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INTERNATIONAL JOURNAL OF
INNOVATIONS IN DENTAL SCIENCES
DECEMBER 2016 / VOL 1 / ISSUE 1
General Information
The Journal, INTERNATIONAL JOURNAL OF INNOVATIONS IN DENTAL SCIENCES,
will target the Dental Academicians and Clinicians and will provide them a platform to improve
their knowledge and practice. This Journal will pave the way for Dentists throughout the world
to share their clinical experiences and scientific knowledge. The subjects to be covered in this
journal includes ALL THE BRANCHES OF DENTISTRY AND RELATED SUBJECTS. This
Journal presents the comprehensive aspects of Dentistry, organized to coincide with topics of
recent advancement and Research, as objective. It offers strong theory and concepts, as well as
highly instructive clinical practice applications.
Intended readership of the Journal includes, Research scholars in Dentistry, Under graduates &
Post Graduates students of Dentistry. This Journal will be made available online, throughout the
world. This will attract the readers and authors to publish their works. Articles about
interrelationships between oral and systemic health and advanced technologies and techniques
such as oral, plastic and reconstructive surgery, and dental implant surgery are also welcomed in
addition to the articles from other branches of Dentistry and other related fields.
As it targets the Academicians in the field of Dentistry (and related fields), it will be soon
subscribed by the libraries of renowned Dental institutions. The journal will be peer-reviewed by
double blind peer-review method. The articles submitted will be sent to the reviewers for their
genuine opinion and feedback about the article. Reviews, case reports, original research,
newsletters and different opinions and updates in the field of Dentistry are welcome for
publication.
Editor in Chief
Dr. Prabhu Manickam Natarajan, BDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), MDS,
PhD (Periodontics),
College of Dentistry, Gulf Medical University, United Arab Emirates.
Mobile: + 971 56 213 4322 Email ID: [email protected]
For Submissions: Send your article to [email protected]
Cover page
Contribution
Dr. V. Gopinath, MDS (Periododontics) M.B.A., FCIP.
No.18/3, Thirumalai Raja Street, Ayanavaram, Chennai – 600 023.
Email id – [email protected]
Phone no. – +919840180899, +919425294377.
INTERNATIONAL JOURNAL OF
INNOVATIONS IN DENTAL SCIENCES
EDITORIAL BOARD
EDITOR IN CHIEF
Dr. Prabhu Manickam Natarajan, BDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), MDS, PhD
(Periodontics), College of Dentistry, Gulf Medical University, United Arab Emirates.
ASSOCIATE EDITOR
Dr. S. Bhuminathan, BDS, MFDS RCPS (Glasgow), MDS, PhD (Prosthodontics), Registrar,
Bharath University, India.
JOINT EDITOR
DR. Venkatesh Jayaraman, BDS, MDS, MBA (Hospital Management), Annamalai University, India.
EDITORIAL BOARD MEMBERS
Dr. Mohamed Said Hamed, PhD, UAE.
Dr. Haifa Hannawi, PhD, UAE.
Dr. Sura Ali Ahmed Ali, PhD, UAE.
Dr. Hossam Eid Abdelmagyd, DDSc, Egypt.
Dr. J.Sabarinathan, MFDS RCPSG, MDS, Malaysia.
Dr. Goran Tosic, PhD, Greece.
Dr. Dusan Surdilovic, PhD, Serbia.
Dr. Walid Elsayed, PhD, Egypt.
Dr. Ahmed Atif Shon, PhD, Egypt.
Dr. Hoda Gaffar, PhD, Saudi Arabia.
Dr. Ravichandran, MDS, UAE.
Dr. Riaz Ahmed, MDS, Doha.
Dr. Sivaram, MDS, MFDS RCPS, M Ortho, Muscat.
Dr. Mohammad Elyasi, DMD, Iran.
Dr. Talal Attasi, DMD, Germany.
Dr. Omar Barakat, DMD, New Zealand.
Dr. Jayantha Padmanabhan, MDS, India.
Dr. Chitraa R Chandran, MDS, India.
Dr. Krishnan, MDS, India.
Dr. Rajasekar, MDS, India.
Dr. V.Bhaskar, MDS, India.
Dr. Sugumaran, MDS, India.
Dr. Srinivas Rao, MDS, India.
Dr. Kurinji Kumaran, MDS, PhD, India.
Dr. Sivakumar Palanivelu, MDS, India.
Dr. Lakshmisree, MDS, India.
Dr. Julius, PhD, India.
Dr. Gnana Shanmugham, MDS, India.
Dr. Aravindha Babu, MDS, India.
Dr. Sreedevi Kannan, MDS, India.
Dr. Bhuvana Birla, MDS, India.
Dr. Mahalakshmi, PhD, India.
Dr. Balaguhan, MDS, FCFS,FIBOMS, MBA (Hospital Management), India.
Dr. Rajaraman, MDS, India.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
i
INTERNATIONAL JOURNAL OF
INNOVATIONS IN DENTAL SCIENCES
SECTION EDITORS
ORTHODONTICS
Dr. M.S.Kannan, MDS,
HOD, Department of Orthodontics, SBDCH, India.
ORAL AND MAXILLOFACIAL SURGERY & IMPLANT DENTISTRY
Dr. Kamaraj, MDS, MFDS RCPS Glasgow, MFGDP RCS Eng,
HOD, Department of Oral& Maxillofacial Surgery, PIDC, Malaysia.
ORAL MEDICINE AND RADIOLOGY
Dr. Sicher Ram Shetty, MDS, PhD,
GMU, UAE.
PERIODONTICS
Dr. Gopinath Vivekanandan, MDS, MBA.
HOD, Department of Periodontology, CDCRI, Rajnandgaon, India.
CONSERVATIVE DENTISTRY AND ENDODONTICS
Dr. Syed M. Ali, MDS,
American Mission Hospital, Bahrain.
PROSTHODONTICS
Dr. Karthi Kumar Murari, MDS,
HOD, Department of Prosthodontics, IBN SINA Hospital, UAE.
PEDODONTICS & PREVENTIVE DENTISTRY
Dr. R. Veerakumar, MDS,
HOD, Department of Pedodontics, PDC, India.
ORAL AND MAXILLOFACIAL PATHOLOGY
Dr. Ajay Telang, MDS,
HOD, Department of Oral & Maxillofacial Pathology, PIDC, Malaysia.
GENERAL DENTISTRY
Dr. Annapoorna Sivaram, BDS, MSc, MPDC (RCS Ed),
Muscat.
Dr. Huei Yinn, BDS,
Pahang, Malaysia.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
ii
INTERNATIONAL JOURNAL OF
INNOVATIONS IN DENTAL SCIENCES
Vol.1, Issue.1, Dec 2016
CONTENTS
Sl.
Title and Authors
No
Editorial
1
1
Analgesics Used In Periodontal Surgery
Dr. Prabhu MN
2
2
Tooth Brush Injury: A Case Report
Veerakumar.R, Pavithra.J, Rohini.M, Suganya.M
10
3
Erythema Multiforme Major:
Case Report & Review of Literature
Dr. R. S. Sathawane, Dr. Samiksha Tripathi, Dr. Abhijeet Deoghare
13
4
Prevalence of Aggressive Periodontitis and its
Associated Systemic Manifestations in Moradabad,
India - A Cross-Sectional Survey
Karthik Krishna. M, Keerti Sharma , Lumbini Pathivada
19
5
Osteoporosis and Periodontal Disease - A Review
V.Gopinath, M.N.Prabhu, Hema Suryawanshi
27
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
iii
INTERNATIONAL JOURNAL OF
INNOVATIONS IN DENTAL SCIENCES
EDITORIAL
Dear Readers and Authors of the Journal,
I am pleased to welcome you to International Journal of Innovations in Dental Sciences.
This is a fully open access, internationally peer-reviewed Journal with emphasis on the
publication of high-quality practical and clinical research in all areas of Dentistry.
During the last two decades, the research activity in the field of Dentistry has increased
tremendously. More and more Clinicians and Researchers worldwide are developing
newer systems and devices, or studying natural pattern of changes, happening in
Dentistry.
The purpose of this Journal is to offer a multi-disciplinary analysis and updates of issues
happening in the international arena of Dentistry. The Journal will strive to combine
academic excellence with professional relevance and a strong focus on Clinical
Research. My aim is to encourage an inter-disciplinary dialogue with and between our
authors and readers; that requires intelligibility across the borders of the authors’
specialties. The intellectual appeal of Dentistry has linked numerous fields from various
disciplines, an interdisciplinary phenomenon which I have tried to capture in this
Journal.
The entire editorial team will remain devoted to focusing on improving further the
quality of the Journal and to raise its standards.
I hope you will join me and will continue to support the Journal as readers, reviewers,
contributors, and promoters and share the excitement regarding this novel approach
and find the Journal, a useful new tool for your progress and development.
Regards
Dr. Prabhu Manickam Natarajan.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
1
Prabhu . MN : Analgesics used in Periodontal Surgery
ANALGESICS USED IN PERIODONTAL SURGERY
[
Dr. Prabhu MN,
College of Dentistry, Gulf Medical University, United Arab Emirates
Address For Correspondence
Dr. Prabhu, MDS, MFDS RCPS (Glasgow), MFGDP RCS (Eng), Ph.D (Periodontics)
College of Dentistry, Gulf Medical University, United Arab Emirates
Email id – [email protected]
Phone no. – +971562134322
A B S T R A C T
Periodontal surgical procedures commonly require the support of the analgesics as part of home care
management. There are a wide range of analgesics which are available for management of the postoperative pain following a periodontal surgery. Acetaminophen, nonsteroidal anti-inflammatory drugs and
opioids are the commonly used analgesics in Dentistry. They have specific advantages, disadvantages,
indications and contraindications. This article provides a brief review of their role in the management of
postoperative pain following a Periodontal surgery.
KEY WORDS: analgesics, post-operative pain, periodontal surgery, pain control, therapeutic dose.
INTRODUCTION
The first considerations in pain control are to
prevent discomfort by proper local
procedures and to eliminate the cause of pain
already present. Analgesic drugs are only
secondary to these efforts.
The selection of an analgesic for any
particular case is essentially a matter of
matching the potency of an analgesic against
the severity of the pain present or
anticipated. This rather simplistic concept
becomes complicated when you consider the
importance of the emotions on pain and pain
control. Numerous analgesics are available,
and the recent introduction of new agents
provides even more options from which
to choose1 One must never lose sight of the
fact that the psychologic makeup of a patient
is an extremely important factor in the
selection of the proper analgesic. Healthy
patients have approximately the same
capacity to perceive pain, but their reaction
to what they perceive may vary widely.
Discomfort that requires no analgesic in one
patient may require aspirin or acetaminophen
in another and even codeine, meperidine, or
morphine in others. Thus knowing one’s
patients is of considerable value.
Predisposition toward a greater reaction to
pain has been said to be associated with
emotional instability, fatigue, youth, the
female sex, fear, and apprehension
(Monheim, 1969). Fear and apprehension are
of particular significance and are the basis of
the potentiation of analgesics by sedatives.
A range of analgesic potencies will be
required in alleviating discomfort from
periodontal
infections
and
temporomandibular joint dysfunction as well
as varying degrees of postoperative
discomfort, but proper local treatment
wsill usually allow complete pain control
with mild analgesics such as aspirin or
acetaminophen. Only in extensive cases,
where local treatment is restricted or when
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
the patient is hypersensitive to discomfort,
are more potent analgesics required.
Routine post-operative. discomfort often
requires no analgesic, and when one is
required, aspirin or acetaminophen is
frequently adequate
have been demonstrated, notably those
with the coumarin anticoagulants and the
sulfonylurea hypoglycemics. The clinician
should also recognize the danger of
aspirin overdose in infants and children.
Only in extensive osseous cases, where
there has been heavy trauma, where
wound closure has been inadequate, or
again where the patient is hypersensitive
to discomfort, will more potent agents be
required.5
When aspirin should be avoided,
acetaminophen (Tylenol, Tempra, Nebs)
is an excellent substitute. In the same
dosage as aspirin (650 mg (10 grains)
every 4 hours) this drug equals aspirin in
analgesic and antipyretic potency. At this
time acetaminophen is not believed to
have anti-inflammatory effects. It is not
known whether the absence of this effect
is important in situations with a
significant inflammatory component, as in
most dental cases requiring an analgesic.
Although acetaminophen appears to have
the same drug interactions as noted earlier
for aspirin, it does not have the adverse
gastrointestinal
effects
or
the
antiprothrombin and antiplatelet effects of
aspirin. Acetaminophen should also be
safe in cases of aspirin allergy5.
ASPIRIN
Most pain of periodontal origin can be
effectively controlled by aspirin alone
(650 mg (10 grains) every 4 hours).
Analgesic,
antipyretic,
and
antiinflammatory effects are provided. Many
practitioners are too quick to go to more
potent drugs with greater toxicity and
more troublesome side effects and could
make a greater use of aspirin alone.
However, the clinician should be aware
of the adverse effects of this drug. Aspirin
causes gastric irritation, especially if taken
on an empty stomach, and should be
avoided in people with ulcers or other
gastrointestinal
difficulties.
Many
individuals are allergic to aspirin and
obviously should not be given this drug or
any combination product containing it.
Aspirin is known to prolong prothrombin
time and inhibit platelet function.
However, this is not likely to be clinically
significant in the practice of periodontics
except in patients with peptic ulcer,
hemorrhagic disease, or those on
anticoagulant therapy. The practitioner
should also be aware of the clinically
important aspirin drug interactions that
ACETAMINOPHEN
Acetaminophen is indicated for the
management of mild to moderate pain if
there is a contraindication to an NSAID.
Excessive doses can lead to irreversible
liver damage and thus caution must be
exercised in patients with a history of
liver disease or alcoholism. Long-term
use should be avoided as it may lead to
renal toxicity. For the management of
severe pain acetaminophen is usually
insufficient by itself, although it may be
used in combination with an opioid such
as codeine or oxycodone.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
TABLE - 1 1
a
Drug (Brand name )
Dose
(mg)
Frequency
Daily
maximum
(mg)
Adults
Acetaminophen
500-1000
q4-6h
4,000
325-1000
q4-6h
4,000
Celecoxib (Celebrex)
200
Once/day
Diflunisal (Dolobid)
500
q12h
1,500
Acetylsalicylic
(Aspirin)
acid
400
Etodolac (Ultradol)
200-400
q6-8h
1,200
Floctafenine (Idarac)
200-400
q6-8h
1,200
Flurbiprofen
(Ansaid)
50
q4-6h
300
Ibuprofen (Orudis)
400
q4-6h
2,400
Ketoprofen (Orudis)
25-50
q6-8h
300
Ketorolac (Toradol)
10
q4-6h
40 (5 days
max)
Naproxen (Anaprox,
Naprosyn)
275/250
q6-8h
1,375
Rofecoxib (Vioxx)
50
Once/day
50 (5 days
max.)
Acetaminophen
(Tylenol,
Tempra)
Ibuprofen
(Children’s Advil)
1015mg/kg
q4-6h
65 mg/kg
Age 2-12
10 mg/kg
q6-8h
Over age of 12
200400mg
q4h
Children
b
1,200
NSAIDS
NSAIDS have been used as interestingly
as analgesics
not just as anti
inflammatory agents since the mechanism
of action od acetylsalicylic acid was
discovered approximately 30years ago.
Clinical trials have shown repeatedly that
by themselves NSAIDS are effective for
the management of any management of
dental pain, whether mild moderate or
severe.2-5
Optimal use of these drugs reside in
understanding their mechanism of action
on arachidinic acid cascade. NSAIDS
block the cyclooxygenase enzymes which
exist in 2 forms known as cyclooxygenase
1(cox-1) cyclooxygenease 2(cox-2).cox-1
is responsible for synthesis of several
mediators including the prostaglandins
that protect the gastric mucosa and that
regulate the renal blood flow, and
thromboxanes that initiate platelet
aggregation.
Analgesic
and
antiinflammatory actions are their main
properties .these actions combined with
their inhibition of uterine contraction
make th3m effective for the management
of menstrual pain.
Dosing regimens for the NSAIDS tested
in a dental pain model is listed in table 1
studies have shown that NSAIDS may be
all that is required to manage any level of
post operative pain.2,3,4 It has been
suggested that NSAIDS can be more
effective analgesics if they are given early
enough and in sufficient doses to prevent
the synthesis of prostaglandins, as
opposed to prescribing them to deal with
the pain once prostaglandins have been
already formed .Therefore one should
consider an initial loading dose such as
the double maintenance dose which will
allow therapeutic levels to be reached
more
rapidly.
post
operative
administration of NSAIDS may reduce
the need for analgesics postoperatively.
Consideration canthus be give to either
preoperative dosing or atleast to
beginning the dosing immediately after
surgery, before the offset of local
anaesthesia.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
IBUPROFEN
Commercial Products :
Motrin, Advil, Nuprin Structure
2-p-isobutylphenyl proprionic acid
Mode of Action
Non-steriodal anti-inflammatory agent
which reduces prostaglandin activity by
inhibiting prostatalgin synthetase. Has
anti-inflammatory, analgesic, and some
antipyretic activity.
Periodontal Indications
Control of postsurgical pain. Peak blood
levels obtained within one to two hours,
stays active as an analgesic for four to six
hours. Prolonged use has been shown to
cause a small reduction in bone loss due
to periodontal disease, but further studies
are needed before ibuprofen is used in this
manner.
Precautions Ibuprofen inhibits platelet
aggregation but this effect usually
causes small changes in bleeding time in
normal patients. This is less than that seen
with aspirin. Patients on anticoagulant
therapy or with intrinsic bleeding
disorders can be at risk for hemostatic
problems with the concurrent use of
ibuprofen.
Patients with decreased renal or liver
function, heart failure or under diuretic
therapy can be at risk for liver
dysfunction, renal failure, and fluid
retention while taking Ibuprofen.
Drug Interactions
Anticoagulants-see precautions
Methotrexate – Ibuprofen can enhance the
toxicity of methotrexate. Lithium –
Ibuprofen can increase toxicity of lithium
Diuretics such as furosemide and
thiazides can have less effect tin patient
using Ibuprofen
How Prescribed : Available in USA
without prescription in 200 mg dosage.
Usual prescription is for 400 mg
ibuprofen every four hours to six hours as
needed for control of post surgical pain
for one to five days.
DIFLUNISAL
Commercial Products Dolobid
Structure:2-4-difluoro-4-hydroxy-3biphenyl, carboxylic acid.
Derivative of salicyclic acid similar to
aspirin. Mode of Action Non steroidal
anti-inflammatory agent.
Peripherally acting analgesic with antiinflammatory and some antipyretic
effects. It is a prostaglandin synthesase
inhibitor.
Periodontal Indications
Control of postsurical pain. Peak blood
levels obtained within two to three
hours, and stays active as an analgesic
for eight hours.
Dosage Adults an initial loading dose
of 1000mg diflunisal followed by
recommended for pregnancy or nursing
women.
Side Effects Gastrointestinal problems
like nausea, dyspepsia, heartburn,
vomiting, and abdominal pain can occur
and more severe problems such as gastric
ulceration and bleeding can occur. Sleep
disorder, fatigue, tinnitus and skin
disorder occur infrequently, i.e. less then
1 in 200 with short term use.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
Contraindication History of intolerance to
diflunisal, aspirin or other non- steroidal
anti-inflammatory drugs.
Precautions Diflunisal inhibits platelet
aggregation but has less effect than aspirin
and has minimal effects in short term use,
ie., less than 7 days. Patients on
anticoagulant therapy or with intrinsic
bleeding disorders can be at risk for
hemostatic
problems
with
the
concurrent use of diflunisal. Patient
with decreased renal or liver functions,
heart failure or under diuretic therapy can
be at risk for liver dysfunction , renal
failure and fluid retention while taking
diflunisal. Patients using beta blockers or
ACE inhibitors can have complications if
NSAIDS are used that can result in
increased blood pressure.
Drug Interactions
How Prescribed. An initial loading dose
of 1000 mg followed by 500 mg
Coumarin type anticoagulants see
precautions every 8 to 12 hours as needed
for control of postsurgical pain for one to
five days
NAPROXEN
Commercial Products
Naprosyn, Alleve, Anaprox
Structure: 5-6 methoxy-d-methyl
2-naphthaleneacetic acid, methoxy
Mode of Action
Non-steroidal anti-inflammatory agent
which reduces prostaglandin activity.
Has anti-inflammatory analgestic and
some antipyretic activity.
Periodontal Indications
Dosage
Adults 500 mg naproxen followed by
250 mg every 6 to 8 hours. Do not
exceed 1250 mg per day. Not
recommended for pregnant or nursing
women.
Side Effects Gastrointestinal problems
like constipation, heartburn pain, nausea,
dyspepsia and diarrhea. Severe problems
like gastric ulceration and bleeding are
present in 1 to 4 per cent of patients
using naproxen for prolonged periods
up to one year. Short term use does not
cause changes in blood coagulation.
Changes in vision, hearing disorders
and vertigo have also bee reported with
Naproxen.
Contraindication
History of allergic
reactions to naproxen other non- steroidal
anti-inflammatory drug and aspirin.
Naproxen inhibits platelet aggregation
but this effect.
Control of postsurgical pain. Peak blood
levels obtained in two to four hours,
stays active as an analgesic for six to
eight hours usually causes small changes
in bleeding time in normal patients. This
is less than that seen with aspirin. Patients
on anticoagulant therapy or with intrinsic
bleeding disorders can be at risk for
hemostatic problems with the concurrent
use of ibuprofen Precautions.
Patients with decreased renal or liver
function, heart failure or under diuretic
therapy can be at risk for liver
dysfunction renal failure, and fluid
retention while taking Naproxen.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
Drug Interactions
How Prescribed Available in USA
without prescription. Usual prescription is
500 mg followed by 250 mg every 6 to 8
hours as needed for control of post
surgical pain for one to five day
Opioids
Opioid analgesics may be used to
manage dental pain. They should be
considered if acetaminophen or an NSAID
alone will not be sufficient.
Patients using beta blockers or ACE
inhibitors can have complications if
NSAIDS are used that can result in
increased blood pressure.
Effects of opioids
Analgesia is the primary action of
opioids, affecting both
the pain
threshold and pain reaction. Although
high doses can be very effective for the
relief of severe pain, opioids are most
often accompanied by unacceptable side
effects. Prescribing opioids for dental pain
should be considered only in combination
with an NSAID or acetaminophen. Opioids
can be prescribed alone if the patient
already has a prescription for an NSAID or
is taking acetaminophen appropriately. If
an opioid is necessary, codeine should be
the first to consider. Formulations
combining acetaminophen or ASA with
codeine are available
and popular
because of ease of administration. If
codeine is insufficient, the next opioid to
consider is oxycodone. This drug is
most commonly available with either
ASA or acetaminophen1,7.
Use of analgesics in pregnancy and
lactation 8
Optimal management of dental pain
during pregnancy is removal of the source
of pain using local anesthesia. If, however,
postoperative pain is present, an analgesic
may be necessary and should be made
available. Acetaminophen is clearly the
analgesic of choice in all stages of
pregnancy. T he use of NSAIDS is less
favorable, particularly late in pregnancy.
NSAIDS may predispose to ineffective
contractions during labour, increased
bleeding during delivery or premature
closure of
the ductus arteriosus of
the heart. NSAIDS are therefore
contraindicated in the third trimester.
If acetaminophen is insufficient, opioids
are considered
acceptable during
pregnancy provided they are given for a
short duration. Chronic opioid use can
result in fetal dependence, premature
delivery and growth retardation1,8.
As with pregnancy, acetaminophen is the
analgesic of choice in lactation. ASA and
diflunisal may increase bleeding and
should be avoided if possible. Opioids are
considered safe in lactation.
General Guidelines for
Use 1 ,6
Analgesic
Eliminate the source of pain, if at
all possible and Individualize regimens
based on pain severity and medical
history. Always it should be noted that
the dose of
nonopioid should be
increased before adding an opioid and
Optimize dose and frequency before
switching. With regards to NSAIDS,
consideration should be given to
Preoperative and Loading dose. Care
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
should be taken to avoid chronic
use of any analgesic
whenever
possible and reduce the dose and
duration of any NSAID or opioid in the
elderly, always. Overall prescribing
recommendations.1 A protocol, or
algorithm, for analgesic use is presented
below.
IF MILD TO MODERATE
POSTOPERATIVE PAIN IS EXPECTED
ACETAMIN OPHEN
IF 1,000 MG OF ACETAMINOPHEN IS
INSUFFICIENT (I.E. FOR MODERATE TO
SERVE PAIN)
IF NO
CONTRAINDIC
IF NSAIDS
CONTRAINDICATE
IF CONCERNS
REGARDING
GASTRIC BLEEDING
OR IF ELDERLY
ADD CODEINE TO
ACETAMINOPHEN
IF MORE
ANALGESIA IS
ADD OXYCODONE WITH
ACETAMINOPHEN
ADD CODEINE TO NSAID,
ACETAMINOPHEN OR
ASA
ADD OXYCODONE WITH
ACETAMINOPHEN OR
ASA
CONCLUSION
Nonsteroidal anti-inflammatory drugs
(NSAIDS) are a chemically heterogenous
group of compounds that have antiinflammatory, analgesic and antipyretic
effects and share common therapeutic
action and toxic effects. The principal
mechanism of action of NSAIDS is the
inhibition of cyclooxygenase ,the enzyme
responsible for the biosynthesis of
prostaglandins.
Patients have variability in their
susceptibility to the analgesic effect of the
various non-steriodal anti-inflammatory
agents and so when these drugs are used it
may be necessary to change to another
agent in this group in order to get
acceptable analgesia. In order to get peak
levels to the analgesic agent at the time
the local analgesia is wearing off, the
appropriate time for the patient to take
these tablets is based on the
pharmacodynamics of each agent.
Acetaminophen and Ipubrufen work best
if given at the end of the surgical
procedures, longer acting agents like
diffunisal may be more effective given
immediately prior to the surgery
The non-steroidal anti-inflammatory
agents and acetaminophen have very few
side
effects
or
contraindication,
particularly when used for short periods of
time as suggested after Periodontal
surgery. The adverse effects of these
agents have one-half to one-tenth the
frequency reported for long term
utilization.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Prabhu . MN : Analgesics used in Periodontal Surgery
Analgesics are a second –best means of
managing pain; the nest means is to
remove the source as quickly as possible
.we have numerous analgesics at our
disposal. Our goal should be use these
drugs optimally to treat pain most
effectively.
REFERENCES
7. Haas DA. Opioid agonists and
antagonists. In: Dionne RA, Phero
JC, Becker DE, editors. Pain and
anxiety
control
in
dentistry.
Philadelphia: W.B. Saunders; 2002.
p. 114-28.
8. Haas DA, B. Pynn B, Sands T. Drug
use for the pregnant or lactating
patient. Gen Dent 2000; 48(1):54-60
1. Daniel A. Haas. An update on
analgesics for the management of acute
postoperative dental pain. J Can Dent
Assoc. 2002; 68(8):476-82.
2. Ahmad N, Grad HA, Haas DA,
Aronson KA, Jokovic A and Locker
D. The efficacy of non-opioid
analgesics for post-operative dental
pain: a meta-analysis. Anesth Prog
1997; 44(4):119-26.
3.
Dionne
RA,
Berthold
CW.
Therapeutic uses of non-steroidal
anti-inflammatory drugs in dentistry.
Crit Rev Oral Biol Med 2001;
12(4):315-30.
4.
Dionne
RA,
Gordon
SM.
Nonsteroidal anti-inflammatory drugs
for acute pain control. Dent Clin
North Am 1994; 38(4):645-67.
5. Hersh EV, Moore PA, Ross GL.
Over-the-counter
analgesics
and
antipyretics: a critical assessment.
Clin Ther 2000; 22(5):500-48.
6. Haas DA. Drugs in dentistry. In,
Compendium
of Pharmaceuticals
and Specialties (CPS). 31st ed.
Toronto (ON): Webcom Limited;
2002. p. L26-L29.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
9
Veera Kumar et. al : Tooth Brush Injury
TOOTH BRUSH INJURY: A CASE REPORT
Veerakumar.R1 Pavithra.J2 Rohini.M2 Suganya.M2
PRIYADARSHINI DENTAL COLLEGE AND HOSPITAL,THIRUVALLUR.
1.
Professor, Head of the Department, Department of Pedodontics and Preventive Dentistry
Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India
2.
Senior Lecturer Department of Pedodontics and Preventive Dentistry
Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India
Address For Correspondence
Dr. R. Veerakumar, MDS
Professor and Head, Department of Pedodontics and Preventive Dentistry
Priyadarshini Dental College and Research Institute, Thiruvallur (T.N.), India
Email id – [email protected]
ABSTRACT :
Toothbrush is used as an aid for cleaning and maintaining the oral hygiene over centuries. But improper usage
of tooth brushes can cause significant damage to the oral cavity. Especially, this occurs in young children who
tend to play with their toothbrushes. This article describes about the toothbrush injury while brushing the teeth
vigorously. Diagnosis and management of such traumatic injury is illustrated in this article.
Key words: Tooth brush, Injury, Trauma, Soft palate
INTRODUCTION:
Tooth brush plays a major role in
prevention and maintenance of oral health.
Dentists recommend usage of toothbrush as
a cleaning aid. Usage of tooth brush has
reduced incidence of dental caries and
periodontal problems. However, improper
usage of toothbrush results in damage to
tooth structure as well as the oral tissues
especially in children.
This paper describes a toothbrush injury
to soft tissue over the soft palate due to
vigorous brushing which needed surgical
intervention to achieve wound closure.
CASE REPORT:
A young girl of age 12 years , accidentally
injured while brushing her teeth vigorously
which resulted in laceration of soft palate.
The child was reported to the Emergency
medicine department evaluated by our oral
medicine and radiology staff and referred
to our department of Pedodontics.
The child was cooperative with little
distress. The vital signs were normal.
There was no active bleeding but the site
was tender. Oral mucosa was peeled
exposing the underlying connective tissue
medial
to
the
pterygomandibular
raphae[Fig-1].
Initially, the wound was evaluated and it
was irrigated with copious amount of saline
and was sutured with 3.0 nylon sutures
under Local anaesthesia [Fig-2] [Fig- 3].
The patient was discharged on the same
day and was prescribed oral antibiotics and
analgesics. One week later wound had
healed
well
without
postoperative
complications [Fig-4].
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Veera Kumar et. al : Tooth Brush Injury
Fig- 4 Post-operative photograph showing
healed site
[Fig-1] Photograph showing traumatic tooth
brush injury to soft palate.
DISCUSSION:
Although toothbrush is essential for
maintaining oral hygiene, their improper
usage can lead to various complaints from
simple ulcers to serious life threatening
injuries. Impaled toothbrush traumas are
mostly caused while playing with
toothbrush in mouth1. Such trauma may
lead to injuries. Oro-pharyngeal trauma
due to tooth brush can lead to pharyngeal
abscess, carotid artery thrombosis,
mediastinitis or death2,4,7.
Fig- 2 Photograph showing wound closure
Fig-3 Photograph showing sutures over the
wound
Ebenezer et al1 described a case where a
child fell while playing with his sibling
with toothbrush
in
his
mouth.
Toothbrush is impaled deeply into the
buccal
mucosa reaching the masseter
muscle. The toothbrush was surgically
removed and healing occurred without
complications. Rodkowaski et al3 described
a survey on traumatic injuries to oral
cavities. Out of 77 cases, 23 cases were
injuries to soft palate and tonsilar region
with median age of 4 years and average age
of 3 years.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
11
Veera Kumar et. al : Tooth Brush Injury
Sagar et al6 in his study eloborated an
impaled toothbrush into oral cavity due to
fall from bike with toothbrush in his mouth.
Impalement had caused injury to internal
carotid artery which needed immediate
surgical intervention to safe patient’s life.
REFERENCES:
The penetrating injuries can result in
serious complications, all patients who
present with such injuries should be
examined immediately for
2) S.Kumar, R.Gupta, R. Aroraand
S.Saxena: Severe oropharyngeal trauma
caused by toothbrush – case report and
review of 13 cases British dental journal
volume 205 No. 8 OCT 25 2008.
Airway obstruction
Soft tissue injury
Abscess, swelling and discharge.
Neurological alterations
If the injury caused by the brush is
superficial
topical
antibiotics
and
analgesics are to be given. If the tooth
brush has caused lacerating injuries as in
our case debridement and sutures can be
placed. If the tooth brush caused severe
penetrating injury, it should carefully
examined and removal of the same to done
in local or general anaesthesia according
to the severity of impalement. Tetanus
toxoid injection should be given along with
antibiotic and analgesic cover.
CONCLUSION:
Through our case, we would like to deliver
a fact that daily chores such as tooth
brushing can cause injuries to oral cavity.
Thus, children should be under
parental supervision
while brushing
their teeth.
They should be reported to hospital
even if the injury is minor as
complications may arise.
1) Ebenezer J.A, Adhikarid D.B, Mathew
G.C.C, Chacko R. K.: A unusualtooth
brush injury. Journal of Indian Society
of Pedodontics
and
Preventive
Dentistry December 2007.
3) Rodkowski D, Mcgill. J.T, Healy.G.B,
Jones. D.T: Penetrating trauma of
oropharynx in children: Laryngoscope
103, Sep 1993.
4) Moriarty KP, Harris BH, BenitezMarchand
K;
Carotid
artery
thrombosis and stroke after blunt
pharyngeal injury. The Journal of
Trauma [1997, 42(3):541-543].
5) Soose.R.J, Simons.J.P, Mandell.D.L;
Evaluation and Management of
Pediatric Oropharyngeal Trauma Arch
Otolaryngol
Head Neck Surg.
2006;132(4):446-451.
6) Sagar S, Kumar N, Singhal M, Kumar
S, Kumar: A rare case of lifethreatening penetrating oropharyngeal
trauma caused by toothbrush in a
child: Journal of Indian Society of
Pedodontics and Preventive Dentistry
Apr - June 2010, Issue2 ,Vol 28
7) SasakiT, Toriumi S,
Asakage T,
KimitakaKaga, YamaguchiD, Yahagi
N. The Toothbrush: A Rare but
Potentially Life-Threatening Cause of
Penetrating Oropharyngeal Trauma in
Children. American Academy of
Paediatrics May 2004.
8) Law RC, Fouque CA, Waddell A,
Cusick: Penetrating intra-oral trauma
in children. BMJ 1997;314:50-1
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
12
Sathawane et. al : Erythema Multiforme Major : Case Report and Review
ERYTHEMA MULTIFORME MAJOR: CASE REPORT AND
REVIEW OF LITERATURE
Dr. R. S. SATHAWANE1,
Dr. SAMIKSHA TRIPATHI2, Dr. ABHIJEET DEOGHARE3
1.
PROFESSOR, HEAD OF DEPARTMENT, Department of Oral Medicine and Radiology
2.
POST GRADUATE STUDENT, Department of Oral Medicine and Radiology
3.
READER, Department of Oral Medicine and Radiology
CHHATTISGARH DENTAL COLLEGE AND RESEARCH INSTITUTE, RAJNANDGAON (C.G.), INDIA.
ADDRESS FOR CORRESPONDENCE
Dr. Samiksha Tripathi, D/o Chandra Kant Tripathi, Manager, Ultratech Cement, QTR No.- 3064, Grasim
Vihar, Rawan, Dist - Baloda Bazar, Chhattisgarh. Pincode – 493196.
Email id – [email protected]
Phone no. – +919009904195, +919826725406
ABSTRACT
Erythema multiforme is an acute mucocutaneous disorder that occurs with varying degrees of blistering and
ulceration. We report a case of major erythema multiforme managed with systemic steroids. A 45-year-old male had
cutaneous target lesions and ulcerative lesions throughout the oral cavity and lips, which had been diagnosed as
erythema multiforme major. This episode was related to neither drug intake nor herpetic infection, which suggests
that the erythema multiforme was of idiopathic origin. This hypothesis was supported by negative serology for
herpes simplex virus. Excisional biopsy of an intact bulla was performed and the diagnosis was confirmed as
erythema multiforme major. The patient was treated with Prednisolone in a tapering dose for 2 months to control and
completely cure the disease.
Key-words: Erythema multiforme, Immune disorder, Target lesion.
INTRODUCTION
Erythema multiforme (EM) is a rare, acute
immune-mediated mucocutaneous disorder, a
widespread hypersensitivity reaction, caused by
the appearance of cytotoxic T lymphocytes in the
epithelium that induce apoptosis in keratinocytes,
leading to satellite cell necrosis.1 Despite being
frequently caused by, or at least associated with,
infection or drug therapy, the pathogenic
mechanism of EM stays vague, and as a result
there are no evidence-based, reliably effective
therapies. Oral manifestations may occur
independently or precede cutaneous involvement.2
The present article discusses a case of 45-year old
male who was clinically and histopathologically
diagnosed as erythema multiforme and reviews
aspects of EM as relevance to dental practice.
CASE HISTORY
A 45-year old male patient presented to the
outpatient department of our institute with
complains of painful oral ulceration and
hemorrhagic crusts on the lips. History revealed
that complaints started around 2 months back.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Sathawane et. al : Erythema Multiforme Major : Case Report and Review
Initially there was erythema in the oral cavity and
over lips, due to which patient experienced
burning and pain during mastication. Pain was
gradual in onset, moderate to severe in intensity,
continuous in duration, aching type. There was
no history of referred/radiating pain. Soon
vesicles and ulcers appeared at these sites.
Vesicles first appeared on lips, buccal mucosa
bilaterally, followed by hard palate and then onto
tongue and upper and lower labial mucosa.
Vesicles ruptured to form encrustations over lips.
History of itching and burning sensation present
in the perioral region. Also history of dysphonia,
odynophagia and dysarthria was present. No
history of any concomitant symptoms associated
with pain nor febrile episode was present. There
was no history of any drug intake before the onset
of these lesions. History of similar lesions starting
primarily in the hands, legs & then moving
centripetally toward the trunk, neck, inguinal,
genital area and on external nares and near inner
canthus of right eye 1 ½ months back. No history
of previous episodes of ulcerations elsewhere in
the body. Patient went to a private medical
practitioner, got medicated and was referred to the
college for further needful treatment.
On clinical examination, dark brown and red
colored encrustations were present on lips. Lips
were edematous and erythema was present around
encrustations (Fig. 1). Bleeding ulcers and
localized areas of erythema were present on hard
palate, buccal mucosa, tongue and gingivae (Fig.
2). None of the lymph nodes were palpable.
Diagnostically significant finding was the
presence of multiple target lesions on the trunk
(Fig. 3). Nikolsky's sign was negative. Other
systemic examination was normal. Clinically,
diagnosis of erythema multiforme was made.
Routine hematological investigations were within
normal range.
Biopsy from the lesion on
histopathological examination (H&E and PAS
stain) revealed intercellular edema, sub-basilar
separation of epithelium from underlying
connective tissue along with degeneration of basal
cells at few places and connective tissue showing
numerous bundles of collagen fibres, fibroblast,
muscle tissue and blood vessels surrounded by
dense chronic inflammatory cells (Fig. 4).
Oral prednisolone at the dose of 20 mg twice daily
was started along with local application of potent
steroid - Clobetasol ointment thrice daily. Also
oral supplementations were prescribed, to improve
the overall condition of the patient. Within 15
days, there was decrease in the severity of the
mucosal and skin lesions and prednisolone was
tapered over next 15 days and stopped after further
tapering till all lesions healed. Mouthwashes
consisting of local anesthetics and antiseptics
were added for symptomatic treatment.
Complete hematological investigations were
routinely done during the course of treatment
which were within normal limits.
In addition, no oral or skin lesions developed
during the 2 months of treatment, the patient is
still under follow-up and the disease is currently
under control (Fig. 5).
DISCUSSION
Erythema multiforme (EM) is an acute,
usually
self-limiting,
immune-mediated,
blistering, ulcerative condition affecting the skin
and/or mucous membranes, including the oral
cavity.2,3,4 EM has been classified into a
number of variants, mainly minor and major forms
(Table 1).2,3.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Sathawane et. al : Erythema Multiforme Major : Case Report and Review
Type of
Erythema
multiforme
EM Minor
(EMm)
EM Major
(EMM)
Characteristic features
Skin lesions
·
Involves less than 10% of
the body surface area
Mucosal lesions
·
Uncommon
·
Most commonly oral
mucosa
·
Ocasionally EMm that
only affects the oral
mucosa may arise
Skin lesions
·
Involves less than 10% of
the body surface area but
more severe than EMm
Mucosal lesions
·
Involves two or more
mucous membranes with
more
variable
skin
involvement. Oral lesions
are usually widespread and
severe
`
Once in a while it may be associated with
prodromal symptoms, which typically occur 7 to
14 days before development of cutaneous lesion.
The classic skin lesion of EM is a target or iris
lesion or bull’s eye distributed symmetrically on
the extremities and trunk and characterized by
concentric erythematous rings separated by rings
of near normal color with lesion size ranging from
2 to 20 mm with central area of necrosis or
crusting. Less commonly macules, papules or
plaques are manifested. Complete recovery from
an EM attack typically occurs within 1 to 4
weeks, with transient hypo/hyperpigmentation. 3,6
Oral mucosal lesions occur in more than 70% of
EM cases. 3 The lesions show considerable
variability in the appearance, ranging from diffuse
oral erythema, to multifocal superficial
ulcerations, thus the term multiforme. Initially,
vesicles or bullae may be present, which rupture
causing hemorrhagic crustations. Any area of the
mouth may be involved, with buccal mucosa,
palate, and tongue being most frequently affected.
In most cases, lip lesions show hemorrhagic
crustations. There may be mild to severe oral and
perioral pain that may interfere with functional
activities like speech, eating, swallowing and fluid
intake, debilitating the health of the patient.
Intraoral and perioral lesions heal without
EM arises as a result of immune-complex
mechanisms involving antigen-antibody reactions
that target small blood vessels in the skin or
mucosa. In approximately, 90% of cases, the
precipitating event relates to infection, with the
herpes simplex virus (HSV) playing a
The diagnosis of EM is chiefly based on the
history
and
clinical
presentation,
as
histopathologic
features
and
laboratory
predominant role in 70% to 80% of cases.5 Other
triggering factors may include medications,
especially sulfonamides, NSAIDS, penicillins, and
investigations are nonspecific. 2,3,4
anticonvulsants. 3
Corticosteroids are the most commonly used
drugs in the management of EM, regardless of
lack of evidence2 EMm may respond to topical
corticosteroids. Patients with EMM ought to be
scarring.6
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Sathawane et. al : Erythema Multiforme Major : Case Report and Review
treated
with
systemic
corticosteroids
(prednisolone 0.5–1.0 mg/kg/day tapered over 7–
10 days) or azathioprine, or both or other
immunomodulatory
medications
such
as
cyclophosphamide, dapsone,
cyclosporine,
levamisole,
thalidomide
or
interferon-a. 7
Cyclosporine given intermittently may control
recurrent EM.8
.
Fig. 1: Ulcers and hemorrhagic crusts on the
lower lip during the first episode of EM
Fig. 2: Bleeding ulcers and localized areas of
erythema on buccal mucosa, hard palate,
gingivae and tongue
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Sathawane et. al : Erythema Multiforme Major : Case Report and Review
Fig. 3: Characteristic target lesions seen
on the trunk, back, extremities
Fig. 4: Microphotograph (H&E, 10x) showing
histopathological features suggestive of EM
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Sathawane et. al : Erythema Multiforme Major : Case Report and Review
4. Osterne, Brito, Pacheco et al. Management of
Erythema Multiforme Associated with
Recurrent Herpes Infection: A Case Report.
www.cda-adc.ca/jcda • October 2009, Vol.
75, No. 8.
5.
Fig. 5: Intra-oral and Extra-oral post steroid
therapy photographs of the patient, showing
almost completely healed lesions
ACKNOWLEDGEMENT
We acknowledge the help and guidance from Dr.
Shivmurthy, Professor and Head, Department of
Oral and Maxillofacial Surgery and Dr. Gandhi,
Head of Department of General Surgery,
Chhattisgarh Dental College and Research
Institute, Rajnandgaon (C.G.).
REFERENCES
1. Siegel MA, Balciunas BA. Oral presentation
and management of
vesiculobullous
disorders. Semin Dermatol 1994; 13:78–86.
2. Parvinderjit S. Kohli, Jasbir Kaur. Erythema
Multiforme-Oral Variant: Case Report and
Review of Literature. Indian J Otolaryngol
Head Neck Surg 2011 63(Suppl 1):S9–S12;
DOI 10.1007/s12070-011-0169.
Watanabe R, Watanab H, Sotozono C, et al.
Clinical factors differentiating erythema
multiforme majus from Stevens-Johnson
syndrome (SJS)/toxic epidermal necrolysis
(TEN). Eur J Dermatol 2011; 21(6):889-94.
6. Williams PM, Conklin RJ. Erythema
multiforme: a review and contrast from
Stevens- Johnson syndrome/toxic epidermal
necrolysis. Dent Clin North Am 2005;
49(1):67-76.
7. Stewart MG, Duncan III NO, Franklin DJ
et al. Head and neck manifestations of
erythema multiforme in children. Otolaryngol
Head Neck Surg 1994; 111:236–242.
8. Schofield JK, Tatnall FM, Leigh IM. Recurrent
erythema multiforme: clinical features and
treatment in a large series of patients. Br J
Dermatol 1993; 128:542–545.
3. Samim Firoozeh, Zed Christopher, Williams
Michele P.Erythema multiforme-A review of
Epidemiology,
Pathogenesis,
Clinical
Features, and Treatment. Dent Clin N Am 57
(2013) 583-596.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
18
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
PREVALENCE OF AGGRESSIVE PERIODONTITIS AND ITS
ASSOCIATED SYSTEMIC MANIFESTATIONS IN MORADABAD,
INDIA – A CROSS –SECTIONAL SURVEY
Karthik Krishna M1, Keerti Sharmab 2, Lumbini Pathivada3
1.
Professor, Department Of Periodontology, Teerthanker Mahaveer Dental College And
Research Centre, Moradabad, Uttar Pradesh, India
2.
Senior Resident, Department Of Periodontology, Teerthanker Mahaveer Dental College And
Research Centre, Moradabad, Uttar Pradesh, India
3.
Assistant Professor, Department Of Paedodontics and Preventive Dentistry, Teerthanker
Mahaveer Dental College And Research Centre, Moradabad, Uttar Pradesh, India
Corresponding author: Karthik Krishna M Phone: +917830104004
Address:
Dept. of Periodontology, Teerthanker Mahaveer Dental College and Research Centre,
Delhi
Road,
Bagadpur,
Moradabad,
U.P.
Pin:
244001
e-mail:
[email protected]
ABSTRACT
Purpose: The aim of the present study was to determine the prevalence of aggressive periodontitis
and its association with systemic and stress conditions in Moradabad district, Uttar Pradesh, India.
Materials and Methods: Study population included 3000 patients (1872 males; 1128 females) with
mean age of 30.99. Detailed case histories were taken, clinical examination and radiographic
evaluation were performed and study population was divided into three groups: gingivitis (GS),
chronic periodontitis (CP) and aggressive periodontitis (AP). Systemic manifestations of fatigue,
weight loss and loss of appetite were assessed and stress was evaluated based on the Hospital anxiety
and depression (HAD) scale according to which subjects were classified as non-case (NC), borderline
case (BC) and positive case (PC).
Results: Forty four patients were diagnosed with aggressive periodontitis (25 = LAP; 19 = GAP).
Within the AP groups, prevalence rates of fatigue were 20% (LAP) and 15.78% (GAP), weight loss
were 4% (LAP) and 10.52% (GAP) and loss of appetite were 8% (LAP) and 15.78% (GAP). Based
on HA scores, percentages of NC, BC and PC in LAP group were 44 %, 28% and 28%, respectively,
whereas in GAP group percentage of both NC and BC was 31.5% and PC was 37%. Based on HD
scores, percentages of NC, BC and PC in LAP group were 68%, 20% and 12% whereas in GAP group
percentage was 57.89% for NC and 21.05% for both BC and PC.
Conclusion: The frequency of systemic manifestations such as fatigue, weight loss and loss of
appetite was significantly greater in aggressive periodontitis. Significant co-relation between
aggressive periodontitis and chronic stress states was observed with greater predilection in GAP
subjects.
Keywords: aggressive periodontitis, stress, anxiety, depression, systemic conditions.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
INTRODUCTION
Periodontitis is a multifactorial disease that
involves infection and inflammation of
supporting periodontal tissues. Over the
years, this condition has been subject to
categorization into multiple forms based on
characteristics
such
as
etiology,
predisposing
factors
and
rate
of
progression.23 Aggressive periodontitis
encompasses rapidly progressive forms of
the disease, characterized by severe
destruction of periodontal ligament and
alveolar bone in otherwise systemically
healthy individuals. Other characteristics
include lack of heavy plaque or calculus
deposits, an early age of onset and familial
pattern of distribution suggestive of a
genetic trait.2, 15, 24, 31, 32
In India, several studies have been
conducted to determine the prevalence of
gingivitis and periodontitis and associated
risk factors.5, 9, 12, 28, 30 A national oral
health survey done in the year 2002-03
revealed prevalence rates of gingivitis and
periodontitis ranging from 41.8% to 92.9%
and from 0.2% to 29.1%, respectively.19
However, most of these studies have not
differentiated between the chronic and
aggressive forms of periodontitis.
One of the factors that can play a
contributory role in the pathogenesis of
periodontal diseases is the psychological
condition of stress. Chronic states of stress
have known to affect the patho-physiology
of disease either primarily by altering the
host immune response or secondarily
through changes in health related behaviour
such as smoking, diet and oral hygiene.7, 8
Several studies have reported an association
of psychological events such as anxiety and
depression with the onset and progression of
chronic forms and, to a lesser extent, with
aggressive forms of periodontitis.3, 11, 13,
14, 18 However till date, data on the
prevalence rates of aggressive periodontitis
and its association with psychological
conditions in Indian populations is lacking.
The aim of this cross-sectional study was to
determine the prevalence of localized and
generalized
forms
of
aggressive
periodontitis and their association with
systemic and psychological factors in
Moradabad district, Uttar Pradesh, India.
MATERIALS AND METHODS
The study utilized a convenience sampling
model for selecting the subjects. The
methodology was reviewed and cleared by
the Ethical Committee of Teerthanker
Mahaveer Dental College and Research
Centre, Moradabad.
Calculation of Sample Size
A pilot study was conducted among 120
subjects in Moradabad district. Based on the
results obtained, the main sample size was
calculated to be 2495. In order to
compensate for any dropouts or patient
refusal, a final sample size of 3000 subjects
was decided upon.
Schedule of the Study
The study was planned over a period of 9
months and a detailed schedule was
prepared well in advance by informing and
obtaining consent from the respective
authorities. The methodology & advantages
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
of performing this study were explained and
informed consent of each participating
subject were obtained. Detailed dental and
medical histories of each subject were
recorded, including presence of any
systemic manifestations such as loss of
appetite, weight loss and fatigue.
The gingival status of study subjects was
assessed by measuring the Gingival Index
(GI) scores. Scoring was recorded for six
permanent teeth in each patient and final GI
value for each patient was calculated. Based
on the clinical and radiographic evaluations,
the study subjects were categorized into the
following groups: gingivitis (G), chronic
periodontitis
(CP)
and
aggressive
periodontitis (AP). Subjects diagnosed
with AP were further categorized into
localized (LAP) and generalized forms
(GAP).
The levels of anxiety and depression were
determined by utilizing the Hospital
Anxiety and Depression (HAD) Scale, a 14point self-report screening scale comprising
of two 7-point sections: one each for anxiety
and depression (table 1). Based on score
obtained a subject can be categorized as a
non-case (NC), borderline case (BC) or case
(C).34
Statistical Analysis
All the study variables were subjected to
statistical analysis using relevant software
(SPSS v.20). The Pearsons Chi-square test
was used to compare between percentages
and the differences in post-hoc test were
used to analyze the differences in socio-
demographic
characteristics,
manifestations and HAD scores.
systemic
RESULTS
This cross- sectional survey included 3000
patients (1872 males and 1128 females). 44
patients were diagnosed with aggressive
periodontitis (25=LAP; 19=GAP). The
number of females with aggressive
periodontitis was significantly higher than
that of males. The 3000 subjects were
divided into four age groups: < 20yrs, 20-30
yrs, 31- 40 yrs and > 40 yrs. The average
age of the study population was 30.99.
Majority of AP subjects were recorded in
the 20-30 yrs age group (table 1).
Table 1: Distribution of study subjects
based on sex and age group variables
Variable
Sex
Age
GS
CP
AP
TOTAL
Male
1091
682
19
1872
Female
600
583
25
1128
<20 Yrs
459
30
8
497
20-30
Yrs
756
232
30
1018
31-40
Yrs
290
402
5
697
>40 Yrs
186
601
1
788
The frequencies of systemic manifestations
of fatigue and weight loss were significantly
greater in AP subjects whereas loss of
appetite was reported more frequently in the
CP group. Within the AP group,
distributions of anorexia and weight loss
were higher in GAP subjects whereas
fatigue was observed to be higher in LAP
subjects. The differences were statistically
significant (table 2).
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
21
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
Table 2: Differential distribution of
systemic manifestations in the study
population
Systemic
Manifestation
GS
CP
LAP
GAP
Fatigue
321
253
5
3
Loss of
Appetite
68
38
2
3
Weight Loss
67
39
1
2
HAD scale scores for both anxiety and
depression were observed to be significantly
higher in AP subjects with highest
distribution of borderline and positive cases
in this group. Negative cases were more
frequently observed in the GS group. Within
the AP group, the distribution of borderline
and positive cases were higher in GAP
subjects. The differences were statistically
significant (table 3).
Table 3: Distribution of study population
based on HAD scale
HAD Scale
Parameters
Anxiety
Depression
`
NC
BC
PC
Mean
(±
SD)
NC
BC
PC
Mean
(±
SD)
CS
CP
LAP
GAP
1100
253
338
6.97
(±
3.3)
1437
186
68
5.72
(±
3.46)
11
7
7
8.08
(±
3.1)
17
5
3
6.64
(±
2.5)
6
6
7
8.84
(±
2.4)
11
4
4
7.31
(±
3.2)
11
7
7
8.08
(±
3.1)
17
5
3
6.64
(±
2.5)
DISCUSSION
This cross-sectional study was to determine
the prevalence of aggressive periodontitis in
Moradabad district its association with
systemic
manifestations
including
psychological states in Moradabad district.
To our knowledge, this is the first survey
conducted to determine the prevalence of
aggressive forms of periodontitis in this
region.
The prevalence of AP was observed to be
higher in females as compared to males, a
finding that is consistent with previous
studies based on prevalence of AP in
diverse populations.4, 10,
17,
22
However, limited studies reported no
significant gender predilection or higher
prevalence in males.6, 20, 27 Within age
groups, highest distribution of AP cases was
observed in the 21-30 years age group,
confirming the fact that AP is usually
manifested earlier in life in susceptible
individuals. Subjects diagnosed with LAP
were
comparatively
higher,
albeit
marginally, as compared to those with GAP.
Previous studies have reported such
marginal difference or a significantly higher
prevalence of LAP cases.4, 10, 16, 26
The variation in prevalence ratios among
sex, age or type of AP in these several
studies may reflect the influence of the
genetic suspectibility of diverse ethnic
groups or the affect of environmental
factors such as socio-economic status and
geographical location. However, studies
determining prevalence ratios of AP in
Indian populations, which would have
provided more relevant data for comparison
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
22
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
with the current study, are unfortunately
lacking.
A sizeable number of subjects in AP group
experienced one or more systemic
symptoms that could not be related to
disease or external factors. A significantly
high number of AP patients had reported
fatigue followed by loss of appetite and
weight loss with higher prevalence of the
latter two conditions when compared with
GS and CP subjects.
A study done
previously in a Jordanian population that
followed a similar methodology for
evaluating systemic manifestations in
aggressive periodontitis subjects, a higher
prevalence of loss of apetitte and depressive
mood was observed in AP cases as
compared to CP and control groups.1
Based on the study results, the systemic
manifestations of fatigue, loss of appetite
and weight loss as well as anxiety and
depression were strongly associated with
aggressive
periodontitis.
Rapidly
progressive periodontitis (RPP) progresses
in phases of activity and quiescence and the
active phase may be associated with
systemic manifestations such as fatigue,
weight loss, and loss of appetite.25 In the
present study, positive cases for anxiety and
depression
were
significantly more
prevalent in AP group and significantly
higher in GAP group as compared to
LAP group. Yet again, these findings
could be correlated with those of the
Jordanian study.
It would be of interest to know how anxiety
and depression states influence periodontal
disease. A probable mechanism is the
deregulation of the immune system,
mediated
primarily
through
the
hypothalamic– pituitary–adrenal (HPA) and
sympathetic–adrenal medullary
axes.
Activation of the HPA axis by stress
initiates a sequence of events, culminating
in the release of glucocorticoids into the
circulation. The glucocorticoids produce
several effects throughout the body,
including suppression of inflammation,
altered cytokine profiles, elevated blood
glucose levels, and altered levels of
certain growth factors.21
Also, activation of the autonomous nervous
system results in release of catecholamines
which in turn stimulate hormonal secretion
of norepinephrine and epinephrine from the
adrenal medulla, resulting in a range of
effects capable of modulating immune
responses. Catecholamines can also
contribute to the development of
hyperglycemia by directly stimulating
glucose production and interfering with the
tissue disposal of glucose. Through these
immunomodulatory and hyperglycaemic
effects, stress can enhance the susceptibility
of periodontal tissues to microbial infection
and breakdown.29, 33.
A situation wherein onset of aggressive
periodontitis precedes the development of
anxiety and depression was also considered
in the present study. This situation may
arise, in part, from the concern of losing
teeth at an early age among individuals with
AP resulting in a chronic state of stress. In
addition, aspects such as employment levels
and socio-economic status may influence
the quality of life and contribute to anxiety
and depression. Unfortunately, these aspects
could not be researched meticulously in this
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
23
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
study and hence their association with
anxiety and depression could not be
evaluated.
5.
Doifode VV, Ambadekar NN,
Lanewar AG. Assessment of oral
health status and its association with
some epidemiological factors in
population of Nagpur, India. Indian J
Med Sci 2000; 54:261-9.
6.
Ereş G, Saribay A, Akkaya M.
Periodontal treatment needs and
prevalence of localized aggressive
periodontitis in a young Turkish
population. J Periodontol. 2009;80
(6):940-4.
7.
Freeman R, Goss S. Stress measures
as predictors of periodontal disease-a
preliminary
communication.
Community Dent Oral Epidemiol
1993: 21: 176–177.
8.
Glaser R, Glaser JK. Stress
damages
immune system
and
health.
Discovery
Med
2005;5(26):Pages 165-169.
9.
Greene JC. Periodontal disease in
India: report of an epidemiogical
study. J Dent Res 1960; 39:302-12.
10.
Hermes CR, Baumhardt SG, Rösing
CK. Occurrence of aggressive
periodontitis
in patients at a dental school in
southern Brazil. Acta Odontol
Latinoam. 2013;26(2):84-8.
11.
Hugoson A, Ljungquist B, Breivik
T. The relationship of some
negative events and psychological
factors to periodontal disease in an
adult Swedish population 50 to 80
years of age. J Clin Periodontol 2002:
29: 247–253.
CONCLUSION
The present study observed a significant
association of systemic manifestations as
well as anxiety and depression with
both localized and generalized forms
of aggressive periodontitis. However, this
study being cross-sectional, the aspect of
these stress events preceeding or succeeding
breakdown of periodontal tissues could not
be further evaluated. Further studies,
preferably longitudinal, are required to
enable us to better understand this
relationship
REFERENCES
1.
Ababneh KT, Taha AH, Abbadi MS,
Karasneh JA, Khader YS. The
association of aggressive and chronic
periodontitis
with
systemic
manifestations and dental anomalies
in a jordanian population: a case
control study. Head Face Med.
2010;29(6):30.
2.
Albandar JM, Brown LJ. Clinical
features of early-onset periodontitis. J
Am Dent Assoc 1997; 128:1393-9.
3.
Aleksejuniene J, Holst D, Eriksen
HM, Gjermo P. Psychosocial
stress, lifestyle and periodontal
health. J Clin Periodontol 2002: 29:
326–335.
4.
Arowojolu MO, Nwokorie CU.
Juvenile periodontitis in
Ibadan,
Nigeria.
East
Afr
Med J.
1997;74(6):372-5.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
24
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
12.
13.
14.
15.
16.
17.
18.
Jagadeesan M, Rotti SB, Dananbalan
M. Oral Health status and risk factors
for dental and periodontal diseases
among rural women in Pondicherry.
Indian J Community Med 2000;
25:31-8.
Johannsen A, Rydmark I, Soder B,
Asberg M. Gingival inflammation,
increased periodontal pocket depth
and elevated interleukin-6 in gingival
crevicular fluid of depressed women
on long-term sick leave. J Periodontal
Res 2007: 42: 546–552.
Johannsen A, Rylander G, Soder B,
Asberg M. Dental plaque, gingival
inflammation, and elevated levels of
interleukin-6 and cortisol in gingival
crevicular fluid from women with
stress-related
depression
and
exhaustion. J Periodontol 2006: 77:
1403–1409.
Lang N, Bartold PM, Cullinan M.
“Consensus
report:
aggressive
periodontitis,”
Annals
of
Peridontology 1999; 4:53.
Löe H, Brown LJ. Early onset
periodontitis in the United States
of
America.J
Periodontol.
1991;62(10):
608-16.
López NJ, Ríos V, Pareja MA,
Fernández O. Prevalence of juvenile
periodontitis in Chile. J Clin
Periodontol.1991;18(7): 529-33.
Lopez R, Ramirez V, Marro P,
Baelum V. Psychosocial distress
and periodontitis in adolescents.
Oral Health Prev Dent 2012: 10:
211–218.
19.
Mathur B, Talwar C. National oral
health survey and flouride mapping
2002-2003. India. New Delhi: Dental
Council of India; 2004.
20.
Melvin WL, Sandifer JB, Gray JL.
The prevalence and sex ratio of
juvenile periodontitis in a young
racially
mixed
population.J
Periodontol. 1991;62(5): 330-4.
21.
Miller
DB,
O’Callaghan
JP.
Neuroendocrine aspects of the
response to stress. Metabolism 2002;
51: 5–10.
22.
Nassar MM, Afifi O, Deprez RD. The
prevalence of localized juvenile
periodontitis in Saudi subjects. J
Periodontol. 1994;65(7):698-701.
23.
Newman
MG,
Takei
HN,
Klokkevold PR, Carranza FA. In:
Carranza's
(ed)
Clinical
Periodontology.
Saunders 2010:
103-104.
24.
Novak MJ, Novak KF. Early–onset
periodontitis. Curr Opin Periodontol
1996;3:45.
25.
Page RC, Altman LC, Ebersole JL,
Vandesteen GE, Dahlberg WH,
Williams BL, Osterberg
SK:
Rapidly progressive periodontitis. A
distinct clinical
condition.
J
Periodontol 1983; 54: 197-209.
26.
Sadeghi R. Prevalence of aggressive
periodontitis in 15-18 year old
school-children in Tehran, Iran.
Community Dent Health. 2010;
27(1):57-9.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
25
Karthik Krishna et al : Prevalence of Aggressive Periodontitis and Systemic Manifestations
27.
Saxby MS. Juvenile periodontitis: an
epidemiological study in the west
Midlands of the United Kingdom.
J Clin Periodontol. 1987;14(10):
594-8.
28.
Shah N, Pandey RM, Duggal R,
Mathur VP, Ranjan K. Oral Health in
India: A Report of the multi centric
study, Directorate General of Health
Services, Ministry of Health and
family welfare, Government of India
and World Health Organisation
Collaborative Program, December
2007.
29.
Silverman MN, Sternberg EM.
Glucocorticoid
regulation
of
inflammation and its functional
correlates: from HPA axis to
glucocorticoid receptor dysfunction.
Ann N Y Acad Sci 2012; 1261:
55–63.
30.
Singh GP, Soni BJ. Prevalence of
periodontal diseases in urban and
rural areas of Ludhiana, Punjab. Ind J
Commun Med 2005; 30:128-9.
31.
Tonetti M, Mombelli A. Early onset
periodontitis. Annals Periodontol
1999; 4:39-53.
32.
Van Dyke TE, Dave S. Risk factors
for periodontitis. J Int Acad
Periodontol. 2005; 7:3-7.
33.
Webster MJI, Glaser R. Stress
hormones and immune function. Cell
Immunol 2008; 252: 16–26.
34.
Zigmond AS, Snaith RP. "The
hospital anxiety and depression
scale".
Acta
Psychiatrica
Scandinavica 1983; 67: 361–370.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Gopinath et.al : Osteoporosis and Periodontal Disease
OSTEOPOROSIS AND PERIODONTAL DISEASE – A REVIEW
Dr. V. GOPINATH1, Dr.M.N.PRABHU2. Dr. HEMA SURYAWANSHI3,
1.
Professor, Head of the Department, Department of Periodontology.
Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India
2.
Professor Department of Periodontology. Gulf University, U.A.E.
3.
Professor, Dean and Head of the Department, Department of oral and maxillofacial pathology
Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India.
Address For Correspondence
Dr. V. Gopinath, MDS, M.B.A., FCIP.
Professor and Head, Department of Periodontology.
Chhattisgarh Dental College and Research Institute, Rajnandgaon (C.G.), India
Email id – [email protected]
Phone no. – +919840180899, +919425294377
ABSTRACT
Osteoporosis and periodontal diseases are bone resorptive diseases. Osteoporosis and osteopenia are
characterized by reductions in bone mass and may lead to skeletal fragility and fracture. In most women, bone
mass reaches its peak in the third decade of life and declines thereafter. This decline in bone mass is accelerated
with the onset of menopause, and oral symptoms are also found in addition to the systemic manifestations of
menopause. This review deals with the assessment ,mechanism and treatment of osteoporosis.
KEY WORDS:
Osteoporosis,
therapy
Bone
mineral
density,
Dual
Energy
INTRODUCTION
Osteoporosis and periodontal diseases have
been considered as the bone resorptive
diseases. Both Osteoporosis and osteopenia
are characterized by reductions in bone
mass and may lead to skeletal fragility and
fracture. In postmenopausal women, bone
mass reaches its peak in the third decade of
life (age 20 to 30) and declines thereafter.
This decline in bone mass is accelerated
with the onset of menopause, and oral
symptoms are also found in addition to the
systemic manifestations of menopause. An
X-Ray
absorptiometry,
Hormone replacement
increased incidence is observed of oral
discomfort, including pain, a burning
sensation, dryness, and altered taste
perception, as well as a debated rise in the
prevalence of periodontal disease.
Periodontitis, an inflammatory disease
characterized by resorption of the alveolar
bone as well as loss of the soft tissue
attachment to the tooth, is a major cause of
tooth loss in adults. Since loss of alveolar
bone is a prominent feature of periodontal
disease, severe osteoporosis could be
suspected of being an aggravating factor in
the case of periodontal destruction. In
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
27
Gopinath et.al : Osteoporosis and Periodontal Disease
recent years, there has been increasing
interest in the interrelationship between
systemic osteoporosis, oral bone loss, tooth
loss, and periodontal disease1
DEFINITION
Osteoporosis is defined as a skeletal
disorder characterized by compromised
bone strength predisposing an individual to
an increased risk of fractures.2 Bone
strength primarily reflects the integration of
bone density and bone quality. Bone
density is expressed as grams of mineral
per unit area or volume, and in any given
individual, is determined by peak bone
mass and amount of bone loss.Bone quality
refers to architecture, turnover, damage
accumulations (e.g. Microfractures) and
mineralization. The standard deviation is
determined by certain established criteria
namely: T-score which is defined as the
number of standard deviations above or
below the average Bone mineral density
(BMD) value for young healthy white
women and Z-score which is defined as the
number of standard deviations above or
below the average BMD for age and sex
matched controls.
CLASSIFICATION
Following classification is based on
standard deviation: The various methods
for assessing bone are as follows3,4:
A) Systemic bone:
a) Absorptiometry
Single photon absorptiometry
Dual photon absorptiometry
b) Dual Energy X-Ray Absorptiometry
(DEXA) c) Quantitative Computed
Tomography (QCT) d) Measurement
from radiographs
Measurement of cortical thickness
and other indices
Fractal dimension e) Ultrasound
B) Intra-oral Sites (Research tools):
a) Adaptation of absorptiometry or DEXA
b) Measurement from panoramic films
c) Cortical thickness and other indices
d) Measurement from intra-oral films
e) Measurement of bone or ridge height
f) Apparent bone density expressed as
arbitrary units based on the reference
wedge
g) Digital
subtraction
radiography
(changes in bone height (mm) or
density (mg/mm2)
h) Fractal dimension i) Microdensitometry
j) Pixel intensity analysis
ASSESSMENT OF OSTEOPOROSIS
Osteoporosis is usually be assessed by a
measurement of bone mineral density
(BMD). BMD is expressed in terms of the
number of standard deviations (SD) from
the mean of healthy individuals, matched to
age and sex (the Z-score), and the number
of SD from the mean of healthy young sexmatched individuals (the T-score).5
According
to
the
World
Health
Organization, Osteoporosis is considered to
be present when BMD is 2.5 SD below the
BMD of the young normal individual.
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Gopinath et.al : Osteoporosis and Periodontal Disease
Osteopenia is defined as bone density
levels between 1 SD and 2.5 SD below
normal
BMD.
Fracture
risk
is
approximately doubled for every 1 SD
below the young adult mean BMD.6 There
are several tools available to measure
BMD. The most widely used tool for
assessing Osteoporosis is dual-energy x-ray
absorptiometry (DXA). Non-invasive DXA
is reliably used around the world to identify
patients with low BMD because of its high
precision and resolution, high accuracy,
low radiation dose, and low cost.7
DXA remains the gold-standard assessment of
osteoporosis. Dual-photon absorptiometry
(DPA) is similar in concept to DXA,
however, it is not as advantageous because
it has a longer scan time and shorter source
life.8 Prior to the development of
Computerized Densitometry, Digital x-ray
radiogrammetry (DXR) was used. This less
precise technique estimates BMD by
evaluating a standard radiograph of the
hand9.
A less common assessment test used by 2
studies in this review is the Quantitative
Ul- trasound (QUS) of the calcaneal and
phalanges.10,11 It provides a measure of
skeletal status by determining a Stiffness
Index (SI), a measure of bone strength,
which is sensitive to bone structure.
Another type of osteoporosis assessment
method measures the thickness of the
mandibular inferior cortex (MIC) below the
mental foramen on a dental panoramic
radiograph (DPR).12 The cortical bone was
chosen over the trabecular bone due to its
greater consistency among readings, which
may be due to trabecular bone being more
easily influenced by dental infections.13
The porosity of the MIC is classified using
the Klemetti Index.12 This classification
system is an excellent means to determine
undiagnosed osteoporosis.14 Based on MIC
findings of erosion or thin cortical width on
DPR, younger postmenopausal women
could be identified as osteoporotic.15 A
decrease in MIC thickness by 1 mm was
shown to increase the likelihood of
osteoporosis by 47%. Mild to moderate
MIC erosion on the DPR correctly reflected
the presence of osteoporosis 83% of the
time, and a normal MIC reading predicted a
normal BMD 60% of the time.16 This
means that normal spine BMD would
correlate with normal MIC evaluations on
DPR greater than half the time. This
method has great potential because DPRs
are taken as part of routine dental
examinations.
ASSESSMENT
DISEASE
OF
PERIODONTAL
Many dental conditions affect the
postmenopausal age group, including tooth
loss and periodontal disease and prevalence
increases with age.17 In the reviewed
studies, periodontal disease was assessed
with a diversity of outcome measures. In
general, studies lacked concise and widely
accepted assessment criteria for diagnosing
periodontal disease, making comparisons
among
studies
and
conclusions
challenging. Gomes-Filho proposed a gold
standard of the combination of periodontal
bone resorption (>3 mm) with 3 other
clinical parameters for the disease: Pocket
depth (PD) (>4 mm), clinical attachment
level (CAL) (>3 mm) and Bleeding upon
probing (BOP).18 These 3 clinical parameters
had the greatest frequency among the
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Gopinath et.al : Osteoporosis and Periodontal Disease
reviewed studies, with probing depth used
17% of the time, CAL 13% and BOP 15%,
confirming that Gomes-Filho made a
logical choice.
RELATIONSHIP BETWEEN OSTEOPOROSIS
AND
PERIODONTAL
DISEASES
There is interrelationship between systemic
osteoporosis, oral bone loss, tooth loss, and
periodontal
disease.
It
has
been
hypothesized that the breakdown of
periodontal tissue may, in part, be related to
systemic conditions that also predispose the
patient to osteoporosis/osteopenia. Kribbs19
showed no significant differences in
periodontal measurements (mean probing
depth and attachment loss) between
osteoporotic and normal groups. Another
cross-sectional study demonstrated that
periodontal attachment loss was correlated
with tooth loss, but not with vertebral or
proximal femur bone density20. Elders and
coworkers21
examined
periodontal
condition and measured lumbar bone
mineral density (lumbar BMD) in 286
female volunteers between 46 and 55 years
of age. No significant correlation was
observed between the clinical parameters of
periodontitis (mean probing depth,
occurrence of bleeding after probing and
number of missing teeth) and the lumbar
BMD, nor was a significant relation
observed between the bone mass
measurements and alveolar bone height.
Thus, they concluded that systemic bone
mass was not an important factor in the
pathogenesis
of
periodontitis.
No
statistically significant differences were
found in gingival bleeding, probing pocket
depth, gingival recession and marginal
bone level between 15 women with
osteoporosis21 and healthy subjects22. No
statistically significant association between
the parameters of periodontal disease and
measures of systemic BMD were found
even after controlling some potential
confounding factors of age, smoking and
number of remaining natural teeth,
(Weyant et al)23. Other authors have found
a significant relation between systemic
osteoporosis and loss of periodontal
tissue.24,25 A case-control study comparing
12 osteoporotic fracture women and 14
normal women found that there was
significantly greater loss of periodontal
attachment in the osteoporotic women than
in the normal women.24 Similar findings
were shown in a cross-sectional
investigation of the association between
systemic BMD and periodontal status. In
that study, thirty post- menopausal, AsianAmerican women were screened for
osteoporosis and chronic periodontitis.
Periodontal assessments included tooth
loss, plaque index, probing depths, and
clinical attachment levels.
Statistically
significant negative correlations were
found between BMD and tooth loss and
BMD and clinical attachment loss that were
independent of plaque scores.25 In another
study controlling for known confounders,
the relationship between systemic bone
mineral density and periodontal disease in
70 postmenopausal Caucasian women aged
51 to 78 was investigated. BMD was
assessed by dual-energy x-ray. The severity
of periodontal disease was represented by
clinical attachment loss and interproximal
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
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Gopinath et.al : Osteoporosis and Periodontal Disease
alveolar bone loss (ABL). It was found that
Mean ABL and BMD are correlated with
each other. Clinical attachment loss
appeared to be related to skeletal bone
mineral density consistently at all regions
of the skeleton, but the results did not reach
the level of statistical significance.26 For a
2-year longitudinal clinical study, the
alveolar bone height and density changes in
21 osteoporotic/osteopenic women were
compared with those of 17 women with
normal lumbar spine BMD. These subjects
were postmenopausal women having a
history of periodontitis and participating in
a periodontal maintenance program. The
results
indicated
that
osteoporotic/
osteopenic women exhibited a higher
frequency of loss in alveolar bone height
and crestal bone density relative to women
with normal BMD.27 However, these
results should be interpreted with caution
since the compared groups are small.
Variety of methods used to assess
osteoporosis and periodontitis, as well as
varying definitions of outcomes of interest.
If osteoporosis is a predisposing factor for
periodontal tissue destruction, then a
relationship should exist between measures
of systemic bone mineral density
and
periodontal tissue destruction. However,
previous studies have failed to establish a
strong relationship. Possible explanations
for this could be lack of precise methods
for assessment of bone density and
confounding of the result by other factors
such as age, gender, smoking, remaining
nature teeth, hormone intake, exercise of
jaw bone, and most importantly the host
susceptibility to dental plaque and oral
hygiene status. Moreover, the crosssectional studies have their own limitations,
since little information is available about
the pattern of disease progression during
the short period of the study, nevertheless,
most osteoporosis and periodontal disease
progress in a chronic pattern. Although
findings of these studies regarding the
association between osteoporosis and
periodontal disease are still controversial,
with Increases in the number of aged
patients in Taiwan society, the dialogue
among medical and dental professional in
this field provides a unique viewpoint in
achieving and maintaining patients’
optimal health. Clearer understanding of
this relationship may aid health care
providers in their efforts to detect and
prevent osteoporosis and periodontal
disease.28 To date, few longitudinal studies
have been performed. To better evaluate
the relationship between bone mineral
density and periodontal disease, additional
prospective longitudinal studies with
further analysis of possible confounding
factors for osteoporosis and periodontal
disease in larger cohorts of postmenopausal women are needed. However,
dentists must bear in mind that the primary
etiology of periodontal disease is
pathogenic bacterial plaque in a susceptible
patient. Therefore, if good oral hygiene is
combined with regular check-ups, the
effects that any of osteoporotic factors may
exert on the periodontal tissues can be
minimized.
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Gopinath et.al : Osteoporosis and Periodontal Disease
RISK FACTORS FOR OSTEOPOROSIS
AND PERIODONTAL DISEASES
Risk factors for osteoporosis can be
divided into non-modifiable and modifiable
(Table 1). The non -modifiable risk factors
for osteoporosis include gender, age, early
menopause, thin or small body frame, race,
and heredity. Lack of calcium and vitamin
D, lack of exercise, smoking, and alcohol
consumption are modifiable risk factors.
Low bone mass, certain medications,
propensity to falling, and systemic diseases
such
as
hyperparathyroidism
and
hyperthyroidism are modifiable to some
extent.
Calcium-regulating hormones, disorders
such as anorexia nervosa or bulimia, and
genetic abnormalities may also play a role
in decreased bone density.29
Bone loss in women occurs most rapidly
in the years immediately following
menopause when natural levels of estrogen
are greatly reduced. In most women, bone
mass reaches its peak in the third decade of
life and declines30,31 thereafter This decline
in bone mass accelerates with the onset of
menopause. While estimates of the rate of
postmenopausal bone loss may differ by
population and measurement technology, a
rate on the order of 32,33 0.5% to 1.0%
per year has been reported.
Table 1.
Risk Factor
ModiHow Modifiable
fiable
Gender
No
Age
No
Early menopause
No
Risk Factor
ModiHow Modifiable
fiable
Low bone mass
Yes
Treatment of
osteoporosis or
osteopenia
Thin, smallframed body
No
Race
No
Lack of calcium
Yes
Diet high in
calcium
or vitamin D
Lack of exercise
Yes
Weight-bearing
Exercise
Smoking
Yes
Smoking
cessation
Alcohol
Yes
Decreased
alcohol
consumption
Heredity
No
To
Diseases
Treatment
some
(e.g., hyperparathyroidism) extent
Certain
medications
(e.g., steroids)
To
Alter treatment
some
extent if feasible
Propensity to
falling
To
Physical therapy,
some neurological
extent treatment if
possible
MECHANISM OF ASSOCIATION
BETWEEN OSTEOPOROSIS AND
PERIODONTAL DISEASES
Mechanisms by which osteoporosis or
systemic bone loss may be associated with
periodontal attachment loss, loss of
alveolar bone height and tooth loss is
shown in Fig(1) First, low bone mineral
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Gopinath et.al : Osteoporosis and Periodontal Disease
density in the oral bone may be associated
with low systemic bone. This low bone
density or loss of bone mineral density may
lead to a rapid resorption of alveolar bone
along with periodontal disease caused by
periodontal bacteria as it intensifies the
bone loss.
Second, systemic factors affecting bone
remodeling may also modify local tissue
response
to
periodontal
infections.
Individuals with systemic bone loss are
known to have increased systemic
production of cytokines (i.e.interleukin-1
and interleukin-6) that may have an effect
on bone throughout the body, including the
bones of oral cavity. Periodontal infection
has been shown to increase the local
cytokine production that, in turn, increases
local osteoclast activity resulting in
increased bone resorption.
Third, genetic factors that predispose a
person to systemic bone loss also influence
or predispose a person to periodontal
destruction. Lastly, certain lifestyle factors
such as cigarette smoking and suboptimal
calcium intake, amongst others, may put
individuals at risk for development of both
osteopenia and periodontal disease34. It has
been hypothesized that osteoporosis may
cause decreased alveolar bone density,
which in turn, may be more susceptible to
resorption by the effect of co-existing or
subsequent periodontal infection and
inflammation.
IMPLICATION FOR THE TREATMENT
OF PATIENT’S WITH OSTEOPOROSIS
AND PERIODONTITIS
Implications for treatment of patients with
osteoporosis and periodontitis: Medications
and strategies in current use for
osteoporosis prevention and treatment
include
bisphosphonates,
Selective
Estrogen Receptor modulators (SERMs),
BACTERIAL CHALLENGE
PERIODONTAL HEALTH
OSTEOPOROSIS & PERIODONTAL DISEASE
CYTOKINES
PreOSTEOCLAST
OSTEOCLAST
PHYSIOLOGIC BONE RESORPTION
PERIODONTAL BONE RESORPTION
Fig 1: MECHANISM OF ASSOCIATION BETWEEN
OSTEOPOROSIS AND PERIODONTAL DISEASE
calcitonin, Hormone Replacement Therapy
(HRT) and Nutritional Supplements of
Calcium and Vitamin D. Anti-resorptive
medications: These groups of medications
act on resorption phase without affecting
the formation in osteoporosis. The
bisphoshonates have been shown to prevent
alveolar
resorption
and
preserve
mandibular bone mass in animals, but their
exact role has not been clearly established
in human studies. Also, the retention of
teeth has been reported to be higher in
patients on HRT35.Nishida et al36 surveyed
the dietary intake of calcium and
periodontal examination on 12,000 adults.
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Gopinath et.al : Osteoporosis and Periodontal Disease
It was found that there was inverse
association between dietary calcium intake
and level of periodontal disease, controlling
for smoking and age.
ORAL BONE
LOW BONE DENSITY + LOW SYSTEMIC BONE
RAPID RESORPTION OF ALVEOLAR BONE
PERIODONTAL BACTERIA
AFFECT LOCAL TISSUE RESPONSE TO
PERIODONTAL INFECTIONS
SYSTEMIC BONE LOSS [*genetic factors +
environmental factors predispose]
INCREASED CYTOKINE PRODUCTION
EFFECTS BONE (BODY + ORAL CAVITY)
INCREASED OSTEOCLASTIC ACTIVITY
INCREASES BONE RESORPTION
PERIODONTAL DISEASE
Model describing various activity of
osteoporosis leading to periodontal disease
CONCLUSION
Periodontal diseases are multi- factorial
disease and the main etiologic factor is
microbial plaque. Osteoporosis is not the
cause for the onset of periodontal disease,
but after outbreak of the disease, it may be
a predisposing factor in the exacerbation, or
persistence of the disease. In patients with
preexisting periodontitis there is more
tendency of alveolar bone loss than in
patients with osteoporosis. The low
systemic bone mass density is also
considered to be one of the risk factor of
the periodontal disease.
ACKNOWLEDGEMENT
The Authors wish to thank Dr. Priya Kolhe,
BDS for her help in drawing figure.
REFERENCES
1. Yun-linlai;
osteoporosis
and
periodontal disease ; Journal of chinese
medical association2004;67;387-88
2. NIH Consensus Development Panel on
Osteoporosis Prevention, Diagnosis,
and Therapy. Osteoporosis Prevention,
Diagnosis, and Therapy. JAMA: The
Journal of the American Medical
Association. 2001 Feb 14;285(6):
785–95.
3. Wahner HW. Use of densitometry in
management of osteoporosis. In:Marcus
R, Feldman D, Kelsey J,eds. Osteoporosis
San
Diego:
Academic
Press
1996;23:1055-1074.
4. Anna N Law, Anne-Marie Bollen, SsuKuang Chen. Detecting osteoporosis
using dental radiographs: A comparison of
four methods. JADA 1996;127:17341742.
5. Assessment of fracture risk and its
application
to
screening
for
postmenopausal osteoporosis. Report of a
WHO study group. World Health Organ
Tech Rep Ser. 1994;843:1-129
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
34
Gopinath et.al : Osteoporosis and Periodontal Disease
6. Wasnich R. Bone mass measurement:
Prediction of risk. Am J Med. 1993;95
(5A): 6S-10S.
7. Jeffcoat MK, Lewis CE, Reddy MS,
Wang CY, Redford M. Post-menopausal
bone loss and its relationship to oral bone
loss. Periodontol 2000. 2000;23:94-102.
8. Tezal M, Wactawski-Wende J, Grossi SG,
Ho AW, Dunford R, Genco RJ. The
relationship between bone mineral density
and periodontitis in postmenopausal
women. J Periodontol. 2000;71(9):14921498.
9. Swezey RL, Draper D, Swezey AM. Bone
densitometry: Comparison of dual energy
x-ray absorptiometry to radiographic
absorptiometry. J Rheumatol. 1996;23(10)
: 1734- 1738.
10. Drozdzowska B, Pluskiewicz W, Michno
M. Tooth count in elderly women in
relation to their skeletal status. Maturitas.
2006;55(2):126-131.
11. Vishwanath SB, Kumar V, Kumar S,
Shashikumar P, Shashikumar Y, Patel PV.
Correlation of periodontal status and bone
mineral density in postmenopausal
women: A digital radiographic and
quantitative ultrasound study. Indian J
Dent Res. 2011;22(2):270-276.
12. Bollen AM, Taguchi A, Hujoel PP,
Hollender LG. Case-control study on selfreported osteoporotic fractures and
mandibular cortical bone. Oral Surg Oral
Med Oral Pathol Oral Radiol Endod.
2000;90(4):518-524.
13. Taguchi A, Sanada M, Krall E, et al.
Relationship between dental panoramic
radiographic findings and biochemical
markers of bone turnover. J Bone Miner
Res. 2003;18(9):1689-1694.
14. Klemetti E, Kolmakov S, Kroger H.
Pantomography in assessment of the
osteoporosis risk group. Scand J Dent Res.
1994;102(1):68-72.
15. Persson RE, Hollender LG, Powell LV, et
al. Assessment of periodontal conditions
and systemic disease in older subjects. I.
focus on osteoporosis. J Clin Periodontol.
2002;29(9):796-802.
16. Taguchi A, Tsuda M, Ohtsuka M, et al.
Use of dental panoramic radiographs in
identifying younger postmenopausal
women with osteoporosis. Osteoporos Int.
2006;17(3):387-394.
17. Henriques PS, Pinto Neto AM.
Association between tooth loss and bone
mineral
density
in
brazilian
postmenopausal women. J Clin Med Res.
2011; 3(3):118-123.
18. Gomes-Filho IS, Passos Jde S, Cruz SS,
et al. The association between
postmenopausal
osteoporosis
and
periodontal disease. J Periodontol. 2007;
78(9): 1731-1
19. Kribbs PJ. Comparison of mandibular
bone in normal and osteoporotic women. J
Prosthet Dent 1990;63:218-22.
20. Hildebolt CF, Pilgram TK, Dotson M,
Yokoyama-Crothers N, Muckerman J,
Hauser J, et al. Attachment loss with
postmenopausal age and smoking. J
Periodontal Res 1997;32: 619-25.
21. Elders PJ, Habets LL, Netelenbos JC, van
der Linden LW, van der Stelt PF. The
relation between periodontitis and
systemic bone mass in women between 46
International Journal of Innovations in Dental Sciences / December 2016 / Vol 1 / Issue 1
35
Gopinath et.al : Osteoporosis and Periodontal Disease
and 55 years of age. J Clin Periodontol
1992;19:492-6.
22. Lundstrom A, Jendle J, Stenstrom B, Toss
G, Ravald N. Periodontal conditions in
70-year-old women with osteoporosis.
Swed Dent J 2001;25:89-96.
23. Weyant RJ, Pearlstein ME, Churak AP,
Forrest K, Famili P,Cauley JA. The
association between osteopenia and
periodontal attachment loss in older
women. J Periodontol 1999; 70:982-91.
24. Von Wowern N, Klausen B, Kollerup G.
Osteoporosis: a risk factor in periodontal
disease. J Periodontol 1994;65:1134-8.
25. Mohammad AR, Hooper DA, Vermilyea
SG, Mariotti A, Preshaw PM. An
investigation of the relationship between
systemic bone density and clinical
periodontal status in post-menopausal
Asian-American women. Int DentJ
2003;53:121-5.
26. Tezal M,Wactawski-Wende J, Grossi SG,
Ho AW, Dunford R, Genco RJ. The
relationship between bone mineral density
and periodontitis in postmenopausal
women. J Periodontol 2000;71:1492-8.
27. Payne JB, Reinhardt RA, Nummikoski
PV, Patil KD. Longitudinal alveolar bone
loss in postmenopausal osteoporotic/
osteopenic women. Osteoporos Int 1999;
10:34-40.
28. Shen EC, Gau CH, Hsieh YD, Chang CY,
Fu E. Periodontal status in postmenopausal Osteoporosis: A preliminary
clinical study in Taiwanese women.
J Chin Med Assoc 2004;67: 389-93.388
30. Melton L.J. Epidemiology of Fractures,
In: Riggs BL,
Melton LJ, eds.
Osteoporosis: Etiology, Diagnosis and
Management. New York: Raven Press;
1988:133-154.
31. Lindsay R. Estrogens, bone mass and
Osteoporotic Fracture. Am
J Med
1991;91(suppl. 5B):10S-13S.
32. Kellie SE, Brody JA. Sex-specific and
race-specific hip fracture rates. Am J
Public Health 1990;80:326-328.
33. Villa ML, Nelson L. Race, ethnicity and
osteoporosis. In: Marcus R, Feldman D,
Kelsey J, eds. Osteoporosis San Diego:
Academic Press;1996:435-447.
34. Tezal M, Wactawski-Wende J, Grossi SG,
Ho AW, Dunford R, Genco RJ. The
Relationship Between Bone Mineral
Density
and
Periodontitis
in
Postmenopausal Women. Journal of
Periodontology. 2000 Sep;71(9):1492–
8.International Journal of Therapeutic
Applications, Volume 32, 2016, 11-19.
35.Ronderos M, Jacobs DR, Himes JH,
Pihlstrom BL. Associations of periodontal
disease with femoral bone mineral density
and estrogen replacement therapy: crosssectional evaluation of US adults from
NHANES III. J Clin Periodontol. 2000
Oct;27(10):778–86.
36. Nishida M, Grossi SG, Dunford RG, Ho
AW, Trevisan M, Genco RJ. Calcium and
the Risk For Periodontal disease ; J
periodontal 2000 Jul; 71(7);1057-66.
29) Marjorie jeffcoat; osteoporosis and oral
oral bone loss; J periodontal; Nov 2005
(suppl.); vol76;2125 -2132.
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36
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