March 2014 - New York State Dental Association

Transcription

editorial
Dream Job
S
Now there’s confirmation that dentistry is a compelling career choice.
canning the Internet recently, I came across
an article from US News and World Report on the
top 10 careers for 2014. The number-one career was
software developer. This came as no surprise to me,
as computers have just about taken over our lives.
They are ubiquitous, performing innumerable functions, from cooking our dinner, to keeping our
vehicles running properly and our homes warm.
Someone has to program them to work correctly.
Career number two was computer systems analyst. Again, no surprise. With all the computers out
there, specialists will be needed to keep them running properly so that all the computers can communicate with each other.
The real surprise came in the career listed at
number three: dentistry. The article stated that,
according to the Bureau of Labor Statistics, dentistry
is expected to add over 23,000 jobs by the year 2022.
That is a 16 percent increase in the number of dentists
currently employed. Dentists, it seems, have a wonderful career because their incomes are excellent; job
stress is relatively low; they have a great deal of independence; and job satisfaction is high. Physicians, by
comparison, occupy the number-eight career.
I really shouldn’t be surprised by dentistry’s
high standing. Dentistry is a unique career in that
it lets you work at your own pace, do the things you
like to do, refer out the things you don’t, work the
hours you want and be your own boss most of the
time. Pretty good work if you can get it.
I remember when I decided I wanted to be a
dentist. I was a senior in high school and had to
select the college I wanted to attend. But first, I had
to decide what I actually wanted to do with my life
after college. During my formative years, I had been
4
march 2014 • The New York State Dental Journal
exposed to many different occupations. Some
appealed to me; others didn’t. For some reason, the
dentists I met and became friends with impressed
me the most. To a man—and at that time most
dentists were men, particularly in Utica, NY—they
seemed the most satisfied with their career choice.
So I selected my college with dental school in
mind, one of the reasons why I went to the
University at Buffalo for my undergraduate degree.
Buffalo had a dental school, and it was a very good
dental school. I thought I might have an added
advantage getting into dental school as a UB alum.
That thinking may have been wrong, but it worked
for me. Eight years later, I graduated from UB
School of Dental Medicine. Following a residency
in orthodontics at the University of Connecticut
School of Dental Medicine, I had attained my goal
of being an orthodontist.
I have never been sorry for my career choice. It
has been everything I had hoped for and then some.
I have met some remarkable people during my
career, both patients and other dentists. The patients
I have treated have been, for the most part, wonderful. Sure, there are always those patients who, no
matter how hard you try or what you do, are never
pleased with the outcome. Thankfully, the dissatisfied have been few and far between. Most patients
appreciate all you do for them and are truly thankful for the care you provide.
There is no better feeling in the world than to see
a patient once treatment is completed beaming because
you were able to give him or her a beautiful smile. It
took a long time—usually two years—but these patients
are truly pleased with the way they look. Since I work
mostly with children and teens, being an orthodontist
NYSDA
has helped keep me young at heart. However,
since 25 percent of my practice are adults, my
older patients help keep me grounded in reality.
The best of both worlds!
Since I have my own practice and am a
solo practitioner, I am also my own boss. This
is another reason why I chose a career in dentistry. My father had worked in corporate
America, and, while he was treated well for
most of his working life, his career ended on
the whim of his boss. He had no control over
the decision. I never wanted to be placed in
that position. I will succeed or fail due to my
own efforts and not because of some arbitrary
reason from someone higher up.
Dentistry also allows me to pursue other
activities and passions. Since you decide how
much you want to work and you set your
own hours, you have much more flexibility
when it comes to pursuing other interests.
Knowing many dentists, I have found that
those interests are vast and varied. There are
other careers that allow this, but I have to
believe dentistry is at the top of that list.
Dentistry has, moreover, allowed me to
expand my list of friends and acquaintances.
Through my involvement in organized dentistry,
I have met many wonderful dentists from all
areas of our country and the world. This has
helped me to understand that we all have similar problems and responsibilities. Even though
we may practice alone, we are not alone; help
can be only a phone call away. Being the caring
individuals they are, dentists tend to respond
positively to calls for assistance.
To me, dentistry is really the number-one
career choice. It has been my career for over
35 years, and I have loved just about every
minute of it. The people I have met, those I
have treated over the years, those I have
helped, have given me a wonderful sense of
satisfaction and accomplishment. I wouldn’t
trade it for any other career.
There is an old saying: Do what you love and
you won’t work another day in your life. That is
how I feel about dentistry. I haven’t worked all
these years; I have just enjoyed myself.
D.D.S.
Directory
OFFICERS
Joel M. Friedman, President
525 E. 68th St., New York, NY 10065
John J. Liang, President Elect
2813 Genesee St., Utica, NY 13501
David J. Miller, Vice President
467 Newbridge Rd., East Meadow, NY 11554
Mark J. Weinberger, Treasurer
78 Southbury Road, 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
P. Deborah Weisfuse, Immediate Past President
12 E. 41st St., #1100, New York, NY 10017
NY – Edward J. Miller Jr
121 E. 60th St., #7A, New York, NY 10022
2 - Craig S. Ratner
7030 Hylan Blvd., Staten Island, NY 10307
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 – Jeffrey A. Baumler
2145 Lancelot Drive, Niagara Falls, NY 14304
9 – Stuart H. Coleton
7 Stone Rd., Chappaqua, NY 10514
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
Awards
Lawrence E. Volland
115 Professional Parkway, Lockport, NY 14094
Dental Benefit Programs
Eugene G. Porcelli
601 Franklin Ave., #211, Garden City, NY 11530
Dental Education & Licensure
Rekha C. Gehani
35-40 82nd St., #1F, Jackson Heights, NY 11372
Dental Health Planning & Hospital Dentistry
Carl H. Tegtmeier
359 E. Main St., #2C, Mt. Kisco, NY 10549
Dental Practice
Bijan Anvar
15 Rocky Rd., Larchmont, NY 10538
Ethics
Richard B. Serchuk
5 Valentines Ln., Old Brookville, NY 11545
Governmental Affairs
Prabha Krishnan
110-45 Queens Blvd., #108, Forest Hills, NY 11375
Membership & Communications
Maria C. Maranga
508 Main Rd., PO Box 170, Aquebogue, NY 11931
Nominations
P. Deborah Weisfuse
12 E. 41st St., #1100, New York, NY 10017
Peer Review & Quality Assurance
Jeffrey M. Galler
18 Copper Beech Lane, Lawrence, NY 11559
Professional Liability Insurance
Roland C. Emmanuele
4 Hinchcliffe Dr., Newburgh, NY 12550
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 • march 2014
5
Invisalign
Current Guidelines for Effective Treatment
Daniel A. Kuncio, D.D.S.
A b st r a c t
Invisalign is an increasingly popular technique for
aligning teeth and correcting malocclusions orthodontically. This article analyzes the current professional
literature published on Invisalign and the benefits and
risks of using the technique for both patients and doctors. The steady increase in the number of cases treated with Invisalign and where the technique is going in
the future is investigated. Ten guidelines for Invisalign
treatment and patient selection are given, along with
case examples.
Align Technology revolutionized orthodontic tooth movement with
its invention and marketing of the Invisalign system. Although the
idea of moving teeth naturally using clear thermoplastic aligners to
apply pressure to the dentition has been around for many decades,
Align’s engineers applied new CAD/CAM and mass customization
technologies to greatly increase the use of aligners. According to
Align’s website, Invisalign has been used to treat over 2.4 million
patients worldwide, with over 80,000 dentists trained in the technique. Since its founding in 1997, Align has earned over 500 patents
for its technologies and has another 200 patents pending. These are
without debate impressive numbers, as are Align’s financial figures
that show record revenue of $164.5 million in the third quarter of
2013 alone.1
So, what has created such an upswing in demand? Certainly
there are major advantages to using Invisalign over fixed appliances
(braces). The aligners can be removed for eating, brushing and intimacy; patients experience less dental pain, have better oral hygiene
and fewer dietary restrictions; and the treatment planning software
(ClinCheck) is an excellent tool for visualizing and analyzing potential treatment outcomes, especially when preparing for future
restorative work.2,3
Of course, there is also the “invisibility” factor, but lingual braces
are probably more undetectable to laypeople than Invisalign, and
have been around for decades. They’re just not as comfortable and
cannot be removed.4
These are all valid and important points, but my inkling is
that the more significant factors in these surging sales of Invisalign are Align’s massive advertising campaign, Internet groupdiscount companies like Groupon and Living Social driving down
the cost to the patient, and Invisalign’s relative ease of use for the
practitioner. A PVS impression or digital tooth scan is the major
pretreatment step in the Invisalign technique. And the most laborious clinical step is bonding the composite attachments to teeth,
which can usually be done in one step from a template. Both of
these procedures can even be done by certified dental assistants,
leaving the doctor only the treatment planning and interproximal
reduction (IPR) to complete.5 Research presented at the AADR
meeting found that Invisalign cases used significantly less chair
time than conventional braces treatment, and had an overall
shorter treatment time.6
But if you step back and take a look at the big picture, this is
a potentially precarious position for the treating doctor. He or she
takes 100% of the responsibility for the outcome of each case (see
Invisalign’s terms and conditions1); is confronted with a public
perception (and hi-tech computer software) that Invisalign is a
product that can place teeth virtually anywhere in the mouth with
relative ease no matter who the doctor is; and is facing shrinking
profit margins, forcing more production and, therefore, less clinical time with each patient.
A look at the published research on the Invisalign technique
reveals mixed results. The last systematic review was in 2005,
and it yielded inconclusive results—another published review is
overdue.7 Invisalign has been proven to resolve moderate anterior
tooth crowding predictably, but treatment outcome studies have
highlighted Invisalign’s weaknesses compared to conventional
braces in treating anterior-posterior discrepancies, large rotation-
11
Figure 1. Typical attachment protocol with G4 attachments. Some patients may be disappointed with esthetics on maxillary anterior teeth, so our practice makes sure to show potential
patients this example, both with and without aligners in. Then potential downside of not having
those attachments is discussed.
Figure 2. Perfect Invisalign candidate: full adult dentition; no large vertical, transverse or anterior-posterior problems; reciprocal space closure needed (equal space closure in anterior to posterior and posterior to anterior directions) so as not to require special anchorage considerations,
like elastics or mini-implants.19 Treatment time: 20 months; 1 refinement.
12
MARCH 2014 • The New York State Dental Journal
al movements and the extrusion of teeth.8,9,10 More post-treatment relapse of anterior dental alignment has also been found in
Invisalign cases.11 Two independent studies recommend leaving
the aligners in the mouth for longer than the two-week intervals
the company advocates, probably for better bone and periodontal
ligament (PDL) formation.11,12
Align has attempted to improve treatment outcomes with
several generations of composite tooth attachments and softer,
more resilient, aligner material.1 Even though the theory behind
these improvements seems sound, Align does not publish its internal clinical findings and, thus, the data cannot be peer-reviewed.
The time is now. We need blind, randomized, prospective studies
comparing the outcomes of Invisalign to traditional braces. And
if we really want a modern study, Invisalign treatment should
be compared to fixed appliances using digital treatment planning
software (Insignia or Suresmile). Surely, with thousands of practitioners all over the world using both techniques, such a study
could be done.
There are several published Invisalign case studies that show
impressive space closure, crowding alignment and moderate open
bite correction.13,14 The Invisalign website and other case reports
show patients who almost certainly feel they have a more attractive
smile—and the improved quality of life that such changes bring
should not be dismissed.1,15 But many of these published cases
have occlusions that stand little chance of passing the American
Board of Orthodontics (ABO) standards and could potentially
make patients more prone to future dental problems.16,17,18
This is the dilemma that all clinicians using Invisalign face: At
what point, if ever, do the esthetic concerns trump the health issues?
Is a beautiful smile worth an increased chance of certain dental
problems later on in life? I’m sure many patients would say yes and
many doctors would say no. But if we clinicians are not satisfying
our patients’ demands, we’d all be out of business very soon.
I believe the solution is not only studying the literature and
educating ourselves as to the capabilities of the Invisalign appliances, but also having an honest conversation with our patients
about what these appliances can and cannot do; what has a high
percentage chance of working; what is risky even with multiple
refinements (ordering more aligners from a new scan or impression); and what the potential consequences can be. This conversation should be documented and signed by the patient.
To help dentists navigate this challenging terrain, I have provided basic guidelines below for case selection and general advice
and troubleshooting tips. This list is certainly not comprehensive,
but should, I hope, help the thousands of Invisalign clinicians in
New York State.
1. Until you decide to invest in a digital tooth scanner (only the
iTero and 3M True Definition brands are currently compatible with Invisalign), try a two-phase PVS impression with
putty to make a quick custom tray and then a light body wash
(Genie or Henry Schein brand is fine). True, it’s an extra
step, but you or your assistant will get a perfect impression
every time, which will eliminate redoes and will capture that
elusive distal side of the upper second molars. An excellent
impression leads to better results. Take the bite registration
first and use it to measure the correct size of impression tray,
avoiding multiple fittings.
2. Use Invisalign’s new G4 composite attachments, but note
that the well on these attachments is usually much smaller, making the use of heavier filled composites challenging.
Flowable composite (Kerr brand) is easier to place, but these
resins tend to shrink more and abrade faster, preventing full
expression of the aligner. Align claims to have unpublished
Figure 3. Invisalign combined with restorations (veneers on maxillary lateral incisors and composite bonding on mandibular central incisor, done by Zenovia D. Kuncio, DDS). Mandibular incisor was
extracted to relieve crowding and address tooth-size discrepancy. Treatment was effectively simulated with ClinCheck software. Maxillary laterals were difficult to rotate and extrude, and black triangles persisted in mandibular anterior due to tipping of teeth—Invisalign cannot move tooth bodily
without perfect attachment or complete contact-free side to upright after tipping. Patient was offered
lingual and esthetic fixed appliances (Incognito/Simpliclear), but chose Invisalign with restorations
for removable feature. Treatment time: 21 months; 2 refinements.
studies on composite attachments as well, but it’s hard to see
how the attachment/aligner interface will ever be as accurate as a wire/bracket interface. Theoretically, using a digital
scanner, a clinician should be able to bond attachments first
and then have the aligners manufactured. But, as of this publication, Align does not seem to be pursuing that avenue.
3. Use the Align-issued Ivoclar (or other similar density composite) if you have large spaces to close or root movement to
accomplish. Overcorrect these movements in the refinement
phase (after most other problems have been corrected) and
instruct the patient to use Aligner Chewies as often as possible to help seat the aligner and create the correct force vectors. Even using all of these steps, however, will not guarantee that the clinician will be able to diverge roots for implant
spaces—we’ve needed to switch to braces at least temporarily
in every such case thus far.
4.Make sure the patient is aware that Invisalign attachments are
not “invisible” to other people (Figure 1). Currently, G4 attachments cannot be placed on the lingual side of teeth, so
another outcome/esthetics decision needs to be made and
documented.
5. Try Brasseler coarse strips in the mini-stripper handle for patient comfort and ease of use for IPR of .2 mm or less. If more
reduction is indicated, break the contact with the strips and
Figure 4. Patient had moderate crowding and posterior crossbite, but insisted on Invisalign
appliances. We discussed limitations of Invisalign with potential consequences and treatment
plan was signed. He ended up with excellent esthetic improvement, but posterior crossbite
remains, as does small open bite, affecting anterior guidance. Better functional result was probably obtainable with fixed appliances, but patient is extremely satisfied with esthetic results. Did
we do our job? Treatment time: 20 months;1 refinement.
The New York State Dental Journal • MARCH 2014
13
use the Brasseler double-sided mesh disk. Postpone all IPR as
far into treatment as possible to get clear access through the
contact point (expand and procline teeth first). This will ensure more accurate measuring with the IPR gauge. Tell the Invisalign tech the exact ClinCheck stage you wish to start your
IPR and where. Attempt mostly posterior IPR unless you want
to change the shape of the anterior teeth for esthetic reasons.
6. Do not attempt rotations over 30° unless you plan to use
fixed appliances to align the rotated teeth first. If using Invisalign only and the tooth is not in an esthetic area, do not
attempt to rotate the tooth at all, because the subsequent
aligners will not fit and a new PVS impression or scan will be
needed almost immediately. If a tooth is rotated 20° to 30°
and is in an important esthetic area, you can attempt the
correction with large buccal and lingual rectangular Ivoclar
attachments, but educate the patient that several refinements
may be needed and do not promise a 100% correction.
7. Overcorrect space closure with a “C-chain” aligner that
will overcorrect all anterior spaces with three extra aligners at the end. You may not need all of these extra aligners,
but you can sometimes avoid doing an entire refinement to
close a small gap.
8.Ask the patient to leave the final three aligners in for three
weeks each (unless using an accelerator like AcceleDent or
Propel). This should allow for better bone and PDL formation toward the end of treatment and will, it is hoped, lead
to better, more stable final results.11 Patients stop feeling the
aligner forces after only a few days, but if they move to the
next aligner too soon, they can potentially damage tissues.19
As always, compliance is a major factor with Invisalign and
22-hour/day wear is a must (Figure 2), as is nightly retainer
wear after treatment or a fixed retainer.
9. Do not attempt the extrusion of teeth unless you plan and
discuss with the patient the use of elastics or fixed appliances, or possible restorations (Figure 3). Due to the “watermelon seed” effect, every rotational force put on a tooth
with Invisalign has an inherent intrusive vector.20 Anterior
open bites are corrected with intrusion of posterior teeth and
subsequent bite closure, not extrusion of anterior teeth.14
10. Do not promise to correct skeletal Class II or Class III malocclusions, posterior crossbites, severe open bites (larger than
2 mm), or TMD symptoms with Invisalign (Figure 4). Advanced users have had some success correcting these conditions, but these techniques require full orthodontic records
with a traced cephalometric radiograph and are beyond the
scope of this article.
The bottom line to general practitioners is please use the Invisalign technique cautiously and conservatively. Invisalign has
and will continue to produce thousands of beautiful smiles and
healthy occlusions and is our first choice for removable esthetic
orthodontic treatment—we prefer Invisalign over ClearCorrect
14
and other clear aligners due to the superior treatment planning
software—but is most certainly not for every patient and is extremely case-sensitive. Seek the guidance of your trusted orthodontist to select the cases that have a high probability of success,
and keep patients informed about issues that might not be completely corrected. Don’t forget that Align’s primary responsibility
is to its shareholders. The patients are our responsibility. p
Dr. Kuncio is an orthodontist in private practice on the
upper west side of Manhattan who has treated or supervised the treatment of hundreds of Invisalign cases since
2006. He is a diplomate of the American Board of Orthodontics and a clinical attending and assistant professor of orthodontics at Montefiore Medical Center/Albert
Einstein College of Medicine, New York, NY. Dr. Kuncio
has no financial affiliation with Align Technology or any
other dental company. Queries about this article can be sent to Dr. Kuncio at
[email protected].
References
1. 2. The Invisalign website. http://www.invisalign.com. 2012.
Schaefer I, Braumann B. Halitosis, oral health and the quality of life during treatment
with Invisalign and the effect of low-dose chlorhexidine solution. J Orofac Orthop 2011;
71(6):430-41.
3. Miller K. A comparison of treatment impacts between Invisalign aligner and fixed appliances therapy during the first week of treatment. Am J of Orthod Dentof Orthop
2007;131(3):302.e1-302.e9.
4. Shalish M, Cooper-Kazaz R, Ivgi I, Canetti L, Tsur B, Bachar E, Chaushu S. Adult patients’
adjustability to orthodontic appliances. Part 1: a comparison between Labial, Lingual and
Invisalign. Eur J Orthod 2011; (Epub).
5. New York State Department of Education website. http://www.op.nysed.gov/prof/dent/
dentasst.htm. 2011.
6. Orthodontic Products website. http://www.orthodonticproductsonline.com/newsbites/2012-04-16-04.asp. 2012.
7. Lagravere MO, Flores-Mir C. The treatment effects of Invisalign orthodontic appliances: a
systematic review. JADA 2005;136:1724-1729.
8. Krieger E, Seiferth J, Marinello I, Jung BA, Wriedt S, Jacobs C, Wehrbein H. Invisalign treatment in the anterior region: were predicted tooth movements achieved? J Orofac Orthop
2012; 73(5): 365-376.
9. Djeu G, Shelton C, Maganzini AL. Outcome assessment of Invisalign and traditional orthodontic treatment compared with the American Board of Orthodontics objective grading
system. Am J Orthod Dentofacial Orthop 2005;128(3):293-298.
10. Kravitz N, Kusnoto B, BeGole E, Obrez A, Agran B. How well does Invisalign work? A prospective clinical study evaluating the efficacy of tooth movement with Invisalign. Am J
Orthod Dentof Orthop 2009;135(1):27-35.
11. Kuncio D, Shelton C, Maganzini AL, Freeman K. Invisalign and traditional orthodontic
treatment postretention outcomes using the American Board of Orthodontics Objective
Grading System. Angle Orthod 2007;77(5):864-869.
12. Vardimon AD, Robbins D, Brosh T. In-vivo von Mises strains during Invisalign treatment.
Am J Orthod Dentof Orthop 2010;138(4):399-409.
13. Boyd RL. Esthetic orthodontic treatment using the Invisalign appliance for moderate to
complex malocclusions. J of Dental Education 2008;72(8):948-967.
14. Schupp W, Haubrich J, Neumann I. Treatment of anterior open bite with the Invisalign
system. J Clin Othod 2010;44(8):501-507.
15. Olsen J, Inglehart MR. Malocclusions and perceptions of attractiveness, intelligence, and
personality, and behavioral intentions. Am J Orthod Dentof Orthop 2011;140:669-79.
16. Nicozisis J. Aligners can for your cants. Orthodonic Products 2013; 8:16-19.
17. American Board of Orthodontics website. http://www.americanboardortho.com. 2013.
18. Stenik A, Espeland L, Berg RE. A 57-year follow-up of occlusal changes, oral health, and
attitudes towards teeth. Am J Orthod Dentof Orthop 2011;139:S102-8.
19. Proffit, WR. Contemporary Orthodontics, 3rd Ed. 2000; pg. 296-304, 347-348.
20. Hahn W, Engelke B, Jung K, Dathe H, Fialka-Fricke J, Kubein-Meesenburg D, Sadat-Khonsari R. Initial forces and moments delivered by removable thermoplastic appliances during
rotation of an upper incisor. Angle Orthodontist 2010; 80(2): 239-246.
pediatric dentistry
Elements in Oral Health Programs
Anty Lam, R.D.H., M.P.H.
A b st r a c t
Demographically, dental caries remains the single
most common disease of childhood. Various campaigns have been carried out to promote and to improve the oral health of children. However, the prevalence of dental caries was still more than 50% in many
communities. This article reviews different approaches used in dental health programs in industrialized
and developing countries. To build a comprehensive
oral health preventive program, three elements are
essential. They are oral health education/instruction,
primary prevention measures and secondary prevention measures.
Demographically, dental caries remains the single most common
disease of childhood.1 According to the Report of the U.S. Surgeon
General in 2000, tooth decay is five-times more common than
asthma and seven-times more common than hay fever. It affects
more than one-fourth of U.S. children ages 2 to 5 and half of
those ages 12 to 15.2,3
The World Health Organization (WHO) also considers dental caries the most important global oral health burden. And a
global strategy for preventing oral health diseases was formulated
26
and endorsed in 2000 by the Fifty-third World Health Assembly.4,5 Before that, the WHO had partnered with the Fédération
Dentaire Internationale (FDI) to formulate global goals for oral
health to be achieved by the year 2000.6 One of the goals was
to declare 50% of 5- to 6-year-olds free of dental caries. Various
campaigns have been carried out to promote and to improve the
oral health of children to reach the goal. However, the prevalence
of dental caries was still more than 50% in many communities.
It is not only children in developing countries, but those in
developed countries with low socio-economic status as well who
suffer from a similar pattern of dental decay. For instance, in the
United States, about half of all children and two-thirds of children
ages 12 to 19 from low-income families have had dental decay.2
Nevertheless, many reports suggest there was a decline in dental
caries in the past decades observed in many developed countries
as a result of a number of public health measures, coupled with
changing living conditions, lifestyles and improved self-care practices. However, it must be stressed that dental caries, as a disease,
is not eradicated but only controlled to a certain degree.
Oral Hygiene in Children
Poor oral hygiene leads to the development of gingivitis. Epidemiological studies have found that oral hygiene in children is worse
in developing countries and in low socio-economic groups.7,8 Gingivitis can be prevented by practicing good personal oral hygiene
practices, including brushing and flossing, which are also impor-
tant in controlling the advancement of periodontal lesions.5 The
2001 Grant Makers in Health Issue Dialogue observed that “One
proven strategy for reaching children at high-risk for dental disease is providing oral and dental health services in school-based
health centers….”9
The American Dental Association (ADA) also addresses the fact
that tooth decay remains the single most common chronic disease
of children. Resolution 38H-2010, passed by the ADA House of
Delegates, recognizes the benefits of school-based oral health programs in preventing and controlling dental caries in children and
adolescents.10 In fact, a number of community oral health programs
for children have been conducted in school/kindergarten. Some examples are the ones in Milwaukee, WI, Brazil and Ecuador.11-13 To
facilitate the operation of these community oral health programs,
the involvement of school staff, community clinics, dental hygienists and health educators is feasible and appropriate.
people’s lives, when lifelong oral health-related behaviors, as
well as beliefs and attitudes, are being developed.
l School can provide a supportive environment for promoting
oral health. Access to safe water, for example, may allow for
general and oral hygiene programs. Also, a safe physical environment in school can help reduce the risk of accidents and
concomitant dental trauma.
l The burden of oral disease in children is significant. Most
established oral diseases are irreversible and will last a lifetime and have an impact on the quality of life and general
health.
l School policies, the physical environment and education for
health are essential for attainment of oral health and to control risky behaviors, such as the intake of sugary foods and
drinks, use of tobacco and alcohol consumption.
l Schools can provide a platform for providing oral health care,
that is, preventive and curative services.
Oral health education is considered important to preventing
Elements in Oral Health Programs
and treating oral diseases as evidenced in
There are three main elements in most
the Knowledge Attitude Behavior (KAB)
oral health programs. They are: oral
model. The Health Belief Model (HBM)
health education/instruction; primary
The American Dental
also posits that individuals must perceive
prevention measures, which can be chairthemselves to be at risk before they will
side and non-chairside; and secondary
Association (ADA) also
take actions to reduce risky behaviors
prevention measures, which refer to early
or to engage in healthy alternative bedetection and treatment. Frazier and his
addresses the fact that
haviors. Through education, people can
co-workers surveyed prevention programs
tooth decay remains the
acquire the knowledge to identify their
for children in Japan, Singapore, Sweden
risk and the impetus to practice healthy
and the United Kingdom and concluded
single
most
common
chronic
alternative behaviors.
that it is essential to include these three
Kay and Locker reviewed the efprogram elements to build a comprehendisease of children.
fectiveness of dental health education
sive oral health preventive program.14
and reported that very few definitive
conclusions about the effectiveness of
Oral Health Education/Instruction
oral health promotion can be drawn from currently available
Oral health education/instruction usually refers to oral hygiene
evidence.16 Knowledge levels can almost always be improved by
instruction and/or oral health education. These instructional
activities aim to promote oral health practices and to improve
oral health promotion initiatives, but whether these shifts in
awareness and attitudes toward dental health. They target not
knowledge and attitudes can be causally related to changes in
only children, but also their parents, teachers and health workers.
behavior or clinical indices of disease has not been established.
Oral health education and instructional activities for children,
Although there are studies conducted in China and in England
parents, teachers and health workers are commonly carried out
reporting that oral health education had an effect in improving
in schools and clinics. Reinforcing and teaching toothbrushing
the dental health of children,17,18 several other studies in differis generally accepted to be a main component in oral hygiene inent countries, such as the ones conducted in Zimbabwe, Belstruction. Oral health education is usually carried out through
gium and Indonesia, concluded that the involvement of primary
presentations, games or printed materials. Schools are often
healthcare personnel and school teachers in providing schoolselected because they provide good access to children, parents,
based oral health education had little significant effect on caries
teachers and health workers. The WHO supports programs carprevention in children.19-21
15
ried out in schools. Arguments in favor of promoting dental
health through schools include:
Primary Prevention Measures
l Students can be accessed during their formative years, from
Fluoride agents are commonly used as a primary prevention
childhood to adolescence. These are important stages in
measure. It is generally agreed that the use of fluorides has led
27
to a significant decline in dental caries.22,23 Research has shown
that fluoride is most effective in preventing dental caries when a
low level of fluoride is constantly maintained in the mouth.24,25
The provision of fluoride can be through drinking water, salt,
mouthrinse or toothpaste, and various forms of professionally
applied fluorides, such as gels and varnishes. Of these modalities,
water fluoridation is considered the most cost-effective way to
prevent caries formation. It has been suggested that the most potent effect of water fluoridation is not so much preventing new lesions from appearing, but remineralizing existing carious lesions
and, thus, slowing down or even arresting the caries process.26
Although there is evidence of merits in water fluoridation,
health authorities in many countries still have implementation
problems. The lack of a safe networked water supply system and
the absence of government willingness/support are difficulties
in developing countries. In industrialized countries, worry from
unjustified claims of harmful effects and freedom-of-choice and
autonomy arguments from anti-fluoridationists may affect the
decision to add fluoride to the water.
When water fluoridation is not feasible, WHO recommends
considering the use of salt fluoridation techniques to prevent
dental caries.27 Unlike water fluoridation, which requires a reliable water supply, salt fluoridation is less dependent on infrastructure and can achieve wide coverage. It is a less politically
sensitive issue that allows for freedom of choice. And it has been
reported to have an effect on preventing dental caries. In some
areas of France and Germany, domestic fluoridation salt has a
market share of more than 50%.28 In Jamaica, the reduction of
caries in children has been noticed since implementation of salt
fluoridation.29 Although there is increased use of fluoridated salt
in Europe, Central and South America, the population coverage
is still not large.
The most common products for self-application are fluoride
toothpastes and mouthrinses. A review of fluoride toothpaste by
Cochrane Collaboration, using random effects meta-analyses,
found that fluoride toothpaste is efficacious in preventing caries in children.30 The review also found that the effect of fluoride toothpaste increased with higher baseline levels of D(M)
FS, higher fluoride concentration, higher frequency of use and
supervised brushing. Fluoride toothpaste can be used in community-based preventive programs. A study in China found that
brushing with fluoride toothpaste for three years arrested 45% of
the proximal and 23% of the buccal and palatal carious lesions
in primary anterior teeth.31 It demonstrated that daily toothbrushing with fluoride toothpaste could be an effective program
to control the caries problem in children. Since the use of fluoride toothpaste in developing countries like China, especially in
rural areas, can be inhibited by its relatively high cost and poor
distribution, the development of the fluoride toothpaste market
in these countries presents a challenge to manufacturers and to
dental public health workers.32
28
Although fluoride mouthrinse is not as popular as fluoride
toothpaste for self-application, there are studies that report that
mouthrinse is effective in caries prevention in children. A metaanalysis conducted by Cochrane Collaboration suggested that
the supervised regular use of fluoride mouthrinse reduced caries
incrementally in children.33 However, fluoride rinses may not
be suitable for young children, because they are likely to swallow the solution posing a risk for fluorosis. On the other hand,
rinsing appears to have a greater effect in older children aged 10
or above.34,35
Fissure sealant application is another procedure that has
been demonstrated to be effective in preventing caries in children.
Although the prevalence among U.S. children and adolescents of
one or more sealed permanent tooth surfaces increased about
13% during the period 1988-1994 to 1999-2002, it is still well
below the objective set by the Healthy People 2010 document,
which is 50% of sealant use among this population.
Many states have used government money to initiate sealant utilization programs to meet the objective delineated in the
Healthy People 2010 document.36 Examples of community-based
sealant promotion programs targeted to high-risk school children
include Sealant Saturdays in Salt Lake City, UT, and the Dental Initiatives of the Academic Health Center at the University
of Minnesota; Dental Sealant Program of the Department of
State Health Services, Texas; Seal a Smile Program of Wisconsin
Oral Health Program; Dental Sealant Grant Program of Illinois
Department of Public Health; and the Rural School-Based Oral
Health Program for South Texas.37 School-based dental sealant
programs also have significant accomplishments. Those programs
in Arizona, Illinois, New Mexico, Michigan and Ohio have been
named as successful practices in the Association of State & Territorial Dental Directors May 2011 Report.38
Secondary Prevention Measures
Dental screening is the usual strategy used in early detection and
treatment service. A study in Sweden pointed out the importance
of early detection and prevention of caries in the primary dentition.39 In industrialized countries, dental treatments are often
carried out in either standing dental clinics or provided through
a “mobile dental clinic” housed in a van that travels to various
places. These methods are neither available nor affordable in developing countries,40 where the cost of basic sets of instruments,
dental materials and infection control products is too high and
training for primary health workers to undertake basic oral care is
inadequate. In these situations, a new approach to oral healthcare
is needed.
The Commonwealth Dental Association (CDA) and the
WHO held a workshop in 1996 on equity in oral health. One
of the many challenges addressed at the workshop was how to
provide funding to treat the massive amount of caries in children
in developing countries.41 Managing caries through minimal
invasions and low-cost methods is imperative. Caries-arresting
treatment that aims to halt or slow down disease progression is
a practical solution to minimize children’s discomfort and other
problems due to dental caries.
Studies on xylitol chewing gum showed the effect of the gum
on arresting caries in children.42,43 Other studies showed similar
results from using chlorehexidine varnish.44,45 Moreover, a minimal intervention treatment using professionally applied topical
silver fluoride, followed by stannous fluoride solution, was found
to be effective in arresting caries in primary molars.46 The School
Dental Service in Western Australia has used a 40% silver fluoride solution as the standard treatment for deep carious lesions
in primary teeth with good results.47 In China and Japan, silver
ammonia fluoride or silver diamine fluoride (SDF) has been used
successfully for arresting caries in children for many years.48,49 A
recent review found that SDF is a simple and cost-effective agent
that has significant and substantial benefit in arresting and preventing caries.50
Another systemic review by Rosenblatt concluded that SDF
appears to meet the criteria of both the WHO Millennium Goals
and the U.S. Institute of Medicine’s criteria for 21st century medical care.51
The use of glass ionomer in atraumatic restorative treatment
(ART) is another useful method for treating dental caries in pre-
school children in developing countries. The short treatment time
and simple and minimal armamentarium of ART makes it affordable for treating children. An evaluation of ART restorations
placed in children in China showed promising results.52 Another
study in Tanzania reported a good success rate with ART over six
years.53 The WHO Collaborating Centre performed a meta-analysis and found it appears there is no difference in survival results
between single-surface ART restorations and amalgam restorations in permanent teeth over the first three years.54
The advantages of ART sealants and restorations then are: it
requires simple instruments and materials; the cost is low; it is
flexible; and it is user friendly, especially for children. Dr. R.G.
deAmorim commented in a journal article that the accumulating
evidence of ART has suggested that it can be as good as or even
better than conventional treatment.55
Conclusion
In summary, most articles on prevention describe how the programs were run; few studies have proper evaluations. Evidencebased studies are essential to evaluate the outcome of these
programs. It is difficult to have appropriate study design for evaluation; and a randomized clinical trial model may not be applicable because of ethical issues. However, as there are a number
of effective prevention methods available, we can provide feasible
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29
prevention care to children after careful consideration of the cultural, social, economic and healthcare settings in which they live. p
Queries about this article can be sent to Ms. Lam at [email protected].
References
1.
Dye BA, Tan S, Smith V, et al. Trends in oral health status: United States, 1988–1994 and
1999–2004. Vital Health Stat 2007:11(248):1–92.
2.
U.S. Department of Health and Human Services (USDHHS). Oral Health in America: A
Report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services. National Institute of Dental and Craniofacial Research, National Institutes of Health.
2000.
3.
Oral Health - Preventing Cavities, Gum Disease, Tooth Loss, and Oral Cancers: At A Glance
2010. Center for Disease and Prevention.
4.
Oral Health - Strategies and Approaches in Oral Disease Prevention and Health Promotion.
World Health Organization 2011.
5.
Strategies for oral disease prevention and health promotion - Oral Health within WHO
strategic directions. World Health Organization 2011.
6.
Federation Dentaire Inernationale/World Health Organization 1982. Global goals for oral
health in the year 2000. Int Dent J; 32:74-7.
7.
Lam A, Chu CH. Oral health of children in rural area of Philippines. JDR
2010;89(A):1270.
8.
Lam A, Chu CH. Oral health of children in rural areas of Myanmar. JDR 2011;90(A):
1210.
9.
Grant Makers in Health Issue Dialogue: Filling the Gap: Strategies for Improving Oral
Health. Issue Brief. Washington; May 2001.
10.ADA News - House resolution addresses school-based oral health programs. November 1,
2010.
11.Columbia St. Mary’s – A Passion for Patient Care. Milwaukee, WI. Available from: http://
www.columbia-stmarys.org/Smart_Smiles. Accessed on July 20, 2011.
12.Child Family Health International. San Francisco, CA. Available from: http://www.cfhi.
org/web/index.php/program/show/id/315. Accessed on July 20, 2011.
13. Over the Rainbow – Health & Education Services. Cedar Falls, IA. Available from: http://
www.over-therainbow.org/oralhealthpromotion.html. Accessed on July 20, 2011.
14. Frazier PJ, Jenny J, Johnson BG. Preventive dental programs for school-age children in 8
countries: pilot survey, 1979. Int Dent J 1982;32:204-214.
15. Oral Health Promotion Through Schools. WHO Information Series on School Health.
Document 11. Geneva: World Health Organization 2003.
16. Kay E, Locker D. A systematic review of the effectiveness of health promotion aimed at
improving oral health. Community Dent Health 1998;15:132-144.
17.Rong WS, Bian JY, Wang WJ, Wang JD. Effectiveness of an oral health education and
caries prevention program in kindergartens in China. Community Dent Oral Epidemiol
2003;31:412-416.
18. Worthington HV, Hill KB, Mooney J, Hamilton FA, Blinkhorn AS. A cluster randomized
controlled trial of a dental health education program for 10-year-old children. J Public
Health Dent 2001;61(1):22-27.
19. Frencken JE, Borsum-Andersson K, Makoni F, Moyana F, Mwashaenyi S, Mulder J. Effectiveness of an oral health education programme in primary schools in Zimbabwe after 3.5
years. Community Dent Oral Epidemiol 2001;29,4:253-259.
20. Vanobbergen J, Declerck D, Mwalili S, Martens L. The effectiveness of a 6-year oral health
education programme for primary schoolchildren. Community Dent Oral Epidemiol
2004;32:173-182.
21.Hartono SW, Lambri SE, van Palenstein Helderman WH. Effectiveness of primary schoolbased oral health education in West Java, Indonesia. Int Dent J 2002;52(3):137-43.
22. Featherstone JD. Prevention and reversal of dental caries: role of low level fluoride. Community Dent Oral Epidemiol 1999;27:31-40.
23. Featherstone JD. The science and practice of caries prevention. J Am Dent Assoc 2000;
131(7): 887-899.
24. Fluorides and oral health WHO Technical Report Series No. 846 Geneva: World Health
Organization;1994.
25. Oral Health Fact sheet No.318. World Health Organization. February 2007.
26. Lawrence HP, Sheiham A. Caries progression in 12- to 16-year-old schoolchildren in fluoridated and fluoride-deficient areas in Brazil. Community Dent Oral Epidemiol 1997;25:402411.
27. Petersen PE, Lennon MA. Effective use of fluorides for the prevention of dental caries in the
21st century: the WHO approach. Community Dent Oral Epidemiol 2004;32:319-321.
28.Meyer J, Marthaler TM, Burgi H. The change from water to salt as the main vehicle for
community-wide fluoride exposure in Basle, Switzerland. Community Dent Oral Epidemiol
2003;31:401-402.
29.Meyer-Lueckel H, Satzinger T, Kielbassa AM. Caries prevalence among 6- to 16-year-old
students in Jamaica 12 years after the introduction of salt fluoridation. Caries Res 2002;
36:170-173.
30
30.Marinho VC, Higgins JP, Sheiham A, Logan S. Fluoride toothpastes for preventing dental
caries in children and adolescents. Cochrane Database Syst Rev 2003b;1:CD002278.
31. Lo ECM, Schwarz E, Wong MCM. Arresting dentine caries in Chinese preschool children.
Int J Paediatr Dent 1998;8:253-260.
32.Burt BA, Eklund SA. Dentistry, Dental Practice and the Community. 5th Ed.Philadelphia:
W. B. Saunders 1999, 279-314.
33.Marinho VC, Higgins JP, Logan S, Sheiham A. Fluoride mouthrinses for preventing dental
caries in children and adolescents. Cochrane Database Syst Rev 2003a; (3): CD002284.
34.Bell RM, Klein SP, Bohannan HM, Disney JA, Graves RC, Madison R. Treatment effects in
the national preventive dentistry demonstration program. Santa Monica: Rand Corporation, 1984.
35. Poulsen S, Kirkegaard E, Bangsbo G, Bro K. Caries clinical trial of fluoride rinses in a Danish
public child dental service. Community Dent Oral Epidemiol 1984;12:283-287.
36.Beltran-Aguilar ED, Barker LK, Canto MT, et al. Surveillance for dental caries, dental sealants, tooth retention, edentulism, and enamel fluorosis—United States, 1988-1994 and
1999-2002. MMWR Surveill Summ 2005;54:1-43.
37. Lam A. Increase in utilization of dental sealants. J Contemp Dent Pract 2008; 9:81-87.
38.Best Practice Approach Reports—School-based Dental Sealant Programs. Association of
State & Territorial Dental Directors. May 14, 2011.
39.Alm A, Wendt LK, Koch G. Dental treatment of the primary dentition in 7-12 year-old
Swedish children in relation to caries experience at 6 years of age. Swed Dent J 2004; 28:6166.
40. Frencken JE, Pilot T, Songpaisan Y, Phantumvanit P. Atraumatic Restorative Treatment
(ART): rationale, technique and development. J Public Health Dent 1996;56:135-140.
41.Commonwealth Dental Association and World Health Organization. Proceedings of a
workshop on Promoting Equity in Oral Health, Cape Town 1-3 April 1996. NG Med. University of the Western Cape.
42.Makinen KK, Makinen PL, Pape HR Jr, Allen P, Bennett CA, Isokangas PJ, Isotupa KP. Stabilisation of rampant caries: polyol gums and arrest of dentine caries in two long-term cohort
studies in young subjects. Int Dent J 1995;45:93-107.
43. Duane B. Xylitol gum, plaque pH and mutans streptococci. Evid Based Dent 2010;
11(4):109-10.
44. Garcia MB, Nör JE, Schneider LG. A model for clinical evaluation of the effect of antimicrobial agents on caries dentine. Amer J Dent 2000;14:119-122.
45. Paula VA, Modesto A, Santos KR, Gleiser R. Antimicrobial effects of the combination of
chlorhexidine and xylitol. Br Dent J 2010 Dec 18;209(12):E19. Epub 2010 Oct 1.
46.Craig GG, Powell KR, Cooper MH. Caries progression in primary molars: 24-month results
from a minimal treatment programme. Community Dent Oral Epidemiol 1981;9:260265.
47. Gotjamanos T. Pulp response in primary teeth with deep residual caries treated with silver
fluoride and glass ionomer cement (‘atraumatic’ technique). Austral Dent J 1996;41:328334.
48.Chu CH, Lo EC, Lin HC. Effectiveness of silver diamine fluoride and sodium fluoride varnish in arresting dentin caries in Chinese pre-school children. J Dent Res 2002; 81:767770.
49. Yamaga R, Nishino M, Yoshida S, Yokomizo I. Diamine silver fluoride and its clinical application. J Osaka Univ Dent Sch 1972;12:1-20.
50.Chu CH, Lo EC. Promoting caries arrest in children with silver diamine fluoride: a review.
Oral Health Prev Dent 2008; 6:315-321.
51.Rosenblatt A, Stamford TCM, Niederman R. Silver Diamine Fluoride: A caries “silver-fluoride bullet.” J Dent Res 2009; 88(2):116-125.
52.
Lo ECM, Holmgren CJ. Provision of atraumatic restorative treatment (ART) restorations to
Chinese preschool children—a 30-month evaluation. Int J Paediatr Dent 2001;11:3-10.
53.Mandari GJ, Frencken JE, van‘t Hof MA. Six-year success rates of occlusal amalgam and
glass-ionomer restorations placed using three minimal intervention approaches. Caries Res
2003;37:246-253.
54. Frencken JE, Van ‘t Hof MA, Van Amerongen WE, Holmgren CJ. Effectiveness of singlesurface ART restorations in the permanent dentition: a meta-analysis. J Dent Res 2004;
83:120-123.
55. de Amorim RG, Leal SC, Frencken JE. Survival of atraumatic restorative treatment (ART)
sealants and restorations: a meta-analysis. Clin Oral Investig 2011; Jan 28. (Epub ahead of
print)
Pediatric Dentistry
Riga-Fede Disease
Case Report
Jessica Lee, D.D.S.; Louis Mandel, D.D.S.
A b st r a c t
Riga-Fede disease results when an infant’s instinctive
tongue thrusting and raking motion over recently
erupted primary mandibular incisors causes a traumatic ulceration of the tongue and/or mouth floor.
The symptoms and therapeutic approach to the condition are highlighted in this case report.
Riga-Fede disease (RFD) is a reactive traumatic mucosal disease
in infants, characterized by an uncommon self-limiting persistent
ulceration of the oral mucosa.1,2 It was first described clinically by
Riga in 1881. In 1890, Fede added a histologic description.2,3
The ulceration is a result of repetitive trauma to the oral
mucosa by teeth and usually involves the ventral surface of the
tongue. An instinctive infantile reflex tongue thrust3-5 leads to
a raking motion of the tongue over the incisal edges of recently
erupted primary mandibular incisors. Inevitably, an ulceration of
the tongue’s ventral surface results. However, the lingual frenum,
mucosa of the lips, buccal mucosa, mouth floor, and even the
dorsum of the tongue if contact with maxillary teeth occurs, all
can become involved.1,4,6,7
Natal teeth, those that are present at birth, and neonatal
teeth that erupt in the first 30 days after birth are the causes of
RFD. Although RFD is usually seen soon after birth, coinciding
with deciduous tooth eruption at 6 to 8 months, it is also observed in infants up to 2 years of age.1,3,8,9 Traumatic ulcerative
granuloma with stromal eosinophilia is the diagnostic term used
to describe the identical condition in children older than 2 and
36
in adults.1,10,11 The incidence of RFD in the presence of natal/
neonatal teeth has been reported to be 6% to 10%.8,11 Because
of the oral discomfort that is present, feeding problems with nutritional deficiencies, retarded growth, dehydration and infection
can result.9,11,12 Prompt care is necessary to avoid these sequela.
Furthermore, an early accurate diagnosis is mandatory in order to
differentiate RFD from serious neurologic and hereditary disorders that present similar oral ulcerations.
The authors present a case of RFD that was previously undiagnosed by the infant’s pediatrician and dentist. The purpose
of the report is to highlight the etiology, symptomatology and
therapeutic approach to RFD. The profession’s familiarity with
the entity will avoid known complications, the patient’s chronic
discomfort and needless parental concern.
Case Report
A 9-month-old female was seen in the oral surgery clinic of
Columbia University College of Dental Medicine. The infant’s
mother was concerned about an ulceration that was present in
the anterior mouth floor. The mother said she first noticed the
lesion three weeks previously and had sought professional advice,
but no diagnosis had been made. The mother believes a feeding
problem has developed and this has heightened her concern.
A previous examination by the infant’s pediatrician indicated
that the baby was thriving normally and was in excellent health.
The intraoral examination revealed a non-suppurating ulcerative
From the Department of Oral and Maxillofacial Surgery, Columbia University
College of Dental Medicine, New York, NY.
lesion, measuring about 1.3 cm in diameter, that involved the anterior mouth floor, lingual frenum and the ventral surface of the
tongue (Figure 1). The ulcer had a gray-white surface, reflecting
the presence of a necrotic slough. Mandibular deciduous central
incisors, with distinctive mammelons, were noted to be in their
normal eruptive position.
The source of the problem became quite evident during the
examination. The infant constantly thrust her tongue anteriorly
out of the mouth and over the incisal edges of the deciduous centrals. In so doing, the tongue carried forward the lingual frenum
and the mouth floor. The involuntary repetitive action brought
these anatomic mucosal structures into continuous contact with
the mammelons of the erupted teeth. The ulcer’s location corresponded perfectly with those mucosal areas that rubbed against
the mandibular primary anterior teeth.
A diagnosis of RFD was made. Conservative therapeutic treatment involved referring the infant to the pediatric dentist, with
the recommendation that the sharp incisal edges of the deciduous anterior teeth be smoothed by disking. Our follow-up phone
call, five weeks later, revealed that the ulcer had disappeared three
weeks after the teeth were disked.
Discussion
The classic ulcer associated with RFD can also herald the existence of underlying developmental or neurologic disorders. Familial dysautonomia (Riley-Day syndrome) is an inherited disorder that affects the autonomic nervous system with a variable
symptom complex that includes insensitivity to pain, loss of tears,
poor growth, a labile blood pressure and frequent emetic episodes.
Lesch-Nyhan syndrome, an X-linked recessive disorder of purine
metabolism, is best known for its classic diagnostic characteristic,
a severe compulsive self-injurious patient behavioral pattern. Additionally, the persistent motor disorder associated with cerebral
palsy can include involuntary tongue thrusting activity that may
lead to tongue ulceration.6
Histologic analysis of the ulcer will reveal a chronic ulceration surrounded by a dense mixed inflammatory granulation
tissue infiltrate consisting largely of lymphocytes, macrophages,
mast cells and numerous eosinophils.2,3,6 Due to the large number
of eosinophils, it is often classified as a subtype of the traumatic ulcerative granuloma with stromal eosinophilia (TUGSE).4,10
However, TUGSE differs clinically from RFD in that the ulcers
are seen in adults and involve oral regions other than the tongue.
Biopsy is rarely indicated in cases of RFD, because a diagnosis can
be made on the basis of the history and clinical features of the
lesion. When the clinical symptoms do not resolve within two
weeks after standard treatment, biopsy can be performed to rule
out an infectious or neoplastic etiology.1,2,6
Figure 1. Ulceration involving anterior mouth floor and ventral surface of tongue
(arrow).
Treatment
The aim of therapy for RFD is to minimize trauma. Standard treatment options for RFD begin and typically end with conservative
therapies such as disking down the sharp incisal edges of teeth and/
or placing composite resins on the edges of the teeth. Both techniques are usually combined with a topical corticosteroid because
of its anti-inflammatory action.1,4,7-9,12 Extraction of the culpable
teeth is an option, but its effect on the eruption of the permanent
teeth must be considered.7-9,12 Recurrence of the ulcerative lesion is
not expected once healing has occurred following therapy.6 p
Queries about this article can be sent to Dr. Mandel at [email protected].
References
1.
Eley KA, Watt-Smith PA, Watt-Smith SR. Deformity of the tongue in an infant: Riga-Fede
disease. Paediatr Child Health 2010;15:581-2.
2.Ceyhan AM, Yidirim M, Poasak PY, Akkaya VB, Ayata A. Traumatic lingual ulcer in a child:
Riga-Fede disease. Clin Exp Dermatol 2008;34:186-8.
3.
Zaenglein Al, Chang MW, Meehan SA, Axelrod FB, Orlow SJ. Extensive Riga-Fede disease of
the lip and tongue. J Am Acad Dermatol 2002;47:445-7.
4.Baghdad ZD. Riga-Fede disease: report a case and review. J Clin Pediatr Dent 2001; 25:209-13.
5.
Domingues-Cruz J, Herrara A, Fernandez-Crehuet P, Garcia-Bravo B, Camacho F. Riga-Fede
disease associated with postanoxic encephalopathy and trisomy 21: a proposed classification. Pediatr Dermatol 2007; 24:663-5.
6.
Taghi A, Motamdi MK. Riga-Fede disease: a histological study and case report. Indian J Dent
Res 2009;20:227-9.
7.Choi SC, Park JH, Choi YC, Kim G-T. Sublingual traumatic ulceration (a Riga-Fede disease):
report of two cases. Dent Traumatol 2009;25:e48-50.
8.Buchanan S, Jenkins CR. Riga-Fedes syndrome: natal or neonatal teeth associated with
tongue ulceration. Case Report. Austral Dent J 1997; 42: 225-7.
9.Hegde RJ. Sublingual traumatic ulceration due to neonatal teeth (Riga-Fede disease). J Indian Soc Pedod Prev Dent 2005;23:51-2.
10. Elzay RP. Traumatic ulcerative granuloma with stromal eosinophilia (Riga-Fede’s disease and
traumatic eosinophilic granuloma). Oral Surg Oral Med Oral Pathol 1983; 55:487-506.
11. Padmanabhan MY, Pandey RK, Aparna R, Radhakrishnan V. Neonatal sublingual traumatic
ulceration-case report and review of the literature. Dent Traumatol 2010;26:490-5.
12.Baroni A, Capristo C, Rossiello L, Faccenda F, Satriano RA. Lingual traumatic ulceration
(Riga-Fede disease). Int J Dermatol 2006; 45:1096-7.
37
dental manpower
Use of Oral Healthcare and Need to
Expand Population That is Served
A Commentary
H. Barry Waldman, D.D.S., M.P.H., Ph.D.; Steven P. Perlman, D.D.S., M.Sc.D., D.H.L. (Hon.)
A b st r a c t
General population demographics are undergoing
dramatic changes. Long-term customary populations
that provided the bulwark for successful dental practices are being replaced by the many minority populations. Despite these significant general population
developments, the demographic profile of the dental
profession has experienced (and, apparently, based on
dental student populations, will continue to experience) limited changes. The economic strength of the
profession may well be predicated upon its responses
to these developments. The question remains, “Is the
l The rising proportion of those over 65 years old (projected
to increase from 48 million in 2015 to 92 million in 2060)
could significantly increase dental expenditures, “…buoying
up the dental economy for years to come.”1
Unfortunately, waiting decades for the number of seniors
to almost double and boost the economics of dentistry is not a
viable option for current practitioners. Similarly, relying solely
on emphasizing efforts to increase the use of services by the
traditional consumers of oral healthcare may have its limitations. Maybe by “accentuating the negative” component of the
2012 report on dental expenditures from the federal Agency for
Health Care Research and Quality, we can tell the story that
could direct the profession as it seeks to expand its services to
the general population.2
profession preparing for them?”
In mid-April 2013, the lead headline of the ADA News announced, “Baby Boomers Boost Utilization: Older Patients Show
Raise in Dental Expenditures.”1 However, the information contained in paragraphs of the column that followed emphasized a
different story. It included:
lAmericans aren’t spending any more on dental care than
they were five years ago.
lAfter decades of steady growth, national dental expenditures began to slow in the 2000s, years before the economy
soured.
l Once the great recession hit in 2008, national dental expenditures leveled off and have remained flat ever since.
38
March 2014 • The New York State Dental Journal
Non-use of Services
Percent with No Expenses
Almost half of youngsters and teenagers (ages 5 to 17 years) were
reported to have had no expenditures for dental services in 2010,
followed by two-thirds of younger adults (18 to 44 years) and
more than half of the population 45 years and older. Among other demographic cohorts, dental expenditures were reported by a
smaller percent of:
l Men than women.
l Minority groups, in particular Hispanics, than white nonHispanics.
l Middle income and poor populations than higher income
populations.
“More than 4 million children aged 17
tations in the availability of dentists to provide access to care. For
example, the death of Deamonte Driver in 2007 was headlined
as, “For the Want of a Dentist.” And follow-up statements in the
Washington Post made the case that “Twelve-year-old Deamonte
Driver died of a toothache Sunday. A routine, $80 tooth extraction might have saved him… If Medicaid dentists weren’t so hard
to find.”5
and younger had unmet dental need in
2011 because their families could not
afford dental care….”6
Ongoing Crisis in Dental Care
The Centers for Disease Control and Prevention reported that in
lResidents in non-metropolitan statistical areas (MSA) than
the second half of the last decade, almost one-quarter (23.7%) of
those in MSA.
adults 20 to 64 years had untreated dental caries.7
l Uninsured individuals than privately insured and government covered program groups.
Table 1
lResidents of the Southern Region than in all other cenDental Services—Median and Mean Expenses per Person with Expenses: 20102
sus regions (Table 1).
Mean and Median per Person Expenses
It is estimated that almost 60% of the population (183.9
million individuals) reported no expenditures for dental
services. Among those who spent money for services, the
average individual expended $666 in 2010, with a median
expenditure of $236—which would indicate that of those
who spent money for care, half expended a relatively small
amount of money (that is, less than $236) and half (or possibly a small component) expended a much greater amount
of money to raise the overall national mean level to $666
(Table 1).
Payment for Dental Services
Out-of-pocket spending represented 44% of all dental service costs. By contrast, out-of-pocket spending represented
14% for all healthcare expenditures for the total population—including 17% of the costs for youngsters < 18years;
15% for the 18- to 64-year population; and 12% for the 65+
year population.3 In essence, spending for dental services “is
felt” to a greater extent than for total health services.
l Private insurance does not cover 54% of dental expenses.3
l Medicaid provided 6% of all expenditures for dental services. However, it represented 42% of costs for children
less than 5 years, 21% for the Hispanic population, 38%
for the poor population and 73% for the 65+ population with public insurance (Table 2). At the same time,
studies suggest that fewer than 25% of all dentists accept Medicaid patients and fewer than 10% have at least
30% of their practice represented by Medicaid beneficiaries.4
Yes, there are explanations, including inadequate fee
schedules and Byzantine bureaucratic impediments. However, from the prospective of the public, the results are limi-
Population characteristics
Population
(in
millions)
Percent
with
Expenses
Per person
with Expenses
Total
308.6
40.4% $236
Age in years
Under 65
Under 5
5-17
18-44
45-64
65 & over
267.4
21.3
53.6
111.1
81.5
41.2
40.1
18.9
54.1
34.2
44.5
42.4
228
125
188
240
273
296
642
234
678
547
759
814
Gender
Male
Female
151.6
157.0
37.2
43.5
230
242
644
684
Race/ethnicity
White, non-Hispanic
Black, non-Hispanic
Native American
Asian
Hispanic
198.7
37.4
6.6
15.5
50.3
45.8
30.5
38.1
36.3
28.0
252
166
235
247
177
710
466
560
668
566
Health insurance status
< 65 yrs, private
< 65 yrs, public
< 65 yrs, uninsured
65+ yrs, Medicare only
65+ yrs, Medicare & private
179.4
47.8
40.2
15.7
20.8
48.1 30.7
15.6
32.0
55.1
250
129
210
294
308
687
410
574
758
860
Poverty status
Poor
Middle income
High income
46.8
93.0
111.7
25.9
37.9
53.9
151
227
268
447
672
735
Metropolitan statistical areas (MSA)
MSA
Non-MSA
260.1
48.4
41.1
37.1
240
222
674
620
Census region
Northeast
Midwest
South West
55.5
66.9
114.0
72.2
41.9
45.6
35.8
41.9
226
240
215
280
689
642
589
776
Median
Mean
$666
The New York State Dental Journal • March 2014
39
The 2012 report “Dental Care Crisis in America” by the Subcommittee on Primary Health and Aging of the U.S. Senate Committee on Health, Education, Labor & Pensions goes further in
describing the need for dental health services. It found that:
l “More than 47 million people live in places where it is difficult to access dental care.
lAbout 17 million low-income children received no dental
care in 2009.
l One fourth of adults in the U.S. ages 65 and older have lost
all of their teeth.
l Low-income adults are almost twice as likely as higher-income adults
to have gone without a dental checkup in the previous year.
lBad dental health impacts overall health and increases the
risk for diabetes, heart disease and poor birth outcomes.
l There were over 830,000 visits to emergency rooms across
the country for preventable dental conditions in 2009—a
16% increase since 2006.
lAlmost 60% of kids ages 5 to 17 have cavities—making tooth
decay five-times more common than asthma among children
of this age.
l Nearly 9,500 new dental providTable 2
ers are needed to meet the coun2
Dental Services—Distribution of Sources of Payment: 2010
try’s current oral health needs.
Percent Distribution of Total Expenses by Source
lHowever, there are more dentists
of Payment
retiring each year than there are
Total
dental school graduates to re
Expenses
Out of
Private
place them.”8
(in billions)
Pocket
Insurance
Medicare Medicaid Other
Total
$59.7
44.3%
46.1%
0.7%
5.7%
3.2%
Somehow the problem seems
to
be
“poverty” and “the dentist,”
Age in Years
rather than the inadequacies of the
Under 65
47.8
38.0
51.9
*0.2
6.7
3.3
Under 5
.9
13.7
40.5
*0.0
42.4
*3.4
system to provide sufficient resources
5-17
8.2
25.6
48.5
*0.0
21.9
4.0
to support the needed care.
18-44
15.8
34.6
58.3
*0.0
3.8
3.3
45-64
65 & over
22.9
11.9
45.6
69.5
49.2
22.7
*0.4
3.0
1.9
*1.7
3.0
3.1
Gender
Male
Female
27.0
32.7
41.7
46.4
47.5
44.9
*0.7
0.8
6.0
5.4
4.0
2.6
Race/ethnicity
White, non-Hispanic
Black, non-Hispanic
Native American
Asian
Hispanic
46.8
4.0
1.1
2.4
5.3
46.2
32.3
37.4
42.7
38.9
47.5
43.5
41.0
50.8
34.0
0.8
*0.5
*0.8
*0.3
*0.4
2.8
17.4
16.2
3.2
21.0
2.7
6.3
*4.5
*3.0
5.7
41.3
4.0
2.5
3.3
38.1
16.8
70.0
81.8
60.0
*0.0
*0.0
*0.0
*0.0
*2.1
*0.0
9.0
0.6
73.5
*0.0
*0.0
1.3
7.6
30.0
9.2
8.2
66.6
32.1
*0.6
*0.0
*0.6
4.2
17.3
39.7
46.6
14.3
46.4
*0.5
*0.7
38.5
*0.3
7.1
2.1
Metropolitan statistical
areas (MSA)
MSA
Non-MSA
51.3
8.4
43.0
52.2
47.3
38.3
0.7
*0.8
5.8
5.0
3.2
3.7
Census region
Northeast
Midwest
South West
10.6
14.4
17.6
17.1
40.6
45.9
45.2
44.3
49.8
45.0
44.7
46.0
*0.6
*0.
*1.0
0.9
7.1
5.5
5.2
5.4
1.9
3.1
3.9
3.5
Health insurance status
< 65 yrs, private
< 65 yrs, public
< 65 yrs, uninsured
65+ yrs, Medicare only
65+ yrs, Medicare
& private
Poverty status
Poor
Middle income
High income
* Relative standard error equal to or greater than 30%.
40
National Demographic Changes
The reality is that the majority of
births in the United States occur
among Hispanic, black and Asian
mothers. It is evidence that white
Americans will become a minority nationwide within about three
decades and will “…be reliant on
younger minorities and immigrants
for our future demographic and economic growth.” (emphasis added)7
If current trends continue, the
nation’s population will rise to 438
million in 2050, from 296 million in 2005. And fully 82% of the
growth during this period will be due
to immigrants arriving from 2005
to 2050 and their descendants. The
Pew Research Hispanic Center projections indicate that nearly one-infive Americans (19%) will be foreign
born in 2050, surpassing the historic
peaks for immigrants as a share of
the U.S. population—almost 15% in
1890 and 1910.10
By 2050, the nation’s racial and
ethnic mix will look quite different
than it does now. Non-Hispanic
whites, who made up 67% of the population in 2005, will be 47%
in 2050. Hispanics will rise from 14% of the population in 2005
to 29% in 2050. Blacks were 13% of the population in 2005 and
will be roughly the same proportion in 2050. Asians, who were
5% of the population in 2005, will be 9% in 2050.10
Minorities, classified as those of any race other than nonHispanic, single-race whites, currently constitute about a third
of the U.S. population, according to Census figures. In 2042, minorities are projected to become the majority, making up more
than half the population. Minority children are projected to reach
that milestone even sooner. By 2023, the Census Bureau reports
“… more than half of all children will be minorities.”11
“New census estimates foretell profound
Dental Profession Demographic Changes
Dental School Graduates
Between 2001 and 2010, the continuing increase in the proportion of female representation among graduates, from 37.5% to
45.3%, was the major demographic change. During the same period, the proportion representations among graduates included:
l Non-Hispanic white—decreased from 62% to 58.4%.
lAsian—decreased from 26.5% to 25.0%.
lHispanic—increased from 4.9% to 6.1%.
lBlack—increased from 4.9% to 5.5%.
l Native American—increased from 0.6% to 0.7%.12
Compared to the general population, Asian students were
over-represented among graduates, and other minorities continued to be under-represented among dental school graduates during the past decade.
Disability Prevalence
No review of underserved populations would be complete without reference to individuals with disabilities. Approximately 56.7
million people living in the United States in 2010 (18.7% of the
population) had some kind of disability. About 12.6%, or 38.3
million people, had a severe disability. This number has continued to increase and will enlarge much further as the expanding
aging population reaches into their 70s, 80s, 90s and beyond.15 In
2010, almost 29% of individuals with disabilities (many of whom
are dependent upon the Medicaid program for care) did not ob-
demographic change for the country.”9
tinue to experience) limited changes. The proverbial roles of increasing “minority power” and “minority practitioner role models” are essential factors in: 1. developing legislative support for
the needed health services of minority populations; and 2. increasing the demand for all oral healthcare from providers with
whom minority populations could identify.
Dentists
In 2010, 80.3% of the 175,000 dentists were non-Hispanic
whites; 19.7% were members of minority groups (13.7% Asian,
5.7% Hispanic and 0.3% black).13 The shortage of Hispanic dentists has been emphasized previously by the National Hispanic
Medical Association.14
Overview
Decades of studies and reports based on race/ethnicity, income,
residency locations and insurance have emphasized the disparities in the delivery of dental care to the general population. The
layout of most tables in these reports (e.g., Tables 1 & 2) “accentuated the positive” use of services by non-Hispanic white
middle- and higher-income populations with insurance. The tables usually compare and recognize the inadequacies for minority
populations. But general population demographics are undergoing dramatic changes with the result that the long-term customary populations that provided the bulwark for successful dental
practices are being replaced by the many minority populations.
Despite these dramatic general population developments,
the demographic profile of the dental profession has experienced
(and, apparently, based on dental student populations, will con-
41
tain dental services because of cost.16 Also, Medicaid dentists are
“…so hard to find.”5
The reality is that changes are coming. The question remains,
“Is the profession preparing for them?”p
Queries about this article can be sent to Dr. Waldman at [email protected].
References
1.
Soderlund K. Baby boomers boost utilization: older patients show rise in dental expenditures. ADA News 2013;44:1,4.
2.Agency for Health Care Research and Quality. Medical expenditure panel survey: 2010. Web
site: http://meps.ahrq.gov Accessed June 7, 2013.
3.Carper K, Machlin S. National Health Care Expenses in the U.S. Civilian Noninstitutionalized Population, 2010. Statistical Brief #396. January 2013. Agency for Healthcare Research
and Quality, Rockville, MD. Web site: http://www.meps.ahrq.gov/mepsweb/data_files/
publications/st396/stat396.pdf Accessed June 9, 2013.
4.
Friedman E. Access to dental care: a national scandal. Web site: http://www.hhnmag.com/
hhnmag/HHNDaily/HHNDailyDisplay.dhtml?id=2540006049 Accessed June 10, 2013.
5.
Otto M. For want of a dentist. Washington Post. February 28, 2007. Web site: http://www.
washingtonpost.com/wp-dyn/content/article/2007/02/27/AR2007022702116.html Accessed June 10, 2013.
6.
Palmer C. Children’s dental visits, unmet need: data from 2011 National Health Interview
Survey. ADA News, March 21, 2013. Web site: http://www.ada.org/news/8420.aspx Accessed June 13, 2013.
7.Centers for Disease Control and Prevention. Health United States 2011. Web site: http://
www.cdc.gov/nchs/data/hus/hus12.pdf Accessed June 10, 2013.
42
March 2014 • The New York State Dental Journal
8.A Report from Chairman Bernard Sanders of the Subcommittee on Primary Health and
Aging: U.S. Senate Committee on Health, Education, Labor & Pensions. Dental Crisis In
America: The need to expand services, February 29, 2012. Web site: http://www.sanders.
senate.gov/imo/media/doc/DENTALCRISIS.REPORT.pdf Accessed June 10, 2013.
9.Roberts S. For whites, more deaths than births, data shows. NY Times, June 6, 2013. pA16.
10. Passel J, Cohn D. Pew Research Hispanic Center. U.S. Population Projections: 2005-2050.
Web site: http://www.pewhispanic.org/2008/02/11/us-population-projections-2005-2050.
Accessed June 13, 2013.
11.CNN.com.Minorities expected to be majority in 2050. Web site: http://www.cnn.
com/2008/US/08/13/census.minorities Accessed June 13, 2013.
12.American Dental Association. 2010-2011 Survey of Dental Education. Academic programs,
enrollment and graduates –Vol. 1 May 2012. Web http://www.ada.org/sections/professionalResources/pdfs/survey_ed_vol1.pdf Accessed June 12, 2013.
13.Census Bureau, 2012 Statistical Abstract of the United States. Web site: http://www.census.
gov/compendia/statab/2012edition.html Accessed June 13, 2013.
14. National Hispanic Medical Association. Diversity in the health professions. Shortage of
Hispanic dentists. Web Site: http://www.slideshare.net/dentistryinfo/shortage-of-hispanic-dentists Accessed June 13, 2013.
15.Brault MW. Americans with Disabilities: 2010. Current Population Reports. P70-131. Web
site: http://www.census.gov/prod/2012pubs Accessed February 15, 2013.
16. National Center for Health Statistics. Health, United States, 2011: With Special Feature on
Socioeconomic Status and Health. Hyattsville, MD. 2012. Web site: http://www.cdc.gov/
nchs/data/hus/hus11.pdf Accessed February 14, 2013.
restorative dentistry
Histologic Findings within Peri-implant Soft Tissue
in Failed Implants Secondary to Excess Cement
Report of Two Cases and Review of Literature
Naomi Ramer, D.D.S.; Chandur Wadhwani, B.D.S., M.S.D.; Andrew Kim, D.D.S.;
Dwight Hershman, D.D.S.
A b st r a c t
A link has been established between peri-implant disease and excess cement extrusion in cement-retained
implant restorations. The histologic findings of two
patients with failed implants secondary to residual
excess cement are reported here. If excess cement is
detected early and adequately removed, resolution
can occur in the majority of situations. Simple recommendations are proposed, with the intention of
preventing further implant failures from residual excess cement.
Cementation of an implant prosthesis is an accepted protocol.
Advantages include less demanding surgical placement of the
implant, simpler laboratory techniques, passive fit, esthetics and
control of the occlusion.1-2 Disadvantages are unpredictable retention and resistance, and the detrimental effect of cement flow
into the soft tissues that can be difficult to remove.2
The soft tissue attachment onto the implant surface is more
delicate than that seen at the natural tooth surface due to the
lack of Sharpey’s fiber insertion, the reduced number of collagen fibers and the direction in which these fibers run.2-3 Cement
extrusion into the sulcular area may result in soft tissue swelling, soreness and bleeding, or exudation on probing.2,4 In some
instances, the excess cement has been considered the cause of
implant failure.2,5
We report here on two cases of failed implants with histologic evidence of excess cement within the soft tissue surrounding these implants and foreign body inflammation. The intent of
this publication is to increase awareness of the detrimental effects
of incomplete cement removal or residual excess cement, and to
provide clinicians with simple recommendations to minimize
further implant failures.
Case Reports
Case One
In June 2009, a 44-year-old female in good general health was
referred by her general dentist to an oral and maxillofacial surgeon for extraction of the mandibular left first molar (#19)
(Figure 1A). The treatment plan was to extract tooth #19 and
immediately place a dental implant. After local anesthesia was
obtained, the tooth was atraumatically extracted. The surgical
site revealed an inadequate amount of alveolar bone for the
planned procedure and, thus, the decision was made to place
freeze-dried human bone graft material (Oragraft; Life Net Health) in
the extraction socket and postpone placement of a dental implant for several months.
The patient returned to the office in March 2010 for evaluation of the previously placed graft in the edentulous area of tooth
#19 and implant consultation (Figure 1B). The patient was ad-
43
Figure 1A. Case One preoperative radiograph. Taken in June
2009 of endodontically failed tooth #19.
Figure 1B. Post-extraction radiograph with replacement bone
graft of edentulous #19 area left mandible. Radiograph taken
March 2010.
Figure 1C. Post-insertion radiograph taken Aug. 26, 2010,
of Nobel Biocare replace select screw implant.
Figure 1D. Hematoxylin and eosin-stained section (20x
magnification) demonstrating multiple foci of black exogenous
cement deposits in several areas. Stroma is highly vascularized fibrous tissue and contains scattered acute and chronic
inflammatory cells.
Figure 1E. Hematoxylin and eosin-stained section (40x magnification) demonstrates multinucleated giant cells and foci of
black cement particles within fibrous tissue stroma. Scattered
inflammatory cells are also noted.
Figure 1F. Hematoxylin and eosin-stained section (10x magnification) shows squamous surface mucosa overlying inflamed
fibrous tissue and spicule of residual necrotic bone.
vised to wait an additional six months. On August 26, 2010, the
patient returned to the oral and maxillofacial surgeon for implant
placement. A Nobel Biocare replace select implant (Nobel Biocare;
Yorba Linda, CA) was inserted (Figure 1C) in the edentulous space
#19. The implant was allowed to heal for four months. In December 2010, the patient returned to her general dentist for restoration of the implant. A ceramo-metal crown was subsequently
fabricated and cemented.
On October 14, 2011, the patient returned to the practice of
the now-deceased oral and maxillofacial surgeon with excessive
bone loss and granulation tissue around #19 implant. The implant was removed, along with the friable surrounding soft tissue
and ostectomy contents, which were placed in a bottle of 10%
formalin and sent to the oral and maxillofacial pathology laboratory for histopathologic evaluation.
Hematoxylin and eosin-stained sections of the specimen
(Figure 1D) revealed foci of black amorphous exogenous cement
scattered throughout the fibrous stroma. These foci were accompanied by an acute and chronic inflammatory cell infiltrate and
multinucleated foreign body type giant cells (Figure 1E). Surface
mucosa overlying inflamed fibrous tissue containing a spicule of
residual necrotic bone (Figure 1F) was also noted. The final pathology report included a diagnosis of acute and chronic inflammatory reaction with foci of exogenous matter consistent with cement. The ICD-9 code for foreign body granuloma accompanied
the diagnosis.
44
Case Two
In January 2006, a 57-year-old male presented to an oral and
maxillofacial surgeon. He had been referred by his general dentist
for placement of dental implants in the edentulous right mandible. Two implants (Nobel Biocare replace select) were placed in the
edentulous right mandible in the area of the second premolar and
second molar sites (Figure 2A).
Four months after the implants were placed they were evaluated for clinical integration (Figure 2B). The patient returned to
the general dentist for fabrication of abutment crown restorations. Individual ceramo-metal crowns were fabricated and cemented onto the implants.
On October 26, 2011, the patient presented with excessive
bone loss around a failing implant at the mandibular second molar
site. This implant was removed, along with the hyperplastic soft
tissue surrounding the failed implant, which was placed in a bottle
of 10% formalin and sent to the oral and maxillofacial pathology laboratory for histopathologic examination. A bone graft using
a mineralized allograft material (Puros; Zimmer Dental, Warsaw, IN) was
placed in the surgical defect (Figure 2C) for a future implant.
Hematoxylin and eosin-stained sections of the tissue (Figure
2D) showed scattered foci of black particulate exogenous cement
material throughout the inflamed fibrous tissue stroma. The final
pathology report included a diagnosis of acute and chronic inflammatory reaction, with foci of exogenous matter, consistent
with cement, and ICD-9 coded for foreign body granuloma.
Discussion
The cemented crown was introduced for esthetic reasons and
to compensate for loosening problems encountered with screwretained restorations4,6 The initial disadvantage associated with
cemented restorations was lack of retrievability when problems
occurred that required crown removal. Another problem is the
difficulty associated with visualization and with removing excess
cement at the crown margins.4 Residual excess cement (REC) is
a common complication of cement-retained prosthesis and has
been linked to peri-implant disease,7-8 which can result in a local
inflammatory process and has been documented as a cause of
peri-implant disease.2,5
In a published study by Wilson,9 peri-implant disease was
first diagnosed in test implants loaded from four months to more
than nine years after cementation of single-unit fixed partial dentures. Case Two in our series occurred five and a half years after
final cementation. Wilson9 noted that if the REC is identified and
adequately removed, resolution of peri-implant disease can occur
in the majority of situations. The proposed etiology for the periimplant disease in the Wilson study was bacterial colonization
of the cement; however, in the two examples cited in our case
report, it may well be due to a foreign body reaction.
Prevention of cement extrusion during the restoration process beyond the restorative cement margins cannot be underestimated; however this may be more difficult than it appears.10 In
vitro model systems have demonstrated the difficulty in controlling and removing REC by visual and tactile means,11 even when
supra-gingival crown/abutment margins were placed.12
Radiographic evaluation allows for a non-invasive evaluation of the site, with the potential to locate REC. Detection is
influenced by factors such as composition of the cement, amount
and site.13-14 Other disciplines within dentistry have required radiopacity specifications for cements.15 No mandatory minimal
standard specifications exist for implant cements.16
The radiopacity of some commonly used cements has been
documented, and a large variability in radiographic detection
ability was reported.13 Some cements have high radiographic density, which allows for easy radiographic detection; others cannot
be detected even at 2 mm thickness.10 The radiographic material
varies directly with the third power of the atomic number of the
absorber elements.14 For this reason, the zinc found in zinc phosphate and zinc oxide eugenol cements is highly detectable. This is
in contrast to the low atomic number elements found in acrylic
urethane cements, which are difficult to detect radiographically
unless the manufacturer purposefully adds agents containing
higher atomic numbers to increase the radiopacity.
The failure of complete seating of the crown during cementation has also been reported.9 In this situation, excess cement
is allowed to be extruded during placement. This can occur for
several reasons, including too much cement placed within the
crown, tight proximal contact, tight fit of the crown, inadequate
Figure 2A. Case Two radiograph taken January 2006 following insertion of
screw dental implants #29 and #31.
Figure 2B. Radiograph taken before prosthetics; April 2006.
Figure 2C. radiograph taken October 2011 following removal of failed implant
#31 and replacement bone graft for future implant.
Figure 2D. Hematoxylin and eosin-stained section (20x magnification) depicts
highly vascularized fibrous tissue containing several foci of black exogenous cement particles and scattered acute and chronic inflammatory cells in stroma.
45
cement space, not following cement manufacturer’s recommendations regarding working and setting time and inadequate pressure application while seating the crown. Some of these issues are
readily highlighted with a pre-cementation radiograph, allowing
for corrective adjustment and complete seating.
Comparison of a post-cementation radiograph with a precementation film can be useful for visualizing incomplete seating
of the crown and for providing a means of determining if residual
excess cement is present, given that the cement is radiopaque
enough and at a site that allows for detection.
The importance of postoperative appointments for implant
patients following cementation of the restoration cannot be overemphasized.4 A recommendation of one week, followed by onemonth, three-month and six-month postoperative appointments
following cementation of prosthesis has been proposed.4 Should
peri-implant complications suggest the possibility of residual excess cement, treatment would include conservative exploratory
surgery to confirm initial diagnosis and to evaluate the extent of
the problem; removal of the excess cement; and replacement of
the existing restoration, if indicated, to restore the health of the
surrounding tissues.4
46
Summary
This article describes two patients with failed implants secondary
to REC and the histologic findings of foreign body inflammation
and foci of exogenous cement within the tissues surrounding the
failed dental implants. By understanding the issues, the clinician
may be able to more readily diagnose problems early and gain
clearer understanding of an important factor when selecting a cement for implant restorations, that is, the ability to readily detect
excess cement with intraoral radiography. If detected early and
adequately removed, resolution of peri-implant disease can occur
in most cases. p
Queries about this article can be sent to Dr. Ramer at [email protected].
References
1. Hebel KS, Gajjar RC. Cement-retained versus screw-retained implant restorations: achieving optimal occlusion and esthetics in implant dentistry. J Prosthet Dent 1997; 77:28-35.
2. Wadhwani C, Pineyro A. Technique for controlling the cement for an implant crown. J
Prosthet Dent 2009;102:57-58.
3. Salvi GE, Lang NP. Diagnostic parameters for monitoring peri-implant conditions. Int J
Oral Maxillofac Implants 2004; 19 Suppl:116-27.
4. Pauletto N, Lahiffe BJ, Walton JN. Complications associated with excess cement around
crowns on osseointegrated implants: a clinical report. Int J Oral Maxillofacial Implants
1999;14:865-868.
5. Gapski R, Neugeboren N, Pomerantz AZ, Reissner MW. Endosseous implant failure influenced by crown cementation: a clinical case report. Int J Oral Maxillofac Implants
2008;23:943-946.
6. Avivi-Arber L, Zarb GA. Clinical effectiveness of implant-supported single-tooth replacement: the Toronto study. Int J Oral Maxillofac Implants 1996;11:311-321.
7. Quirynen M, DeSoete M, Van Steenberghe. Infectious risks for oral implants: a review of the
literature. Clin Oral Impl Res 2002;13:1-19.
8. Lee A, Okayasu K, Wang HL. Screw-versus cement-retained implant restorations: current
concepts. Implant Dent 2010;19;8-15.
9. Wilson TG. The positive relationship between excess cement and peri-implant disease: a
prospective clinical endoscopic study. J Periodontol 2009;80:1388-1392.
10. Wadhwani C, Rapoport D, LaRosa S, Hess T, Kretschmar S. Radiographic detection and
characteristic patterns of residual excess cement-retained implant restorations: a clinical
report. J Prosthet Dent 2012 Mar;107(3):151-7.
11. Agar JR, Cameron SM, Hughbanks JC, Parker MH. Cement removal from restorations luted
to titanium abutments with simulated subgingival margins. J Prosthet Dent 1997;78:43-7.
12. Linkevicius T, Vindasiute E, Puisys A, Peciuliene V. The influence of margin location on the
amount of undetected cement excess after delivery of cement-retained implant restorations.
Clin Oral Impl Res 2011; 000-000 (Epub ahead of print).
13. Wadhwani C, Hess T, Faber T, Pineyro A, Chen CSK. A descriptive study of the radiographic
density of implant restorative cements. J Prosthet Dent 2010;103:295-302.
14. White SC, Pharoah MJ. Oral radiology, 6th Ed: Principles and Interpretation. St. Louis:
Elsevier. 2009, p.152-3; p.14.
15. International Organization for Standardization. ISO 6876:2002. Dental root canal sealing
materials. Geneva: ISO;200. Available at: http://222.iso.ch/iso/en/prods-services/ISOstore/store.html
16. International Organization for Standardization. ISO 4049:2009. Dentistry-polymer based
restorative materials Geneva: ISO;2009. Available at http://www.iso.ch/iso/en/prods-services/ISOstore/store.html. Accessed September 16, 2009.
oral surgery
Myositis Ossificans of Infraorbital
Musculature in Uncontrolled Diabetic
Mohan Baliga, M.D.S.; Joanna Baptist, M.D.S.
A b st r a c t
Myositis ossificans traumatica is a form of dystrophic
calcification that leads to heterotopic ossification of
intramuscular connective tissue. It is rare in the orofacial region. A history of trauma, conventional radiography and computed tomography, along with histopathological examination, can be used effectively to
diagnose this condition. We present a unique case of
infected myositis ossificans traumatica in the infraorbital region in an uncontrolled diabetic.
Myositis ossificans is a non-neoplastic, heterotropic bone formation within muscle or fascia1 broadly classified into myositis
ossificans progressiva (MOP) and myositis ossificans traumatica
(MOT).2 MOT is a rare sequelae of acute trauma, burns, surgical manipulation, repeated injury or inflammation,1,2 with the
first evidence of a calcified mass appearing from between 3 weeks
to more than 20 years.3 Thighs, arms, shoulders and hands are
the commonly affected sites.4 MOT in the head and neck region
is unusual. Within the maxillofacial region, involvement of the
medial pterygoid, temporalis, masseter, buccinator, platysma and
sternocleidomastoid muscles have been reported.5,6,7,8 To the best
of our knowledge, this may be the first case of myositis ossificans
traumatica in the infraorbital region in an uncontrolled diabetic.
Case Report
A 34-year-old uncontrolled diabetic male patient was referred to
the department with a bony, hard swelling in the infraorbital region that had been present for the past year. The patient was involved in a traffic accident one and half years ago, during which
he reportedly injured the right infraorbital region. This area subsequently healed without surgical intervention. Three months after the first injury, the patient sustained a blunt trauma in the
same region, following which he noticed a swelling that gradually increased in size. Initially the swelling was asymptomatic, but
later, it became painful. Associated with the swelling was a pus
discharge, for which he underwent wound exploration. As the
swelling and discharge persisted, he was referred to our department for opinion and further management.
On physical examination, the patient was afebrile with a diffuse, tender, firm-to-hard swelling in the right infraorbital region.
The overlying skin was erythematous with a solitary draining sinus (Figure 1). There was no associated paraesthesia or epiphora.
Orbital examination was within normal limits. Foci of infection
from intraoral and paranasal sinuses were ruled out.
A paranasal sinus view revealed a diffuse radiopacity in the
right infraorbital region (Figure 2). A CT scan showed normal
paranasal sinuses and a radiodense region superficial to the right
zygomatic bone (Figure 3), suggestive of MOT.
Prior to surgical intervention, detailed hematological and
biochemical investigations showed altered levels of plasma glu-
47
Figure 1. Preoperative photograph showing swelling in right infraorbital region with solitary draining
sinus.
Figure 2. Paranasal sinus view showing diffuse radiopacity in
right infraorbital region over zygomatic bone.
cose (376mg/dl), glycosylated hemoglobin (11.1%), total cholesterol (229 mg/dl) and triglycerides (749mg/dl).
After obtaining glycemic control, an infraorbital incision was
placed along the existing scar. The pathologic mass was excised,
along with the sinus tract, and sent for histopathological examination. Primary closure was achieved after thorough debridement
of the infected area, and scar revision was done. There were no
immediate postoperative complications.
Histopathological examination revealed a moderately collagenous connective tissue stroma with a dense mixed inflammatory cell infiltrate, skeletal muscle degeneration, perineural and
perivascular inflammation with focal areas of heterotopic calcification scattered in the tissue specimen. The patient is on constant
follow-up with strict advice on lifestyle modifications. At the sixmonth follow-up, there was evidence of a residual, inconspicuous
mass.
Discussion
Myositis ossificans is categorized clinically into four variants:
myositis ossificans traumatica (MOT; associated with a history
of trauma);3,9 myositis ossificans progressiva (MOP; autosomal
dominant disease characterized by symmetric congenital malformations of the hands and feet with progressive heterotopic ossification of soft connective tissue);10 myositis ossificans associated with paraplegia (a disease process where tissue atrophy and
degeneration may promote metaplastic ossification); and pseudo
48
Figure 3. CT scan showing radiodense region superficial to right
zygomatic bone.
malignant myositis ossificans (where a history of trauma is absent).3
MOT is the most common extra-skeletal bone-forming lesion.1 Although it may occur at any age and without any sex predilection, it is generally reported in young adult males. This may
be because young males are more prone to accidents and are actively involved in contact sports.11
The clinical features include pain, tenderness, soft-to-firm
tissue swelling with decreased range of function. A history of
trauma to the region may or may not be elicited.12
Many theories have been proposed to explain the etiopathogenesis for MOT. The three most widely accepted are: implantation of osteogenic cells from active periosteum into muscle;13,14
bone formed from mesenchymal stem cells that retain their ability to differentiate along bone-forming lines; and over production
of bone morphogenic protein4 (BMP 4) in response to injury.15
Our literature review showed only one reported case of MOT
in the periorbital region. This was an intraorbital mass that presented with diplopia due to restricted movements of the involved
eye. This was attributed to the change in configuration of the orbit and change in orientation of muscle fibers.11 Our case had
no functional deficit, as the calcific mass was in the infraorbital
region superficial to the zygomatic bone and did not involve any
of the extraocular musculature.
Early lesions appear as amorphous calcification within soft
tissue on a conventional radiograph. As they mature, they appear
more well-circumscribed, with a ring of calcification around a
relatively radiolucent central portion. A longstanding lesion will
appear diffusely calcified.16 A similar appearance can be seen on a
computed tomogram. The biochemical findings are almost always
within normal limits,11 but there are some reported cases of elevated alkaline phosphatase levels due to disease progression.17
The conventional treatment for MOT is surgical excision of
the ossified mass. However, recurrences are common, especially
when the mass is removed at an early stage.18 The recurrences are
presumed to occur as a result of surgical hemorrhage and inadequate physical therapy. Nonsurgical therapy and prevention of
postsurgical recurrence have been suggested. A low dose of radiation is believed to have anti-inflammatory actions. This is thought
to inhibit mesenchymal cell differentiation in osteoblasts.19 Disodium etidronate (a bisphosphonate) is generally used for MOT to
decrease bone mineralization and is known to cause osteomalacia
in long-term use.20 Many authors recommend its use as a supplement to surgical treatment to prevent recurrence.
Intra-lesional steroid injections have had anecdotal success.21
NSAIDs like endomethacin decrease the synthesis of prostaglandins E and F and also inhibit differentiation of pre-osteoblasts.22
Warfarin interferes with Vitamin K-dependent production of osteoclastin, thereby preventing heterotopic bone formation.1 Retinoids have also been studied for prophylaxis against MOT, as they
inhibit mesenchymal differentiation into cartilage and bone.23 A
more recent treatment strategy includes bone morphogenic protein type I receptor inhibition to reduce heterotopic ossification.24
Spontaneous regression of MOT has also been reported.25
Conclusion
A detailed history and thorough clinical examination, along with
conventional radiography and computed tomography, is most
often adequate to diagnose MOT. This can be supplemented by
histopathology to confirm the diagnosis. We suggest surgery as
an option in rapidly growing, symptomatic, painful lesions, and
in cases where the surgery will not create additional functional
deficits. Alternative nonsurgical treatment modalities may be
considered alone or in combination with surgical intervention,
depending on the individual patient need. Whatever the mode of
treatment employed, periodic and long-term follow-up is absolutely essential. p
4. Yazici M, Etensel B, Gursoy MH, Aydogdu A, Aydin ME. Non-traumatic myositis ossificans
with an unusual location: case report. J Pediatr Surg 2002;37:1621-22.
5. Parkash H, Goyal M. Myositis ossificans of the medial pterygoid muscle: a cause for temporomandibular joint ankylosis. Oral Surg Oral Med Oral Pathol 1992;73:27-28.
6. Tong KA, Christiansen EL, Heisler W, Hinshaw Jr DB, Hasso AN. Myositis ossificans traumatica of the medial pterygoid muscle. J Orofacial Pain 1994; 8:223-26.
7. Kruse AL, Dannemann C, Grätz KW. Bilateral myositis ossificans of the masseter muscle
after chemoradiotherapy and critical illness neuropathy—report of a rare entity and review
of literature. Head Neck Oncol 2009 Aug 12;1:30.
8. Uematsu Y, Nishibayashi H, Fujita K, Matsumoto H, Itakura T. Myositis ossificans of
the temporal muscle as a primary scalp tumor. Case report. Neurol Med Chir (Tokyo)
2005;45(1):56-8.
9. Manzano D, Silván A, Saez J, Moreno JC. Myositis ossificans of the temporalis muscle. Case
report. Med Oral Patol Oral Cir Bucal 2007 Aug 1;12(4):E277-80.
10. Kaplan FS, Tabas JA, Zasloff MA. Fibrodysplasia ossificans progressive: a clue from the fly?
Calcif Tissue Int 1990; 47:117-25.
11. Ajike SO, Mohammed A, Adebayo ET, Ononiwu CN, Omisakin OO. Myositis ossificans
circumscripta of the supra-orbital region: a case report. Ann Afr Med 2007;6(4):203-6.
12. Jepsen MC, Graham SM. Traumatic myositis ossificans of the levator scapulae muscle. Am
J Otolaryngol 1998;19:433.
13. Takahashi K, Sato K. Myositis ossificans traumatica of the medial pterygoid muscle. J Oral
Maxillofac Surg 1999;57:451-56.
14. Cushner FD, Morwessel RM. Myositis ossificans traumatic. Orthop Rev 1992; 21:1319.
15. Marx RE. Inflammatory, Reactive, and Infectious Diseases. Marx RE, Diane Stern (eds).
Oral and Maxillofacial Pathology- A Rationale for Diagnosis and Treatment, 1st Ed. Illinois:
Quintessence. 2003, pp 32.
16. Ackerman LV. Extra-osseous localized non-neoplastic bone and cartilage formation (socalled myositis ossificans). J Bone Joint Surg Am 1958;40;279.
17. Spinazze RP, Heffez LB, Bays RA. Chronic progressive limitation of mouth opening. J Oral
Maxillofac Surg 1998;56:1178.
18. Mulherin D, Schow CE. Traumatic myositis ossificans after genioplasty. J Oral Surg 1980;
38:786.
19. Anglen JO, Moore D. Prevention of heterotopic bone formation after acetabular fracture fixation by single-dose radiation therapy: a preliminary report. J Orthop Trauma
1996;10:258.
20. Ayers DC, Evarts CM, Parkinson JR. The prevention of heterotopic ossification in high risk
patients by low-dose radiation therapy after total hip arthroplasty. J Bone Joint Surg 1986;
68A: 1423.
21. Molloy JC, Mcguirk RA. Treatment of traumatic myositis ossificans circumscripta: use of
aspiration and steroids. J Trauma 1976;16:851.
22. Randelli G, Romano CL. Prophylaxis with Indomethacin for heterotopic ossification after
chiari osteotomy of the pelvis. J Bone Joint Surg Am 1992;74:1344.
23. Vernale CA. Traumatic myositis ossificans of the masseter muscle. Oral Surg Oral Med Oral
Pathol 1968;26:8.
24. Yu PB, Deng DY, Lai CS, Hong CC, Cuny GD, Bouxsein ML, et al. BMP type I receptor
inhibition reduces heterotopic ossification. Nat Med 2008;14:1363-69.
25. Rooser B, Herrlin K, Rydholm A, et al. Pseudomalignant myositis ossificans. Clinical, radiologic and cytologic diagnosis in 5 cases. Acta Orthop Scand 1989; 60:457-60.
Queries about this article can be sent to Dr. Baptist at [email protected].
References
1. Kim DD, Lazow SK, Har- El G, Berger JR. Myositis ossificans traumatica of masticatory musculature: a case report and literature review. J Oral Maxillofac Surg
2002;60:1072-76.
2. Aoki T, Naito H, Ota Y, Shiiki K. Myositis ossificans traumatica of masticatory musculature:
review of literature and report of a case. J Oral Maxillofac Surg 2002;60:1083-88.
3. Steiner M, Gould AR, Kushner GM, Lutchka B, Flint R. Myositis ossificans traumatica of the
masseter muscle: review of the literature and report of two additional cases. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod. 1997;84(6):703-7.
49
dental malignancy
Oral Osteosarcoma
A Case Report and Analysis of Previously Reported Cases
Shiva Shirazian, D.D.S., M.Sc.; Farzaneh Agha-hosseini, D.D.S., M.Sc.
A b st r a c t
Osteosarcoma is the most common malignancy of
mesenchymal cells after hematopoietic neoplasms.
Most originate within bones, but the occurrence of
this malignancy in the jaw bones is rare. There is controversy about the characteristics of this tumor in the
literature. The aim of this paper was to collect the
previous reported data and provide a statistical analysis of them. Additionally, we have reported a case of
mandibular osteosarcoma.
Osteosarcoma (OS) is a malignant bone tumor that most frequently affects long bones.1,2 It accounts for approximately 40%
to 60%3,4 of primary malignant bone tumors. Its annual incidence is relatively rare, about 2 per 1 million people,5 or 0.07
in 100000.6 About 10% of osteosarcoma occurs in the head and
neck region,2-5 with jaws affected most frequently.2,4,5 It rarely occurs in the ethmoid and sphenoid bones.4 The prevalence in the
jaws is about 4%.7
The etiology of the tumor is unknown, but major risk factors include previous radiotherapy,2,4,8,9 Paget’s disease,2,4 fibrous
dysplasia,4,7 chronic osteomyelitis, myositis ossificans, trauma4
and Li-Fraumani syndrome.3 OS is categorized primarily as osteoblastic, chondroblastic and fibroblastic.2,7 In addition, it can
50
be classified as telangiectatic, fibrohistiocytic or juxtacortical
tumors (parosteal and periosteal), according to the histologic
appearance.10 The few case reports published during the last 50
years result in scattered, and even controversial, demographic
characteristics of OS. We have tried to find the previous case
reports and analyze their data to attain more complete information about jaw OS. In addition, we report on a case of mandibular OS.
Methods and Materials
To find all accessible data about OS, we searched Medline and
Scholar Google using the key words osteosarcoma (bone or jaw),
malignancy (head and neck or jaw or oral), and chondroblastic osteosarcoma. We searched these data bases until September
2009; no language was restricted. We found 21 oral chondroblastic osteosarcoma articles. Extracted data consist of age, sex,
involved jaw, location of lesion, chief complaint of patients, treatment plan, histological type and survival recorded and analyzed
with Mann-Whitney, chi-square and survival analysis.
Case Report
A 50-year-old man, presenting with a right mandibular extensive
swelling, was referred to the Department of Oral Medicine, Faculty of Dentistry, Tehran University of Medical Sciences. His chief
complaint was pain and limited mouth opening. The swelling had
begun two months previously and had grown rapidly. During this
time, his lesion was diagnosed as a tooth abscess and was treated
with antibiotics by his dentist.
Intraoral examination showed an approximately 3 cm diameter, painful, hard, dome-shaped buccolingual mass on the right
retromolar and molar areas of the mandible. Ulcerative mucosa
covered the lesion on the buccal side (Figure 1). There was no
paresthesia over the inferior alveolar nerve and no evidence of
lymph node involvement.
A panoramic radiograph showed a radiopaque lesion with
poorly circumscribed borders and no evidence of bone destruction (Figure 2). An incisional biopsy was performed. Microscopic
examination demonstrated a neoplastic tissue consisting of areas of osteoid and chondroid formation, surrounded by a cellular
stroma and fibroblastic bundles. The diagnosis of chondroblastic
osteosarcoma was established. The patient was referred to the Department of Oncology, where he underwent surgical resection of
the lesion.
Discussion
Mesenchymal malignant cells of OS are able to produce osteoid
or immature bone.3 OS is the most common malignant bone tumor, but its occurrence in the jaw is rare,7 and most published literature comprises a small series or case report (Table 1). Despite
some case series, there is no comprehensive information about
this disease and controversy exists about the demographic characteristics of it among authors. To achieve our goal, we searched
Medline and Scholar Google databases and found the full text of
21 articles. After data extraction of each case from all reports, we
analyzed them.
The results showed patients’ ages range from 8 to 81 years
(mean: 35.43± 15.52). The disease was more prevalent in males
than in females (59.7% vs. 40.3%). There was no significant difference between males and females with respect to age (MannWhitney: P=0.136). Although the mandible was a common location of JOS in some reports,2-4 11 others reported that the maxilla
can be involved more frequently.6,7 Our analysis showed that
OS occurred 49.6% of the time in the mandible and 45.4% in
the maxilla. In 5.0% of the cases it occurred in other areas, such
as the orbit, nasal cavity and ethmoid sinus. Males and females
showed no significant difference with regard to the location of
disease (x2=1.44; P=0.487).
The chief complaints of patients were swelling alone (60.8%),
swelling and pain (15.7%), swelling and tooth mobility (9.8%),
swelling and loss of sensation (7.8%), previous fibrous dysplasia
(3.9%), and tooth mobility and loss of sensation (2.0%). This
is consistent with other reports that concluded that the most
51
Table 1
Demographic Characteristics of Previous Case Reports
N
Author
Year
Age
Sex
Location
Chief
Complaint
Treatment
Histologic
Type
Survival (M)
1
McGuff5
2008
38
F
Max
P & Sw
C then S
Ch
2
Amaral7
2008
38
F
Max
F.D + P
palliative C
Ch
3
Fernandes3
2007
41
6M
10 F
9 Man
7 Max
Sw14/14,
L.T3/14,
P2/14
S 14,
C4
8 Ch
4Os
4
Gerressen16
2006
60
M
Max
?
S+C
Ch
5
Ogunlewe1
2006
29.4±
13.6
12 M
5F
8 Man
9 Max
Sw12/17,
P/Sw3/17,
T/ Sw1/17
S. ± postop. R
8 Ch,
6 F,
3 Os
6
Ghavami14
2006
33
F
Man
?
?
Ch
S + C ,S + R.
Experience
Cases
47
-
-
6
-
-
46
10 (1993-2003)
year Balltimore
16
Died
-
-
21 (1983-2003)
Lagos, Nigeria
17
?
-
-
Ch
18
-
-
3-9
7
De Biase15
2005
54
M
Man
P Sw+ Pa+
paroxytic P
8
Silva17
2005
32
M
Man
Sw
S+C
Ch
?
-
-
2 Ch,
8 Os
2.7-93.0
14( 1983-2001)
10
Os
?
-
9
9
Nakayama18
2005
33.6
10 M
5 Man
5 Max
-
2 preop C,
3 postop C,
5 unknown
10
Frei19
2004
?
?
Max
?
?
2004
25-67
6M
3F
5 Man
4 Max
-
S 5, S + R + C 3, S
+C1
-
38
25 (1974-1998)
Tokyo, Japan
20
11
Yamaguchi
12
Li21
2003
39.8
1.26 M
1F
57.4% Man
32.8% Max.
?
?
16.4 Ch,
55.7Os,
21.3 F
39.1%recurrence, 8.7%
metastasis to
lung
Shanghai,China
61
13
Youssef9
2003
81
F
Max.
Sw
S
Ch
?
-
-
2003
29
12 M
13 F
10 Man
15 Max
-
S 32%, S+C 36% ,
S+R4%, S+C+R12%,
C4%, R4%, C+R4%,
without information 4%
72% Ch,
28% Os
72
43
(1958-2001)
Sao Paulo, Brazil
25
-
2
14
Junior
15
Kaushik22
2002
18
M
Max & Man
Sw(F.D)
S + C and R
Ch
48
-
16
Mutafoglu
Uysal23
2001
17
M
Max
?
S + postop.R
Ch
46
-
17
Mardinger6
2001
33
9M
5F
6 Man
8 Max
Sw, Sw +
T.M, Sw +
LoS, T.M +
LoS
14 S, 5 postop.R 2
postop C,1 preop C
and postop. R
6
3
4
1
Ch,
Os,
F,
F.H
17 - 88
10 year
(1989-1998)
Israel
14
1 Ch,
9 Os,
2 F,
1
Par
6 - 180
15 years
(1981-1996)
Washington, USA
17
(13 primary
tumors, 4
recurrence )
5/13 Man
3/13 Max
5/13 others
-
3 S, ,4 preop.
C+S+ postop.C,
1 preop.C+S+
postop.C+postopR,
1S+ postop.C, 1
preop. C+S +postop.R,
1S+postop.R, 1
preop.C+ postop.
C+postop.R, 1
preop.C +S+ postop.R
1997
40.9
8M
5F
Altuwairgi13
1996
41
37
F
M
Max.
Max
Sw
T.M
Preop.C, S, R
C+S+R
Ch
Ch
48
24
-
-
20
Kawasaki24
1996
50
F
Man
P,Sw
S
Ch
15
-
-
21
Regezi10
1987
31
10 M
7F
10 Man
7 Max
Sw, P , Pa
16 S, 1 S+C
5 Ch,
3Os,5F,2
Par,1 Tel, 1
Ch.sarc
-
Michigan,USA
17
18
Oda
19
4
C:chemotherapy, Ch:chondroblastic, Ch.sarc:chondrosarcomas, F:fibroblastic, F.D:fibrous dysplasia,F.H: fibrous histocytoma-like, LoS:loss of sensation ,L.T:loosening of teeth,
Man:mandible, Max:maxilla, M:months, Os:osteoblastic, P:pain, Pa:paresthesia, Par:parosteal, Postop: postoperative, Preop: preoperative, R:radiotherapy, S:surgery,
Sw:swelling, Tel: telangiectatic, T.M: tooth mobility,? : Data were not accessible, -: not determined in the article
52
Table 2
Frequency of Different Treatment Plans in Various Sites
Treatment
Preoperative
chemotherapy
& surgery
Palliative
chemotherapy
Primary
surgery &
chemotherapy
Surgery
Surgery &
chemotherapy &
radiotherapy
Surgery &
radiotherapy
Preoperative
chemotherapy
& surgery &
radiotherapy
Chemotherapy
& surgery &
chemotherapy
Radiotherapy
Chemotherapy
& radiotherapy
Maxilla
2
66.7%
1
33.3%
10
45.5%
12
36.4%
7
70.0%
8
88.9%
2
50.0%
0
.0%
0
.0%
0
.0%
Mandibular
1
33.3%
1
33.3%
11
50.0%
19
57.6%
3
30.0%
1
11.1%
1
25.0%
4
100.0%
0
.0%
1
100.0%
Other
0
.0%
1
33.3%
1
4.5%
2
6.1%
0
.0%
0
.0%
1
25.0%
0
.0%
1
100.0%
0
.0%
Total
3
100.0%
3
33.3%
22
100.0%
33
100.0%
10
100.0%
9
100.0%
4
100.0%
4
100.0%
1
100.0%
1
100.0%
In our analysis, the range of survival was 2.7 to 180 months, with
a mean of 51.13±38.74 months. But there was no significant difference between various treatment protocols and survival rates
(P=0.49). The survival rate was similar between males and females statistically (P=0.79). Histological types were chondroblastic
(54%), osteoblastic (35%) and fibroblastic (11%), and had no significant differences in maxilla, mandible or other areas (x2=4.82;
P=0.31). Histological types were similar between males and females
statistically (x2=0.25; P=0.88). The mandible may be involved more
frequently, but the difference in survival among patients with jaw
OS of the mandible versus maxilla was not statistically significant.3
Chart 1: Frequency Percent of Different Treatment Plans of Oral OS
40
35
30
25
20
15
10
5
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em
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ot
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ra
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r
ap
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ra
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di
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er
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op
er
at
iv
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ra
Pr
e
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he
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ot
ot
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eo
pe
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er
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py
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y
er
rg
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ra
py
ra
er
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he
y
py
&
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ar
im
Pr
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al
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e
0
Su
common clinical appearance of jaw OS can be painless swelling as the first sign, in 85% to 95.5% cases.1,3,6 Frequencies of
chief complaint were similar statistically among males and females (x2=6.49; P=0.261). The chief complaint of patients had
no correlation with the involvement of sites—maxilla, mandible
or other areas (x2=10.94; P=0.54). Although there are different
treatment plans for this lesion, the most common treatment in
previous case reports was surgery alone, in 36.7% of cases (Chart
1). There was significant difference between the location of lesions and various treatment plans (x2=36.87; P=0.005).
The survival rate among patients may depend on different
factors, like age, CT pattern of osteogenesis, treatment
plan, early diagnosis and adequate surgical resection.3,7 Our finding is in agreement with Fernandes
et al., who divided their patients into younger or older
than 40 years. Despite a higher mean survival rate in
young patients than in old ones, there was no significant difference between them. Fernandes et al.3
explained that survival was increased among patients
younger than 40 years, but this was not statistically
significant.3 We found no correlation between age
and the survival rate of patients (P=0.154). But August and colleagues reported that prognosis may be
influenced by the patient's age.12
Prognostic factors include the size of tumor, the
histologic grade at the time of diagnosis and tumor
necrosis after preoperative chemotherapy. The latter is
the most reliable and statistically significant factor.13
Different treatment regimens, like chemotherapy or
radiotherapy, for OS do not change the prognosis,2,6,14
but radical surgery may provide a better prognosis.6
The expression of P53 protein is associated with high
grade and aggressive tumors, but the author could not
find any relation between the positivity of P53 and
prognosis or detect a worse survival rate in patients
with tumors positive for this protein.2 Some poor
prognostic factors are age over 60 years, non-mandibular location, tumor size >6 cm and positive resection
margins.15
53
In our investigation, the survival rate had no correlation with location of lesion (P=0.87) and histological type (x2=58.69; P=0.45).
But some authors believed chondroblastic OS comprises about half
of the jaw OS and has a slightly better survival rate.2 The differential diagnosis of jaw OS includes the following: chondrosarcoma;
Ewing sarcoma; bone metastasis; fibrous dysplasia; osteomyelitis;
and, even, lesions that do not usually affect the jaw bones, such as
fibrosarcoma, liemyosarcoma or rhabdomyosarcoma.7 p
Queries about this article can be sent to Dr. Shirazian at [email protected].
Figure 1. Exophitic mass in buccal and lingual of posterior of right molar area of mandible.
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destruction.
54
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