the new york state dental journal

Volume81 Number 5 August/September 2015

30 Rheumatoid Arthritis and Periodontal Disease: An Update

Archana Venkataraman, B.D.S.; Khalid Almas, B.D.S., M.Sc., FDSRCS
It is possible that individuals manifesting both rheumatoid arthritis and periodontal
disease suffer from a unifying underlying systemic deregulation of the inflammatory
response. Data suggest that periodontal therapies, combined with routine RA treatments,
further improve RA status.

37 Epithelial and Fibrous Hyperplasia: An Oral Manifestation of

Tuberous Sclerosis Complex
Sandra U. Mbibi, D.D.S.; Stuart L. Segelnick, D.D.S., M.S.; Mea A. Weinberg, D.M.D., R.Ph, M.S.D.
Classic characteristics of tuberous sclerosis complex, an autosomal dominant disorder, are
examined through case study of 13-year-old female with past medical history of TSC.

42 Ortho-Perio Interrelationship: Treatment Challenges

Nidhi Rathore, B.D.S., M.D.S.; Asavari Desai, B.D.S., M.D.S.; Mridula Trehan, B.D.S., M.D.S.;
Cover: Interventions to prevent, minimize or Vikas Jharwal, B.D.S., M.D.S.; Lakshmi Puzhankara, B.D.S., M.D.S.; Anand Marya, B.D.S.
treat periodontitis in arthritis patients will
definitely promise a better quality of life for Certain periodontal treatment modalities need to be undertaken before commencing
these patients. orthodontic treatment. And some periodontal procedures are required after active orth-
odontic treatment. Review of precautions and clinical techniques necessary to preserve
integrity of already compromised periodontium.
2 Editorial
The future is in our hands 48 Methadone Maintenance Therapy and the Dental Patient
George Raymond, D.D.S.; William Maloney, D.D.S.
4 Attorney on Law Patients undergoing methadone maintenance therapy experience higher incidence of
It was a very good year rampant caries, xerostomia, bruxism and poor oral hygiene. A review of pharmacology,
systemic effects, drug interactions and oral manifestations and discussion of possible
8 Letters modifications to treatment and considerations in dental therapies.

10 Perspectives 52 Differential Diagnosis of Periapical Radiolucent Lesion

Predictability in treatment Matthew Malek, D.D.S.; Lina M. Cortes, D.D.S.; Asgeir Sigurdsson, D.D.S., M.S.;
Paul A. Rosenberg, D.D.S.
14 Association Activities Methodical approach to diagnosing periapical radiolucency that could not be diagnosed
using basic clinical and radiographic findings is described. Case report and review of
61 General News literature.

66 Component News 57 Plasma Cell Gingivitis: An Occasional Case Report

M.B. Mishra, M.D.S.; Swati Sharma, M.D.S.; Alok Sharma, M.D.S.
77 Read, Learn, Earn Case report emphasizes need for comprehensive history taking, careful clinical examina-
tion and appropriate diagnostic tests to arrive at definitive diagnosis and treatment plan
80 Classifieds for gingival conditions that are refractory to conventional therapy and to exclude certain
malignancies and oral manifestations of systemic diseases.
83 Index to Advertisers

88 Addendum

The New York State Dental Journal is a peer reviewed

publication. Opinions expressed by the authors of material
included in The New York State Dental Journal do not
necessarily represent the policies of the New York State
Dental Association or The New York State Dental Journal.
EZ-Flip version of The NYSDJ is available at www. Use your smartphone to scan this QR Code and access the current online version
nysdental.org and can be downloaded to mobile devices. of The New York State Dental Journal.
editorial
Dentistrys Demise is not Inevitable
The will to change and a lot of creative thinking are key to the professions survival.
A n opinion piece by Marko Vujicic, Ph.D.,
chief economist and vice president of the ADA
Health Policy Institute, that appeared in June in the
Journal of the American Dental Association
(Where Have all the Dental Care Visits Gone)
got me thinking. In his article, Dr. Vujicic discussed
the current state of dentistry in the United States
and speculated on where these trends may lead in
the future. The picture he paints is gloomy. It seems
dentistry never really recovered from the Great
Recession the way other segments of the economy
did. However, the downturn in dentistry began
early in this century, when the number of adult
visits to the dentist began to decline. They have
since leveled off. But dental schools are graduating
more and more new dentists, while older dentists
are not retiring at the rate they once did. This is
leading to a glut of dentists with more time on their
hands and more holes in their schedules.
Since the passing of the Affordable Care Act,
the number of children seeking care has grown
exponentially. But most of these patients are not
being seen in traditional settings. Rather, they are
being treated in federally qualified health centers
(FQHCs). This is most likely due to the increased
number of children covered under Medicaid.
Adults, meanwhile, are visiting hospital emer-
gency rooms in greater numbers to obtain relief
from acute dental problems, with no thought given
2 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
to the need for ongoing dental care or to the long-
term consequences of poor dental care. The cost of
dental care is a factor as well, with more adults,
especially those in the middle and higher income
ranges, using their discretionary income for vaca-
tions, consumer electronics and the like. And, while
the ACA mandated dental coverage for children,
there is no such mandate for adult dental coverage.
Even in states where there is Medicaid coverage for
adults, reimbursement rates are so low, most den-
tists do not see Medicaid patients.
Dr. Vujicic pointed out that these and other
factors may be contributing to the downward
trend in adult dental visits. The fact that Congress
did not make adult dental care part of the ACA
leads to the belief that dentistry is not an essential
service of health care. Likewise, people do not
place significant value on dental care, which
places further downward pressure on the econom-
ics of dentistry. And, finally, expansion in dental
services appears to be focused on three groups of
patients: children, senior citizens and those receiv-
ing Medicaid. The traditional middle-aged adult
no longer sees the benefit of dental care over the
long run.
Dr. Vujicic ended his piece with a series of
challenging and thought-provoking questions on
the future of dentistry and whether the dental pro-
fession can adapt to potential changes.
 THE NEW YORK STATE DENTAL JOURNAL

EDITOR
Kevin J. Hanley, D.D.S.

MANAGING EDITOR
Mary Grates Stoll

ADVERTISING MANAGER
Jeanne DeGuire

ART DIRECTORS
Kathryn Sikule / Ed Stevens

EDITORIAL REVIEW BOARD

Frank C. Barnashuk, D.D.S.
David A. Behrman, D.M.D.
Michael R. Breault, D.D.S.
Ralph H. Epstein, D.D.S.
Daniel H. Flanders, D.D.S.
Joel M. Friedman, D.D.S.
Chester J. Gary, D.D.S., J.D.
G. Kirk Gleason, D.D.S.
John T. Grbic, D.M.D., M.S., MMSc.
Dentistry must educate the public and the medical community as to the impor- Brian T. Kennedy, D.D.S.

tance of good dental health to the overall well-being of the individual. We have the
science to demonstrate this link; we have to do a better job of conveying it to the
public at large.
Cost is a large impediment to adults seeking care. We need to ask ourselves if
there are ways to reduce costs so that the patient is served well and properly and
the dentist is able to maintain a good standard of living. We all know how difficult
it is to run a practice in todays economy. Can we run our practices more effi-
ciently, or are there ways to economize so that savings can be made that can be
passed on to our patients? Are reimbursement rates from insurance companies a
stumbling block to a profitable dental practice? Do traditional delivery systems
constitute the most efficient way to deliver good dental care to our patients, or are
there alternative systems that would do the job better? These are all difficult ques-
tions that need answers if dentistry is to survive as a profession.
Dentistry is at a crossroad. The road we take will dictate what dentistry will
look like in the future. We deliver the best oral health care in the world. We need
to find innovative ways to finance and deliver cost-effective care to more people
more efficiently. At the same time, we must instill in the general population the
idea that dentistry is important to their health and well-being.
Changes are coming. It is inevitable. Nothing stays the same. If you remain
stagnant, you get run over as the world moves past you. We need to embrace
change, but we also have to be the agents of that change. In that way, we will be
the ones who control the outcome, adding to the possibility of our survival. We
need to be innovative. We must think outside the box to solve the problems we
face. If not us, then who? I would not want someone who knows nothing about
dentistry deciding dentistrys future. How about you?
I didnt think so.
Stanley M. Kerpel, D.D.S.
Elliott M. Moskowitz, D.D.S., M.Sd
Francis J. Murphy, D.D.S.
Eugene A. Pantera Jr., D.D.S.
Robert M. Peskin, D.D.S.
Georgios Romanos, D.D.S.,
D.M.D., Ph.D., Prof.Dr.med.dent
Robert E. Schifferle, D.D.S., MMSc., Ph.D.
PRINTER
Fort Orange Press, Albany
NYSDJ (ISSN 0028-7571) is published six times a year,
in January, March, April, June/July, August/September
and November, by the New York State Dental Association,
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Postmaster: Please send change of address to the New
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D.D.S.

The New York State Dental Journal AUGUST/SEPTEMBER 2015 3

 PERSPECTIVES
Wisdom
Experience and conviction come into play when the dentist and patient disagree on the treatment plan.
Paul S. Apfel, D.D.S.
ABSTRACT
Restorative dentists are often faced with the challenge
of weighing best practice treatment plans against the
treatment requests of their patients. I believe we all
must ask ourselves prior to performing any dental
procedure, How do I know this restoration will be
successful, given the multitude of physiological, path-
ological and anatomical limitations that can affect
the prognosis? There is no restorative dental proce-
dure that is free of risk. The purpose of this article is
to examine an interesting and somewhat controver-
sial restorative case that illuminates perception and
judgment and the consequences of risk assessment.
As health care professionals, we are obligated to perform the best
we can every day and to improve upon what we learned yesterday.
Every great accomplishment starts with the decision to try and to
trust that little voice in our head. Its difficult to mature into ones
greatest self, but its a tragedy to let fear stop us. So understand
right now that fear is only as deep as our mind allows it to be.
Theres a saying I learned shortly after graduating from dental
school: You have to be willing to lose the patient before you can tru-
ly keep him or her. Its application to dentistry is rather straightfor-
ward. We need to recommend a treatment plan that is based upon
sound scientific principles and that has the patients best oral health
10 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
interests in mind. To prejudge and propose treatment that falls short
of the benchmark for what we believe is appropriate, necessary and
predictable because that little inner voice is forewarning patient re-
fusal is a window to the fear and anxiety pervasive in the relationship
between patient and dentist. How ironic that it is the dentist who
may become anxious anticipating that the recommended treatment
will cause the patient to say no, or worse, goodbye.
Who wants to lose a patient? Definitely not me. And if my guess
is correct, not you either! Walt Disney once said, When you believe
in a thing, believe in it all the way, implicitly and unquestionably.
Each of us has several unique beliefs regarding patient care. We each
manage the doctor-patient interpersonal relationship differently.
We also have preconceptions regarding dental procedures, restor-
ative materials, prognoses and the quality of laboratory prosthetics.
We use these principles and morals to regulate our behavior in the
operatory. And we often apply them in our daily lives outside of the
office. William Whewell (1794-1866), English scientist, philosopher
and theologian, envisioned prudence as the virtue by which we se-
lect right means for given ends, while wisdom implies the selection
of right ends as well as right means. All of us possess knowledge and
the skills to perform a multitude of procedures. Questioning which
treatment options are wise and which minimize risk, while maximiz-
ing predictability, is whats important.
As an experienced practitioner, educator and author, I share
with you now a simple restorative dental predicament that ex-
emplifies the challenges we face in our practices when a patient
refuses a treatment plan we have judged to be the most appropri-
ate and predictable given the particular clinical circumstances.
The Patient Said No
A 58-year-old female who had been a patient of my dental prac-
tice for 19 years came into the office missing an extensive DO
amalgam restoration from her mandibular right second bicuspid
(tooth #29). During her emergency visit, recurrent caries was
present, and both the lingual and buccal cusps were undermined.
The tooth was asymptomatic, according to the patient; a periapi-
cal X-ray (Dexis, LLC) revealed dental caries down to the osseous
level (Figure 1). My patient requested that I just refill it.
Clinical examination revealed that any attempt to restore
the tooth would likely result in endodontic treatment, a post/
core procedure and a crown restoration. However, because dental
caries had extended to the osseous level, crown-lengthening sur-
gery would be required. Consequently, this patient would require Figure 1. Preop emergency visit X-ray.
removal of a minimum of 3 mm to 4 mm of bone (1 mm to 2
mm for ferrule, and an additional 2 mm to allow for the dento-
gingival complex or DGC.)1 In addition, bone would need to be
removed from the mesial of the molar or a vertical defect would
be created.
To further complicate the situation, the root of this premolar
tooth had a disto-angular dilaceration. As a result, the ability to
insert a post would be compromised (far less than an insertion
to one-half the root supported by bone), thereby amplifying an
unfavorable crown-root ratio.2,3
Given these restorative compromises, my recommendation
was to extract the premolar and replace it with an implant-sup-
ported crown. We know from an abundance of available clinical
data that the success rate for a single implant in the mandible is
usually over 97 percent.4,5,6 The predictability, therefore, for this
type of restoration far exceeds the long-term predictability in this
particular situation for a root canal, compromised post/core and
crown restoration with osseous crown lengthening. My patients
response to my treatment recommendation was an adamant no
Figure 2. Nobel Biocare Replace Select dental implant with provisional abutment.
and a repeat request that I just fill it.
Again, I discussed the considerable loss of tooth structure
and the poor predictability if the tooth was restored as she de-
sired. The success rate for an implant-supported restoration also
precludes the preparation of otherwise healthy adjacent teeth for Missing the Larger Picture
a three-tooth, fixed partial denture.7 However, when offered as a Predictability is defined as the ability to declare or tell in advance;
viable alternative restoration, she refused this option as well. She to prophesy. Almost 30 years in practice has given me knowledge
appeared annoyed and said she might seek treatment elsewhere. and experience with treatment predictability. As practitioners, we
In spite of her visibly growing hostile demeanor, I maintained a know that the very best clinical restorations, once exposed to the
smile as we sat face-to-face in the operatory. I recommended we detrimental effects of a watery bacterial-inhabited oral environ-
take a short break so she could think about my suggestions, and I ment and to harmful occlusal forces, can, unfortunately, fail pre-
removed myself from the operatory. I proceeded to go straight to maturely. We also know procedures that on the surface suggest
my private office, where I sat at my desk trying to absorb the con- questionable outcomes, given the same parameters, can last for
flicting thoughts about my long-time patient leaving my practice decades.
because she didnt want to accept treatment that I believed was The presentation of the radiograph in Figure 1 has evoked
most predictable. In fact, my dental assistant pleaded with me to chatter from dentists at continuing education seminars through-
reconsider so we dont lose her. out the country, as well as a steady wave of hands from colleagues

The New York State Dental Journal AUGUST/SEPTEMBER 2015 11


Figure 3. Clinical photograph of provisional implant abutment.
Figure 4. Clinical photograph of completed implant-supported ceramo-metal crown.
ready to debate my position and restorative philosophy. Doctors
in attendance have affirmed that their patients will not pay for
implants. Theyve suggested that they can start the root canal and
bill the insurance company right away. And they have questioned
even, Where is it written that a crown has to last 5 to 10 years
or, perhaps, even longer?
The apparent need for immediacy in operatory production
often interferes with the development of sound and predictable
treatment plans. This seems to be a pervasive topic of discussion
when it comes to offering a patient an implant-supported resto-
ration requiring a dental team approach. Doctors have told me
repeatedly that they need to be productive. Consequently, they
12 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
prefer to commence treatment now, if possible, as opposed to
after the patient consults with a specialist. They subscribe to the
old proverb a bird in the hand is worth more than two in the
bush and often dont see the larger picture.
This start it now philosophy too often seems to be an over-
whelming, driving force, especially in times of economic adver-
sity. Life is about choices, and nothing can be more rewarding
than to offer our patients treatment options that are predictable
and evidence-based. The restorative dentist is responsible for co-
ordinating development of these predictable treatment plans. Di-
agnostic casts and record bases can be obtained, in addition to
laboratory wax-ups, stents, and implant radiographic and surgical
guides, all of which are prerequisites to predictable dental implant
placement. I cant think of a better immediate scenario.
I returned to my patient in the operatory and, in spite of my
rationale for my treatment recommendations, she again refused.
She said she was very upset and left my office. I couldnt help
thinking of what I had learned early in my career: You have to
be willing to lose a patient before you can truly keep them. I
repeated to myself that I was offering the most appropriate and
predictable restorative treatment for my patient. No patient is
ever happy when he or she returns with a failed restoration and is
told he or she has to spend more money and more time to fix it
again. Failures create tension in the doctor-patient relationship.
Predictability Wins Out
Every decision we make has consequences and costs. Yielding to
the temptation to comply and treat according to the demands of
our patients when we believe it is not a best practice, may result
in premature failure with significant professional, financial and
emotional consequences. Theres the financial cost to the patient
and doctor, as well as the emotional cost to both if the restoration
fails. In addition, there is the possibility of a lawsuit. The bond of
implied trust is damaged, often irreversibly.
Several weeks passed and my patient returned for another
consultation. She appeared calm and asked me to explain the im-
plant procedure. After our discussion, she finally agreed to have
an implant-supported crown. Ultimately, her bicuspid was ex-
tracted and a dental implant was placed (Figures 2,3,4).
While there often are multiple treatment options, there
exists only one diagnosis. We must consider the needs and
wants of the patient and balance those against sound clinical
data while considering restorative options in terms of their pre-
dictability. To know how to do a dental procedure well is often
not enough. Questioning whether it is a wise procedure and in
the best interest of the patient is equally as important. Theres
a famous quote by legendary coach John Wooden: If you dont
take the time to do it right the first time, when will you find the
time to do it over?
I was delighted when my patient returned and accepted the pro-
cedure, which both the periodontist and I believed was most
predictable. But I can never forget that feeling of loss when she
walked out of my office previously.
Wisdom has been defined as the use of the best means for
attaining the best ends. It implies the union of high mental and
moral excellence. Knowledge and wisdom, far from being one,
often times have no connection. Knowledge dwells in heads re-
plete with thoughts of other men; wisdom, in minds attentive to
their own, said Whewell.
In conclusion, another well-known quote comes to mind.
Never let your fear steer your present or decide your future.
And, remember, courage is not the absence of fear, but rather the
judgment that something else is far more important. p
Queries about this article can be sent to Dr. Apfel at papfel@aol.com.
REFERENCES
1. Daniela ED, Kalizia MO,Clarissa RF, et al. Surgical crown lengthening: a 12-month study-
radiographic results. J Applied Oral Sci 2007; Aug; 15(4): 280284.
2. Heydecke G, Peters MC, The restoration of endodontically treated, single-rooted teeth with
cast or direct post and cores: a systematic review. J Prosthet Dent 2002 Apr;87(4):380-386.
The New York State Dental Journal AUGUST/SEPTEMBER 2015
3. Slutzky-Goldberg I, Slutzky H, Gorfil C, Smidt A. Restoration of endodontically treated
teeth: review and treatment recommendations. Int Journal of Dentistry 2009; 150251 doi:
10.1155/2009/150251. Epub 2010 Jan 26.
4. Jung RE, Zembic A, Pjetursson BE, et al. Systematic review of the survival rate and incidence
of biological, technical, and aesthetic complications of single crowns on implants. Clin Oral
Implants Res 2012;23 (suppl 6):2-21.
5. Lang NP, Pun L, Lau KY, et al. A systematic review of survival and success rates of implants
placed immediately into fresh extraction sockets after at least 1 year. Clin Oral Implants Res
2012;23 (suppl 5);39-66.
6. Onur G, Hakan B, Esma G, Altug C, Emre M, Canan B. Evaluation of possible prognos-
tic factors for the success, survival, and failure of dental implants. Implant Dentistry
2014;23:44-50.
7. Sadan A, Salinas TJ, Block MS. Fixed partial denture or single-tooth implant restoration?
Statistical considerations for sequencing and treatment. J Oral Maxillofac Surg 2004; Sept
(62) 9 Suppl 2: 2-16.
Paul S. Apfel, D.D.S., is co-director of the dental implant postgraduate
fellowship program and chief of prosthetics, Department of Dental Medicine,
North Shore University Hospital, Manhasset, NY. He is in private practice in
Huntington, NY.
13
 Workshop participants mull over possible solutions to eradicating early childhood caries.

Workshop Focuses on Improving

Childrens Dental Health
Pediatric and dental health professionals meet in Albany to develop strategies for doing away with early childhood caries.

C
G. Kirk Gleason, D.D.S.

oncerns about the well-being of children brought close
to 40 professionals to Albany in June to participate in a two-day
workshop devoted to the Current State of Childrens Dental
Health. The workshop was sponsored by the New York State
Dental Foundation. Moderator was Meg Atwood, R.D.H., M.P.S.,
associate professor in the Department of Dental Hygiene at Or-
ange County Community College.
Among those gathered for the event in the Legislative Office
Building were dentists, registered dental hygienists, educators and
public health workers, with representatives from six of the best
practices throughout New York State. Their objective was to learn
about and develop strategies for treating, reducing and eradicat-
ing early childhood caries (ECC). They were motivated by the
awful knowledge that ECC can result in pain, increased risk of
future caries, missed school days, visits to the ER and inpatient
hospitalizations.
Kara Williams, M.P.H., from the Health Foundation for
Western and Central New York (HFWCNY) described an initia-
tive named CHOMPERS! The program was developed to pro-
vide dental care to more preschool-aged children through edu-
cation, treatment and prevention. So far, it has brought portable
dental care to seven sites throughout Central and Western New
York. Through education, it has successfully helped families
change their behavior and has heightened their caries preven-
tion knowledge.
Bridget Walsh, M.P.H., from the Schuyler Center for Analysis
and Advocacy (SCAA) discussed Keep NY Smiling, a project that
has brought together SCAA, the Childrens Dental Health Project,
the Centers for Disease Control, the New York State Department
of Health and HFWCNY to reduce ECC through the adoption of
evidence-based prevention strategies tailored to individual com-
munities. As such it takes into account local leadership, dental
health statistics and existing programs. Once a strategy is chosen,
it is incorporated into the infrastructure of an existing program,
thereby reducing costs and initial set-up time.
Melinda Clark, M.D., FAAP, from Albany Medical Center
and Albany Medical College explained how the separation of
medicine and dentistry is having a detrimental effect on oral

26 AUGUST/SEPTEMBER 2015 The New York State Dental Journal

health. She referred to oral health issues as a silent epidemic
and the most common unmet health need. Noting that oral
health issues are largely preventable, Dr. Clark called on primary
care physicians to screen and assess ECC risk in the children
they see, often 13 times in the first 36 months of life. Primary
care physicians can be an excellent resource for ECC prevention,
she said, when another dental home is unavailable. In addition
to screening and risk assessment, pediatricians are now required
to apply fluoride varnish on patients ages 5 and younger two to
four times a year. This ensures that every child receives the ECC
prevention benefits of fluoride varnish, regardless of whether he
or she visits a dentist.
Dara Rosenberg, D.D.S., M.S., M.P.H., of St. Barnabas Hospi-
tal Health System in the Bronx described her participation in the
DentaQuest ECC Collaborative, a national initiative designed to
foster the spread of an alternative disease management model of
ECC care that is focused on prevention and minimally invasive
treatment rather than on restorative and surgical treatment. By
participating in the collaborative and focusing on high-risk pa-
tients under 5 years of age, by providing families with self-man-
agement goals and increasing patient return rates, St. Barnabas
was able to reduce ECC rates. Moving forward, Dr. Rosenberg has
joined the NYS ECC Learning Collaborative as expert faculty to
test these methods in more facilities in the state.
Christie Custodio-Lumsden, Ph.D., M.S., R.D., C.D.N.,
from Columbia University College of Dental Medicine dis-
cussed the MySmileBuddy iPad-based family intervention devel-
oped by a multidisciplinary team of Columbia-affiliated faculty.
MySmileBuddy relies upon lay health workers using the interac-
tion between these workers and families to achieve the follow-
ing: engage, educate and train families; assess ECC risk; indi-
vidualize risk and provide analysis for it; set family specific goals;
individualize action plans with family input; and offer continu-
ous support and encouragement to families. So far, this family-
to-family approach has been successful at reducing ECC rates.
Its success is more remarkable considering that technology is
ever changing, lay health workers have a high turnover rate, the
population is difficult to reach because of cultural and language
barriers and, as with most groups, the population MySmileBud-
dy serves has many misconceptions about oral health, ECC and
the importance of preventive care.
The final best practice presentation came from Tony Men-
dicino, D.D.S., and Carly Sisson from Finger Lakes Commu-
nity Health. Finger Lakes has created a TeleHealth network, a
component of which is TeleDentistry. As part of TeleDentistry,
when Dr. Mendicino comes across a patient whose dental care
needs are beyond what his clinic has resources for, Dr. Men-
dicino videoconferences an initial patient visit with a pediat-
The New York State Dental Journal AUGUST/SEPTEMBER 2015
ric dentist at Eastman Dental Clinic in Rochester. During the
real-time videoconference, X-rays and photographs are shared
with the dentist at Eastman. This process allows the patient
and dentist to become acquainted without the patient need-
ing to travel to Rochester. Using this approach has reduced
the no-show rates for patient appointments at Eastman. The
TeleDentistry program has successfully expanded access to care
where dentists are few to none and has connected patients to
a source of care.
During day two of the workshop, participants were asked
which best practice, best practices or components of multiple best
practices could be adopted in communities throughout the state
where there may be limited access to care, cultural differences be-
tween patients and dentists, lower socioeconomic status, lack of
preventative knowledge and providers that do not accept children
or certain insurance coverage.
Dental health education emerged as a common initiative
no matter the community situation. With the help of health
professionals, parent groups and trusted community figures
especially when cultural barriers are presentdefining oral
health, stressing the importance of children 5 years and younger
visiting the dentist, and reframing dental decay as a preventable
disease using methods that engage the parents, rather than rep-
rimand or lecture them, would begin to change the focus away
from treatment and towards prevention.
Additionally, participants suggested utilizing available re-
sources whenever possible. By training pediatricians on the ben-
efits of fluoride varnish and how to apply it and by teaching lay
health workers and school nurses how to incorporate dental
health concerns into their communications with families, com-
munities without dental health providers would still have access
to preventive measures and the educational resources they would
ordinarily receive only at a dental home.
Participants agreed a broader reaching TeleDental program
would be an excellent resource for reducing ECC, but they cited
start-up costs as the largest barrier to adopting this program in
communities throughout the state. A mobile dental unit would
be a more practical approach, but the services it can offer tend to
be more limited.
For more information on the workshop or to join an advisory
committee on childrens dental health needs, please contact Mer-
cedes Susi at msusi@nysdental.org. p
Dr. Gleason is chair of the New York State Dental Foundation Board
of Trustees.
27
 disease management
Rheumatoid Arthritis and Periodontal Disease
An Update
Archana Venkataraman, B.D.S.; Khalid Almas, B.D.S., M.Sc., FDSRCS
ABSTRACT
A review of the epidemiological, pathological and
immunological relationships between two chronic
inflammatory diseases: rheumatoid arthritis (RA)
and periodontal disease (PD). RA is a chronic inflam-
matory disease of the joints, characterized by loss
of connective tissue and mineralized structures, the
so-called synovial membrane. Periodontitis is the
inflammatory destruction of the periodontal attach-
ment and alveolar bone.
While the etiology of these two diseases may differ,
the underlying pathogenic mechanisms are similar.
And it is possible that individuals manifesting both PD
and RA may suffer from a unifying underlying system-
ic deregulation of the inflammatory response. There is
an overproduction of a variety of cytokines and MMPs
that appears to be common in both diseases. Oral
health parameters should be more closely monitored
in patients with RA, an autoimmune disease. Data sug-
gest that periodontal therapies combined with routine
RA treatments further improve RA status. Interven-
tions to prevent, minimize or treat periodontitis in ar-
thritis patients will definitely promise a better quality
of life for these patients.
30 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
Rheumatoid arthritis (RA) is a chronic inflammatory disease of
the joints characterized by loss of connective tissue and mineral-
ized structures, the so-called synovial membrane.1 It affects ap-
proximately 1% of the total world population.2 It affects women
about three-times more often than men. Prevalence varies from
0.2% to 1.0% in various European, North American, Asian and
Australian populations.3 The prevalence of periodontal disease
has increased two-fold among patients with rheumatoid arthritis
compared to the general population.4 It affects all races, but is
more common in Pima Indians5 and in the Chippewa Indians.6
Synovial and adjacent soft tissue inflammation may be initi-
ated by a number of microbial factors, including bacterial DNA,
heat shock proteins and lipopolysaccharides.7 MMPs, cathep-
sins and osteoclast activation contribute to bone resorption.8,9 A
number of cytokines, like TNF-a, IL-1 and macrophage colony-
stimulating factor (MCSF), are also involved.10 Epigenetic changes
through the regulation pro-inflammatory response through
NF k B regulation affecting TNF alpha may be crucially involved
in the pathology of RA and other chronic inflammatory diseases.
Chronic periodontitis and RA appear to share many common
pathological features. Oxygen metabolism has an important role
in the pathogenesis of both CP and RA. However, the presence of
RA seems not to affect local and systemic Oxidative Stress Index
values in patients with chronic periodontitis.11
RA can affect any joint, but it is usually found in metacarpo-
phalangeal, proximal interphalangeal and metatarsophalangeal
joints, as well as in the wrists and knee. The clinical presentation
of RA varies, but insidious onset of pain with symmetric swelling
of small joints is the most frequent finding. RA onset is acute or
subacute in about 25% of patients, but its patterns of presen-
tation also include palindromic onset, monoarticular presenta-
tion, extra-articular synovitis, polymyalgic-like onset and general
symptoms. Morning stiffness duration is related to disease ac-
tivity.12 Synovitis, destruction of cartilage and bone tissue of the
joints, ultimately leads to physical impairment and disabilities.13
Periodontitis
Periodontitis is characterized by the inflammatory destruction of
the periodontal attachment and alveolar bone. Its clinical appear-
ance can be influenced by congenital, as well as acquired factors.
Periodontal disease (PD) is one of the most common chronic dis-
orders of infectious origin known in humans, with a prevalence
of 10% to 60% in adults, depending upon the diagnostic crite-
ria.14 Patients affected by PD respond to bacterial dental plaque
biofilm by mobilizing their defensive cells and releasing cytokines
like interleukin-1, tumor necrosis factor-a, and interleukin-6,
which lead to tissue destruction by stimulating the production of
the collagenolytic enzymes: matrix metalloproteinase.15
According to the NHANES 1999 to 2004 data, older adults,
black and Hispanic adults, current smokers, and those with lower
incomes and less education are more likely to have periodontal
disease. It is estimated that 48.2%, or approximately half the
United States adults aged 30 years, had periodontitis in the pe-
riod 1988 to 1994, and that the prevalence of periodontitis was
underestimated by the NHANES III (1988-1994) Survey.16
Diagnosis of RA
RA is an autoimmune condition diagnosed as chronic inflamma-
tory polyarthritis when five or more joints are affected.3 Diagnosis
is based upon clinical history, physical examination, blood count
(ESR, C-reactive protein) and immunoglobulin rheumatoid fac-
tor (RF). Imaging methods are used to assess various joints. RA
manifests typically with the signs of inflammation, with the af-
fected joints being swollen, warm, painful and stiff. This inflam-
mation leads to tendon tethering, erosion and destruction of
joint surfaces.17
Chronic, plaque-associated inflammation of the periodon-
tium is among the most common oral diseases and has a preva-
lence of 80% to 90%,18 resulting in soft and hard periodontal
tissue destruction and, ultimately, tooth loss.19 Both the amount
and virulence of the microorganisms and the resistance factors
of the host (risk factors and immune status) are crucial for the
initiation and progression of the periodontal destruction.20
To arrive at a periodontal diagnosis, the dentist must rely
upon such factors as: 1. presence or absence of clinical signs of
inflammation (e.g., bleeding upon probing); 2. probing depths;
3. extent and pattern of loss of clinical attachment and bone; 4.
patients medical and dental histories; and 5. presence or absence
of miscellaneous signs and symptoms, including pain, ulceration,
and amount of observable plaque and calculus.
The New York State Dental Journal AUGUST/SEPTEMBER 2015
It has also been known for some years now that patients with PD
not only suffer from local loss of connective and hard tissue, but
also have an increased risk of developing systemic diseases.21 This
interrelation is referred to as periodontal medicine. Risk factors
common to both diseases are listed in Table 1. Periodontal disease
is significantly higher in non-smoking, treatment-naive rheuma-
toid arthritis patients.22
Plausible Link between RA and PD
Both are chronic inflammatory reactions in an immunogeneti-
cally susceptible host.23
Link via citrullination of proteins: Citrullination, also termed
deamination, is a modification of arginine side chains catalyzed by
peptidylarginine deaminase (PAD) enzymes. This post-translational
modification has the potential to alter the structure, antigenicity
and function of proteins.
In RA, antibodies to cyclic citrullinated peptides are used in
clinical diagnosis. The citrullinated antigens are fibrinogen, vi-
mentin, collagen Type II and alpha-enolase, all of which are ex-
pressed in the joint.24 P. gingivalis produces a microbial enzyme,
equivalent to the human PAD enzyme. It has been thought to
represent a susceptibility factor for RA. The antigens generated
by this enzyme lead the production of rheumatoid factor and
local inflammation of both the gingivae and synovium.25 PAD
leads to the citrullination of putative RA autoantigen, which in
association with major histocompatibility complex molecules and
antigen-presenting cells, leads to the production of anti-cyclic
citrullinated peptide antibodies (anti-CCP antibody).26 Periodon-
tal diseases in RA patients are associated with high titres of anti-
citrullinated protein antibodies (ACPAs).22
Detection of Bacterial DNA in the Synovial Fluid of RA Patients
It has been reported that P. gingivalis, Tannerella forsythia, and
P. intermedia have been identified in synovial fluid samples from
RA and psoriatic arthritis patients using the checkerboard DNA
DNA-hybridization.27 A recent cross-sectional study involving
19 subjects with periodontitis and refractory RA has shown that
TABLE 1
Common Risk Factors for Rheumatoid Arthritis and
Periodontal Diseases
Individual Age
Risk Factor Gender
Body mass
Genetic factors (ILb, polymorphism and HLA gene association)
Systemic diseases
Exogenic Nutritive factors
Risk Factors Socioeconomic status
Psychological factors like stress
Lifestyle: Cigarette smoking and Alcohol consumption
31
P. intermedia (89.4%), P. gingivalis (57.8%) and P. nigrescens
(21.0%) were frequently detected with PCR.25 These two stud-
ies clearly demonstrate that chromosomal DNA from bacteria
associated with PD is present in serum and synovial fluid from
patients with RA.
P. gingivalis and rheumatoid arthritis
P. gingivalis is the main organism associated with chronic PD. It is a
gram-negative anaerobic bacteria, the fimbriae of which allow bind-
ing of the bacterial cell to host proteins.28 P. gingivalis is the sole
microorganism documented to express peptidylarginine deaminase
(PAD), which allows individuals with periodontitis to be exposed to
citrullinated antigens, predisposing them to development of anti-
cyclic citrullinated peptide (CCP) antibodies.25 Thus, oral bacterial
infection (P. gingivalis) may play a role in citrullination and be in-
volved in loss of self-tolerance and development of RA.29
The IgG and IgA antibody levels against P. gingivalis, together
with other periodontopathic organisms, such as P. intermedia, P.
nigrescens and T. forsythia, were higher in serum and synovial fluid
from RA patients when compared with controls. The presence of
these antibodies could be important in the etiopathogenesis of RA
and could represent a potential connection between periodontal
and joint diseases.30,31 Heat shock proteins (HSP 60) from P. gingi-
valis can trigger molecule-linking infectious periodontitis and au-
toimmune atherosclerosis.32,33 Data suggest that HSPs are signifi-
cant factors also in RA and are related to citrullination.34,35
Role of IL-17
IL-17, a proinflammatory cytokine contributes to bone destruc-
tion in RA but, at the same time, is essential in the host innate
immune defense against pathogens such as P. gingivalis.36 While
recent evidence has shown that Th17 cells are more osteoclas-
togenic than other T helper subsets such as Th1 or Th2, and ab-
lation of IL-17 signaling prior to the onset of infection with P.
gingivalis increases susceptibility to periodontal bone loss.37
IL-17 stimulates the generation and mobilization of neutro-
phils and plays an important role in the defense of extracellular
bacteria.38 Th17 cells and IL-17 play an important role in the patho-
genesis of RA. Th17 cells are also present in chronic periodontal
disease.39 IL-17 can be found in periodontal lesions and potentially
plays a role in the etiopathogenesis of periodontal disease. The P.
gingivalis antigen stimulates the T cells to express IL-17.39
IL-1
Cytokines are the main mediators of the immune response, in-
flammation and tissue destruction in both diseases. Elevated
serum levels of TNF alpha released in response to lipopolysac-
charide and other bacterial products induce the production of
CRP (C reactive protein), and IL-1.IL-1 facilitates the migration
of polymorphnuclear cells into the synovial tissue.
32 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
A high level of IL-1 causes increased production of nitric oxide
killing of chondrocytes. IL-1 also regulates NFKB-osteoprotegrin-
RANKL and induces osteoclast activation. These inflammatory
processes result in osteolysis in both RA and PD.17 There are in-
creased levels of IL-1 in synovial tissue macrophages and gingival
crevicular fluid in patients with RA and PD.40 Studies in animal
models have shown high levels of tissue MMPs, tumor necrosis
factor-a and IL-1 in both diseases, indicating a similar pattern
of tissue destruction.41
Role of Genetics and Epigenetics
It has also been reported that human leukocyte antigen (HLA)
genes are directly associated with RA and PD. These are powerful
risk factors for both diseases, further suggesting a close connec-
tion. The main HLA marker for both diseases is the highly poly-
morphic HLA-DRB1 locus.42,43
Smoking
There is a clustering of RA risks associated with smoking, a pres-
ence of shared epitope alleles and the presence of ACPA.21 Smok-
ing is a risk factor for PD, possibly through the effects of nico-
tine on inflammatory cytokine profiles44 and MMP-3 activity45 or
through direct effects on P. gingivalis gene expression.
Metallomatrix Proteinases
Under a clinically healthy gingival situation, collagen decompos-
ing MMP and tissue inhibitors of MMP (TIMPs), for example,
are always to be found. In PD, TIMPs are overbalanced in favor of
the MMPs. A key enzyme for the tissue destruction in PD, MMP-
8 in its active form decomposes fibrillar collagen structures and
also is associated with alveolar bone destruction. A recent study46
showed lower MMP-8 levels in the healthy control group than in
the RA group with gingivitis, in the RA group with PD or in the
systemically healthy PD group (P < 0.05).47
In contrast, MMP-13 levels were similar in all groups (P
> 0.05). RA patients with gingivitis or PD had similar MMP-8,
MMP-13 and TIMP-1 levels as did the systemic healthy control
group (P > 0.05). This study indicates that the simultaneous ap-
pearance of RA and PD has no influence on the investigated pa-
rameters. Increased MMP-8 levels in the gingival sulcus fluid can
be found in periodontal inflammation.
Markers of Inflammation in RA and PD
The synovial fluid is rich in proinflammatory cytokines. Several
interleukins, IL-1, IL- 6, IL- 8, IL-15, IL- 17,48 as well as NF-KB
ligand (RANKL), can be associated with RA. Similar proinflam-
matory cytokines have also been associated in periodontitis.49
Mechanisms of Tissue Destruction in RA and PD
The mechanisms of alveolar bone destruction in PD and articular
surfaces in RA are similar. There is an overproduction of a variety of
cytokines and MMPs that appear to be common in both diseases.40
PD and RA both have persistent high levels of proinflammatory cy-
tokines, including IL-1 and tumor necrosis factor-alpha (TNF-a),
and low levels of cytokines that suppress the imunoinflammatory
response, such as IL-10 and transforming growth factor- (TGF-
).50 These cytokines, together with low levels of metalloproteinase
inhibitors (TIMPs) and high levels of MMPs and prostaglandin E2
(PGE2), are associated with disease activity.40
Many studies have been made to find the association between
RA and PD among humans (Table 2) and in animals (Table 3).
Management
1. Rheumatology patients should be referred to dental care for
scaling, root planing and dental surgery if needed, as peri-
odontitis is also associated with an increased risk of prema-
ture atheroma.
2. Treatment modalities may include medications, efforts to re-
duce joint stress, physical therapy and surgical intervention.
Non-steroidal anti-inflammatory agents (NSAIDs, such as
aspirin, ibuprofen, COX-2 inhibitor) corticosteroids and dis-
ease-modifying anti-rheumatic drugs (DMARDs) are com-
monly used to treat RA. In addition, injectable gold therapy
(until late 1990s), cyclosporine, diet and climate-humidity
change are considered.17
3. Anti-inflammatory treatments of periodontitis have also
been proposed. Lipoxin antagonizes P. gingivalis-induced cell
activation dependent upon leukocyte-platelet interaction
through down regulation of CD11b/CD18.55,56 Administra-
tion of omega-3 polyunsaturated fatty acids, plus low dose
aspirin, as an adjunctive treatment to regenerative periodon-
tal therapy, provides additional clinical benefits.57 Adjunctive
sub-antimicrobial dose of doxycycline in periodontal therapy
suppresses proinflammatory cytokines and regulates the in-
flammatory response to therapy.58
4. Tetracycline, non-steroidal anti-inflammatory drugs (NSAIDs)
and bisphosphonates are used in the treatment of both RA
and PD.
5. Treatment with anti-TNF alpha medication is commonly
used to control for the inflammatory process in RA. Such
therapy may also be relevant for the management of peri-
odontitis.17 Two studies57,59 that assessed the effects of anti-TNF
alpha in the treatment of RA demonstrated that anti-TNF
alpha therapy resulted in clinical benefits with regard to peri-
odontal conditions.
6. Immunization with cysteine proteases purified P. gingivalis
against periodontitis may have significance in prevention
and management of RA through humoral factors and in im-
pacting cytokine production and control of infection and in-
flammation.60
The New York State Dental Journal AUGUST/SEPTEMBER 2015
7. Data suggest that oxidative stress is profound in RA. So medi-
cation used to manage oxidant/antioxidant imbalance may
be an alternative treatment in RA.17 Administration of ome-
ga-3 fatty acid reduces the extent of swollen and tender joints
in patients with RA.61 Dietary intake of polyphenols inter-
feres with P. gingivalis, suggesting that polyphenols in diet
may be useful in the management of PD.62 Dietary factors
like micronutrients and non-nutrient dietary components
can modify epigenetic markers.63
Role of Medical/Dental Professionals
1. To maintain good oral health, RA patients are encouraged
to brush and floss regularly and to see a dental professional
twice a year.
2. Periodontist consultation is necessary to decide the course of
treatment for gingivitis. Reduction in the oral contribution
to the total inflammatory burden following the favorable
periodontal treatment outcome is highly desirable.
3. Maintaining the complete health of RA patients should be a
collaborative effort. It is important that both the dental and
medical professionals work together when treating a patient
with RA. This partnership will definitely influence the oral
and overall health of these patients.53
4. Chronic periodontitis and RA appear to share many common
pathological features. Oxygen metabolism has an important
role in the pathogenesis of both CP and RA. However, the pres-
ence of RA seems not to affect local and systemic Oxidative
Stress Index values in patients with chronic periodontitis.63
Conclusions and Clinical Implications in Health Care
There is a strong association between RA and periodontitis. Inter-
ventions to prevent, minimize or treat periodontitis in arthritis
patients will definitely promise a better future for these patients.
Periodontal disease is prevalent and often severe in patients with
RA; the prevalence of periodontitis in RA was 97.5%. The preva-
lence of mild (12.5%) to moderate (75%) periodontitis was sig-
nificantly elevated in RA patients.64
Significant evidence suggests that citrullination may link
periodontal disease with RA. Genetic factors are driving the host
responses to chronic diseases with a complex pathogenesis. The
oral systemic link cannot be ignored any longer. We have to act
on this new knowledge about the relationship between periodon-
tal diseases and systemic diseases.
In the future, more effective therapeutic approaches will in-
clude multiple, synergistic host modulation therapies combined
with treatments that target the microbial etiology. Additional
studies are needed to better understand these mechanisms and
help in maintaining the overall health of an individual.
Chronic periodontitis and RA appear to share many common
pathological features. Oral health parameters should be moni-
33
TABLE 2
Association Studies between Rheumatoid Arthritis and Periodontitis (Human Studies)

First Author Study Design Clinical Data Lab Data Findings Conclusion
& Reference and Characteristics
Ribeiro et 42 patients PPD,CAL ESR GROUP 2: More reduction on PPD Periodontal treatment with SRP
al.,200551 Group 1 (G1) -16 RF 4mm than GROUP 1 might have an effect on the ESR
Group 2 (G2)-26 Drug therapy reduction.
G1:OHI+tooth cleaning ESR was significantly reduced in G2
G2:SRP after SRP
Ortiz et RCT PD,CAL,BOP,GI,PI,RA ESR In patients receiving periodontal treat- Control of periodontal infection
al.,200952 40 pts with mod / disease activity ment, there is sig decrease in mean by SRP and oral hygiene in sub-
severe periodontitis scores(DAS-28) DAS28,ESR and serum TNF alpha jects with moderate periodontitis
20 test: SRP might contribute to reduction in
20 control: No therapy No sig decrease in patients who did signs and symptoms of RA and
20 pts: Anti-rheumatic not receive treatment reduction in serum levels of TNF
drugs alpha.
20 pts: Anti TNF alpha drug therapy: sig
Anti-rheumatic drugs improvement in CAL,BOP,PD,GI
+anti TNF alpha drug
Pischon et Association between PI, GI ,PD, CAL Subjects with RA had a sig 8.05 fold Subjects with RA have signifi-
al.,200853 RA and periodontitis increased odds of periodontitis. cantly increased attachment loss
was examined in compared to controls.
57 pts with RA and PI: Accounted for 12.4%, GI:11.1%,
52 healthy controls PI and GI combination:13.4% of
matched by age and the association between RA and
gender periodontitis.
Ziebolz et 60 RA pts. Pool samples 24pts-Gingivitis No association was found
al.,20111 Periodontal classifica- for PCR analysis 18 pts-moderate periodontitis between RF on periodontal
tion was assessed with for presence of 23pts -severe periodontitis classification and microbiologic
periodontal screening 11 periodontal parameters.
index PSR/PSI pathogens No sig influence of RF on periodon-
1: healthy tal classification and microbiological
2: gingivitis parameters.
3: moderate
periodontitis Smoking showed a sig influence on
4: severe periodontitis this classification and in the case of
E. corrodens.
Leksell et Case-control study. Plaque, calculus, Serum, RF, CRP, 68% JIA and 12% controls had pain 1.Children with JIA have more
al.,201211 Subjects between 10 PPD, CAL, and ESR, salivary when opening the mouth. 12% JIA oral ulcerations, discomfort,
and 19 years 41 juve- mucosal lesions flow rate. had intraoral ulcers. 32% JIA but plaque, BOP, and gingival
nile idiopathic arthritis dental radiographs. none in control group had increased hyperplasia.
(JIA) on DMARDS.41 Child health assess- PPD/IA+ subjects on anti-TNF-a had
control subjects. ment questionnaire lower BOP scores. Medications; 2. Children with JIA on
Stanford HAQ dis- Anti-TNF-a, DMARD, NSAIDS, and anti-TNF-a had less gingivitis.
ability index. methotrexate.

TABLE 3
Association Studies between Rheumatoid Arthritis and Periodontitis (Animal Studies)

First Author Aim Data Findings Conclusion

Collection
Trombone AP et Basis of A.a and P.g Higher severity PD in the genetically inflammation Interaction between
al., 201041 induced PD and pristane- prone acute inflammatory reactivity maximum (AIR max) Exp PD and arthritis in
induced arthritis (PIA) mice strain was associated with higher levels of TNF- mice involves a shared
interaction in mice was alpha, IL-1beta, IL-17, MMP-13, and RANKL. hyper-inflammatory
examined. genotype and func-
PD/PIA co-induction resulted in higher levels of IL-1be- tional interferences in
ta, IFN-gamma, IL-17, RANKL, and MMP-13 levels. innate and adaptive
immune responses.

Cantley et al., To develop an animal
201154 model to assess the
relationship between pre-
existing periodontitis and
experimental arthritis (EA)
in mice.
Alveolar bone and joint Mice with pre-existing periodontitis developed more Pre-existing periodon-
changes were assessed. severe arthritis. titis exacerbated
Histological and Mice with periodontitis only also showed bone loss experimental arthritis in
immunohistochemistry. within the radiocarpal joint. mouse model.
Serum levels of C-reactive Evidence of alveolar bone loss in mice with EA alone.
protein.

34 AUGUST/SEPTEMBER 2015 The New York State Dental Journal

tored more closely in patients with RA, an autoimmune disease.
Interventions to improve oral pathology may have direct and in-
direct systemic benefits. In most patients with RA, the condition
will necessitate few or no changes in routine dental care. How-
ever, considerations include the patients ability to maintain ad-
equate oral hygiene, xerostomia and its related complications, the
patients susceptibility to infections, impaired hemostasis, and
untoward drug actions and interactions.
Patients with RA may require antibiotic prophylaxis because
of joint replacement and/or immune suppression, glucocortico-
steroid replacement therapy and modifications in oral hygiene
procedures. Intra- and extraoral conditions, such as ulcerations,
gingival overgrowth, disease-associated periodontitis and tem-
poromandibular pathology, also need to be recognized. Oral
health care providers need to recognize and identify modifica-
tions of dental care based upon the medical status of patients
with RA.65
It is hoped that this review will help health care professionals
better understand the RA and PD mechanisms and improve the
quality of life of their patients. p

Authors do not have any conflict of interest in reviewing the topic. Queries
about this article can be sent to Dr. Almas at khalidalmas9@gmail.com.

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31. Ronnelid J, Lysholm J, Engstrom-Laurent A, Klareskog L, Heyman B. Local anti-type II colla-
gen antibody production in rheumatoid arthritis synovial fluid. Evidence for an HLA-DR4-
restricted IgG response. Arthritis Rheum 1994;37:10231029.
32. Choi J, Lee SY, Kim K, Choi BK. Identification of immunoreactive epitopes of the Porphy-
romonas gingivalis heat shock protein in periodontitis and atherosclerosis. J Periodontal Res
2011;46:2405.
33. Seymour GJ, Ford PJ, Cullinan MP, Leishman S, Yamazaki K. Relationship between peri-
odontal infections and systemic disease. Clin Microbiol Infect 2007;13:310.
34. Bodnr N, Szekanecz Z, Prohszka Z, Kemny-Beke A, Nmethn-Gyurcsik Z, Gulys K, et
al. Anti-mutated citrullinated vimentin (anti-MCV) and anti-65kDa heat shock protein
(anti-hsp65): new biomarkers in ankylosing spondylitis. Joint Bone Spine 2012;79:6366.
35. Wu CT, Ou LS, Yeh KW, Lee WI, Huang JL. Serum heat shock protein 60 can predict remis-
sion of flare-up in juvenile idiopathic arthritis. Clin Rheumatol 2011;30:95965.
36. Yu JJ, Ruddy MJ, Conti HR, Boonanantanasarn K, Gaffen SL. The interleukin-17 receptor
plays a gender-dependent role in host protection against Porphyromonas gingivalis-induced
periodontal bone loss. Infect and Immun 2008;76:420613
37. Yu JJ, Gaffen SL. Interleukin-17: a novel inflammatory cytokine that bridges innate and
adaptive immunity. Front Biosci 2008;13:170-7.
38. Tesmer LA, Lundy SK, Sarkar S, Fox DA. Th17 cells in human disease. Immunol Rev 2008;
223:87-113.
39. Cardoso CR, Garlet GP, Crippa GE, Rosa AL, Jnior WM, Rossi MA, Silva JS. Evidence of
the presence of T helper type 17 cells in chronic lesions of human periodontal disease. Oral
Microbiol Immunol 2009;24:1-6.
40. Bartold PM, Marshall RI, Haynes DR. Periodontitis and rheumatoid arthritis: a review. J
Periodontol 2005;76:2066-74.
41. Trombone AP, Claudino M, Colavite P, de Assis GF, Avila-Campos MJ, Silva JS, et al. Peri-
odontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype
and functional immunological interferences. Genes Immun 2010;11:47989.
42. Marotte H, Farge P, Gaudin P, Alexandre C, Mougin B, Miossec P. The association between
periodontal disease and joint destruction in rheumatoid arthritis extends the link between the
HLA-DR shared epitope and severity of bone destruction. Ann Rheum Dis 2006;65:9059.
43. Weyand CM, Goronzy JJ. Association of MHC and rheumatoid arthritis. HLA polymor-
phisms in phenotypic variants of rheumatoid arthritis. Arthritis Res 2000;2:2034.
44. de Heens GL, Kikkert R, Aarden LA, van der Velden U, Loos BG. Effects of smoking on the
ex vivo cytokine production in periodontitis. J Periodontal Res 2009;44:2834.
45. Zhang W, Song F, Windsor LJ. Cigarette smoke condensate affects the collagen-degrading
ability of human gingival fibroblasts. J Periodontal Res 2009;44:704-13.
46. Taba M Jr, Kinney J, Kim AS, Giannobile WV. Diagnostic biomarkers for oral and periodon-
tal diseases. Dent Clin North Am 2005;49:551-71.
47. Biyikoglu B, Buduneli N, Kardesler L, Aksu K, Pitkala M, Sorsa T. Gingival crevicular fluid
MMP-8 and -13 and TIMP-1 levels in patients with rheumatoid arthritis and inflammatory
periodontal disease. J Periodontol 2009;80:130714.
48. Astry B, Harberts E, Moudgil KD. A cytokine-centric view of the pathogenesis and treatment
of autoimmune arthritis. J Interferon Cytokine Res 2011;31:92740.
36 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
49. Hernndez M, Dutzan N, Garca-Sesnich J, Abusleme L, Dezerega A, Silva N, et al. Host-
pathogen interactions in progressive chronic periodontitis. J Dent Res 2011;90:116470.
50. Arend WP, Dayer JM. Cytokines and cytokine inhibitors or antagonists in rheumatoid ar-
thritis. Arthritis Rheum 1990;33:305-15.
51. Ribeiro J, Leo A, Novaes AB. Periodontal infection as a possible severity factor for rheuma-
toid arthritis. J Clin Periodontol. 2005; 32:412-6.
52. Ortiz P, Bissada NF, Palomo L, Han YW, Al-Zahrani MS, Panneerselvam A, Askari A. Peri-
odontal therapy reduces the severity of active rheumatoid arthritis in patients treated with
or without tumor necrosis factor inhibitors. J Periodontol 2009;80:535-40.
53. Pischon N, Pischon T, Krger J, Glmez E, Kleber BM, Bernimoulin JP, Landau H, Brink-
mann PG, Schlattmann P, Zernicke J, Buttgereit F, Detert J. Association among rheumatoid
arthritis, oral hygiene, and periodontitis. J Periodontal 2008;79:979-86.54. Cantley MD,
Haynes DR, Marino V, Bartold PM. Pre-existing periodontitis exacerbates experimental ar-
thritis in a mouse model. J Clin Periodontol 2011;38: 532-41.
55. Brgeson E, Lnn J, Bergstrm I, Brodin VP, Ramstrm S, Nayeri F, et al. Lipoxin A4 in-
hibits Porphyromonas gingivalis-induced aggregation and reactive oxygen species produc-
tion by modulating neutrophil-platelet interaction and CD11b expression. Infect Immun
2011;79:148997.
56. Pouliot M, Clish CB, Petasis NA, Van Dyke TE, Serhan CN. Lipoxin A(4) analogues inhibit
leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins
in periodontal disease. Biochemistry 2000;39:4761-8.
57. Elkhouli AM. The efficacy of host response modulation therapy (omega-3 plus low-dose as-
pirin) as an adjunctive treatment of chronic periodontitis (clinical and biochemical study).
J Periodontal Res 2011;46:2618.
58. Emingil G, Grkan A, Atilla G, Kantarci A. Subantimicrobial-dose doxycycline and cyto-
kine-chemokine levels in gingival crevicular fluid. J Periodontol 2011;82:4526144.
59. Al-Katma MK, Bissada NF, Bordeaux JM, Sue J, Askari AD. Control of periodontal infection
reduces the severity of active rheumatoid arthritis. J Clin Rheumatol 2007;13:1347.
60. Page RC, Lantz MS, Darveau R, Jeffcoat M, Mancl L, Houston L, et al. Immunization of
Macaca fascicularis against experimental periodontitis using a vaccine containing cysteine
proteases purified from Porphyromonas gingivalis. Oral Microbiol Immunol 2007;22:1628.
61. Bahadori B, Uitz E, Thonhofer R, Trummer M, Pestemer-Lach I, McCarty M, et al. Omega-3
Fatty acids infusions as adjuvant therapy in rheumatoid arthritis. J Parenter Enteral Nutr
2010; 34:1515.
62. Bonifait L, Grenier D. Cranberry polyphenols: potential benefits for dental caries and peri-
odontal disease. J Can Dent Assoc 2010;76:a130.
63. McKay JA, Mathers JC. Diet induced epigenetic changes and their implications for health.
Acta Physiol (Oxf) 2011;202:10318.
64. Esen C, Alkan BA, Krnap M, Akgl O, Iskoglu S, Erel O. The effects of chronic periodontitis
and rheumatoid arthritis on serum and gingival crevicular fluid total antioxidant/oxidant
status and oxidative stress index. J Periodontol 2012; 83:773-91-15.
65. Treister N, Glick M. Rheumatoid arthritis: a review and suggested dental care consider-
ations. J Am Dent Asso. 1999;130:689-98.
Dr. Venkataraman Dr. Almas
Archana Venkataraman, B.D.S., is a resident in the Division of Periodontics, Indiana University
School of Dentistry.
Khalid Almas, B.D.S., M.Sc., FDSRCS, is professor of periodontology, University of Dammam,
College of Dentistry, Dammam, Saudi Arabia. He is former clinical professor, Division of Periodontol-
ogy, and director of predoctoral periodontics and fellowship in advanced periodontics, University of
Connecticut Health Center, School of Dental Medicine, Farmington, CT.
 disease management
Epithelial and Fibrous Hyperplasia: An Oral
Manifestation of Tuberous Sclerosis Complex
A Case Study
Sandra U. Mbibi, D.D.S.; Stuart L. Segelnick, D.D.S., M.S.; Mea A. Weinberg, D.M.D., R.Ph, M.S.D.
ABSTRACT
The authors present a case study of a 13-year-old fe-
male with a past medical history of tuberous sclerosis
complex (TSC), an autosomal dominant disorder. It
usually presents with a triad of epilepsy, mental de-
ficiency and facial angiofibromas that are often dis-
tributed around the nose, cheek and chin, and are
frequently shaped like butterfly wings. In addition,
oral manifestations include gingival enlargement and
developmental enamel pitting on the facial aspect of
the anterior permanent dentition in 50% to 100% of
patients. The patients chief complaint was gingival
enlargement and gingival bleeding. The histology of
the excised gingival tissue revealed epithelial and fi-
brous hyperplasia, consistent with TSC.
Tuberous sclerosis complex (TSC), also known as Bournevilles
disease or epiloia, is an autosomal dominant disorder with a
neurological manifestation. It was first documented in 1862 by
Von Recklinghausen in a brief report and then more thoroughly
described in 1880 by Desire-Magloire Bourneville, who observed
that the disease was only suspected in patients that presented
with mental retardation and fits.1,2
In 1908, Vogt described TSC as a disorder that presents with a
triad of epilepsy, mental deficiency and facial angiofibromas that
are often distributed around the nose, cheek and chin, and are
The New York State Dental Journal AUGUST/SEPTEMBER 2015
frequently shaped like butterfly wings.2,3 With the advent of new
techniques for genetic studies, it is currently understood that TSC
is an autosomal dominant disease with high penetrance, and that
males and females have a 50% chance of passing the affected gene
to their offspring.4 It is caused by inactivating mutations of TS1
and TS2 tumor suppressor genes located on chromosomes 9q34
and 16p13.3, respectively, leading to cellular hyperproliferation
and harmatoma formation in different organs of the body, most
commonly, the kidneys, heart, eyes, gingiva, skin and brain.2,5,6
No single organ is affected in every patient diagnosed with TSC;
and there is no proof that any single clinical or radiographic sign
present in one organ is absolutely specific for TSC.6
Diagnosis is usually made by clinical, pathologic and/or radio-
graphic findings. Because of the variation in symptoms of TSC dis-
order, the diagnosis of TSC has been divided into major and minor
criteria. A patient is said to definitely have TSC if he or she presents
with two major features or one major feature and two or more minor
features.7-10 Probable TSC diagnosis is reached if a patient presents
with one major and one minor feature, while a diagnosis of pos-
sible TSC is made if the patient presents with one major feature or
two or more minor features (Table 1).7-10 However, patients should
be considered for the syndrome if they present with a history of sei-
zures and hypomelanotic lesions, as 90% of patients present with
seizures and up to 98% present with skin lesions.7,10
Oral manifestations of TSC include developmental enamel
pitting on the facial aspect of the anterior permanent dentition in
50% to 100% of patients.2,11,12 The pathogenesis of pitted enamel
hypoplasia in TSC is not understood. Previous studies suggest that
the pits extend to the dentoenamel junction. The pits appear to
37
 TABLE 1
Tuberous Sclerosis (TS) Diagnostic Criteria9
Major Features
1. Facial angiofibromas or forehead plaque.
2. Non-traumatic ungual or periungual fibroma. result from a reduction in the amount of enamel matrix formed.
3. Hypomelanotic macules (more than three).
This may be because of a primary defect in odontoblasts, or in
4. Shagreen patch (connective tissue nevus).
5. Multiple retinal nodular hamartomas. ameloblasts, or may be the result of defective interaction between
6. Cortical tuber. odontoblasts and ameloblasts.13
7. Subependymal nodule.
However, enamel pitting is not unique to TSC; it is also as-
8. Subependymal giant cell astrocytoma.
9. Cardiac rhabdomyoma, single or multiple. sociated with other abnormalities of amelogenesis, including pit-
10. Lymphangiomyomatosis. ted amelogenesisimperfecta, vitamin D-dependent rickets, epi-
11. Renal angiomyolipoma.
dermolysis-bullosa-dystrophica, pseudo-hypoparathyroidism and
Minor Features tricho-dento-osseous syndrome.1 Since enamel pits might be the
1. Multiple randomly distributed pits in dental enamel. most common oral manifestation of TSC, they may be a helpful
2. Hamartomatous rectal polyps.
3. Bone cysts. marker in the diagnosis of this disorder.13
4. Cerebral white matter migration lines. Multiple fibrous papules that present clinically as gingival en-
5. Gingival fibromas. largement are the second most common oral finding of TSC, affect-
6. Non-renal hamartoma.
7. Retinal achromic patch. ing 11% to 56% of patients. The fibrous papules are seen predomi-
8. Confetti skin lesions. nantly on the anterior gingival mucosa, although the lips, buccal
9. Multiple renal cysts. mucosa, palate and tongue may be involved.11,12 Less common oral
Definite TSC: Either two major features or one major feature with two minor features. manifestations include hemangiomas, facial asymmetry, high arched
Probable TSC: One major feature and one minor feature. palate, bifid uvula, lip/palate, delayed eruption and diastemas.11,12,14
Possible TSC: Either one major feature or two or more minor features.
Because of the varying clinical manifestations, the prevalence
and incidence of TSC differs among epidemiological studies. Inci-
dence of TSC varies from 1:10000 to 1:100000, depending upon
the study.5 A study showed that 1:8000 newborns and 1:6000
adults have the disorder.4,6 Differences in data may be explained
by diagnostic criteria and partial forms of presentation of the dis-
order.4 Both sexes are affected in a similar frequency, but women
may show more prominent signs. There are no reports showing
disproportionate involvement in a particular ethnic group.6

Figure 1. Reveals facial angiofibromas consisting of blood vessels and fibrous tissue, and
Shagreens patch on the back, Periungual fibromas (Koenens tumor) on thumb.
Figure 2. Gingival overgrowth between #23 and #24 showing low smile line.
Case Report
A 13-year-old female presented to Brookdale University Hospital
dental clinic for comprehensive dental care and gingival bleed-
ing from the areas of overgrowth. She had been an inconsistent
patient since 2004. A medical clearance from her primary care
physician, dated June 2008, described her past medical history as
tuberous sclerosis with skin lesions/seizure disorder and learn-
ing issues and two small rhabdomyomas in the left ventricle with
good heart function, and shagreens patch on her back. She is
on Keppra (levetiracetam) 250 mg two times a day and has no
known drug allergies. Extraoral exam shows facial angiofibromas;
no swelling, no lymphadenopathy and no tempro-mandibular
disorder were observed (Figure 1).
The intraoral exam showed missing permanent first molars
(#3, #14, #19, #30), which were extracted in 2006. Notes from
her clinic chart stated the first molars were extracted due to
dysmorphic and abnormal development; hypoplastic maxillary
central incisors (#8 and #9), gingival enlargement about 2 cm by
1 cm on facial gingival papilla between #23 and #24; gingival en-
largement also observed between facial papilla of #7,#8, #9 and
lingual of #6 and #7; ankylosed and over-retained primary tooth
#K, edge-to-edge incisal occlusion, and rotated #28 (Figures 2-4).

38 AUGUST/SEPTEMBER 2015 The New York State Dental Journal

Methods
On Sept. 25, 2012, the patient presented for a gingivectomy on
the maxillary anterior region; a gingivectomy was achieved previ-
ously on the mandibular anterior region. Her medical history was
reviewed. She was administered 72 mg 2% lidocaine with 0.034
mg epinephrine for local infiltration of the buccal and palatal
gingiva, from tooth #6 to #11. Using an 11- and 15-blade scalpel,
a gingivectomy was performed on the lingual and facial gingival
of teeth #6 to #11; crown lengthening was performed on tooth
#9; and an enameloplasty, to reduce bulbous enamel, on facial
cervical third of #8 and #9 (Figure 5). Tissue from the papillary
overgrowth from the palatal area between teeth #6 and #7 was Figure 3. Gingival overgrowth of facial papilla and gingival margins of #6 through #11.
sent to the laboratory for biopsy. Hemostasis was achieved with
gauze, and a Coe-pak was placed in incised areas. The patient was
advised to take ibuprofen every four to six hours when needed
for pain and to return in two weeks for postop and again at two
months (Figure 6).
The pathology report, dated 10/01/2012, of gingival tissue fix-
ated in formalin, measuring 1.5 cm x 0.7 cm x 0.3 cm, showed ker-
atotic, stratified squamous epithelium covering a core of dense and
cellular fibrous connective tissue. Numerous enlarged stellate-shaped
fibroblasts, some containing multiple nuclei, were seen in the lesional
stroma. Scattered lymphocytes and plasma cells were also seen. The
diagnosis was epithelial and fibrous hyperplasia (Figure 7).
Figure 4. Panoramic radiograph.

Discussion
TSC is an autosomal dominant neuro-cutaneous disorder char-
acterized by the development of multiple hamartomas distributed
throughout the body, skin, brain, heart, kidneys, liver and lungs.15
Two-thirds of the patients report sporadic mutations. It is usually
associated with the classic of mental retardation (in 70% of cas-
es), seizures (in 90% of cases) and angiofibromas (95% of cases).
However, this classic triad is only present in 29% of patients with
the disorder; 6% of these patients lack all three.2,16 Oral mani-
festations such as enamel pitting and fibromatous growth of the
gingiva are also seen in patients with TSC, and are considered
minor features of the disorder.7,16,17
Figure 5. Anatomical crown exposure and gingivectomy.
In the case presented here, the patient appeared with the
classic triad of history of seizure disorder, learning issues and
angiofibromas, with a butterfly-like pattern on the face;18,19 In
addition, a consultation with her primary care physician revealed
she had cardio-rhabdomyomas, facial angiofibromas and periun-
gual fibromas (Koenens tumor); these are all major features of
the disorder. Thus, her diagnosis of TSC is definite.
Her chief complaint was gingival overgrowth that bleeds
when she brushes, which affects her home care and negatively
affects her quality of life. She was not concerned about her esthet-
ics but, rather, difficulty brushing and flossing. We decided on
minimal gingival reduction and restorative treatment until she
was older. Her treatment plan included oral hygiene instructions, Figure 6. Two-month postsurgery.

The New York State Dental Journal AUGUST/SEPTEMBER 2015 39


Figure 7. Dense fibrous connective tissue is noted subjacent to surface mucosa
(hematoxylin and eosin, 10x).
mechanical debridement and periodontal re-evaluation, at which
time a gingivectomy was recommended and completed to provide
improved function, esthetics and, thus, improved quality of life.8
The differential diagnosis of these gingival lesions includes
the gingival overgrowth induced by medications such as calcium
channel blockers, phenytoin (Dilantin), or cyclosporine. The pa-
tient in this case is on Keppra (levetiracetam), which is one of the
new antiepileptic drugs that pose less of a chronic risk of gingival
enlargement.20 It is noteworthy that uniform and generalized gin-
gival enlargement, the common pattern of gingival enlargement
induced by other epileptic drugs, was not observed in this case;14
thus, Keppra was least likely the cause of the sporadic gingival
enlargements observed.
Also, in the literature, gingival enlargement due to familial
or medication causes are histologically described as showing elon-
gated, narrow rete ridges, which was also not observed histologi-
cally in this case.8
Excised tissue from a gingivectomy submitted to the lab was
diagnosed as epithelial and fibrous hyperplasia. In the literature,
histology of the enlarged gingiva of TSC has been described as
showing keratotic stratified squamous epithelium overlying dense
fibrous connective tissue, surrounded by abundant distinctive
pleomorphic stellate-shaped cells with multiple nuclei present,8,14

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40 AUGUST/SEPTEMBER 2015 The New York State Dental Journal

which we saw in this case. Thus, we can deduce that the gingival
overgrowth in this case was most likely primarily a result of the
TSC disorder. However, some literature also observes numerous
dilated capillaries histologically;8,14 but these were not observed
in this case.
The recurrence of these lesions in the gingival tissue after gingi-
vectomy and periodontal care is rare, probably because of the effec-
tiveness of the treatment.14 However, there can be possible rebound
of gingival enlargement with anti-seizure medications; thus, routine
recall and plaque control are strongly advised after gingivectomy.8,11
17. Gupta S, Bhowate R, Degwekar SS. Clinical and radiological findings related to tuberous
sclerosis complex: a case report. J Contemp Dent Pract 2008 May 1;9(4):85-91.
18. Arajo Lde J, Muniz GB, Santos E, Ladeia JP, Martelli H Jr, Bonan PR. Tuberous sclerosis
complex diagnosed from oral lesions. Sao Paulo Med J 2013; 131(5):351-5.
19. Prabhu S, Mahesh KP. Tuberous sclerosis with oral angiofibroma: case report. Br J Oral
Maxillofac Surg 2010 Apr;48(3):205-7.
20. Asconap JJ. Some common issues in the use of antiepileptic drugs. Semin Neurol 2002
Mar;22(1):27-39.

Dr. Mbibi Dr. Segelnick Dr. Weinberg

Conclusion
Signs and symptoms of TSC vary, with many cases going undiag-
nosed.15 Dentists should be aware of the oral clinical manifesta-
tions of TSC, which include enamel pits and gingival overgrowth.
The 2012 International Tuberous Sclerosis Complex Clinical Con-
sensus Conference concluded that skin and oral lesions are com-
mon in TSC and that early intervention, including genetic counsel-
ing, may help to increase the quality of life of these patients.10 p
Sandra U. Mbibi, D.D.S., was a graduate resident in the Pediatric Dental Department, Brookdale
University Medical Center, Brooklyn. NY. She is currently in the private practice of pediatric dentistry
in League City, TX.
Stuart L. Segelnick, D.D.S., M.S., is clinical associate professor, Department of Periodontology
and Implant Dentistry, New York University College of Dentistry, New York, NY, and section chief of
periodontics, Brookdale University Medical Center, Brooklyn, NY. He is a diplomate of the American
Board of Periodontology.

Mea A. Weinberg, D.M.D., R.Ph, M.S.D., is clinical professor, Department of Periodontology

The authors thank Dr. Stephanie Wetzel and Dr. Renee Reich for the histology
and Implant Dentistry, New York University College of Dentistry, New York, NY. She is a diplomate of
report and description used in preparation of this manuscript. Queries about
the American Board of Periodontology.
this article can be sent to Dr. Segelnick at EperioDr@aol.com

REFERENCES
1. Flanagan N, OConnor WJ, McCartan B, Miller S, McMenamin J, Watson R. Develop-
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2. Stalker HJ (editor), Zori R T (director). Tuberous Sclerosis. R. C. Phillips Units Newsletter
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4. Napolioni V, Curatolo P. Genetics and molecular biology of tuberous sclerosis complex.
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fibroma-like tumor of maxillofacial region associated with tuberous sclerosis. Pathol Oncol
Res 2004;10(4):237-9. Epub 2004 Dec 27.
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Chimenos-Kstner E, Rosell-Llabrs X. Tuberous sclerosis and its oral manifestations. A
clinical case. Med Oral 2004 May-Jul;9(3):216-23.
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The New York State Dental Journal AUGUST/SEPTEMBER 2015 41

 Orthodontics
Ortho-Perio Interrelationship
Treatment Challenges
Nidhi Rathore, B.D.S., M.D.S.; Asavari Desai, B.D.S., M.D.S.; Mridula Trehan, B.D.S., M.D.S.;
Vikas Jharwal, B.D.S., M.D.S.; Lakshmi Puzhankara, B.D.S., M.D.S.; Anand Marya, B.D.S.
ABSTRACT
It is an undisputed fact that sound periodontal health
is a prerequisite for successful orthodontic therapy.
Various complex dental problems necessitate a mul-
tidisciplinary approach; there cannot be a better
example than an ortho-perio interaction. Certain
periodontal treatment modalities need to be under-
taken before commencing orthodontic treatment.
And some periodontal procedures are required after
active orthodontic treatment. The aim of this article
is to familiarize clinicians in the field of both peri-
odontics and orthodontics with the precautions and
clinical techniques necessary to preserve the integrity
of already compromised periodontium.
The cornerstone to a successful orthodontic outcome in a peri-
odontally compromised patient depends upon the patients peri-
odontal health before, during and after active orthodontic treat-
ment. Periodontal disease can result in pathologic migration of
involved teeth, which clinically manifests as rotation, elongation
and spacing, or crowding of the incisors.1 These changes might
complicate long-term periodontal care by reducing the efficacy
of plaque control. They can also compromise the esthetics and
function of the dentition.2 However, if high quality periodontal
intervention is performed, and the patient is able to maintain
optimal oral hygiene to control the disease, then fixed appliance
42 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
treatment can be carried out safely and satisfactorily, even in the
presence of previous alveolar bone loss.
Thus, the primary aim before commencing orthodontic treat-
ment is to stabilize the periodontal condition.3 The aim of this article
is to review the benefits of integrating orthodontics and periodontics
in the management of periodontally compromised patients.
Treating Periodontally Compromised Patients
Before commencing orthodontic treatment, it is mandatory to
assess the status of the periodontium. Periodontal screening and
recording is highly sensitive in detecting deviations from peri-
odontal health. The Michigan O probe and the Marquis probe
serve as alternative means of detecting periodontal disease. With
proper probe angulation, depth of interproximal osseous defects
can be evaluated precisely. OPG serves as an excellent tool for
generalized screening; however, the bitewing radiograph is the
best diagnostic tool for evaluating periodontal osseous lesions, as
it allows better crestal bone evaluation. IOPA may also serve as a
viable option for interproximal bone level assessment.4
Laboratory markers can supplement these findings to predict
high risk sites in these patients. These tests for causative factors
include cultures, DNA probes, enzyme-linked immunosorbent
assay (ELISA) and benzoyl DL-arginine naptylthylamide (BANA).
Tests for susceptible hosts include polymorphonuclear leukocyte
chemotaxis, markers for inflammation, tissue damage and cell
death (collagenase, elastase, prostaglandins, etc.).5 Prostaglandin
E2 is reported to be a principal mediator of periodontal tissue de-
struction. Its high levels indicate active disease, whereas low levels
are seen in sites of remission and areas with no attachment loss.6
Initial scaling and root planing performed prior to orthodontic
treatment must be followed by an observation period of four to six
months to allow tooth movement to occur in healthy tissues and
to assess the patients motivation for oral hygiene maintainence.7
Assessment of advanced mobility is important. In clench-
ers and bruxers, extensive osseous breakdown can be prevented
if a nightguard or biteplate appliance is used during orthodontic
treatment.4
Patients who run a high risk of developing sites with addi-
tional attachment loss include those with multiple residual prob-
ing depths greater than or equal to 6 mm and bleeding on probing
at three-month re-evaluation after periodontal therapy.8
Periodontal surgical procedures should be reserved for cases
where suppuration from one or more sites is seen and bleeding on
probing occurs despite good oral hygiene, in addition to increased
pocket depth.7
Age per se is not a contraindication to orthodontic treat-
ment. The difference is that tissue response to orthodontic forces
is much slower in adults than in children and teenagers.9
Orthodontic and Periodontal Treatment
Comprehensive assessment and occlusal adjustments are man-
datory, as occlusal interferences promote dental jiggling, ag-
gravate attachment loss, bone loss10 and significantly decrease
potential re-attachment after periodontal treatment.11
Gingival grafting should be considered prior to orthodontic
treatment for areas with less than 2 mm of attached gingiva, denti-
tions with prominent roots, areas of gingival recession, root expo-
sure and when orthodontic treatment includes moving the teeth
facially.4 As these are high risk areas for future gingival recession
and bone dehiscences,2 reevaluation by a periodontist is needed.
Grafting enhances the type of tissue around the tooth and controls
inflammation during orthodontic treatment. However, when lin-
gual tooth movement is planned, the soft tissue margin migrates
coronally, thereby reducing gingival recession and dehiscence with-
out the need for a gingival augmentation procedure.12 Traditional
methods for root coverage are gingival and pedicle grafts; however,
connective tissue grafts have now become the treatment of choice,
as they are more esthetic, less traumatic and provide a greater de-
gree of root coverage than traditional methods.4
Periodontal osseous defects, like osseous craters, three-wall
defects and furcation defects, need to be treated before begin-
ning orthodontic treatment. Osseous craters should be treated
preorthodontically, as treatment increases the ability to maintain
interproximal areas during orthodontic treatment and because
they do not improve with orthodontic treatment. Shallow craters
(4 mm to 5 mm pocket) may be maintained nonsurgically.
Three-wall defects are amenable to correction with regenera-
tive periodontal therapy using bone grafts. They must be reeval-
uated after three months for assessment of sulcular depth and
The New York State Dental Journal AUGUST/SEPTEMBER 2015
amount of bone regeneration. Orthodontic therapy can be initi-
ated only if the periodontium remains stable over the next three
to six months after periodontal therapy.
Furcation defects should be treated preorthodontically by
hemisection procedures in cases where the hemisected molar
will be used as an abutment for a bridge following orthodontics.
In this case, hemisection is performed after endodontic therapy,
followed by orthodontic treatment, which involves placing the
brackets on the root fragments. Open coil spring can then be used
to separate the roots, allowing for a more favorable restoration
and eliminating the furcation problem, thus enabling the patient
to maintain the area with greater efficiency.4
Precautions during Orthodontic Treatment
During orthodontic treatment, oral hygiene instruction should
be reinforced, and professional tooth cleaning should be done
every three months.7 The biological rationale for using a three-
month periodontal maintenance schedule is based upon the ob-
servation that repopulation of subgingival pathogenic bacteria
generally takes six to eight weeks to occur after the pocket has
been cleansed thoroughly.13 Periodontal reexamination at every
6- to 12-month interval should include recording of probing
depths, bleeding on probing, suppuration, gingival recession,
and bone level assessment through radiographs, depending
upon the situation.7
Orthodontic appliances and mechanics should be kept
as simple as possible, as they have a tendency to accumulate
plaque.14 Use of steel ligatures is opted on all brackets rather than
elastomeric modules, as the latter attracts more plaque.15 Self-
ligating brackets may be a better alternative than conventional
brackets.16 Bonded molar attachments are preferred over molar
bands, as the bands present with greater gingival inflammation,
plaque accumulation and loss of attachment.6
Bone level must be used as a guide to position brackets in
patients with advanced horizontal bone loss. If the interproximal
bone is oriented in the same direction as the marginal ridge dis-
crepancy, then leveling the marginal ridge will help level the bone.
However, in case of unequal discrepancy between marginal ridge
and interproximal bone, the bone should be leveled orthodonti-
cally and any discrepancy in marginal ridge should be equilibrat-
ed to achieve the best occlusal results and improve periodontal
health. Recall visits should be planned every two to three months
during leveling to control inflammation interproximally.4
As the center of resistance of the involved teeth moves more
apically, due to significant alveolar bone loss, teeth become more
prone to tipping. There is also expression of greater moments and
a higher extrusive component of the applied force.17 Implant-
orthodontic anchorage has become a valid treatment option
in such cases to allow better control of tooth movement in all
three dimensions with no loss of anchorage.2 Lighter orthodontic
43
forces should be applied, as greater orthodontic force can further
weaken the periodontium.18
When the treatment plan includes attempting orthodontic
intrusion and formation of new attachment, scaling is suggested
at shorter intervals than normal because intrusion shifts supra-
gingival plaque to a subgingival location.19 Forces for intrusion
must be kept very low (5 gm to 15 gm/tooth).20 During orth-
odontic extrusion, gingival sulcus depth can be maintained and
periodontal pocket formation can be prevented, provided oral hy-
giene is well controlled. But as potential risk for relapse exists, the
use of fixed permanent or semi-permanent retainers is recom-
mended.21 Orthodontic therapy involving bodily tooth movement
may enhance the rate of destruction of the connective tissue at-
tachment at teeth with inflamed, infrabony pockets.22
Furcation defects require special attention in patients under-
going orthodontic treatment, as molars will usually require bands
with tubes and attachments, which may impede the patients access
to buccal furcation for home care. Reevaluation and instrumenta-
tion of furcation defects during orthodontic treatment every two
to three months is required. In cases where root proximity is exac-
erbated due to molar supraeruption, orthodontic intrusion results
in leveling of bone and opening up of embrasure space between the
44 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
molar roots, thus making home care and periodontal maintenance
easy. Orthodontic decrowding in the anterior region will improve
the embrasure forms and maintain healthy and esthetic papillae.4
Periodontal Procedures after Orthodontic Treatment
Following orthodontic treatment, the patient should remain on
a three-month periodontal maintenance program and should be
reassessed to evaluate further periodontal needs.23 A new set of
periapical radiographs are advised after six months to allow for
bone remodeling, cessation of tooth mobility and narrowing of
periodontal ligament.4
A gingival grafting procedure might be considered after orth-
odontic treatment in cases where it has to be performed for cos-
metic reasons and also for areas of borderline attached gingiva
that have become narrower during orthodontic treatment. When
the orthodontic treatment plan does not include moving the
roots apart, it is advisable to perform the hemisection after treat-
ment. The molar to be hemisected thus remains intact during
treatment, thereby simplifying the finishing and tooth movement
for the orthodontist.4 Surgical removal of the maxillary labial fre-
num is delayed until after orthodontic treatment, unless the tis-
sue prevents space closure.24
Semi-permanent or permanent retention is required, as these cas- in removing plaque due to the presence of the orthodontic
es show a marked tendency to return to their pretreatment posi- appliance.37
tion following active appliance therapy.21 Thin flexible spiral wire 2. Gingivitis and gingival enlargement is observed soon after
(FSW)25-27 and a modified A-splint28 have been recommended as placement of a fixed appliance. However, it rapidly improves
optimal long-term retainers. A modified A-splint has the advantage within 48 hours of appliance removal. Increase in probing
of being invisible after placement and home care instructions are depth during orthodontic treatment has been attributed to
simplified involving conventional floss threaders.28 A removable gingival enlargement.20
plate or spring retainer should be avoided because of the high risk 3. A generalized increase in salivary bacterial counts is seen af-
of jiggling of teeth, which can lead to attachment loss and bone ter orthodontic band placement.20 However, pathogen level
resorption. The patient should be reinstructed about oral hygiene was not found to be significantly higher after 12 months of
measures following appliance removal in order to prevent labial orthodontic treatment.38
gingival recession, which may occur as the result of overzealous 4. Uncontrolled intrusive forces may result in root resorption,
brushing, as the cleaning becomes easier after decrowding.7 pulp disorders,39 alveolar bone resorption and a concentrat-
ed stress within the apical part of the ligament.40 Intrusion,
Beneficial Effects of Orthodontic Therapy on Periodontium when attempted in poor oral hygiene conditions, may result
The benefits of orthodontic treatment for establishment of a sta- in the formation of infrabony defects and loss of connective
ble periodontal status in cases of loss of periodontal support have tissue attachment, as intrusive forces displace supragingival
been confirmed in large scale studies, regardless of the applied plaque apically.36
orthodontic technique.29 5. Gingival invaginations occur during orthodontic treatment
1. It improves oral hygiene maintenance by eliminating dental with extraction space closure. These may become sites where
crowding, which serves as a facilitating factor for periodon- dental plaque can get embedded, thus acting as a risk factor
tal disease.30 A lesser number of periodontal pathogens are for the occurrence of periodontal disorders during orthodon-
found in sites of aligned teeth.31 tic treatment.20
2. It results in vertical occlusal impact along the long axis of the
teeth, thereby allowing uniform distribution of the applied
muscle force throughout the dental arch, thus preventing
damage to the periodontium. It also improves the position-
ing of abutment teeth for fixed prostheses.30
3. Orthodontic extrusion of teeth is useful in reducing half-wall
infrabony defects,32 tooth lesions between the cementoenamel
junction and coronal third of the root, angular defects and iso-
lated periodontal pockets.33 It increases bone ridge height, as well
as quantity of attached gingiva by forcing coronal migration of
the root.33 And it helps achieve favorable crown-root ratio.30
4. The combination of orthodontic intrusion and periodontal
treatment improves compromised periodontal conditions,
provided oral hygiene is maintained and tissues are healthy.34
5. Orthodontic tooth uprighting may facilitate improvement of
gingival architecture20 and correction of bony vertical defects
in mesially tipped molars.30
6. Orthodontic treatment eliminates occlusal interferences,
which may lead to periodontal breakdown,35 and also de-
creases the effects of bruxism during orthodontic therapy.30

Possible Adverse Effects of Orthodontic Procedures

1. In the presence of plaque, orthodontic forces can cause an-
gular bony defects and attachment loss, especially with tip-
ping and intruding movements.36 Orthodontic therapy,
when performed in patients with active periodontal disease,
can accelerate attachment loss because of greater difficulty

The New York State Dental Journal AUGUST/SEPTEMBER 2015 45

6. Marginal ridges, if leveled orthodontically in cases where the
interproximal bone is flat and only the marginal ridge is at
different levels, may result in hemiseptal defects. In these
cases, ideal treatment would be equilibration of the crown to
level the marginal ridge and endodontic therapy if required,
followed by full crown restoration.4
Discussion
There have been various controversies with regard to orthodontic
techniques, brackets, archwires and periodontal treatment mo-
dalities to be used in periodontally compromised patients.
Minibrackets and low profile brackets may be preferred be-
cause of their smaller size. Complicated wire configurations in-
corporating loops may be avoided because of their higher ten-
dency to accumulate plaque.
Tipping appliances such as tipedge brackets may be pre-
ferred in cases of horizontal bone loss, as they will move the
crown quickly without apical root movement3 and, thus, prevent
formation of periodontal defects.
Heat-activated NiTi wires may be preferred over normal NITi
wires, as they exert low and intermittent forces. Chun et al. sug-
gested surface modification of orthodontic archwires with photo-
catalytic TiO2 as a way to prevent development of dental plaque
during orthodontic treatment.24
Guided tissue regeneration (GTR) techniques may be use-
ful when orthodontic treatment aims to extrude or intrude teeth
with intraosseous defects or to upright molars with mesioangular
lesions, as they result in the formation of new supracrestal and
PDL collagen fibers on the tension side and, thus, help in trans-
ferring the orthodontic force stimulus to the alveolar bone.41
Hemiseptal defects present around tipped teeth and supraerupted
teeth improve with orthodontic therapy alone involving uprighting
and intrusion, respectively, of the involved teeth without requiring any
periodontal intervention other than scaling and root planing. How-
ever, the teeth must be stabilized for at least six months on completion
of orthodontic treatment and must be reassessed later.4 With orth-
odontic molar uprighting, osseous defects are eliminated, provided the
furcation is not involved; however, it aggravates a periodontal problem
if attempted in cases with furcation involvement.42
Adjunctive periodontal procedures like mucogingival surger-
ies, crown lengthening procedures, alveolar ridge augmentation
and placement of dental implants may be undertaken to facilitate
the achievement of orthodontic treatment goals.24
In cases of impaired manual dexterity, powered toothbrushes
may be prescribed to improve the efficacy of plaque removal.
Conclusion
Orthodontic treatment is no longer a contraindication in the peri-
odontally compromised patient.43 The maintenance of healthy
periodontal tissues throughout active orthodontic treatment is
46 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
of paramount importance to ensure a healthy periodontium. A
successful orthodontic outcome can thus be achieved with an in-
tegrated ortho-perio approach. p
Queries about this article can be sent to Dr. Rathore at nidhirathore11@gmail.com.
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dontics: Current Principles and Techniques, 2nd ed. St Louis: Mosby. 1994; p. 542-626.
15. Forsberg CM, Brattstrom V, Malmberg E, et al. Ligature wires and elastomeric rings: two
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tans and Lactobacilli. Eur J Orthod 1991;17:416-420.
16. Alves de Souza R, Borges de Arau, Jo Maganani MB, Nouer DF, Oliveira da Silva, Klein MI, Sal-
lum EA, et al. Periodontal and microbiologic evaluation of two methods of archwire ligation:
ligature wire and elastomeric rings. Am J Orthod Dentofacial Orthop 2008;134:506-512.
17. Melsen B. Limitations in adult orthodontics. In: Melsen B, ed. Current Controversies in
Orthodontics. Chicago: Quintessence. 1991; p. 147-180.
18. Williams S, Melsen B, Agerbaek N, Asboe V. The orthodontic treatment of malocclusion in
patients with previous periodontal disease. Br J Orthod 1982; 9:178-184.
19. Melsen B, Agerbaek N, Markenstam G. Intrusion of incisors in adult patients with marginal
bone loss. Am J Orthod Dentofacial Orthop 1989;96:232241.
20. Aous Dannan. An update on periodontic-orthodontic interrelationships. J Indian Soc Peri-
odontol 2010;14:66-71.
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port: an experimental study in dogs. Eur J Orthod 1980;2:51-7.
22. Wennstrom JL, Stokland BL, Nyman S, Thilander B. Periodontal tissue response to orthodontic
movement of teeth with infrabony pockets. Am J Orthod Dentofacial Orthop 1993;103:313-9.
23. Axelsson P, Lindhe J. The significance of maintenance care in the treatment of periodontal
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24. Vinod K, Reddy YG, Reddy VP, Nandan H, Sharma M. Orthodontic-periodontics interdisci-
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Orthod 1983;17:838-844.
26. Zachrisson BU. Adult Retention: A New Approach. In: Graber LW, editor. Orthodontics:
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27. Dahl EH, Zachrisson BU. Long-term experience with direct-bonded lingual retainers. J Clin
Orthod 1991;25:619-630.
28. Moskowitz EM, Kaner C. Predictable retention for the periodontally compromised patient.
J Clin Orthod 2004;38(1):14-16.
29. Nelson PA, Artun J. Alveolar bone loss of maxillary anterior teeth in adult orthodontic
patients. Am J Ortho Dentofac Orthop 1997;111:328-34.
30. Marinho Del Santo. Periodontium and orthodontic implications: clinical applications. Int
J of Stomatological Research 2012;1(3);17-23.
31. Lindhe J, Svanberg G. Influences of trauma from occlusion on progression of experimental
periodontitis in the beagle dog. J Clin Periodontol 1974;1:3-14.
32. Lino S, Taira K, Machigashira M, Miyawaki S. Isolated vertical infrabony defects treated by
orthodontic tooth extrusion. Angle Orthod 2008;78:728-736.
33. Bach N, Baylard JF. Orthodontic extrusion: periodontal considerations and applications. J
Can Dent Assoc 2004;70(11):775-80.
34. Melsen B, Agerbaek N, Erikson J, Terp S. New attachment through periodontal treatment
and orthodontic intrusion. Am J Orthod Dentofacial Orthop 1988;94:104-16.
35. Gazit E, Lieberman M. The role of orthodontics as an adjunct to periodontal therapy. Refuat
Hapeh Vehashinayim 1978;27:5-125-1.
36. Ericsson I, Thilander B, Lindhe J, Okamoto H. The effect of orthodontic tilting movements
on the periodontal tissues of infected and non-infected dentitions in dogs. J Clin Periodon-
tol 1977;4:27893.
37. Zachrisson BU. Cause and prevention of injuries of teeth and supporting structures during
orthodontic treatment. Am J Orthod 1976;69:285-300.
38. Thornberg MJ, Riolo CS, Bayirli B, Riolo ML, Van Tubergen EA, Kulbersh R. Periodontal
pathogen levels in adolescents before, during, and after fixed orthodontic appliance therapy.
Am J Orthod Dentofacial Orthop 2009;135:958.
39. Wennstrom JL, Lindhe J, Sinclair F, Thilander B. Some periodontal tissue reactions to orth-
odontic tooth movement in monkeys. J Clin Periodontol 1987;14:1219.
40. Stenvik A, Mjor IA. Pulp and dentine reactions to experimental tooth intrusion. A histologic
study of the initial changes. Am J Orthod 1970;57:37085.
41. Diedrich PR. Guided tissue regeneration associated with orthodontic therapy. Semin Or-
thod 1996;2:39-45.
42. Burch JG, Bagci B, Sabulski D, Landrum C. Periodontal changes in furcations resulting from
orthodontic uprighting of mandibular molars. Quintessence Int. 1992;23:509-513.
43. Re S, Corrente G, Abundo R, Cardaropoli D. Orthodontic treatment in periodontally com-
promised patients: 12-year report. Int J Periodontics Restorative Dent 2000;20:31-9.

Dr. Rathore Dr. Desai Dr. Trehan Dr. Jharwal

Dr. Puzhankara Dr. Marya

Nidhi Rathore, B.D.S., M.D.S., is senior lecturer, Department of Orthodontics and Dentofacial
Orthopedics, Eklavya Dental College and Hospital, Rajasthan University of Health Sciences, Kotputli,
Rajasthan, India.

Asavari Desai, B.D.S., M.D.S., is senior lecturer, Department of Orthodontics and Dentofacial
Orthopedics, Manipal College of Dental Sciences, Manipal University, Mangalore, Karnataka, India.

Mridula Trehan, B.D.S., M.D.S., is professor and head of the Department of Orthodontics and
Dentofacial Orthopedics, Mahatma Gandhi Dental College and Hospital, Mahatma Gandhi University of
Medical Sciences and Technology, Jaipur, Rajasthan, India.

Vikas Jharwal, B.D.S., M.D.S., is senior lecturer, Department of Orthodontics and Dentofacial
Orthopedics, Mahatma Gandhi Dental College and Hospital, Mahatma Gandhi University of Medical
Sciences and Technology, Jaipur, Rajasthan, India.

Lakshmi Puzhankara, B.D.S., M.D.S., is senior lecturer, Department of Periodontology and

Oral Implantology, Amrita School of Dentistry, Kochi, Kerala, India.

Anand Marya, B.D.S., is a third-year postgraduate student, Department of Orthodontics, College

of Dentistry, University of the East, Manila, Philippines.

The New York State Dental Journal AUGUST/SEPTEMBER 2015 47

 the addict patient
Methadone Maintenance Therapy
and the Dental Patient
George Raymond, D.D.S.; William Maloney, D.D.S.
ABSTRACT
Methadone is a Schedule II drug best known for its
use in the treatment of opioid dependence. Dental
providers should be aware of the oral and systemic
effects of methadone. In patients undergoing metha-
done maintenance therapy, there is a higher incidence
of rampant caries, xerostomia, bruxism and poor oral
hygiene. A review of the pharmacology, systemic ef-
fects, drug interactions and oral manifestations is
presented, as well as possible modifications to treat-
ment and specific considerations in dental therapies.
Methadone was approved by the Food and Drug Administration
in 1972 as a treatment for opioid addiction. Research began in
1964 at Rockefeller Hospital in the then-Rockefeller Institute for
Medical Research.1
Methadone prevents cravings while blocking the euphoric
effects of heroin to establish abstinence.2,3 Originally the hope
was that refraining from heroin would decrease criminal activity
as well but, according to a 2009 Cochrane review, methadone
maintenance treatments decreased the likelihood that heroin-
dependent patients would use heroin, but it did not change crime
or mortality rates.4
There are currently over 1,400 methadone maintenance
therapy (MMT) centers in the United States.5 There are well-
documented drug interactions with methadone that will be dis-
cussed, along with the effect of alcohol on methadone levels.
48 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
Pharmacology
Methadone occurs in R-enantiomeric and S-enantiomeric forms,
with the majority of activity due to the activity of R-methadone.
It is a lipid soluble drug; estimates of the half-life are between 15
to 55 hours.6,7 Methadone has high oral bioavailability, so it gives
reliable effects when administered orally; both tolerance and physi-
ological dependence develop more slowly than with morphine.8
Methadone exerts its activity through binding to and activat-
ing opioid receptors centrally and in the periphery. This activity
produces the effects common to all opioid agonists: analgesia,
euphoria, constipation, sedation, respiratory depression, nausea
and miosis. Additionally, methadone antagonizes N-methyl-D-
aspartate receptors, which may increase its effectiveness in the
treatment of neuropathic pain compared with other opioids.9
Methadone binds directly to proteins and to plasma proteins,
chiefly albumin, globulins, and alpha 1-acid glycoprotein. Steady
state is not attained until methadone is fully distributed and
bound in tissues. Therefore, blood levels continue to rise slow-
ly for four to six weeks. Although patients sometimes complain
about drug formulation changes (tablets versus liquid; differing
flavors), there are no correlated changes in pharmacokinetics or
dynamics.7
The route of metabolism of methadone is hepatic and in-
volves the cytochrome p-450-related enzymes. The methadone is
broken down into two biologically inactive metabolites, a pyrro-
line and a pyrrolidine, which are further metabolized.1,10,11 These
are eliminated by the kidney and excreted through the bile. In
total, nine metabolites have been identified, including two minor
active metabolites, methadol and normethadol.12
Most patients require a dose of 60 mg to 120 mg/day to achieve
the optimum therapeutic effects of methadone. Compared to
those on lower doses, patients on higher doses are shown to stay
in treatment longer, use less heroin and other drugs, and have
lower incidence of HIV infection. Some patients need even higher
doses for fully effective treatment.13
Systemic Manifestations
In a well-controlled methadone maintenance therapy patient,
the two most common side effects are constipation and sweat-
ing.1,14 Other side effects include sedation, nausea, vertigo, em-
esis and pruritis.1,15
Metabolism of methadone can be affected by interactions of
other medications, such as phenytoin, carbamazepine, rifampi-
cin, fluconazole and some protease inhibitors. These drugs cause
an increase in the metabolism of methadone.16 If taken concur-
rently, erythromycin and ketoconazole may enhance the risk of
a methadone overdose in susceptible individuals due to their
potential to inhibit the metabolism of methadone. Fluoxetine
(Prozac) can also increase the plasma concentration of metha-
done, as can other selective serotonin reuptake inhibitors.16-18
Higher doses of methadone (200 mg to 400 mg/day) have
been implicated in prolongation of the QT interval on electro-
cardiogram and, possibly, with Torsades de pointes.1 Torsades is a
form of ventricular tachycardia manifested by episodes of alter-
nating polarity with the amplitude of the QRS complex twisting
around an isoelectric baseline. The rhythm usually starts with a
pre-ventricular contraction and is preceded by a widening of the
QT interval.19
The New York State Dental Journal AUGUST/SEPTEMBER 2015
FIGURE 1
Oral Manifestations of Methadone Use22-27
Increased Caries Risk Rampant.
Decay Periodontal Disease.
Xerostomia.
Bruxism Candidiasis.
Methadone levels are also affected by the regular intake of more
than four alcoholic beverages a day. Studies performed on 129
long-term MMT men and women indicated that although one
quarter of the cohort reported four or more drinks a day, there
were no significant changes in liver enzymes after three years of
MMT.1,20 These findings indicate that MMT does not potentiate
alcohol-induced hepatotoxicity.1,20
Dental Manifestations
Residual effects from heroin addiction are often prevalent in
MMT patients. Rampant caries, poor oral hygiene, xerostomia
and periodontal disease are frequently lingering effects of the
time spent abusing opioids.
The MMT patient may present as part of a referral program,
or be genuinely interested in restoring his or her oral health. Her-
oin addiction produces xerostomia with hypoglycemia. Individu-
als combat this with frequent ingestion of sugar (chocolate, sugar
cubes), resulting in rampant caries.21 The altered taste preference
for sweet foods seen in heroin addiction continues into many pa-
tients on MMT. This high cariogenic diet is compounded in these
49
patients by their dental phobias and poor oral hygiene, with many
MMT patients exhibiting a fear of needles, especially in the hands
of others, which further accentuates heightened anxiety.22,23
The dental provider is at times posed with a significant clini-
cal decision when a MMT patient presents with pain. At times,
the patient may have simulated symptoms, seeking a prescrip-
tion for a narcotic. Tolerance is achieved to the analgesic effect of
methadone so a patients usual MMT dose cannot be considered
to be analgesic. Premedication with a non-steroidal anti-inflam-
matory, such as ibuprofen, 600-800mg, one to two hours prior
to the procedure, has been demonstrated to lower postoperative
pain and to result in a decreased need for opiates.24 Patients on
MMT should be maintained on their current dose and, if needed,
receive additional opiate analgesics for pain, often at higher doses
than usually given and at shorter dispensing intervals.24,25
Bruxism has been reported more frequently in opioid-de-
pendent individuals and may be attributed to a general increase
in neurosis in this cohort of patients.22,26 Abfraction lesions are
also commonly found on former opioid abusers and may require
treatment. The overall oral health of a patient in this category is
often poor and may require multiple visits to restore to optimal
health. Unrealistic expectations may also exist in the MMT pa-
tient. As such, it is imperative to be empathetic yet direct about
the prognosis of dental treatment.
Caries prevention should be stressed and various treatment
modalities, such as home fluoride treatments, adjunctive oral
hygiene devices and nutritional support, are possible avenues to
be explored with the patient. Many MMT patients combat xe-
rostomia by simply drinking copious amounts of water. Water
is a poor substitute for saliva, because it lacks certain necessary
ions, buffering capacity, lubricating mucins and protective pro-
teins.27 Many of the saliva substitutes available on the market
today may be suggested for xerostomia. It should be noted that
if they contain sorbitol, their use reinforces the need for topical
fluoride treatments.
Conclusion
The dental care of a patient engaged in methadone maintenance
therapy is multifaceted. The importance of educating the patient
about oral hygiene and proper diet is paramount. The dental pho-

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50 AUGUST/SEPTEMBER 2015 The New York State Dental Journal

bias of these patients require attention to insure the completion 25. Peng PW, Tumber PS, Gourlay D. Review article: Peri-operative pain management of pa-
tients on methadone therapy. Can J Anaesth 2005;52(5):513-23.
of dental treatment. Depending upon the dosage and stage of 26. Colon PG Jr. Dental disease in the narcotic addict. Oral Surg Pral Med Oral Pathol
therapy in the methadone program, shorter appointments may 1972;33:905-910.
27. Ciancio S, editor. ADA/PDR Guide to Dental Therapeutics. 4th ed.Chicago:ADA/Thomson
be required or appointments set around the patients schedule of PDR. 2006;pp 31-32.
methadone ingestion. Attention should be given as well to avoid-
ing prescribing any narcotic pain relievers when possible. And the
practitioner needs to be aware that the methadone might mask
dental pain in the earlier stages. This information should be re-
layed to the patient to reinforce the importance of follow-up ex-
aminations at proper time intervals. p Dr. Raymond Dr. Maloney

Queries about this article can be sent to Dr. Maloney at wjm10@nyu.edu. George Raymond, D.D.S., is clinical instructor in the Department of Cariology and Comprehensive
Care, New York University, New York, NY.
REFERENCES
1. Kreek MJ, Borg L, Ducat E., Ray B. Pharmacotherapy in the treatment of addiction: metha- William James Maloney, D.D.S., is clinical associate professor in the Department of Cariology
done. J Addict Dis 2010 Apr;29(2):200-16. and Comprehensive Care, New York University College of Dentistry, New York, NY.
2. Brondani M, Park P. Methadone and oral health: a brief review. J Dental Hygiene
2011;85:92-98.
3. Farnsworth N. Oral health project for people on methadone programs & with substance
abuse issues in the outer metropolitan region. Department of Health (internet). 2004.
Available from: www.health.vic.gov.au/healthpromotion/downloads/fr_knox.pdf
4. Mattick RP, Breen C, Kimber J, Davoli M. Methadone maintenance therapy versus no opioid
replacement therapy for opioid dependence. Cochrane Database Syst Rev. 2003 CD002209.
5. National Institute on Drug Abuse. Study Supports Methadone Maintenance in Thera-
peutic Communities. Retrieved from http://www.drugabuse.gov/news-events/nida-
notes/2010/12/study-supports-methadone-maintenance-in-therapeutic-communities.
Accessed March 29, 2013.
6. Brown R, Kraus C, Fleming M, Reddy S. Methadone: applied pharmacology and use as
adjunctive treatment in chronic pain. Postgrad Med J 2004;80:650-659.
7. Eap CB, Buclin T, Baumann P. Inter-individual variability of the clinical pharmacokinetics
of methadone: implications for the treatment of opioid dependence. Clin Pharmacokinet
2002;41:1153-1193.
8. Katzung B, editor. Basic & Clinical Pharmacology. 7th ed. Stamford: Appleton & Lange.
1998; pp. 504-505.
9. Inturrisi CE. Clinical pharmacology of opioids for pain. Clin J Pain 2002;18:S313.
10. Ferrari A, Coccia CP, Bertolini A, Sternieri E. Methadone metabolism, pharmacokinetics
and interactions. Pharmacol Res 2004;50:551-559.
11. Lugo RA, Satterfield KL, Kern SE. Pharmacokinetics of methadone. J Pain Palliat Care Phar-
macother 2005;19:13-24.
12. Felder C, Uehlinger C, Baumann P, Powell K, Eap CB. Oral and intravenous methadone use:
some clinical and pharmacokinetic aspects. Drug & Alcohol Dependence 1999;55:137-43.
13. CDC Department of Health and Human Services. Methadone management therapy. Febru-
ary 2002. Available at www.cdc.gov/idu.
14. Kreek MJ. Medical safety and side effects of methadone in tolerant individuals. JAMA
1973;223:665-668.
15. Gutstein HB, Akil H. Opioid Analgesics. In: Brunton L, Lazo JS, Parker KL., editors. Good-
man and Gilmans the Pharmacological Basis of Therapeutics. 11th ed. New York: McGraw-
Hill. 2005; pp.547-590.
16. Corkery J, Fabrizio S, Ghodse A, Oyefeso A. The effects of methadone and its role in fatali-
ties. Hum Psychopharmacol Clin Exp 2004;19:565-576.
17. Furet Y, Gibier L, Clarte C. Aspects pharmacologiques des programmes de substitution pour
les toxicomanes aux opiaces [Pharmacologic aspects of substitution programs for opiate
addiction]. Revue Med Tours 1999;33:153-158.
18. Bertschy G, Baumann P, Eap CB, Baettig D. Probable metabolic interaction between metha-
done and fluvoxamine in addict patients. Ther Drug Monitor 1994;16:42-45.
19. Ferri F, editor. Practical Guide to the Care of the Medical Patient. 5th ed. St. Louis:Mosby.
2001;pp 151-154.
20. Kreek MJ. Plasma and urine levels of methadone. NY State J Med 1973;73:2773-2777.
21. Sheedy J. Methadone and caries. Case reports. Australian Dental J 1996;4(6):367-9.
22. Titsas A, Ferguson MM. Impact of opioid use on dentistry. Australian Dental J
2002;47(2):94-98.
23. Scheutz F. Anxiety and dental fear in a group of parenteral drug addicts. Scand J Dent Res
1986;94:241-247.
24. Patton L, editor. The ADA Practical Guide to Patients with Medical Conditions. 1st ed. Iowa:
Wiley-Blackwell. 2012;pp 344-346.

The New York State Dental Journal AUGUST/SEPTEMBER 2015 51

 differential diagnosis
Differential Diagnosis of a
Periapical Radiolucent Lesion
A Case Report and Review of the Literature
Matthew Malek, D.D.S.; Lina M. Cortes, D.D.S.; Asgeir Sigurdsson, D.D.S., M.S.; Paul A. Rosenberg, D.D.S.
ABSTRACT
This article demonstrates a methodological approach
to diagnosing a periapical radiolucency that could not
be diagnosed using only basic clinical and radiograph-
ic findings. The patient was a 59-year-old Hispanic
female with a small tender mass on the lower gingi-
va associated with tooth #25. Radiographic appear-
ance demonstrated a well-defined radiolucent lesion
at the apices of the mandibular incisors. The patient
had no significant medical history. Cone-beam com-
puted tomography (CBCT) showed bony expansion
of the buccal plate. Differential diagnosis included
non-endodontic unilocular radiolucent lesions in
the anterior mandibular region. Biopsy findings were
consistent with periapical cemento-osseous dysplasia
(PCOD). In conclusion, clinical appearance of PCOD
varies from non-expansile and asymptomatic to being
expansile and sometimes symptomatic. In the latter
cases, it may be necessary to use additional diagnostic
tools to confirm the diagnosis.
52 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
Establishing an accurate diagnosis for a periapical lesion may be
challenging, especially when the nature of the lesion cannot be
determined through basic diagnostic tests. The most important
question to be addressed is the origin of the lesion, since radio-
graphic bone changes that mimic lesions of endodontic origin
may occur as a consequence of neoplastic and developmental al-
terations.1
The initial diagnostic step is to determine whether the le-
sion is of endodontic origin. This is most often accomplished
through use of high-quality radiographs and a thorough clinical
examination, including sensibility tests. Interpretation of periapi-
cal radiography may lead to subjective conclusions;2 and there is
insufficient evidence to determine the diagnostic accuracy of pulp
sensibility tests.3 Therefore, relying solely upon periapical radio-
graphs and inconclusive clinical tests may lead to misdiagnosis
and unnecessary treatment for a healthy tooth with a periapical
radiolucency.4,5
When diagnosing an apical radiolucent lesion seemingly
associated with vital teeth, the clinician should follow an or-
ganized thought process to reach a definite diagnosis.6 Some
lesions may be accurately diagnosed through radiographs and
clinical findings.7 But in cases where the diagnosis is not clear,
the clinician would benefit from other diagnostic methods to
further evaluate the lesion. Studies have shown that a high-
resolution, three-dimensional technique, such as cone-beam
computed tomography (CBCT), can be valuable in diagnosing ly calcified periapical osteopetrosis;12 odontogenic keratocyst
periapical lesions.8 Biopsy and histopathological analysis of the (OKC),13 which is also referred to as keratocystic odontogenic
lesion can provide definitive confirmation of the diagnosis of a tumor; simple bone cyst (traumatic bone cyst);14 and central
suspected lesion.9 Few authors have strongly suggested biopsy ossifying fibroma.12
and the sequential histopathological analysis for cases that the We also took into consideration certain systemic diseases. For
initial diagnostic tests indicate a lesion of non-endodontic ori- example, hyperparathyroidismincluding renal osteodystrophy
gin.1 However, biopsy has been recommended only if there are may manifest as radiolucent areas in the anterior mandible area.15
concerns about the clinical diagnosis and not as a routine audit
to merely confirm the clinical diagnosis.10
The following case report demonstrates a thought process
that includes the use of different diagnostic modalities in a se-
quential manner to reach a definite diagnosis.

Case Report
A 59-year-old Hispanic female was presented for the purpose of
root canal treatment on the mandibular right central incisor. Her
chief complaint was pain upon palpation around the gingival tis-
sue of the mandibular central incisors. Her medical history was
noncontributory (Figure 1).

Figure 1. Preoperative intraoral image. Arrow is pointing to area of gingival mucosa where
Radiographic Appearance
hard swelling was palpable.
The radiograph showed a relatively well-defined radiolucency
with slightly irregular borders at the apices of the mandibular left
and right central incisors (Figure 2). No caries, restorations or
fractures were present on the mandibular anterior teeth. Intraoral
and radiographic examination revealed normal probing depths
and mild-to-moderate generalized chronic periodontitis. A small
tender mass was noted on the gingival mucosa of the mandibular
right central incisor.
All four mandibular incisors responded normally to Endo Ice
(Coltene/Whaledent Inc., Newark, NJ) and to the electrical pulp tester
(Sybron Endo, Orange, CA). No percussion sensitivity was detected
on the four anterior incisors, but the gingival mucosa around the
apex of the mandibular right central and lateral incisors was sen-
sitive to palpation. Figure 2. Preoperative periapical ra- Figure 3. Sagittal section of mandibular right
diograph of mandibular anterior teeth, central incisor, showing extent of expansion.
Cone Beam Computed Tomography (CBCT) revealing periapical radiolucency.
In order to evaluate the nature and extent of the lesion and its
expansion, we utilized a CBCT. On panoramic reconstruction, we
noted a large lytic lesion in relation to the mandibular anterior
teeth. In the cross-section view, the lesion appeared to have ex-
panded the mandibular cortices and measured approximately 10
mm 7 mm. The lesion extended from the apex of the mandibu-
lar left central incisor to the apex of the mandibular right lateral
incisor (Figures 3, 4).
Considering tooth vitality, the differential diagnosis includ-
ed non-endodontic unilocular radiolucent lesions that can be
found in the anterior mandibular region. These lesions include
Figure 4. Inferior view of axial section showing labial extension of lesion and its relation to
the following: periapical cemento-ossesous dysplasia (PCOD);9 roots of mandibular incisors. Arrows are pointing to bony expansions on buccal and lingual plates.
central giant cell granuloma (CGCG);6 ameloblastoma;11 poor-

The New York State Dental Journal AUGUST/SEPTEMBER 2015 53

Metastatic carcinomas16,17 may also present with the same mani-
festation. Metastases to the mandible are four-times more com-
mon than those to the maxilla. And the most common primary
tumor sites are breast, lung, kidney, thyroid and prostate.18 Since
the patients medical history was unremarkable, hyperparathyroid-
ism and renal osteodystrophy were unlikely. But the patient could
have a metastasis without having a primary lesion diagnosis.
Figure 5. Histology slide with x20 magnification, demonstrates cellular fibrovascular tissue
with plump fibroblasts and scattered foci of new bone, osteoid and cementum-like material
with associated osteoblasts and osteoclasts.
Figure 6. Postoperative,
one-year follow-up radiograph
shows scattered radio-opaque
calcific areas in lesion.
54 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
Because the clinical and radiographic findings did not yield a
definitive diagnosis (see "Discussion" that follows), we recom-
mended an incisional biopsy.
Biopsy
We performed an incisional biopsy under local anesthesia with
68 mg (2 carpules of 1.7 cc) lidocaine 2% with 1:100,000 epi-
nephrine, using a full thickness flap with sulcular incision with
two vertical releases at distal of mandibular canines. After flap
reflection, we performed an osteotomy, exposing and incising 5
mm x 5 mm x 5 mm3 of the lesion.
Histopathological Analysis
Histological sections demonstrated cellular fibrovascular tissue
with plump fibroblasts and scattered foci of new bone, osteoid
and cementum-like material with associated osteoblasts and os-
teoclasts. There were also a few infiltrating chronic inflammatory
cells. The histopathological diagnosis was benign fibro-osseous le-
sion and in view of the radiographic findings was consistent with
periapical cemento-osseous dysplasia (Figure 5).
We informed the patient of the diagnosis and explained the
prognosis to her, which based upon the self-limiting, non-progres-
sive nature of the lesion, was considered to be good. At the one-year
follow-up, radio-opaque areas were visible in the lesion; all four
anterior mandibular teeth responded normally to pulp tests; and
while the patient still experienced some mild sensation upon pal-
pation, the tender mass on the labial mucosa was gone (Figure 6).
Discussion and Review of Literature
PCOD was originally classified as a type of cementoma. In 1992,
it was removed from the World Health Organization (WHO)
classication of odontogenic tumors and placed among the bro-
osseous bone lesions.18 This lesion, along with focal cemento-osse-
ous dysplasia and florid cemento-osseous dysplasia, form cemento-
osseous dysplasia (osseous dysplasia), one of the most common
groups of fibro-osseous lesions encountered in clinical practice.19
PCOD has three radiographic features that indicate stages
from early formation to maturation: 1. osteolytic; 2. cementoblas-
tic; and 3. mature. In the early stage of osteolytic, lesions are well-
dened radiolucencies at the apex of one or more teeth.18 The his-
tologic appearance demonstrates fibrous connective tissue mixed
with woven bone, lamellar bone and cementoid particles. This ap-
pearance changes with the stage of maturation, such that as the
lesion matures, the ratio of fibrous connective tissue to mineralized
material decreases.19 The calcied structures in the osteolytic stage
are of insufcient size to be observed radiographically.18
PCOD is a benign, slowly growing tumor.20 In most cases, no
further treatment is necessary after its diagnosis.18 In some cases,
when a cemento-osseous lesion becomes significantly sclerotic,
it tends to become hypovascular and prone to necrosis. The ad-
dition of an inflammatory component to the disease would basi-
cally turn this process into a chronic osteomyelitis involving dys-
plastic bone and cementum. In such instances, further treatment
may be necessary.19
The etiology of the lesion is not well understood. Based on its
origin, it consists of three variations: 1. originating from periodon-
tal ligament tissue; 2. originating from medullary bone tissue; and
3. resulting from the simultaneous involvement of both tissues.12
There have also been reports of autosomal dominant PCOD.21
PCOD predominantly involves the apical areas of vital man-
dibular incisors. There is a marked predilection for female pa-
tients; and most cases affect the African-American population.
Most patients are between the ages of 30 and 50 when diagnosed
initially; in fact, PCOD is almost never found in individuals
younger than 20.19,20,22 PCOD has also been found in the max-
illa; in rare cases, it may be present simultaneously in both the
mandible and the maxilla.23
PCOD is asymptomatic and is usually discovered upon a ra-
diographic examination. Radiographically, the lesion may demon-
strate variable appearances based upon the stage of its maturation:
The New York State Dental Journal AUGUST/SEPTEMBER 2015
from a well-circumscribed radiolucent lesion, to a mixed radio-
lucent/radiopaque one; and at its final stage, a radiopaque lesion
involving the apices of one or several teeth. Individual lesions are
rarely more than 10 mm in diameter;19 most are less than 5 mm.22
No systemic disease has been found to be significantly as-
sociated with this condition. Clinically, no misalignment in local
structures, including the teeth, and usually no soft tissue reac-
tion or discoloration have been found to be significantly associ-
ated with PCOD.19,20 The lesion is self-limiting, and progressive
growth rarely happens.19
Differentiating PCOD from other radiolucent lesions may be
possible through radiograph and clinical findings.6 However, the
differential diagnosis of PCOD may vary according to the stage of
development of the lesion. The most difficult stage in diagnosing
PCOD is its early stage. There are a number of reported cases in
which an incorrect diagnosis of PCOD resulted in inappropriate
treatment.22,24,25 This is because in the initial osteolytic stage, the
radiolucent appearance mimics periapical periodontitis,19 which
may cause diagnostic difficulty.9 Moreover, in this early stage, a
neoplastic process (ossifying fibroma) or simple bone cyst cannot
be ruled out by radiographic assessment alone.12
55
In this case, the presence of pain upon palpation and buccal ex-
pansion did not completely match the classic features of PCOD.
Some studies have described PCOD as non-expansile.20,27,28 In
one such study, the authors considered the non-expansile nature
of this lesion to be a key criterion in distinguishing this lesion
from other expansile lesions.20 Moreover, some other lesions may
also create bony expansion, thus creating a need for further inves-
tigation. For instance, ossifying fibroma (cementifying fibroma)
may cause bony expansion.12,19 And cystic ameloblastoma (one of
the most commonly reported benign lesions mimicking an end-
odontic lesion)1 may also cause enlargement of the jaws without
pain or paresthesia.11,29 OKC may be associated with bony expan-
sion.13 And traumatic bone cysts have also been reported to cause
expansion.2 CGCG, which mostly occurs in the anterior man-
dible of young females, may also cause bone expansion.18 In a
recent study on lesions mimicking lesions of endodontic origin,1
it was found that swelling and pain were the most frequently cited
symptoms of malignant lesions (46.6%), whereas benign lesions
presented these associated symptoms in only 10.8% of all cases.
Because of these uncertainties, a CBCT was obtained to fur-
ther evaluate the extent of the lesion. Its results confirmed the bony
expansion of the lesion. We then opted to perform an incisional
biopsy; the histopathologic report was consistent with the early (os-
teolytic) stage of PCOD. We informed the patient of the diagnosis
and her prognosis, and will continue to review her status every six
months to monitor any changes in the size and density of the lesion.
Conclusion
An accurate diagnosis of this lesion required knowledge of biology
and pathology, as well as the ability to interpret and utilize various
diagnostic tools. Differential diagnosis is the first step in diagnosis.
And the various possibilities should be ruled out one by one using a
methodological approach until one reaches a definite diagnosis. An
important caveat to this approach is to avoid using diagnostic tools
solely for the purpose of screening or confirming a well-established
diagnosis. In the case presented here, due to the expansile nature
of the lesion and sensitivity to palpation, we deemed the use of
additional diagnostic tools necessary to confirm the diagnosis. p
Queries about this article can be sent to Dr. Malek at matthewmalek@nyu.edu.
REFERENCES
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2. Reit C. The influence of observer calibration on radiographic periapical diagnosis. Int Endod
J 1987;20(2):75-81.
3. Mejre IA, Axelsson S, Davidson T, et al. Radiological diagnosis of periapical bone tissue
lesions in endodontics: a systematic review. Int Endod J 2012;45(9):783-801.
4. Galgano C, Samson J, Kffer R, et al. Focal cemento-ossesous dysplasia involving a man-
dibular lateral incisor. Int Endod J 2003;36(12):907-11.
5. Bhaskar SN. Oral surgery-oral pathology conference No. 17, Walter Reed Army Medical Center. Periapi-
cal lesions-types, incidence, and clinical features. Oral Surg Oral Med Oral Pathol 1966;21(5):657-71.
6. Morton TH. Differential diagnosis of periapical radiolucent lesions. Dent Clin North Am
1979;23(4):519-41.
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7. Resnick CM, Novelline RA. Cemento-osseous dysplasia, a radiological mimic of periapical
dental abscess. Emerg Radiol 2008;15(6):367-74.
8. Lofthag-Hansen S, Huumonen S, Grndahl K et al. Limited cone-beam CT and intraoral
radiography for the diagnosis of periapical pathology. Oral Surg Oral Med Oral Path Oral
Radiol Endod 2007;103(1):114-19.
9. Rosenberg PA, Frisbie J, Lee J, et al. Evaluation of pathologists (histopathology) and radiolo-
gists (cone beam computed tomography): differentiating radicular cysts from granulomas.
J Endod 2010;36(3):423-28.
10. Peters E, Lau M. Histopathologic examination to confirm diagnosis of periapical lesions: a
review. J Can Dent Assoc 2003;69(9):598-600.
11. Kaufman AY, Dayan D, Horowitz I. Cystic ameloblastoma-an endodontic differential diag-
nostic problem. J Endod 1987;13(7):358-361.
12. Kawai T, Hiranuma H, Kishino M, et al. Cemento-osseous dysplasia of the jaws in 54 Japa-
nese patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87(1):107-14.
13. Nohl FS, Gulabivala K. Odontogenic keratocyst as periradicular radiolucency in the anterior
mandible. Oral Surg Oral Med Oral Pathol 1996;81(1):103-9.
14. Hansen LS, Sapone J, Sproat RC. Traumatic bone cysts of jaws. Oral Surg Oral Med Oral
Pathol 1974;37(6):899-910.
15. Loushine RJ, Weller RN, Kimbrough WF, et al. Secondary hyperparathyroidism: a case re-
port. J Endod 2003;29(4):272-4.
16. Fujihara H, Chikazu D, Saijo H, et al. Metastasis of hepatocellular carcinoma into the mandible
with radiographic findings mimicking a radicular cyst: a case report. J Endod 2010;36(9):1593-6.
17. Khalili M, Mahboobi N, Shams J. Metastatic breast carcinoma initially diagnosed as pulpal/
periapical disease: a case report. J Endod 2010;36(5):922-5.
18. Sapp JP, Eversole LR, Wysocki GP. Contemporary Oral and Maxillofacial Pathology. 2nd ed.
Missouri: Mosby, 2003;95-98.
19. Chi AC, Bone Pathology in: Neville BW, Damm DD, Allen CM, et al. Oral and Maxillofacial
Pathology. 3rd ed. St. Louis: Saunders, 2009:613-77.
20. Zegarelli EV, Kutscher AH, Napoli N, et al. The cementoma - a study of 230 patients with
435 cementomas. Oral Surg Oral Med Oral Pathol 1964;17:219-24.
21. Sedano HO, Kuba R. Gorlin RJ. Autosomal dominant cemental dysplasia. Oral Surg Oral
Med Oral Pathol 1982;54(6):642-6.
22. Waldron CA. Fibro-osseous lesions of the jaws. J Oral Maxillofac Surg 1985;43(4):249-62.
23. Falace DA, Cunningham CJ. Periapical cemental dysplasia: simultaneous occurence in mul-
tiple maxillary and mandibular teeth. J Endod 1984;10(9):455-56.
24. Smith S, Patel K, Hoskinson AE. Periapical cemental dysplasia: a case of misdiagnosis. Br
Dent J 1998;185(3):122-3.
25. Wilcox LR, Walton RE. A case of mistaken identity: periapical cemental dysplasia in an
endodontically treated tooth. Endod Dent Traumatol 1989;5(6):298-301.
26. Alsufyani NA, Lam EW. Osseous (cemento-osseous) dysplasia of the jaws: clinical and ra-
diographic analysis. J Can Dent Assoc 2011;77:1-8.
27. Brannon RB, Fowler CB. Benign fibro-osseous lesions: a review of current concepts. Adv
Anat Pathol 2001;8(3):126-43.
28. Eversole R, Su L, ElMofty S. Benign fibro-osseous lesions of the craniofacial complex. A
review. Head Neck Pathol 2008;2(3):177-202.
29. Faitaroni LA, Bueno MR, De Carvalhosa AA, et al. Ameloblastoma suggesting large apical
periodontitis. J Endod 2008;34(2):216-9.
Dr. Malek Dr. Cortes Dr. Sigurdsson Dr. Rosenberg
Matthew Malek, D.D.S., is clinical assistant professor and director of the Advanced Education
Program in Endodontics, New York University, New York, NY. He is a diplomate of the American Board
of Endodontics and in private practice limited to endodontics in Manhattan.
Lina M. Cortes, D.D.S., is in full-time private practice limited to endodontics in San Antonio, TX.
Asgeir Sigurdsson, D.D.S., M.S., is associate professor and chairperson of the Department
of Endodontics, New York University, New York, NY. He is a diplomate of the American Board of
Endodontics.
Paul A. Rosenberg, D.D.S., is professor in the Department of Endodontics, New York University,
New York, NY. He is a diplomate of the American Board of Endodontics.
 clinical diagnosis
Plasma Cell Gingivitis
An Occasional Case Report
M.B. Mishra M.D.S.; Swati Sharma, M.D.S.; Alok Sharma, M.D.S.
ABSTRACT
Plasma cell gingivitis, an infrequently observed oral
condition, has been clinically characterized by diffuse
gingival enlargement, erythema and sometimes des-
quamation. These lesions are usually asymptomatic,
but invariably the patient will complain of a burn-
ing sensation in the gingiva and bleeding from the
mouth. The diagnosis requires hematological screen-
ing in addition to clinical and histopathological ex-
aminations. This case report outlines one such case of
plasma cell gingivitis in a 15-year-old female caused
by use of an herbal, homemade toothpowder. The case
presented here highlights the adverse effects and irra-
tional use of herbal agents in dentifrices. At the same
time, it emphasizes the need for comprehensive his-
tory taking, careful clinical examination and appro-
priate diagnostic tests in order to arrive at a definitive
diagnosis and treatment plan for gingival conditions
that are refractory to conventional therapy and to ex-
clude certain malignancies and oral manifestations of
systemic diseases.
Plasma cell gingivitis (PCG) is an uncommon inflammatory
condition of uncertain etiopathogenesis. PCG has been clini-
The New York State Dental Journal AUGUST/SEPTEMBER 2015
cally characterized by diffuse gingival enlargement, erythema and
sometimes desquamation.1-3 These lesions are usually asymptom-
atic, but invariably the patient will complain of a burning sensa-
tion in the gingiva4 and bleeding from the mouth.5-8
PCG is known by a variety of other names. They include
atypical gingivostomatitis,9 idiopathic gingivostomatitis,4 allergic
gingivostomatitis10 and plasmacytosis of the gingiva.11 A localized
lesion called plasma cell granuloma has also been reported by
Phadnaik et al.12
Although the etiopathogenesis of PCG is still not clearly
understood, it is considered a hypersensitivity reaction to some
antigens, such as the components of chewing gums and dentifric-
es.3,5,13-14 Flavoring agents added to chewing gums and dentifrices
can produce an inflammatory reaction in both free and attached
gingiva. The most prominent microscopic picture of plasma cell
gingivitis is diffuse and massive infiltration of plasma cells into
the sub-epithelial connective tissue, resulting in disruption or
damage to the basement membrane. The capillaries in the con-
nective tissue may also become dilated.6-8
It is important to be able to differentiate PCG from other
mucous membrane lesions affecting the gingival tissues. Often,
microscopic examination is necessary to make this distinction.
The diagnosis requires hematological screening in addition to
clinical and histopathological examination. Pathological changes
in this condition are clinically similar to those of pemphigus,
pemphigoid, desquamative gingivitis, lichenoid or allergic reac-
tions, anti-seizure (such as Dilantin) or calcium channel blocker
hyperplasia and a leukemic infiltrate, which must be differenti-
ated through hematologic and serologic testing.3,11-14 It has been
57
Figure 1. Preoperative view.
Figure 3. Histopathological picture showing dense infiltration of lymphocytes with scattered
plasma cells and neutrophilic abscesses.
observed that histopathological changes of PCG mimic those of
multiple myeloma or solitary plasmacytoma.3
This case report concerns plasma cell gingivitis in a 15-year-
old female caused by the use of herbal, homemade toothpowder.
Case Report
A 15-year-old female was referred to the Department of Periodon-
tics and Oral Implantology at Mahatma Gandhi Dental College
and Hospital, Jaipur, Rajasthan, India, with a chief complaint of
red swollen gums. It was associated with bleeding on slight provo-
cation and pain when eating hard food.
The patient had neither relevant medical history nor any his-
tory of mouth breathing. However, her oral hygiene history was
significant, revealing a recent use of herbal toothpowder made
at home. The contents of this toothpowder were grounded black
pepper, black salt, alum and ajwain. The patient had been rub-
bing the powder on her teeth and gums twice daily for the last six
months. There was associated gingival bleeding on slight provoca-
58 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
Figure 2. Preoperative view showing heavy accumulation of plaque and deposits.
Figure 4. Histopathological picture showing thickened epithelium with widened rete-pegs.
tion. The patient first noticed a mild reddish discoloration around
five months ago, which progressively increased in size without
any apparent discomfort.
Clinical examination revealed severe inflammation of the
gingival tissues extending from the free gingival margin to the
mucogingival junction in both the maxillary and mandibular
arches. Gingival enlargement was Grade III (Bokenkamp et al.;
1994) in the maxillary and mandibular anterior sextant; the
entire tissue was a bright fiery red, moderately thick and edem-
atous, with profuse bleeding on gentle manipulation (Figure
1). The gingiva in the posterior region of both arches was rela-
tively less edematous. The entire length of gingival tissue was
easily reflectable, which exposed heavy plaque accumulation
around the teeth in the maxillary and mandibular anterior sex-
tants (Figure 2). Nikolskys sign was negative, with no blister
formation. The patient exhibited mild clinical attachment loss
in relation to the maxillary and mandibular anterior sextant
and the maxillary first molars. Based upon the history and

Figure 5. Six months postoperative view.
clinical signs, a provisional diagnosis of plasma cell gingivitis
was made.
Laboratory investigations included routine blood exami-
nation, peripheral blood smear and erythrocyte sedimentation
rate. Antibody titer of immunoglobulins was also assessed. Un-
der local anesthesia, an incisional biopsy was taken from the
right mandibular anterior region for histopathological (HPE)
examination.
Blood test results revealed total leukocyte count (TLC) and
differential leukocyte count (DLC) within normal limits. How-
ever, red blood cells (RBCs) showed mild anisocytosis with hypo-
chromasia. Serum IgG and serum IgM levels were within normal
limits (991 mg/L & 202 mg/L, respectively). However, serum IgE
level (512 IU/ml) was considerably higher than the normal range
(1.4-300 IU/ml).
Histopathologic Findings
HPE of the biopsy specimen of the gingival tissue was carefully
examined under different magnifications. HPE showed hyper-
plastic epithelium at places, with erosion at several spots. The
epithelial cells in certain areas exhibited hydropic degenera-
tion. The rete-ridges were also found widened. Underlying con-
nective tissue had dense aggregates of infiltration of plasma
cells supported by fibrous connective tissue. Multiple neutro-
philic abscesses were found, depicting acute exacerbation. HPE
findings confirmed the diagnosis of plasma cell gingivitis (Fig-
ures 3,4).
Clinical Management
The patient was advised to immediately stop using the offending
powder preparation for toothbrushing and to avoid possible al-
lergens, such as chewing gums, cosmetics and food additives. A
super soft toothbrush with an over-the-counter toothpaste was
prescribed, and proper brushing technique for care of edematous
bleeding gingival was demonstrated.
Nonsurgical therapy included thorough oral prophylaxis,
strict oral hygiene instructions and 0.2% Chlorhexidine mouth-
wash. There was a significant reduction in the inflammation of
The New York State Dental Journal AUGUST/SEPTEMBER 2015
the gingival tissue after nonsurgical therapy. However, the in-
flammatory enlargement still persisted in the mandibular left
quadrant and maxillary quadrant, extending from right maxillary
canine to left maxillary second molar region. Because of this, a
surgical approach was planned in those regions.
An internal beveled incision was made and a full thickness
periodontal flap was raised. Thorough debridement with root
planing and irrigation was done. After positioning the flap and
suturing, a Coe-pack was placed, and postoperative analgesics
and antibiotics were prescribed for five days. Appropriate instruc-
tions for wound care were given, and the patient was recalled
after one week for suture removal. Clinically, there was excellent
resolution of inflammation, and the entire phase was unevent-
ful. The patient was advised to maintain strict oral hygiene and
was recalled after one, three and six months. After six months,
clinically, the entire gingival tissue appeared healthy with normal
morphology (Figure 5). The patient has been put on regular recall
visits every three months.
Discussion
Plasma cell gingivitis is a rare benign condition of the gingiva
characterized by sharply demarcated edematous and erythema-
tous gingivitis, often extending to the mucogingival junction.14,16
The etiology of plasma cell gingivitis is not clearly known,17 but
because of the obvious presence of plasma cells, many authors
believe it is an immunological reaction to allergens, among
them, the ingredients of toothpaste, chewing gum and oral care
products.5 Cases related to the use of herbal toothpaste have
been reported.14 It has been suggested that strong spices and
some herbs, such as chili, pepper and cardamom, may be impor-
tant triggering factors.14,16
Three categories of plasma cell gingivitis have been proposed
based upon the etiology of the condition.18 They are:
1. Lesions caused by an allergen.
2. Neoplastic lesions.
3. Lesions of unknown cause.
The case report presented here was Type 1. Usually, the pa-
tient presents with edematous and inflamed gingiva on the labial
aspect of the anterior region of the maxillary arch. A tendency
for gingival bleeding upon gentle tissue manipulation is invari-
ably present in all cases. Similar findings were present in our case
where Grade III gingival enlargement was noticed in the maxillary
and mandibular anterior sextant and moderate enlargement in
the posterior aspect. The entire tissue was bright red, moderately
thick and edematous.
Differential diagnosis of this condition is very important
because of the similarity with other aggressive conditions.
Pathological changes in this condition are clinically similar to
those of pemphigus, pemphigoid, desquamative gingivitis, li-
59
chenoid or allergic reactions, anti-seizure (such as Dilantin)
or calcium channel blocker hyperplasia and a leukemic infil-
trate, the latter needing to be differentiated through hema-
tologic and serologic testing.3,11-14 A negative Nikolskys sign,
a thorough medical history and age of the patient helped ex-
clude these clinical entities. The presence of atypical plasma
cells in the microscopic examination suggested malignancy,
such as multiple myeloma and solitary myeloma.8,19 However,
such condition was also ruled out considering the age of the
patient. Aggregates of plasma cells upon microscopic examina-
tion might cause concern of a plasma cell dyscrasis, notably,
multiple myeloma or plasmacytoma. However, in contrast to
malignant plasma cell lesions, the plasma cells in PCG are nor-
mal and are found within a connective tissue matrix rather
than replacing the background stroma.
The histopathological picture revealed that the underlying
connective tissue had a dense infiltration of plasma cells; multiple
neutrophilic abscesses were found, thus depicting acute exacer-
bation. Hence, a confirmatory diagnosis of plasma cell gingivitis
was made.
Once the diagnosis of plasma cell gingivitis is made, the
screening of various antigenic substances must be done. In the
case presented here, the patient had switched to an herbal tooth-
paste fabricated at home and consisting of alum, black pepper,
black salt and ajwain. Alum (although used as an astringent)
and pepper have already been reported as potential allergens in
the literature.
The case presented here highlights the adverse effects and
irrational use of herbal dentifrices. This case also illustrates
the need to explore a patients individual background and hab-
its when several possible etiologic agents have been eliminated
and the desired clinical results are not obtained with conven-
tional therapy.
Conclusion
This case highlights the adverse effects and irrational use of herb-
al agents in dentifrices. Plasma cell gingivitis is a diagnosis of
exclusion, distinguished primarily by the histologic findings of a
marked submucosal infiltrate, after excluding certain conditions.
It emphasizes the need for comprehensive history taking,
careful clinical examination and appropriate diagnostic tests in
order to arrive at a definitive diagnosis and treatment plan for
gingival conditions that are refractory to conventional therapy
and exclude certain malignancies and oral manifestations of sys-
temic diseases. p
The authors report no potential conflict of interest relevant to this article. Queries
about this article can be sent to Swati Sharma at drswatinagpal@gmail.com.
60 AUGUST/SEPTEMBER 2015 The New York State Dental Journal
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Dr. Mishra Dr. Swati Sharma Dr. Alok Sharma
M.B. Mishra, M.D.S., is professor and head of the Department of Periodontics at Mahatma Gandhi
Dental College & Hospital, Jaipur, Rajasthan, India.
Swati Sharma, M.D.S., is senior lecturer, Department of Periodontics, Mahatma Gandhi Dental
College & Hospital, Jaipur, Rajasthan, India.
Alok Sharma, M.D.S., is associate professor, Jaipur Dental College, Jaipur, Rajasthan, India.