dental journal march-april

ISSN 2229-6360

MultidisciplinaryDENTISTRY

Indian Journal of

Volume 1, Issue 3March-April 2011

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© Copyright 2011 IJCP Publications Pvt. Ltd.All rights reserved.

Dr KK Aggarwal, on behalf of IJCP PublicationsPvt. Ltd. and Published at E - 219, Greater Kailash, Part - 1, New Delhi - 110 048

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Indian Journal of Multidisciplinary Dentistry does not guarantee, directly or indirectly,the quality or efficacy of any product or service described in the advertisements or othermaterial which is commercial in nature in this issue.

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http://ebook.ijcpgroup.com/ijmd/index.htm

IJMD’s Editorial Panel

Associate Editor N Aravindha Babu

Editor-in-Chief KMK Masthan

Executive Editor S Bhuminathan

Indian Journal of

Multidisciplinary DentistryIndian Journal of

Multidisciplinary Dentistry

IJMD Advisory BoardProsthodontics Mahesh Verma Srinisha J Raghavendra Jayesh S Sanjna Nayar

Conservative Dentistry/Endodontics Sukumaran VG Subbiya A Swaminathan S (Singapore)

Implantology John W Thurmond (USA)

Genetics Aravind Ramanathan

Oncology Abraham Kuriakose M

Oral and Maxillofacial Surgery Ramakrishna Shenoi Vijay Ebnezer Raj Kutta (USA)

Oral Pathology and Microbiology Vinay K Hazarey Ipe Vargese V Puneet Ahuja

Orthodontics Krishna Nayak US Dhandapani G Murali RV Deepak C

Pharmacology Muthiah NS Elumalai M

General Medicine Rajendran SM

Periodontics Chandrasekaran SC Ash Vasanthan (USA)

Oral Medicine and Radiology Selva Muthu Kumar SC Nalini Aswath

Pedodontics Krishan Gauba Ashima Gauba

Biochemistry Julius A

Microbiology Mahalakshmi K

IJCP’s Editorial PanelDr KK Aggarwal

CMD, Publisher and Group Editor-in-Chief

Dr Veena AggarwalJoint MD & Group Executive Editor

Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean

Harvard Medical SchoolGroup Consultant Editor

Anand Gopal Bhatnagar Editorial Anchor

Dr Deepak ChopraChief Editorial Advisor


Advisory BodiesHeart Care Foundation of India, Non-Resident Indians Chamber of Commerce & Industry, World Fellowship of Religions

IJMD is included in the databases of Genamics JournalSeek along with Ulrich International periodical directory and Index Copernicus International, Ltd.

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ContentsFrom 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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Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 3, March-April 2011124

From the editor-in-chieF

Our 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-speciality consider it beneath their pride even to enroll in such workshops. Now who is the loser?

Dr KMK MasthanProfessor and Head, Department of Oral Pathology and Microbiology Sree Balaji Dental College and Hospital, Chennai

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...

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

From the desk oF iJcP GrouP editor-in-chieF

Poorly 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.

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

n n n

Dr KK AggarwalPadma Shri and Dr BC Roy National Awardee

Sr. Physician and Cardiologist, Moolchand MedcityPresident, Heart Care Foundation of India

Group Editor-in-Chief, IJCP Group Editor-in-Chief, eMedinewS

Chairman Ethical Committee, Delhi Medical CouncilDirector, IMA AKN Sinha Institute (08-09)

Hony. Finance Secretary, IMA (07-08)Chairman, IMA AMS (06-07)

President, Delhi Medical Association (05-06)[email protected]

http://twitter.com/DrKKAggarwalKrishan Kumar Aggarwal (Facebook)

Diabetes Mellitus and Dental Infections

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

Imaging 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

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:

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

Comparative Study of Manual Cephalometric Tracing and Computerized Cephalometric Tracing in Digital Lateral Cephalogram for Accuracy and Reliability of LandmarksRV Murali*, MR Sukumar**, t faisal tajir†, S Rajalingam‡

*Professor and Head**Professor †Associate Professor‡Postgraduate StudentDept. of Orthodontics and Dentofacial OrthopedicsSree Balaji Dental College and Hospital, ChennaiAddress for correspondence Dr RV MuraliProfessor and HeadDept. of Orthodontics and Dentofacial OrthopedicsSree Balaji Dental College and HospitalsPallikaranai, Chennai - 600 100E-mail: [email protected]

review article


review article

Good quality radiographs without any artifacts z

that might interfere with the location of the anatomical points.No craniofacial deformity or asymmetry. z

Patient biting in occlusion (maximum inter- z

cuspation).Permanent dentition with no missing teeth. z

No excess soft tissue (as determined from the z

radiographs) that could interfere with locating anatomical points.

All the lateral cephalometric radiographs were acquired using the same digital cephalometer (Orthophos XG5 - Sirona Dental Systems GmbH) set at x1.25 magnification, as recommended by the manufacturer.

Digital tracing

The digital images were stored in a laptop (Hp pavilion dv 2000 screen resolution 1074 × 728 pixels) and then imported into the software program (Vistadent by GAC International, New York).

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 structures and double images, the mid-point was chosen by construction.

A total of 33 anatomical landmarks (Fig. 1) were defined on each radiograph and following 37 parameters were calculated:

Skeletal variables 16-(Fig. 2) z

Dental variables 10-(Fig. 3) z

Soft tissue variables 11-(Fig. 4) z

Statistical Analysis

Statistical analysis was undertaken using SPSS 16.0 version statistical software program. No differentiations were made for age or gender. For

figure 1. Landmarks used.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, GI´-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.

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).

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

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review article

table 1. Variables UsedSkeletal variablesSNA (°) SNA angle

SNB (°) SNB angle

ANB (°) ANB angle

Nperp-A (mm) Maxillary position

Nperp-Pog (mm) Mandibular position

Cond-A (mm) Effective maxillary length

Cond-Gn (mm) Effective mandibular length

Max-Mand (mm) Maxillomandibular difference

Wits (mm) Distance of A and B on occlusal plane

Ba N-NA (°) Formed by connecting the Sella-Nasion plane to A point

SpP-GoMe (°) Angle of palatal to mandibular plane

SN-GoMe (°) Angle of anterior cranial base to mandibular plane

(S-Go:N-Me) Ratio of posterior and anterior facial height

ArGo-Me (°) Gonial angle

ANS-Me (mm) Lower facial height

Go-Me (mm) Mandibular length

Dental variablesIMPA (°) Angle of axis of 1l to mandibular. Base

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

1l-NB (mm) Distance of labial outline of 1l to N-B

Overjet (mm) Overjet

Overbite (mm) Overbite

Interincisal (°) Interincisal angle

SpP-OcP (°) Angle of palatal to occlusal plane

MeGo-OcP (°) Angle of mandible to occlusal plane

Soft tissue variablesGl’-Sn (mm) Upper facial height

Sn-Me’ (mm) Lower facial height

Sn-stm-s (mm) Upper lip length

Stm-i-Me’ (mm) Lower lip length

Stm-s - Stm-i (mm) Interlabial gap

SnPerp-Ls (mm) Distance of upper lip to SnPerp

SnPerp-Li (mm) Distance of lower lip to SnPerp

SnPerp-Pog’ (mm) Distance of chin to SnPerp

CotgSnLs (°) Nasolabial angle

Ls-NsPog’ (mm) Upper lip to esthetic line

Li-NsPog’ (mm) Lower lip to esthetic line

figure 3. Dental variables used.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 (°), 10-MeGo-OcP (°).

figure 4. Soft tissue variables used.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),8-SnPerp-Pog’ (mm), 9-CotgSnLs (°), 10-Ls-NsPog’ (mm),11-Li-NsPog’ (mm).

and Vistadent tracing was evaluated using t-test. A level of p < 0.05 was considered to be significant.

Results

Statistical evaluation of skeletal, dental, soft tissue variables between Group I (manual tracing), Group II (Vistadent) (Table 2) shows the following variables were significant (p < 0.05) Nperp-Pog (p = 0.032),

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review article

table 2. Statistical Evaluation of Skeletal, Dental, Soft Tissue VariablesVariables Group I (Manual tracing) Group II (Vistadent tracing) t-test

Skeletal variables

SNA (°)

SNB (°)

ANB (°)

Nperp-A (mm)

Nperp-Pog (mm)

Cond-A (mm)

Cond-Gn (mm)

Max-Mand (mm)

Wits (mm)

Ba N-NA (°)

SpP-GoMe (°)

SN-GoMe (°)

(S-Go:N-Me)

ArGo-Me (°)

Dental variables

IMPA (°)

Max1-NA (°)

Mand1-NB (°)

1u-NA (mm)

1l-NB (mm)

Overjet (mm)

Overbite (mm)

Interincisal (°)

SpP-OcP (°)

MeGo-OcP (°)

Soft tissue variables

Gl’-Sn (mm)

Sn-Me’ (mm)

Sn-stm-s (mm)

Stm-s - Stm-i (mm)

Stm-i-Me’ (mm)

SnPerp-Ls (mm)

SnPerp-Li (mm)

SnPerp-Pog’ (mm)

CotgSnLs (°)

Ls-NsPog’ (mm)

Li-NsPog’ (mm)

83.1125 ± 0.38702

78.1000 ± 0.41687

5.0000 ± 0.22482

1.6250 ± 0.47480

–4.3125 ± 0.46370

94.7125 ± 0.52561

120.2430 ± 0.82898

24.5075 ± 0.52171

3.6125 ± 0.37134

64.0125 ± 0.34641

23.1375 ± 0.62041

31.4500 ± 0.68416

68.7550 ± 0.59614

123.9512 ± 0.65214

104.9812 ± 0.94918

30.7225 ± 0.84037

31.7625 ± 0.80967

6.8375 ± 0.27047

7.8125 ± 0.27736

6.1400 ± 0.28670

2.3538 ± 0.20749

111.8340 ± 1.37505

7.6750 ± 0.41346

16.8000 ± 0.43043

66.3750 ± 0.56485

66.6875 ± 0.72114

19.8700 ± 0.28302

4.5688 ± 0.44851

44.7688 ± 0.53931

–4.5875 ± 0.23647

–0.5375 ± 0.54131

10.7875 ± 0.69552

99.5375 ± 1.11590

–1.2625 ± 0.31684

2.6500 ± 0.43248

83.6125 ± 0.40702

78.4000 ± 0.45687

5.2000 ± 0.24482

0.9875 ± 0.36608

–6.7000 ± 0.77936

95.2125 ± 0.5451

119.2420 ± 0.79898

24.0375 ± 0.51171

3.3125 ± 0.36134

64.3625 ± 0.36641

23.4375 ± 0.63041

30.9500 ± 0.66416

67.0625 ± 0.55099

122.4422 ± 0.68085

102.7622 ± 0.93866

30.2225 ± 0.83269

32.1100 ± 0.92365

6.2375 ± 0.25047

6.4375 ± 0.29059

6.0875 ± 0.28865

2.2125 ± 0.22398

112.5232 ± 1.48505

7.3750 ± 0.40346

16.0000 ± 0.41043

65.7750 ± 0.53485

66.1875 ± 0.71114

20.3700 ± 0.33302

4.4488 ± 0.43851

44.0688 ± 0.49931

–4.0125 ± 0.19035

–0.5625 ± 0.42166

9.1625 ± 0.60860

97.4875 ± 1.13419

–0.9625 ± 0.29684

2.0500 ± 0.40248

NS

NS

NS

NS

***

NS

NS

NS

NS

NS

NS

NS

***

NS

***

NS

***

NS

NS

NS

NS

NS

NS

NS

NS

NS

NS

NS

NS

NS

NS

***

***

NS

NS

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


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 variablesSNA (°)SNB (°)ANB (°)Nperp-A (mm)Nperp-Pog (mm)Cond-A (mm)Cond-Gn (mm)Max-Mand (mm) Wits (mm)Ba N-NA (°)SpP-GoMe (°)SN-GoMe (°)(S-Go:N-Me)ArGo-Me (°)ANS-Me (mm)Go-Me (mm)Dental variablesIMPA (°)Max1-NA (°)Mand1-NB (°)1u-NA (mm)1l-NB (mm)Overjet (mm)Overbite (mm)Interincisal (°)SpP-OcP (°)MeGo-OcP (°)Soft tissue variablesGl’-Sn (mm)Sn-Me’ (mm)Sn-stm-s (mm)Stm-s - Stm-i (mm)Stm-i-Me’ (mm)SnPerp-Ls (mm)SnPerp-Li (mm)SnPerp-Pog’ (mm)CotgSnLs (°)Ls-NsPog’ (mm)Li-NsPog’ (mm)

83.7000 ± 0.7507178.5667 ± 0.824465.1333 ± 0.370561.5000 ± 0.73773

–6.0333 ± 0.9103395.6000 ± 0.99146119.5000 ± 1.4025823.7667 ± 0.800413.5333 ± 0.46420

64.1333 ± 0.5925522.0667 ± 0.8853029.7667 ± 1.0257468.6000 ± 0.85715

123.1000 ± 1.1520668.4667 ± 1.2051075.4667 ± 1.01113

106.6667 ± 1.3513230.4667 ± 1.2500432.7667 ± 1.543766.2000 ± 0.330107.7333 ± 0.454695.8667 ± 0.397502.7433 ± 0.25260

111.8333 ± 2.271306.7333 ± 0.63415

15.2069 ± 0.71813

65.5667 ± 0.8230666.0333 ± 1.1904619.5900 ± 0.505435.0300 ± 0.55602

43.8333 ± 0.86287-4.4000 ± 0.27332-0.2667 ± 0.768549.9000 ± 0.82539

97.1667 ± 1.89202–1.0000 ± 0.431501.9667 ± 0.62969

83.7667 ± 0.7499978.6333 ± 0.810115.1667 ± 0.374731.5333 ± 0.74546

–6.0333 ± 0.8963395.6667 ± 0.99808119.5667 ± 1.4163923.8000 ± 0.819873.4667 ± 0.46420

64.2000 ± 0.6203422.1333 ± 0.8863429.8333 ± 1.0395468.7333 ± 0.86561

123.1333 ± 1.1643568.5333 ± 1.1984075.5333 ± 0.99969

106.8000 ± 1.3402730.4333 ± 1.2527532.7333 ± 1.546926.2667 ± 0.324957.8000 ± 0.450805.9000 ± 0.402152.8100 ± 0.25910

111.9000 ± 2.266376.8000 ± 0.63499

15.1034 ± 0.72829

65.6333 ± 0.8255766.1000 ± 1.1845319.6167 ± 0.50685.0467 ± 0.55588

43.8733 ± 0.86766–4.4667 ± 0.41725–0.3000 ± 0.7763010.8333 ± 0.8297499.6333 ± 1.89772–0.9333 ± 0.447042.0333 ± 0.65026

0.1610.1610.5730.5731.0000.1610.1610.5730.1610.3260.1610.1610.0430.5730.0210.161

0.0730.5730.5730.1610.1610.5730.1610.1610.1610.184

0.1610.1610.1180.2830.0900.3260.5730.0420.0320.1610.083


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table 4. Statistical Evaluation of Skeletal, Dental, Soft Tissue Variables: Vistadent Tracing and Retracing after 1-week - 30 SamplesVariables tracing-initial Retracing 1-week after Paired t-test

Sig p < 0.05

Skeletal variablesSNA (°)SNB (°)ANB (°)Nperp-A (mm)Nperp-Pog (mm)Cond-A (mm)Cond-Gn (mm)Max-Mand (mm)Wits (mm)Ba N-NA (°)SpP-GoMe (°)SN-GoMe (°)(S-Go:N-Me)ArGo-Me (°)ANS-Me (mm)Go-Me (mm)Dental variablesIMPA (°)Max1-NA (°)Mand1-NB (°)1u-NA (mm)1l-NB (mm)Overjet (mm)Overbite (mm)Interincisal (°)SpP-OcP (°)MeGo-OcP (°)Soft tissue variablesGl’-Sn (mm)Sn-Me’ (mm)Sn-stm-s (mm)Stm-s - Stmi (mm)Stm-i-Me’ (mm)SnPerp-Ls (mm)SnPerp-Li (mm)SnPerp-Pog’ (mm)CotgSnLs (°)Ls-NsPog’ (mm)Li-NsPog’ (mm)

83.7000 ± 0.750778.5667 ± 0.82455.1333 ± 0.37060.9333 ± 0.5929

–6.4667 ± 1.065495.6000 ± 0.9915119.5000 ± 1.402623.7667 ± 0.80043.3667 ± 0.4806

64.1333 ± 0.592522.0667 ± 0.885329.7667 ± 1.025768.2667 ± 0.8853

121.0667 ± 1.125466.0000 ± 1.232775.4667 ± 1.0111

104.3333 ± 1.349630.4800 ± 1.262732.6700 ± 1.48776.2000 ± 0.33016.4333 ± 0.49295.8567 ± 0.40582.6633 ± 0.2602

111.8333 ± 2.27136.7333 ± 0.6341

15.2069 ± 0.7181

65.5667 ± 0.823166.0333 ± 1.190519.5900 ± 0.50545.0300 ± 0.5560

43.8333 ± 0.8629–3.9667 ± 0.2733–0.4000 ± 0.58058.4000 ± 0.8525

98.1667 ± 1.8920–1.0000 ± 0.43151.9667 ± 0.6297

83.8000 ± 0.751278.6000 ± 0.82855.2000 ± 0.36010.9000 ± 0.5899

–6.4000 ± 1.086695.6667 ± 0.9981119.5333 ± 1.402623.8333 ± 0.80103.4000 ± 0.4997

64.1667 ± 0.595222.1000 ± 0.870129.8000 ± 1.026570.1667 ± 0.9149

123.3333 ± 1.152068.3333 ± 1.209575.5333 ± 1.0134

104.6000 ± 1.313630.4700 ± 1.261032.6700 ± 1.48776.2667 ± 0.32856.5333 ± 0.49535.8833 ± 0.40382.6867 ± 0.2590

111.9333 ± 2.28486.8333 ± 0.6362

15.2759 ± 0.7343

65.6667 ± 0.829566.0667 ± 1.187019.6167 ± 0.50685.0800 ± 0.5689

43.8733 ± 0.8564–4.0667 ± 0.2874–0.3333 ± 0.59189.3333 ± 0.8608

100.6333 ± 1.8977–1.0000 ± 0.43152.0333 ± 0.6370

0.0830.5730.1610.5730.1610.1610.5730.1610.5730.5730.5730.5730.2800.1610.5730.161

0.0880.7940.1610.1610.0830.6080.0900.0830.0830.424

0.0830.3260.1030.1540.1030.0830.1610.0470.0321.0000.161


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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 VariablesSNA (°)SNB (°)ANB (°)Nperp-A (mm)Nperp-Pog (mm)Cond-A (mm)Cond-Gn (mm)Max-Mand (mm)Wits (mm)Ba N-NA (°)SpP-GoMe (°)SN-GoMe (°)(S-Go:N-Me)ArGo-Me (°)ANS-Me (mm)Go-Me (mm)Dental variablesIMPA (°)Max1-NA (°)Mand1-NB (°)1u-NA (mm)1l-NB (mm)Overjet (mm)Overbite (mm)Interincisal (°)SpP-OcP (°)MeGo-OcP (°)Soft tissue variablesGl’-Sn (mm)Sn-Me’ (mm)Sn-stm-s (mm)Stm-s - Stm-i (mm)Stm-i-Me’ (mm)SnPerp-Ls (mm)SnPerp-Li (mm)SnPerp-Pog’ (mm)CotgSnLs (°)Ls-NsPog’ (mm)Li-NsPog’ (mm)

83.7667 ± 0.7499978.6333 ± 0.810115.1667 ± 0.374731.5333 ± 0.74546

–6.0333 ± 0.8963395.6667 ± 0.99808119.5667 ± 1.4163923.8000 ± 0.819873.4667 ± 0.46420

64.2000 ± 0.6203422.1333 ± 0.8863429.8333 ± 1.0395468.7333 ± 0.86561

123.1333 ± 1.1643566.5333 ± 1.1984075.5633 ± 0.99969

106.8000 ± 1.3402730.4333 ± 1.2527532.7333 ± 1.546926.2667 ± 0.324957.1000 ± 0.450805.9000 ± 0.402152.8100 ± 0.25910

111.9000 ± 2.266376.8000 ± 0.63499

15.1034 ± 0.72829

65.6333 ± 0.8255766.1000 ± 0.1663719.6167 ± 0.50685.0800 ± 0.5689

43.8733 ± 0.8564–4.0667 ± 0.2874–0.3333 ± 0.59189.7333 ± 0.8608

102.6333 ± 1.8977–1.0000 ± 0.43152.0333 ± 0.6370

83.8000 ± 0.751178.6000 ± 0.82855.2000 ± 0.36010.9000 ± 0.5899

–5.4000 ± 1.086695.6667 ± 0.9981119.5333 ± 1.402623.8333 ± 0.80103.4000 ± 0.4997

64.1667 ± 0.595222.1000 ± 0.870129.8000 ± 1.026570.1667 ± 0.9149

123.3333 ± 1.152068.3333 ± 1.209575.5333 ± 1.0134

104.6000 ± 1.313630.4700 ± 1.261032.6700 ± 1.48776.2667 ± 0.32856.8333 ± 0.49535.8833 ± 0.40382.6867 ± 0.259

111.9333 ± 2.28486.8333 ± 0.6362

15.2759 ± 0.7343

65.6667 ± 0.829566.0667 ± 1.187019.6167 ± 0.50685.0800 ± 0.5689

43.8733 ± 0.8564–4.0667 ± 0.2874–0.3333 ± 0.59188.3333 ± 0.8608

100.6333 ± 1.8977–1.0000 ± 0.43152.0333 ± 0.6370

0.9750.9770.9490.5080.0431.0000.9870.9770.9220.9690.9790.9820.0230.9030.0340.989

0.2460.9840.9771.0000.6460.9770.7380.9920.9710.895

0.9770.9841.0000.9671.0000.4330.9730.0340.0470.9150.971


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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

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.


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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 ReadingCelik E, Polat-Ozsoy O, Toygar Memikoglu TU. 1. Comparison of cephalometric measurements with digital versus conventional cephalometric analysis. Eur J Orthod 2009;31(3):241-6.Gonçalves FA, Schiavon L, Pereira Neto JS, Nouer DF. 2. Comparison of cephalometric measurements from three radiological clinics. Braz Oral Res 2006;20(2):162-6.Geelen W, Wenzel A, Gotfredsen E, Kruger M, 3. 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.

Quintero JC, Trosien A, Hatcher D, Kapila S. Cranio-4. facial imaging in orthodontics: historical perspective, current status, and future developments. Angle Orthod 1999;69(6):491-506.Lim KF, Foong KW. Phosphor-stimulated computed 5. cephalometry: reliability of landmark identification. Br J Orthod 1997;24(4):301-8.Gregston MD, Kula T, Hardman P, Glaros A, Kula K. 6. A comparison of conventional and digital radiographic methods and cephalometric analysis software: I-Hard tissue. Semin Orthod 2004;10(3):204-11.Martins LP, Pinto AS, Martins JCR, Mendes AJD. Error 7. reproducibility of cephalometric analysis of Steiner and Ricketts, the conventional method and the computerized method. Orthodontics 1995;28(1):4-17.Ricketts MM. Perspectives in the clinical application 8. of cephalometries. The first fifty years. Angle Orthod 1981;51(2):115-50.Sandler PJ. Reproducibility of cephalometric measure-9. ments. Br Orthod 1988;15(2):105-10.Yu SH, Nahm DS, Baek SH. Reliability of 10. landmark identification on monitor-displayed lateral cephalometric images. Am J Orthod Dentofacial Orthop 2008;133(6):790.e1-6; discussion e1.Santoro M, Jarjoura K, Cangialosi TJ. Accuracy of 11. digital and analogue cephalometric measurements assessed with the sandwich technique. Am J Orthod Dentofacial Orthop 2006;129(3):345-51.Sayinsu K, Isik F, Trakyali G, Arun T. An evaluation of 12. the errors in cephalometric measurements on scanned cephalometric images and conventional tracings. Eur J Orthod 2007;29(1):105-8.Baumrind S, Frantz RC. The reliability of head film 13. measurements. Landmark identification. Am J Orthod 1971;60(2):111-27.Baumrind S, Frantz RC. The reliability of head film 14. measurements. 2. Conventional angular and linear measures. Am J Orthod 1971;60(5):505-17.Trindade Junior AS, Adams GA, Capelozza Son L. 15. Rapid maxillary expansion: a prospective cephalometric analysis. Orthodo 1999;32(1):45-56.Williams S, Leighton BC, Nielsen JH. Linear evaluation 16. of the development of sagittal jaw relationship. Am J Orthod 1985;88(3):235-41.Chen YJ, Chen SK, Chang HF, Chen KC. Comparison 17. of landmark identification in traditional versus computer-aided digital cephalometry. Angle Orthod 2000;70(5):387-92.

n n n


Peripheral 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, ChandigarhAddress for correspondenceDr Renu YadavHouse No.: 924, Ashirwad EnclaveSector-49-A, Chandigarh -160 047E-mail: [email protected]

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, amelo-blastoma of the gingiva

Peripheral Ameloblastoma: Review of Literature and Case PresentationRenu Yadav*, Anubha Gulati**, Rahul Sharma†, Satya narain†

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.

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figure 1. No bone involvement is seen in the IOPA. figure 2. Surface epithelium showing acanthosis (H&E stain, X10).

figure 3. Islands and cords of odontogenic epithelium showing microcysts and central polygonal cells surrounded by ameloblast-like cells (H&E stain, X10).

figure 4. Island exhibiting squamous metaplasia of the central stellate reticulum-like cells (H&E stain, X40).

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

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.


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The 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

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


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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.

Acknowledgement

We thank Mr. Tarsem Raj for his skillful technical assistance.

ReferencesEl-Mofty SK, Gerard NO, Farish SE, Rodu B. Peripheral 1. ameloblastoma: a clinical and histologic study of 11 cases. J Oral Maxillofac Surg 1991;49(9):970-4; discussion 974-5.Schaberg SJ, Antimarino RF, Pierce GL, Crawford BE. 2. Peripheral ameloblastoma. Report of a case. Int J Oral Surg 1983;12(5):344-7.Martelli-Júnior H, Souza LN, Santos LA, Melo-Filho 3. MR, De Paula AM. Peripheral ameloblastoma: a case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;99(5):E31-3.Wettan HL, Patella PA, Freedman PD. Peripheral 4. ameloblastoma: review of the literature and report of recurrence as severe dysplasia. J Oral Maxillofac Surg 2001;59(7):811-5.Shetty K. Peripheral ameloblastoma: an etiology 5. from surface epithelium? Case report and review of literature. Oral Oncol Extra 2005;41(9):211-5.Lecorn DW, Bhattacharyya I, Vertucci FJ. Peripheral 6. ameloblastoma: a case report and review of the literature. J Endod 2006;32(2):152-4.Philipsen HP, Reichart PA, Nikai H, Takata T, 7. Kudo Y. Peripheral ameloblastoma: biological profile based on 160 cases from the literature. Oral Oncol 2001;37(1):17-27.Gomes CC, Garcia BG, Gomez RS, de Freitas JB, 8. Mesquita RA. A clinical case of peripheral amelo-blastoma. Braz J Oral Sci 2007;6(21):1364-6.Vanoven BJ, Parker NP, Petruzzelli GJ. Peripheral 9. ameloblastoma of the maxilla: a case report and literature review. Am J Otolaryngol 2008;29(5):357-60.Ide F, Mishima K, Miyazaki Y, Saito I, Kusama K. 10. 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.Woo SB, Smith-Williams JE, Sciubba JJ, Lipper S. 11. 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.Zhu EX, Okada N, Takagi M. Peripheral ameloblastoma: 12. case report and review of literature. J Oral Maxillofac Surg 1995;53(5):590-4.WHO classification of tumors. Pathology and 13. Genetics of Head and Neck Tumors Chapter 6. Odontogenic tumors; IARC: Lyon 2006:297-8.


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Pekiner FN, Özbayrak S, Şener BC, Olgaç V, 14. Sinanoğlu A. Peripheral ameloblastoma: a case report. Dentomaxillofac Radiol 2007;36(3):183-6.Mintz S, Anavi Y, Sabes WR. Peripheral ameloblastoma 15. of the gingiva. A case report. J Periodontol 1990;61(10):649-52.Redman RS, Keegan BP, Spector CJ, Patterson RH. 16. Peripheral ameloblastoma with unusual mitotic activity and conflicting evidence regarding histogenesis. J Oral Maxillofac Surg 1994;52(2):192-7.Orsini G, Fioroni M, Rubini C, Piattelli A. Peripheral 17. ameloblastoma: a report of 2 cases. J Periodontol 2000; 71(7):1174-6.Neville BW, Damm DD, Allen CM, Bouquot JE. Oral 18. and maxillofacial pathology. In: Odontogenic Cysts and Tumors. 3rd edition, Neville BW, Damm DD, Allen CM, Bouquot JE (Eds.), Elsevier: Noida 2009:710.Shiba R, Sakoda S, Yamada N. Peripheral amelo-19. blastoma. J Oral Maxillofac Surg 1983;41(7):460-3.Gurol M, Burkes EJ Jr. Peripheral ameloblastoma. 20. J Periodontol 1995;66(12):1065-8.Smullin SE, Faquin W, Susarla SM, Kaban LB. Peripheral 21. desmoplastic ameloblastoma: report of a case and literature review. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105(1):37-40.Isomura ET, Okura M, Ishimoto S, Yamada C, 22. Ono Y, Kishino M, et al. Case report of extragingival peripheral ameloblastoma in buccal mucosa. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2009;108(4):577-9.Ramnarayan K, Nayak RG, Kavalam AG. Peripheral 23. ameloblastoma. Int J Oral Surg 1985;14(3):300-1.Patrikiou A, Papanicolaou S, Stylogianni E, 24. Sotiriadou S. Peripheral ameloblastoma. Case report

and review of the literature. Int J Oral Surg 1983;12(1):51-5.Califano L, Maremonti P, Boscaino A, De Rosa G, 25. Giardino C. Peripheral ameloblastoma: report of a case with malignant aspect. Br J Oral Maxillofac Surg 1996;34(3):240-2.Gardner DG. Peripheral ameloblastoma: a study of 21 26. cases, including 5 reported as basal cell carcinoma of the gingiva. Cancer 1977;39(4):1625-33.Ng KH, Siar CH. Peripheral ameloblastoma with clear 27. cell differentiation. Oral Surg Oral Med Oral Pathol 1990;70(2):210-3.Curtis NJ, Zoellner H. Surgical management of an 28. ameloblastoma in soft tissues of the cheek. Br J Oral Maxillofac Surg 2006;44(6):495-6.Kishino M, Murakami S, Yuki M, Iida S, Ogawa I, 29. Kogo M, et al. An immunohistochemical study of the peripheral ameloblastoma. Oral Dis 2007;13(6):575-80.Lentini M, Simone A, Carrozza G. Peripheral 30. ameloblastoma: use of cytokeratin 19 and Ber-EP4 to distinguish it from basal cell carcinoma. Oral Oncol Extra 2004;40(6-7):79-80.Anneroth G, Johansson B. Peripheral ameloblastoma. 31. Int J Oral Surg 1985;14(3):295-9.Ide F, Kusama K, Tanaka A, Sakashita H. Peripheral 32. ameloblastoma is not a hamartoma but rather more of a neoplasm. Oral Oncol 2002;38(3):318-20.Tajima Y, Kuroda-Kawasaki M, Ohno J, Yi J, 33. Kusama K, Tanaka H, et al. Peripheral ameloblastoma with potentially malignant features: report of a case with special regard to its keratin profile. J Oral Pathol Med 2001;30(8):494-8.Ide F, Kusama K. Difficulty in predicting biological 34. behavior of peripheral ameloblastoma. Oral Oncol 2004;40(6):651-2.

n n n


Periodontitis, 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, RMDCHAnnamalai University, Chidambaram, Tamil NaduAddress for correspondenceDr S Lakshmi SreeAishwaryam, 7(110), 8th Cross, Kanagasabai Nagar Chidambaram, Tamil Nadu - 608 001E-mail: [email protected]

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

Antioxidants in Periodontal Diseases: A Review

S lakshmi Sree*, R Mythili**

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

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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)

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 z

Lipid peroxidation (through activation of cyclo- z

oxygenases and lipo-oxygenases).

Protein damage, including gingival hyaluronic acid z

and proteoglycans.8

Oxidation of important enzymes e.g. antiproteases z

such as α1-antitrypsin.Stimulation of pro-inflammatory cytokine release z

by monocytes and macrophages by depleting intracellular thiol compounds and activating nuclear factor kB (NFkB).

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.

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; NFkB = 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.

Periodontal Pathogens

LPS DNA

Inflammatory cytokines,

chemokines, adhesion

molecules, etc. e.g. TNF-α, IL-1, IL-8

GM-CSF, E-selectin

Cell wall components

TNF-α LPS

IL-8 GM-CSF E-selectin LPS TNF-α

Crevicular/Junctional epithelium + other PDL cells

Receptor-mediated

Activation of NFkB & AP-1

Nonreceptor-mediated

TIMPs ↓

MMPs ↑

Osteoclast Activation/

Differentiation

Oxidative Stress

Recruitment and activation of hyper-responsive PMNL

Release of traditional inflammatory mediators

Generation of oxidation products-

Lipid peroxides, oxidized proteins

Inactivation of TIMPs

tissue Damage

Fibroblast generation of

ROSPMNL generation

of ROS


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Garrett et al9 demonstrated both in vivo and in vitro that when free oxygen radicals were generated in the bone environment, osteoclasts were formed and bone resorption occurred. Few studies have addressed the degradation of the periodontal extracellular matrix by ROS. Earlier studies by Bartold et al8 demonstrated the in vitro ability of ROS particularly the OH° species, to degrade hyaluronan and proteoglycans extracted from porcine gingivae and within cryostat sections of tissue.

Proteoglycans and glycosaminoglycans (GAGs) when exposed to a broad-spectrum of ROS species of differing reactivity and over differing periods of time were found to undergo chain depolymerization and residue modification to varying degrees, particularly in the presence of the highly reactive OH° species. Moreover, the nonsulfated GAG, hyaluronan was identified as being more susceptible to degradation by ROS than sulfated GAG.1

The highly reactive OH° species was also shown to exert the most detrimental degradative effects on the small chondroitin sulfate, proteoglycans from alveolar bone, compared to other ROS.1

Antioxidants: What are they and how do they Act?

“An antioxidant is any substance that, when present at low concentrations compared to those of an oxidizable substrate, significantly delays or prevents oxidation of that substrate”.2

Several biologically important compounds have been reported to have antioxidant functions. These include vitamin C (ascorbic acid), vitamin E (α-tocopherol), vitamin A, b-carotene, metallothionein, polyamines, melatonin, nicotinamide adenine dinucleotide phosphate (NADPH), adenosine, co-enzyme Q-10, urate, ubiquinol, polyphenols, flavonoids, phyto estrogens, cysteine, homocysteine, taurine, methionine, S-adenosyl-L-methionine, resveratrol, nitroxides, reduced glutathione (GSH), glutathione peroxidase (GPX), superoxide dismutase (SOD), catalase (CAT), nitric oxide synthase (NOS), heme oxygenase-1 (HO-1) and eosinophil peroxidase (EPO).10

A functional classification of antioxidant systems based on the way they act (Niki 1996) appears to be the most useful (Table 1).2

Superoxide Dismutase

Superoxide dismutase (SOD) is an antioxidant enzyme that catalyses the dismutation of the highly reactive superoxide anion to O2 and to the less reactive species H2O2, accelerating it upto 10,000 times.2

2O2°¯ + 2H+ H2O2 + O2

In humans, there are three forms of SOD: Cytosolic Cu/Zn-SOD, mitochondrial Mn-SOD and extracellular SOD (EC-SOD). Though, Cu/Zn-SOD is believed to play a major role in the first-line of antioxidant defense, recent reports have revealed that Mn-SOD is essential for life whereas Cu/Zn-SOD is not.10 SOD has been localized within human periodontal ligament and may represent an important defense mechanism with in gingival fibroblasts against excess superoxide release.11

Catalase

Catalase (CAT) is an antioxidant enzyme, which contains heme bound iron and is mainly located in peroxisomes.2 It reacts very efficiently with H2O2 to form water and molecular oxygen and with hydrogen donors (methanol, ethanol, formic acid or phenols) with peroxidase activity.10

SOD

table 1. A Functional Classification of Antioxidant Systemstypes of defense system

Mode of action Examples

Preventive antioxidants

Suppress the formation of FR: Nonradical decomposition of LOOH and H2O2

Catalase, GPX and serum-transferase

Sequestration of metal by chelation

Transferrin, ceruloplasmin, albumin, haptoglobin

Quenching of active O2 SOD, carotenoidsRadical- scavenging antioxidants

Scavenge radicals to inhibit chain initiation and break chain propagation

Lipophilic: Ubiquinol, vitamin A, vitamin E, carotenoids Hydrophilic: Uric acid, ascorbic acid, albumin, bilirubin

Repair and de novo enzymes

Repair the damage and reconstitute membranes

DNA repair enzymes, protease, transferase, lipase


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2H2O2 H2O + O2

ROOH + AH2 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

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

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

GPX

CAT

CAT


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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, α-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

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


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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.

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Ellis SD, Tucci MA, Serio FG, Johnson RB. Factors for 35. progression of periodontal diseases. J Oral Pathol Med 1998;27(3):101-5.

Katsuragi H, Hasegawa A, Saito K. Distribution of 36. metallothionein in advanced periodontitis patients. J Periodontol 1997;68(10):1005-9.

Chang YC, Lai CC, Lin LF, Ni WF, Tsai CH. The 37. up-regulation of heme oxygenase-1 expression in human gingival fibroblasts stimulated with nicotine. J Periodontal Res 2005;40(3):252-7.

Tuter G, Kurtiş B, Serdar M. Interleukin-1beta and 38. thiobarbituric acid reactive substance (TBARS) levels after phase I periodontal therapy in patients with chronic periodontitis. J Periodontol 2001;72(7):883-8.

Borges I Jr, Moreira EA, Filho DW, de Oliveira TB, da 39. Silva MB, Frõde TS. Proinflammatory and oxidative stress markers in patients with periodontal disease. Mediators Inflamm 2007;2007:45794.


Esthetic 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 LecturerDept. of Periodontology and Oral ImplantologySree Balaji Dental College and Hospital, ChennaiAddress for correspondenceDr Jebin Paul Nesaline JDept. of Periodontology and Oral Implantology Sree Balaji Dental College and Hospital, Chennai - 600 100E-mail: [email protected]

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

Minimally Invasive Atraumatic Extraction of Fractured Tooth Using Implant Drills and Immediate Implant PlacementJebin Paul nesaline J* SC Chandrasekaran**, Bhaskar Jayaraman†, Jumshad B Mohamed‡

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

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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

figure 1. Preoperative clinical photograph. figure 2. Preoperative radiograph.

was 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

figure 3. Fractured crown removed. figure 4. Tapered fissure airotor bur used to widen the root canal.

figure 5. Pilot implant drill used to thin the root canal wall. figure 6. Periapical granuloma removed in totality.


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figure 12. Cyanoacrylate tissue adhesive between flap and implant.

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

figure 7. Extraction socket. figure 8. Post extraction periapical radiograph.

figure 9. Bone graft placed. figure 10. Implant placed.

figure 11. Wrench break at 40 Ncm.

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


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figure 15. Three-month postoperative radiograph. figure 16. One-year postoperative clinical photograph.

figure 13. Temporary restoration. figure 14. Three-month postoperative clinical photograph.

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.

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

figure 17. One-year postoperative radiograph.


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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

ReferencesYalcin S, Aktas I, Emes Y, Kaya G, Aybar B, Atalay B. 1. A technique for atraumatic extraction of teeth before immediate implant placement using implant drills. Implant Dent 2009;18(6):464-72.Becker W, Goldstein M. Immediate implant placement:2. treatment planning and surgical steps for successful outcome. Periodontology 2008;47(1):79-89.Barzilay I. Immediate implants: their current status. 3. Int J Prosthodont 1993;6(2):169-75.Schropp L, Isidor F. Timing of implant placement 4. relative to tooth extraction. J Oral Rehabil 2008;35 (Suppl 1):33-43.Novaes AB Jr, Novaes AB. Immediate implants placed 5. into infected sites: a clinical report. Int J Oral Maxillofac Implants 1995;10(5):609-13.Villa R, Rangert B. Early loading of interforaminal 6. implants immediately installed after extraction of teeth presenting endodontic and periodontal lesions. Clin Implant Dent Relat Res 2005;7(Suppl 1):S28-S35.Chen ST, Darby IB, Adams GG, Reynolds EC. A 7. prospective clinical study of bone augmentation techniques in immediate implants. Clin Oral Implants Res 2005;16(2):176-84.Covani U, Cornelini R, Barone A. Buccolingual 8. remodeling around implants placed into immediate extraction sockets: a case series. J Periodontol 2003;74(2):268-73.Paolantonio M, Dolci M, Scarano A, d’Archivio D, 9. 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.Grisdale J. The use of cyanoacrylates in periodontal 10. therapy. J Can Dent Assoc 1998;64(9):632-3.Vasenius J. Is n-butyl-2-cyanoacrylate a biocompatible 11. coating material for biodegradable fracture fixation devices: an experimental study on rats. Clin Mater 1988;3(2):133-43.

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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

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

Rhinocerebral Mucormycosis with Palatal Involvement Associated with Diabetes Mellitus Type II: A Case ReportKMK Masthan*, n Aravindha Babu**, Jagdish Rajguru†

*Professor and Head**Associate ProfessorDept. of Oral Pathology and MicrobiologySree Balaji Dental College and Hospital, Chennai†Senior Lecturer, Saraswathi Dental College and Hospital, LucknowAddress for correspondenceDr N Aravindha BabuAssociate Professor Dept. of Oral Pathology and MicrobiologySree Balaji Dental College and Hospital, ChennaiE-mail: [email protected]

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 z

Zygomycetes - class n

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R


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Mucorales - order

Mucoraceae - family

Absidia - genus

Mucor

Rhizomucor

Rhizopus - species

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 years back for high increase in glucose and hematuria.

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, mucormycosis and midline lethal granuloma. CT scan suggested soft tissue mass in the left maxillary sinus eroding and destroying medial and lateral wall of maxillary sinus (Fig. 2).

Hemogram showed mild polymorphonuclear leukocytosis. Biochemical investigation showed HbA1C of 8.7%. Random blood sugar was 193 mg/dl and associated with ketonuria. An incisional biopsy was done under glycemic control. Histopathological examination was characterized by nonseptate hyphae with acute right angle branchings suggestive of mucor species with focal areas of necrosis and thrombi

figure 1a and B. Extraoral and intraoral patient picture.

figure 2. CT scan reveal soft tissue mass in left maxillary sinus.

figure 3. H&E aseptate hyphae branching at acute angle (10x and 40X).

formation (Fig. 3). Periodic acid-Schiff (PAS) stain suggested a final diagnosis of mucormycosis (Fig. 4a and b).

The patient was started on IV amphotericin B 60 mg in four divided doses, cefotaxime lg b.i.d. and metronidazole 500 mg t.d.s. Amphotericin-induced nephrotoxicity was monitored carefully. Surgical debridement of the necrotic tissues was done under general anesthesia and a temporary palatal obturator was given.


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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

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 z

are acidic)Blood dyscrasias, leukemia z


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Malignant conditions, lymphoma z

Renal failure z

Burns z

Protein-calorie malnutrition z

Cirrhosis z

Corticosteroid, immunosuppressive therapy z

Solid organ transplants or bone marrow z

transplantsDeferoxamine therapy z

Deficient T-cell immunity z

Immaturity and low birth weight z

Severe and prolonged neutropenia z

Relationship between Predisposing Condition and Site of Infection25

Predisposing condition Predominant site of infectionDiabetic ketoacidosis RhinocerebralNeutropenia Pulmonary and disseminatedCorticosteroids Pulmonary, disseminated or

rhinocerebralDesferoxamine DisseminatedMalnutrition GastrointestinalTrauma, catheter/injection site, skin laceration

Cutaneous/subcutaneous

Due to limitations of imaging studies, diagnosing mucormycosis almost always requires histopathologic evidence of fungal invasion of the tissues. Culturing organisms from a potentially infected site is rarely sufficient to establish the diagnosis of mucormycosis because the causative agent is ubiquitous, may colonize normal persons and is a relatively frequent laboratory contaminant. Additionally, the organism may be killed during tissue grinding, which is routinely used to process tissue specimens for culture. Thus, a sterile culture does not rule out the infection. Furthermore, waiting for the results of the fungal culture may delay the institution of appropriate therapy. There are no reliable serologic, PCR-based or skin tests for mucormycosis.

Therefore, the diagnosis should be made by biopsy of infected tissues. The biopsy should demonstrate the characteristic wide, ribbon-like, aseptate hyphal elements that branch at right or obtuse angles. The organisms are often surrounded by extensive necrotic

debris. Other fungi, including Aspergillus, Fusarium, or Scedosporium spp., may look similar to the Mucorales on biopsy. However, these molds have septae, are usually thinner and branch at acute angles. The genus and species of the infecting organism may be determined by culture. It is rarely isolated from cultures of blood, cerebrospinal fluid, sputum, urine, feces or swabs of infected areas.

Treatment

Factors to be considered before treatment are, rapidity of diagnosis, reversal of the underlying predisposing factors, appropriate surgical debridement of infected tissue and appropriate antifungal therapy. Therefore, the recommended dose of amphotericin B deoxycholate has been 1-1.5 mg/kg/day, which results in a very high toxicity rate.

Prognosis

Rhinocerebral mucormycosis has a higher survival rate than pulmonary or disseminated mucormycosis because rhinocerebral disease can frequently be diagnosed earlier and the most common underlying cause, diabetic ketoacidosis, can be treated readily.

ReferencesPillsbury HC, Fischer ND. Rhinocerebral mucor-1. mycosis. Arch Otolaryngol 1977;103(10):600-4.McNulty JS. Rhinocerebral mucormycosis: predisposing 2. factors. Laryngoscope 1982;92(10 Pt 1):1140-3.Abedi E, Sismanis A, Choi K. Pastore P. Twenty-five 3. years’ experience treating cerebro-rhino-orbital mucor-mycosis. Laryngoscope 1984;94(8):1060-2.Peterson KL, Wang M, Canalis RF, Abemayor E. 4. Rhinocerebral mucormycosis: evolution of the disease and treatment options. Laryngoscope 1997;107(7): 855-62.Thajeb P, Thajeb T, Dai D. Fatal strokes in patients with 5. rhino-orbito-cerebral mucormycosis and associated vasculopathy. Scand J Infect Dis 2004;36:643-8.Dhiwakar M, Thakar A, Bahadur S. Improving outcomes 6. in rhinocerebral mucormycosis - early diagnostic pointers and prognostic factors. J Laryngol Otol 2003;117(11):861-5.Morrison VA, McGlave PB. Mucormycosis in the 7. BMT population. Bone Marrow Transplant 1993;11 (5):383-8.Talmi YP, Goldschmied-Reouven A, Bakon M, 8. Barshack I, Wolf M, Horowitz Z, et al. Rhino-orbital and rhino-orbito-cerebral mucormycosis. Otolaryngol Head Neck Surg 2002;127(1):22-31.


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Husain S, Alexander BD, Munoz P, Avery RK, 9. 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.

Gleissner B, Schilling A, Anagnostopolous I, Siehl I, 10. Thiel E. Improved outcome of zygomycosis in patients with hematological diseases? Leuk Lymphoma 2004;45(7):1351-60.

Tryfon S, Stanopoulos I, Kakavelas E, Nikolaidou A, 11. Kioumis I. Rhinocerebral mucormycosis in a patient with latent diabetes mellitus: a case report. J Oral Maxillofac Surg 2002;60(Suppl 2):328-30.

Prabhu RM, Patel R. Mucormycosis and entomo-12. phthoramycosis: a review of the clinical manifestations, diagnosis and treatment. Clin Microbiol Infect 2004;10(Suppl 1):31-47.

Khor BS, Lee MH, Leu HS, Liu JW. Rhinocerebral 13. mucormycosis in Taiwan. J Microbiol Immunol Infect 2003;36(4):266-9.

Blonde L. State of diabetes care in the US. Am J Manag 14. Care 2007;13(Suppl 2):S36-40.

Paultauf A. Mycosis mucorina. Virchows Arch Path Anat 15. 1885;102:543-64.

Petrikkos G, Skiada A, Sambatakou H, Toskas A, 16. 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.

Joshi N, Caputo GM, Weitekamp MR, Karchmer AW. 17. Infections in patients with diabetes mellitus. N Engl J Med 1999;341(25):1906-12.Lee FYW, Mossad SB, Adal KA. Pulmonary 18. mucormycosis: the last 30 years. Arch Intern Med 1999;159:1301-9.Tuqsel Z, Sezer B, Akalon T. Facial swelling and palatal 19. ulceration in a diabetic patient. Oral Surg Oral Pathol Oral Radiol Endod 2004;98:630-6.Jayachandran S, Kritika C. Mucor mycosis presented 20. as palatal perforation. Indian J Dent Res 2006;17(3): 139-42.Klemptner A. Pulmonary mucormycosis in a patient 21. with COPD. Am Fam Physician 1999;59(9): 2428,2430.Marr KA, Carter RA, Crippa F, Wald A, Corey L. 22. Epidemiology and outcome of mould infections in hematopoietic stem cell transplant recipients. Clin Infect Dis 2002;34(7):909-17.Bhansali A, Bhadada S, Sharma A, Suresh V, 23. 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.Spellberg B, Edwards Jr, Ibrahim A. Novel perspectives 24. on mucormycosis: pathophysiology, presentation, and management. Clin Microbiol Rev 2005;18(3):556-9.Roden MM, Zaoutis TE, Buchanan WL, Knudsen TA, 25. 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.

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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

Full Mouth Rehabilitation of a Patient with Severely Attrited DentitionSanjna nayar*, u Aruna**, Sharmila Hussain†, S Bhuminathan†, Raghavendra Jayesh S‡

*Professor**Senior Lecturer†Associate Professor‡Professor, Dept. of ProsthodonticsSree Balaji Dental College and Hospital, ChennaiAddress for correspondence Prof. Dr Sanjna NayarProfessor, Dept. of ProsthodonticsSree Balaji Dental College and Hospital, Pallikaranai, Chennai - 600 100E-mail: [email protected]

Full 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

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.


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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

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 1. Preoperative intraoral view of the patient. figure 2. Face bow transfer. figure 3. Diagnostic wax-up.

figure 4. Silicone index. figure 5. Group function occlusion (left-side).


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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.

DiscussionFull mouth rehabilitation involves the procedures necessary to produce a healthy, esthetic, well-

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


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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.

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.

ReferencesDawson PE. Functional occlusion from TMJ to smile 1. design. Mosby St. Louis, Elsevier. 2007:18-26, 27-32, 75-83, 429-52.Binkley TK, Binkley CJ. A practical approach to full 2. mouth rehabilitation. J Prosthet Dent 1987;57(3): 261-6.Rivera-Moreles WC, Mohl ND. Restoration of vertical 3. dimension of occlusion in the severely worn dentition. Dent Clin North Am 1992;36(3):651-64.Lucia VO. Modern Gnathological concept: updated. 4. Quintessence, Chicago, 1983.Lynch CD, McConnell RJ. Prosthodontic management 5. of the curve of Spee: use of the Broadrick flag. J Prosthet Dent 2002;87(6):593-7.Christensen GJ. Treating bruxism and clenching. J Am 6. Dent Assoc 2000;131(2):233-5.Schuyler CH. The function and importance of incisal 7. guidance in oral rehabilitation, 1963. J Prosthet Dent 2001;86(3):219-32.Pokorny PH, Wiens JP, Litvak H. Occlusion for fixed 8. prosthodontics: a historical perspective of gnathological influence. J Prosthet Dent 2008;99(9):299-313.Bloom DR, Padayachy JN. Increasing occlusal 9. vertical dimension- Why, When and How. Br Dent J 2006;200(4):199-203.Goldman I. The goal of full mouth rehabilitation. 10. J Prosthet Dent 1952;2(2):246-51.


The 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

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.

*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, ChennaiAddress for correspondenceDr RV Murali Professor and Head, Dept. of Orthodontics and Dentofacial OrthopedicsSree Balaji Dental College and Hospital, Pallikaranai, Chennai - 600 100E-mail: [email protected]

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

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Interdisciplinary Management of Deep Bite in an Adult PatientRV Murali*, BS KulaRashmi**, Issa fathima Jasmine†


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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

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

figure 1. Extraoral view of the patient.

figure 2. Preoperative photo showing the deep bite.

figure 3. Acrylic crown on 32, 41 and attrited 31.

figure 4. Self-ligation bra-ckets bonded on all teeth.


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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 of an initial 0.016-in Nitinol, followed by 0.018 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.

Prosthetic Finishing

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.

ReferencesMoyers RE, Riolo ML. Early treatment. In: Handbook 1. of Orthodontics. 4th edition, Moyers RE (Eds.), Year Book Medical Publishers Inc: Chicago, III 1988:422-6.Nanda R. Correction of deep over bite in adults. Dent 2. Clin North Am 1997;41(1):67-87.

figure 5. After debonding. figure 6. Postoperative - Frontal view.

figure 7. Postoperative - Right view.

figure 8. Postoperative - Left view.


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Dermaut LR, De Pauw G. Biomechanical aspects of 3. 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.Seong-Hun Kim, Young-Guk Park, Kyurhim Chung. 4. Severe Class II anterior deep bite malocclusion treated with a C-lingual retractor. Angle Orthodont 2004;74(2):280-5.Dake ML, Sinclair PM. A comparison of the Ricketts 5. and Tweed-type arch leveling techniques. Am J Orthod Dentofacial Orthop 1989;95(1):72-8.Wylie WL. Overbite and vertical facial dimensions in 6. terms of muscle balance. Angle Orthod 1994;14:13-7.Melsen B, Agerbaek N, Markenstam G. Intrusion of 7. incisors in adult patients with marginal bone loss. Am J Orthod Dentofacial Orthop 1989;96(3):232-41.

Burzin J, Nanda R. The stability of deep overbite 8. correction. In: Retention and Stability in Orthodontics. Nanda R, Burstone CJ (Eds.), W.B. Saunders Co: Philadelphia, Pa 1993:61-79.Arunpraditkul S, Saengsanon S, Pakviwat W. Fracture 9. resistance of endodontically treated teeth: three walls versus four walls of remaining coronal tooth structure. J Prosthodont 2009;18(1):49-53.Harradine NW. Self-ligating brackets and treatment 10. efficiency. Clin Orthod Res 2001;4(4):220-7.Eberting JJ, Straja SR, Tuncay OC. Treatment time, 11. outcome, and patient satisfaction comparisons of Damon and conventional brackets. Clin Orthod Res 2001;4(4): 228-34.Damon DH. The Damon low-friction bracket: a 12. biologically compatible straight-wire system. J Clin Orthod 1998;32(11):670-80.

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*Reader**Senior Lecturer†Professor‡Professor and HeadDept. of Oral and Maxillofacial SurgerySree Balaji Dental College and Hospital, ChennaiAddress for correspondenceDr AbudakirDept. of Oral and Maxillofacial SurgerySree Balaji Dental College and HospitalPallikaranai, Chennai - 600 100E-mail: [email protected]

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

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Submental Intubation - A Case Report

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

Open 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 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 an hour. The patient exhibited profuse nasal bleeding, with laceration all over the face and contusions.


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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.

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 1:1,00,000 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 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

figure 1. Preoperative frontal view. figure 2. Preoperative profile view.

figure 4. 3D CT scan.figure 3. Derangement of occlusion.


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figure 5. Oral endotracheal intubation. figure 6. Submental incision.

figure 7 a and b. Submental intubation in position.

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 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 was then secured to the skin of the submental area (Figs. 7 a and b) by

strong silk sutures 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.

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

A B


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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

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

ReferencesSmoot EC 3rd, Jernigan JR, Kinsley E, Rey RM Jr. 1. A survey of operative airway management practices for midface fractures. J Craniofac Surg 1997; 8(3):201-7.Taher AA. Nasotracheal intubation in patients with facial 2. fractures. Plast Reconstr Surg 1992;90(6):1119-20.Bernard AC, Kenady DE. Conventional surgical 3. tracheostomy as the preferred method of airway management. J Oral Maxillofac Surg 1999;57(3):310-5.Taicher S, Givol N, Peleg M, Ardekian L. Changing 4. indications for tracheostomy in maxillofacial trauma. J Oral Maxillofac Surg 1996;54(3):292-5; discussion 295-6.Wood DE. Tracheostomy. Chest Surg Clin N Am 5. 1996;6(4):749-64.Hernandez Altemir F. The submental route for 6. endotracheal intubation. A new technique. J Maxillofac Surg 1986;14(1):64-5.Schütz P, Hamed HH. Submental intubation versus 7. tracheostomy in maxillofacial trauma patients. J Oral Maxillofac Surg 2008;66(7):1404-9.Amin M, Dill-Russell P, Manisali M, Lee R, Sinton I. 8. Facial fractures and submental tracheal intubation. Anaesthesia 2002;57(12):1195-9.Caubi AF, Vasconcelos BC, Vasconcellos RJ, de 9. 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.Júnior SM, Asprino L, Moreira RW, Moraes MD. 10. A retrospective analysis of submental intubation in maxillofacial trauma patients. J Oral Maxillofac Surg 2011 Feb. 28.Eipe N, Neuhoefer ES, La Rosee G, Choudhrie R, 11. Samman N, Kreusch T. Submental intubation for cancrum oris: a case report. Paediatr Anaesth 2005;15(11): 1009-12.Biglioli F, Mortini P, Goisis M, Bardazzi A, Boari N. 12. Submental orotracheal intubation: an alternative to tracheotomy in transfacial cranial base surgery. Skull Base 2003;13(4):189-95.


Titanium 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.

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

Comparison of Enzyme Alkaline Phosphatase Levels Around Healthy and Diseased Implants: A Clinical StudyMn 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

*Associate Professor, Dept. of Periodontics Tagore Dental College and Hospital, Chennai **Professor, Dept. of PeriodonticsMeenakshi Ammal Dental College and Hospital, ChennaiAddress for correspondenceDr MN PrabhuAssociate Professor, Dept. of Periodontics Tagore Dental College and Hospital, ChennaiE-mail: [email protected]

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{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

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

4000

3000

2000

1000

0

865

3302

Successful FailureImplant

Mea

n al

kalin

e ph

osph

atas

e -

mea

n

figure 1. Increased levels of alkaline phosphatase in the diseased implants.


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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

ReferencesNewman MG, Fleming TF. Periodontal considerations 1. of implants and associated microbiota. J Dent Educ 1988;52(12):737-44. Socransky SS, Haffajee AD, Goodson JM, Lindhe J. 2. New concepts of destructive periodontal disease. J Clin Periodontol 1984;11(1):21-32.Ishikawa I, Cimasoni G. Alkaline phosphatase in human 3. gingival fluid and its relation to periodontitis. Arch Oral Biol 1979;15(12):1410-4.Lang NP, Adler R, Joss A, Nyman S. Absence of bleeding 4. on probing. An indicator of periodontal stability. J Clin Periodontol 1990;17(10):714-21.Rams TE, Link CC Jr. Microbiology of failing dental 5. implants in humans: electron microscopic observations 1983;11(1):93-100.Chapple IL, Garner I, Saxby MS, Moscrop H, 6. 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.Binder TA, Goodson JM, Socransky SS. Gingival fluid 7. levels of acid and alkaline phosphatase. J Periodontal Res 1987;22(1):14-9.Chapple IL, Glenwright HD, Matthews JB, Thorpe 8. 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.Lamster IB, Oshrain RL, Gordon JM. Enzyme activity 9. in human gingival crevicular fluid: considerations in data reporting based on analysis of individual crevicular sites. J Clin Periodontol 1986;13(8):799-804.Polson AM, Goodson JM. Periodontal diagnosis. 10. Current status and future needs. J Periodontol 1985; 56(1):25-35.McCulloch CA. Host enzymes in gingival crevicular 11. fluid as diagnostic indicators of periodontitis. J Clin Periodontol 1994;21(7):497-506.

n n n


Sterilization 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

Sterilization Protocol for Orthodontic and Endodontic InstrumentsMadhuri 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

*Professor and Head, Dept. of Orthodontics **Assistant ProfessorDept. of Orthodontics and Dentofacial Orthopedics†Assistant ProfessorDept. of Conservative Dentistry and Endodontics Priyadarshini Dental College and Hospital, Thiruvallur, Tamil NaduAddress for correspondencePriyadarshini Dental College and HospitalVGR Nagar, ThiruvallurPandur - 631 203, Tamil NaduE-mail: [email protected]

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.

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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 z 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 z (utility) gloves are meant to be used while cleaning instruments and environmental surfaces.Hand washing: z 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 nonsurgical procedures. For surgical procedures, an antimicrobial hand scrub should be used.Face masks z protect the oral and nasal mucosa from body fluid spatters. They should be changed when visibly soiled or wet.

table 1. Category of InstrumentsCategory Definition ExampleCritical Penetrates soft tissue, contacts bone, enters

into or contacts the bloodstream or other normally sterile tissue.

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.

Semi critical Contacts mucous membrane or nonintact skin; will not penetrate soft tissue, contact bone, enter into or touch other normally sterile tissue

Dental mouth mirror, amalgam condenser, reusable dental impression trays, dental handpieces, orthodontic pliers, elastomeric ligatures.

Noncritical Contacts intact skin Dental chair unit, light switch, handles.

Protective eye wear z is indicated to shield the eyes from spatters.Protective clothing: z 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 z can be done by three methods.

Proper patient positioning n

Use of high volume evacuation n

Use of rubber dam n

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 z

Sterilization z

Storage z

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.


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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 z °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

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 antiviral 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.


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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 z

Five seconds - reamers, files, broaches, burs, z

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.

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 z

depending on the capacity of the unit.Thorough rinsing with distilled water as tap water z

may contain impurities and pH imbalances which may cause corrosion.Complete moisture removal by drying with oil- z

free compressed air.Dry heat sterilization at 190°C for 6-12 minutes. z

Never expose the instruments to more than 193°C.Position the instruments in the ‘open’ position to z

ensure thorough sterilization of joints.Using silicone bases lubricants for the instrument z

joints. Oil based lubricants are not recommended as they tend to clog the pliers.Storage in a dry area free from moisture and z

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.


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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 z

depending on the capacity of the unitThorough rinsing with distilled water z

Complete moisture removal by drying with z

oil-free compressed airDry heat sterilization at 190°C for six minutes. z

Storage in a dry area free from moisture and z

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.

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 z

under running tap water.Immerse the impression along with the tray in z

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 z

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.


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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.

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 z

method, when used according to manufacturer’s instructions, will not corrode or dull carbide burs. Steam autoclaves –121°C (250°F) for 20 minutes z

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: z The hardness of water, excess mineral content and pH imbalances play an important role in instrument corrosion.High temperatures: z Using temperatures above the current manufacturer recommendation of 193°C results in corrosion of the instruments being sterilized.Moisture and insufficient drying: z 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: z 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: z Instruments sterilized by immersion in chemical solutions are reported to be associated with pitting corrosion.Enzymes: z Enzymatic cleaning solutions are known to have corrosive effects on the instruments and are not recommended.


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Aging of instruments: z 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.

ReferencesMatlack RE. Instrument sterilization in orthodontic 1. offices. Angle Orthod 1979;49(3):205-21.Buckthal JE. Survey of sterilization and disinfection 2. procedures. J Clin Orthod 1988;22(1):22-8.Cash RG. Trends in sterilization and disinfection 3. procedures in orthodontic offices. Am J Orthod Dentofacial Orthop 1990;98(4):292-9.Crawford JJ. Clinical asepsis in dentistry. P8RA Kolstad, 4. Publisher 1978.MMWR perspectives on the control of viral hepatitis 5. Type B centre for disease control US Dept of health, Ed and Welfare 1976;25:17.Boyd KS, Sonntag KD, Crawford JJ. Efficacy of 6. sterilization of endodontic files after autoclaving in a synthetic sponge. Int Endod J 1994;27(6):330-3.Vélez AE, Thomas DD, del Rio CE. An evaluation of 7. sterilization of endodontic instruments in artificial sponges. J Endod 1998;24(1):51-3.Mazzocchi AR, Paganelli C, Morandini C. Effects of 8. 3 types of sterilization on orthodontic pliers. J Clin Orthod 1994;XXVIII:644-7.Wichelhaus A, Brauchle G, Mertmann M, Sander 9. FG. Corrosion of orthodontic pliers using different sterilization procedures. J Orofac Orthop 2004; 65(6):501-11.

Jones ML. An initial assessment of the effect on 10. orthodontic pliers of various sterilization and disinfection regimes. Br J Orthod 1989;16(4):251-8.

Patel MP. Development of a self-disinfecting alginate 11. impression material. Biological and Medicinal Research, University of London, 2009.

Miller JA, Harrower KM, Costello MJ. A novel method 12. of sterilizing orthodontic instruments. Aust Orthod J 1992;12(3):151-2.

Nisalak P, Prachyabrued W, Leelaprute V. Glass bead 13. sterilization of orthodontic pliers. J Dent Assoc Thai 1990;40(4):177-84.

Smith GE. Glass bead sterilization of orthodontic 14. bands. Am J Orthod Dentofacial Orthop 1986;90(3):243-9.

Hohlt WF, Miller CH, Need JM, Sheldrake MA. 15. Sterilization of orthodontic instruments and bands in cassettes. Am J Orthod 1990;98(5):411-6.

George O, Benoit F, Rapin C, Aranda L, Berthod 16. P, Steinmetz P, et al. Effect of surgical sterilization procedures on orthodontic pliers: a preliminary report. Eur Cells Materials 2005;10(Suppl 4):13.

Wichelhaus A, Bader F, Sarder FG, Krieger D, 17. Merters T. Effective disinfection of orthodontic pliers. J Orofac Orthop 2006;67(5):316-36.

Dowsing P, Benson PE. Molar band re-use and 18. decontamination: a survey of specialists. J Orthod 2006;33(1):30-7; discussion 28.

Benson PE, Douglas CW. Decontamination of 19. orthodontic bands following size determination and cleaning. J Orthod 2007;34(1):18-24.

Mayberry DR, Allen R, Close J, Kinney DA. Effects of 20. disinfection procedures on elastomeric ligatures. J Clin Orthod 1996;30(1):49-51.

Jeffries CL, von Fraunhofer JA. The effects of 2% 21. alkaline glutaraldehyde solution on the elastic properties of elastomeric chain. Angle Orthod 1991;61(1):25-30.

Blair FM, Wassell RW. A survey of the methods of 22. disinfection of dental impressions used in dental hospitals in the United Kingdom. Br Dent J 1996; 180(10):369-75.

Hooks TW, Adrian JC, Gross A, Bernier WE. Use of 23. the carbon dioxide laser in sterilization of endodontic reamers. Oral Surg Oral Med Oral Pathol 1980;49(3):263-5.

Venkatasubramanian R, Jayanthi, Das UM, 24. 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.


case rePort

Information for Authors

Manuscripts should be prepared in accordance with the ‘Uniform requirements for manuscripts submitted to biomedical journals’ compiled by the International Committee of Medical Journal Editors (Ann. Intern. Med. 1992;96:766-767). The Journal strongly disapproves of the submission of the same articles simultaneously to different journals for consideration as well as duplicate publication and will decline to accept fresh manuscripts submitted by authors who have done so.

The boxed checklist will help authors in preparing their manuscript according to our requirements. Improperly prepared manuscripts may be returned to the author without review. The checklists should accompany each manuscript.

Covering Letter: The covering letter should explain if there is any deviation from the standard IMRAD format (Introduction, Methods, Results and Discussion) and should outline the importance of the paper. Principal/Senior author must sign the covering letter indicating full responsibility for the paper submitted, preferably with signatures of all the authors. Articles must be accompanied by a declaration by all authors stating that the article has not been published in any Journal/Book. Authors should mention complete designation and departments, etc., on the manuscript.

Manuscript: Three complete sets of the manuscript should be submitted and preferably with a CD; typed double spaced throughout (including references, table and legends to figures). The manuscript should be arranged as follow: Covering letter, Checklist, Title page, Abstract, Keywords (for indexing, if required), introduction, Methods, Results, Discussion, References, Tables, Legends to Figures and Figures. All pages should be numbered consecutively beginning with the title page.

Types of Submission: Original Research articles, Review articles, Case reports and Clinical study

Title Page: Should contain the title, short title, names of all the authors (without degrees of diplomas), names and full location of the departments and institutions where the work was performed, name of the corresponding authors, acknowledgement of financial support and abbreviations used. The title should be of no more than 80 characters and should represent the major theme of the manuscript. A subtitle can be added if necessary.

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 and fax numbers, e-mail and postal addresses of the author to whom communications are to be sent should be typed in the lower right corner of the title page.

Abstract: The abstract of not more than 200 words. It must convey the essential features of the paper. It should not contain abbreviations, footnotes or references.

Introduction: The introduction should state why the study was carried out and what were its specific aims/objectives were.

Material and Methods: Theses should be described in sufficient details to permit evaluation and duplication of the work by others. Ethical guidelines followed by the investigations should be described.

Results: These should be concise and include only the tables and figures necessary to enhance the understanding of the text.

Discussion: This should consist of a review of the literature and relate the major findings of the article to other publications on the subject. The particular relevance of the results to healthcare in India should be stressed, e.g., practically and cost.

References: These should conform to the Vancouver style. References should be numbered in the order in which they appear in the texts and these numbers should be inserted above the lines on each occasion the author is cited.

Tables: These should be typed double spaces on a separate sheet and figure number (in Roman Arabic numerals) and title above the table and explanatory notes below the table.

Legends: These should be typed double spaces on a separate sheet and figure numbers (in Arabic numerals) corresponding with the order in which the figures are presented in the text. The legend must include enough information to permit interpretation of the figure without reference to the text.

Figures: Two complete sets of glossy prints of high quality should be submitted. The labeling must be clear and neat. All photomicrographs should indicate the magnification of the print. Special features should be indicated by arrows or letters which contrast with the background. The back of each illustration should bear the first author’s last name, figure number and an arrow indicating the top. This should be written lightly in pencil only. Please do not use a hard pencil, ball point or felt pen. Color illustrations will be accepted if they make a contribution to the understanding of the article. Do not use clips/staples on photographs and artwork. Illustrations must be drawn neatly by an artist and photographs must be sent on glossy paper. No captions should be written directly on the photographs or illustration. Legends to all photographs and illustrations should be typed on a separate sheet of paper. All illustrations and figures must be referred to in text and abbreviated as ‘Fig’.

Please complete the following checklist and attach to the manuscript:

1. Classification (e.g. original article, review, etc.)_________________

2. Total number of pages____________________________________

3. Number of tables________________________________________

4. Number of figures_______________________________________

5. Special requests_________________________________________

6. Suggestions for reviewers (name and postal address)

Indian 1.______________ Foreign 1. _______________

2._____________________ 2._______________

7. All author’s signatures____________________________________

8. Corresponding author’s name, current postal and e-mail address and telephone and fax numbers

__________________________________________________________

Dr KMK Masthan

Professor and Head Department of Oral Pathology and Microbiology

Sree Balaji Dental College and Hospital Velachery Main Road, Narayanapuram, Pallikaranai

Chennai - 600 100, E-mail: [email protected], [email protected]

For Editorial Correspondence

Indian Journal of

Multidisciplinary Dentistry

ISSN 2229-6360

MultidisciplinaryDENTISTRY

Indian Journal of


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© Copyright 2011 IJCP Publications Pvt. Ltd.All rights reserved.

Dr KK Aggarwal, on behalf of IJCP PublicationsPvt. Ltd. and Published at E - 219, Greater Kailash, Part - 1, New Delhi - 110 048

[email protected], [email protected]

The copyright for all the editorial material contained in this journal, in the form of layout,content including images and design, is held by IJCP Publications Pvt. Ltd. No part ofthis publication may be published in any form whatsoever without the prior writtenpermission of the publisher.

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Editorial PoliciesThe purpose of IJCP Academy of CME is to serve the medical profession and provide printcontinuing medical education as a part of their social commitment. The information andopinions presented in IJCPgroup publications reflect the views of the authors, not those of thejournal, unless so stated. Advertising is accepted only if judged to be in harmony with thepurpose of the journal; however, IJCP group reserves the right to reject any advertising at itssole discretion. Neither acceptance nor rejection constitutes an endorsement by IJCP groupof a particular policy, product or procedure. We believe that readers need to be aware of anyaffiliation or financial relationship (employment, consultancies, stock ownership, honoraria,etc.) between an author and any organization or entity that has a direct financial interest in thesubject matter or materials the author is writing about. We inform the reader of any pertinentrelationships disclosed.Adisclosure statement, where appropriate, is published at the end ofthe relevant article.

Indian Journal of Multidisciplinary Dentistry does not guarantee, directly or indirectly,the quality or efficacy of any product or service described in the advertisements or othermaterial which is commercial in nature in this issue.

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