
Fissured tongue
Cheilitis
Aphthous stomatitis
Delayed tooth eruption
Diminished size of teeth
Salivary gland dysfunction
Problems in enamel formation
incisors are always affected. Aine also states that symmetrically
and chronologically distributed enamel defects are strongly associated with CD.11 Other studies have demonstrated the elevated
prevalence of enamel defects in both incisors and molars.38-39 The
defects are usually bilateral and symmetrical in the affected stages. These affected teeth share parallel developmental stages. The
cause of these dental enamel defects is unknown.40 Patients with
CD do not show a greater susceptibility to caries. Table 2 shows
the dental and oral manifestations of CD.
It is apparent that dentists have a unique ability to aid in the
diagnosis of an ailment that has puzzled diagnosticians for decades.
The existence of a pattern of clear, symmetrical, chronological
enamel defects has been well documented. Dentists who suspect
CD from the dental and oral manifestations should refer the patient to the proper medical professional for a definitive diagnosis.
Pathophysiology
A unique feature of CD, compared to other autoimmune diseases,
is the knowledge of a definitive environmental prompt (gluten)
that is required for the disease to occur. Gluten and other prolinerich proteins are poorly digested in the normal human small intestinal tract due to a lack of prolyl endopeptidases. This can lead
to gluten peptides as much as 10 to 15 amino acids in length.41
Gliadin is a glycoprotein extract from gluten that is believed to
affect the enterocytes of individuals afflicted with CD, mainly via
the overexpression of IL-15 in the intestine.42
Another key component of the disease is the tissue enzyme
transglutaminase. It is believed that if transglutaminase is not activated, gliadin is less immunogenic and may not stimulate T cells
as effectively.43 When activated, this enzyme is important in the
pathogenesis of CD in that the enzyme crosslinks ingested gliadin
and causes specific deamidation of glutamine into glutamic acid
and gliadin peptides. When such deamidation occurs, the gliadin
peptides can be presented in a more effective manner to gliadin
reactive CD 4 T cells, thereby increasing its immunogenicity.44
Histologically it has been shown that two and a half hours after the ingestion of wheat gluten, there is a deterioration of villus
architecture, distortion of microvillus structure, disorganization
of the intermicrovillus pit region, and an increase in lysosomelike bodies in the apical cytoplasm of the luminal enterocytes,
as well as pronounced hypertrophy of the rough endoplasmic reticulum of these cells.45 Also, at high magnification, CD patients
exhibit enterocytes that are irregular in size and shape, with a decrease and disruption of the glycocalyx. Reductions in the length
and density of the microvillus were also clearly identified.46
The Marsh classification system is used to organize histology
findings and is grouped into three categories: infiltrative, hyperplastic or destructive. These three categories share the common
features of increased intraepithelial lymphocytes, decreased enterocyte height, crypt hyperplasia and villous atrophy to different
degrees.47
The New York State Dental Journal • JUNE/JULY 2014
47
Immunochemistry of the small intestine of patients shows villous
atrophy, crypt hyperplasia and elevated levels of intraepithelial
lymphocytes.47,48 These intraepithelial lymphocytes are localized
between intestinal epithelial cells at the basolateral side of the epithelium and are thought to play an important role in immunosurveillance of the epithelium. In the lamina propria, CD4 cells elicit
an immune response and intraepithelial lymphocytes acquire activating natural killer receptors and the ability to lysis stressed epithelial cells independent of T-cell receptor signaling, which likely
contributes to the typical tissue damage seen in celiac disease.48
21.
Conclusion
CD is often misdiagnosed and can cause the patient much suffering. Once diagnosed, the individual can live a happy and full life.
As in the case of many other systemic disorders, the dentist plays
a unique and vital role in diagnosing CD in their patients. In this
regard, the dentist can provide a service to the patient, which can
tremendously increase the patient’s quality of life. p
29.
Queries about this article can be sent to Dr. Maloney at [email protected].
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ds00319/dsection=symptomsrash.
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de Paor L. The People of Ireland. In: The People of Ireland, edited by P. Loughrey. Belfast:
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Aine L, Maki M, Reunala T. Coeliac-type dental enamel defects in patients with dermatitis
herpetiformis. Acta Derm Venereol (Stockh) 1992;72:25-27.
Smith DMH, Miller J. Gastroenteritis, coeliac disease and enamel hypoplasia. Br Dent J
1979;147:91-95.
Prati C, Santopadre A, Baroni C. Ritardata erupcione, hipoplasia dello smalto e carie in
corso di malatia celiaca delli infanzia. Min Stom 1987;36:749-752.
Aine L. Permanent tooth dental enamel defects leading to the diagnosis of coeliac disease.
Br Dent J 1994;177:253-254.
Bucci P, Carile F, Sangianantoni A, D’angio F, Santarelli A, Lo Muzio L. Oral apthous ulcers
and dental enamel defects in children with coeliac disease. Acta Paediatrica 2006;95:203-207.
Mariani P, Mazzilli MC, Margutti G, Lionetti P, Triglione P, Petronzelli F, et al. Coeliac
disease, enamel defects, and HLA typing. Acta Paediatr 1994;83:1272-1275.
Ventura A, Martelossi S. Dental enamel defects and coeliac disease. Arch Dis Child
1997;77:91.
Hill ID, Dirks MH, Liptak GS, Colletti RB, Fasano A, et al. Guideline for the diagnosis and
treatment of celiac disease in children: recommendations of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition. J Pediatr Gastroenterol Nutr
2005;40:1-19.
Priovolou CH, Vanderas AP, Papagiannoulis L. A comparative study on the prevalence of
enamel defects and dental caries in children and adolescents with and without coeliac
disease. Eur J Paediatr Dent 2004;5:102-106.
Patinen P, Aine L, Collin P, Hietanen J, Korpela M, Enckell G, et al. Oral findings in coeliac
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Rasmusson CG, Eriksson MA. Celiac disease and mineralisation disturbances of permanent
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Martelossi S, Torre G, Zanatta M, Del Santo M, Not T, Clarich G, et al. Dental enamel
defects and screening for coeliac disease. Pediatr Med Chir 1996;18:579-581.
Martelossi S, Torre G, Zanatta M, Del Santo M, Not T, Clarich G, et al. Dental enamel
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Aine L. Coeliac-type permanent-tooth enamel defects. Ann Med 1996;28:9-12.
Ballinger A, Hughes C, Kumar P, Hutchinson I, Clark M. Dental enamel defects in coeliac
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Maki M, Aine L, Lipsanen V, Koskimies S. Dental enamel defects in first-degree relatives of
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Aine L. Dental enamel defects and dental maturity in children and adolescents with coeliac
disease. Proc Finn Dent Soc;82 Suppl 1986;3:1-71.
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Smith DM, Miller J. Gastroenteritis, coeliac disease and enamel hypoplasia. Br Dent J
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31. Rasmussen P, Espelid I. Celiac disease and the teeth. Nor Tannlaegeforen Tid 1979;89:578583.
32. Sedghizadeh PP, Shuler CF, Allen CM, Beck FM, Kalmar JR. Celiac disease and recurrent
aphthous stomatitis: a report and review of the literature. Oral Surg Oral Med Oral Pathol
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33. Meini A, Pillan MN, Plebani A, Ugazio AG, Majorana A, Sapelli PL. High prevalence of
DRW10 and DQW1 antigens in celiac disease associated with recurrent aphthous stomatitis. Am J Gastroenterol 1993;88:972.
34. Aydemir S, Tekin NS, Aktunc E, Numanoglu G, Ustundag Y. Celiac disease in patients having recurrent aphthous stomatitis. Turk J Gastroenterol 2004;15:192-195.
35. Patial RK. Recurrent aphthous ulcers in subclinical coeliac disease. J Assoc Physicians India
2003;51:80.
36. Biel K, Bohm M, Luger TA, Bonsmann G. Longstanding oral aphthae—a clue to the diagnosis of coeliac disease. Dermatology 2000;200:340.
37. Lahteenoja H, Toivanen A, Viander M, et al. Oral mucosa changes in coeliac patients on a
gluten-free diet. Eur J Oral Sci 1998;105:899-906.
38. Andersson-Wenckert I, Blomsquist HK, Fredikzon B. Oral health in coeliac disease and
cow’s milk protein intolerance. Swed Dent J 1984:8:9-14.
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40. Wierink CD, Van Diermen DE, Aartman IHA, Heymans HSA. Dental enamel defects in
children with coeliac disease. International Journal of Paediatric Dentistry 2007;17:163168.
41. Kagnoff M. AGA Institute Medical Position Statement on the Diagnosis and Management
of Celiac Disease. Gastroenterology 2006;131:1977-1980.
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2003;125:730-745
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gliadin epitopes deamidated in situ by endogenous tissue transglutaminase. Eur J Immunol.
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the small intestine of coeliac patients to wheat gluten. Gut 1989 Jan;30(1):78-85.
46. Magliocea FM, Bonamico M, Petrozza V, Correr S, Montouri M, Triglione P, Carpino F.
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2010 Oct;62(10):641-51.
endodontics
The Plasma-Rich in Growth Factor as a
Suitable Matrix in Regenerative Endodontics
A Case Series
Hengameh Bakhtiar, D.D.S., M.Sc.; Mehdi Vatanpour, D.D.S., M.Sc.; Arezoo Rayani, D.D.S.;
Fina Navi, D.D.S., M.Sc.; Ehsan Asna-Ashari, D.D.S., M.Sc.; Anahid Ahmadi, D.D.S;
Hamid Jafarzadeh, D.D.S., M.Sc.
ABSTRACT
The aim of this report is to describe the positive effect
of plasma-rich in growth factor (PRGF) on pulp regeneration and apex formation in cases with necrotic
pulps and open apices. After access cavity preparation
and cleaning of the canal, triple antibiotic paste was
inserted into the canals for the purpose of disinfection. After two weeks, apical bleeding was mechanically created by insertion of a #80 file through the
apex. PRGF obtained from the patient was centrifuged and injected into the canals up to the level of
the cementoenamel junction; the teeth were restored
temporarily. The patients returned for review two
weeks later. If there was absence of pain, swelling, fistula or any other complication, the teeth were sealed
with MTA and composite. At 22 months follow-up,
complete apex closure in two teeth and apical closure
and continued increase of dentinal wall thickness in
two other cases were evident.
Endodontic treatment of teeth with necrotic pulps and open apices can be a great challenge for practitioners, because it is very
difficult to achieve complete cleaning/filling and a tight seal with
traditional techniques and materials. Moreover, these teeth have
thin dentinal walls, which leaves them susceptible to subsequent
fracture after endodontic treatment.1-3
As stated by Torabinejad and Turman,4 “the ideal outcome
for a tooth with an immature root and necrotic pulp would be the
regeneration of pulp tissue into a canal capable of promoting the
continuation of normal root development.” Thus, regenerative
endodontics may be a suitable alternative for conventional root
canal treatment in teeth with necrotic pulps and open apices.4-6
Revascularization of immature avulsed teeth has been welldocumented. However, it has also been shown that infection may
arrest the progress of revascularization and continued development of the root.7,8 And it has been indicated that even in the
presence of a large periapical lesion, vital pulp tissue and Hertwig’s epithelial root sheath are possible.9,10 This tissue could proliferate if canal cleaning and disinfection is performed thoroughly
and the previously existent inflammatory process is reversed.8,11
The thickening of dentinal walls and apex maturation may be
observed in teeth with necrotic pulps and open apices.1,4,8,10,12,13
To increase the success rate of a pulp regeneration procedure,
use of a suitable physical scaffold for supporting cell growth and
The New York State Dental Journal • JUNE/JULY 2014
49
Figure 1A. Initial radiograph of case; 1B. Three-month follow-up
radiograph; 1C. Six-month follow-up; 1D. Nine-month follow-up; 1E.
22-month follow-up.
Figure 2A. Initial radiograph of case; 2B. Radiograph three months
after treatment; 2C. Radiograph six months after treatment; 2D.
Radiograph nine months after treatment; 2E. Radiograph at 22-month
follow-up.
Figure 3A. Initial radiograph of case; 3B. Radiograph three months
after treatment; 3C. Radiograph six months after treatment; 3D.
Radiograph nine months after treatment. 3E. Radiograph at 22-month
follow-up.
50
JUNE/JULY 2014 • The New York State Dental Journal
differentiation is mandatory. For example, platelet-rich plasma
(PRP) has been used for this procedure and seems to be a suitable
material.2,4,14
Another scaffold that might be ideal for this procedure is
plasma-rich in growth factor (PRGF). It has been shown to be
enriched with PDGF, TGF1, TGFb1, TGFb2, FGF, VEGF, EGF and
ILGF1.12,15 Considering the effect of PRGF on Hertwig’s epithelial
root sheath and the increase of alkaline phosphatase activity, acceleration of osteogenic differentiation of human dentinal stem
cells seems to be possible.16 It has been hypothesized that after
root canal disinfection with a paste mixture of three antibiotics,
formation of the blood clot would serve as a matrix that could
speed up the differentiation of the remaining progenitor cells.17
This case series describes the effect of PRGF on pulp regeneration and apex formation in four cases with necrotic pulps and
open apices in children 6 to 11 years old. All treatment procedures were performed in the Endodontic Department, Faculty of
Dentistry, Islamic Azad University, Tehran, Iran. The medical history of all patients was non-contributory.
Case One
The patient was an 11-year-old girl with a history of trauma to
both maxillary central incisors. During extraoral examination,
an acute apical abscess with swelling at the anterior area of the
maxilla was present. On intraoral examination, no soft tissue
abnormality was present. Both incisors were sensitive to percussion and palpation tests. Cold test using refrigerant spray (Coltène/
Whaledent, Switzerland) and the electric pulp test (Parkell, New York)
induced no response on either incisor. Control teeth had no sensitivity to percussion and palpation; however, the response to
the cold test was positive. During periodontal examination, no
periodontal pocket was observed. A periapical radiograph showed
both central incisors had immature roots, thin dentinal walls and
open apices (Figure 1A).
On the basis of these findings, the pulpal diagnosis was
necrosis and the periapical diagnosis was acute apical abscess
for both teeth. Abscess drainage was done via labial mucosa
without antibiotic prescription. The common treatment protocol used for all patients presented in this case series (application of PRGF for a regenerative endodontic procedure) was
applied to both incisors.
Case Two
The patient was an 8-year-old girl with a history of trauma (three
months earlier) to the right central incisor. On extra- and intraoral examination, everything was normal. Both incisors were
sensitive to percussion and palpation tests. Cold test and electric pulp test induced no response on the right central incisor.
Control teeth had no sensitivity to percussion and palpation, in
addition to a positive response to cold test. During periodontal
examination, no periodontal pocketing was observed. A periapical
radiograph showed that both central incisors had thin dentinal
walls and open apices (Figure 2A).
On the basis of these findings, the pulpal diagnosis was necrosis, and the periapical diagnosis was acute apical periodontitis.
The common treatment protocol was performed for this patient.
Case Three
The patient was an 8-year-old girl with a history of trauma to
the anterior area of the maxilla. The patient’s parents reported
that her right central incisor had been avulsed in an accident
four months earlier. No replantation had been done for this
tooth. On extra- and intraoral examination, everything was
normal. The left central incisor was sensitive to percussion.
Cold test and electric pulp test induced no response on this
incisor. Control teeth had no sensitivity on percussion and
palpation, in addition to the positive responses to the cold test.
No periodontal pocketing was present. A periapical radiograph
showed the left central incisor had thin dentinal walls and an
open apex (Figure 3A).
On the basis of these findings, pulpal diagnosis was necrosis,
and the periapical diagnosis was acute apical periodontitis. The
common treatment protocol was performed for this patient.
Common Treatment Protocol
Prior to treatment, the patients’ parents were told that the treatment protocol was an attempt to help apex maturation and thickening of the dentinal walls. They were also told that the success of
this treatment is not definite. They signed the informed consent
form.
The patients received local anesthesia of 2% lidocaine with
1:80,000 epinephrine (Darou Pakhsh, Tehran, Iran), and the teeth
were isolated with a rubber dam. An access cavity was prepared
using fissure diamond burs (Dentsply/Maillefer, Tulsa, OK). A new
bur was used for each tooth. In all patients, no hemorrhage was
observed on entering the root canals. The working length of
each canal was determined using a #80 K-file (Maillefer, Dentsply,
Switzerland) and a periapical radiograph. The canals were irrigated with 8 ml of 0.5% sodium hypochlorite (NaOCl), followed
by normal saline prior to placement of triple antibiotic paste
(consisting of 500 mg metronidazole, 100 mg minocycline and
200 mg ciprofloxacin) to avoid the unwanted interaction of antibiotics with NaOCl.
After drying the canals with sterile paper points (Ariadent Co,
Tehran, Iran), a thick paste mixture of triple antibiotics was prepared. For each case, a freshly prepared paste was used. This paste
The New York State Dental Journal • JUNE/JULY 2014
51
was prepared from the powder after removal of the sugar coating
with a scalpel blade. The pills were crushed individually in separate mortars and each antibiotic ground to a fine powder. Equal
amounts of antibiotics (1:1:1) were combined on a mixing pad.
The powders were then mixed with an MP carrier (equal amounts
of macrogel ointment and propylene glycol) with the proportion
of 1:6 (1 part MP to 6 parts mixed antibiotics). The antibiotic
mixture was inserted in the coronal two-thirds of the canal using
a carrier (Q-106, Beijing, China) and packed using #80 paper points
(Ariadent Co, Tehran, Iran). For the temporary sealing of the access
cavity, Cavit (ESPE, Seefeld, Germany) was used.
For preparation of PRGF, 10 ml of patient blood was poured
into sterile tubes containing 5 ml of 3.8% sodium citrate. The
blood-filled laboratory tubes were centrifuged with 460 g speed
for 8 minutes. Plasma was consequently divided into different
layers. The third layer formed in the tube precisely on top of
the red blood cells layer. It contained x4 time concentration
PRGF, of which 0.5 ml was used for this study. 0.5 ml of CaCl2
was added to the separated solution to activate release of the
growth factors.
After two weeks, all patients were asymptomatic. At this appointment, triple antibiotic paste was removed and apical bleeding
was mechanically created by inserting a #80 file to within 1 mm
of the radiographic apex. The PRGF obtained from the previously
centrifuged patient’s blood was injected into the canals to the level
of the cementoenamel junction. This was done to help position the
growth factors to the apical portion of the canals. The teeth were
temporarily restored using Cavit (ESPE, Seefeld, Germany).
The patients returned for follow-up two weeks later. In the
absence of pain, swelling, fistula or any other complication, the
teeth were sealed with MTA (ProRoot, Dentsply, USA) and composite
(3M ESPE, Ontario, Canada), a thin layer of MTA at the floor of the
cavity, and composite for restoring the cavity.
Follow-up sessions at 3, 6, 9 and 22 months were scheduled
for all patients so the apical closure could be evaluated. At the
first three-month follow-up, increased dentinal wall thickness
in all four cases and apical closure in at least one case were
visible (Figures 1B, 2B, 3B). At the six-month follow-up, an increase in dentinal wall thickness was evident in one case and
apical closure in all other cases (Figures 1C, 2C, 3C). At the
nine-month radiographic follow-up, resolution of the periapical
lesion, apical closure and continued increase of dentinal wall
thickness in both incisors of Case 1 were evident (Figure 1D).
An increase in dentinal wall thickness was evident in Case 2
(Figure 2D). And increasing thickness in the dentinal walls and
apical closure were observed in Case 3 (Figure 3D). All three
patients remained asymptomatic.
At the 22-month follow-up, complete closure of the apex in
Case 1 (Figure 1E), apical closure and continued increase of dentinal wall thickness in Case 2 (Figure 2E) and Case 3 (Figure 3E)
were evident.
52
JUNE/JULY 2014 • The New York State Dental Journal
Discussion
Mechanical instrumentation of canals with necrotic pulps and
open apices is futile in immature teeth because of the weak dentinal walls, so disinfection of these canals is restricted to irrigation and intracanal medicament.1 This may induce regeneration
of pulp tissues in these teeth and thereby increase the likelihood
of the root length and apical closure.4 The cases presented here
can be added to previously reported cases1,4,8,10,12,13,18 to form the
basis for future studies.
For successful regenerative endodontics in teeth with necrotic pulps and open apices, the removal of infection from the canal,
a hermetic coronal seal, a physical scaffold for the promotion
of growth/differentiation and some molecules for stimulation of
stem cells are mandatory.4 In the cases presented here, disinfection was obtained with NaOCl and triple antibiotic paste, as proposed by other researchers.4,13
Banchs and Trope8 studied revascularization of immature
necrotic but adequately disinfected premolars with a suitable
matrix. The triple antibiotic paste was used. Apical closure, increased dentinal wall thickness, and the disappearance of both
periradicular radiolucency and sinus tract were evident at followup. Chueh et al.10 studied 23 teeth with necrotic pulps and open
apices where canals were irrigated with 5.25% NaOCl without
mechanical instrumentation. Calcium hydroxide was used, and
canals were filled only if they remained symptomless at followup. All teeth with necrotic pulps and open apices showed signs of
root formation within 10 to 20 months (mean 16 months). Since
2.5% NaOCl affects vital pulp and periapical cells, 0.5% NaOCl
was used in this study, but with an increased volume, as suggested
by Banchs and Trope.8
A component of tissue engineering with great importance is
using a physical scaffold. This scaffold should be able to provide a
correct position of cell location and also regulate differentiation.
These scaffolds may be natural or synthetic. Although most studies have considered only the blood clot as the scaffold, PRP2,4,14
has been introduced as a suitable scaffold.
In the cases presented here, PRGF was used as the scaffold.
PRGF is a combination of autologous proteins prepared from
PRP. It provides platelet-enriched plasma that contains no leukocytes.19 It may be considered a natural growth factor composite to
help endodontic regeneration. It has important advantages. It is
an autologous product, and so avoids the risk of disease transmission. It can facilitate the simultaneous action of growth factors
and provide a safe and effective biocompatible agent that can be
resorbed by the body after initiating local regeneration.20,21 It may
limit inflammation, suppress cytokine release and induce tissue
regeneration.22 However, PRGF has only limited potential in local
bone formation in animals.23
Although the number of cases presented here is small, it’s
possible that pulp regeneration in teeth with necrotic pulps and
open apices is predictable if the suggested protocol is followed.
In these circumstances, PRGF may be a suitable scaffold for pulp
regeneration. Additional clinical trials may further assess the
suitability of PRGF for pulp regeneration. More research on the
origin and cellular nature of the newly formed tissue would be
beneficial. p
Queries about this article can be sent to Dr. Jafarzadeh at [email protected], or [email protected]
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