ISSN 2229-6360

Volume 1, Issue 3
March-April 2011

Indian Journal of
Volume 1, Issue 3, March-April 2011, Indian Journal of Multidisciplinary Dentistry, Page (121-180)

Multidisciplinary
DENTISTRY

http://ebook.ijcpgroup.com/ijmd/index.htm
Indian Journal of
Multidisciplinary Dentistry Volume 1, Issue 3
March-April 2011

IJMD’s Editorial Panel

Editor-in-Chief
KMK Masthan
Executive Editor Associate Editor
S Bhuminathan N Aravindha Babu

IJMD Advisory Board

Prosthodontics Oral and Maxillofacial General Medicine
Mahesh Verma Surgery Rajendran SM
Srinisha J Ramakrishna Shenoi
Raghavendra Jayesh S Vijay Ebnezer Periodontics
Sanjna Nayar Raj Kutta (USA) Chandrasekaran SC
Ash Vasanthan (USA)
Conservative Dentistry/ Oral Pathology and
Endodontics Microbiology Oral Medicine and
Vinay K Hazarey Radiology
Sukumaran VG
Ipe Vargese V Selva Muthu Kumar SC
Subbiya A
Puneet Ahuja Nalini Aswath
Swaminathan S (Singapore)

Orthodontics Pedodontics
Implantology
Krishna Nayak US Krishan Gauba
John W Thurmond (USA)
Dhandapani G Ashima Gauba
Murali RV
Genetics Deepak C Biochemistry
Aravind Ramanathan Julius A
Pharmacology
Oncology Muthiah NS Microbiology
Abraham Kuriakose M Elumalai M Mahalakshmi K

IJCP’s Editorial Panel

Dr Sanjiv Chopra Dr KK Aggarwal
Prof. of Medicine & Faculty Dean CMD, Publisher and Group
Harvard Medical School Editor-in-Chief
Group Consultant Editor Dr Veena Aggarwal
Joint MD & Group Executive Editor
Dr Deepak Chopra Anand Gopal Bhatnagar
Chief Editorial Advisor Editorial Anchor
IJMD is included in the databases of Genamics JournalSeek along with Ulrich
International periodical directory and Index Copernicus International, Ltd.
Advisory Bodies
Heart Care Foundation of India, Non-Resident Indians Chamber of Commerce & Industry,
World Fellowship of Religions
Contents
From the Editor-in-chief 124

From the Desk of IJCP Group Editor-in-Chief

Diabetes Mellitus and Dental Infections 125

review article
Comparative Study of Manual Cephalometric Tracing and Computerized Cephalometric
Tracing in Digital Lateral Cephalogram for Accuracy and Reliability of Landmarks 126

Peripheral Ameloblastoma: Review of Literature and Case Presentation 135

Antioxidants in Periodontal Diseases: A Review 140

Case report
Minimally Invasive Atraumatic Extraction of Fractured Tooth Using Implant Drills and Immediate
Implant Placement 147

Rhinocerebral Mucormycosis with Palatal Involvement Associated with Diabetes Mellitus Type II:
A Case Report 152

Full Mouth Rehabilitation of a Patient with Severely Attrited Dentition 157

Interdisciplinary Management of Deep Bite in an Adult Patient 161

Submental Intubation – A Case Report 165

clinical study
Comparison of Enzyme Alkaline Phosphatase Levels Around Healthy and Diseased Implants:
A Clinical Study 169

Sterilization Protocol for Orthodontic and Endodontic Instruments 172

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 From the Editor-in-chief
xxxxxxxxx
Dr KMK Masthan
Professor and Head, Department of Oral Pathology and Microbiology
Sree Balaji Dental College and Hospital, Chennai
O
ur second issue had some additions like the
orderly arrangement of articles and advisory
board members and some deletions like
leaving out some extraneous names. I received some
suggestions like grouping of articles according to
the sub-specialties and maintaining the same e-link
for the subsequent issues. The second suggestion, I
have requested our IJCP editorial team to consider
whereas the first suggestion, in my opinion defeats the
whole purpose of a multi disciplinary journal and the
intention towards an interdisciplinary discussion. Let us
consider, for example, a learned discussion on implants.
It consists of a surgical phase for placing an implant, a
periodontic part for abutment attachment and the most
difficult prosthodontic part of providing an esthetically
pleasing tooth attachment. In addition, the role of a
radiologist is paramount in deciding a safe location for
the implant so that sinus space is not breached and
an inadvertent nerve damage is not encountered. Now,
which speciality can hold a proprietary interest in that?
If the history of implantology is reviewed, the implants
were introduced and promoted by general dentists
with support from engineering, metallurgy and pure
research like animal studies.
I have seen heated discussions when this subject
is broached and I feel that we are looking at the
whole concept with tunnel vision. Dentistry was
divided into several branches and will continue to
be divided further in the future into several more
because the sheer amount of literature, armamentarium,
techniques and the skill were and are becoming too wide
for one singe dental professional to master in his or
her limited undergraduate and postgraduate academic
time window. But any dental/medical education is
a continuous lifelong process and an intellectual
pursuit and the speciality sticker should in no way
act as a barrier for someone who thirsts at knowledge
and wants to master newer technologies and
procedures. My view is supported by CDE/CME
program which are enthusiastically attended by several
undergraduates since they do not recognize any such
mental blocks, whereas the postgraduates of one sub-
specialty consider it beneath their pride even to enroll
in such workshops. Now who is the loser?
124
Another sensitive subject that deserves our time and
attention is myopic jurisdictional attitude of some
of our fellow professionals. I have come across such
situations, where a periodontist is criticized for doing
RCTs and an oral pathologist is denied access to
clinical cases. Now, how will the periodontist treat an
endo-perio lesion if he should not do RCTs and how
will an oral pathologist learn clinical features of an oral
disease if he does not get a chance to see the patient?
Are we there for patients and their problems or are
the patients there for providing us a prestigious degree
and a lucrative income? Patient’s welfare must come
first and the right to educate a student adequately and
comprehensively utilizing all available resources must
come second.
Another incident that merits mention is an article that
was submitted. We had received a wonderful article,
painstakingly written on Oral Radiology from a junior
staff member from a dental college that I am familiar
with. Then I received an urgent request from the author
withdrawing the article. When I enquired why, I was
told a shocking and a staggering reply. The HOD does
not like the juniors to publish even though the author
had the grace to put the HOD as the first author.
When the Dental Council is making the publications
a mandatory requirement and the institutions are
literally begging the staff members to publish and the
whole profession stands to benefit by publications,
the HOD does not like the juniors to get the credit
that the junior truly deserves. The institution will
also suffer due to lesser number of publications at the
time of inspections. Monumental egos, unreasonable
insecurities and personal prejudices have no place in a
profession that is growth-bound and let us remember
nature has a way of weeding out such impediments.
Now, that our journal has gained some popularity
and is privileged to be included in databases of several
indexing bureaus, I make an appeal to the readers and
authors to recommend some sponsors and advertisers
since more funds will help us to elevate the journal to
a higher standard.
My wholehearted thanks to IJCP for accommodating
my nagging demands and bringing out wonderful
issues.
Best wishes...
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 From the Desk of IJCP Group Editor-in-Chief
xxxxxxxxx
Diabetes Mellitus and Dental Infections

Dr KK Aggarwal
Padma Shri and Dr BC Roy National Awardee
Sr Physician and Cardiologist, Moolchand Medcity
President, Heart Care Foundation of India
Group Editor-in-Chief, IJCP Group
Editor-in-chief, eMedinewS
Chairman Ethical Committee, Delhi Medical Council
Director, IMA AKN Sinha Institute (08-09)
Hony. Finance Secretary, IMA (07-08)
Chairman, IMA AMS (06-07)
President, Delhi Medical Association (05-06)
emedinews@gmail.com
http://twitter.com/DrKKAggarwal
Krishan Kumar Aggarwal (Facebook)

P
oorly controlled diabetes is a risk factor for increased severity of periodontitis and poor response to
periodontal treatment. Patients may present with xerostomia, candidiasis, and caries as well as periodontal
disease. Patients with poor control of diabetes and severe periodontitis show improvement in their A1C
levels, as well as decrease in periodontal inflammation, with treatment of the periodontitis1,2 not all studies confirm
improvement in glycemic control, however.3-5
There is no strong scientific evidence on the effects of periodontal treatment on glycemic control and systemic
inflammation.6 Efforts should be made to counsel all diabetics to take care of their dental hygiene and if an
infection is present to control it simultaneously.
And much more in this issue...

References
1. Stewart JE, Wager KA, Friedlander AH, Zadeh HH. The effect of periodontal treatment on glycemic control in patients
with type 2 diabetes mellitus. J Clin Periodontol 2001;28(4):306-10.
2. Kiran M, Arpak N, Unsal E, Erdoğan MF. The effect of improved periodontal health on metabolic control in type 2
diabetes mellitus. J Clin Periodontol 2005;32(3):266-72.
3. Aldridge JP, Lester V, Watts TL, Collins A, Viberti G, Wilson RF. Single-blind studies of the effects of improved periodontal
health on metabolic control in type 1 diabetes mellitus. J Clin Periodontol 1995;22(4):271-5.
4. Christgau M, Palitzsch KD, Schmalz G, Kreiner U, Frenzel S. Healing response to non-surgical periodontal therapy in
patients with diabetes mellitus: clinical, microbiological, and immunologic results. J Clin Periodontol 1998;25(2):112-24.
5. Promsudthi A, Pimapansri S, Deerochanawong C, Kanchanavasita W. The effect of periodontal therapy on uncontrolled
type 2 diabetes mellitus in older subjects. Oral Dis 2005;11(5):293-28.
6. Salvi GE, Carollo-Bittel B, Lang NP. Effects of diabetes mellitus on periodontal and peri-implant conditions. Update on
associations and risks. J Clin Periodontol 2008;35(Suppl 8):349.

n n n

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 125

 review article

Comparative Study of Manual Cephalometric Tracing and Computerized

Cephalometric Tracing in Digital Lateral Cephalogram for Accuracy and
Reliability of Landmarks
RV Murali*, MR Sukumar**, T Faisal Tajir†, S Rajalingam‡

Abstract
Introduction: The purpose of the study was to evaluate the skeletal, dental and soft tissue variables accuracy and reliability
in digital cephalogram by two methods of tracing - i.e., manual tracing and computerized (Vistadent) cephalometric tracing.
Material and methods: A sample of 80 pre-treatment standardized lateral cephalogram were analyzed by a single observer,
who performed the manual and computerized tracings of all 80 radiographs. Thirty-three anatomical landmarks were defined
on each radiograph by a single investigator and 37 variables were calculated. Data were subjected to statistical analysis.
Statistical analysis was undertaken using SPSS 16.0 version statistical software program. No differentiations were made
for age or gender. For statistical evaluation of the principal data, differences in measurements between manual tracing and
Vistadent tracing were evaluated using t-test. A level of p < 0.05 was considered to be significant. To evaluate the method error,
30 randomly selected radiographs were retraced 1-week after the initial measurements and paired t-test was done. The retracing
values of manual and Vistadent tracing was evaluated using t-test. A level of p < 0.05 was considered to be significant. Results
and conclusions: Most of the variables showed consistency between the two methods except for Pog-Nperp, Jarabak ratio,
ANS-Me, IMPA, L1-NB, SnPerp-Pog’ and nasolabial angle. The study indicates that most of the variables show consistency
between manual tracing and computerized tracing while most of the cephalometric variables were reliable.

Key words: Skeletal variables, dental variables, soft tissue variables, computerized tracing, manual tracing

I
maging is one of the most ubiquitous tools
orthodontists use to measure and record the
size and form of craniofacial structures. Despite
the diverse image acquisition technologies currently
available, standards have been adopted in effort to
balance the anticipated benefits with associated costs
and risks. Because of these considerations, orthodontists
routinely use an array of two-dimensional static imaging
techniques to record the three-dimensional anatomy of
craniofacial region.4
In orthodontics cephalometric radiography is an
essential tool for studying growth and development
of the facial skeleton, diagnosis and treatment
planning, and evaluating pre- and post-treatment
changes.8,13,14 However, despite its widespread use in
orthodontics, the technique is time consuming and
*Professor and Head
**Professor
†
Associate Professor
‡
Postgraduate Student
Dept. of Orthodontics and Dentofacial Orthopedics
Sree Balaji Dental College and Hospital, Chennai
Address for correspondence
Dr RV Murali
Professor and Head
Dept. of Orthodontics and Dentofacial Orthopedics
Sree Balaji Dental College and Hospitals
Pallikaranai, Chennai - 600 100
E-mail: muralikothai@gmail.com
has several drawbacks, including a high-risk of error in
tracing, landmark identification and measurement.9,14
Cephalometric errors can be divided into those
related to acquisition, identification, and technical
measurement. Reproducibility of measurements by the
operator is also a significant factor in determining
the accuracy of any method of analysis. The use of
computers in treatment planning is expected to reduce
the incidence of personal errors due to operator fatigue
and provide standardized, fast and effective evaluation
with a high rate of reproducibility. The literature
contains only a few studies comparing the accuracy
of digital cephalometric measurements with the hand-
tracing method.3,6,11 There is still a need to evaluate any
possible differences in errors between newly emerging
cephalometric software and earlier programs.
Hence, the present study was undertaken to evaluate
the skeletal, dental, soft tissue variables accuracy and
reliability in digital cephalogram by two methods
of tracing: i.e., manual tracing and computerized
cephalometric tracing (Vistadent).
Material and Methods
Pre-treatment lateral cephalometric radiographs of 80
patients were randomly selected from the archives of
dental OPG X-ray Center with the following criteria:

126 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

 Review Article

 Good quality radiographs without any artifacts
that might interfere with the location of the
anatomical points.
 No craniofacial deformity or asymmetry.
 Patient biting in occlusion (maximum inter-
cuspation).
 Permanent dentition with no missing teeth.
 No excess soft tissue (as determined from the
radiographs) that could interfere with locating
anatomical points.
statistical evaluation of the principal data, differences
in measurements between hand tracing and Vistadent
tracing was evaluated using t-test. A level of p < 0.05
was considered to be significant. To evaluate the
method error, 30 randomly selected radiographs were
retraced 1-week after the initial measurements and
paired t-test was done. The retracing values of hand
Gi
N

All the lateral cephalometric radiographs were acquired

S
using the same digital cephalometer (Orthophos
XG5 - Sirona Dental Systems GmbH) set at x1.25 Po
Co Or

magnification, as recommended by the manufacturer. Ar ANS Ns

Ba Aplu A Cotg
PNS Sn
Digital Tracing Lslu
Ls
Is 11 Stm-s
ppOcP Stm-i
The digital images were stored in a laptop (Hp pavilion Li 11 Li
Sto
Is1u

dv 2000 screen resolution 1074 × 728 pixels) and then Go

Ap 11 B

imported into the software program (Vistadent by Gn

Pog
Pog

GAC International, New York). Me

Me

Figure 1. Landmarks used.

Manual Tracing
For manual tracing the digital images were printed on
dry imaging recording film. Manual tracing was carried
out in a darkened room using an illuminated viewing
screen with a black surround to reduce extraneous
light. Each X-ray was firmly secured to the surface
of a viewing box and a sheet of fine grade, semi-matt
acetate tracing paper taped over the X-ray. Using
a hard 3H pencil, landmarks were identified by a
single point, in a predetermined order. For bilateral
N-Nasion, S-Sella turcica, Co-Condylon, Po-Porion, Ba-Basion, Ar-Articulare,
Go-Gonion, Me-Menton, Pog-Pogonion, Gn-Gnathion, B-B point, A-A
point, Or-Orbitale, Sn-Subnasale, Sto-Stomion, ANS-Anterior nasal spine,
PNS-Posterior nasal spine, Ap1u-Apex of 1u, Ls1u-Labial outline of upper
incisor, Is1u-Incision superior, Is1l-incision inferior, Li1l-Labial outline of
lower incisor, Ap1l-Apex of 1l, ppOcP-Posterior point of occlusal plane,
Gl´-Soft tissue glabella, Ns-Tip of the nose, Cotg-Columella tangent point,
Ls-Labrale superior, Stm-s-Stomion superius, Stm-I-Stomion inferius, Li-Labrale
inferior, Pog´-Soft tissue pogonion, Me´-Soft tissue menton.
2
1

structures and double images, the mid-point was 10

chosen by construction.
3

A total of 33 anatomical landmarks (Fig. 1) were

6 4
defined on each radiograph and following 37 parameters
were calculated: 11 7
9

 Skeletal variables 16-(Fig. 2)

 Dental variables 10-(Fig. 3) 14 15
5
 Soft tissue variables 11-(Fig. 4) 16

Statistical Analysis
Statistical analysis was undertaken using SPSS
16.0 version statistical software program. No
differentiations were made for age or gender. For
Figure 2. Skeletal variables used.
1-SNA (°), 2-SNB (°), 3-ANB (°), 4-Nperp-A (mm), 5-Nperp-Pog (mm),
6-Cond-A (mm), 7-Cond-Gn (mm), 8-Max-Mand (mm), 9-Wits (mm),
10-Ba N-NA (°), 11-SpP-GoMe (°), 12-SN-GoMe (°), 13-Jarabak ratio
(S-Go:N-Me), 14-ArGo-Me (°), 15-ANS-Me (mm), 16-Go-Me (mm).

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 127

 Review Article

Table 1. Variables Used

Skeletal variables
SNA (°) SNA angle
SNB (°) SNB angle
ANB (°) ANB angle
Nperp-A (mm) Maxillary position
Nperp-Pog (mm) Mandibular position
8 Cond-A (mm) Effective maxillary length
9 7
4
Cond-Gn (mm) Effective mandibular length
5
6
Max-Mand (mm) Maxillomandibular difference
10
1
2
Wits (mm) Distance of A and B on occlusal plane
3
Ba N-NA (°) Formed by connecting the Sella-
Nasion plane to A point
SpP-GoMe (°) Angle of palatal to mandibular plane

Figure 3. Dental variables used. SN-GoMe (°) Angle of anterior cranial base to
mandibular plane
1-IMPA (°), 2-Max1-NA (°), 3-Mand1-NB (°), 4-1u-NA (mm), 5-1l-NB
(mm), 6-Overjet (mm), 7-Overbite (mm), 8-Interincisal (°), 9-SpP-OcP (°), (S-Go:N-Me) Ratio of posterior and anterior facial
10-MeGo-OcP (°). height
ArGo-Me (°) Gonial angle
ANS-Me (mm) Lower facial height
Go-Me (mm) Mandibular length
Dental variables
IMPA (°) Angle of axis of 1l to mandibular. Base
1 Max1-NA (°) Angle of axis of 1u to N-A
Mand1-NB (°) Angle of axis of 1l to N-B
1u-NA (mm) Distance of labial outline of 1u to N-A
6
10 3
1l-NB (mm) Distance of labial outline of 1l to N-B
2 Overjet (mm) Overjet
11
7
Overbite (mm) Overbite
Interincisal (°) Interincisal angle
4
8
SpP-OcP (°) Angle of palatal to occlusal plane
MeGo-OcP (°) Angle of mandible to occlusal plane
Figure 4. Soft tissue variables used. Soft tissue variables
1-Gl’-Sn (mm), 2-Sn-Me’ (mm), 3-Sn-stm-s (mm), 4-Stm-i-Me’ (mm),
5-Stm-s - Stm-i (mm), 6-SnPerp-Ls (mm), 7-SnPerp-Li (mm), Gl’-Sn (mm) Upper facial height
8-SnPerp-Pog’ (mm), 9-CotgSnLs (°), 10-Ls-NsPog’ (mm), Sn-Me’ (mm) Lower facial height
11-Li-NsPog’ (mm).
Sn-stm-s (mm) Upper lip length

and Vistadent tracing was evaluated using t-test. Stm-i-Me’ (mm) Lower lip length

A level of p < 0.05 was considered to be significant. Stm-s - Stm-i (mm) Interlabial gap
SnPerp-Ls (mm) Distance of upper lip to SnPerp
Results SnPerp-Li (mm) Distance of lower lip to SnPerp
SnPerp-Pog’ (mm) Distance of chin to SnPerp
Statistical evaluation of skeletal, dental, soft tissue
CotgSnLs (°) Nasolabial angle
variables between Group I (manual tracing), Group II
Ls-NsPog’ (mm) Upper lip to esthetic line
(Vistadent) (Table 2) shows the following variables
Li-NsPog’ (mm) Lower lip to esthetic line
were significant (p < 0.05) Nperp-Pog (p = 0.032),

128 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

 Review Article

Table 2. Statistical Evaluation of Skeletal, Dental, Soft Tissue Variables

Variables Group I (Manual tracing) Group II (Vistadent tracing) t-test
Skeletal variables
SNA (°) 83.1125 ± 0.38702 83.6125 ± 0.40702 NS
SNB (°) 78.1000 ± 0.41687 78.4000 ± 0.45687 NS
ANB (°) 5.0000 ± 0.22482 5.2000 ± 0.24482 NS
Nperp-A (mm) 1.6250 ± 0.47480 0.9875 ± 0.36608 NS
Nperp-Pog (mm) –4.3125 ± 0.46370 –6.7000 ± 0.77936 ***
Cond-A (mm) 94.7125 ± 0.52561 95.2125 ± 0.5451 NS
Cond-Gn (mm) 120.2430 ± 0.82898 119.2420 ± 0.79898 NS
Max-Mand (mm) 24.5075 ± 0.52171 24.0375 ± 0.51171 NS
Wits (mm) 3.6125 ± 0.37134 3.3125 ± 0.36134 NS
Ba N-NA (°) 64.0125 ± 0.34641 64.3625 ± 0.36641 NS
SpP-GoMe (°) 23.1375 ± 0.62041 23.4375 ± 0.63041 NS
SN-GoMe (°) 31.4500 ± 0.68416 30.9500 ± 0.66416 NS
(S-Go:N-Me) 68.7550 ± 0.59614 67.0625 ± 0.55099 ***
ArGo-Me (°) 123.9512 ± 0.65214 122.4422 ± 0.68085 NS
Dental variables
IMPA (°) 104.9812 ± 0.94918 102.7622 ± 0.93866 ***
Max1-NA (°) 30.7225 ± 0.84037 30.2225 ± 0.83269 NS
Mand1-NB (°) 31.7625 ± 0.80967 32.1100 ± 0.92365 ***
1u-NA (mm) 6.8375 ± 0.27047 6.2375 ± 0.25047 NS
1l-NB (mm) 7.8125 ± 0.27736 6.4375 ± 0.29059 NS
Overjet (mm) 6.1400 ± 0.28670 6.0875 ± 0.28865 NS
Overbite (mm) 2.3538 ± 0.20749 2.2125 ± 0.22398 NS
Interincisal (°) 111.8340 ± 1.37505 112.5232 ± 1.48505 NS
SpP-OcP (°) 7.6750 ± 0.41346 7.3750 ± 0.40346 NS
MeGo-OcP (°) 16.8000 ± 0.43043 16.0000 ± 0.41043 NS
Soft tissue variables
Gl’-Sn (mm) 66.3750 ± 0.56485 65.7750 ± 0.53485 NS
Sn-Me’ (mm) 66.6875 ± 0.72114 66.1875 ± 0.71114 NS
Sn-stm-s (mm) 19.8700 ± 0.28302 20.3700 ± 0.33302 NS
Stm-s - Stm-i (mm) 4.5688 ± 0.44851 4.4488 ± 0.43851 NS
Stm-i-Me’ (mm) 44.7688 ± 0.53931 44.0688 ± 0.49931 NS
SnPerp-Ls (mm) –4.5875 ± 0.23647 –4.0125 ± 0.19035 NS
SnPerp-Li (mm) –0.5375 ± 0.54131 –0.5625 ± 0.42166 NS
SnPerp-Pog’ (mm) 10.7875 ± 0.69552 9.1625 ± 0.60860 ***
CotgSnLs (°) 99.5375 ± 1.11590 97.4875 ± 1.13419 ***
Ls-NsPog’ (mm) –1.2625 ± 0.31684 –0.9625 ± 0.29684 NS
Li-NsPog’ (mm) 2.6500 ± 0.43248 2.0500 ± 0.40248 NS

***p < 0.05 ; NS - Not significant.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 129

 Review Article

Table 3. Statistical Evaluation of Skeletal, Dental, Soft Tissue Variables: Manual Tracing and Retracing after
1-week - 30 Samples
Variables Tracing-initial Retracing 1-week after Paired t-test
Sig p < 0.05

Skeletal variables
SNA (°) 83.7000 ± 0.75071 83.7667 ± 0.74999 0.161
SNB (°) 78.5667 ± 0.82446 78.6333 ± 0.81011 0.161
ANB (°) 5.1333 ± 0.37056 5.1667 ± 0.37473 0.573
Nperp-A (mm) 1.5000 ± 0.73773 1.5333 ± 0.74546 0.573
Nperp-Pog (mm) –6.0333 ± 0.91033 –6.0333 ± 0.89633 1.000
Cond-A (mm) 95.6000 ± 0.99146 95.6667 ± 0.99808 0.161
Cond-Gn (mm) 119.5000 ± 1.40258 119.5667 ± 1.41639 0.161
Max-Mand (mm) 23.7667 ± 0.80041 23.8000 ± 0.81987 0.573
Wits (mm) 3.5333 ± 0.46420 3.4667 ± 0.46420 0.161
Ba N-NA (°) 64.1333 ± 0.59255 64.2000 ± 0.62034 0.326
SpP-GoMe (°) 22.0667 ± 0.88530 22.1333 ± 0.88634 0.161
SN-GoMe (°) 29.7667 ± 1.02574 29.8333 ± 1.03954 0.161
(S-Go:N-Me) 68.6000 ± 0.85715 68.7333 ± 0.86561 0.043
ArGo-Me (°) 123.1000 ± 1.15206 123.1333 ± 1.16435 0.573
ANS-Me (mm) 68.4667 ± 1.20510 68.5333 ± 1.19840 0.021
Go-Me (mm) 75.4667 ± 1.01113 75.5333 ± 0.99969 0.161

Dental variables
IMPA (°) 106.6667 ± 1.35132 106.8000 ± 1.34027 0.073
Max1-NA (°) 30.4667 ± 1.25004 30.4333 ± 1.25275 0.573
Mand1-NB (°) 32.7667 ± 1.54376 32.7333 ± 1.54692 0.573
1u-NA (mm) 6.2000 ± 0.33010 6.2667 ± 0.32495 0.161
1l-NB (mm) 7.7333 ± 0.45469 7.8000 ± 0.45080 0.161
Overjet (mm) 5.8667 ± 0.39750 5.9000 ± 0.40215 0.573
Overbite (mm) 2.7433 ± 0.25260 2.8100 ± 0.25910 0.161
Interincisal (°) 111.8333 ± 2.27130 111.9000 ± 2.26637 0.161
SpP-OcP (°) 6.7333 ± 0.63415 0.161
6.8000 ± 0.63499
MeGo-OcP (°) 15.2069 ± 0.71813 0.184
15.1034 ± 0.72829
Soft tissue variables
Gl’-Sn (mm) 65.5667 ± 0.82306 65.6333 ± 0.82557 0.161
Sn-Me’ (mm) 66.0333 ± 1.19046 66.1000 ± 1.18453 0.161
Sn-stm-s (mm) 19.5900 ± 0.50543 19.6167 ± 0.5068 0.118
Stm-s - Stm-i (mm) 5.0300 ± 0.55602 5.0467 ± 0.55588 0.283
Stm-i-Me’ (mm) 43.8333 ± 0.86287 43.8733 ± 0.86766 0.090
SnPerp-Ls (mm) -4.4000 ± 0.27332 0.326
–4.4667 ± 0.41725
SnPerp-Li (mm) -0.2667 ± 0.76854 0.573
–0.3000 ± 0.77630
SnPerp-Pog’ (mm) 9.9000 ± 0.82539 0.042
10.8333 ± 0.82974
CotgSnLs (°) 97.1667 ± 1.89202 0.032
99.6333 ± 1.89772
Ls-NsPog’ (mm) 0.161
–1.0000 ± 0.43150
Li-NsPog’ (mm) –0.9333 ± 0.44704
1.9667 ± 0.62969 0.083
2.0333 ± 0.65026

130 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

 Review Article

Table 4. Statistical Evaluation of Skeletal, Dental, Soft Tissue Variables: Vistadent Tracing and Retracing after
1-week - 30 Samples
Variables Tracing-initial Retracing 1-week after Paired t-test
Sig p < 0.05

Skeletal variables
SNA (°) 83.7000 ± 0.7507 83.8000 ± 0.7512 0.083
SNB (°) 78.5667 ± 0.8245 78.6000 ± 0.8285 0.573
ANB (°) 5.1333 ± 0.3706 5.2000 ± 0.3601 0.161
Nperp-A (mm) 0.9333 ± 0.5929 0.9000 ± 0.5899 0.573
Nperp-Pog (mm) –6.4667 ± 1.0654 –6.4000 ± 1.0866 0.161
Cond-A (mm) 95.6000 ± 0.9915 95.6667 ± 0.9981 0.161
Cond-Gn (mm) 119.5000 ± 1.4026 119.5333 ± 1.4026 0.573
Max-Mand (mm) 23.7667 ± 0.8004 23.8333 ± 0.8010 0.161
Wits (mm) 3.3667 ± 0.4806 3.4000 ± 0.4997 0.573
Ba N-NA (°) 64.1333 ± 0.5925 64.1667 ± 0.5952 0.573
SpP-GoMe (°) 22.0667 ± 0.8853 22.1000 ± 0.8701 0.573
SN-GoMe (°) 29.7667 ± 1.0257 29.8000 ± 1.0265 0.573
(S-Go:N-Me) 68.2667 ± 0.8853 70.1667 ± 0.9149 0.280
ArGo-Me (°) 121.0667 ± 1.1254 123.3333 ± 1.1520 0.161
ANS-Me (mm) 66.0000 ± 1.2327 68.3333 ± 1.2095 0.573
Go-Me (mm) 75.4667 ± 1.0111 75.5333 ± 1.0134 0.161
Dental variables
IMPA (°) 104.3333 ± 1.3496 104.6000 ± 1.3136 0.088
Max1-NA (°) 30.4800 ± 1.2627 30.4700 ± 1.2610 0.794
Mand1-NB (°) 32.6700 ± 1.4877 32.6700 ± 1.4877 0.161
1u-NA (mm) 6.2000 ± 0.3301 6.2667 ± 0.3285 0.161
1l-NB (mm) 6.4333 ± 0.4929 6.5333 ± 0.4953 0.083
Overjet (mm) 5.8567 ± 0.4058 5.8833 ± 0.4038 0.608
Overbite (mm) 2.6633 ± 0.2602 2.6867 ± 0.2590 0.090
Interincisal (°) 111.8333 ± 2.2713 111.9333 ± 2.2848 0.083
SpP-OcP (°) 6.7333 ± 0.6341 6.8333 ± 0.6362 0.083
MeGo-OcP (°) 15.2069 ± 0.7181 15.2759 ± 0.7343 0.424
Soft tissue variables
Gl’-Sn (mm) 65.5667 ± 0.8231 65.6667 ± 0.8295 0.083
Sn-Me’ (mm) 66.0333 ± 1.1905 66.0667 ± 1.1870 0.326
Sn-stm-s (mm) 19.5900 ± 0.5054 19.6167 ± 0.5068 0.103
Stm-s - Stmi (mm) 5.0300 ± 0.5560 5.0800 ± 0.5689 0.154
Stm-i-Me’ (mm) 43.8333 ± 0.8629 43.8733 ± 0.8564 0.103
SnPerp-Ls (mm) –3.9667 ± 0.2733 –4.0667 ± 0.2874 0.083
SnPerp-Li (mm) 0.161
–0.4000 ± 0.5805 –0.3333 ± 0.5918
SnPerp-Pog’ (mm) 0.047
8.4000 ± 0.8525 9.3333 ± 0.8608
CotgSnLs (°) 0.032
98.1667 ± 1.8920 100.6333 ± 1.8977
Ls-NsPog’ (mm) 1.000
–1.0000 ± 0.4315 –1.0000 ± 0.4315
Li-NsPog’ (mm) 0.161
1.9667 ± 0.6297 2.0333 ± 0.6370

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 131

 Review Article

Table 5. Manual Tracing: Vistadent Tracing 1-week Later

Variables Manual tracing 1-week later Vistadent tracing 1-week later t-test
Sig p < 0.05

Skeletal Variables
SNA (°) 83.7667 ± 0.74999 83.8000 ± 0.7511 0.975
SNB (°) 78.6333 ± 0.81011 78.6000 ± 0.8285 0.977
ANB (°) 5.1667 ± 0.37473 5.2000 ± 0.3601 0.949
Nperp-A (mm) 1.5333 ± 0.74546 0.9000 ± 0.5899 0.508
Nperp-Pog (mm) –6.0333 ± 0.89633 –5.4000 ± 1.0866 0.043
Cond-A (mm) 95.6667 ± 0.99808 95.6667 ± 0.9981 1.000
Cond-Gn (mm) 119.5667 ± 1.41639 119.5333 ± 1.4026 0.987
Max-Mand (mm) 23.8000 ± 0.81987 23.8333 ± 0.8010 0.977
Wits (mm) 3.4667 ± 0.46420 3.4000 ± 0.4997 0.922
Ba N-NA (°) 64.2000 ± 0.62034 64.1667 ± 0.5952 0.969
SpP-GoMe (°) 22.1333 ± 0.88634 22.1000 ± 0.8701 0.979
SN-GoMe (°) 29.8333 ± 1.03954 29.8000 ± 1.0265 0.982
(S-Go:N-Me) 68.7333 ± 0.86561 70.1667 ± 0.9149 0.023
ArGo-Me (°) 123.1333 ± 1.16435 123.3333 ± 1.1520 0.903
ANS-Me (mm) 66.5333 ± 1.19840 68.3333 ± 1.2095 0.034
Go-Me (mm) 75.5633 ± 0.99969 75.5333 ± 1.0134 0.989
Dental variables
IMPA (°) 106.8000 ± 1.34027 104.6000 ± 1.3136 0.246
Max1-NA (°) 30.4333 ± 1.25275 30.4700 ± 1.2610 0.984
Mand1-NB (°) 32.7333 ± 1.54692 32.6700 ± 1.4877 0.977
1u-NA (mm) 6.2667 ± 0.32495 6.2667 ± 0.3285 1.000
1l-NB (mm) 7.1000 ± 0.45080 6.8333 ± 0.4953 0.646
Overjet (mm) 5.9000 ± 0.40215 5.8833 ± 0.4038 0.977
Overbite (mm) 2.8100 ± 0.25910 2.6867 ± 0.259 0.738
Interincisal (°) 111.9000 ± 2.26637 111.9333 ± 2.2848 0.992
SpP-OcP (°) 6.8000 ± 0.63499 6.8333 ± 0.6362 0.971
MeGo-OcP (°) 15.1034 ± 0.72829 15.2759 ± 0.7343 0.895
Soft tissue variables
Gl’-Sn (mm) 65.6333 ± 0.82557 65.6667 ± 0.8295 0.977
Sn-Me’ (mm) 66.1000 ± 0.16637 66.0667 ± 1.1870 0.984
Sn-stm-s (mm) 19.6167 ± 0.5068 19.6167 ± 0.5068 1.000
Stm-s - Stm-i (mm) 5.0800 ± 0.5689 5.0800 ± 0.5689 0.967
Stm-i-Me’ (mm) 43.8733 ± 0.8564 43.8733 ± 0.8564 1.000
SnPerp-Ls (mm) –4.0667 ± 0.2874 –4.0667 ± 0.2874 0.433
SnPerp-Li (mm) –0.3333 ± 0.5918 –0.3333 ± 0.5918 0.973
SnPerp-Pog’ (mm) 9.7333 ± 0.8608 8.3333 ± 0.8608 0.034
CotgSnLs (°) 102.6333 ± 1.8977 100.6333 ± 1.8977 0.047
Ls-NsPog’ (mm) –1.0000 ± 0.4315 –1.0000 ± 0.4315 0.915
Li-NsPog’ (mm) 2.0333 ± 0.6370 2.0333 ± 0.6370 0.971

132 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011


Jarbak ratio (p = 0.021), ANS-Me (p = 0.043), IMPA
(p = 0.032), Mand1-NB (p = 0.043), SnPerp-Pog’
(p = 0.041) and CotgSnLs (p = 0.023). When comparing
hand tracing initial and Retracing 1-week later
(Table 3), Jarabak ratio (p = 0.043), ANS-Me
(p = 0.021), Snperp-Pog’ (p = 0.042) and nasolabial
angle (p = 0.032) showed significant difference.
Between Vistadent tracing initial and retracing 1-week
later (Table 4), Snperp-Pog’ (p = 0.047) and CotgSnLs
(p = 0.032) showed significant difference. When
comparing hand and vistadent retracing 1-week later
(Table 5), Nperp-pog (p = 0.043), Jarabak ratio
(p = 0.023), ANS-Me (p = 0.034), Snperp-Pog’
(p = 0.034) and CotgSnLs (p = 0.047) showed
significant difference.
Discussion
Landmark identification from digital images can
be affected by several factors such as spatial and
contrast resolution of the display device, background
luminance level and luminance range of the display
system, brightness uniformity, extraneous light
in the reading room, displayed field size, viewing
distance magnification functions and user interface as
stated by Yu et al.10 Linear measurements may be
affected by the inclination of the reference line, and
angular measurements cannot indicate correctly
the jaw relationship in the case of extreme facial
divergence as stated by Williams et al.16 Therefore, it is
reasonable to evaluate a set of structural relationships
by multiple cephalometric parameters rather than by
a single parameter. This is the reason why as many as
37 variables were included in our customized
cephalometric analysis.
The cephalometric radiographs used in this study
were randomly selected and represented the quality of
daily routine work. The skeletal, dental and soft tissue
variables used in this study were commonly used
cephalometric variables for orthodontic diagnosis,
treatment planning and evaluation of treatment
results.
Landmark identification is greatly affected by operator
experience, which might be as important as the
tracing method itself. Because interoperator error has
in general been found to be greater than intraoperator
error as stated by Sayinsu et al,12 to minimize the error
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Review Article
all measurements in this study were carried out by
one examiner. In this study, the overall differences of
landmark location between the two modalities were
statistically significant. The extent of difference for
each landmark depends on the radiographic
complexities, which are also associated with the
reliability of landmarks. The representation of
head films and observers should be considered as
possible sources of error when comparing computer-
aided cephalometric analysis based on conventional
radiographs and digitized images.
Between hand tracing and Vistadent tracing, out of
16 skeletal variables compared, three variables showed
significant difference i.e., Pog-N-perp (p = 0.032),
Jarabak ratio (p = 0.021) and ANS-Me (p = 0.043).
The uncertainty in locating the Me and Gn points
may be caused by the difficulty of delineating a
landmark on a curved anatomical boundary. Lim and
Foong,5 in his article ‘Phosphor-stimulated computed
cephalometry, reliability of landmark identification’
stated anatomical landmarks with low radiodensity,
e.g., orbitale; a point and those ending in thin taper,
e.g., anterior and posterior nasal spine tend to be less
reliable. Chen et al17 assessed landmark identification on
digital images in comparison with those obtained from
original radiographs and reported low reproducibility
for Go, Me, and Po25. Santoro et al11 evaluated the
accuracy of cephalometric measurements obtained
with digital tracing software compared with equivalent
hand-traced measurement and reported differences
between the two methods for SNA, ANB, S-Go:
N-Me, U1/L1, L1-GoGn and N-ANS:ANS-Me were
statistically significant.
Among the 10 dental variables compared, two showed
significant difference i.e., IMPA (p = 0.032) and
L1-NB (p = 0.043). The significant measurement
difference for L1-NB angle could be due to differences
in the horizontal component of the location of
Gonçalves et al2 in comparison of cephalometric
measurements from three radiological clinics stated
IMPA cephalometric measurements presented
with statistically significant difference. In order to
determine the error of both conventional and digitized
cephalometric methods, a study by Martins et al7
demonstrated that regardless of the method used, the
incorporation of errors may occur, particularly for
those measurements involving incisors, which present
a greater number of errors.
133
 Review Article
Among the soft tissue variables SnPerp-Pog’
(p = 0.041) and nasolabial angle (p = 0.023) showed
significant difference. The results of nasolabial
angle coincides with the results of Celik et al1
nasolabial angle, depends on landmarks that are placed
on a curve with wide radii which show proportionally
greater errors of measurements as reported by
Baumrind and Frantz.13,14 This type of error can
be made regardless of the method (digital-manual)
used for measurement as reported by Sayinsu et al.12
When comparing hand tracing, initial and retracing
1-week later, out of 16 skeletal variables two variables
Jarabak ratio (p = 0.043) and ANS-Me (p = 0.021)
showed significant difference. Among the soft tissue
variables SnPerp-Pog’ (p = 0.042) and nasolabial angle
(p = 0.032) showed significant difference. Between
Vistadent tracing, initial and retracing 1-week later,
among the soft tissue variables SnPerp-Pog’ (p = 0.047)
and nasolabial angle (p = 0.032) showed significant
difference.
When comparing hand and Vistadent retracing 1-week
later, out of 16 skeletal variables three variables - Nperp-
Pog (p = 0.043), Jarabak ratio (p = 0.023), ANS-Me
(p = 0.034) showed significant difference. Among
the soft tissue variables SnPerp-Pog’ (p = 0.034)
and nasolabial angle (p = 0.047) showed significant
difference.
Conclusion
The study indicates that most of the variables show
consistency between manual tracing and computerized
tracing while most of the cephalometric variables were
reliable.
Suggested Reading
1. Celik E, Polat-Ozsoy O, Toygar Memikoglu TU.
Comparison of cephalometric measurements with digital
versus conventional cephalometric analysis. Eur J Orthod
2009;31(3):241-6.
2. Gonçalves FA, Schiavon L, Pereira Neto JS, Nouer DF.
Comparison of cephalometric measurements from three
radiological clinics. Braz Oral Res 2006;20(2):162-6.
3. Geelen W, Wenzel A, Gotfredsen E, Kruger M,
Hansson LG. Reproducibility of cephalometric
landmarks on conventional film, hardcopy, and monitor-
displayed images obtained by the storage phosphor
technique. Eur J Orthod 1998;20(3):331-40.
134
4. Quintero JC, Trosien A, Hatcher D, Kapila S. Cranio-
facial imaging in orthodontics: historical perspective,
current status, and future developments. Angle Orthod
1999;69(6):491-506.
5. Lim KF, Foong KW. Phosphor-stimulated computed
cephalometry: reliability of landmark identification.
Br J Orthod 1997;24(4):301-8.
6. Gregston MD, Kula T, Hardman P, Glaros A, Kula K.
A comparison of conventional and digital radiographic
methods and cephalometric analysis software: I-Hard
tissue. Semin Orthod 2004;10(3):204-11.
7. Martins LP, Pinto AS, Martins JCR, Mendes AJD. Error
reproducibility of cephalometric analysis of Steiner and
Ricketts, the conventional method and the computerized
method. Orthodontics 1995;28(1):4-17.
8. Ricketts MM. Perspectives in the clinical application
of cephalometries. The first fifty years. Angle Orthod
1981;51(2):115-50.
9. Sandler PJ. Reproducibility of cephalometric measure-
ments. Br Orthod 1988;15(2):105-10.
10. Yu SH, Nahm DS, Baek SH. Reliability of
landmark identification on monitor-displayed lateral
cephalometric images. Am J Orthod Dentofacial Orthop
2008;133(6):790.e1-6;discussion e1.
11. Santoro M, Jarjoura K, Cangialosi TJ. Accuracy of
digital and analogue cephalometric measurements
assessed with the sandwich technique. Am J Orthod
Dentofacial Orthop 2006;129(3):345-51.
12. Sayinsu K, Isik F, Trakyali G, Arun T. An evaluation of
the errors in cephalometric measurements on scanned
cephalometric images and conventional tracings. Eur J
Orthod 2007;29(1):105-8.
13. Baumrind S, Frantz RC. The reliability of head film
measurements. Landmark identification. Am J Orthod
1971;60(2):111-27.
14. Baumrind S, Frantz RC. The reliability of head film
measurements. 2. Conventional angular and linear
measures. Am J Orthod 1971;60(5):505-17.
15. Trindade Junior AS, Adams GA, Capelozza Son L.
Rapid maxillary expansion: a prospective cephalometric
analysis. Orthodo 1999;32(1):45-56.
16. Williams S, Leighton BC, Nielsen JH. Linear evaluation
of the development of sagittal jaw relationship. Am
J Orthod 1985;88:(3)235-41.
17. Chen YJ, Chen SK, Chang HF, Chen KC. Comparison
of landmark identification in traditional versus
computer-aided digital cephalometry. Angle Orthod
2000;70(5):387-92.
n n n
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Peripheral Ameloblastoma: Review of Literature and
Case Presentation
Renu Yadav*, Anubha Gulati**, Rahul Sharma†, Satya Narain†
Abstract
Peripheral ameloblastoma (PA) is a rare soft tissue neoplasm of odontogenic origin that arises in the tooth-bearing gingiva of
the maxilla and mandible. This article describes a case of PA located in the lingual gingiva of the mandible in a 48-year-old
male with a review of the English literature.
Key words: Peripheral ameloblastoma, lingual gingiva, soft tissue ameloblastoma, extraosseous ameloblastoma, ameloblastoma
of the gingiva
P
eripheral ameloblastoma (PA) is a relatively
uncommon odontogenic tumor that is
histologically identical to the classic intraosseous
ameloblastoma.1 It originates in the soft tissues of
the oral cavity namely alveolar mucosa or gingiva.2
It accounts for 1-5% of all ameloblastomas.3,4 Kuru,
first reported PA in 1911.5,6 However, Philipsen et al
stated that what Kuru described was not a peripheral,
but rather an intraosseous ameloblastoma having
penetrated through the alveolar bone, fused with the
oral epithelium and eventually presented itself clinically
as a ‘peripheral lesion’.
They also supported the fact that the first completely
documented case of a PA must be attributed to
Stanley and Krogh, who defined the clinical and
histopathologic characteristics of the lesion in 1959.5-8
This article describes a case of gingival PA of the
mandible and reviews the English literature.
Case Report
A 48-year-old male patient reported to our OPD with
a complaint of growth on the lingual aspect of the left
side of the mandible. The growth had been present for
the previous 1-year and was slowly increasing in size.
The intraoral examination disclosed a nontender mass
*Assistant Professor
**Associate Professor, Dept. of Oral Pathology
†
Associate Professor, Dept. of Oral Surgery
Dr HSJ Institute of Dental Sciences and Hospital, Chandigarh
Address for correspondence
Dr Renu Yadav
House No.: 924, Ashirwad Enclave
Sector-49-A, Chandigarh -160 047
E-mail: renyadava@gmail.com
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
review article
extending from the lingual gingiva spanning from the
mandibular left central incisor to the left canine. The
growth was ovoid, reddish grey in color, firm and fixed
to the underlying structures and measured 1 × 1 cm2
approximately. All the involved teeth tested vital.
The patient had a very poor oral hygiene and also
suffered from generalized periodontitis. The patient’s
social history was significant for use of chewing betel
nut quid and consumption of alcohol for the past
five and 15 years, respectively. The radiographic
examination did not reveal any signs of bone
involvement (Fig. 1).
The differential diagnosis included: Pyogenic
granuloma, peripheral ossifying fibroma and benign
fibrous lesion. The growth was surgically excised
under local anesthesia. The mass could be easily
separated from the underlying bone but there was
profuse bleeding associated with it. The surgical wound
healed uneventfully.
On microscopic examination, the tissue depicted dense
connective tissue stroma containing islands and cords
of odontogenic epithelium. Some portion of the lesion
was covered by stratified squamous epithelium with
mild acanthotic changes (Fig. 2).
Many islands and cords showed microcyst formation
and central polygonal cells surrounded by ameloblast-
like cells (Fig. 3). Some islands exhibited squamous
metaplasia of the central stellate reticulum-like cells
(Fig. 4). The histologic findings were consistent with a
diagnosis of peripheral ameloblastoma, follicular type
with acanthomatous changes.
135
 Review Article
Figure 1. No bone involvement is seen in the IOPA.
Figure 3. Islands and cords of odontogenic epithelium
showing microcysts and central polygonal cells surrounded
by ameloblast-like cells (H&E stain, X10).
Discussion
A review of the English literature disclosed 70 well-
documented cases of PA till 2005.5 Since, then very
few cases have been reported.3,6,9,10 PA is also known
as mucosal, extramedullary, extraosseous, soft tissue
ameloblastoma or ameloblastoma of the gingiva.7,11
According to Buchner and Sciubba, PA is defined
as a tumor with the histologic characteristics of an
intraosseous ameloblastoma but occurring in the soft
tissue overlying the tooth-bearing regions of the maxilla
and mandible.11,12 According to WHO classification
(2005), “the extraosseous/PA is the extraosseous
counterpart of the intraosseous solid/multicystic
ameloblastoma”.13
PA is a painless, sessile, firm and exophytic growth
with relatively smooth sometimes granular, pebbly,
papillary or warty surface.7,14 The color of the lesion
136
Figure 2. Surface epithelium showing acanthosis (H&E
stain, X10).
Figure 4. Island exhibiting squamous metaplasia of the central
stellate reticulum-like cells (H&E stain, X40).
varies between normal or pink and red or dark red.7
During mastication, the PA may become traumatized,
and the lesion may thus show an ulcerated surface or
may appear keratotic (frictional keratosis). The duration
of the lesion is reported to be anywhere between two
days and 20 years, and the size ranges from 0.3 to 4.5
cm in diameter with a mean of 1.3 cm.7 According to
Shetty,5 the average size of the lesion measured
between 1 and 2 cm. Pekiner et al reported the average
size range to be between 0.5-2.0 cm. In a study by
Mintz et al, the tumors ranged between 0.2 and 4.0 cm
in diameter, with a mean of 1.4 cm.15 In the present
case, the growth was 1 cm in diameter and had been
present for the past 1-year.
The lesions are primarily extraosseous and the bone
changes are seldom present.14 There is no report of
any radiological evidence of bone involvement7 in the
literature which was also true in the present case. The
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

small lesions have an inferior margin that is usually
superficial to the cortical bone. The large lesions have
an advancing margin that produces a cup-shaped
resorption of the cortical plate. Occasionally, there will
be a superficial saucerization of the cortical plate seen
radiologically or at surgery.14 Cupping or saucerization
is thought to be due to pressure resorption6,16 in
contrast to resorption caused by neoplastic invasion.7
PA is rarely the initial presenting diagnosis to be made.7
The differential diagnosis must be made with fibrous
nodule, gingival tumors, peripheral odontogenic
fibroma, peripheral ossifying fibroma, pyogenic
granuloma, peripheral giant-cell granuloma, papilloma,
peripheral squamous odontogenic tumor and other
hyperplastic swellings superficial to the alveolar
ridge.3,7,14,17 When the PA arises on the edentulous
alveolar mucosa in denture wearing patients, the PA
may be diagnosed as denture irritation hyperplasia.
However, the final diagnosis requires histologic
evaluation.7
PA accounts for 1-10% for all ameloblastomas.18
According to Philipsen et al PA comprises 2-10%
of all ameloblastomas. They also mentioned that PA
is in fact more prevalent than hitherto anticipated7
whereas according to WHO, PA comprises 1.3-10%
of all ameloblastomas.8,13 The age range of the patients
with PA as reported by Philipsen et al is between
9 and 92 years at the time of diagnosis with an overall
average of 52.1 years.6-8 Pekiner et al and Shiba et al
have documented patients’ age range to be between
23-82 years.14,19 According to Gurol et al the average
age was 62 years.20 The PA is more commonly seen
in men with a male-to-female ratio of 1.9:1.7,8,13 In a
study by El-Mofty and Gurol, no gender predilection
was found.1,20 A male-to female ratio of 1.7:1 has been
observed by Mintz and Buchner in their studies.15,16
Mandible has been clearly the most common site of
occurrence for PA.7,12,15,20,21 The maxilla-to-mandible
ratio is 1:2.46,13 with the mandibular premolar region to
be the most common site of involvement15,19 followed
by anterior mandibular region and maxillary tuberosity.
In the mandible, the lingual aspect of the gingiva is
the most common site of involvement.7 According to
Zhu et al’s study of 16 cases, the sites of involvement
in the mandible were the canine-premolar region,
molar region, incisor region while in the maxilla, the
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Review Article
tuberosity region was the most common followed by
premolar region.12 In the present case the lesion was
found in the mandibular anterior region and the age
of the patient was 48 years which is well within the
age range mentioned in the literature.
In Philipsen et al’s study, the extragingival lesions were
not accepted under the diagnosis of PA.7 They further
quoted that the extragingival lesions most likely
represent basal cell adenomas with a histopathological
resemblance to an ameloblastoma or the rare
ameloblastoid variant of the squamous cell carcinoma.
It is characteristic that all cases reported as extragingival
PA developed around the orifices of either the Stensen’s
duct or the Wharton’s duct and could thus represent
tumors of salivary origin. In addition seven cases of
extragingival PA have been reported out of which six
were found in the buccal mucosa and one in the floor
of the mouth.22,23
Two histogenetic origins for the PA have been proposed.
Tumors that show complete separation from overlying
surface epithelium probably arise from odontogenic
epithelial remnants. Tumors showing direct extension
from the surface epithelium may arise from the basal
cell layer of the overlying epithelium,9,10,24,25 although
a collision phenomenon cannot be entirely ruled
out.1,17,26 The gross specimen consists of a firm to
slightly spongy mass of pink to pinkish grey color.
The cut surface may contain minute cystic spaces filled
with clear, pale yellow fluid.7 Histologically, the tissue
is composed of islands and strands of odontogenic
epithelium, usually resembling the follicular pattern
of intraosseous ameloblastoma. Most of the islands
exhibit palisading of columnar basal cells and a stellate
reticulum is seldom conspicuous.7,14 The epithelial
islands commonly exhibit the acanthomatous variant
of this pattern, with central areas of keratin formation,
or the cystic pattern. In some lesions, the epithelial
strands are in continuity with the surface epithelium
and appear to arise from this origin. The epithelial
islands and strands are usually surrounded by fibrous
tissue.14 Literature reveals a documented case of a
PA with clear cells differentiation. The lesion in this
case depicted a follicular pattern with few islands
exhibiting acanthomatous changes. The clear cells have
vesicular, centrally placed nuclei and faintly granular
or vacuolated cytoplasm.27 Redman et al reported 0.4
mitotic figures per field (207 in 477 fields) and those
137
 Review Article
numbers seemed to be more frequent in inflamed
than in noninflamed portions of the overlying
stratified squamous epithelium.16 Mintz et al in their
review of literature stated that the acanthomatous
type was the most prevalent followed by plexiform
and follicular types. In their study, another set of
cases was reported as combinations of reticular,
basaloid, and/or acanthomatous type.15 Curtis and
Zoellner also reported a case of acanthomatous
from of PA.28 Mintz et al reported a case of
metastasis to cervical lymph nodes which reported
to have occurred two days post surgery of a follicular
PA.15 In the literature there are no reports of
malignant extragingival PA, whereas several cases of
gingival PA with malignancy have been reported.22
An immunohistochemical study performed by
Kishino et al suggests that PA originates from
odontogenic epithelial remnants rather than from the
gingival epithelium, and the Ki-67 labeling index of
the tumor is a good prognostic indicator.29 PA could
be differentiated from basal cell carcinoma with
immunohistochemical staining for cytokeratin-19
and Ber-EP4 where use of CK-19 shows positivity
for ameloblastic cells and Ber-EP 4 shows positivity for
neoplastic basal cells.30
The recommended treatment for peripheral
ameloblastoma differs from the treatment of other
forms of ameloblastoma because the tumor is usually
small and remains localized to the superficial soft
tissue.14 Most lesions are successfully managed with
local excision that includes a small margin of normal
tissue.14,31,32 The inferior margin should include the
periosteum to ensure that bone penetration has not
occurred.
According to Ide et al en bloc resection seems curative
when PA presents as a large papillary tumor (larger
than 1.5-2.0 cm) with an erosion of the underlying
bone.32,33 Ide et al34 suggested that large size (over 2
cm in diameter) is a powerful predictor of aggressive
behavior of PA, no matter how bland.34 PA does not
show invasive behavior and conservative excision is
the treatment of choice. The recurrence rate is low
(16-19%).8,13 Long-term follow-up is recommended24,31
especially for lesions with aggressive behavior.13,22,33
The present case was treated by surgical excision with
wide margins and has not shown any recurrence in the
2-year follow-up.
138
Acknowledgement
We thank Mr. Tarsem Raj for his skillful technical
assistance.
References
1. El-Mofty SK, Gerard NO, Farish SE, Rodu B. Peripheral
ameloblastoma: a clinical and histologic study of 11
cases. J Oral Maxillofac Surg 1991;49(9):970-4;
discussion 974-5.
2. Schaberg SJ, Antimarino RF, Pierce GL, Crawford BE.
Peripheral ameloblastoma. Report of a case. Int J Oral
Surg 1983;12(5):344-7.
3. Martelli-Júnior H, Souza LN, Santos LA, Melo-Filho
MR, De Paula AM. Peripheral ameloblastoma: a case
report. Oral Surg Oral Med Oral Pathol Oral Radiol
Endod 2005;99(5):E31-3.
4. Wettan HL, Patella PA, Freedman PD. Peripheral
ameloblastoma: review of the literature and report of
recurrence as severe dysplasia. J Oral Maxillofac Surg
2001;59(7):811-5.
5. Shetty K. Peripheral ameloblastoma: an etiology
from surface epithelium? Case report and review of
literature. Oral Oncol Extra 2005;41(9):211-5.
6. Lecorn DW, Bhattacharyya I, Vertucci FJ. Peripheral
ameloblastoma: a case report and review of the
literature. J Endod 2006;32(2):152-4.
7. Philipsen HP, Reichart PA, Nikai H, Takata T,
Kudo Y. Peripheral ameloblastoma: biological profile
based on 160 cases from the literature. Oral Oncol
2001;37(1):17-27.
8. Gomes CC, Garcia BG, Gomez RS, de Freitas JB,
Mesquita RA. A clinical case of peripheral ameloblastoma.
Braz J Oral Sci 2007;6(21):1364-6.
9. Vanoven BJ, Parker NP, Petruzzelli GJ. Peripheral
ameloblastoma of the maxilla: a case report and literature
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10. Ide F, Mishima K, Miyazaki Y, Saito I, Kusama K.
Peripheral ameloblastoma in-situ: an evidential fact of
surface epithelium origin. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod 2009;108(5):763-7.
11. Woo SB, Smith-Williams JE, Sciubba JJ, Lipper S.
Peripheral ameloblastoma of the buccal mucosa: case
report and review of the English literature. Oral Surg
Oral Med Oral Pathol 1987;63(1):78-84.
12. Zhu EX, Okada N, Takagi M. Peripheral ameloblastoma:
case report and review of literature. J Oral Maxillofac
Surg 1995;53(5):590-4.
13. WHO classification of tumors. Pathology and
Genetics of Head and Neck Tumors Chapter 6.
Odontogenic tumors; IARC: Lyon 2006:297-8.
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14. Pekiner FN, Özbayrak S, Şener BC, Olgaç V,
Sinanoğlu A. Peripheral ameloblastoma: a case report.
Dentomaxillofac Radiol 2007;36(3):183-6.
15. Mintz S, Anavi Y, Sabes WR. Peripheral ameloblastoma
of the gingiva. A case report. J Periodontol
1990;61(10):649‑52.
16. Redman RS, Keegan BP, Spector CJ, Patterson RH.
Peripheral ameloblastoma with unusual mitotic activity
and conflicting evidence regarding histogenesis. J Oral
Maxillofac Surg 1994;52(2):192-7.
17. Orsini G, Fioroni M, Rubini C, Piattelli A. Peripheral
ameloblastoma: a report of 2 cases. J Periodontol 2000;
71(7):1174-6.
18. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral
and maxillofacial pathology. In: Odontogenic Cysts and
Tumors. 3rd edition, Neville BW, Damm DD, Allen
CM, Bouquot JE, (Eds.), Elsevier: Noida 2009:710.
19. Shiba R, Sakoda S, Yamada N. Peripheral ameloblastoma.
J Oral Maxillofac Surg 1983;41(7):460-3.
20. Gurol M, Burkes EJ Jr. Peripheral ameloblastoma.
J Periodontol 1995;66(12):1065-8.
21. Smullin SE, Faquin W, Susarla SM, Kaban LB. Peripheral
desmoplastic ameloblastoma: report of a case and
literature review. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 2008;105(1):37-40.
22. Isomura ET, Okura M, Ishimoto S,
Ono Y, Kishino M, et al. Case
extragingival peripheral ameloblastoma
mucosa. Oral Surg Oral Med Oral Pathol
Endod 2009;108(4):577-9.
23. Ramnarayan K, Nayak RG, Kavalam AG. Peripheral
ameloblastoma. Int J Oral Surg 1985;14(3):300-1.
24. Patrikiou A, Papanicolaou S, Stylogianni E,
Sotiriadou S. Peripheral ameloblastoma. Case report
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and review of the literature. Int J Oral Surg
1983;12(1):51‑5.
25. Califano L, Maremonti P, Boscaino A, De Rosa G,
Giardino C. Peripheral ameloblastoma: report of a
case with malignant aspect. Br J Oral Maxillofac Surg
1996;34(3):240-2.
26. Gardner DG. Peripheral ameloblastoma: a study of 21
cases, including 5 reported as basal cell carcinoma of the
gingiva. Cancer 1977;39(4):1625-33.
27. Ng KH, Siar CH. Peripheral ameloblastoma with clear
cell differentiation. Oral Surg Oral Med Oral Pathol
1990;70(2):210-3.
28. Curtis NJ, Zoellner H. Surgical management of an
ameloblastoma in soft tissues of the cheek. Br J Oral
Maxillofac Surg 2006;44(6):495-6.
29. Kishino M, Murakami S, Yuki M, Iida S, Ogawa I,
Kogo M, et al. An immunohistochemical study of the
peripheral ameloblastoma. Oral Dis 2007;13(6):575‑80.
30. Lentini M, Simone A, Carrozza G. Peripheral
ameloblastoma: use of cytokeratin 19 and Ber-EP4
to distinguish it from basal cell carcinoma. Oral
Oncol Extra 2004;40(6-7):79-80.
31. Anneroth G, Johansson B. Peripheral ameloblastoma.
Int J Oral Surg 1985;14(3):295-9.
32. Ide F, Kusama K, Tanaka A, Sakashita H. Peripheral
ameloblastoma is not a hamartoma but rather more of a
Yamada C, neoplasm. Oral Oncol 2002;38(3):318-20.
report of
33. Tajima Y, Kuroda-Kawasaki M, Ohno J, Yi J,
in buccal Kusama K, Tanaka H, et al. Peripheral ameloblastoma
Oral Radiol with potentially malignant features: report of
a case with special regard to its keratin profile.
J Oral Pathol Med 2001;30(8):494-8.
34. Ide F, Kusama K. Difficulty in predicting biological
behavior of peripheral ameloblastoma. Oral Oncol
2004;40(6):651-2.
n n n
139
 review article

Antioxidants in Periodontal Diseases: A Review

S Lakshmi Sree*, R Mythili**

Abstract
Periodontal disease is considered an inflammatory disorder that damages tissue through the complex interactions between
periodontopathic bacteria and host defense systems. It is likely that the role of reactive oxygen species (ROS) is common
to both bacterial- and host-mediated pathways of tissue damage. In recent years, there has been a tremendous expansion in
the medical and dental research concerned with free radicals (FR), ROS and antioxidant defense mechanisms. This review is
intended to provide a critical up-to-date summary of the field with particular emphasis on the evidence for oxidative damage
and compromised antioxidant status in periodontal diseases.

Key words: Reactive oxygen species/free radicals, antioxidants, polymorphonuclear neutrophils, periodontal disease

P
eriodontitis, an inflammatory disease, is
considered to be initiated and perpetuated by
a small group of predominantly gram-negative,
anaerobic or microaerophilic bacteria that colonize the
subgingival area. Bacteria cause the observed tissue
destruction directly by toxic products and indirectly by
activating host defense systems (i.e. inflammation).1
Polymorphonuclear Leukocytes: A Key
Role in Periodontitis
Polymorphonuclear leukocytes (PMNs) are the
predominant leukocytes in blood and constitute the
primary cellular host resistance factor against infection.2
In the oral cavity, following plaque accumulation
and the development of clinical inflammation, 90%
of leukocytes that enter the gingival crevicular fluid
(GCF) and 50% of those that infiltrate junctional
epithelium are PMNs.3
PMNs possess at least two main pathways for
controlling micro-organisms (i.e., oxidative and
nonoxidative) which either kill bacteria, influence
bacterial growth or modify bacterial colonization in
relation to the periodontium.4 Upon recognition of a
*Reader
**Professor and Head, Division of Periodontia, RMDCH
Annamalai University, Chidambaram, Tamil Nadu
Address for correspondence
Dr S Lakshmi Sree
Aishwaryam, 7(110), 8th Cross, Kanagasabai Nagar
Chidambaram, Tamil Nadu - 608 001
E-mail: periolakshmi@gmail.com
phagocytic or soluble stimulus, both neutrophils and
macrophages experience a ‘respiratory burst’, which is
characterized by an increase in oxygen consumption,
activation of the hexose-monophosphate (HMP)
shunt and generation of free radicals (FR), reactive
species and their metabolic products.5 At sites of chronic
inflammation, there is considerable over production of
FR and reactive species.
Free Radicals Definition and Formation
A FR may be defined as an atomic or molecular
species capable of independent existence with one or
more unpaired electrons in its structure.6 FR can be
positively (NAD°+) or negatively charged (O2°¯) or
electrically neutral (OH°).
A feature of the reactions of FR is that they tend to
proceed as chain reactions, one radical begets another
one and so on.6 The reactive species including reactive
oxygen species (ROS), reactive chlorine species (e.g.,
HOCl hypochlorous acid) and reactive nitrogen species
(RNS) are produced in large quantities by activated
neutrophils.7
ROS Definition and Formation
In recent years the term ROS has been adopted to
include molecules such as hydrogen peroxide (H2O2),
hypochlorous acid (HOCl) and singlet oxygen (1O2),
which whilst not radicals in nature, are capable of
radical formation in the extra- and intracellular
environments.3

140 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

 Review Article

The most important species implicated in inflammatory
injuries to tissues are the hydroxyl (OH°) radical,
the superoxide anion (O2°¯), the nitric oxide (NO°)
radical (where ‘°’ signifies an unpaired electron) and
hypochlorous acid, hydrogen peroxide and 1O2, which
are ROS.3
Potential Mechanisms for Periodontal
Tissue Destruction by ROS (Fig. 1)
 Protein damage, including gingival hyaluronic acid
and proteoglycans.8
 Oxidation of important enzymes e.g. antiproteases
such as α-1antitrypsin.
 Stimulation of pro-inflammatory cytokine release
by monocytes and macrophages by depleting
intracellular thiol compounds and activating
nuclear factor kB (NFkB).

Whilst most ROS have extremely short half-lives as
10–9 to 10–6 s (Pryor 1986), they can cause substantial
tissue damage by initiating free radical chain reactions.
Different mechanisms, which mediate tissue damage,
include the following:3
 DNA damage
 Lipid peroxidation (through activation of cyclo-
oxygenases and lipo-oxygenases).
Recent reports1 have also suggested that ROS are
produced by osteoclasts at the ruffled border/bone
interface and may play a role in resorption. However,
certain ROS, such as superoxide and hydrogen peroxide
have been found to play a role in the activation of
osteoclasts, rather than in the direct degradation
of the bone matrix, whilst NO has been found to
inhibit bone resorption.

Periodontal Pathogens

LPS DNA Cell wall components

Crevicular/Junctional Inflammatory
TIMPs ↓
cytokines,
epithelium + other PDL cells IL-8
MMPs ↑ chemokines,
Receptor mediated adhesion GM-CSF
TNF-α E-selectin
Osteoclast molecules, etc.
Activation of NF-κB & AP-1 LPS LPS
Activation/ e.g. TNF-α, IL-1, IL-8
GM-CSF, TNF-α
Differentiation Nonreceptor mediated
E-selectin

Fibroblast Recruitment and

generation of activation of hyper-
Oxidative ROS responsive PMNL
Stress PMNL generation
of ROS

Release of traditional
inflammatory mediators
Generation of
Tissue
oxidation products -
Damage Lipid peroxides,
oxidized proteins

Inactivation of TIMPs

Figure 1. Simplified diagram illustrating a central role of ROS in generating chronic inflammation and tissue damage in
response to periodontal pathogens.
MMP = Matrix metalloproteinase; TIMP = Tissue inhibitor of matrix metalloproteinase; NF-κB = Nuclear factor kappa B; AP-1 = Activating protein-1;
PDL = Periodontal ligament; TNF = Tumor necrosis factor; IL = Interleukin; GM-CSF = Granulocyte-macrophage colony-stimulating factor;
LPS = Lipopolysaccharide; ROS = Reactive oxygen species.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 141

 Review Article

Garrett et al9 demonstrated both in vivo and in vitro Table 1. A Functional Classification of Antioxidant
that when free oxygen radicals were generated in Systems
the bone environment, osteoclasts were formed and Types of Mode of action Examples
bone resorption occurred. Few studies have addressed defense
the degradation of the periodontal extracellular matrix system
by ROS. Earlier studies by Bartold et al8 demonstrated Preventive Suppress the formation Catalase, GPX and
antioxidants of FR: Nonradical serum-transferase
the in vitro ability of ROS particularly the OH° species,
decomposition of
to degrade hyaluronan and proteoglycans extracted LOOH and H2O2
from porcine gingivae and within cryostat sections
Sequestration of metal Transferrin,
of tissue. by chelation ceruloplasmin,
albumin, haptoglobin
Proteoglycans and glycosaminoglycans (GAGs) when
Quenching of active O2 SOD, carotenoids
exposed to a broad-spectrum of ROS species of
differing reactivity and over differing periods of time Radical- Scavenge radicals to Lipophilic: Ubiquinol,
scavenging inhibit chain initiation vitamin A, vitamin E,
were found to undergo chain depolymerization and antioxidants and break chain carotenoids
residue modification to varying degrees, particularly propagation Hydrophilic: Uric
in the presence of the highly reactive OH° species. acid, ascorbic acid,
Moreover, the nonsulfated GAG, hyaluronan was albumin, bilirubin
identified as being more susceptible to degradation by Repair and Repair the damage DNA repair
ROS than sulfated GAG.1 de novo and reconstitute enzymes, protease,
enzymes membranes transferase, lipase
The highly reactive OH° species was also shown to
exert the most detrimental degradative effects on the
small chondroitin sulfate, proteoglycans from alveolar Superoxide Dismutase
bone, compared to other ROS.1
Superoxide dismutase (SOD) is an antioxidant enzyme
Antioxidants: What are they and how do that catalyses the dismutation of the highly reactive
they Act? superoxide anion to O2 and to the less reactive species
“An antioxidant is any substance that, when present at H2O2, accelerating it upto 10,000 times.2
low concentrations compared to those of an oxidisable 2O2°¯ + 2H+ SOD
H2O2 + O2
substrate, significantly delays or prevents oxidation of
that substrate”.2 In humans, there are three forms of SOD: Cytosolic
Cu/Zn-SOD, mitochondrial Mn-SOD and extra-
Several biologically important compounds have been cellular SOD (EC-SOD). Though, Cu/Zn-SOD
reported to have antioxidant functions. These include is believed to play a major role in the first-line of
vitamin C (ascorbic acid), vitamin E (α-tocopherol), antioxidant defense, recent reports have revealed
vitamin A, b-carotene, metallothionein, polyamines, that Mn-SOD is essential for life whereas Cu/Zn-SOD
melatonin, nicotinamide adenine dinucleotide is not.10 SOD has been localized within human
phosphate (NADPH), adenosine, co-enzyme Q-10, periodontal ligament and may represent an important
urate, ubiquinol, polyphenols, flavonoids, phytoe- defense mechanism with in gingival fibroblasts against
strogens, cysteine, homocysteine, taurine, methionine, excess superoxide release.11
S-adenosyl-L-methionine, resveratrol, nitroxides,
reduced glutathione (GSH), glutathione peroxidase Catalase
(GPX), superoxide dismutase (SOD), catalase (CAT),
Catalase (CAT) is an antioxidant enzyme, which
nitric oxide synthase (NOS), heme oxygenase-1
contains heme bound iron and is mainly located in
(HO-1) and eosinophil peroxidase (EPO).10
peroxisomes.2 It reacts very efficiently with H2O2 to
A functional classification of antioxidant systems based form water and molecular oxygen and with hydrogen
on the way they act (Niki 1996) appears to be the donors (methanol, ethanol, formic acid or phenols)
most useful (Table 1).2 with peroxidase activity.10

142 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011


2H2O2 CAT H2O + O2
ROOH + AH2 CAT H2O + ROH + A
Thus, CAT protects cells from hydrogen peroxide
generated within them. Even though CAT is not
essential for some cell types under normal conditions,
it plays an important role in the acquisition of tolerance
to oxidative stress in the adaptive response of cells.
Reduced Glutathione
Glutathione (GSH) is an essential tripeptide with
many important functions. Glutathione’s three major
roles in the body are summarized by the letters
AID-Antioxidant, Immune booster and Detoxifier -
three critical processes driven by GSH.
In its reduced form GSH is an important antioxidant
(radical scavenger), a property bestowed upon it by
its central thiol containing cysteine amino acid. It is
also regarded as a pivotal molecule to the immune
system especially for regulation of interleukin-2 (IL-2)
dependent T-lymphocyte proliferation.3
GSH has a dual role. It reacts directly with FR, but
it also is alternatively a substrate or a co-factor of a
transferase (GSH-tr), a peroxidase (GSH-PX) or a
reductase (GSH-red). Oxidized glutathione (GSSG)
is made by joining two GSH molecules by their -
SH groups, losing the two hydrogens and forming
a disulfide bridge. The reaction is catalyzed by a
GSH-PX that detoxifies H2O2 very efficiently.2
GPX
2GSH + H2O2 2GSSG + 2H2O
Glutathione Peroxidase
Glutathione peroxidase (GPX) is selenium containing
peroxidase, which catalyses the reduction of a variety
of hydroperoxides (ROOH and H2O2) using GSH,
thereby protecting mammalian cells against oxidative
damage. There are at least five GPX isoenzymes found
in the mammals normally-GPX1, GPX2, GPX3,
GPX4, and GPX5.
Although GPX shares the substrate, H2O2 with CAT, it
alone can react effectively with lipid and other organic
hydroperoxides. The glutathione redox cycle is a major
source of protection against low levels of oxidant stress,
whereas CAT becomes more significant in protecting
against severe oxidant stress.10
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Review Article
Plasma Antioxidant Status in Periodontal
Diseases
In periodontal literature, early studies of individual
antioxidant micronutrients were unconvincing in
their associations between dietary antioxidant intake
and periodontitis. Few studies (Nishada et al 2000,
Amarasena et al 2005, Chapple et al 2007) that have
explored individual antioxidant scavengers in serum or
plasma have shown only mildly compromised levels
in periodontitis subjects relative to healthy controls,
except where smoking is a co-factor.12
Sobaniec and S Lotowska (2000) reported lower
serum antioxidant enzyme levels in ligature-induced
periodontitis in a rat model.12
Abnormally high levels of hydroperoxide and
compromised serum co-enzyme Q10 and vitamin E
were observed in Papillon-Lefèvre syndrome subjects,
suggesting substantial oxidative stress in these
subjects and a potential role for specified antioxidant
therapies.13
An inverse relationship was found between serum
vitamin C concentrations and antibody levels to
porphyromonas gingivalis (Pussinen et al 2003).12
Panjamurthy et al14 observed lower plasma vitamin C,
vitamin E and reduced GHS in periodontitis subjects.
However, antioxidant enzyme levels were raised and
the authors attributed this to a protective response to
oxidative stress.
Total antioxidant capacity (TAOC) concentration
was found to be reduced in serum and plasma of
periodontitis patients.15,16
Tamaki et al17 observed a positive correlation between
plasma oxidative status and clinical attachment loss
in patients in the maintenance phase of periodontal
treatment. They suggested that a systemic increase in
oxidative stress may influence the rate of progression of
periodontal disease.
Low levels of a number of carotenoids, in particular
b-cryptoxanthin and b-carotene were found to be
associated with an increased prevalence of periodontitis
in the year 60-70 year old men.18
Though, these studies reveal an antioxidant compromise
in the plasma of periodontitis patients, the changes in
143
 Review Article
antioxidant status lack relevance or significance, given
their low concentrations and rates of activity, relative
to the antioxidant scavengers.
Salivary Antioxidant Status in Periodontal
Diseases
Moore et al,19 who were the first to explore salivary
total antioxidant activity found no difference in TAOC
levels in periodontitis and nonperiodontitis subjects.
The predominant antioxidant component of saliva was
uric acid (>70% of antioxidant activity).
However, Chapple et al20 found lower total antioxidant
concentration in the saliva of periodontitis patients
when compared to periodontally healthy controls.
Similar results were observed in a larger cohort study21
and in small case-control studies (Diab Ladki et al12
and Brock et al15). Lower TAOC was reported in
women than men. A higher level of protein carbonyls
(oxidative stress) was found in periodontitis patients
than in controls.21
Salivary antioxidant levels (SOD, GPX, reduced GHS,
ascorbic acid, a-tocopherol) were observed to be lower
in periodontitis patients22,23 as well as in patients under
antiepileptic therapy with gingival hyperplasia.24
Markers of oxidative damage such as malondial-
dehyde23,25 8-hydroxy-deoxy-guanosine23,26 were found
to be higher in saliva of patients with periodontitis
which decreased following initial treatment appro-
aching the mean control values.26
Overall, the relevance of saliva as a medium for
assessing surrogate markers of reactive oxygen and
antioxidant species in periodontitis patients must be
open to question. Moreover, saliva contains GCF and
the contribution of GCF antioxidants to saliva will
vary according to the degree of salivary stimulation.27
GCF Antioxidant Status in Periodontal
Diseases
GCF is the most appropriate fluid to sample
when investigating biomarkers of tissue events in
periodontium.
Guarnieri et al28 observed spontaneous generation
of superoxide in the GCF of periodontitis subjects,
with no differences in antioxidant scavenging capacity
144
between cases and controls. However, no difference was
reported in the SOD activity in GCF of periodontitis
subjects.29
Reduced GSH was the most important antioxidant in
GCF with levels 1,000-fold higher than paired plasma
samples27 and was significantly lower in periodontitis
relative to matched control subjects.22
The antioxidant enzyme GPX correlated negatively with
pocket depth and attachment loss and increased post-
therapy (Hung et al 2000).12 However, significantly
greater levels of GPX, lactoferrin, myeloperoxidase and
IL-1b in the GCF were in periodontally diseased sites
when compared to healthy sites.30,31
Studies investigating oxidative stress and antioxidant
status both locally and peripherally (in serum, saliva
and GCF) in periodontitis patients reported higher
levels of malondialdehyde and total oxidant status,
which decreased following Phase I therapy.32-34
Tsai et al22 reported a positive correlation between
GCF lipid peroxidation and periodontopathogens
and a negative correlation between GCF GPX and
periodontopathogens. They concluded that the
increased levels of lipid peroxidation with decreased
level of antioxidants provided the evidence that
oxidative stress, after the stimulation of periodonto-
pathogens might play a role in the pathogenesis of
periodontitis.
A negative correlation between serum and GCF
TAOC and gingival inflammation was reported in
miniature poodle dogs (Pavlica et al 2004).12 Similarly,
TAOC in the GCF of periodontitis subjects was
significantly lower.15 Based on GCF studies, it can be
concluded that local antioxidant scavenging defenses
are compromised in periodontitis, but whether this
represents a predisposition to disease or results from
the inflammatory lesion is not clear.
Periodontal Tissue Antioxidant Status in
Periodontal Diseases
Gingivitis subjects exhibited higher levels of GSH in
gingival tissue samples when compared to controls
(Giorgi et al, 1992).12 Tissue levels of CAT and
SOD decreased with increasing pocket depth in
periodontitis patients scheduled for extractions.35
On the contrary, higher levels of SOD activity was
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

observed in the GCF and gingival tissue samples of
periodontitis patients.29
Smokers with periodontitis exhibited increased
levels of metallothionein (a radical scavenging
and preventive antioxidant) in the gingival tissue
indicating a protective response to the increased
inflammation in these patients.36 Another study in
smokers37 observed higher levels of HO-1 antioxidant
enzyme levels in smokers with periodontitis than in
nonsmoker periodontitis patients. Higher levels of
thiobarbituric acid reactive substances (TBARS),
a marker of oxidative stress was found in the
gingival tissue obtained from unresolved pockets
following Phase I therapy in patients with chronic
periodontitis.38 In a similar study, Panjamurthy
et al14 also observed higher levels of TBARS and
enzyme antioxidants with lower levels of scavenging
antioxidants in the gingival tissue of periodontitis
subjects when compared to controls.
Recently, Borges et al39 reported increased activities
of myeloperoxidase, GPX, glutathione-S-transferase,
oxidized GSH and higher levels of TBARS in gingival
tissue of chronic periodontitis patients when compared
to controls, suggesting a correlation between oxidative
stress biomarkers and periodontal diseases. Biopsy
studies are difficult to implement for ethical and
technical reasons, but the limited data so far confirm
the presence of more significant oxidative stress in the
periodontal tissues of diseased periodontium relative
to control tissue and the apparent upregulation of
antioxidant enzyme systems.
Conclusion
Whilst a myriad of possible mechanisms leading to the
destruction of periodontal tissues exist, ROS would
appear to play a significant role in the pathology of
periodontal diseases. Oxidative stress observed in a
diseased periodontium could result directly from excess
ROS activity or antioxidant deficiency or indirectly by
creating a pro-inflammatory state. Novel adjunctive
antioxidant and anti-inflammatory strategies to the
traditional periodontal therapy can help us in achieving
good clinical results.
References
1. Waddington RJ, Moseley R, Embery G. Reactive oxygen
species: a potential role in the pathogenesis of periodontal
diseases. Oral Dis 2000;6(3):138-51.
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2. Battino M, Bullon P, Wilson M, Newman H.
Oxidative injury and inflammatory periodontal
diseases: the challenge of antioxidants to free radicals
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1999;10(4):458‑76.
3. Chapple IL. Reactive oxygen species and antioxidants
in inflammatory diseases. J Clin Periodontol 1997;24(5):
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4. Miyasaki KT. The neutrophil: mechanisms of
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1991;62(12):761‑74.
5. Firatli E, Unal T, Onan U, Sandalli P. Antioxidative
activities of some chemotherapeutics. A possible
mechanism in reducing gingival inflammation. J Clin
Periodontol 1994;21(10):680-3.
6. Halliwell B. Tell me about free radicals, doctor: a review.
J Royal Soc Med 1989;82(12):747-52.
7. Halliwell B. Oral inflammation and reactive species: a
missed opportunity? Oral Dis 2000;6(3):136-7.
8. Bartold PM, Weibkin OW, Thonard JC. The effect of
oxygen-derived free radicals on gingival proteoglycans
and hyaluronic acid. J Periodont Res 1984;19(4):
390‑400.
9. Garrett IR, Boyce BF, Oreffo RO, Bonewald L, Poser
J, Mundy GR. Oxygen-derived free radicals stimulate
osteoclastic bone resorption in rodent bone in vitro and
in vivo. J Clin Invest 1990;85(3):632‑9.
10. Matés JM. Effects of antioxidant enzymes in the
molecular control of reactive oxygen species toxicology.
Toxicology 2000;153(1-3):83-104.
11. Jacoby BH, Davis WL. The electron microscopic
immunolocalization of a copper-zinc superoxide
dismutase in association with collagen fibers of perio-
dontal soft tissues. J Periodontol 1991;62(7):413‑20.
12. Chapple IL, Matthews JB. The role of reactive oxygen
and antioxidant species in periodontal tissue destruction.
Periodontol 2000 2007;43:160-232.
13. Battino M, Ferreiro MS, Bompadre S, Leone L,
Mosca F, Bullon P. Elevated hydroperoxide levels and
antioxidant patterns in Papillon-Lefèvve syndrome.
J Periodontol 2001;72(12):1760-6.
14. Panjamurthy K, Manoharan S, Ramachandran CR. Lipid
peroxidation and antioxidant status in patients with
periodontitis. Cell Mol Biol Lett 2005;10(2):255‑64.
15. Brock GR, Butterworth CJ, Matthews JB, Chapple IL.
Local and systemic antioxidant capacity in periodontal
health. J Clin Periodontol 2004;31(7):515-21.
16. Pendyala G, Thomas B, Kumari S. The challenge of
antioxidants to free radicals in periodontitis. J Indian
Soc Periodontol 2008;12(3):79-83.
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17. Tamaki N, Tomofuji T, Maruyama T, Ekuni D,
Yamanaka R, Takeuchi N, et al. Relationship
between periodontal condition and plasma reactive
oxygen metabolites in patients in the maintenance
phase of periodontal treatment. J Periodontol
2008;79(11):2136‑42.
18. Linden GJ, McClean KM, Woodside JV, Patterson
CC, Evans A, Young IS, et al. Antioxidants and
periodontitis in 60-70-year-old men. J Clin Periodontol
2009;36(10):843-9.
19. Moore S, Calder KA, Miller NJ, Rice-Evans CA.
Antioxidant activity of saliva and periodontal disease.
Free Radic Res 1994;21(6):417-25.
20. Chapple IL, Mason GI, Garner I, Matthews JB, Thorpe
GH, Maxwell SR, et al. Enhanced chemiluminescent
assay for measuring the total antioxidant capacity of
serum, saliva and crevicular fluid. Ann Clin Biochem
1997;34(Pt 4):412-21.
21. Sculley DV, Langley-Evans SC. Periodontal disease is
associated with lower antioxidant capacity in whole
saliva and evidence of increased protein oxidation. Clin
Sci (Lond) 2003;105(2):167-72.
22. Tsai CC, Chen HS, Ho YP, Ho KY, Wu YM,
Hou GL. Periodontopathogens and oxidative stress in
periodontal diseases. Paper 0595, 81st General Session
of International Association for Dental Research June
25-28, 2003.
23. Canakci CF, Cicek Y, Yildirim A, Sezer U, Canakci V.
Increased levels of 8-hydroxydeoxyguanosine and
malondialdehyde and its relationship with antioxidant
in saliva of periodontitis patients. Eur J Dent
2009;3(2):100‑6.
24. Sobaniec H, Sobaniec W, Sendrowski K, Sobaniec S,
Pietruska M. Antioxidant activity of blood serum and
saliva in patients with periodontal disease treated due to
epilepsy. Adv Med Sci 2007;52(Suppl 1):204-6.
25. Khalili J, Biloklytska HF. Salivary malodialdehyde
levels in clinically healthy and periodontal diseased
individuals. Oral Dis 2008;14(8):754-60.
26. Takane M, Sugano N, Iwasaki H, Iwano Y, Shimizu N,
Ito K. New biomarker evidence of oxidative DNA
damage in whole saliva form clinically healthy and
periodontally diseased individuals. J Periodontol
2002;73(5):551-4.
27. Chapple IL, Brock G, Eftimiadi C, Matthews JB.
Glutathione in gingival crevicular fluid and it relation
to local antioxidant capacity in periodontal health and
disease. Mol Pathol 2002;55(6):367-73.
28. Guarnieri C, Zucchelli G, Bernardi F, Scheda M,
Valentini AF, Calandriello M. Enhanced superoxide
production with no change of the antioxidant activity in
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gingival fluid of patients with chronic adult periodontitis.
Free Radic Res Commun 1991;15(1):11-6.
29. Alkalin FA, Toklu E, Renda N. Analysis of superoxide
dismutase activity in gingiva and gingival crevicular fluid
in patients with chronic periodontitis and periodontally
healthy controls. J Clin Periodontol 2005;32(3):238-43.
30. Tsai CC, Wei PF, Ho KY. Proinflammatory cytokines
and oxidative stress in periodontal diseases. Paper 2275,
IADR/AADR/CADR 80th General Session. March 6-9,
2002.
31. Wei PF, Ho KY, Ho YP, Wu YM, Yang YH, Tsai CC.
The investigation of glutathione peroxidase, lactoferrin,
myeloperoxidase and interleukin-1beta in gingival
crevicular fluid: implications for oxidative stress in human
periodontal diseases. J Periodontal Res 2004;39(5):
287-93.
32. Tsai CC, Chen HS, Chen SL, Ho YP, Ho KY, Wu YM,
et al. Lipid peroxidation: a possible role in the induction
and progression of chronic periodontitis. J Periodontal
Res 2005;40(5):378-84.
33. Akalin FA, Baltacioglu E, Alver A, Karabulut E.
Lipid peroxidation levels and total oxidant status in
serum, saliva and gingival crevicular fluid in patients
with chronic periodontitis. J Clin Periodontol
2007;34(7):558-65.
34. Wei D, Zhang XL, Wang YZ, Yang CX, Chen G.
Lipid peroxidation levels, total oxidant status and
superoxide dismutase in serum, saliva and gingival
crevicular fluid in patients with chronic periodontitis
before and after periodontal therapy. Aust Dent J
2010;55(1):70-8.
35. Ellis SD, Tucci MA, Serio FG, Johnson RB. Factors for
progression of periodontal diseases. J Oral Pathol Med
1998;27(3):101-5.
36. Katsuragi H, Hasegawa A, Saito K. Distribution of
metallothionein in advanced periodontitis patients.
J Periodontol 1997;68(10):1005-9.
37. Chang YC, Lai CC, Lin LF, Ni WF, Tsai CH. The
up-regulation of heme oxygenase-1 expression in
human gingival fibroblasts stimulated with nicotine.
J Periodontal Res 2005;40(3):252-7.
38. Tuter G, Kurtiş B, Serdar M. Interleukin-1beta and
thiobarbituric acid reactive substance (TBARS) levels
after phase I periodontal therapy in patients with chronic
periodontitis. J Periodontol 2001;72(7):883-8.
39. Borges I Jr, Moreira EA, Filho DW, de Oliveira TB, da
Silva MB, Frõde TS. Proinflammatory and oxidative
stress markers in patients with periodontal disease.
Mediators Inflamm 2007;2007:45794.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 Case report

Minimally Invasive Atraumatic Extraction of Fractured Tooth

Using Implant Drills and Immediate Implant Placement
Jebin Paul Nesaline J* SC Chandrasekaran**, Bhaskar Jayaraman†, Jumshad B Mohamed‡

Abstract
Implant placement has been a constant challenge in the field of dentistry. This case report demonstrates a novel extraction of
fractured tooth at the cervical region. The tooth was endodontically treated two years back and radiograph revealed periapical
radiolucency. The technique involves atraumatic extraction of root using implant drills followed by placing bone graft and
immediate implant placement.

Key words: Atraumatic extraction, immediate implant

E
sthetic and functional components play an
integral part in periodontal practice. Implants
today have cascading effect from yesteryears.
Extraction was done after thinning the root walls with
the help of the implant drills.1 Extraction of the root
with periapical lesion was done in totality.2 Implant
sites were prepared and filled with bone graft* and
then implants were inserted.
Immediate implants are placed into a prepared
extraction socket following tooth removal. Short-term
animal and human studies have shown these implants
to be comparable with implants placed into healed
bone. The advantages of this procedure include fewer
surgical sessions, elimination of the waiting period
for socket healing, shortened edentulous time period,
reduced overall cost, as well as preservation of bone
height and width.3 Although immediate implants is
more demanding both surgically and prosthetically,
compared to the conventional placement technique,
the advantages make it very appealing to patients
in need of both extraction and implant placement
in one sitting. Implant placement in the esthetic
zone is a technique-sensitive procedure with little
*Postgraduate Student
**Professor and Head
†
Professor
‡
Senior Lecturer
Dept. of Periodontology and Oral Implantology
Sree Balaji Dental College and Hospital, Chennai
Address for correspondence
Dr Jebin Paul Nesaline J
Dept. of Periodontology and Oral Implantology
Sree Balaji Dental College and Hospital, Chennai - 600 100
E-mail: dr.jebin@yahoo.co.in
room for error. Several authors have reported success
rates of more than 95%2,4 for implants placed into
fresh extraction sites. This case report demonstrates
minimally invasive extraction without flap reflection
and immediate implant placement with single-stage
surgical procedure in the esthetic zone. Peri-implant
bone defect was minimal, as the implant chosen
was wider than the dimensions of the extraction
socket. Nevertheless, the periapical void was filled with
bone graft*.
Case History
A 27-year-old female patient presented to the Dept.
of Periodontology and Oral Implantology, Sree Balaji
Dental College and Hospital complaining of mobile
anterior tooth. On clinical examination, tooth number
21 was found to be fractured with the fracture line
running subgingivally (Fig. 1). Radiograph confirmed
that root canal treatment was performed on the tooth
previously with a periapical lesion in relation to tooth
#21 (Fig. 2). The patient was given the option of
extraction followed by immediate implant placement.
Pros and cons of the procedure were explained to
the patient and informed consent was obtained.
Preoperative evaluation included study of diagnostic
casts, photographs, periapical radiograph and
computerized tomography for assessment of implant
size, position of implant and anatomical landmarks.
Surgery was performed according to standard
protocols. After administration of local anesthesia
(2% lignocaine 1:80,000 adrenaline), the fractured
crown was removed (Fig. 3). Root extraction was

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 147

 Case Report
Figure 1. Preoperative clinical photograph.
Figure 3. Fractured crown removed.
Figure 5. Pilot implant drill used to thin the root canal wall.
initiated with airotor using tapering fissure bur
(Fig. 4) to widen the root canal so as to accommodate
the initial 2 mm implant drill (Fig. 5). Progressive
implant drills upto 3.3 mm were used to thin the
root wall. Mosquito artery forceps was used to remove
the root and the periapical granuloma in totality
148
Figure 2. Preoperative radiograph.
Figure 4. Tapered fissure airotor bur used to widen the
root canal.
Figure 6. Periapical granuloma removed in totality.
(Fig. 6). The root was extracted atraumatically without
flap reflection (Fig. 7). A periodontal probe was used
to explore and estimate the integrity of the bony walls
of the alveolus and periapical radiographs were taken
to confirm the total removal of the tooth remnants
(Fig. 8). It was planned to fill the periapical void
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Figure 7. Extraction socket.
Figure 9. Bone graft placed.
Figure 11. Wrench break at 40 Ncm.
with bone graft (Fig. 9) prior to implant placement*.
The socket was prepared with sequential drills to place
a 4.8 mm diameter implant. After osteotomy, the
periapical void was filled with bone graft* followed by
4.8 × 14 mm implant #placement (Fig. 10). Primary
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Case Report
Figure 8. Post extraction periapical radiograph.
Figure 10. Implant placed.
Figure 12. Cyanoacrylate tissue adhesive between flap
and implant.
stability was confirmed by the wrench breaking at
40 Ncm (Fig. 11). Since primary closure was not
possible it was decided to close the minor space between
implant and gingiva with one layer of cyanoacrylate
tissue adhesive$ (Fig. 12). Temporary restoration was
149
 Case Report
Figure 13. Temporary restoration.
Figure 15. Three-month postoperative radiograph.
Figure 17. One-year postoperative radiograph.
provided using an adhesive resin bridge (Fig. 13).
After surgery postoperative instructions along with
antibiotics and analgesics were prescribed for five days.
Patient was placed on regular maintenance protocol.
150
Figure 14. Three-month postoperative clinical photograph.
Figure 16. One-year postoperative clinical photograph.
At the end of three months soft tissue and radiographic
findings were clinically acceptable (Figs. 14 and 15).
One-year postoperative clinical and radiograph shows
that the implant is both functionally and esthetically in
good condition (Figs. 16 and 17).
Discussion
Minimally invasive extraction without flap reflection
and immediate implant placement with single-stage
surgical procedure is a sensitive technique. Many
clinicians postpone treatment of sites exhibiting
infection. Novaes et al5 and Villa and Rangert6
recently reported on a case series of patients where
implants were installed immediately after extraction,
and where the extracted teeth exhibited signs of
periodontal or endodontic infections. At two years
post-treatment, the cumulative survival rate was 100%.
In immediate implant placement, it is very important
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

to preserve the continuity of the bone surrounding
the root for primary stability and long-term success,
especially in upper incisors.7
In this case we used a novel atraumatic technique for
extraction of teeth to prevent damage to the labial
plate and preserve periodontium. Since, the fracture
line runs subgingivally, implant drills were used in
the root canal for thinning and to prevent damage to
the labial plate.8 Implant socket was prepared slightly
palatal to achieve primary stabilization. In this case
periapical granuloma was removed in totality and the
void debrided and filled with bone graft*.
Schirolli9 reported using a tapered design implant
protecting integrity of buccal bone and enable the
use of a longer implant to achieve primary stability.
Primary stability was achieved with the wrench
breaking at 40 Ncm (Fig. 11). Minor space between
the gingiva and the implant was occluded with one
layer of formulated cyanoacrylate tissue adhesive$.
N-butyl cyanoacrylate is an effective tissue adhesive
which is hemostatic and bacteriostatic.10
N-butyl-2-cyanoacrylate polymer did not delay bone
healing and was well-tolerated by rat’s cancellous
bone tissue without signs of foreign body reaction
or prolonged inflammation reaction.11 The soft
tissue healing and morphology were satisfactory and
additional mucogingival surgery was not required
before definitive prosthetic rehabilitation. Successful
application of this technique can minimize the need
of regenerative procedures after extraction thereby
reducing the chair-side time. Long-term clinical trials
are needed to confirm the present result.
*Bio-Oss bone graft®
#
Zimmer Tapered Swiss Plus®
$
Periacryl tissue adhesive
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Case Report
References
1. Yalcin S, Aktas I, Emes Y, Kaya G, Aybar B, Atalay B.
A technique for atraumatic extraction of teeth before
immediate implant placement using implant drills.
Implant Dent 2009;18(6):464-72.
2. Becker W, Goldstein M. Immediate implant placement:
treatment planning and surgical steps for successful
outcome. Periodontology 2008;47(1):79-89.
3. Barzilay I. Immediate implants: their current status.
Int J Prosthodont 1993;6(2):169-75.
4. Schropp L, Isidor F. Timing of implant placement
relative to tooth extraction. J Oral Rehabil 2008;35
(Suppl 1):33‑43.
5. Novaes AB Jr, Novaes AB. Immediate implants placed
into infected sites: a clinical report. Int J Oral Maxillofac
Implants 1995:10(5):609-13.
6. Villa R, Rangert B. Early loading of interforaminal
implants immediately installed after extraction of teeth
presenting endodontic and periodontal lesions. Clin
Implant Dent Relat Res 2005:7(Suppl 1):S28-S35.
7. Chen ST, Darby IB, Adams GG, Reynolds EC. A
prospective clinical study of bone augmentation
techniques in immediate implants. Clin Oral Implants
Res 2005;16(2):176-84.
8. Covani U, Cornelini R, Barone A. Buccolingual
remodeling around implants placed into immediate
extraction sockets: a case series. J Periodontol
2003;74(2):268-73.
9. Paolantonio M, Dolci M, Scarano A, d’Archivio D,
di Placido G, Tumini V, et al. Immediate implantation in
fresh extraction sockets. A controlled clinical and
histological study in man. J Periodontol 2001;72(11):
1560-71.
10. Grisdale J. The use of cyanoacrylates in periodontal
therapy. J Can Dent Assoc 1998;64(9):632-3.
11. Vasenius J. Is n-butyl-2-cyanoacrylate a biocompatible
coating material for biodegradable fracture fixation
devices: an experimental study on rats. Clin Mater
1988;3(2):133-43.
n n n
151
 case report

Rhinocerebral Mucormycosis with Palatal Involvement

Associated with Diabetes Mellitus Type II: A Case Report
KMK Masthan*, N Aravindha Babu**, Jagdish Rajguru†

Abstract
Zygomycosis or mucormycosis is an increasingly frequent life-threatening infection caused by opportunistic fungal organisms
of the class zygomycetes. The pathognomonic feature is the presence of invasive aseptate mycelia that are larger than other
filamentous fungi with the hyphae exhibiting right angle and haphazard branching. Usually classified as rhinocerebral,
disseminated and cutaneous types, this classification serves as important predictor of pathogenesis and prognosis. These occur
mostly in immunosuppressed patients including individuals with diabetes (43% exhibit the rhinocerebral form) and patients
with organ transplants and hematologic malignancies. Without early aggressive treatment, the disease follows a dismal and fatal
course. Early recognition and aggressive treatment have reduced the mortality and morbidity. We present a case of rhinocerebral
mucormycosis with palatal perforation who presented with a slowly progressive swelling of the left cheek.

Key words: Mucormycosis, palatal perforation, diabetes mellitus, hematuria

R hinocerebral mucormycosis continues to be the

most common form of the disease, accounting
for between one-third and one-half of all cases
of mucormycosis.1 About 70% of rhinocerebral cases
(occasionally referred to as craniofacial) are found
in diabetic patients in ketoacidosis.2 More rarely,
rhinocerebral mucormycosis has also occurred in
patients who received a solid organ transplant or those
with prolonged neutropenia.1,3-6 Recently, rhinocerebral
disease has been an increasing problem in patients
undergoing hematopoietic stem cell transplantation.7,8
These cases have largely been associated with steroid
use for graft versus host disease. The initial symptoms
of rhinocerebral mucormycosis are consistent with
either sinusitis or periorbital cellulitis9 and include eye
or facial pain and facial numbness, followed by the
onset of conjunctival suffusion, blurry vision and soft
tissue swelling.4,10 Fever is variable and may be absent
in upto half of cases;11 white blood cell counts are
typically elevated, as long as the patient has functioning
bone marrow.12 If untreated, infection usually spreads
from the ethmoid sinus to the orbit, resulting in
*Professor and Head
**Associate Professor
Dept. of Oral Pathology and Microbiology
Sree Balaji Dental College and Hospital, Chennai
†
Senior Lecturer, Saraswathi Dental College and Hospital, Lucknow
Address for correspondence
Dr N Aravindha Babu
Associate Professor
Dept. of Oral Pathology and Microbiology
Sree Balaji Dental College and Hospital, Chennai
E-mail: dr_aravindmsdc@yahoo.co.in
loss of extraocular muscle function and proptosis.
Marked chemosis may also be seen. The infection may
rapidly extend into the neighboring tissues. Onset
of signs and symptoms in the contralateral eye, with
resulting bilateral proptosis, chemosis, vision loss and
ophthalmoplegia, is an ominous sign that suggests the
development of cavernous sinus thrombosis. Upon visual
inspection, infected tissue may appear normal during
the earliest stages of spread of the fungus. Infected
tissue then progresses through an erythematous phase,
with or without edema, before onset of a violaceous
appearance and finally the development of a black,
necrotic eschar as the blood vessels become thrombosed
and tissue infarction occurs.6,13
Infection can sometimes extend from the sinuses into
the mouth and produce painful, necrotic ulcerations of
the hard palate. Fungal pathogens are subdivided into
superficial fungi (restricted to the epithelial surface)
and deep fungi (those that invade deep organs and
tissues). Most are considered opportunistic (infecting
only immunocompromised hosts) and others truly
pathogenic (capable of infecting normal persons).14
Mucormycosis (zygomycosis) is an increasingly
emerging life-threatening infection. Paultauf first
reported it as causing disease in humans in 1885.15
Classification of mucormycosis:16
 Zygomycotina - phylum
n Zygomycetes - class

152 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

 Case Report

 Mucorales - order
 Mucoraceae - family
 Absidia - genus
 Mucor
 Rhizomucor
 Rhizopus - species
Figure 1a and B. Extraoral and intraoral patient picture.
 Cunninghamellacaeae

Case Report
A 60-year-old male patient reported to Dept. of Oral
and Maxillofacial Pathology of Sree Balaji Dental
College and Hospital with a chief complaint of pain
and swelling in the left upper back region since four
days. History revealed that left upper first molar
was extracted 15 days back due to compromised
periodontal status in a private clinic.
Past medical history revealed that the patient is a non-
insulin-dependent diabetes mellitus (NIDDM) and
under medication. Patient had been hospitalized few
Figure 2. CT scan reveal soft tissue mass in left maxillary
years back for high increase in glucose and hematuria. sinus.
Extraoral manifestation showed diffuse swelling over
the left upper cheek region, with signs of inflammation
(Fig. 1a).
Intraorally a linear ragged ulcer with 0.5 × 2 cm
dimension appreciated in the mid palatine region
(hard palate). The border of the ulcer was raised,
erythematous with lateral area of exposed bone
(Fig. 1b).
Provisional diagnosis was given as squamous cell
carcinoma of palate, necrotizing sialometaplasia, Figure 3. H&E aseptate hyphae branching at acute angle
mucormycosis and midline lethal granuloma. CT scan (10x and 40X).
suggested soft tissue mass in the left maxillary sinus
eroding and destroying medial and lateral wall of formation (Fig. 3). Periodic acid-Schiff (PAS)
maxillary sinus (Fig. 2). stain suggested a final diagnosis of mucormycosis
(Fig. 4a and b).
Hemogram showed mild polymorphonuclear
leukocytosis. Biochemical investigation showed HbA1C The patient was started on IV amphotericin B
of 8.7%. Random blood sugar was 193 mg/dl and 60 mg in four divided doses, cefotaxime lg b.i.d. and
associated with ketonuria. An incisional biopsy was metronidazole 500 mg t.d.s. Amphotericin-induced
done under glycemic control. Histopathological nephrotoxicity was monitored carefully. Surgical
examination was characterized by nonseptate hyphae debridement of the necrotic tissues was done under
with acute right angle branchings suggestive of mucor general anesthesia and a temporary palatal obturator
species with focal areas of necrosis and thrombi was given.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 153

 Case Report
Figure 4a. PAS stain showing hyphae (10x).
Figure 4b. PAS stain showing hyphae (40x).
Discussion
Mucormycosis is an opportunistic and fulminant, fungal
infection caused by a member of the class zygomycetes.
It is commonly found in soils, manure and decaying
organic matter. These fungi are primitive, fast growing,
terrestrial, largely saprophytic aerobic fungi with a
cosmopolitan distribution. It is an umbrella term
encompassing all mucormycotic infections regardless
of the etiologic agents. Based on clinical presentation
and the involvement of a particular anatomic site,
mucormycosis can be divided into at least six clinical
categories: i) Rhinocerebral, ii) pulmonary, iii)
cutaneous, iv) gastrointestinal, v) disseminated and iv)
miscellaneous.17
The organisms colonize the oral mucosa, nose,
paranasal sinuses and throat. Mucor favors an acidic
pH and glucose-rich medium, whereas rhizopus is
frequently noted in patients using desferoxamine due
to its affinity for an iron-rich environment. The fungi
154
invade the vessels causing embolization and subsequent
necrosis of surrounding tissue, thus spreading through
the bloodstream.17 In immunocompromised individuals
it spreads rapidly along neurovascular structures,
eroding the bone of the sinus wall spreading into the
orbit, the retro-orbital area and the brain.
Infectious diseases caused by mucormycosis have
risen significantly over the past decade. Patients with
diabetes, malignancies, solid organ or bone marrow
transplants or iron overload and those receiving
immunosuppressive agents, desferoxamine therapy
or broad-spectrum antimicrobial drugs are at highest
risk for mucormycosis. Although mucormycosis can
be seen in nondiabetic and metabolically controlled
diabetic patients, diabetic patients with sustained
hyperglycemia, particularly those with ketoacidosis
are more susceptible to mucormycosis.18,19 Diabetes
mellitus (DM) is a predisposing factor in 36-88% of
all mucormycosis cases.18-20 Moreover, mucormycosis
was found to be the first clinical manifestation of some
patients who had undiagnosed DM. Type 1, type 2 and
secondary DM have all been reported as risk factors in
patients with mucormycosis.18,19
The most common clinical manifestation found
in mucormycosis patients with DM is sinus disease
(66%), followed by pulmonary mucormycosis
(16%), whereas 19% and 60% of cancer patients had
sinus disease and pulmonary disease, respectively.20
The overall survival rate of diabetic patients
with mucormycosis who undergo treatment is
approximately 60%.21 Perineural spread with invasion
of nerves, blood vessels, cartilage, bone and meninges
is common and may result in thrombosis and nerve
dysfunction. Rhinocerebral mucormycosis is the most
common type, causing paranasal sinus infection,
usually extending to the orbit, hard palate and brain.22
Clinically, nasal obstruction, bloody nasal discharge,
facial pain, headache, facial swelling and cellulitis with
visual disturbances and concurrent proptosis may be
appreciated. Cranial nerve involvement may manifest
as facial paralysis and blindness, lethargy, seizures and
subsequent death.23
Predisposing conditions for zygomycosis:14,24
 Uncontrolled diabetes (particularly patients who
are acidic)
 Blood dyscrasias, leukemia
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 Case Report

 Malignant conditions, lymphoma debris. Other fungi, including Aspergillus, Fusarium,

 Renal failure or Scedosporium spp., may look similar to the
Mucorales on biopsy. However, these molds have
 Burns
septae, are usually thinner and branch at acute angles.
 Protein-calorie malnutrition The genus and species of the infecting organism may
 Cirrhosis be determined by culture. It is rarely isolated from
 Corticosteroid, immunosuppressive therapy cultures of blood, cerebrospinal fluid, sputum, urine,
 Solid organ transplants or bone marrow feces or swabs of infected areas.
transplants
Treatment
 Deferoxamine therapy
Factors to be considered before treatment are, rapidity
 Deficient T-cell immunity
of diagnosis, reversal of the underlying predisposing
 Immaturity and low birth weight factors, appropriate surgical debridement of
 Severe and prolonged neutropenia infected tissue and appropriate antifungal therapy.
Therefore, the recommended dose of amphotericin
Relationship between Predisposing Condition and B deoxycholate has been 1-1.5 mg/kg/day, which
Site of Infection25 results in a very high toxicity rate.
Predisposing condition Predominant site of infection
Diabetic ketoacidosis Rhinocerebral Prognosis
Neutropenia Pulmonary and disseminated Rhinocerebral mucormycosis has a higher survival
Corticosteroids Pulmonary, disseminated or rate than pulmonary or disseminated mucormycosis
rhinocerebral because rhinocerebral disease can frequently be
Desferoxamine Disseminated diagnosed earlier and the most common underlying
Malnutrition Gastrointestinal cause, diabetic ketoacidosis, can be treated readily.
Trauma, catheter/injection Cutaneous/subcutaneous
site, skin laceration References
1. Pillsbury HC, Fischer ND. Rhinocerebral mucor-
mycosis. Arch Otolaryngol 1977;103:(10)600-4.
Due to limitations of imaging studies, diagnosing
2. McNulty JS. Rhinocerebral mucormycosis: predisposing
mucormycosis almost always requires histopathologic factors. Laryngoscope 1982;92:(10 Pt 1)1140-3.
evidence of fungal invasion of the tissues. Culturing 3. Abedi E, Sismanis A, Choi K. Pastore P. Twenty-five
organisms from a potentially infected site is rarely years’ experience treating cerebro-rhino-orbital mucor-
sufficient to establish the diagnosis of mucormycosis mycosis. Laryngoscope 1984;94(8):1060-2.
because the causative agent is ubiquitous, may colonize 4. Peterson KL, Wang M, Canalis RF, Abemayor E.
normal persons and is a relatively frequent laboratory Rhinocerebral mucormycosis: evolution of the disease
and treatment options. Laryngoscope 1997;107:(7)
contaminant. Additionally, the organism may be 855‑62.
killed during tissue grinding, which is routinely used 5. Thajeb P, Thajeb T, Dai D. Fatal strokes in patients with
to process tissue specimens for culture. Thus, a sterile rhino-orbito-cerebral mucormycosis and associated
culture does not rule out the infection. Furthermore, vasculopathy. Scand J Infect Dis 2004;36:643-8.
waiting for the results of the fungal culture may 6. Dhiwakar M, Thakar A, Bahadur S. Improving outcomes
delay the institution of appropriate therapy. There in rhinocerebral mucormycosis - early diagnostic
pointers and prognostic factors. J Laryngol Otol
are no reliable serologic, PCR-based or skin tests for 2003;117(11):861‑5.
mucormycosis.
7. Morrison VA, McGlave PB. Mucormycosis in the
Therefore, the diagnosis should be made by biopsy BMT population. Bone Marrow Transplant 1993;11
(5):383-8.
of infected tissues. The biopsy should demonstrate
8. Talmi YP, Goldschmied-Reouven A, Bakon M,
the characteristic wide, ribbon-like, aseptate hyphal Barshack I, Wolf M, Horowitz Z, et al. Rhino-orbital
elements that branch at right or obtuse angles. The and rhino-orbito-cerebral mucormycosis. Otolaryngol
organisms are often surrounded by extensive necrotic Head Neck Surg 2002;127(1):22-31.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 155

 Case Report
9. Husain S, Alexander BD, Munoz P, Avery RK,
Houston S, Pruett T, et al. Opportunistic mycelial fungal
infections in organ transplant recipients: emerging
importance of non-Aspergillus mycelial fungi. Clin
Infect Dis 2003;37(2):221-9.
10. Gleissner B, Schilling A, Anagnostopolous I, Siehl I,
Thiel E. Improved outcome of zygomycosis in patients
with hematological diseases? Leuk Lymphoma
2004;45(7):1351-60.
11. Tryfon S, Stanopoulos I, Kakavelas E, Nikolaidou A,
Kioumis I. Rhinocerebral mucormycosis in a patient
with latent diabetes mellitus: a case report. J Oral
Maxillofac Surg 2002;60(Supll 2):328-30.
12. Prabhu RM, Patel R. Mucormycosis and entomo-
phthoramycosis: a review of the clinical manifestations,
diagnosis and treatment. Clin Microbiol Infect
2004;10(Suppl 1):31-47.
13. Khor BS, Lee MH, Leu HS, Liu JW. Rhinocerebral
mucormycosis in Taiwan. J Microbiol Immunol Infect
2003;36(4):266-9.
14. Blonde L. State of diabetes care in the US. Am J Manag
Care 2007;13(Suppl 2):S36-40.
15. Paultauf A. Mycosis mucorina. Virchows Arch Path Anat
1885;102:543-64.
16. Petrikkos G, Skiada A, Sambatakou H, Toskas A,
Vaiopoulos G, Giannopoulou M, et al. Mucormycosis:
ten-year experience at a tertiary-care center in Greece.
Eur J Clin Microbiol Infect Dis 2003;22(12):753-6.
17. Joshi N, Caputo GM, Weitekamp MR, Karchmer AW.
156
Infections in patients with diabetes mellitus. N Engl J
Med 1999;341(25):1906-12.
18. Lee FYW, Mossad SB, Adal KA. Pulmonary
mucormycosis: the last 30 years. Arch Intern Med
1999;159:1301-9.
19. Tuqsel Z, Sezer B, Akalon T. Facial swelling and palatal
ulceration in a diabetic patient. Oral Surg Oral Pathol
Oral Radiol Endod 2004;98:630-6.
20. Jayachandran S, Kritika C. Mucor mycosis presented
as palatal perforation. Indian J Dent Res 2006;17(3):
139-42.
21. Klemptner A. Pulmonary mucormycosis in a patient
with COPD. Am Fam Physician 1999;59(9):
2428,2430.
22. Marr KA, Carter RA, Crippa F, Wald A, Corey L.
Epidemiology and outcome of mould infections in
hematopoietic stem cell transplant recipients. Clin
Infect Dis 2002;34(7):909-17.
23. Bhansali A, Bhadada S, Sharma A, Suresh V,
Gupta A, Singh P, et al. Presentation and outcome of
rhino-orbital-cerebral mucormycosis in patients with
diabetes. Postgrad Med J 2004;80:670-4.
24. Spellberg B, Edwards Jr, Ibrahim A. Novel perspectives
on mucormycosis: pathophysiology, presentation, and
management. Clin Microbiol Rev 2005;18(3)556-9.
25. Roden MM, Zaoutis TE, Buchanan WL, Knudsen TA,
Sarkisova TA, Schaufele RL, et al. Epidemiology and
outcome of zygomycosis: a review of 929 reported cases.
Clin Infect Dis 2005;41(5):634-53.
n n n
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 case report

Full Mouth Rehabilitation of a Patient with

Severely Attrited Dentition
Sanjna Nayar*, U Aruna**, Sharmila Hussain†, S Bhuminathan†, Raghavendra Jayesh S‡

Abstract
The treatment involving the facial esthetics is not only demanding for the patient but also tasking for the clinician. It
involves the astute skill of the prosthodontist, maintaining the health of all the oral structures. This clinical report describes
the prosthodontic management of a 37-year-old male patient with severe attrition of natural dentition. The treatment plan
was executed keeping in mind not only the worn down dentition but also treating the whole stomatognathic system. Utmost
care was taken to achieve harmonious occlusion with no possible occlusal interferences which will further initiate the habit
of bruxism and thereby cause more wear of teeth. The treatment was spread over a period of time so as to achieve perfect
harmony within the masticatory system. The step-wise treatment procedure followed while treating this case has been
presented in a simple and systematic manner.

Key words: Attrition, esthetics, anterior deprogramming, anterior guidance, group function occlusion

F
ull mouth rehabilitation is a challenging
treatment modality that enhances the
appearance of the patient and corrects
imperfections in the occlusion. It is a combination
of the science of neuromuscular dentistry with the
flourish of artistic dentistry. Vertical dimension,
centric relation, speech and muscle tone are it’s
essential elements. The practitioner needs to analyze
each aspect carefully with regard to existing natural
dentition and its relationship with the stomatognathic
system. Full mouth rehabilitation tends to create
smile that is not only esthetic but also functionally
comfortable.1
The complexity in treating full mouth rehabilitation
cases is not only because of its long treatment time
but also at times the lack of clarity in the treatment
objective. A case has to be treated not only by correcting
worn out, broken or discolored teeth but also requires
treating the oral cavity holistically. Every patient with
extreme tooth wear has unique treatment needs.2
The steps in treatment of these patients include a
*Professor
**Senior Lecturer
†
Associate Professor, Dept. of Prosthodontics
‡
Professor, Dept. of Prosthodontics
Sree Balaji Dental College and Hospital, Chennai
Address for correspondence
Prof. Dr Sanjna Nayar
Professor, Dept. of Prosthodontics
Sree Balaji Dental College and Hospital, Pallikaranai, Chennai - 600 100
E-mail: Sanjna101@yahoo.com
comprehensive examination, diagnostic mounting and
diagnostic wax-up, careful planning and sequencing
of various steps, discussion with the patient of the
different treatment alternatives and careful execution
of the treatment plan.3
Case Report
A 37-year-old male patient reported with severely
attrited maxillary and mandibular teeth. The patient’s
main concern was to improve his appearance. Complete
medical and dental history was obtained. The patient
gave a history of previously done root canal treatment
in mandibular anteriors. He also gave a history of
wearing nightguard for the past five years to prevent
further attrition due to night grinding. The patient did
not have any symptoms of temporomandibular joint
(TMJ) disorder.
Extraoral examination revealed no facial asymmetry or
muscle tenderness. The mandibular movements were
normal. Intraoral examination revealed overclosure,
generalized severely worn dentition.
The mandibular anteriors were severely worn
down till the gingival level (Fig. 1). The posterior
teeth showed marked areas of attrition but with
no complaints of dentinal sensitivity. The patient
was explained about the treatment plan. The
aim of the treatment was to improve esthetics and
restore occlusion so as to achieve optimum oral health
for the patient.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 157

 Case Report
Procedure
The patient underwent oral prophylaxis and was given
instructions for oral hygiene maintenance. Panoramic
radiograph was taken to assess the proximity of the
dentin to the pulp in the attrited teeth. Maxillary and
mandibular impressions were made with irreversible
hydrocolloid and study models were poured with
dental stone for the purpose of diagnosis and treatment
planning. Anterior deprogramming device was used
to guide un-interfered movement of mandible to
centric relation by bilateral manipulation.1,4 Low
fusing compound was used as the material for anterior
deprogramming. The maxillary study model was
mounted on a semi-adjustable articulator by means
of facebow transfer using an arbitrary face bow and
the mandibular model was mounted using a centric
interocclusal bite record (Fig. 2).
The study models were analyzed, diagnostic wax-up was
done and the treatment plan was formulated (Fig. 3). Putty
index of the diagnostic wax-up was made section-wise
which will help in fabricating the provisional restorations
later. The anterior wax-up was checked to see if the
Figure 1. Preoperative intraoral view of the patient.
Figure 4. Silicone index.
158
anterior guidance provided the required posterior
disclusion. A medium, thermoplastic occlusal splint
was fabricated and given to the patient for duration of
four weeks to avoid occlusal interference and provide
break in muscle engram.
Replacing the anteriors and harmonizing the anterior
guidance forms the first step in treatment. The
mandibular anteriors were prepared to receive full
coverage metal ceramic crowns, gingival displacement
was done. Impressions were made with single step
putty-wash technique using addition silicone material
and casts poured using type IV dental stone.
The anterior guidance was established using anterior
plane and esthetics as guide. Provisional restorations
were fabricated for the mandibular anteriors with
autopolymerizing resin using the putty index and
were re-shaped in the mouth to achieve ideal contour
and cemented using eugenol free temporary luting
cement. The maxillary anteriors were not modified as
the patient did not want to interfere with his obvious
natural appearance.
Figure 2. Face bow transfer. Figure 3. Diagnostic wax-up.
Figure 5. Group function occlusion (left-side).
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Figure 6. Group function occlusion (right-side).
The anterior replacement was followed by management
of the posteriors. To achieve the goals diagnostic
wax-up was made in the articulated models, which
served as a guide for the opposing tooth preparations.
A putty index was fabricated for the wax-up in each
quadrant which served not only as a guide for the
tooth preparation in each quadrant but also in the
fabrication of provisional restoration (Fig. 4). The plane
of occlusion was determined using Broadrick’s occlusal
plane analyzer.5 The mock wax-up was done for all
the four posterior quadrants. All occlusal interferences
were removed in the articulator. Silicone indices were
made prior to the tooth preparation for achieving the
perfect occlusion in provisional restorations.
The posterior quadrants were prepared for full coverage
metal ceramic crowns. Mandibular posteriors were
prepared followed by the maxillary posteriors. Gingival
displacement was done and impression was made
with single step putty-wash technique using addition
silicone material. The working casts were articulated
using facebow transfer and interocclusal centric record
at previously determined vertical dimension. The
provisional restorations were fabricated using putty
index by the indirect technique, it was finished and
corrected for occlusal interferences and luted with
eugenol free temporary luting cement. The patient was
assessed for adequate esthetics and functional harmony.
The final restorations were fabricated and cemented with
Type I Glass ionomer cement. The scheme of occlusion
given to the patient was group function occlusion
(Figs. 5 and 6). In the post-treatment phase the patient
was instructed oral hygiene maintenance and was
advised six monthly check-up.
Discussion
Full mouth rehabilitation involves the procedures
necessary to produce a healthy, esthetic, well-
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Case Report
functioning masticatory system.3 Treating the full
mouth rehabilitation patients involves not only the
esthetic coverage restorations but also the meticulous
planning of posterior occlusion. The rule of thumb
is to follow the same occlusion unless the complete
posterior occlusion needs to be modified.
The three prime requirements of full mouth
rehabilitation are healthy TMJ, harmonious anterior
guidance and noninterfering posteriors.1 These three
factors are interrelated and any disharmony between
these will affect the stomatognathic system. This patient
presented with severe attrition of teeth. Attrition is
wear due to tooth-to-tooth friction. This kind of wear
results from bruxism and empty mouth parafunction
and leads to loss of clinical crown height.1 Full mouth
rehabilitation with crowns and fixed prosthesis is one
of the treatment options for such patients.6
The diagnostic wax-up should always precede the
treatment so as to decide on the appearance, to
remove occlusal interferences and act as a predictor
to the amount of tooth preparation that is required.
Diagnostic wax-up is done to establish the desired
esthetics, tooth contour, position of tooth and occlusal
plane. The wax-up not only helps in assessing the
amount of preparation and modifications necessary but
also makes the fabrication of provisional restoration
less time consuming.
The anterior teeth are usually restored first so as to
achieve functional and esthetically viable anterior
guidance. The objectives while restoring anterior teeth
were achieving adequate esthetics, function (phonetics)
and noninterference in the posterior teeth so as to have
posterior disclusion. Anterior guidance is the dynamic
relationship of the lower anterior teeth against the
upper anterior teeth through all ranges of function.
Anterior guidance plays a very important role in full
mouth rehabilitation following centric relation.1,7
The anterior guidance forms the anterior control to
provide posterior disclusion. The relationship of the
anterior teeth in function is the principal determinant of
posterior occlusal form. The job of anterior guidance is
to protect the posterior teeth from lateral or protrusive
stresses. The facebow transfer is a must to relate the
anterior guidance with the opening and closing axis.
It is required to reproduce the arc of closure from the
patient to the articulator.
The three main things to be taken care of, while
replacing posterior teeth, are achieving posterior
159
 Case Report
disclusion, establishing the plane of occlusion and
deciding the type of occlusal scheme. Disclusion
refers to separation of opposing teeth during eccentric
movements of mandible, as reported by Christensen,
D’Amico.8 Posterior occlusion should have equal
simultaneous contacts so that it does not interfere with
either the TMJs in the back or the anterior guidance
in the front. Occlusal interference can be detrimental
to the health of the patient. Deflective occlusal
interference can cause painful symptoms in the muscle,
teeth or other orofacial structures. A proper plane of
occlusion must permit disclusion of all the teeth on the
balancing side when the mandible is moved laterally.
The reconstruction of vertical dimension of occlusion
should be done at the centric relation and it should be
acceptable for the patient at the neuromuscular level.9
The patient had severely worn down mandibular
anteriors and wear facets on the canine. Hence group
function occlusion was followed to avoid functional
overload on canines, which can be detrimental to the
overall oral health of the patient. Group function refers
to the distribution of lateral forces to a group of teeth
rather than assigning all forces to one particular tooth.
Lateral pressure is distributed to all working side teeth
in order to prevent overloading of the canine. Little or
no modification was done on the occlusal surface for
this patient to preserve the tooth structure for better
structural durability.
A permissive splint with a medium thermoplastic sheet
was fabricated and given to the patient also to prevent
further tooth damage due to bruxism. A permissive
splint has a smooth surface on one side that allows
the muscle to move the condyles into centric relation
without interference from deflective tooth inclines.1
This eliminates the muscle activity and causes most
of the elevator muscles to release contraction. This is
achieved by separation of all posteriors, allowing only
anterior tooth contact against a smooth surface or by
allowing all the occlusal surfaces to freely guide against
a smooth surface.
The provisional restorations play a critical role in the
successful treatment of the full mouth rehabilitation
patient. Good quality provisional restorations are
essential to achieve predictability with comprehensive
cases involving severe parafunctional habits. The
provisional restorations should be esthetic and also
fulfil the functions so that the effect can be followed
in the temporary before making the final restoration.
160
A properly made provisional restoration psychologically
comforts the patient. The patient should be fully satisfied
with the results of the provisional restoration before
proceeding to the final restorations. The putty index
made on the diagnostic wax-up helps in fabricating a
good provisional restoration in a time saving manner.
The final modifications of the provisionals can be
made in the patient’s mouth. The final restorations
were cemented with temporary luting agent initially
to observe for acceptance from the patient and for
correction of occlusal interferences and then followed
by cementation with permanent luting agent.
Conclusion
Full mouth rehabilitation is a treatment modality
which not only focuses on the esthetics and functional
aspect of the dentition but also improves upon
the health of the whole stomatognathic system.10
A detailed diagnosis and treatment planning is
necessary to achieve predictable success.
References
1. Dawson PE. Functional occlusion from TMJ to smile
design. Mosby St. Louis, Elsevier. 2007:18-26, 27-32,
75-83, 429-52.
2. Binkley TK, Binkley CJ. A practical approach to full
mouth rehabilitation. J Prosthet Dent 1987;57(3):
261-6.
3. Rivera-Moreles WC, Mohl ND. Restoration of vertical
dimension of occlusion in the severely worn dentition.
Dent Clin North Am 1992;36(3):651-64.
4. Lucia VO. Modern Gnathological concept: updated.
Quintessence, Chicago, 1983.
5. Lynch CD, McConnell RJ. Prosthodontic management
of the curve of Spee: use of the Broadrick flag. J Prosthet
Dent 2002;87(6):593-7.
6. Christensen GJ. Treating bruxism and clenching. J Am
Dent Assoc 2000;131(2):233-5.
7. Schuyler CH. The function and importance of incisal
guidance in oral rehabilitation, 1963. J Prosthet Dent
2001;86(3):219-32.
8. Pokorny PH, Wiens JP, Litvak H. Occlusion for fixed
prosthodontics: a historical perspective of gnathological
influence. J Prosthet Dent 2008;99(9):299-313.
9. Bloom DR, Padayachy JN. Increasing occlusal
vertical dimension- Why, When and How. Br Dent J
2006;200(4):199-203.
10. Goldman I. The goal of full mouth rehabilitation.
J Prosthet Dent 1952;2(2):246-51.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 Case report

Interdisciplinary Management of Deep Bite in an

Adult Patient
RV Murali*, BS KulaRashmi**, Issa Fathima Jasmine†

Abstract
The presence of abraded or worn dentition, decreased bony support, temporomandibular joint (TMJ) dysfunction are
challenges in the orthodontic treatment of adults. Deep overbite is one of the most common components of a malocclusion
as well as a major challenge even for a competent orthodontist. Intrusion should be the treatment of choice for adult patients,
who have had significant bone loss around the incisors. In this case report, we document an interdisciplinary approach for the
treatment of deep bite in an adult patient. The treatment of a young adult patient is reported to illustrate the importance of
sequencing treatments from one discipline to another, communication among the team players and the benefits of working
together in an interdisciplinary approach. Orthodontics, endodontics, prosthodontics was combined to achieve the treatment
goals: A bilateral Class I relationship, correction of the anterior deep bite, an esthetic smile displaying four incisors and a
harmonious profile.

Key words: Deep bite, interdisciplinary approach, attrition, intrusion

T
he presence of abraded or attrited dentition,
decreased bony support, temporo-
mandibular joint (TMJ) dysfunction are
challenges in the orthodontic treatment of adults.
Orthodontists often have to resort to less than
ideal treatment to provide an acceptable result.
A comprehensive treatment plan utilizing the combined
expertise of a team of specialists is essential for the
successful outcome.
Deep overbite is one of the most common components
of a malocclusion as well as a major challenge even
for a competent orthodontist. Moyers and Riolo1
reported that deep bite, as a clinical problem, is not
defined in terms of millimeters present today, but in
the light of future changes in esthetics and function.
If left untreated, deep bite can cause attrition of lower
incisors, ulceration of the gingival tissues. The attrition
of lower anterior can be so severe as to have pulpal
involvement, gingival hyperplasia and bone loss.
Nanda2 classified the correction of deep overbite by four
types of tooth movement, i.e., extrusion of posterior
*Professor and Head, Dept. of Orthodontics, Sree Balaji Dental College
and Hospital, Chennai
**Professor, Dept. of Prosthodontics, Asan Dental College and
Hospital, Chennai
†
Lecturer, Dept. of Orthodontics, SRM Dental College, Chennai
Address for correspondence
Dr RV Murali
Professor and Head, Dept. of Orthodontics and Dentofacial Orthopedics
Sree Balaji Dental College and Hospital, Pallikaranai, Chennai - 600 100
E-mail: muralikothai@gmail.com
teeth, flaring of anterior teeth in the case of lingually
tipped incisors, intrusion of incisors and the surgical
method. Among the other types of tooth movement,
Dermaut and De Pauw3 stressed the importance of
intrusion of incisors in adults for whom bite opening
is a goal. Increasing the lower anterior facial height
by extrusion of molars may not always result in a
stable situation in adult patients4 and also difficult
to accomplish as it is opposed by strong muscles of
mastication. In addition, it is less stable in nongrowing
individuals as the extruded posterior teeth would
impinge on the freeway space, leaving the prognosis
for the levelling technique in doubt.5,6
Intrusion should be the treatment of choice for adult
patients, who have had significant bone loss around
the incisors.7 A clinical study by Burzin and Nanda8
showed that the relapse of intruded teeth (intruded an
average of 2.3 mm) is almost insignificant (an average
of 0.15 mm) upto two years after treatment.
In this case report, we document an interdisciplinary
approach for the treatment of deep bite in an adult
patient. The treatment of a young adult patient is
reported to illustrate the importance of sequencing
treatments from one discipline to another,
communication among the team players and the benefits
of working together in an interdisciplinary approach.
The objectives of treatment were to get a good arch
form with an ideal over bite, an esthetic smile
displaying the incisors and a harmonious profile.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 161

 Case Report
Case Report
Pre-treatment Evaluation
A 28-year-old male patient presented with a
complaint of fractured lower anterior crown and was
very eager to have a permanent solution. Extraoral
examination revealed the facial characteristics typical
of a Class I anterior deep bite patient, with short
anterior facial height, deep mentolabial sulcus,
prominent upper lip, an everted lower lip and increased
interlabial gap (Fig. 1). The incision-stomion distance,
which represents the extent of maxillary central incisor
crown display when the lips are in a relaxed position,
was 6 mm (3-4 mm is esthetically pleasing).
The intraoral examination revealed a Class I molar
relationship with an anterior deep overbite, reduced
overjet and crowding in upper arch. The crowns in 31,
32 and 41 were fractured (Figs. 2 and 3). There was no
centric relation-centric occlusion (CR-CO) discrepancy
on closure. Skeletal and dental characteristics showed a
flat occlusal plane and retroclined upper incisors. TMJ
was normal. The maxillary and mandibular midline
coincided with the facial midline.
Treatment Plan
The treatment objectives based on the results of
cephalometric and study model analyses were to
establish a Class I canine relationship, create ideal
overjet and overbite and correct the incisor lingual
Figure 1. Extraoral view Figure 2. Preoperative photo
of the patient. showing the deep bite.
Figure 3. Acrylic crown on Figure 4. Self-ligation bra-
32, 41 and attrited 31. ckets bonded on all teeth.
162
inclination, improve occlusal interdigitation and
improve facial balance and also to provide necessary
space for the mandibular incisor prosthetic crown.
Treatment Progress
The treatment was divided into three phases:
Endodontic, orthodontic and prosthetic phase.
Endodontic Phase
The fractured crowns were removed from 31, 32
and 41. After thorough oral prophylaxis, root canal
therapy was done in 31. A post- and core-restoration
was done in 31. The preservation of tooth structure
is an important factor in the successful restoration of
endodontically-treated teeth. When the restored crown
has 360° of sound coronal tooth structure, four walls
of remaining coronal dentine and extends as far as
possible beyond the margin of the core, there will be a
ferrule effect. There are four advantages of this effect:
Promoting hugging action, preventing the shattering
of the root, reducing the wedging effect of a tapered
dowel and resisting functional lever forces and the
lateral forces exerted during post-insertion.9
Normally, the need for additional root canal retention
through a post can be estimated by comparing the
height (mean height) of the remaining coronal dentin
and that of an ideally prepared tooth.
As a rule of thumb, the required extension of a post
into the root canal apically to the gingival margin
should be the same as the difference between the
mean height of the remaining coronal dentin after
the preparation and the height of an ideal preparation.
To avoid unfavorable stress distributions in the root
during function, a root canal post should never
end at the level of the alveolar crest. Its apical end
should either be coronal to the crest or extend at least
2 mm beyond the crestal level. At the same time, a root
canal post must not extend into the apical third of the
canal in order not to disturb the bacteria-tight
seal provided by the apical root filling. Post- and
core-restoration was done for the lower incisors as
per this rule.
Orthodontic Phase
Self-ligation brackets (0.018 slot) were placed on
all teeth. Temporary acrylic crowns were placed in
32 and 41. Brackets were placed on the crown of 32,
41 and was bonded directly to 31 since there was
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 Case Report

no space for a crown on 31. The most compelling

potential advantages attributed to self-ligating brackets
are reduction in overall treatment time10,11 and less
associated subjective discomfort.12 Other purported
improvements include more efficient chair side
manipulation and promotion of periodontal health
due to poorer bio-hostability. The usual wire sequence
Figure 5. After debonding. Figure 6. Postoperative -
of an initial 0.016-in Nitinol, followed by 0.018 Frontal view.
stainless steel wire, then 0.016 × 0.022 Niti and
0.018 × 0.022. Stainless steel wires (all from 3M
Unitek, Monrovia, Calif ) was followed. Treatment
was initiated with the leveling and intrusion of
the lower anterior dentition. Deep bite was corrected
with accentuated and reverse curve of spee (Fig. 4).
The appliance was debonded after eight months of
active orthodontic therapy.
Figure 7. Postoperative - Figure 8. Postoperative - Left
Prosthetic Finishing Right view. view.

Tooth preparation was done on 31, 32, 41 (Fig. 5).

Cervically, the finish line was 1 mm short of the free
gingival margin. A 0.5 mm horizontal groove was
placed on the lingual surface to assist in confirming a
positive seal of the final restoration.
A polyvinyl siloxane impression was taken and sent to
the lab along with photographs, opposing model and a
bite registration. Upon delivery of the final restoration
from the laboratory, the resin framework fit and the
all-ceramic crowns were evaluated on the stone die for
proper margin fit and path of seating.
To prepare the restoration for bonding, the tissue
surfaces of the restoration were treated with a silane
ceramic primer for 60 seconds and air-dried. A thin
layer of adhesive resin was painted and air-dried. The
tooth preparations were acid-etched with 37% ortho-
phosphoric acid gel for 20 seconds rinsed and blotted
dry. Multiple coats of bonding agent were applied
to each preparation and excess solvents were
evaporated with light compressed air. The resin bridge
framework was cemented with dual cure adhesive
resin. Excess cement was removed and then light
cured. Permanent all ceramic crowns were cemented to
the teeth, to achieve proper esthetics and stabilize the
bite (Figs. 6-8).
Treatment Results
After treatment, a Class I canine relationship with
coincident midlines, correct tooth position and proper
alignment were obtained. Ideal overjet, overbite and
facial balance also were achieved. The post-treatment
facial photographs showed great improvement of facial
esthetics. The orthodontist often acts as co-ordinator
when interdisciplinary treatment is required. In this
case, orthodontics, endodontics, prosthetics were
combined to achieve the treatment goals: A bilateral
Class I relationship, correction of the anterior deep
bite, an esthetic smile displaying four incisors and a
harmonious profile.
Conclusion
As patient’s knowledge about esthetics and function
increases, dentists are challenged to provide services
that will encompass the well-being of the whole patient.
The creation of an esthetic smile with proper phonetics,
balance and function may involve multiple procedures
and disciplines. Correct diagnosis of the problem is the
key to successful treatment. A successful team involves
constant discussion, communication and education in
order to arrive at a common vision. Understanding
patients by discussion about their desires, concerns and
values also enables the team to establish customized
treatment planning.
References
1. Moyers RE, Riolo ML. Early treatment. In: Handbook
of Orthodontics. 4th edition, Moyers RE, (Eds.), Year
Book Medical Publishers Inc: Chicago, III 1988:422-6.
2. Nanda R. Correction of deep over bite in adults. Dent
Clin North Am 1997;41(1):67-87.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 163

 Case Report
3. Dermaut LR, De Pauw G. Biomechanical aspects of
Class II mechanics with special emphasis in deep bite
correction as part of the treatment goal. In: Biomechanics
in Clinical Orthodontics. Nanda R, (Ed.), W.B. Saunders
Co: Philadelphia, Pa 1997:86-98.
4. Seong-Hun Kim, Young-Guk Park, Kyurhim Chung.
Severe Class II anterior deep bite malocclusion
treated with a C-lingual retractor. Angle Orthodont
2004;74(2):280-5.
5. Dake ML, Sinclair PM. A comparison of the Ricketts
and Tweed-type arch leveling techniques. Am J Orthod
Dentofacial Orthop 1989;95(1):72-8.
6. Wylie WL. Overbite and vertical facial dimensions in
terms of muscle balance. Angle Orthod 1994;14:13-7.
7. Melsen B, Agerbaek N, Markenstam G. Intrusion of
incisors in adult patients with marginal bone loss. Am J
Orthod Dentofacial Orthop 1989;96(3):232-41.
164
8. Burzin J, Nanda R. The stability of deep overbite
correction. In: Retention and Stability in Orthodontics.
Nanda R, Burstone CJ, (Eds.), W.B. Saunders Co:
Philadelphia, Pa 1993:61-79.
9. Arunpraditkul S, Saengsanon S, Pakviwat W. Fracture
resistance of endodontically treated teeth: three walls
versus four walls of remaining coronal tooth structure. J
Prosthodont 2009;18(1):49-53.
10. Harradine NW. Self-ligating brackets and treatment
efficiency. Clin Orthod Res 2001;4(4):220-7.
11. Eberting JJ, Straja SR, Tuncay OC. Treatment time,
outcome, and patient satisfaction comparisons of
Damon and conventional brackets. Clin Orthod Res
2001;4(4): 228-34.
12. Damon DH. The Damon low-friction bracket: a
biologically compatible straight-wire system. J Clin
Orthod 1998;32(11):670-80.
n n n
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 case report

Submental Intubation - A Case Report

Abudakir*, Prakash Dhanavelu**, Balakrishnan Ramalingam†, Vijay Ebenezer‡

Abstract
Panfacial trauma is those fractures, which involve frontal bones, zygomaticomaxillary complex, naso orbito ethmoid region,
nasal region, mandible with concomitant occlusal disturbances. These kind of fractures are often associated with CSF rhinorrhea
and base of the skull fracture. Nasal and oral endo tracheal intubation presents a clinical challenge to the anesthesiologists
and also interferes with surgical procedures. The options in these situations are either tracheostomy or submental intubation.
As the tracheostomy needs transtracheal dissection and carries significant morbidity, submental intubation is simple, safe
technique with low morbidity for operative airway management in maxillofacial trauma.

Key words: Panfacial trauma, submental intubation

O
pen reduction and internal fixation of
maxillofacial fractures requires general
anesthesia which necessitates endotracheal
intubation for ventilation. Since almost all maxillo-
mandibular fractures are reduced with the occlusion
as key, oral intubation is often cumbersome and
hence nasoendotracheal intubation is preferred.
But in panfacial fractures where the nasal bones are
fractured, or the anterior skull base is involved, nasal
intubation is difficult and sometimes not indicated.1
Nasal intubation in cases of concomitant anterior skull
base fractures is mostly avoided since there is a risk
of creating a communication between nasal cavity and
anterior cranial fossa, which may cause inadvertent
damage to the brain.2 In such circumstances, when
both oral and nasal routes for intubation cannot be
chosen, tracheostomy is the next, standard route to
the trachea.3 However, there are reports of 14-45%
morbidity and 1.6-16% mortality associated with
tracheostomy procedures.4 It has often been reported
to lead to complications such as bleeding, injury to
*Reader
**Senior Lecturer
†
Professor
‡
Professor and Head
Dept. of Oral and Maxillofacial Surgery
Sree Balaji Dental College and Hospital, Chennai
Address for correspondence
Dr Abudakir
Dept. of Oral and Maxillofacial Surgery
Sree Balaji Dental College and Hospital
Pallikaranai, Chennai - 600 100
E-mail: drabu_dakir@yahoo.co.in
adjacent vital structures especially the vocal chords,
emphysema, pneumothorax or pneumomediastinum,
blockage or displacement of cannula, tracheitis,
cellulitis, tracheal stenosis and tracheoesophageal
fistula, pulmonary atelectasis, tracheoinnominate
fistula, tracheocutaneous fistula, tracheomalacia,
granulation, tracheal stenosis and failure to decannulate.
Though, these complications can be avoided with
care, tracheotomy is generally avoided unless the
patient needs to be kept intubated, for maintaining
airway, even after the surgery.5
A new technique called submental intubation was
published in 1986, that promises to circumvent the
morbidity of tracheostomy and aid ventilation when
the oronasal routes cannot be used.6 This technique
achieved tracheal intubation by passing the tube
through a submental skin incision in the mouth. This
establishes an airway with unhampered intraoperative
access to the dental occlusion and to the nasal pyramid.
The technique has been tried and tested and has now
gained acceptance. This case report details a case of
panfacial trauma in which the patient was treated
under general anesthesia after submental intubation.
Case Report
A 24-year-old Indian male was brought to the hospital
with a severe injury to the face after a road traffic
accident sustained while traveling on a motor cycle.
The patient was conscious, oriented, afebrile. He
reported a loss of consciousness for a period of half

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 165

 Case Report
an hour. The patient exhibited profuse nasal bleeding,
with laceration all over the face and contusions.
The airway was cleared, breathing was ensured, primary
hemostasis obtained and wounds disinfected. The face
exhibited a dish-face deformity, periorbital edema,
subconjunctival ecchymosis and malocclusion (Figs. 1,
2 and 3). The patient also had cerebrospinal fluid (CSF)
rhinorrhea. Radiological (3D CT Scan) examination
(Fig. 4) revealed bilateral fracture of maxilla, symphysis,
left infraorbital region and frontonasal suture region.
An anterior skull base fracture was also present.
The patient was posted for open reduction and
fixation of the fractures under general anesthesia (GA).
Since, there was an obstruction for nasal intubation
and regular oral intubation would be cumbersome
for the procedure, conversion of oral route into the
transcutaneous laterosubmental route was planned.
Figure 1. Preoperative frontal view.
Figure 3. Derangement of occlusion.
166
Procedure
Endotracheal intubation was initially done through the
oral route (Fig. 5) using an 8.0 mm, armored, reinforced,
spiral embedded endotracheal tube with a detachable
connector after induction of GA by standard direct
laryngoscopy. The sealed connector was loosened from
the proximal end of the tube before intubation so that
it could be easily disconnected during the procedure.
The cuff was inflated with about 10 ml of air to
secure the airway from oropharyngeal secretions and
bleeding. The submental skin was scrubbed with
aqueous povidone iodine solution and the site draped.
Lidocaine 2% with 1:100,000 adrenaline was
administered subcutaneously. A 20 mm incision
(Fig. 6) was made at the parasymphyseal region
adjacent to and parallel to the inferior border of the
Figure 2. Preoperative profile view.
Figure 4. 3D CT scan.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Figure 5. Oral endotracheal intubation.
A B
Figure 7 a and b. Submental intubation in position.
mandible in the submental area beside the midline. The
right side was preferred over the left because it allows
better visualization of the position of the tube with
direct laryngoscopy. A curved artery forceps was used
to perform blunt dissection through the subcutaneous
fat, platysma, deep cervical fascia and mylohyoid
muscle. The mucosal layer in the floor of the mouth
was incised over the distal end of the forceps, which
was then opened, creating a tunnel at the junction
of lingual-attached gingiva and free mucosa. At this
point, the endotracheal tube was briefly disconnected
from the breathing circuit and the tube connector
was removed. The distal end of the tube was covered
with a size eight surgical glove finger to facilitate the
passage through the tunnel and prevent entering of
blood and soft tissue, and the tube end, and cuff were
externalized. The deflated pilot tube cuff followed by
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
Case Report
Figure 6. Submental incision.
the endotracheal tube were grasped by artery forceps
and pulled outside in sequence. During this maneuver,
the tube was fixed in the mouth to prevent slipping
from the trachea either manually or with McGill’s
forceps. Then, the surgical glove finger was removed;
the connection tube was restored and ventilation
circuit was re-established. The tube is then secured to
the skin of the submental area (Figs. 7 a and b) by
strong silk suture after verifying unchanged tracheal
insertion of the tube by auscultation of the chest and
checking the proper intraoral positioning of the tube
in the paralingual groove.
Ventilation was continued via orotracheal intubation
until extubation. At the end of the procedure, the
deflated pilot tube cuff and the tube were pulled back
in the reverse order. The skin wound was sutured and
the intraoral wound was left to heal secondarily.
167
 Case Report
Discussion
Nasal intubation is preferred by maxillofacial trauma
surgeons since occlusion needs to be checked. But a
frequent obstacle to nasal intubation is a concomitant
nasal bone fracture, which cannot be appropriately
reduced or manipulated in the presence of a nasal
tube. Nasal intubation can also be complicated
by deviated nasal septum, polyposis, frontal sinus
fracture, anterior skull base fracture or other
intranasal pathologic conditions. In panfacial fractures
where nasoendotracheal intubation is not feasible,
submental intubation is an easier technique with
lower morbidity that allows the surgeon intraoperative
access to the dental occlusion and the nasal pyramid
simultaneously without having the need to switch
the tube in the middle of the procedure. The main
consideration in choosing this method is the anticipated
length of period requiring airway control after the
surgery.7 It is considered an attractive alternative to
tracheostomy in the surgical management of selected
cases of maxillofacial trauma.
Amin et al report utilizing this technique in a
retrospective study for 11 patients with mid-facial
fractures and associated base of skull fractures, and
one patient who underwent an elective Le Fort III
advancement. They conclude that the technique has a
low morbidity and it does not impede the surgical field,
allowing for temporary maxillomandibular fixation
intraoperatively, and nasal assessment, manipulation
and bone grafting, either simultaneously or as an
independent procedure.8
Caubi et al report one intraoperative complication,
when the tracheal pressure increased as a result of
deviation and compression of the tube. However, no
postoperative complaints were reported in this series
of 13 cases.9
Junior SM et al have published a report wherein 3,149
patients, victims of facial trauma, were evaluated:
2,090 patients presented facial fractures; 674 were
submitted to surgery under GA. There were 449 nasal
intubations, 204 oral intubations, six tracheotomies
and 15 submental intubations. Submental intubation
permitted reduction and fixation of all the fractures
without the interference of the tube during surgical
procedure in all of the patients. They have reported no
complications and conclude that submental intubation
is a simple, safe, low morbidity technique for operative
airway management in maxillofacial trauma patients
when there are fractures involving the nasal region and
concomitant dental occlusion disturbances.10
Eipe et al have reported the usage of the same technique
in the treatment of a 12-year-old girl with cancrum
oris who underwent an abbe flap.11
168
Biglioli et al, on evaluation of the safety and efficacy
of submental intubation in 24 patients, report that
the technique is a useful and safe technique for airway
management of craniomaxillofacial traumas and during
transfacial approaches to the cranial base. It avoids the
complications associated with tracheostomy. It also
permits considerable downward retraction of the maxilla
after a Le Fort I osteotomy and is associated with good
clival exposure. The only complication was one case
of superficial infection of the submental wound. They
have concluded that the technique is ideal not only for
trauma treatment but also for oncological cranial base
surgery.12
References
1. Smoot EC 3rd, Jernigan JR, Kinsley E, Rey RM Jr.
A survey of operative airway management practices
for midface fractures. J Craniofac Surg 1997;
8(3):201‑7.
2. Taher AA. Nasotracheal intubation in patients with facial
fractures. Plast Reconstr Surg 1992;90(6):1119-20.
3. Bernard AC, Kenady DE. Conventional surgical
tracheostomy as the preferred method of airway
management. J Oral Maxillofac Surg 1999;57(3):310-5.
4. Taicher S, Givol N, Peleg M, Ardekian L. Changing
indications for tracheostomy in maxillofacial trauma.
J Oral Maxillofac Surg 1996;54(3):292-5; discussion
295-6.
5. Wood DE. Tracheostomy. Chest Surg Clin N Am
1996;6(4):749-64.
6. Hernandez Altemir F. The submental route for
endotracheal intubation. A new technique. J Maxillofac
Surg 1986;14(1):64-5.
7. Schütz P, Hamed HH. Submental intubation versus
tracheostomy in maxillofacial trauma patients. J Oral
Maxillofac Surg 2008;66(7):1404-9.
8. Amin M, Dill-Russell P, Manisali M, Lee R, Sinton I.
Facial fractures and submental tracheal intubation.
Anaesthesia 2002;57(12):1195-9.
9. Caubi AF, Vasconcelos BC, Vasconcellos RJ, de
Morais HH, Rocha NS. Submental intubation in oral
maxillofacial surgery: review of the literature and analysis
of 13 cases. Med Oral Patol Oral Cir Bucal 2008;13(3):
E197-200.
10. Júnior SM, Asprino L, Moreira RW, Moraes MD.
A retrospective analysis of submental intubation in
maxillofacial trauma patients. J Oral Maxillofac Surg
2011 Feb. 28.
11. Eipe N, Neuhoefer ES, La Rosee G, Choudhrie R,
Samman N, Kreusch T. Submental intubation for
cancrum oris: a case report. Paediatr Anaesth 2005;15(11):
1009-12.
12. Biglioli F, Mortini P, Goisis M, Bardazzi A, Boari N.
Submental orotracheal intubation: an alternative to
tracheotomy in transfacial cranial base surgery Skull Base
2003;13(4):189-95.
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Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 clinical study

Comparison of Enzyme Alkaline Phosphatase Levels Around

Healthy and Diseased Implants: A Clinical Study
MN Prabhu*, Jaideep Mahendra**

Abstract
The levels of the enzyme alkaline phosphatase have proved to be a good indicator gingival health and disease. In this study,
their levels were compared around healthy and diseased implants. The enzyme was taken from peri-implant sulcular fluid
of healthy and diseased implants and was estimated. The results indicate an increase in the enzyme levels around diseased
implants when compared to the healthy implants.

Key words: Peri-implant sulcular fluid, alkaline phosphatase, peri-implant sulcus

T
itanium implants are frequently used in
the rehabilitation of totally and partially
edentulous patients. There are two general
types of surgical procedures for the placement and
restoration of missing teeth using endosseous dental
implants. In the first type, the top of the implant is at
the alveolar crest and the mucosa is sutured over the
implant, which result in a submerged surgical approach
(Two-step surgical procedure). The second approach
places the coronal aspect of the implant coronal to the
alveolar crest, and the mucosa is sutured around the
transmucosal aspect of the implant. This results in a
nonsubmerged surgical approach.1
Despite the favorable treatment results in both the
type of surgical procedures, complications may arise
during the maintenance and retention of implants.
The tissues supporting the osseointegrated dental
implants are susceptible to inflammatory disease that
may lead to implant loss.1
The sulcus formed around the prosthesis of the implant
is termed as ‘peri-implant sulcus’ and the fluid found
in this sulcus is called ‘peri-implant sulcular fluid’. It
has been found through different studies that the peri-
implant sulcus simulates the gingival sulcus and the
peri-implant sulcular fluid contents are nearly similar
to that of the gingival sulcular fluid.
*Associate Professor, Dept. of Periodontics
Tagore Dental College and Hospital, Chennai
**Professor, Dept. of Periodontics
Meenakshi Ammal Dental College and Hospital, Chennai
Address for correspondence
Dr MN Prabhu
Associate Professor, Dept. of Periodontics
Tagore Dental College and Hospital, Chennai
E-mail: prabhumds@rediffmail.com
The association among host response and clinical
and radiographic measurements may be useful to
determine the success of the dental implant system
used, to ascertain factors affecting the success of the
therapy, and to identify method-specific problems.
Analysis of the peri-implant sulcular fluid provides a
means by which different aspects of the multifaceted
host response in inflammatory diseases of implants
can be studied. This provides a noninvasive means
of evaluating the role of host response in periodontal
disease. This fluid contains locally and systemically
derived markers of periodontal disease and hence may
offer the basis for a patient-specific diagnostic test for
diseases affecting the supporting apparatus.2
It has been well-established that alkaline phosphatase
enzyme play a crucial role in the pathogenesis
of periodontal disease. Alkaline phosphatase is a
membrane bound glycoprotein produced by many
cells within the area of the periodontium and
gingival crevice. The main sources of the enzyme are
polymorphonuclear leukocytes, bacteria within dental
plaque and osteoblast and fibroblast cells. Alkaline
phosphatase is an important biochemical component
of the gingival crevicular fluid and has demonstrated
a strongly positive relationship between the levels of
the enzyme in the gingival crevicular fluid (GCF) and
previous disease activity.3
It has been proved in a number of clinical studies
that changes occur in the alkaline phosphatase levels
found in the gingival sulcular fluid, with changes
in the health status of the periodontium surrounding
the normal tooth. A similar finding is likely to occur

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 169

 CLINICAL STUDY
around implants.4 In lieu of above, the present study
was undertaken to estimate the levels of enzyme alkaline
phosphatase in peri-implant sulcular fluid surrounding
healthy and diseased implants.
Material and Methods
Fifty male subjects with implant prosthesis were
screened postoperatively and 19 was selected based on
the following inclusion and exclusion criteria.
Inclusion criteria included those patients in whom the
implant was placed at least six months, earlier patient’s
age range was between at least 20-60 years and the
patient who did not have any oral lesions. The subjects
with a history of periodontal treatment in the preceding
six months, intake of nonsteroidal anti-inflammatory
drugs, immunosuppressive drugs, corticosteroids,
antihypertensive drugs, antibiotic therapy and
antiseptic therapy for the preceding six months,
smokers and any underlying systemic conditions were
excluded from the present investigation.5
Selections of healthy and diseased implants were
based on visual inspection of the gingiva and clinical
records obtained within a period of six months prior to
sampling. Failing implants were evidenced by mobility
of the implant, the presence of fistulae or exposed
implant threads or hydroxyapatite coatings.5
Before the collection of the peri-implant sulcular
fluid, all supragingival plaque was removed from each
sampled site. The sites chosen for sample collection
were isolated with cotton roles. The fluid was collected
using standardized filter paper strips held within the
crevice. The strip was inserted into the sulcus or pocket
until slight resistance was felt and was left in place for
20 seconds. Then it was transferred immediately into
plastic vials containing 300 µl of saline with 0.1%
polysorbate 20. The fluid was later eluted from the
paper strips by vortexing the sample at 3,500 rpm for
a period 30 minutes. The strips were then removed
from the vials and the vials were sealed and frozen at
–80°C for subsequent laboratory analysis.5
Alkaline Phosphatase Assay
The assay is based on the 2-stage de-phosphorylation
of dioxetane substrate by the alkaline phosphatase
enzyme. The substrate used in this study was CSPD
which is the acronym for disodium 3-(-4-methoxyspiro
170
{1,2-dioxetane-3,2’-(5’-chloro)tricycle
[3.3.1.13,7]decan}-4-yl)phenyl phosphate. Upon
dephosphorylation by alkaline phosphatase, both a
hydrogen phosphate anion and a metastable chloro-
aryloxide intermediate anion are formed. The
electrophilic nature of the chloro-adamantyl group
contributes to an electron drift which brings about
a quicker fission of the dioxetane ring than that,
occurring the unchlorinated AMPPD assay previously
reported by Chapple et al, 1994. This rapid dissociation
results in a stable chloro-adamantane group and a very
unstable methyl m-oxybenzoate anion, which rapidly
decomposes and in doing so reaches ground state by
emitting a photon of light of wavelength 477 nm.6
Statistical Analysis
The result obtained was statistically analyzed by using
SPSS PC (Statistical Package for Social Science).
Correlation analysis was done to estimate the strength
of linear relationship between alkaline phosphatase
present in each study group.
Results
The alkaline phosphatase levels in the control group
consisting of 10 well-integrated implants were found
to be 865 ± 71.248 (measured in micro-international
units per site).
The alkaline phosphatase levels in the experimental
group consisting of nine failing implants were
found to be 3302 ± 418.426 (measured in micro-
international units per site). The results are represented
4000
Mean alkaline phosphatase - mean
3302
3000
2000
1000 865
0
Successful Failure
Implant
Figure 1. Increased levels of alkaline phosphatase in the
diseased implants.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

diagrammatically using bar graphs (Fig. 1). The results
were found to be statistically significant. The results
clearly indicate that the alkaline phosphatase level in
the peri-implant sulcular fluid of the diseased implants
is more than that in the healthy implants.
Discussion
Alkaline phosphatase is a membrane bound glyco-
protein produced by many cells within the area of
the periodontium and gingival sulcus. The main sources
of the enzyme are polymorphonuclear leukocytes,
bacteria within dental plaque and osteoblast and
fibroblast cells.7
By estimating the levels of the enzyme alkaline
phosphatase, it is able to predict the inflammatory status
within the sulcus surrounding the implant, thereby
giving a chance to make the required modifications
accordingly at an earlier stage much before the disease
progresses.8
The result of this study clearly indicates that the
alkaline phosphatase levels surrounding the failing
implants are increased when compared to successful
implant sulcus. This is in correlation with the results
obtained by Lamster and Polson et al.9,10 It has been
noticed that the levels did not correlate with the sulcus
fluid volume; this suggests that the enzyme here is
largely of endogenous origin, local to the site.
The outcome of this study indicate that assessment of
biochemical mediators, especially alkaline phosphatase,
investigated in this study is a good way to monitor
as inflammation around dental implants. Further
longitudinal studies will open new horizons in the
diagnosis and predictions of the failing implants at an
initial stage.11
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
CLINICAL STUDY
References
1. Newman MG, Fleming TF. Periodontal considerations
of implants and associated microbiota. J Dent Educ
1988; 52(12):737-44.
2. Socransky SS, Haffajee AD, Goodson JM, Lindhe J.
New concepts of destructive periodontal disease. J Clin
Periodontol 1984;11(1):21-32.
3. Ishikawa I, Cimasoni G. Alkaline phosphatase in human
gingival fluid and its relation to periodontitis. Arch Oral
Biol 1979;15(12):1410-4.
4. Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding
on probing. An indicator of periodontal stability. J Clin
Periodontol 1990;17(10):714-21.
5. Rams TE, Link CC Jr. Microbiology of failing dental
implants in humans: electron microscopic observations
1983;11(1):93-100.
6. Chapple IL, Garner I, Saxby MS, Moscrop H,
Matthews JB. Prediction and diagnosis of attachment
loss by enhanced chemiluminiscent assay of crevicular
fluid alkaline phosphatase levels. J Clin Periodontol
1999;26(3):190-8.
7. Binder TA, Goodson JM, Socransky SS. Gingival fluid
levels of acid and alkaline phosphatase. J Periodontal
Res 1987;22(1):14-9.
8. Chapple IL, Glenwright HD, Matthews JB, Thorpe
GH, Lumley PJ. Site-specific alkaline phosphatase
levels in gingival crevicular fluid in health and
gingivitis: cross-sectional studies. J Clin Periodontol
1994;21(6):409‑14.
9. Lamster IB, Oshrain RL, Gordon JM. Enzyme activity
in human gingival crevicular fluid: considerations in
data reporting based on analysis of individual crevicular
sites. J Clin Periodontol 1986;13(8):799-804.
10. Polson AM, Goodson JM. Periodontal diagnosis.
Current status and future needs. J Periodontol 1985;
56(1):25-35.
11. McCulloch CA. Host enzymes in gingival crevicular
fluid as diagnostic indicators of periodontitis. J Clin
Periodontol 1994;21(7):497-506.
n n n
171
 clinical study

Sterilization Protocol for Orthodontic and

Endodontic Instruments
Madhuri M*, Nazeer Ahmed Meeran**, Omer Sheriff†, Vijay C**

Abstract
Pathogenic microbes may be transmitted directly from the dentist to the patient or from the patient to the doctor, and
indirectly from patient-to-patient. The latter may occur via contaminated instruments or surfaces, and is referred to as cross-
contamination. This presents an enormous challenge in the current scenario as it has been proved that blood and saliva are
high-risk sources of contracting hepatitis B, human immunodeficiency virus and herpes. In addition to that mouth is the
reservoir of several pathogens which can be easily transmitted from patient-to-patient or to the doctor. It is a well-known
fact that oral surgeons deal with blood and are supposed to work in a high-risk zone, but very often we tend to give a blind
eye to the fact that the so called ‘blue collared’ specialists, orthodontists and endodontists, too have a high-risk of pricks and
cut injuries with sharp instruments and are only second to oral surgeons in risk for contracting hepatitis B virus. Effective
sterilization and disinfection techniques must be rigidly followed as per the accepted protocols to prevent the incidence of
cross infections in the dental office. This article offers practical guidelines and recommendations for effective sterilization in
the orthodontic and endodontic office. These guidelines are suited for easy implementation with the instrument longevity
in mind. Various sterilization protocols for orthodontic and endodontic instruments are reviewed concomitantly with
relevant scientific data. Additionally, contributory factors of instrument damage are enumerated to emphasize the
importance of adhering to precise protocols and manufacturer recommendations as well as in alleviating some misconceptions
about sterilization-induced instrument damage.

Key words: Sterilization, orthodontic instruments, endodontic instruments, corrosion

S
terilization plays a very important role in the
prevention of cross infection in dental practice.
Sterilization of orthodontic and endodontic
instruments must be done keeping in mind the need
for faster turnaround times and instrument longevity.
Matlack’s1 review of orthodontic offices confirmed this
insufficiency despite the fact that orthodontic and
endodontic offices were at a high-risk of contracting
infections like hepatitis.2,3 Although unlike surgeons,
orthodontists generally do not work in a blood
contaminated area, orthodontic arch wires and ligatures
can traumatize patients’ mucosa, causing bleeding. The
risk of infection is greater for the orthodontist and his
staff than for the patients.4 Saliva is one of the modes
*Professor and Head, Dept. of Orthodontics
**Assistant Professor
Dept. of Orthodontics and Dentofacial Orthopedics
†
Assistant Professor
Dept. of Conservative Dentistry and Endodontics
Priyadarshini Dental College and Hospital, Thiruvallur, Tamil Nadu
Address for correspondence
Priyadarshini Dental College and Hospital
VGR Nagar, Thiruvallur
Pandur - 631 203, Tamil Nadu
E-mail: nazeerortho@yahoo.co.in
for nonparenteral spread of hepatitis B.5 HIV and
herpes virus complex are other high-risk cross infection
spreading through saliva and blood. Instruments
used for root canal therapy are high-risk sources of
infection. Considering the enormity of the challenge
that infectious agents pose as well as their nature to
continuously multiply in real time, the implementation
of effective infection control protocol among all health-
care communities including our dental office is vital.
Against this backdrop, an appraisal of the current
sterilization protocols from an orthodontic and
endodontic perspective is outlined so that it would
facilitate the orthodontist and endodontist in us to make
an informed decision towards effectively implementing
the protocol for our own safety as well as the patients’
welfare. Various methods of sterilization are reviewed
concomitantly with relevant scientific data. Although
the focus of this article is on sterilization protocols
pertaining to orthodontic and endodontic instruments
and materials, it is hoped that these insights will
guide the clinician towards the understanding and
implementation of additional infection control
measures with the overall office in mind.

172 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011


Table 1. Category of Instruments
Category Definition
Critical Penetrates soft tissue, contacts bone, enters
into or contacts the bloodstream or other
normally sterile tissue.
Semi critical Contacts mucous membrane or nonintact skin; Dental mouth mirror, amalgam condenser, reusable
will not penetrate soft tissue, contact bone,
enter into or touch other normally sterile tissue pliers, elastomeric ligatures.
Noncritical Contacts intact skin
Sterilization
Sterilization is the destruction of all microbial forms
including viruses and spores. It is a process that is
intended to kill or remove all types of microorganisms,
with an acceptably low probability of an organism
surviving on any article.
Disinfection
Disinfection refers to the destruction of pathogenic
microorganisms only and is often applied to procedures
which are incapable of destroying spores and certain
resistant pathogenic microorganisms such as tubercle
bacilli and hepatitis viruses.
Barrier Techniques
They form the first-line of defense against infectious
and transmissible disease as well as cross infections.
 Gloves must be worn when skin contact with body
fluids, mucous membranes or contaminated items
and surfaces is anticipated. Between patients, the
gloves must be removed and hands must be washed
and re-gloved. Latex or vinyl gloves should be used
for patient examinations and procedures.
 Heavy rubber (utility) gloves are meant to be used
while cleaning instruments and environmental
surfaces.
 Hand washing: Hands should be washed at the
start of the day, before gloving, after removal
of gloves and after touching any contaminated
surface. Hand washing with water and plain soap
is adequate for patient examination and non-
surgical procedures. For surgical procedures, an
antimicrobial hand scrub should be used.
 Face masks protect the oral and nasal mucosa from
body fluid spatters. They should be changed when
visibly soiled or wet.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
CLINICAL STUDY
Example
Surgical instruments, periodontal scalers, scalpel
blades, surgical dental burs, dental probes, reamers,
files and broaches. Orthodontic tried in preformed
bands may be considered as a critical item as they
have the ability to induce interdental bleeding.
dental impression trays, dental handpieces, orthodontic
Dental chair unit, light switch, handles.
 Protective eye wear is indicated to shield the eyes
from spatters.
 Protective clothing: Aprons, either reusable or
disposable, must be worn in the dental clinic.
They should be changed when visibly soiled or
penetrated by fluids and they should not be worn
outside the work area.
 Limiting contamination can be done by three
methods.
n Proper patient positioning
n Use of high volume evacuation
n Use of rubber dam
The advice sheet for infection control in dentistry
issued from the department of health UK enumerates
three stages for effective decontamination of
instruments namely:
 Presterilization cleaning
 Sterilization
 Storage
Presterilization Cleaning
All the instruments must be thoroughly debrided of
contaminants like blood, saliva and other impurities
before undergoing a sterilization cycle, as retention
of these debris and contaminants may shield the
microorganisms from being destroyed, thus preventing
effective sterilization. Precleaning protocols remove
a large number of microorganisms when carried out
thoroughly and must not be omitted. Precleaning
protocols have conventionally involved initial
debridement of all the contaminated instruments
with the help of a brush and detergent under running
water. Though cost-effective, this poses a risk to the
personnel involved in cleaning the instruments.
173
 CLINICAL STUDY
Ultrasonic baths and instrument washer and
disinfectors have taken their place, which is much
safer than debriding by hand. Special solutions
containing enzymes and having antirust properties
have been recommended for effective breakdown of
the contaminating particles.
Precleaning cycles usually last between 10-15 minutes,
depending on the instrument load. The instruments
can be placed in specially designed cassettes to reduce
the chances of instrument damage. It is very important
that any residual moisture present must be completely
eliminated to prevent instrument corrosion.
Sterilization
Various methods are currently being used for sterili-
zation of orthodontic and endodontic instruments.
Autoclave
Steam autoclave: At 250°F (30 psi), total time about
one hour. There is good penetration and it maintains
integrity of liquids, like hand piece lubricants, due to
the 100% humidity within the chamber.
Disadvantages
Nonstainless steel metal items corrode, use of hard
water may leave deposits, and it may damage plastic
and rubber items. Sharp instruments get dulled.
 Rapid steam autoclave: At 275°F (35 psi), total
time is 15-20 minutes. It is very convenient and
easy to operate.
Disadvantages
Requires use of distilled water and small chamber size
necessitates frequent cycles.
Endodontic reamers and files can be inserted into
synthetic sponges and subjected to autoclaving.
According to Boyd6 and Vélez7 the sponges do not
obstruct the autoclaving process.
Chemiclave or Chemical Vapor Sterilization
It is effective against all fungi, viruses and bacteria
including spores. Two percent glutaraldehyde solution
and chlorine dioxide are commonly used and has
been approved by the ADA. Sterilization time with
2% glutaraldehyde is 10 hours without dilution
and with chlorine dioxide is six hours when mixed
174
according to the manufacturer’s recommendation. It is
recommended only for heat sensitive nonsurgical
instruments and alginate impressions. The main
drawback is that this type of sterilization requires
prolonged immersion and instrument turnover
time is increased. This type of sterilization is not
recommended for dental office instruments as there
is no method available to verify their effectiveness in
providing complete sterilization as well as the fact
that present day protocols are combined with heat
sterilization for maximum sterilization effectiveness.
The other disadvantage is the lingering unpleasant
strong odor in the room where the solution is kept
and requires adequate ventilation.
Pitting type of corrosion have been observed in
orthodontic cutters and pliers8,9 and there is a
compromise in the integrity of the instrument
when subjected to chemical disinfectants. Chrome
plated pliers appeared more resistant to damage and
maintained their appearance better than stainless steel
pliers.10
In dental office chemical sterilization is used to disinfect
alginate impressions before pouring the model.
Recent research11 is directed in finding a alginate
disinfecting solution capable of releasing nitric oxide
(a broad- spectrum antimicrobial agent) with additional
anti-viral activity (herpes simplex virus) which
would be a good alternative to the present chemical
disinfectants.
Sporicidin solution can be used to disinfect rubber
clamps and X-ray holders. For disinfection it requires
10 minutes at room temperature where as for
sterilization 6.75 hours is needed. Tincture of metaphen
1:200 (untinted) can be scrubbed against surface to be
sterilized for sheath of contra-angle and hand piece, tip
of electric pulp tester, tooth clamp and surrounding
area of rubber dam.
Gutta-percha cones are soaked in 5.2% sodium
hypochlorite for 1-minute and then rinsed with
hydrogen peroxide and dried between two layers of
sterile gauze. Dappen dishes can be swabbed with
merthiolate followed by 70% alcohol. Long handle
instruments, tips of cotton pliers, blades of scissors
can be dipped in isopropyl alcohol (90%) and then
subjected to flaming before use.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Glass Bead Sterilization
Glass bead sterilization uses small glass beads
1.2-1.5 mm in diameter. The recommended
temperature is between 217-232°C (424-450°F) and
should not exceed 250°C. The duration of the cycle is
between 3-5 seconds.
In orthodontics, although the possibility of being able
to sterilize 1-2 orthodontic pliers within 30 seconds has
been highlighted with a stress on correct positioning
for maximum effectiveness,12 these recommendations
are deleterious as the instruments are exposed to
higher temperature ranges against most manufacturer
warnings (193°C/380°F). Nisalak13 showed that it was
possible to kill all the vegetative cells and bacterial
spores by scrubbing the contaminated pliers with
alcohol and placing in a glass bead sterilizer for three
minutes and hence can be a useful adjunct when rapid
chair side sterilization is required. Smith14 found that
it was possible to relive a single band of bacteria in 15
seconds at 223°C and could be relieved of spores when
placed for 45 seconds at a temperature of 226°C but
may not practically feasible as sterilization of multiple
tried in bands would require more duration which can
alter the physical properties of the molar bands.
Root canal instruments such as reamers, spreaders,
broaches and files can be effectively sterilized in glass
bead sterilizer at 218-246°C in 10 seconds.
Hot Salt Sterilization
The following endodontic instruments can be sterilized
in hot salt sterilizer. The temperature ranges between
425-475°F.
 Ten seconds paper points, cotton pellets
 Five seconds - reamers, files, broaches, burs,
spreaders, pluggers, any metallic instrument
introduced in the canal, silver cones
It must be made sure that the instruments are immersed
at least a quarter-inch below the salt surface in the
peripheral area as the ideal temperature is present in
the periphery of the sterilizer.
Ethylene Oxide Gas
Kills microorganisms. The total time from start of
cycle to the end of degas is 14 hours. It can be used for
heat sensitive items. The instruments are cool and dry
at the completion of cycle.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
CLINICAL STUDY
Disadvantage
Very long cycle time. If the cycle is interrupted before
completion, there can be possibility of ethylene oxide
exposure. It requires the use of several single use items
that can be purchased only from the manufacturer.
Dry Heat Sterilization
Their main advantage is they do not cause instrument
corrosion and hence recommended for sterilization of
orthodontic pliers and metal hand instruments.
Orthodontic Pliers Sterilization
The current recommendations for effective sterilization
without compromising the longevity of the instruments
have been enumerated below.
 Placement in ultrasonic cleaner for 5-12 minutes
depending on the capacity of the unit.
 Thorough rinsing with distilled water as tap water
may contain impurities and pH imbalances which
may cause corrosion.
 Complete moisture removal by drying with oil-
free compressed air.
 Dry heat sterilization at 190°C for 6-12 minutes.
Never expose the instruments to more than
193°C.
 Position the instruments in the ‘open’ position to
ensure thorough sterilization of joints.
 Using silicone bases lubricants for the instrument
joints. Oil based lubricants are not recommended
as they tend to clog the pliers.
 Storage in a dry area free from moisture and
humidity.
Autoclaving should be a second option and is
recommended only if a dry heat sterilizer is not
available. A shorter cycle at 134°C for three minutes
is recommended due to the deleterious effect it has
on the instruments and the instruments must be freed
of any residual moisture and wrapped before being
subjected to autoclaving.
Contaminated orthodontic instruments and bands
placed in OMS-ASAP system instrument and band
cassettes15 and then subjected to heat sterilization were
also efficiently decontaminated of spores and instrument
cassettes can be useful adjuncts for sterilization.
175
 CLINICAL STUDY
Prion Protection - Sterilization Protocol
for Orthodontic Pliers
Prions are extremely stable group of infectious agents
composed of mainly proteins and are highly resistant
to sterilization. They are able to re-fold into different
structures, which in turn convert normal protein
molecules into abnormal structures. This altered
structure is extremely stable and highly resistant to
conventional sterilization protocols. Prion elimination
requires autoclave cycles at 121°C for 1-hour or 134°C
for at least 18 minutes. The effect of such extreme
Prion sterilization protocols on orthodontic ligature
cutter were recently evaluated,16 and it was found that
surface alterations occurred from the first cycle itself
with a blunting of the cutting edges and reduction in
the instrument efficiency.
According to Wichelhaus17 exclusive chemical methods
are less effective than thermal or physical chemical
methods for efficient disinfection of contaminated
orthodontic pliers and spraying was not an efficient
method which exhibited severe shortcomings. It was
also found that heat sterilization of pliers resulted in
lesser corrosion than cold disinfection.9 Taking these
factors into account, dry heat is the most effective
method of orthodontic plier sterilization without
compromising the instrument efficiency
Molar Bands Sterilization
Several studies18,19 have reported about the need of
effective protocol for sterilization of preformed bands.
The guidelines for sterilization of molar bands are:
 Placement in ultrasonic cleaner for five minutes
depending on the capacity of the unit
 Thorough rinsing with distilled water
 Complete moisture removal by drying with
oil-free compressed air
 Dry heat sterilization at 190°C for six minutes.
 Storage in a dry area free from moisture and
humidity.
The tried in molar bands must be immediately
placed in ultrasonic cleaner and should be stored in
separate containers if it is not possible to sterilize
immediately. Autoclaving of plain bands can be
done but is not recommended for prewelded bands.
Chemical sterilization is a secondary choice because
of the longer time involved as well as the lack of any
indicator for its effectiveness.
176
Elastomeric Chains and Ligatures
Chemicals are not suitable for disinfection of
elastomeric ligatures and E-chains because they alter
and adversely affect the physical properties of the
elastics.20,21 Alcohol wipes are not effective alternatives
because they are not effective in the presence of tissue
proteins found in saliva and blood. The best safeguard
is to use single patient packs to prevent cross infection.
As for E-chains it is best to cut-off some more above
that is required and discard the rest.
Disinfection of Alginate Impressions in the
Dental Office
For disinfection of alginate impressions, 1% sodium
hypochlorite, sodium dichloroisocyanurate and 2%
glutaraldehyde is used. Current recommendations
requires the alginate impression to be immersed in
disinfecting solutions for not more than 10 minutes
as prolonged immersion alters the surface characters of
the impression material.22
Guide lines for sterilization of alginate impressions.
 Rinse the saliva from the surface of the impression
under running tap water.
 Immerse the impression along with the tray in
the disinfectant solution for 10 minutes. Spraying
aerosols is not recommended because it will not
wet the surface of the impression evenly and poses
a health hazard for the operator.
 After 10 minutes thoroughly rinse off the excess
disinfectant from the impression under running
tap water and pour the model.
Hand Piece Asepsis
Although no documented cases of disease transmission
have been associated with dental hand pieces,
sterilization between patients with acceptable methods
that ensure internal as well as external sterility is
recommended. The inside lines of high speed hand
pieces may become contaminated when patient fluids
retract back through air- water opening. If the hand
piece is not properly processed, the retracted fluids
may enter the mouth of the next patient.
Dental units manufactured after the middle 1980s
have antiretraction valves already installed. Since, these
valves fail periodically, retraction must be routinely
checked and the valve replaced when necessary.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011

Retraction is checked by observing the tip of the water
line opening at the hand piece connection when the
water is turned on and then off. If a drop of water
‘hangs’ on the tip, retraction is not occurring. If the
water is drawn back into the line, then retraction is
occurring. For proper sterilization of hand piece, the
manufacturer’s instructions must be followed. First,
the hand piece should be flushed with water by running
it for 20-30 seconds, discharging the water into a
sink or container.
If recommended by the manufacturer, use ultrasonic
cleaner to remove any adherent material, otherwise, it
should be scrubbed thoroughly with a detergent and
hot water. Lubricate high speed hand pieces when
indicated by the manufacturer and spray out excess
lubricant. Depending upon the hand piece, some
must be lubricated before, after or before and after
sterilization or not at all.
Package for sterilization in steam or unsaturated
chemical vapor must be done following the
manufacturer’s directions. If disinfecting a hand piece
that cannot be heat sterilized, spray or saturate with
disinfectant recommended by the manufacturer. The
light port of fiberoptic handpieces is wiped with an
isopropyl alcohol swab after sterilization. Dry heat
sterilization is not recommended for handpieces.
Steps to Properly Sterilize Tungsten
Carbide Burs
This involves a two step process, cleaning and
sterilization.
Cleaning
Step 1: Wear gloves when handling contaminated
instruments. Pre-soak carbide burs in a container of
soapy water to loosen debris Ultrasonic systems may
also be used to loosen debris in burs; however, burs
should be separated from each other in a bur block
during immersion to prevent damage.
Step 2: Brush away remaining debris using a SS White
stainless steel wire brush and rinse burs under running
water.
Step 3: After rinsing, dry burs thoroughly by placing
them on absorbent towels. Pat dry all surfaces.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
CLINICAL STUDY
Sterilization
Proper sterilization of carbide burs is extremely
important because it eliminates the threat of cross
infection of patients and staff with communicable
diseases.
 Dry heat sterilizers –170°C (340°F) for 1-hour. This
method, when used according to manufacturer’s
instructions, will not corrode or dull carbide
burs.
 Steam autoclaves –121°C (250°F) for 20 minutes
at 15 psi. Steam autoclaves will effectively sterilize
carbide burs; however, potential for corrosion is
present.
Avoid cold sterilizing solutions as they contain oxidizing
agents which may weaken carbide burs.
Laser sterilization: Laser sterilization of endodontic
reamers23,24 has been tried recently using carbon dioxide
laser and has been proved to be 100% effective in
completely eliminating the spores and holds excellent
promise as effective method of sterilizing endodontic
instruments in the future.
Factors responsible for instrument damage during
sterilization and methods of prevention:
 Water hardness: The hardness of water, excess
mineral content and pH imbalances play an
important role in instrument corrosion.
 High temperatures: Using temperatures above the
current manufacturer recommendation of 193°C
results in corrosion of the instruments being
sterilized.
 Moisture and insufficient drying: All the
instruments should be completely dried before
being subjected to dry heat as moisture is the
major culprit for corrosion of most instruments in
the dental office.
 Strong detergents: They promote protein
precipitation on the instrument surface, which
can only be removed by vigorous brushing. This
in turn roughens the instrument surface and acts
as a template for the process of corrosion to start.
 Cold sterilization: Instruments sterilized by
immersion in chemical solutions are reported to
be associated with pitting corrosion.
 Enzymes: Enzymatic cleaning solutions are known
to have corrosive effects on the instruments and
are not recommended.
177
 CLINICAL STUDY
 Aging of instruments: Sterilization accelerated
corrosion in instruments which have been
subjected to wear and tear over a long period
of time due to surface roughening and
irregularities.
Conclusion
It is incumbent upon each orthodontist and
endodontist to conduct their practice in a manner
that restricts the spread of infection and cross
contamination. By following the procedures
described here, they can minimize and even prevent
the possibility of crossinfection. This is the best
protection against the transmission of hepatitis
and other diseases. Asepsis in the dental office is of
utmost importance. Sterilization and disinfection
significantly decreases the risk of infectious disease for
the doctor, the staff and the patient. The oral cavity
is the main portal of entry for pathogenic microbes
into the body and asepsis of the instruments and hand
prevents contamination by way of the respiratory
system, blood or saliva.
References
1. Matlack RE. Instrument sterilization in orthodontic
offices. Angle Orthod 1979;49(3):205-21.
2. Buckthal JE. Survey of sterilization and disinfection
procedures. J Clin Orthod 1988;22(1):22-8.
3. Cash RG. Trends in sterilization and disinfection
procedures in orthodontic offices. Am J Orthod
Dentofacial Orthop 1990;98(4):292-9.
4. Crawford JJ. Clinical asepsis in dentistry. P8RA Kolstad,
Publisher 1978.
5. MMWR perspectives on the control of viral hepatitis
Type B centre for disease control US Dept of health,
Ed and Welfare 1976;25:17.
6. Boyd KS, Sonntag KD, Crawford JJ. Efficacy of
sterilization of endodontic files after autoclaving in a
synthetic sponge. Int Endod J 1994;27(6):330-3.
7. Vélez AE, Thomas DD, del Rio CE. An evaluation of
sterilization of endodontic instruments in artificial
sponges. J Endod 1998;24(1):51-3.
8. Mazzocchi AR, Paganelli C, Morandini C. Effects of
3 types of sterilization on orthodontic pliers. J Clin
Orthod 1994;XXVIII:644-7.
9. Wichelhaus A, Brauchle G, Mertmann M, Sander
FG. Corrosion of orthodontic pliers using different
sterilization procedures. J Orofac Orthop 2004;
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10. Jones ML. An initial assessment of the effect on
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disinfection regimes. Br J Orthod 1989;16(4):251-8.
11. Patel MP. Development of a self-disinfecting alginate
impression material. Biological and Medicinal Research,
University of London, 2009.
12. Miller JA, Harrower KM, Costello MJ. A novel method
of sterilizing orthodontic instruments. Aust Orthod J
1992;12(3):151-2.
13. Nisalak P, Prachyabrued W, Leelaprute V. Glass bead
sterilization of orthodontic pliers. J Dent Assoc Thai
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14. Smith GE. Glass bead sterilization of orthodontic
bands. Am J Orthod Dentofacial Orthop
1986;90(3):243‑9.
15. Hohlt WF, Miller CH, Need JM, Sheldrake MA.
Sterilization of orthodontic instruments and bands in
cassettes. Am J Orthod 1990;98(5):411-6.
16. George O, Benoit F, Rapin C, Aranda L, Berthod P,
Steinmetz P, et al. Effect of surgical sterilization
procedures on orthodontic pliers: a preliminary report.
Eur Cells Materials 2005;10(Suppl 4):13.
17. Wichelhaus A, Bader F, Sarder FG, Krieger D,
Merters T. Effective disinfection of orthodontic pliers.
J Orofac Orthop 2006;67(5):316-36.
18. Dowsing P, Benson PE. Molar band re-use and
decontamination: a survey of specialists. J Orthod
2006;33(1):30‑7; discussion 28.
19. Benson PE, Douglas CW. Decontamination of
orthodontic bands following size determination and
cleaning. J Orthod 2007;34(1):18-24.
20. Mayberry DR, Allen R, Close J, Kinney DA. Effects of
disinfection procedures on elastomeric ligatures. J Clin
Orthod 1996;30(1):49-51.
21. Jeffries CL, von Fraunhofer JA. The effects of 2%
alkaline glutaraldehyde solution on the elastic properties
of elastomeric chain. Angle Orthod 1991;61(1):25-30.
22. Blair FM, Wassell RW. A survey of the methods of
disinfection of dental impressions used in dental
hospitals in the United Kingdom. Br Dent J 1996;
180(10):369-75.
23. Hooks TW, Adrian JC, Gross A, Bernier WE. Use of
the carbon dioxide laser in sterilization of
endodontic reamers. Oral Surg Oral Med Oral Pathol
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24. Venkatasubramanian R, Jayanthi, Das UM,
Bhatnagar S. Comparison of the effectiveness of sterilizing
endodontic files by 4 different methods: an in vitro
study. J Indian Soc Pedod Prev Dent 2010;28(1):2-5.
Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011
 Indian Journal of
Case Report
Multidisciplinary Dentistry
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Types of Submission: Original Research articles, Review articles, Case 1. Classification (e.g. original article, review, etc.)_________________
reports and Clinical study
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(without degrees of diplomas), names and full location of the departments 3. Number of tables________________________________________
and institutions where the work was performed, name of the corresponding
4. Number of figures_______________________________________
authors, acknowledgement of financial support and abbreviations used. The
title should be of no more than 80 characters and should represent the 5. Special requests_________________________________________
major theme of the manuscript. A subtitle can be added if necessary.
6. Suggestions for reviewers (name and postal address)
A short title of not more than 50 characters (including inter-word spaces)
for use as a running head should be included. The name, telephone Indian 1.______________ Foreign 1. _______________
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Abstract: The abstract of not more than 200 words. It must convey the
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essential features of the paper. It should not contain abbreviations, footnotes
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or references.
__________________________________________________________
Introduction: The introduction should state why the study was carried out
and what were its specific aims/objectives were.
For Editorial Correspondence
Material and Methods: Theses should be described in sufficient details to
permit evaluation and duplication of the work by others. Ethical guidelines Dr KMK Masthan
followed by the investigations should be described. Professor and Head
Results: These should be concise and include only the tables and figures Department of Oral Pathology and Microbiology
necessary to enhance the understanding of the text. Sree Balaji Dental College and Hospital
Discussion: This should consist of a review of the literature and relate Velachery Main Road, Narayanapuram, Pallikaranai
the major findings of the article to other publications on the subject. The Chennai - 600 100, E-mail: masthankmk@yahoo.com,
particular relevance of the results to healthcare in India should be stressed,
e.g., practically and cost.
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Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011 179