Dentistry Journal by IJCP

Indian Journal of

Multidisciplinary Dentistry

Volume 1, Issue 1 November-December 2010

IJMD’s Editorial Panel Editor-in-Chief KMK Masthan Executive Editor S Bhuminathan

Associate Editor N Aravindha Babu

IJMD Advisory Board Mahesh Verma

Mahalakshmi

Elumalai M

Srinisha J

John W Thurmond (USA)

Rajendran SM

Krishna Nayak US

Ramakrishna Shenoi

Abraham Kuriakose M

Vinay K Hazarey

Krishan Gauba

Raghavendra Jayesh S

Ipe Vargese V

Chandrasekaran SC

Puneet Ahuja

Sukumaran VG

Raj Kutta (USA)

Selva Muthu Kumar SC

Vijay Ebnezer

Swaminathan S (Singapore)

Muthiah NS

Dhandapani G

Nalini Aswath

Murali RV

Ash Vasanthan (USA)

Deepak C

Sanjna Nayar

Subbiya A

Aravind Ramanathan

Julius A

IJCP’s Editorial Panel Dr Sanjiv Chopra Prof. of Medicine & Faculty Dean Harvard Medical School Group Consultant Editor

Dr Deepak Chopra Chief Editorial Advisor

Dr KK Aggarwal CMD, Publisher and Group Editor-in-Chief Dr Veena Aggarwal Joint MD & Group Executive Editor Anand Gopal Bhatnagar Editorial Anchor

IJCP Editorial Board Dr Alka Kriplani Asian Journal of Obs & Gynae Practice Dr VP Sood Asian Journal of Ear, Nose and Throat Dr Praveen Chandra Asian Journal of Clinical Cardiology

Dr Swati Y Bhave Asian Journal of Paediatric Practice Dr Vijay Viswanathan The Asian Journal of Diabetology Dr M Paul Anand, Dr SK Parashar Cardiology

Dr CR Anand Moses, Dr Sidhartha Das Dr A Ramachandran, Dr Samith A Shetty Diabetology Dr Ajay Kumar Gastroenterology Dr Koushik Lahiri Dermatology

Dr Georgi Abraham Nephrology Dr Sidharth Kumar Das Rheumatology Dr V Nagarajan Neurology Dr Thankam Verma, Dr Kamala Selvaraj Obs and Gyne

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

Contents From the Editor-in-chief

From the Desk of IJCP Group Editor-in-Chief

A Message of Good Wishes

original research Treatment Outcome of Unilateral Condylar Fractures Surgical versus Conservative Approach

CASE REPORT Bilateral Keratocystic Odontogenic Tumor of Mandible

Original RESEARCH EGFR and MEK Pathway Independent Constitutive Activation of ERK-1/2 in a Serum Starved Oral Squamous Cell Carcinoma Cell Line

Comparative Evaluation of Resin Tag Formation on Dentin Substrate Using One-step and Two-step Self Etching System

CASE REPORT Recurrent Chronic Suppurative Osteomyelitis: Review of Literature and Report of a Case

Gingival Abscess Revisited

Second Molar with Single Root and Single Canal

REVIEW ARTICLE Finite Element Method in Orthodontics

Original RESEARCH Mineral Loss before and after Bleaching and Mineral Uptake on Application of Remineralizing Agent

REVIEW Article Dental Implants in Children and Adolescents

Marfan Syndrome

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From the Editor-in-chief xxxxxxxxx

Dr KMK Masthan

Professor and Head Department of Oral Pathology and Microbiology Sree Balaji Dental College and Hospital, Chennai

he progress of any science comes from documentation and sharing of ideas by the people who are involved in that science. A journal in my opinion is similar to a conference where we meet our friends and exchange news, concerns and ideas. The difference is here you don’t meet people, only their ideas. The advantage is you don’t have a time frame, you can read it now or tomorrow or two months later. Now let me walk you through how this journal got started. First is about the seeding. About a year ago, when I attended a review meeting at Sree Balaji Dental College. Our college Chairperson Dr Sri Nisha in her address asked the audience “What I see here is eminent Professors and Teachers in Dentistry giving out exemplary performance reports in each of your speciality. It is one thing to tell all this in a review meeting behind closed doors. But is the academic world aware of your performance?” It was a valid and a veiled reference to our number of publications. That question set me thinking. When we have so much clinical material, academic information and research activities being done right under our noses why this issue comes up. I realized that the answer is multifactorial. Foremost is our inertia to document what we do daily. We could collect vital statistics, take photographs of patients, keep copies of radiographs and pathology reports and organize them around a particular theme and present them as articles or we could go through the previously collected data, focus on similarities and deviations and write a review article, or we could identify one of the recent concepts in this fast changing field of dentistry and analyze the concept, do some innovative work on it and present it as a research paper. Again the key word in the above sentence is ‘could’, meaning facilities are available, knowledge is there and only the initiative is required. Basically that amounts to starting trouble of a perfectly functioning vehicle. I thought this required further deliberation. A few weeks later when I brought up the subject with Dr Bhuminathan, Chief Executive Officer of Balaji Dental College, he in his practical way told me “It is one thing to voice our concern about an issue but another to do something to resolve it. You could start a journal and motivate our professional colleagues to publish.’’ This was how the seed was planted. Before that decision, I used to browse through journals in a desultory manner with only two questions in my mind. Anything interesting? Who has written that? Now my view points changed. Who is the Publisher? Is it national or international? Is it Editor screened or peer reviewed? How much would it have cost to bring out the issue? Is there genuinity and/or quality in the articles? Is the journal theme-oriented or institution-oriented?

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

From the Issue Editor In some journals I tried to guess whether the motive is pursuit of knowledge or gratification of egos or plain profit making through advertisements and author contributions. On further discussions with authors who have several publications to their credit, I understood that for a journal three issues are important. First and most important is the reputation of the journal to consistently publish only quality articles. For that an unbiased Editorial Board with an open mind is important. Only then can a well-informed but a junior member of the profession will feel welcome to send his/her article. An article must be publishedbased on its merits and not based on the might of the author. Hence, a Peer Review Committee is mandatory. The Peers should not know who the author is and vice versa and the Peers must judge the article purely on the basis of its merits. That way they will have the freedom to express their constructive, corrective and negative comments without any hesitation. The second issue to consider is the financial commitment. Finance decides how many issues per year can be brought out and how many pages each issue can have. It is the foremost factor in deciding whether the photographs are color or black and white and who and how many are recipients of complimentary copies. Whereas flamboyance and ornamentation is definitely not needed in a journal, thrift will definitely affect the quality of presentations and interfere with wider circulation. So, financial freedom or at least not having the constant worry of finding the money for printing, postage for each issue was definitely needed. Hence, another round of discussions with Dr Bhuminathan who had just been promoted as the Deputy Registrar of Bharat University. His laconic reply was “Helping hands are better than praying lips. You do the spade work. I will find the money’’ He walked his talk and I had the money with no strings attached. That means though the management will finance my dream project, I was in no way obligated except to produce a good quality journal once in two months. The third issue is to generate a voluminous reader population for the journal. Through, my further analysis I realized that a particular speciality journal attracts only that speciality people and an outsider to that speciality either does not bother to read the journal and sometimes feels unwelcome in college and university libraries as if it is a breach to read other speciality journal. When I was a house surgeon 20 years back, I remember reading only BDJ and Triple O, both multispecialty journals. Hence, after consulting with my senior professional colleagues, I contemplated on a multispecialty dentistry journal. My belief was further strengthened when my invitations to stalwarts of different disciplines to join the advisory board were met with immediate acceptance and approval. Now let us get back to articles and authors. Unless you share your ideas, no one will realize that you had ideas to share. It is true that none of us receive any formal training as part of our curriculum to properly document, to organize data and to write for publishing. It is also true that none of us received any formal training to walk. But still we learnt to walk by falling down frequently and learning how to avoid falling. Same way let us change our mindset about willing to try writing articles. Try writing one, let there be mistakes, submit to our journal at ijmdent@gmail.com, we will discuss with you how to avoid the mistakes and refine your article. If you have money and don’t spend it is waste paper and the same way if you have the knowledge and don’t share it is a waste. Hence, mindsets must change. All you need is a change of attitude. In English, if you allot 1-26 to the alphabets, the word ATTITUDE alone gets 100 when you add up the numerals. So let us score 100 by changing our attitude and contributing articles to our journal. Best wishes... n

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

From the Desk of IJCP Group Editor-in-Chief xxxxxxxxx

Dr KK Aggarwal

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

he birth of a child is generally regarded a blessing and a source of great joy though with some anxious moments. So is the case with the launch of a new journal. Sree Balaji Dental College and Hospital, Chennai is bringing out a new journal ‘Indian Journal of Multidisciplinary Dentistry’ which will publish articles covering various aspects of dentistry. It will appear as a bimonthly journal. It gives me immense pleasure as a publisher to launch the first issue of this new journal. IJCP Group is India’s pioneer in medical journalism with a proven track record of Credibility, Innovation and Excellence in healthcare communications. Spreading medical knowledge has been our founding philosophy. The year 2010 marks the 20th year of IJCP Group as a Publishing Group. Indian Journal of Clinical Practice, our flagship journal was launched in June 1990 as a monthly journal. Since, then the amazing progress has been marked by many more achievements notable among those are Medinews, India’s first and most comprehensive medical newspaper and other Specialty Medical Journals. The launch last year of eMedinewS, the first national daily emedical newspaper of the country is yet another feather in the cap of IJCP Group. ‘Indian Journal of Multidisciplinary Dentistry’ is a new addition to our robust publication schedule. I look back on this journey with great pride and happiness and strive to more forwards to achieve new standards of excellence. I compliment and congratulate the Editors of this journal: Dr KMK Masthan (Editor-in-Chief ), Dr S Bhuminathan (Executive Editor) and Dr N Aravindha Babu (Associate Editor) for having taken this initiative to come out with a new journal in Dentistry for dental professionals across the country. Dr KMK Masthan, a renowned dentist, is Professor and Head, Dept. of Oral Pathology and Microbiology at Sree Balaji Dental College and Hospital, Chennai. I also take this opportunity to thank all authors who have contributed to this journal. Dentistry is fast emerging as one of the most important clinical specialities today. It is one speciality where the expertise has endured a turnaround from being curative to a more preventive and cosmetic one. I am sure that this journal would serve as an important learning resource to the dental fraternity, the dental practitioner, including students of the subject. I wish the Editors the very best in this new endeavor and extend my good wishes for the success of this journal. My best wishes for a happy and healthy New Year!! Happy reading….

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

A Message of Good Wishes

Dated: 14th December 2010

Dr Mahesh Verma Director and Principal Maulana Azad Institute of Dental Sciences, New Delhi Acting President, Dental Council of India

MESSAGE

t gives me immense pleasure to hear that Indian Journal of Multidisciplinary Dentistry is going to be launched by IJCP in the month of December 2010 under the guidance of renowned and professional dentists of Sree Balaji Dental College and Hospital.

I would like to congratulate the Editor Dr KMK Masthan and his team for their enthusiasm and flawless efforts to bring out this journal. I am sure that this journal will certainly help dental fraternity to keep themselves abreast with the latest knowhow in the related field and it will also inspire the readers, the dentists, to think in a precise and practical way about all clinical problems. I would also like to extend my good wishes to IJCP Group of Publications. My best wishes for successful publication of this journal. Happy reading…

Prof. (Dr) Mahesh Verma Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

original research

Treatment Outcome of Unilateral Condylar Fractures Surgical versus Conservative Approach Vijay Ebenezer*, Balakrishnan Ramalingam**

Abstract The aim of this study was to compare the outcome of surgical and conservative approaches for the management of displaced unilateral condylar fractures. Twenty-seven patients who reported to our department within a period of two years (2008-2009) were included in our study. All patients selected for the study had unilateral and displaced condylar fractures, with a ramus shortening of more than 3 mm on the fractured side. The 6-month postoperative radiographs were compared and evaluated. Postoperative ascending ramus height was measured on orthopantomograms. The difference obtained between the closed and conservatively treated patient group was evaluated. Occlusion, postoperative mouth opening and lateral excursive movements were included as the other parameters for the comparison. Our small population study concluded that open reduction and fixation of displaced condylar fractures yielded good postoperative results when compared to the conservatively managed patient group. Key words: Condylar fractures, surgical management, conservative management, ascending ramus height

he debate of surgical versus conservative management of condylar fractures has been widely documented over decades. Condylar fractures amount for 25-35% of all fractures occurring in the mandible (Killey, 1968).

lateral movements as the parameters for comparison between surgical and nonsurgical treated groups. Methods Twenty-seven patients with unilateral condylar fractures with or without associated fractures of the mandible who reported to the Dept. of Oral and Maxillofacial Surgery, Sree Balaji Dental College and Hospital, were included in the study. Nearly 60% of patients who reported to our institution were victims of road traffic accidents.

Several authors have supported surgical management of condylar fractures in view of the excellent postoperative mouth opening and lateral movements (Baker, 1998). Surgical procedures in the condylars region, have become simpler owing to the advances in the instrumentation and reduced size and thickness of the hardware used. However, several others are of the opinion that conservative management offers good results as it obviates the need for a difficult surgical access to the temporomandibular joint (TMJ), repositioning of the fractured condyle and avoiding injury to the facial nerve.

All patients were within the age group of 20-35 years and had condylar fractures, with angle between 10-45° between the ascending ramus and the fractured condylar head. The exclusion criteria included edentulous patients where the occlusion could not be checked or patients with history where general anesthesia could not induced.

This study aims at comparing the postoperative ascending ramus height, occlusion, mouth opening and

Ethical Committee clearance from the institution was obtained prior to the study.

*Professor and Head **Associate Professor, Dept. of Oral and Maxillofacial Surgery Sree Balaji Dental College and Hospital, Chennai Address for correspondence Dr Vijay Ebenezer Professor and Head Dept. of Oral and Maxillofacial Surgery Sree Balaji Dental College and Hospital Pallikaranai, Chennai - 600 100 E-mail: drvijayomfs@yahoo.com

Informed consent from all patients were obtained before either conservative or surgical procedures were done. Each patient was administered antibiotics on admission. All the patients were treated between 1st to 5th day following injury. Patients in the surgical group were discharged 72 hours following treatment and in the conservative group 48 hours following intermaxillary fixation. Oral antibiotics were continued Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research Surgical Group

Conservative Group

Preoperative OPG

or stainless steel were selected as standard hardware for fixation in all cases. Patients were discharged three days after surgery. Patients were routinely recalled every week for six weeks; maximal interincisal mouth opening was recorded. Postoperative radiographs were taken every month for six months and ascending ramus height was recorded. Patients were assessed on the basis of the post-treatment radiographs. Anatomic reduction of the fractured condyles were compared between the surgical and the conservatively managed groups. Lateral movements and occlusion were also compared between the two study groups.

Postoperative OPG

A line drawn from the maximum height of the condyle to the lower border of the ramus on both fractured and normal side was used as the guide line for comparison between the conservatively managed and the surgically treated groups. Results

Modified preauricular approach

Intermaxillary fixation

five days following surgical procedures. Patients in the conservative study group were treated with intermaxillary fixation for two weeks followed by soft oral diet for the next 6-8 weeks. Patients who underwent surgery were treated by standard surgical approaches, depending on the level of fracture using preauricular, submandibular and retromandibular approaches. Miniplates, either titanium Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Out of 27 patients with isolated condylar fractures and condylar fractures with other associated fractures, 19 (70%) were male and eight (30%) were female. Isolated condylar fractures were present in 13 cases (48%) and condylar fractures with other associated fractures were present in 14 cases (52%). Road traffic accidents were the main cause of trauma in 16 cases (59%) followed by assault six cases (22%), fall three cases (11%) and sports-related injuries two cases (8%). Left condyle was involved in 15 cases (56%) and the right condyle in 12 cases (44%). There were 12 patients (45%) with subcondylar fractures, 12 patients (45%) with condylar neck fractures and three patients (11%) with condylar head fractures. Out of 27 patients, 16 patients (59%) were treated by closed reduction and 11 patients (41%) were treated by open reduction. In closed reduction group, the maximum interincisal opening ranged from 32 to 41 mm (average 35.75 mm). Six patients (37.5%) in this group, had reduced mouth opening of below 35 mm. In open reduction group, the maximum interincisal opening ranged from 33 to 44 mm (average 37.50 mm); one patient (18%) had reduced mouth opening. Mandibular deviation towards fractured side was noted in six cases (37.5%) of closed reduction group and two cases (18%) of open reduction group. Pain in TMJ was noted in

No. of Patients

Original research 28 26 24 22 20 18 16 14 12 10 8 6 4 2

Patients treated by open method had the advantage of more rapid return to pretraumatic occlusion and enhanced nutrition. On the other hand, nonsurgically treated patients who required intermaxillary fixation and elastic traction had significant disturbances. These findings correlate with the study of Haug (2001).

0 Open Reduction Group

9 Closed Reduction Group

Figure 1. Reduced ascending ramus height.

seven cases (44%) of closed reduction group and three cases (27%) of open reduction group that subsided gradually on follow-up period. Two patients (12.5%) in closed reduction group had malocclusion after removal of IMF which was later managed with elastics. Radiographically vertical ramus height reduction was present in nine patients (56%) of closed reduction group, but open reduction group patients had normal vertical ramus height postoperatively (Fig. 1). Pain on lateral excursion was present in six patients (37.5%) of closed reduction group and three patients (27%) of open reduction group. Discussion In the past decades, several investigations and outcome studies have appeared in the literature that have compared nonsurgical with surgical treatment of mandibular condyle fractures. We have discussed the outcomes of nonsurgical and surgical treatment for mandibular condyle fractures from the results of our study in terms of restoration of the ascending ramus height of the fractured-side compared to the normal side. Out of 27 patients, 16 (59%) patients were treated nonsurgically by intermaxillary fixation for two weeks followed by guiding elastics and physiotherapy. Other 11 patients (41%) were treated surgically by open reduction and rigid internal fixation by miniplate osteosynthesis. Postoperative follow-up period ranged from 3 to 18 months. Mouth opening ranged from 32 to 41 mm in closed reduction group and 33 to 44 mm in open reduction group. Our results showed statistically significant difference in maximal mouth opening. Open group exhibited good mouth opening postoperatively when compared to closed group, which correlates with the study of Eckelt et al (2006) and Vesnaver (2008). 10

Radiographically, vertical ramus height was significantly reduced in nine patients (56%) treated by closed method. Whereas open group had normal vertical ramus height. This finding correlates with the study of Ellis and Throckmorton (2000) and Danda et al (2010). According to Haug et al (2001), there was higher perception of scarring associated with open group when compared to closed group. In our study, all patients who were treated by open method showed an acceptable surgical scar. Based on the above findings it can be concluded that patients treated by closed reduction give reasonably good clinical results, though the condyle is not anatomically normal in radiographs. Whereas patients treated by open reduction show excellent results clinically as well as radiographically, in terms of restoration of ascending ramus height in accordance with the study of Eckelt (2006). Suggested Reading 1. Vesnaver A. Open reduction and internal fixation of intra-articular fractures of the mandibular condyle: our first experiences. J Oral Maxillofac Surg 2008;66(10):2123-9. 2. Montazem AH, Anastassov G. Management of condylar fractures. Atlas Oral Maxillofac Surg Clin North Am 2009;17(1):55-69. 3. Baker AW, McMahon J, Moos KF. Current consensus on the management of fractures of the mandibular condyle. A method by questionnaire. Int J Oral Maxillofac Surg 1998;27(4):258-66. 4. Danda AK, Muthusekhar MR, Narayanan V, Baig MF, Siddareddi A. Open versus closed treatment of unilateral subcondylar and condylar neck fractures: a prospective, randomized clinical study. J Oral Maxillofac Surg 2010;68(6):1238-41. 5. De Rio G, Gamba U, Anghinoni M, Sesenna E. A comparison of open and closed treatment of condylar fractures: a change in philosophy. Int J Oral Maxillofac Surg 2001;30(5):384-9. 6. Ellis E 3rd, Dean J. Rigid fixation of mandibular condyle fractures. Oral Surg Oral Med Oral Pathol 1993;76(1):6-15. Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research 7. Ellis E 3rd, Complications of mandibular condyle fractures.Â Int J Oral Maxillofac Surg 1998;27(4):255-7. 8. Ellis E 3rd, Palomieri C, Throckmorton G. Further displacement of condylar process fractures after closed treatment. J Oral Maxillofac Surg 1999;57(11): 1307-16. 9. Ellis E 3rd, Throckmorton GS, Palomieri C. Open treatment of condylar process fractures: assessment of adequacy of repositioning and maintenance of stability. J Oral Maxillofac Surg 2000;58(1):27-34, discussion 35. 10. Gerbino G, Boffano P, Berrone S. Long-term clinical and radiological outcomes for the surgical treatment of mandibular condylar fractures. J Oral Maxillofac Surg 2009;67(5):1009-14. 11. Assael LA. Open versus closed reduction of adult mandibular condyle fractures: an alternative interpretation of the evidence. J Oral Maxillofac Surg 2003;61(11):1333-9. 12. Nussbaum ML, Laskin DM, Best AM. Closed versus open reduction of mandibular condylar fractures in adults: a meta-analysis. J Oral Maxillofac Surg 2008;66(6):1087-92. 13. Zide MF, Kent JN. Indications for open reduction of mandibular condyle fractures. J Oral Maxillofac Surg 1983;41(2):89-98.

14. Haug RH, Assael LA. Outcomes of open versus closed treatment of mandibular subcondylar fractures. J Oral Maxillofac Surg 2001;59(4):370-5. 15. Rowe and Williams. Maxillofacial Injuries. Vol 1 (1st edition):p337-62. 16. Brandt Haug RH. Open versus closed reduction of adult mandibular condyle fractures: a review of the literature regarding the evolution of current thoughts on management. J Oral Maxillofac Surg 2003;61(11): 1324-32. 17. Eckett U, Schneider M, Erasmus F, Gerlach KL, Kahlisch E, Loukota R, et al. Open versus closed treatment of fractures of the mandibular condylar process: a prospective randomized multi-centre study. J Craniomaxillofac Surg 2006;34(5):306-14. 18. Konstantinovic VS, Dimitrijevic B. Surgical versus conservative treatment of unilateral condylar process fractures: clinical and radiographic evaluation of 80 patients. J Oral Maxillofac Surg 1992;50(4):349-52. 19. Tang W, Gao C, Long J, Lin Y, Wang H, Liu L, et al. Application of modified retromandibular approach indirectly from the anterior edge of the parotid gland in the surgical treatment of condylar fracture. J Oral Maxillofac Surg 2009;67(3):552-8.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

CASE REPORT

Bilateral Keratocystic Odontogenic Tumor of Mandible Yashoda Devi BK*, N Rakesh**, Aarthi Nisha V†, Parimala Sagar‡, Kavitha Prasad§

Abstract Odontogenic keratocyst (OKC) is one of the most common critical cysts of the oral cavity due to its aggressive behaviour and high rate of recurrence. Recently studies prove that this lesion behaves like a tumour both in clinical presentation and histopathology, hence the term was recoined as keratocystic odontogenic tumor. The lesion often involves the jaws extensively and when they are present bilaterally, Gorlin-Goltz syndrome is suspected. The diagnosis should be solely based on histopathological confirmation and computed tomography (CT) can be used as an adjunct to estimate the size, extent and effects on its adjacent structures. Herein, we report a case of bilateral keratocystic odontogenic tumor in a 32-year-old male, which was diagnosed by a series of investigations and treated appropriately. Key words: Odontogenic keratocyst, aggressive, recurrence, computed tomography, enucleation, decompression

he odontogenic keratocyst (OKC), first described by Philipsen in 1956,1 was recently designated by the World Health Organization as a keratocystic odontogenic tumor and was defined as “a cyst arising in the tooth-bearing areas of the jaws, or posterior to the mandibular third molar, and characterized by a thin fibrous capsule and a lining of keratinized stratified squamous epithelium”.2 It may occur in any part of jaws with most lesions occurring in the mandible in the posterior body and ascending ramus.3 The OKC is one of the most aggressive odontogenic cysts owing to its relatively high recurrence rate and its tendency to invade the adjacent tissues.4 Smaller odontogenic keratocysts usually appear as asymptomatic unilocular radiolucencies with corticated borders; larger cysts may be multilocular, cause bony expansion and be accompanied by pain. These lesions are more common in males than females, occur over a wide age range and are typically diagnosed during the 2nd, 3rd or 4th decade.5 The histologic features of OKCs include a thin epithelial lining, usually consisting of fewer than six cell layers in a corrugated or wavy pattern. The underlying connective tissue is composed of thin, irregular bundles of collagen and often contains islands of epithelium that may represent daughter cysts.6 *Professor and Head **Senior Lecturer † PG Student, Dept. of Oral Medicine, Diagnosis and Radiology ‡ Senior Lecturer § Professor, Dept. of Oral and Maxillofacial Surgery MS Ramaiah Dental College and Hospital, Bangalore E-mail: ijmdent@gmail.com

In this article, we present a case of bilateral odontogenic keratocyst with marked buccal cortical expansion which was treated surgically. Case Report A 32-year-old male reported with a chief complaint of swelling in the left lower cheek region from the past six months. History of presenting illness revealed that the swelling was initially small and gradually increased in size. The swelling was also associated with dull, continuous pain that would subside on taking medications. On extraoral examination, gross facial asymmetry was present on left-half of face with a diffuse swelling in the left mandibular angle region. The swelling was roughly oval in shape and measured about 6-8 cm anteroposteriorly. It extended from 2 cm below the zygomatic arch superiorly to 3 cm below the lower border of the mandible inferiorly and upto mental region anteriorly and angle and posterior border of ramus posteriorly. The skin over the swelling was pinchable and the surface was smooth with diffuse borders (Fig. 1). On palpation, the swelling was firm and tender. Intraorally, no growth or mass was present and there was obliteration of the buccal vestibule in relation to 36, 37 and 38. Deep pocket associated with Grade I mobility was present in relation to 38. Marked expansion of the buccal cortical plate was present. Based on history and clinical examination, a provisional diagnosis of ameloblastoma of the left angle and body of the mandible was made. Differential diagnosis included keratocystic Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Case Report Procedure on the Left Side

Figure 1. Swelling on Figure 2. Panoramic radiograph the left angle region. revealing well-defined unilocular radiolucencies bilaterally.

odontogenic tumor, traumatic bone cyst, aneurysmal bone cyst and dentigerous cyst of the mandible. Panoramic radiograph and CT scan of the mandible were done. Panoramic radiograph (Fig. 2) showed two unilocular, radiolucent areas. On the left side, there was a well-circumscribed unilocular radiolucency with scalloped margins and thin radiopaque border involving the body and ramus extensively with ballooning of the inferior cortex and the anterior border of mandible. Displacement of the inferior alveolar canal was also noticed. On the right side, a well-circumscribed, unilocular radiolucency with smooth margins was noticed distal to 48 which was round in shape. CT scan of the mandible revealed evidence of expansile area of low attenuating or hypoattenuating lesion in the anterior aspect of left ramus of mandible with expansion and thinning of the buccal and lingual cortex. Lesion involved the second and third molars measuring about 5 × 3 cm approximately, extending from alveolar process to ramus of mandible. Another expansile, hypoattenuated lesion measuring about 2.1 × 1.4 cm was noticed in the right ramus of mandible. Aspiration with wide bore needle yielded a scanty amount of thick, purulent whitish substance, which on staining showed nucleated squamous cells against a background of keratinous debris. Incisional biopsy of cyst lining was done. The histopathology of the cystic lining showed keratin floating in lumen immediately beneath a thin layer of parakeratin, which lined a squamous epithelial layer that was six cells thick. Based on the clinical examination and investigations a final diagnosis of bilateral OKC was made. Treatment Treatment plan included decompression followed by enucleation. Under strict aseptic conditions, bilateral inferior, lingual and long buccal nerve block was given. Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Semilunar incision in the buccal sulcus measuring about 2 cm was given. Full thickness mucoperiosteum flap was raised. Bur holes were drilled and connected to create a bony window measuring about 1 cm in diameter (Fig. 3). Cystic contents were evacuated and the cavity was thoroughly irrigated with povidoneiodine solution mixed with saline. To maintain the patency of the bony window, an acrylic plate was later designed and delivered to the patient. Patient was instructed to irrigate the cavity with normal saline mixed with betadine solution and report for review once in a month. At one month follow-up, there was a noticeable decrease in the size of the lesion. Enucleation will be done when the surgical morbidity to associated teeth (36, 37) and inferior alveolar canal is minimal i.e. after a period of 6-9 months. Procedure on the Right Side

A similar procedure was carried out on the right side i.e. decompression followed by enucleation. After one month of decompression, patient was taken for enucleation since the size of the cystic tumor was small. Under strict aseptic condition, Ward’s incision was given, full thickness mucoperiosteum was raised. Bony window of about 2 cm was made (Fig. 4). Cystic lining was then slowly separated from the bone till the complete lining was removed. Then the cavity was painted with tincture of benzoin and finally irrigated thoroughly with normal saline and the mucoperiosteum over it was sutured primarily. Post- operatively antibiotics and analgesics were prescribed and healing was uneventful. Patient will be on regular follow-up, periodic panoramic radiographs will be taken and evaluated. Discussion Over a period of 100 years, we have arrived at the conclusion that keratinization can occur in the lining of many different cysts but there is specific type in which the keratin is predominantly of the parakeratinizing variety.7 In comparison to other cysts of the jaws, OKC is unusual because it shows characteristic clinical features, including potentially aggressive behavior, high recurrence rate and an association with nevoid basal cell carcinoma syndrome. Various treatment options are available. The most established methods are simple enucleation when the lesion is small, enucleation with 13

Case Report

Figure 3. Bony window created Figure 4. Bony window created on the left side. on the right side.

liquid nitrogen cryotherapy, enucleation followed by application of Carnoyâ&#x20AC;&#x2122;s solution, marsupialization, peripheral ostectomy, localized en bloc resection or segmental resection of the jaws.8 More recently, decompression technique is being carried out involving decompression of the cyst and regular continued follow up and maintenance over a period ranging from six months to a year, followed by secondary enucleation. This technique is gaining popularity in the treatment of large OKCs. Decompression and marsupialization of the cysts of the jaws were first described by Partsch in the German literature. They are still described as Partsch I procedure. This treatment was put forward at that time as definitive treatment for the cysts, and it consisted of the removal of the overlying epithelium and the deroofing of the cyst, keeping it open with a drain of some kind. This management is often advocated to stop subsequent growth and cause some decrease in size of the cyst to take it away from vital structures such as inferior alveolar nerve or adjacent teeth in the mandible or maxillary sinus or nasal cavity in the maxilla. It also allows subsequent enucleation to be performed with out complication and complete bone fill can be expected. Marsupialization, on the other hand involves converting the cyst into a pouch. This implies a more definitive treatment for the oral cavity and the exposure of the cyst lining to the oral environment. This type of treatment requires commitment and compliance on the part of patients over an extended period of time. Regular recall visits are required to ensure cyst involution and opportunity for appropriate treatment should there be any evidence of recurrence.

This treatment may require at least nine months. However, chances of recurrence and surgical morbidity are less with this procedure. OKCs respond to one of the most noninvasive treatments of all, which reinforces the paradox that accompanies new evidence that they may represent true cystic tumors and they even respond to simple treatment.9 Acknowledgements We would like to thank our Principal and Professor Dr HN Shama Rao for his support and guidance.

References 1. Philipsen HP. Keratocystic odontogenic tumor. In: World Health Organization classification of tumours. Pathology and genetics of the head and neck tumours. Barnes L, Eveson JW, Reichart PA, et al. (Eds.), IARC Press: Lyon, France 2005:306-7. 2. Kramer IRH, Pindborg JJ, Shear M. Histological typing of odontogenic tumours. Springer Verlag Berlin 1992: 35-6. 3. Brannon RB. The odontogenic keratocyst. A clinicopathologic study of 312 cases. Part I. Clinical features. Oral Surg Oral Med Oral Pathol 1976;42(1): 54-72. 4. Partridge M, Towers JF. The primordial cyst (odontogenic keratocyst): its tumour-like characteristics and behavior. Br J Oral Maxillofac Surg 1987;25(4):271-9. 5. Neville B, Damm D, Allen C, Bouquot J. (Eds.). In: Oral and Maxillofacial Pathology. 5th edition. WB Saunders, Philadelphia 1995:497-500. 6. Zachariades N, Papanicolaou S, Triantafyllou D. Odontogenic keratocysts: review of the literature and report of sixteen cases. J Oral Maxillofac Surg 1985;43(3):177-82. 7. Pogrel MA, Schmidt BL. The odontogenic keratocysts, Clin North Am 2003;15:3. 8. Rao HS, Gunachandra, Rao A. Long-standing odontogenic keratocyst: a case report and review of literature. J Oral Surg 2005;4:3 9. Pogrel MA. Decompression and marsupialization as a treatment for the odontogenic keratocyst. Oral Maxillofac Surg Clin North Am 2003;15(3):415-27.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original RESEARCH

EGFR and MEK Pathway Independent Constitutive Activation of ERK-1/2 in a Serum Starved Oral Squamous Cell Carcinoma Cell Line Arvind Ramanathan

Abstract The EGFR/Ras/RAF/MEK/ERK pathway is a major pathway involved in the control of growth signals, cell survival and differentiation. Constitutive activation of ERK-1/2 has been reported in cancers and has often been associated with constitutively active upstream activating signals. To understand the mechanism of activation of ERK-1/2 in oral squamous cell carcinoma (OSCC) we analyzed two cell lines, OSCC-1 and OSCC-2. OSCC-1 expressed physiological level of EGFR, while OSCC-2 had amplified copies of EGFR in the genome and hence overexpressed EGFR protein. Western blot analysis of the cell lysates showed constitutive activation of ERK-1/2 in both cell lines. In OSCC-2 cells, this activation of ERK-1/2 was associated with constitutive activation of upstream molecules - MEK-1/2 and EGFR, whilst in OSCC-1 this was independent of the activation status of MEK or EGFR. Thus, in this study we showed for the first time that the constitutive activation of ERK-1/2 in OSCC may occur independent of upstream activators. Key words: ERK-1/2, MKP-1, constitutive activation, constitutive phosphorylation

itogen-activated protein kinases (MAPKs) are a family of proteins that is comprised of three major groups: ERK-1/2 (extracellular signal-regulated kinase), p38 and JNK/SAPK (c-Jun 1 N-terminal kinase/stress-activated protein kinase). ERK-1/2 (p44/p42) MAPK is activated mainly by mitogenic signals such as EGFR (epidermal growth factor receptor)/Ras/RAF (MAPK kinase kinase)/MEK (MAPK kinase)-dependent pathway that links signals originating on the cell surface to intracellular events 2-6 such as cell growth, cell survival and differentiation. ERK-1/2 is a cytoplasmic protein and the immediate upstream signaling proteins of ERK-1/2 are MEK 1-6 These proteins transmit extracellular andÂ RAF. signals received by EGFR through sequential kination of RAF, MEK and ERK. Activated 7,8 ERK-1/2 translocates into the nucleus, where it 5,9-13 phosphorylates multiple transcription factors, and other substrates depending on its intracellular 9-14 localization and duration of activation. Although the transcription factors are the major targets for MAPKs that are involved in growth stimulation, ERK-1/2 also induces and phosphorylates a dual Address for correspondence Dr Arvind Ramanathan Human Genetics Laboratory, Balaji Dental College and Hospital Bharath University, Chennai E-mail: drarvindram@yahoo.co.in

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

phosphatase MKP1 which acts as a negative regulator 15-18 by inactivating dual-phosphorylated ERK-1/2. Hence, any abnormality that leads to the constitutive activation of ERK-1/2 could possibly cause a malignant transformation. Indeed, abnormalities in activators of ERK-1/2 such as EGFR gene amplification, activating mutations of Ras, N-terminal deletions of RAF and activating mutations of MEK that ultimately results in aberrant ERK-1/2 phosphorylation have been 19-22 associated with malignant transformations. This is also the case for oral squamous cell carcinomas 23,24 (OSCCs) though the mechanism of constitutive phosphorylation in oral cancer cells remains to be studied. In the present study, we analyzed the activation status of ERK-1/2 in two OSCC cell lines, OSCC-1 and OSCC-2 to understand the molecular mechanism of their activation. We found that the constitutive activation of ERK-1/2 in OSCC-2 cells was associated with constitutive activation of both MEK and EGFR in the serum starved cells. However, the activation status of ERK-1/2 in OSCC-1 cells was not associated with upstream activators, as active signal of neither MEK nor EGFR could be detected in the serum starved cells. Thus in this study, we showed for the first time that the constitutive activation of ERK-1/2 in OSCC cells could be associated with a defect in the inactivating machinery. 15

Original research Material and Methods Cell Lines

The human OSCC cell lines OSCC-1 and OSCC2 were used in this study. HaCaT, an immortalized human oral keratinocyte cell line (a gift from Professor NE Fusenig) was used as a control cell line. The cell lines were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) supplemented with 10% FBS (Invitrogen) and 10 µg/ml of gentamycin and were incubated at 37°C with 5% CO2/95% air in a humidified CO2 incubator. Cells growing at a density of 80-90% were used in this study. EGF Stimulation and Lysate Preparation

Prior to experiments, cells were starved of serum for 48 hours in DMEM and then stimulated with EGF with 10 ng/ml for 10 minutes or 10, 30 and 60 minutes for the time course assay. EGF treated cells were then washed twice with ice-cold 1x PBS and lyzed in NP-40 buffer [20 mM Hepes, pH 7.4, 5 mM EDTA, 150 mM NaCl, 0.1% NP-40, 50 mM NaF, 1 mM glycerophosphate, 5 mM Na4P2O7, 1 mM phenylmethylsulfonyl fluoride (PMSF), supplemented with 1 mM of Na3VO4 and one tablet of complete protease inhibitor cocktail per 10 ml]. Lysates were cleared by centrifugation and supernatants were stored at –80°C until further use. Western Blotting

The lysates were quantified and protein concentrations were determined with a DC protein assay kit. An equal amount of total protein was fractionated in a 10% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), transferred to a polyvinylidene fluoride (PVDF) membrane, blocked for one-hour in Tris-buffered saline (pH 7.5) containing 0.5% Tween 20 and 1% skim milk, and incubated with primary antibodies overnight, followed by incubation with secondary antibodies linked to horseradish peroxidase at room temperature for one-hour. Immunoreactive protein bands were detected with an enhanced chemiluminescent (ECL) reagent Antibodies used were as follows: α-phosphotyrosine ERK-1/2 (Y 204), α-ERK-1/2 (K-23), α-ERK2 (D2) and α-MKP1 and α-phospho MEK and α-phospho ERK-1/2 (dual phosphorylation specific). The secondary antibodies used were α-mouse or rabbit IgG linked with HRP. 16

Quantification of Protein Phosphorylation and Expression

For the quantification of protein bands, the image was scanned and the intensity was analyzed using NIH Image J software with default settings. The values of the scanned image were normalized with values of respective loading controls such as ERK-1/2 or ERK-2 alone. The criteria used to determine whether or not ERK-1/2 was constitutively active in a given cell line were based on the intensities of phosphorylated ERK-1/2 in unstimulated cells with reference to an arbitrarily set value of 1. When the value was >1, the cell line was designated as constitutively active for ERK-1/2 and was expressed as fold increase. Results Constitutive Activation of ERK-1/2 in OSCC-1 and OSCC-2 cell lines

The constitutive activation of ERK-1/2 has been observed in several cancers and cancer cell lines and has 20-24 been associated with the genesis of carcinomas. To understand the underlying molecular mechanism, we first examined the status of ERK-1/2 phosphorylation in two OSCC cell lines - OSCC-1 and OSCC-2, and a control cell line - HaCaT after serum starvation. Western blotting of lysates from the above cells lines with antibodies specific for dual-phosphorylated ERK-1/2 showed high levels of dualphosphorylated ERK-1/2 even after 48 hours of serum starvation relative to HaCaT cells (Fig. 1). Serum starved condition was used to evaluate constitutive phosphorylation of ERK-1/2 because no extraneous growth factors would be present under such condition and the detection of undue phosphorylation of ERK-1/2 would apparently reflect an abnormality in either the activation or inactivation machinery in cells. Constitutive Activation of MEK and EGFR in OSCC-2 cell line

To explore the mechanism underlying the constitutive activation of ERK-1/2 we next checked the activation status of MEK in both cell lines, as MEK has been shown to be an immediate upstream 1-6 activating kinase of ERK-1/2. Western blotting with antiphospho MEK showed a high constitutive activation of MEK in one of the cell line OSCC-2, while OSCC-1 showed a weak phosphorylation under Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research HaCaT EGF

OSCC-1 +

OSCC-2 -

Phospho ERK-1/2

Total ERK-2

Fold increase

0.4

2.0

4.0

Figure 1. Constitutive activation of ERK-1/2 in OSCC-1 and OSCC-2 cell lines. Semi-confluent cells were serum-starved for 48 hours, and then stimulated with 10 ng of EGF for 10 minutes. Unstimulated counterparts of each of the cell line served as the respective control. 10 Âľg of total cell lysate were Western blotted and probed with antiphospho ERK-1/2 (top panel). Equal loading was confirmed by probing the membrane of a parallel gel with anti-ERK2 antibody (lower panel). The constitutive activation of phospho ERK-1/2 was expressed as fold increase and was quantified according to the protocol mentioned in the materials and methods section.

A EGF

HaCaT -

OSCC-1 +

OSCC-2 +

Phospho ERK-1/2

Total ERK-2

B EGF

OSCC-1 -

OSCC-2 +

+ Phospho EGFR-Y845

Phospho EGFR-Y1068

Total EGFR

Figure 2. Levels of phosphorylated MEK after serum-starvation (A) and MEK-dependent phosphorylation of ERK-1/2 in OSCC-1 and OSCC-2 cells (B) A: Cell lysates prepared as described in Fig. 1 were Western-blotted and probed with antiphospho MEK antibody (upper panel). Equal loading was confirmed by probing the same filter with anti-MEK (lower panel). B: Cell lysates were probed with antiphospho EGFR-Y845 and -Y1068. Total EGFR was used to detect EGFR amplification. Equal loading was confirmed with anti-MEK antibody as shown in panel A.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research EGF (min)

HaCaT 0

OSCC-1 60

240

OSCC-2 60

240

240 Phospho ERK-1/2

Total ERK 2

Figure 3. Constitutive and sustained activation of ERK-1/2 in OSCC-1 and OSCC-2 cell lines. Serum-starved cells were stimulated with 10 ng/ml of EGF for 0, 10, 30, 60 and 240 minutes. Cell lysates were prepared and 10 µg of total protein was analyzed by Western blot analysis using antibodies that recognized phosphotyrosine-specific ERK-1/2 (top panels). The same membrane was reprobed for total ERK-1/2 to confirm the equal loading of protein in each of the lane (lower panels).

serum starved conditions (Fig. 2A). Immediately upstream to MEK are cRAF-1 and EGFR. Since, EGFR is the first one to be activated in the kinase module, we analyzed its activation status with two phospho-EGFR specific antibodies (Y845, which lies in the activation loop of EGFR and Y1068, which is required for its interaction with Grb2 adapter protein and subsequently for ERK-1/2 signaling pathway). As shown in Figure 2B - top and middle panel, OSCC-2 displayed constitutive phosphorylation of EGFR in unstimulated cells, relative to OSCC-1. Amplified copies of EGFR in OSCC-2 cells were confirmed by reprobing the membrane with antiEGFR antibody (Fig. 2B - bottom panel). Constitutive Activation of ERK-1/2 in OSCC-1 cell line was associated with its Prolonged Activation

To further explore the mechanism of constitutive activation of ERK-1/2 in the two cell lines, we analyzed the inactivation pattern of ERK-1/2 after stimulation with EGF. Activated ERK-1/2 has been reported to have a half-life of around 45 minutes after which it is inactivated by ERK-1/2 specific dual specific phosphatase MKP-1, via a negative feedback mechanism.15-18 Hence, any abnormality in either the activating or inactivating mechanism could potentially lead to the prolonged and subsequent constitutive activation of ERK-1/2. To test this hypothesis we performed a time course assay of the activation and subsequent inactivation pattern of ERK-1/2. Serum starved cells were exposed to EGF for different time points as mentioned in Figure 3 and cell lysates were subjected to Western blot analysis with an antibody that detects tyrosine phosphorylated ERK-1/2. We found sustained activation of 18

ERK-1/2 both in OSCC-1 and OSCC-2 cells but not in the control cell line - HaCaT, in which a gradual decline was observed (Fig. 3, compare areas marked with arrows). Reprobing of the membrane with antiERK-1/2 showed a similar loading of total protein in each lane of each cell line (Fig. 3 - lower panel). These results indicated that EGF elicited different kinetics of activation and inactivation of ERK-1/2 in HaCaT, OSCC-1 and OSCC-2. Discussion We studied the mechanism behind the constitutive activation of ERK-1/2 in two OSCC cell lines, OSCC-1 and OSCC-2. To clarify the molecular mechanisms underlying the sustained activation of ERK, we took advantage of OSCC cell lines with and without EGFR overexpression and examined the phosphorylation status of ERK-1/2 in cells after 48 hours of serum starvation. Serum starved cells were used instead of cells cultured with 10% serum, in order to uncover aberrant signaling from growth factor receptor to ERK-1/2 in the absence of any extraneous growth factors. The two cell lines OSCC-1 and OSCC-2 maintained high levels of phospho ERK-1/2 even when cultured under serumstarved conditions for 48 hours. OSCC-2 with amplified copies of EGFR overexpressed the receptor protein and exhibited constitutive activation of EGFR, MEK and ERK. For this cell line we also analyzed the time course of activation of EGFR after stimulation with EGF with two different phosphorylation-specific antibodies, EGFR-Y845 and EGFR-Y1068. A prolonged activation of EGFR until four hours of EGF treatment was found (Arvind R, unpublished data). Analysis of the phosphorylation of Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research cRAF (S338) also showed high levels of constitutive phosphorylation under serum-starved conditions relative to other OSCC cell lines and the control cell line NIH3T3 (Arvind R, unpublished data). These results were consistent with the idea that the constitutive activation of ERK was due to overexpressed EGFR and a sustained signaling from EGFR to MEK, which is in 22 line with recent reports. We also identified the constitutive activation of ERK-1/2 in OSCC-1 cells. In this cell line the level of phosphorylated MEK and phosphorylated EGFR under serum starved condition was very low relative to serum starved OSCC-2 cells, suggesting an alternate mechanism for its constitutive activation. Dual specific phosphatase-1 (DUSP-1, also called as MKP-1/2) belongs to a family of DUSP, which is transiently synthesized by activated ERK-1/2 to selfinactivate via a negative feedback loop. Hence, it is likely that the constitutive and sustained activation of ERK-1/2 that we observed in serum starved OSCC-1 cells may be due to a defect in the inactivating machinery that may include a reduced level or downregulation of MKP-1/2. Further support for our hypothesis comes from yet another study which showed that sustained activation of ERK-1/2 could induce ubiquitination and degradation of MKP-1 protein.31,32 We believe that a similar mechanism may be operative in OSCC-1 cells since ERK-1/2 activation was found to be constitutive and prolonged. It is also likely that alternate ERK-1/2 activation mechanism mediated by cytokines or other MAPK activating pathways such as MEKK-1 may exist in these cells. Our present study, as such does not attempt to explain the genesis of carcinoma, but only suggests for a possible mechanism of ERK-1/2 activation in OSCC cell lines. Nevertheless our study may serve as a model for the selection of patients for drug therapy. For example EGFR tyrosine kinase inhibitors are being increasingly used in the treatment of cancers with EGFR amplifications, though only with partial success. Inhibition of the EGFR tyrosine kinase activity usually nullifies the ERK-1/2 phosphorylation in a normal cell. However, in cancers with a defective ERK-1/2 inactivation machinery or alternate signaling mechanism, the EGFR inhibitor drugs may not be effective in curtailing the ERK-1/2 activation thus attributing to the partial success of Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

this drug. Indeed, our works in this direction have confirmed that treatment of OSCC-1 cells with the EGFR inhibitor AG1478 failed to abolish ERK-1/2 phosphorylation unlike in HaCaT cells (Arvind R, unpublished data). The low number of cell lines used in this study prevents us from demonstrating categorically the common underlying features. It would be interesting to extend the analysis to a wide range of OSCC cell lines including clinical samples. This would then enable the clinicians to include the status of ERK-1/2 activation and expression level of MKP-1 in the classification criteria for tumors, which eventually would help them to choose appropriate chemotherapeutic agents. Suggested Reading 1. Pearson G, Robinson F, Beers Gibson T, Karandikar M, Berman K, et al. Mitogen-activated protein (MAP) kinase pathways: regulation and physiological functions. Endocr Rev 2001;22(2):153-83. 2. Waskiewicz AJ, Cooper JA. Mitogen and stress response pathways: MAP kinase cascade and phosphatase regulation in mammals and yeast. Curr Opin Cell Biol 1995;7(6):798-805. 3. Huang CY, Ferrell LE Jr. Ultrasensitivity in the mitogenactivated protein kinase cascade. Proc Natl Acad Sci USA 1996;93(19):10078-83. 4. Lewis TS, Shapiro PS, Ahn NG. Signal transduction through MAP kinase cascades. Adv Cancer Res 1998;74: 49-139. 5. Davis RJ. The mitogen-activated protein kinase signal transduction pathway. J Biol Chem 1993;268(20):14553-6. 6. Nishida E, Gotoh Y. The MAP kinase cascade is essential for diverse signal transduction pathways. Trends Biochem Sci 1993;18(4):128-31. 7. Jaaro H, Rubinfeld H, Hanoch T, Seger R. Nuclear translocation of mitogen-activated protein kinase kinase (MEK1) in response to mitogenic stimulation. Proc Natl Acad Sci USA 1997;94(8):3742-7. 8. Adachi M, Fukuda M, Nishida E. Nuclear export of MAP kinase (ERK) involves a MAP kinase kinase (MEK)-dependent active transport mechanism. J Cell Biol 2000;148(5):849-56. 9. Hill CS, Treisman R. Transcriptional regulation by extracellular signals: mechanisms and specificity. Cell 1995;80(2):199-211. 10. Hunter T. Protein kinases and phosphatases: the yin and yang of protein phosphorylation and signaling. Cell 1995;80(2):225-36.

Original research 11. Schaeffer HJ, Weber MJ. Mitogen-activated protein kinases: specific messages from ubiquitous messengers. Mol Cell Biol 1999;19(4):2435-44. 12. Vojtek AB, Cooper JA. Rho family members: activators of MAP kinase cascades. Cell 1995;82(4):527-9.

22. Thomas CY, Chouinard M, Cox M, Parsons S, StallingMann M, Garica K, et al. Spontaneous activation and signaling by overexpressed epidermal growth factor receptors in glioblastoma cells. Int J Cancer 2003;104(1):19-27.

13. Pagon Z, Volker J, Cooper GM, Hansen U. Mammalian transcription factor LSF is a target of ERK signaling. J Cell Biochem 2003;89(4):733-46.

23. Mishima K, Inoue K, Hayashi Y. Overexpression of extracellular-signal regulated kinases on oral squamous cell carcinoma. Oral Oncol 2002;38(5):468-74.

14. Robinson MJ, Cobb MH. Mitogen-activated protein kinase pathways. Curr Opin Cell Biol 1997;9(2):180-6.

24. Mishima K, Yamada E, Masui K, Shimokawara T, Sugimura M, Ichijima K. Overexpression of the ERK/ MAP kinases in oral squamous cell carcinoma. Mod Pathol 1998;11(9):886-91.

15. Cook SJ, Beltman J, Cadwallader KA, McMahon M, McCormick F. Regulation of mitogen-activated protein kinase phosphatase-1 expression by extracellular signal-related kinase-dependent and Ca2+dependent signal pathways in Rat-1 cells. J Biol Chem 1997;272(20):13309-19. 16. Brondello JM, Brunet A, Pouysségur J, McKenzie FR. The dual specificity mitogen-activated protein kinase phosphatase-1 and -2 are induced by the p42/p44 MAPK cascade. J Biol Chem 1997;272(2):1368-76. 17. Keyse SM. An emerging family of dual specificity MAP kinase phosphatases. Biochem Biophys Acta 1995;1265(2-3):152-60. 18. Keyse SM. Protein phosphatases and the regulation of MAP kinase activity. Semin Cell Dev Biol 1998;9(2): 143-52. 19. Cowley S, Paterson H, Kemp P, Marshall CJ. Activation of MAP kinase kinase is necessary and sufficient for PC12 differentiation and for transformation of NIH3T3 cells. Cell 1994;77(6):841-52. 20. Hoshino R, Chatani Y, Yamori T, Tsuruo T, Yashida O, Shimada Y, et al. Constitutive activation of the 41-/43kDa mitogen-activated protein kinase signaling pathway in human tumors. Oncogene 1999;18(3):813-22. 21. Handra-Luca A, Bilal H, Bertrand JC, Fouret P. Extracellular signal-regulated ERK-1/ERK-2 pathway activation in human salivary gland mucoepidermoid carcinoma: association to aggressive tumor behavior and tumor cell proliferation. Am J Pathol 2003;163(3):957-67.

25. Davies SP, Reddy H, Caivano M, Cohen P. Specificity and mechanism of action of some commonly used protein kinase inhibitors. Biochem J 2000;351(Pt1):95-105. 26. Matsumara K. Detection of DNA amplifications and deletions in oral squamous cell carcinoma cell lines by comparative genomic hybridization (CGH). Kokubyo Gakkai Zasshi 1995;62(4):513-31. 27. Wellbrock C, Weisser C, Geissinger E, Troppmair J, Schartl M. Activation of p59 (Fyn) leads to melanocyte dedifferentiation by influencing MKP-1-regulated mitogen-activated protein kinase signaling. J Biol Chem 2002;277(8):6443-54. 28. Barry OP, Mullan B, Sheehan D, Kazanietz MG, Shanahan F, Collins JK, et al. Constitutive ERK1/2 activation in esophagogastric rib bone marrow micrometastatic cells is MEK-independent. J Biol Chem 2001;276(18):15537-46. 29. Grammer TC, Blenis J. Evidence for MEK-independent pathways regulating the prolonged activation of the ERK-MAP kinases. Oncogene 1997;14(14):1635-42. 30. Lin YW, Chuang SM, Yang JL. ERK-1/2 achieves sustained activation by stimulating MAPK phosphatase-1 degradation via the ubiquitin-proteasome pathway. J Biol Chem 2003;278(24):21534-41. 31. Tong Z, Singh G, Rainbow AJ. Sustained activation of the extracellular signal-regulated kinase pathway protects cells from photofrin-mediated photodynamic therapy. Cancer Res 2002;62(19):5528-35.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original RESEARCH

Comparative Evaluation of Resin Tag Formation on Dentin Substrate Using One-step and Two-step Self Etching System Sushil Kumar*, VG Sukumaran**, A Subbiya†, P Vivekanandhan†, V Prakash†

Abstract An evaluation of length and depth of resin tag infiltration was done using four different bonding agents grouped as follows: Group I: ‘One-bottle one-step’ self-etch adhesive (i-bond, kulzer), Group II: ‘Two-bottle one-step’ self-etch adhesive (Adper prompt, 3M), Group III: ‘Two-bottle two-step’ self-etch adhesive (AdheSE, Vivadent) and Group IV: ‘Etch and rinse’ adhesive (Prime and bond NT, Dentsply). The study was conducted using 60 noncarious freshly extracted premolars solely extracted for orthodontic purpose. A standard smear layer was produced by using a wet 600-grit silicon carbide paper to simulate clinical conditions and later the bonding agents applied as per the recommended protocol. Each bonded sample was vertically sectioned to expose the resin-dentin interface to be observed under confocal laser scanning microscope and later images were analyzed using the Ultima Master Program version 4.15. The results were tabulated and statistically analyzed using one-way ANOVA and multiple range tests by Tukey-HSD procedure. Key words: Resin tag, bond strength, hybridization, confocal scanning microscope

he success of adhesion to acid-etched enamel has further propelled Buonocore et al to try the same procedure on dentin. To their dismay, they found that resin-dentin bond strengths were relatively low (5-10 Mpa) as compared to enamel (20-25 Mpa).1-3 They were ignorant of the fact that acid etching of dentin altered its surface from hard mineralized structure to a very soft mineral free collagen rich substrate, which collapsed readily and thereby yielding undesirable bond strength. Similar scientific efforts were advocated by Fusayama (1979) on both enamel and dentin simultaneously to be known as total etch concept. This concept raised a lot of controversy amongst researchers proclaiming that acid etching of dentin caused pulpal death, which led to impeding his further efforts.4 Nakabayashi et al (1982) further worked and claimed Fusayama’s claims of resin bonding to acid-etched dentin. He suggested that there was a dramatic improvement in dentin bonding due to resin infiltration within the demineralized dentin surface as a result of hybrid layer and resin tag formation. These modes of retention via the resin-collagen infiltration became widely accepted as the fundamental basis of dentin adhesion.1,4 *PG Student **Professor and Head, Dept. of Conservative Dentistry and Endodontics † Professor Sree Balaji Dental College and Hospital, Chennai E-mail: ijmdent@gmail.com

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Despite these positive revelations, bonding to wet dentin surface proved to be a formidable obstacle. Hence, generations of bonding agents have been developed with different claims and properties to suit the nature of dentin. Based on the underlying strategy two systems of adhesion have been developed currently, namely ‘etch and rinse’ and ‘self-etch’. The ‘etch and rinse’ adhesives claim to produce relatively high bond strength values to dentin. But the quality and quantity of dentin hydration following rinsing and drying of dentin has resulted in conflicting reports regarding the durability of adhesion. This has further led to the advent of ‘self-etch’ adhesives in which nonrinse acidic monomers are added that simultaneously primed and conditioned dentin. They claimed to exhibit a twofold bonding mechanism, namely micromechanical and chemical bonding which they believed to be advantageous in terms of durability.5,6 The purpose of this study was to evaluate the length and depth of resin tag formation using ‘one-step’ and ‘twostep’ self-etch adhesives (sixth- and seventh-generation) compared with etch and rinse system (fifth-generation) under a confocal laser scanning microscope (CLSM) Material and Methods Methodology

Sixty noncarious freshly extracted human maxillary premolars, extracted for orthodontic reasons were 21

Original research selected for this study. They were stored in normal saline solution for less than one month after extraction. Following ultrasonic cleaning of the teeth, flat dentin surface were created on mid-coronal dentin using a slow speed diamond disc with copious water irrigation. A standard smear layer was produced by wet-sanding the dentin surface with 600-grit silicon carbide paper for 60 seconds. After this procedure the teeth were randomly divided into four groups of 15 specimens each. The bonding agents selected for the study were grouped as follows (n = 15):  Group I: ‘One-bottle one-step’ self-etch adhesive (i-bond, Kulzer)  Group II: ‘Two-bottle one-step’ self-etch adhesive (Adper prompt, 3M)  Group III: ‘Two-bottle two-step’ self-etch adhesive (AdheSE, Vivadent)  Group IV: ‘Etch and rinse’ adhesive (Prime and bond NT, Dentsply) Fluorescent Labeling of Bonding Agents

In this study, Rhodamine B (Batch No. 0496/496/240372, Hichem Lab), which emits fluorescence when exited with 514 nm green light, was used Rhodamine B isothiocyanate is comprised of electroneutral, undissociated molecules which do not dissolve in water and, therefore, lead to a contrast under CLSM. It provides improved resolution and image contrast on laser illumination of the sample components especially around the interface of a fluorescent labeled adhesive within the tissue. It is not labile and fixes well to the material to be examined which is very ideal for resin tag imaging. A few grains of the dye were mixed and dissolved with the bonding agents before their application. Following dissolution of the dye, the bonding agents were applied as per manufacturer’s instructions as follows: Group I: One-bottle One-step Self-etch Adhesive (I-bond)

Immediately after dispensing, soak the applicator tip or a soft disposable brush and apply a copious amount to the entire cavity surface. Apply two additional coats of i-bond slowly and consecutively. Wait for 30 seconds, slight agitation during the dwell time may improve demineralization and diffusion. Keep the coated surface free of contamination. Spread i-bond carefully with a 22

gentle stream of air until no movement of the adhesive film is detectable. Surface should be visibly glossy, both after application of i-bond and after evaporation of the solvent. Light activate for 20 seconds. Group II: Two-bottle One-step Self-etch Adhesive (Adper Prompt)

Dispense one drop of liquid A contained in one-bottle and one drop of liquid B contained in the second bottle into the mixing well; keep the bottles vertical to ensure equal drop size. Mix both components with a disposable applicator until a clear, yellowish solution without streaking results. Brush the adhesive onto the cavity surface, for a treatment surface of approximately 5 × 5 mm, massage it for 15 seconds applying pressure; longer massaging times are required for larger surfaces. The adhesive must be massaged over the entire surface, as this is the step in which the cavity surface is also etched, conditioned and covered with adhesive. Use a gentle stream of air to thoroughly dry the adhesive to a thin film. Rewet the brush tip with adhesive and apply a second coat, this coat does not need to be massaged into the surface. Again, use a gentle stream of air to thoroughly dry the adhesive to a thin film. Harden the adhesive with a light cure unit for 10 seconds. Group III: Two-bottle Two-step Self-etch Adhesive (AdheSE)

AdheSE primer is supplied in one-bottle and AdheSE bond in the second bottle. Apply AdheSE primer for 15 seconds and brush into the prepared dentin surface for another 15 seconds. A strong stream of air is used to disperse the excess primer. Immediately apply AdheSE bond. Without waiting, disperse the AdheSE bond with a very weak stream of air followed by light curing for a period of 20 seconds. Group IV: Etch and Rinse Adhesive (Prime and Bond NT)

Acid condition the cavity surface with 36% phosphoric acid and rinse with water. Following blot drying; dispense prime and Bond NT directly onto a fresh applicator tip. Immediately apply the adhesive thoroughly to wet all cavity surfaces. These surfaces should remain fully wet for 20 seconds and may necessitate additional application of mixed adhesive. Remove solvent by blowing gently with air from a hair drier for at least five seconds. The surface should have Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research a uniform, glossy appearance. Light cure for a period of 10 seconds. To protect the bonding layer, all the bonded surfaces were restored with 2 mm of resin composite (Z100 Restorative, Batch No. 800413, 3M) and cure for 40 seconds. The specimens were stored in normal saline. After 24 hours of storage the teeth were longitudinally sectioned using a slow speed diamond disc under a copious water supply. The sectioned surface was polished with a 600-grit silicon carbide paper. The dentin-adhesive interfacial region was examined using a CLSM. Results All the 60 specimens were bonded with four different adhesive systems namely one-bottle one-step self-etch adhesive (i-bond) - (Group I), two-bottle one-step self-etch adhesive (Adper prompt) - (Group II), two bottle 2-step self-etch adhesive (AdheSE) - (Group III) and etch and rinse (Prime and bond NT) – (Group IV). These specimens were sectioned and observed under CLSM. These images were automatically transferred Table 1. Length of Resin Tags Length of resin tag (µm) Samples

I-Bond Group I

Adper prompt Group II

AdheSE Group III

Prime and Bond Group IV

101.47

40.51

91.73

87.84

146.32

62.08

127.09

93.36

140.37

57.84

84.17

101.49

111.43

46.27

141.10

61.23

127.92

28.76

136.67

104.08

107.12

45.94

76.42

123.25

164.84

60.73

103.36

32.91

103.28

31.47

99.37

53.67

139.53

39.24

81.12

98.28

10.

140.37

52.13

103.14

34.59

11.

134.62

43.26

118.23

58.76

12.

156.25

71.42

127.71

75.04

13.

99.07

49.67

84.56

48.25

14.

106.29

68.01

56.04

81.63

15.

120.32

76.41

67.27

69.21

Mean ±

126.6133

51.5827

99.8687

74.9060

S.D

± 21.2763

± 14.2589

± 25.8574

26.7597

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

to Ultima Master Program Version 4.15 using Tagged Image File Format (TIFF) images. The length and depth of resin tags were evaluated. The results were tabulated and statistically analyzed. Mean and standard deviations were estimated from the sample for each study group. Mean values were compared by oneway ANOVA and multiple range tests by Tukey-HSD procedure was employed to identify the significant groups at 5% level. The lengths of resin tag of four adhesive systems are given in Table 1. The mean, standard deviation and test of significance of mean values between adhesive systems is given in Table 2. The length of resin tag, when compared within the group and among the groups, was found to be statistically significant (p < 0.05). Table 1 shows length of resin tags of four different bonding agents. Group I demonstrated values significantly higher (126.613) compared to Group III (99.686), Group IV (74.906) and Group I (51.582). Discussion Dentin, the fundamental substrate of restorative dentistry determines all restorative parameters along with preventive and disease processes affecting teeth. Its complex structure along with physical/chemical/ physiological relationships is so varied and unique such that a biologic restoration is next to impossible.7,8 Nevertheless, enormous amount of research is focused on understanding its characteristics, properties, histology and structure to develop a suitable restorative which may form a biologic composite.9,10 The fundamental principle of adhesion to dentin is based upon an exchange process by which inorganic tooth material is exchanged for synthetic resin. This process involves two phases; one phase consists of removing calcium phosphate by which microporosities are exposed on the surface of dentin. The other phase involves infiltration and subsequent in situ polymerization of resin within the micro-porosities resulting in hybridization.8,11 Using contemporary adhesives, this interchange of substance between the biomaterial and tooth tissues is carried out in either one, two or three clinical application steps. Consequently, generations of bonding agents have been recognized based on various clinical operatory parameters to accomplish the interchange. However, this classification in generations lacks scientific argumentation and does not permit the adhesives to 23

Original research be categorized-based on objective criteria. According to Van Meerbeek, adhesives can be classified into ‘etch and rinse’ systems which includes the fourth- and fifthgeneration bonding agents and ‘self-etch or no rinse’ systems which includes sixth- and seventh-generation bonding agents. The etch and rinse systems are still considered to be the most effective adhesives in achieving reliable and stable bond strength values. Hence, in most of the laboratory studies, the fifth-generation dentin bonding agents are considered to be the ‘accepted standard’ against which contemporary adhesives are evaluated. But as far as these etch and rinse systems are concerned, following etching, the dentin substrate should be properly dried to facilitate adequate penetration of adhesive resin monomers.5 In simple words, these systems pose a major limitation in the form of how ‘dry is dry’ and how ‘wet is wet’.5,6,12 The quest to overcome those ‘over dry’ or ‘over wet’ phenomena associated with etch and rinse systems resulted in the birth of ‘self-etch systems’. These systems avoid the rinsing and drying steps that may be critical in the hydrated state of etched dentin. Further, self-etched systems are supplied as ‘one-bottle’ and ‘two-bottle’ systems which involve either a ‘onestep’ or a ‘two-step’ technique.13 The adhesives chosen for the study include, one-bottle one-step adhesive (i-bond), two-bottle two-step adhesive (AdheSE), two bottle one-step adhesive (Adper prompt) that were compared with the etch and rinse adhesive (Prime and bond NT). CLSM analysis of hybrid layer and resin tags is a nondestructive evaluation, since the layer visualized can be upto 100 µm below the surface.14 Further, the drying of samples which is indispensable in conventional SEM and TEM is not necessary with CLSM leading to decreased risk of shrinkage or other drying artifacts.14,15 In the samples chosen the mid-coronal section of freshly extracted teeth was specifically selected as forms the domain for the maximum water retained area with respect to dentin structure, for the diameter of dentinal tubules in this area is around 1.2 µm.10 Moreover, the central portion of the mid-coronal dentin surfaces exhibit all their tubuli perpendicular to the surface.13 The ‘one-bottle one-step self-etch’ adhesive (i-bond) demonstrated the longest infiltration of resin tag as evident from Figure 1. This adhesive has urethane dimethacrylate (UDMA), 4-methacryloxyethyl 24

Figure 1. CLSM images of group i (i-bond).

trimellitate anhydrine (4-META), glutaraldehyde and acetone as its major components. Muskaard and Asmussen (1984) reported that glutaraldehyde and HEMA (hydroxyethyl methacrylate) employed as bonding components produced a chemical reaction with amino groups of dentin collagen resulting in a durable bond despite the presence of water.16 This paved the way that bonding agents could be used in the presence of dentinal fluids; if otherwise, the unavoidable humidity of dentinal and intratubular surfaces would prohibit composite resin adhesion capable of contrasting the polymerization contracture as supported by many researchers.1 4-META, another active ingredient of i-bond is the first acidic monomer that was developed. It consists of both hydrophobic and hydrophilic groups and promotes the infiltration of the monomer into the hard tissue.17 Nakabayashi et al demonstrated that addition of 4-META to the luting agent markedly enhanced its adhesion to etched enamel and dentin. Also, he first described the presence of hybrid layer when working with 5% 4-META in methacrylic acid (MMA), initiated by partially oxidized tri-n-butylborane (TBB) in the presence of polymethacrylic acid (PMMA) powder on vital human dentin.17,18 The pH of onebottle one-step self-etch adhesive (i-bond) is 1.6, which falls under the category of intermediary-strong self-etch adhesives. Van Meerbeek classified self-etch systems based on pH of the adhesive. Accordingly, selfetch systems that have a pH of 1 or below are labeled strong, pH of around 2 as mild and pH of around 1.5 as intermediary-strong. i-bond, being an intermediary strong adhesive result in a two-fold build up of the dentinal hybrid layer with a completely demineralized top layer and a partially demineralized base. Following Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research an intermediary-strong self-etch approach, the deepest region of the hybrid layer upto a maximum of 1 µm still contain hydroxyapatite, by which the transition of the hybrid layer to the underlying unaffected dentin is more gradual. These adhesives are more acidic than mild self-etch adhesives, by which better micromechanical interlocking is achieved at enamel and dentin. The residual hydroxyapatite at the hybrid layer base may still allow for chemical intermolecular interaction,11 which has been postulated to be advantageous compared to both strong and mild self-etch system. Further, Kanca et al (1998) stated that primers with either alcohol or acetone-based solvents appeared to act rapidly. He also found that water-based primers based on dried etched dentin surfaces appear to require longer application times than acetone or alcohol-based primers applied to wet-etched dentin surfaces.6 Earlier he also observed that in an acetone-based adhesive, acetone facilitated spreading of the primer over the water-coated surface, chasing the water and carrying primer resins into the dentinal surface. In yet another study comparing generic adhesives using different adhesives, the lowest bond strength values were obtained with water as the solvent,6 the highest when acetone was used as a solvent that was demonstrated from the values obtained depicted in Table 1. The ‘two-bottle one-step self-etch adhesive’ (Adper Prompt) resulted in the formation of shortest resin tags compared to all the groups as shown in Figure 2. Adper prompt self-etch, successor of the original prompt-L-pop adhesive, is composed of methacrylated phosphoric esters, BisGMA, initiators, stabilizers, water, HEMA and polyalkenoic acid. Ibarra and others (2002) suggested that the low bond strength obtained with this system may be due to incomplete

Figure 2. CLSM images of Group II (Adper Prompt).

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

infiltration of the acidic monomers and subsequent partial dissolution of the smear layer, thereby resulting in inconsistent performance in terms of achieving a quality bond.13,19 BisGMA, an ingredient of Adper prompt mixes poorly with water, resulting in the formation of an emulsion and during cure a BisGMA ‘sponge’ or BisGMA ‘droplet’ is formed depending on the geometry of the phase. Therefore, the presence of water will increase the pore size of sponge or increase the distance between the droplets affecting the resin-dentin interface to a large extent.4 Further, Adper prompt has been labeled as a strong self-etch adhesive, having a pH of 1 or below. Van Meerbeek suggested that high acidity would result in rather deep demineralization effects at the dentin surface. This defect can be visualized as ‘collagen expose’ resulting in the discoloration of nearly all hydroxyapatite as shown by Perdigao et al (2002).11 Consequently, the underlying bonding mechanism of strong self-etch adhesive is primarily diffusion based, wherein the diffusion is limited, resulting in a demineralized layer devoid of resin infiltration.11,13 DeMunch et al and others (2005) demonstrated that hybrid layer formed by Adper bond is substantially thinner. This insufficient adhesive infiltration could be attributed to the fact that penetration may have been hampered by an amorphous layer on top of the hybrid layer formed by the polyalkenoic acid copolymer component of the adhesive. Also, a lack of ‘rubbing’ may have caused the reduced penetration, as this can prevent local concentration of polyalkenoic acid. Tay and others (2002) demonstrated that the combination of acidic monomers, HEMA and water does not result in a uniform hydrophobic resin layer, but areas of incomplete polymerization and ‘hydrogel’ formation are present. These areas may then permit water fluxes within the hybrid layer and subsequently accelerate water sorption of the adhesive interface combined with degradation and extraction of resin components that could be detrimental to the bond integrity.13,19 (Hashimoto and others, 2000, Demunk and others 2003). A combination of all these factors, most probably resulted in the less optimal infiltration of the adhesive. AdheSE, a ‘two-bottle, two-step self-etch adhesive’ did produce pronounced resin tags as depicted from Figure 3. Its self-etch capacity is based on phosphoric 25

Original research acid acrylates compared to Adper prompt, which is based on methacrylate phosphoric esters.11,19 The constituents of the adhesive include a primer composed of phosphoric acid acrylate, bis-acrylamide, water, initiators, stabilizers and a bonding component composed of dimethacrylate HEMA and highly dispersed silicon dioxide, initiators and stabilizers. The presence of water/HEMA in AdheSE was found to have a deleterious effect on the dentin surface. In the presence of water, the HEMA molecules will not saturate the collagen mesh fast and efficiently because water will not evaporate as easily and completely as in the case of acetone/HEMA. Moreover, the water molecule will be retained and would thus compete for space with the HEMA molecule within the collagen network resulting in a lower HEMA density inside the collagen mesh.20 Secondly, the presence of water within the collagen would render HEMA to polymerize less efficiently, which would result in lower molecular weight of HEMA and weak interpenetrating network.2,14 Although, it is well-known that HEMA may stabilize the collagen network and improve the monomer diffusion, it is not hydrolytically stable and forms associates in concentrated solution which promotes its hydrolysis. Furthermore, it has to be considered that a high content of monofunctional monomers in the adhesive impair its polymerization rate. This may lead to a significant lower density of cross-linkage in the polymerized adhesive layer, which may result in weakened adhesive bonds, in particular, after storage and swelling in water.13 Also, Pashley et al (1998) showed that HEMA can dramatically lower the vapor pressure of water, i.e., as the concentration of HEMA increases there is a progressive decrease in the partial pressure of water. As the partial pressure drops, it becomes more and more difficult for residual water to be removed from the demineralized dentin.18,20,21 The pH of AdheSE is about 1.5 which is classified as intermediary-strong. When these adhesives are employed, the deepest region of the hybrid layer upto maximum of 1 µm still hydroxyapatite, by which the transition of the hybrid layer to the underlying unaffected dentin is more gradual. These adhesives are more acidic than mild-self-etch systems, by which enhanced micromechanical interlocking is achieved at the dentin interface.3 The residual hydroxyapatite at the hybrid layer base may still allow for chemical inter 26

Figure 3. CLSM images of Group III (AdheSE).

Figure 4. CLSM images of Group IV (Prime and Bond NT).

molecular attraction resulting in two-fold build up of the hybrid layer with a completely demineralized top layer and a partially demineralized base. This gradual transition compared to abrupt transition in the case of strong self-etch adhesives and etch and rinse adhesives could well explain the superior performance of intermediary-strong self-etch adhesives compared to both strong and weak11 as shown by values in Tables 1 and 2 related to both i-bond and AdheSE. The only etch and rinse system used in the study as the Table 2. Mean, Standard Deviation and Tests of Significance Mean Values of Length of Resin Tags among Different Study Groups Groups Length of resin tags

P value*

Significant # Groups at 5% level

Mean ± S.D I

126.613 ± 21.2763

51.582 ± 14.2589

III

98.868 ± 25.8574

0.000

74.906 ± 26.7597

< 0.001

I > III, IV & II

•One way ANOVA was used to calculate the p value. # Multiple range tests by Tukey-HSD procedure was employed to identify the significant groups at 5% level.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research

140

126.613

120 99.868

100 80

74.906

51.582

40 20 0

Control

Group II

Group III

Group I

Figure . CLSM study of resin tag formation comparing 1 step and 2 step self etching systems.

Figure . Confocal laser scanning microscope.

control, prime and bond N.T, demonstrated significant resin tags compared to Adper prompt, however, shorter in length than i-bond and AdheSE as evident from Figure 4. Perdigäo et al (1998) emphasized the superiority of acetone and ethanol over-water. The etch and rinse adhesives usually contain acetone or ethanol which can dislocate water from the dentin surface and from the moist collagen network, thus promoting the infiltration of resin monomers through the nanospaces of the dense collagen web, and enhancing bond strengths.22 This could probably be attributed to the formidable amount of resin tags exhibited by prime and bond NT. However, following etching and rinsing, dehydration of the etched dentin surface through air drying is through to induce surface tension causing the exposed collagen network to collapse, shrink and form a compact coagulate that is impenetrable to the resin ‘dry bonding phenomena’.23 The other alternative is not to over dry the rinsed acid etched dentin so as to keep the surface of the dentin moist and rely on the water chasing capacity of acetone-based primers as in the case of Prime Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

and Bond NT. This clinical technique is commonly referred to as ‘wet bonding’ and has been introduced by Kanca and Gwinnett in the early ‘90s. This ‘wet bonding’ phenomena has been shown repeatedly to enhance bond strength because water preserves the porosity of collagen network available for resin monomer inter diffusion. However, it should be emphasized that wet bonding technique can result in efficient resin interdiffusion, provided the residual water on the dentin surface is eliminated and replaced by monomers.6 The risk that all moisture on the dentin surface is not completely replaced by hydrophilic primer monomers is clinically real and documented as ‘over wetting phenomena’.24 In such over-wet conditions, excessive water that was incompletely removed during priming appeared to cause phase separation of the hydrophobic and hydrophilic monomer components resulting in blisters and globule formation at the resin-dentin interface. Such interface deficiencies undoubtedly weaken the resin-dentin bond. Consequently, wet bonding phenomenon is technique sensitive, especially in terms of the precise amount of moisture that should be retained after conditioning the dentin surface.6,24 Conclusion From the data obtained it may be concluded as follows: ‘One-bottle one-step self-etch’ adhesive (i-bond)  exhibited the longest and deepest infiltration of resin tags as compared to other systems. Yet another interesting finding observed was pH related, intermediary-strong (pH-1.5) was found to impart to the length and depth of resin tag formation to a significant extent. In general, acetone-based adhesives also contributed  significantly to the length and depth of resin tag formation. The above fact-findings may further be supported authentically by microtensile bond strength evaluation and long-term bonding evaluation studies based on clinical trials. Acknowledgement The authors are grateful to Dr N Geetha Priya, I year Postgraduate Student, Dept. of Conservative Dentistry and Endodontics, Sree Balaji Dental College and Hospitals, Chennai, for her sincere efforts in preparing the manuscript of the article.

Original research References 1. Van Meerbeek B, Perdigâo J, Lambrechts P, Vanherle G. The clinical performance of adhesives. J Dent 1998;26(1): 1-20. 2. Eick JD, Robinson SJ, Byerley TJ, Chappelow CC. Adhesives and nonshrinking dental resins of the future. Quintessence Int 1993;24(9):632-40. 3. Finger WJ. Dentin bonding agents. Relevance of in vitro investigations. Am J Dent 1988;1(2):184-8. 4. Jacobsen T, Söderholm KL. Some effects of water on dentin bonding. Dent Mater 1995;11(2):132-6. 5. De Munk J, Van Landuyt K, Poitevin A, Lambrechts P, Braem M, et al. A critical review of the durability of adhesion to tooth tissue: methods and results. J Dent Res 2005;84(2):118-32. 6. Kanca J 3rd. Wet bonding: effect of drying time and distance. Am J Dent 1996;9(6):273-6. 7. Marshall GW Jr. Dentin: microstructure and characterization. Quintessence Int 1993;24(9):606-17. 8. Eick JD, Robinson SJ, Cobb CM, Chappell RP, Spencer P. The dentinal surface: its influence on dentinal adhesion 2. Quintessence Int 1992;23(1):43-51. 9. Anusavice KJ. Phillips’ Science of Dental Materials. 11th edition, Elsevier, Missouri 2003:368-93. 10. Tencate AR. Oral histology, development, structure and function. Mosby Year Book. 3rd edition, 1994:105-7. 11. Van Meerbeek B, De Munck J, Yoshida Y, Inoue S, Vargas M, Vijay P, et al. Adhesion to enamel and dentin: Current status and future challenges. Oper Dent 2003;28(3):215-35. 12. Tay FR, Gwinnett AJ, Pang KM, Wei SH. Structural evidence of a sealed tissue interface with a totaletch wet-bonding technique in vivo. J Dent Res 1994;73(3):629-36. 13. De Munk J, Vargas M, Iracki J, Van Landuyt K, Poitevin A, Lambrechts P, et al. One-day bonding effectiveness of new self-etch adhesives to bur-cut enamel and dentin. Oper Dent 2005;30(1):39-49.

14. Watson TF. Application of confocal Scanning optical microscopy to dentistry. Br Dent J 1991;171(9): 287-91. 15. Watson TF. Facts and artifact in confocal microscopy. Adv Dent Res 1997;11(4):433-41. 16. Goracci G, Bazzucchi M, Mori G, Martinis L. In vivo and in vitro analysis of a bonding agent. Quintessence Int 1994;25(9):627-35. 17. Nakabayashi N, Ashizawa M, Nakamura M. Identification of a resin-dentin hybrid layer in vital human dentin created in vivo: durable bonding to vital dentin. Quintessence Int 1992;23(2):135-41. 18. Chang JC, Hurst TL, Hart DA, Estey AW. 4-META use in dentistry: a literature review. J Prosthet Dent 2002;87(2):216-24. 19. Sensi LG, Lopes GC, Monteiro S Jr, Baratieri LN, Vieira LC. Dentin bond strength of self-etching primers/ adhesives. Oper Dent 2005;30(1):63-8. 20. Pashley EL, Zhang Y, Lockwood PE, Rueggebrg FA, Pashley DH. Effects of HEMA on water evaporation from water-HEMA mixtures. Dent Mater 1998;14(1): 6-10. 21. Moszer N, Salz U, Zimmermann J. Chemical aspects of self-etching enamel-dentin adhesive-review. Dent Mater 2005;21(10):895-910. 22. Perdigäo J, May KN, Wilder AD Jr, Lopes M. The effect of depth of dentin demineralization on bond strengths and morphology of the hybrid layer. Oper Dent 2000;25(4):186-94. 23. Tay FR, Gwinnett JA, Wei SH. Relation between water content in acetone/alcohol-based primer and interfacial ultrastructure. J Dent 1998;26(2):147-56. 24. Tay FR, Gwinnet AJ, Wei SH. The overwet phenomenon: a scanning electron microscopic study of surface moisture in the acid-conditioned, resin-dentin interface. Am J Dent 1996;9(3):109-14. 25. Hashimoto M, Ito S, Tay FR, Sano H, Kaga M, Pashley DH, Fluid movement across the resin-dentin during and after bonding. J Dent Res 2004;83(11):843-8.

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CASE REPORT

Recurrent Chronic Suppurative Osteomyelitis: Review of Literature and Report of a Case Ramakrishna Shenoi*, Vrinda Kolte**, Samprati Badjate†, Vishakha Devrukhkar‡

Abstract Chronic suppurative osteomyelitis (CSO) of the mandible is often considered difficult to treat and may lead to refractory osteomyelitis. This case report describes the successful surgical treatment of CSO of the mandible in a 65-year-old man. Combined surgical and antimicrobial therapy was used to cure CSO of the mandible. Key words: Mandible, osteomyelitis, surgery, hyperbaric oxygen

hronic suppurative osteomyelitis (CSO) is a persistent abscess of the bone that is characterized by the usual complex of the inflammatory process, including necrosis of mineralized and marrow tissues, suppuration and resorption other than sclerosis and hyperplasia. It may result from odontogenic infection, postextraction complication, trauma or irradiation to the mandible. Pathogenic organisms are primarily streptococci (α-hemolytic) and oral anaerobes, particularly Peptostreptococcus, Fusobacterium and Prevotella, the organisms responsible for odontogenic infections.1,2 The typical age of presentation is in the fifties to the sixties, with males more likely to be affected. The commonest site is the posterior body of the mandible. Clinical findings may include local pain and swelling and trismus, but constitutional symptoms are unusual. Radiologic examination discloses radiolucent areas, bony destruction and sequestrum formation. Chronic mandibular osteomyelitis must be differentiated from malignant disease involving the mandible. Diagnosis is accomplished by history, biopsy and culture. CSO is often considered difficult to manage and has been reported to lead to pathologic fracture and even may entail resection of the affected part of the mandible;3 although several authors deduce that CSO can be treated successfully by a combination *Vice Dean and Professor **Professor † Reader ‡ PG Student Dept. of Oral and Maxillofacial Surgery VSPM Dental College and Research Centre, Nagpur E-mail: ijmdent@gmail.com

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

of intravenous antimicrobial therapy and surgery consisting of sequestrectomy or decortication.4-6 The recently advocated use of adjunctive treatment, such as hyperbaric oxygen,7-9 gentamycin or tobramycin beads and heparin streptokinase infusion,10 supposedly leading to better results, suggests a sizable number of refractory cases of CSO. Unfortunately, the total number of reports on the treatment of CSO patients is limited.8,9,11-14 The above mentioned treatment suggestions are often based on series of patients with limited information concerning the exact type of osteomyelitis (suppurative, nonsuppurative, sclerosing); the cause of the osteomyelitis (dentoalveolar infection, trauma, operative procedures); the extent of the lesion (limited to the alveolar process, diffuse) and follow-up. A further compounding factor in comparing reports on chronic osteomyelitis of the mandible is the definition of the classification ‘chronic’. CSO may develop after the acute phase, or without a preceding acute stage.15 According to some authors, osteomyelitis has to exist at least one month before one can classify it as chronic, thereby implying that the disease is refractory to host defences or to initial therapy.7,16 Other authors suggest two months7 or do not specify the duration of symptoms.9, 11 A problem in comparing the effectiveness of treatment in the reported series of CSO patients is the follow up. Since, chronic osteomyelitis may be dormant for long period of time, a follow-up of at least several months seems mandatory for reliable analysis of treatment results. Report of a Case A 65-year-old male patient reported to the Dental OPD of Dept. of Oral Surgery, VSPM’s Dental College and Research Centre, Nagpur, with the chief 29

Case Report complaint of painful swelling in lower left posterior region of jaw since six months. Pain was intermittent and pricking in nature. Swelling was single and diffuse which increased gradually to the present size of 4 Ă&#x2014; 2 cm (Fig. 1). Skin over the swelling was red and edematous tender on palpation, hard in consistency and fixed to the underlying bone. Swelling extended from the symphysis to left angle of mandible in horizontal direction and vertically from corner of mouth to lower border of mandible. Since one month, swelling was associated with pus discharge. Two sinus openings were present in lower border of mandible on left side, with pus discharge (Fig. 2). Sinuses were tender on palpation and fixed to underlying bone. The patient gave a past history of extraction of lower left first and second molar. Patient had similar complaint three years back for which he had undergone sequestrectomy. OPG was taken, which revealed moth eaten appearance of jaw, with small radio-opaque sequestra with

surrounding involucrum (Fig. 3). Considering the extent of disease, a decision was taken for resection of mandible from left side angle to right side lateral incisors followed by reconstruction with titanium reconstruction plate. The resected mandible was sent for histopathological investigations. Hematoxylin and eosin (H&E) staining showed necrotic bony trabeculae with chronic inflammatory cell infiltrate features suggestive of CSO. Postoperative recovery was uneventful (Figs. 4-6). Discussion In the literature on CSO of the mandible, several authors recognize resistance to therapy as an infrequent but possible problem.6,7 The amount of recently published adjunctive treatment modalities suggests, however, a substantial number of problematic cases ofÂ CSO.7-10

Figure 1. Initial presentation of the swelling.

Figure 3. Initial OPG showing the area of mottled radiolucency/radio-opacity.

Figure 2. Initial presentation of the cutaneous sinus.

Figure 4. Extraoral surgical site at one month review.

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Case Report

Figure 5. Extraoral surgical site at one month review.

Figure 6: OPG showing resection of mandible followed by reconstruction.

Regrettably, the methods of treatment as reported in the literature are not uniform, thus obscuring the real number of cases resistant to treatment. Several authors suggest treatment protocols consisting of a combination of surgery and antimicrobial treatment, but they report no results.3,6,7 In other reports, surgery and antimicrobial treatment are not always combined5,9 or the data are unclear.11,12 Surgical treatment includes a gamut of modalities from sequestrectomy and decortication to resection.3,13 The use of antimicrobial agents also differs widely. In Koorbusch13 series of 35 CSO patients, the number of different antibiotics used in a patient ranged from 1 to 5 with a mean of 2.3. The duration of treatment in this series was more than 60 days in 18 patients, and even more than 180 days in two patients. Topazian3 recommends continuing treatment for 2-4 months after resolution of symptoms, whereas Bartkowski et al,10 uses IV therapy for a period of 10-24 days. Antibiotic-impregnated Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

acrylic beads have been used in the treatment of osteomyelitis to deliver high concentrations of antibiotics into the wound bed and in immediate proximity to the infected bone.17-19 Antibiotics in high concentrations may also be placed in direct contact with the bone manually or with an implantable pump.20,21 As suggested in literature, the duration of the process, the formation of granulation tissue and the presence of sequestra in almost all cases make surgery mandatory with simultaneous IV antimicrobial therapy in the management of CSO of the mandible.4,7,22 The type of surgery depends on the extent of the osteomyelitic process. The aim of the surgery is to eliminate all infected and necrotic soft and hard tissue. Incomplete curettage and sequestrectomy leads to persistence of the disease, which may mistakenly be interpreted as resistance to therapy. In cases with limited osteolysis, a sequestrectomy must be performed, followed by elimination of dead space and primary closure of the wound. In more extensive cases, a decortication of the affected part of the mandible5 must be performed in order to remove all affected cortical bone and to facilitate debridement of the underlying cancellous bone. Another advantage of decortication is that the adjacent well-vascularized periosteum can be brought in close contact with the remaining vital bone. The use of hyperbaric oxygen is often described as an adjunct in refractory cases. However, hyperbaric oxygen therapy is expensive and requires specialized equipments which may not be available in all parts of developing countries, which acts as a deterrent for its use. It can be concluded that a protocol consisting of thorough surgical debridement of infected and necrotic tissue, supported by intravenous antimicrobial therapy for one week, followed by oral administration for three weeks, can lead to predictable, good results in cases of CSO of the mandible.23 References 1. Flynn TR. Anatomy and surgery of deep space infections of head and neck. In: Knowledge Update. Rosemont, Ill, 1993. American Association of Oral and MaxillofacialÂ Surgeons. 2. Peterson LJ. Microbiology of head and neck infections, Oral Maxillofac Clin North Am 1999;13:775. 3. Topazian RG. Osteomyelitis of the jaws. In: Oral and Maxillofacial Infections. 3rd edition, Topazian RG, Goldberg MH (Eds.), Saunders: Philadelphia 1994: 251-88.

Case Report 4. Groot RH. Diffuse sclerosing osteomyelitis of the mandible: infection or traction? Thesis. University of Amsterdam 1995:7-39.

15. Shafer WG, Hine MK, Levy BM. A Textbook of Oral Pathology. 4th edition, Saunders: Philadelphia 1983: 498-508.

5. Hjorting-Hansen E. Decortication in treatment of osteomyelitis of the mandible. Oral Surg Oral Med Oral Pathol 1970;29(5):641-55.

16. Mercuri LG. Acute osteomyelitis of the jaws. In: Oral and Maxillofacial Surgery Clinics of North America. Laskin D, Strass R, (Eds.), Saunders: Philadelphia 1991;3: 335-66.

6. Hudson JW. Osteomyelitis of the jaws: a 50-year perspective. J Oral Maxillofac Surg 1993;51(12): 1294-301. 7. Marx RE. Chronic osteomyelitis of the jaws. In: Oral and Maxillofacial Surgery Clinics of North America. Laskin D, Strass R, (Eds.), Saunders: Philadelphia 1991;3:367-81. 8. Calhoun KH, Shapiro RD, Stiernberg CM, Calhoun JH, Mader JT. Osteomyelitis of the mandible. Arch Otolaryngol Head Neck Surg 1988;114(10):1157-62. 9. Taher AA. Osteomyelitis of the mandible in Tehran, Iran. Analysis of 88 cases. Oral Surg Oral Med Oral Pathol 1993;76(1):28-31. 10. Bartkowski SB, Heczko PB, Lisiewicz J, DorozyĂąski J, Kurek M, KuĹ&#x203A;miderski J, et al. Combined treatment with antibiotic, heparin and streptokinase - a new approach to the therapy of bacterial osteomyelitis. J Craniomaxfac Surg 1994;22(3):167-76. 11. Adekeye EO, Cornah J. Osteomyelitis of the jaws: a review of 141 cases. Br J Oral Maxillofac Surg 1985;23(1): 24-35. 12. Daramola JO, Ajagbe HA. Chronic osteomyelitis of the mandible in adults: a clinical study of 34 cases. Br J Oral Surg 1982;20(1):58-62. 13. Koorbusch GF, Fotos R, Goll KT. Retrospective assessment of osteomyelitis. Etiology, demographics, risk factors and management in 35 cases. Oral Surg Oral Med Oral Pathol 1992;74(2):149-54. 14. Ragne A, Rood A. Osteomyelitis of the jaws. Int J Oral Surg 1978;7:523-7.

17. Chisholm BB, Lew D, Sadasivan K. The use of tobramycin-impregnated polymethylmethacrylate beads in the treatment of osteomyelitis of the mandible: report of three cases. J Oral Maxillofac Surg 1993;51(4):444-9; discussion 449-50. 18. Alpert B, Colosi T, van Fraunhofer JA, Seligson D. The in vivo behavior of gentamycin-PMMA beads in the maxillofacial region. J Oral Maxillofacial Surg 1989;47(1):46-9. 19. Grime PD, Bowerman JE, Weller PJ. Gentamycinimpregnated polymethylmethacrylate (PMMA) beads in the treatment of chronic osteomyelitis of mandible. Br J Oral Maxillofac Surg 1990;28(6):367-74. 20. Boda A. Antibiotic irrigation-perfusion treatment of chronic osteomyelitis. Arch Orthop Trauma Surg 1979;95(1-2):31-8. 21. Perry CR, Davenport K, Vossen MK. Local delivery of antibiotics via an implantable pump in the treatment of osteomyelitis, Clin Orthop 1988;(226):222-30. 22. Van Merkesteyn JP, Bakker DJ, Van den Wall I, Kussen GJ, Egyedi P, Van den Akker HP, et al. Hyperbaric oxygen treatment of chronic osteomyelitis of the jaws. Int J Oral Surg 1984;13(5):386-95. 23. Van Merkesteyn JP, Groot RH, Van den Akker HP, Bakker DJ, Brogmeijer-Hoelen AM. Treatment of chronic suppurative osteomyelitis of the mandible. Int J Oral Maxillofac Surg 1997;26(6):450-4.

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CASE REPORT

Gingival Abscess Revisited SC Chandrasekaran*, V Bagavad Gita**, P Preethi†

Abstract Aim: The aim of the present article was to critically evaluate the available literature regarding gingival abscess and highlight a case report. Background: Abscesses are one of the main causes for patients to seek emergency care in the dental clinic. This condition has clinical implications, not only diagnostic, but also, prognostic and therapeutic, in everyday periodontal practice. Case description: This case report especially highlights the prevalence of the use of inappropriate aids to remove impacted food. Conclusion and clinical significance: It becomes necessary that we bear this basic fact in mind when we come across such periodontal emergencies before we arrive at a conclusive diagnosis. Key words: Periodontal emergency, gingival abscess, matchstick

bscesses are one of the main causes for patients to seek emergency care in the dental clinic. Odontogenic abscesses include a broad group of acute infections that originate from the tooth and/the periodontium. Abscesses are associated with an array of symptoms, including a localized purulent inflammation, in the periodontal tissues which causes pain and swelling. Definitions Gingival Abscess

Acute inflammatory condition of the gingiva characterized by purulent exudates without attachment loss. Following traumatic insult: e.g., injury by a fish bone, tooth brush bristle, etc., implantation of virulent bacteria into the gingival connective tissue leads to excessive gingival inflammatory reaction. A gingival abscess was also defined as a localized purulent infection that involves the marginal gingiva or interdental papilla.1 Classification of Abscesses I.  Chronic/acute n Single/multiple n Gingival/periodontal *Professor and Head *Professor † PG Student III Year Dept. of Periodontics Sree Balaji Dental College and Hospital, Chennai E-mail: ijmdent@gmail.com

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II. Gingival abscesses in previously healthy sites and caused by foreign body impaction. n Periodontal abscesses are chronic or acute in relation to a periodontal pocket. n Pericoronal abscesses in incompletely erupted teeth.1 III. Based on etiology n Periodontitis related acute infection originates from bacteria present at the subgingival biofilm in a deepened periodontal pocket. n Nonperiodontal related abscesses when the acute infection originates from bacteria originating from another local source such as foreign body impaction, or from alteration in the integrity of the root leading to bacterial colonization. Impaction of foreign body in the gingival sulcus or periodontal pocket.2 Periodontal Abscesses in the Absence of Periodontitis Periodontal abscesses can also develop in the absence of periodontitis, due to the following causes:  Impaction of foreign bodies,3 such as an orthodontic elastic,4 a piece of dental floss,2 a popcorn kernel,5 a dislodged cemental tear,6 a piece of a toothpick, a corn husk in peri-implant tissues7 or an unknown object.8 Periodontal abscesses caused by foreign bodies, related with oral hygiene aids, have been named ‘oral hygiene abscesses’.  Perforation of the tooth wall by an endodontic instrument.9  Infection of lateral cysts; local factors affecting 33

Case Report the morphology of the root may predispose to periodontal abscess formation. The presence of cervical cemental tears has been related to rapid progression of periodontitis and the development of abscesses.6,10 The presence of external root resorption,11 an invaginated tooth,12 or a cracked tooth,13 have been also suggested as predisposing factors for periodontal abscess formation. Microbiology Review articles have pointed out that purulent oral infections are polymicrobial, and caused by endogenous bacteria.14 However, very few studies have investigated the specific microbiota of a gingival abscess. Hafstrőm et al15 reported a microflora harboring >106 total viable counts per sample. Topoli et al16 and Newman and Sims,17 reported that around 60% of cultured bacteria were strict anaerobes. It was further described that the most frequent type of bacteria were gram-negative anaerobic rods and gram-positive facultative cocci. In general, gram-negatives predominated over grampositives, and rods over cocci with percentages ranging between 40% and 60% for each group.

continuous with no specific aggravating and relieving factors. History revealed that he had pricked the area with a matchstick eight days ago while attempting to remove impacted food. On examination, there was a soft, fluctuant swelling in relation to 26, 27 with pus discharge. The swelling was 3 × 2 mm ovoid in shape, and confined to the marginal gingiva (Fig. 1). On palpation, there was pain and exudate. Intraoral periapical radiograph 26, 27 did not reveal any alterations in bone levels or periapical changes (Fig. 2). Considering the history, symptoms and clinical and radiographic findings, the lesion was provisionally diagnosed to be a gingival abscess. Differential Diagnosis  Acute gingival inflammatory enlargement  Periodontal abscess Management Antibiotics and anti-inflammatory drugs were prescribed. The patient was prescribed amoxycillin

Diagnosis The diagnosis of a gingival abscess is based on the symptoms revealed by the patient, and the signs found during the oral examination. Additional information can be obtained through a careful medical and dental history, and radiographic examination. The diagnosis of a gingival abscess is uncomplicated, as a gingival abscess is confined to marginal gingival tissues, often at previously nondiseased sites. It is often an acute inflammatory response to the impaction of a foreign body or material into the gingiva from the oral surface or from the gingival sulcus. The finding and retrieval of the offending foreign material is, thus, often diagnostic. The diagnosis of a gingival abscess can be made on the basis of a history of 1-2 days of pain and a localized gingival swelling and the clinical finding of a red, shiny swelling confined to the marginal gingival tissues.

Figure 1. Patient presenting with abscess in 26, 27 region.

Case Description A male patient aged 19 years, visited the Periodontics OPD of Sree Balaji Dental College, complaining of pain and swelling in the upper left back tooth region for the past three days. The pain was dull and 34

Figure 2. Intraoral periapical radiograph 26, 27.

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Case Report Discussion Odontogenic infections have various possible sources, including pulp necrosis, periodontal infections, pericoronitis, trauma or surgery.18 Odontogenic or dental abscesses have been defined according to their infection source, as endodontal or periapical abscess, periodontal abscess and pericoronal abscess.19 This nomenclature, however, is somehow confusing, since abscesses of pulp necrosis origin have been referred both as dental or periapical or dentoalveolar abscesses.20 Figure 3. Scaling and root planing done.

Figure 4. Impacted matchstick.

Figure 5. Postoperative picture after a week.

250 mg thrice-daily day and metronidazole 400 mg thrice-daily with ibuprofen 400 mg thrice-daily for three days. Supragingival scaling was done and scaling and root planing was done in relation to 26, 27 under local anesthesia (Fig. 3). During this procedure, the portion of the matchstick (3.5 cm) used to remove the impacted food was retrieved (Fig. 4). The patient was put on maintenance therapy after review was done (Fig. 5). Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Acute dentoalveolar abscesses have been termed as the most common infections in dentistry that demand emergency treatment.21 However, in order to render appropriate therapy, it is important to distinguish among abscesses of endodontal and periodontal origin.22 In nonperiodontitis-related abscesses, impaction of foreign objects and radicular abnormalities are the two main causes. In this case report, the foreign body impacted was a matchstick used to remove impacted food between 26, 27. Gingival abscess formation has also been reported following subepithelial connective tissue graft for root coverage.23 The abscess microflora seems to be similar to that of adult periodontitis, and it is dominated by gram-negative anaerobic rods, including wellknown periodontal pathogens. Complications and consequences include tooth loss and the spread of the infection to other body sites. Diagnosis and treatment is mainly based on empiricism, since evidence-based data are not available. The role of systemic antibiotics, in the treatment of periodontal abscesses, is especially controversial. Recently, a novel vaccine targeting Fusobacterium nucleatum inducing protective immunity provides an alternative option to conventional antibiotic treatments for chronic halitosis-associated with abscesses.24 Conclusion and Clinical Significance Thus, from the above article, it is evident that emergencies are not uncommon in periodontal practice. Eliciting a proper history with systematic clinical and periodontal examination is the key to successful diagnosis and management of periodontal emergencies. This case report especially highlights the prevalence of the use of inappropriate aids to remove impacted food 35

Case Report even among youth in a metropolitan city like Chennai. It is important to bear this basic fact in mind when we come across such periodontal emergencies before we arrive at a conclusive diagnosis. References 1. Carranza FJ. Glickman’s clinical periodontology. 7th edition WB Saunders Company: Philadelphia, 1990. 2. Haney JM, Leknes KN, Lie T, Selvig KA, Wikesjö UM. Cemental tear related to rapid periodontal breakdown: a case report. J Periodontol 1992;63(2):220-4. 3. Kareha MJ, Rosenberg ES, DeHaven H. Therapeutic considerations in the management of a periodontal abscess with an intrabony defect. J Clin Periodontol 1981;8(5):375-86. 4. Hafström CA, Wikström MB, Renvert SN, Dahlén GG. Effect of treatment on some periodontopathogens and their antibody levels in periodontal abscesses. J Periodontol 1994;65(11):1022-8.

12. Chen RJ, Yang JF, Chao TC. Invaginated tooth associated with periodontal abscess. Oral Surg Oral Med Oral Pathol 1990;69(9):659. 13. Trope M, Tronstad L, Rosenberg ES, Listgarten M. Darkfield microscopy as a diagnostic aid in differentiating exudates from endodontic and periodontal abscesses. J Endod 1988;14(1):35-8. 14. Yusof VZ, Ghazali MN. Multiple external root resorption. J Am Dent Assoc 1989;118:453-5. 15. Abrams H, Kopozyk RA, Gingival sequela from a retained piece of dental floss. J Am Dent Assoc 1983;106(1):578. 16. Pini Prato GP, Cortellini P, Clauser C. Fibrin and fibronectin system in a guided tissue regeneration procedure. A case report. J Periodontol 1988;59(10): 679-83. 17. Emslie RD. Some considerations on the role of cementum in periodontal disease. J Clin Periodontol 1978;5(1): 1-2.

5. Rada RE, Bronny AT, Hasiakos PS. Sickle cell crisis precipitated by periodontal infection: report of two cases. J Am Dent Assoc 1987;114(6):799-801.

18. Gill Y, Scully C. Orofacial odontogenic infections: review of microbiology and current treatment. Oral Surg Oral Med Oral Pathol 1990;70(2):155-8.

6. Topoll HH, Lange DE, Müller RF. Multiple periodontal abscesses after systemic antibiotic therapy. J Clin Periodontol 1990;17(4):268-72.

19. Liu PF, Haake SK, Gallo RL, Huang CM. A novel vaccine targeting Fusobacterium nucleatum against abscesses and halitosis. Vaccine 2009;27(10):1589-95.

7. Lewis MA, Meechan C, MacFarlane TW, Lamey PJ, Kay E. Presentation and antimicrobial treatment of acute orofacial infections in general dental practice. Br J Oral Maxillofac Surg 1990;28:359-66.

20. Newman MG, Sims TN. The predominant cultivable microbiota of the periodontal abscess. J Periodontol 1979;50(7):350-4.

8. Meng HX. Periodontal abscess. Ann Periodontol 1999;4:79-83. 9. Gill Y, Scully C. The microbiology and management of acute dentoalveolar abscess: views of British oral and maxillofacial surgeons. Br J Oral Maxillofac Surg 1988;26(6):452-7. 10. Goose DH. Cracked tooth syndrome. Br Dent J 1981;150(8):224-5. 11. Ibbott CG, Kovach RJ, Carlson-Mann LD. Acute periodontal abscess associated with an immediate implant site in the maintenance phase: a case report. Int J Oral Maxillofac Implants 1993;8(6):699-702.

21. van Winkelhoff AJ, Carlee A, de Graaff J. Bacteroides endodontalis and other black-pigmented Bacteroides species in odontogenic abscesses. Infect Immun 1985;49(3):494-7. 22. Tabaqhali S. Anaerobic infections in the head and neck region. Scand J Infect Dis 1988;57:24-34. 23. Vastardis S, Yukna RA. Gingival/soft tissue abscesses following subepithelial connective tissue graft for root coverage: report of three cases. J Periodontol 2003;74(11)1676-81. 24. Ishikawa I, Oda S, Hayashi J, Arakawa S. Cervical cemental tears in older patients with adult periodontitis. Case reports. J Periodontol 1996;67(1):15-20.

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CASE REPORT

Second Molar with Single Root and Single Canal Venugopal Naveenkumar*, Saravanan Poorni**, Dasarathan Duraivel**, Rajamani Indiraâ&#x20AC;

Abstract Molars demonstrate considerable anatomic complexities and abnormalities with respect to number of roots and root canals. This report presents, relatively uncommon clinical cases of maxillary and mandibular second molars with single root and single canal along with substantial data on the incidence of single canal in this tooth. Key words: Second molars, second molars with single canal, single rooted second molar

he variability of root canal system in molars poses a constant challenge to endodontic diagnosis and therapeutics. A thorough knowledge of internal and external anatomy, coupled with a correct diagnosis and appropriate cleaning and shaping of the root canal system, will lead to a successful treatment outcome.1 Slowey emphasized that root canal morphology was limitless in its variability and clinicians must be aware that anatomic variations constitute a formidable challenge to endodontic success.2 In the past years, the morphology of molars has been reviewed extensively. A survey of literature revealed that there is a wide range of variation in the number of canals in each root, number of roots and incidence of conical roots. Very few articles have reported the presence of second molars with single root and single canal. This clinical article presents a few cases of maxillary and mandibular second molars with single root and single canal. Case Report Case 1

A 40-year-old female patient reported to the Department of Conservative Dentistry and Endodontics at Ragas Dental College with the complaint of pain in the posterior left mandibular region for the past two weeks. *Senior Lecturer, Dept. of Conservative Dentistry and Endodontics, Karpaga Vinayaga Institute of Dental Sciences, Chennai **Senior Lecturer â&#x20AC; Professor and Head, Dept. of Conservative Dentistry and Endodontics, Ragas Dental College and Hospital, Chennai Address for correspondence Dr Saravanan Poorni Senior Lecturer Dept. of Conservative Dentistry and Endodontics Ragas Dental College and Hospital, 2/102, East Coast Road Uthandi, Chennai - 600 119 E-mail: poorniis@yahoo.com

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She gave a history of intermittent pain in the same region for the past three months. Her past medical history was found to be noncontributory. Clinical examination revealed a carious left mandibular second molar (37) with tenderness on percussion. The clinical findings, radiographic findings and vitality tests led to a diagnosis of irreversible pulpitis with acute apical periodontitis of the left mandibular second molar (37), necessitating endodontic therapy. Radiographic evaluation of the involved tooth indicated an unusual anatomy of conical root with a single canal (Fig. 1). The tooth was anesthetized using 2% lignocaine with 1:80,000 adrenaline and isolated using rubber dam. Endodontic access cavity was established. The pulp chamber frequently flushed with 5% sodium hypochlorite to remove debris and bacteria. Inspection of the pulp chamber revealed a single canal orifice in the center of the floor of the pulp chamber. Canal patency was checked with #10 K-file. Working length radiograph was taken (Fig. 2) and the presence of single canal was confirmed. Cleaning and shaping was performed using a step back technique

Figure 1. Preliminary radiograph showing single canal of left mandibular second molar (37).Â

Case Report with K files under abundant irrigation with 5% sodium hypochlorite solution in a 5 ml syringe and EDTA. The root canals were dried with paper points and obturated with cold, laterally condensed gutta-percha and AH plus resin sealer (Fig. 3). Case 2

A male patient with spontaneous pain in the second maxillary right molar (17) was seen. Endodontic treatment was indicated because of irreversible acute pulpitis. After anesthesia and rubber dam placement, crown access was performed and the coronal pulp tissue was removed, showing a single root canal opening at the center of the pulp chamber floor. The working length radiograph confirmed the presence of single root and single canal. Biomechanical preparation was performed using the step back technique K files under abundant irrigation with 5% sodium hypochlorite solution in a 5 ml syringe and EDTA. The root canals were dried with paper points and obturated with cold, laterally condensed gutta-percha and AH plus resin sealer (Fig. 4). Postoperative radiographs of three other mandibular and maxillary molars with single root and single canal treated in the department are shown in Figures 5-7.

Discussion A thorough understanding of root canal anatomy and morphology is essential for achieving high levels of success in endodontic treatment. Failure to recognize variations in root or root canal anatomy can result in unsuccessful endodontic treatment. As with most posterior teeth, the maxillary and mandibular second molars have several variants in its canal configurations. The standard description of the mandibular second molar is of two roots and two, three or four root

Figure 4. Postoperative radiograph of second maxillary right molar (17) showing single canal.

Figure 2. Working length estimation radiograph.

Figure 5. Radiograph of maxillary left second molar (27) showing completed root canal treatment.

Figure 3. Postoperative radiograph of mandibular left second molar (Note the single obturated canal).

Figure 6. Postobturation radiograph of right mandibular second molar (47).

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Case Report

Figure 7. Radiograph showing obturated right mandibular second molar (47).

canals and that of maxillary second molar is three roots and two, three or four canals. However, maxillary and mandibular second molars with a conical root and wide single root canal are also reported and the occurrence in mandibular molar is described more often than in the corresponding maxillary second molars.1 Weine et al in a study evaluated 75 human extracted second molars and found one tooth (1.3%) with one root canal.3 Hartwell et al reported that the incidence of single canal in maxillary second molar is 0.6%.4 More recently, Peikoff et al5 reported 3.1% of endodontically treated maxillary second molars with one root and canal. Tamse et al6 reported the occurrence of bilateral symmetry in 89.65% of cases with single conical rooted mandibular second molar. Sert et al7 in a study found that gender plays an important role in determining canal morphology and that both gender and ethnic origin should be considered during preoperative evaluation stage of root canal therapy. Manning et al8 in a study reported that Asians have a higher frequency of single rooted mandibular second molars. The morphological variant of single root and single canal is easily detected in routine radiographs. However, care should be taken to assess the correct anatomy on the preoperative radiograph to rule out the clinical condition of two roots, one buccal and one palatal that could be superimposed on the diagnostic radiograph.1 Careful inspection through angled radiographs (20º mesial or distal shift in horizontal angle) prior to and during endodontic therapy aids in identifying extra roots or canals. The incidence of canal bifurcation in a root is usually identified in radiographs using the ‘fast break’ guideline. Fast break guideline states that the sudden disappearance or narrowing of the canal infers the presence of canal division.9 An examination of the pulp chamber floor offers clues to the location of orifices and to the type of canal system present.

When only one canal is present, it usually lies in the centre of the root. A root always contains a root canal even though one is not visible on a radiograph and is difficult to locate and negotiate.9 Instrumentation is one of the key factors in the success of endodontic therapy; therefore, the clinician should be aware of all the anatomical variants and aberrant canal configurations. The clinician should then perform a thorough examination of the pulp chamber to insure complete debridement of all canals. This increases the chance for long-term successful endodontic therapy.10 Conclusion Ambiguity in the canal morphology of the second molars is quite common. An astute clinician always looks for canal variations. Knowledge of possible variations in the internal anatomy of teeth is important for successful endodontic therapy. References 1. Fava LR, Weinfeld I, Fabri FP, Pais CR. Four second molars with single roots and single canals in the same patient. Int Endod J 2002;33(2):138-42. 2. Slowey RR. Radiographic aids in the detection of extra root canals. Oral Surg Oral Med Oral Pathol 1974;37(5):762-72. 3. Weine FS, Pasiewicz RA, Rice RT. Canal configuration of mandibular second molar using a clinically oriented in vitro method. J Endod 1988;14(5):207-13. 4. Hartwell G, Bellizzi R. Clinical investigation of in vivo endodontically treated mandibular and maxillary molars. J Endod 1982;8(12):555-7. 5. Peikoff MD, Christie WH, Fogel HM. The maxillary second molar: variations in the number of roots and canals. Int Endod J 1996;29(6):365-9. 6. Tamse A, Kaffe I. Radiographic survey of the prevalence of conical lower second molar. Int Endod J 1981;14(3):188-90. 7. Sert S, Bayirili GS. Evaluation of the root canal configurations of mandibular and maxillary permanent teeth by gender in Turkish population. J Endod 2004;30(6):391-8. 8. Manning SA. Root canal anatomy of mandibular second molars. Part II. C-shaped canals. Int Endod J 1990;23(1):40-5. 9. Vertucci FJ. Root canal morphology and its relationship to endodontic procedures. Endod Top 2005;10(1):3-29. 10. Baugh D, Wallace J. Middle mesial canal of the mandibular first molar: a case report and literature review. J Endod 2004;30(3):185-6.

n Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

n 39

REVIEW ARTICLE

Finite Element Method in Orthodontics N Raj Vikram*, Y Mohamed Hashir*, MK Karthikeyan**

Abstract Finite element analysis (FEA) is a commonly applied experimental research technique which enables us to study the effects of geometrical and material variations under load and internal mechanical process. In the last decade the application of a well-proven predictive technique, the finite element method (FEM), originally used in structural analysis has revolutionized dental biomedical research. Key words: Finite element method, finite element analysis

n the field of dentistry a variety of sophisticated procedures and equipment are used, which are based on basic concepts of engineering. A composition of finite (countable) number of elements forms the basis for finite element analysis (FEA). It is a commonly applied experimental research technique which enables us to study the effects of geometrical and material variations under load and internal mechanical process. The analysis shows areas of internal stress concentration and consequently predictions can be made of possible failure. In the last decade the application of a well-proven predictive technique, the finite element method (FEM), originally used in structural analysis has revolutionized dental biomedical research. FEA was introduced originally as a method for solving structural mechanical problems, which was later recognized as a general procedure for numerical approximation to all physical problems that can be modeled by a differential equation description. FEA has also been applied to the description of physical form changes in biologic structures particularly in the area of growth and development and various branches of dentistry. FEM, which is an engineering method of calculating stresses and strains in all materials including living tissues has made it possible to adequately model the tooth and periodontal structure for scientific checking and validating the clinical assumptions. Melsen, Cattaneo, Dalstra1 in 2005 have illustrated FEM as a tool to study orthodontic tooth movement. *Senior Lecturer **Professor, Dept. of Orthodontics and Dentofacial Orthopedics Thai Moogambigai Dental College and Hospital, Chennai E-mail: ijmdent@gmail.com

Finite Element Method Finite analysis solves a complex problem by redefining it as the summation of the solution by a series of interrelated simpler problems. The first step is to subdivide (i.e. discretize) the complex geometry into a suitable set of smaller ‘elements’ of ‘finite’ dimensions when combined from the ‘mesh’ model of the investigated structures. Each element can adapt a specific geometric shape (i.e., triangle, square, tetrahedron, etc.) with a specific internal strain function. Using these functions and the actual geometry of the element, the equilibrium equations between the external forces acting on the element and the displacements occurring on its nodes can be determined (Figs. 1 and 2). Information needed by the software to perform the task/application:  Coordinates of the nodal points  Number of nodes for each element  Young’s modulus and Poissons ratio of the material modelled by different elements  The initial and boundary conditions  External forces applied on the structure The boundary condition of these models is defined so that all the movements at the base of the model are restrained. This manner of restraining prevents the model from any rigid body motion while the load is acting. The human tooth is highly irregular in shape, such that it cannot be represented in a two-dimensional (2-D), space and the actual loading cannot be simulated without taking the third-dimension (3-D) into Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article

(a)

Figure 2. A finite element tooth model with different parameters and zones of tooth material, enamel, filling material, root canal filling, dentine and cementum, cancellous bone and cortical bone, gingival. 



(b) 



(c)

Figure 1. (a) A 3-D FEM model of a central incisor; (b,c) FEM model of a tooth with surrounding periodontal ligament and alveolar bone.

consideration. The distribution of various materials of the tooth structure does not show any symmetry. Therefore, a 3-D modeling with the actual dimension must be preferred for a reliable analysis. Applications of FEM  FEA has been applied to the description of form changes in biological structures (morphometrics), particularly in the area of growth and development. Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

The knowledge of physiological values of alveolar stresses is important for the understanding of stress-related bone remodeling and also provides a guideline reference for the design of dental implants. FEM is also useful for structures with inherent material homogeneity and potentially complicated shapes such as dental implants. Analysis of stresses produced in the periodontal ligament when subjected to orthodontic forces. To study stress distribution in tooth in relation to different designs. To optimize the design of dental restorations. To investigate stress distribution in tooth with cavity preparation. The type of predictive computer model described may be used to study the biomechanics of tooth movement, whilst accurately assessing the effect of new appliance systems and materials without the need to go to animal or other less representative models.

Advantages of FEM  It does not require extensive instrumentation.  Any problems can be split into smaller number of problems.  It is an noninvasive technique.  3-D model of the object can be easily generated with FEM.  The actual physical properties of the materials involved can be simulated. 41

Review Article 



 

Reproducibility does not affect the physical properties involved. The study can be repeated as many times as the operator wants. There is close resemblance to natural conditions. Static and dynamic analysis can be done.

Disadvantages of FEM The tooth is treated as pinned to the supporting bone, which is considered to be rigid and the nodes connecting the tooth to the bone are considered fixed. This assumption will introduce some error however, maximum stresses are generally located in the cusp area of the tooth. The progress in the FEA will be limited until better defined physical properties for enamel, dentin and periodontal ligament and cancellous and cortical bone are available. FEM and Dentistry In the general field of medicine, FEM has been applied mainly to orthopedic research in which the mechanical responses of bony structures relative to external forces were studied. The first FEM study in dentistry appeared in 1974, where Farah and Craig2 did a finite element stress analysis in a restored asymmetric first molar. The application of this theory is relatively new in orthodontic research. It is the development of powerful mainframe computers with extensive memory and improved softwares that has now placed FEA in the hands of orthodontic researchers It has been shown that the FEM can be applicable to the problem of the strain-stress levels induced in internal structures. This method also has the potential for equivalent mathematic modeling of a real object of complicated shape and different materials. Thus, FEM offers an ideal method for accurate modeling of the tooth-periodontium system with its complicated 3-D geometry. The force systems that are used on an orthodontic patient can be complicated. The FEM makes it possible to analytically apply various force systems at any point and in any direction. It is very important to keep in mind that the FEM will give the results based upon the 42

nature of the modeling systems and, for that reason, the procedure for modeling is most important. FEM Studies in Orthodontics FEM has been broadly applied in orthodontic research. Yettram et al3 were amongst the first to employ a 2-D FEM of a maxillary central incisor to determine the instantaneous center of rotation of this tooth during translation. Halazonetis4 used a similar 2-D model to determine periodontal ligament (PDL) stress distribution following force application at varying distances from the center of resistance of a maxillary incisor. Using more complex 3-D models, McGuinness and Wilson et al,5 Tanne et al6 have studied moment to force ratios and stress distributions during orthodontic tooth movement. In the field of dentofacial orthopedics, finite element models has been employed to evaluate the stress distribution-induced within the craniofacial complex during the application of protraction headgear, orthopedic chin cup forces and conventional headgear forces.7,8 Mechanical Properties of Bone and FEM Bone is a living tissue that models and remodels throughout life, thus continuously changing its mechanical behavior. Moreover, a clear discrimination between cortical and trabecular bone is not a straightforward procedure especially in the transition areas. Having this in mind, it is anyway important to have a mathematical description (i.e., Young’s moduli and Poisson’s ratio) for both cortical and trabecular bone properties. In cortical bone, the osteons are aligned to the bone’s long-axis or in case of short-bones along the direction of forces, therefore, cortical bone exhibits a higher Young’s modulus. Cortical bone as well as trabecular bone has viscoelastic properties. This means that it has different values for ultimate strength and stiffness depending on the strain rate during loading. In addition to this the mechanical properties of the bone are also depend on age and thus the level of mineralization Tanne et al9 investigated stress distributions in the craniofacial complex by means of the FEA. An Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article orthopedic 1.0 kg force was applied on the first molars of the model in the anterior direction parallel to the occlusal plane. The model was restrained at the region around the foramen magnum, where no linear and angular displacements were allowed. Stress distributions produced only by an anteriorly directed force applied to the maxillary first molars were investigated. Large compressive stresses were found in the bones around the maxillofacial sutures in addition to tensile stresses in the maxillary bone. These biomechanical changes in the sutures were caused by counterclockwise rotation and upward displacement of the complex. They concluded that orthopedic maxillary protraction forces applied in more downward directions and/ or at more anteriorly located teeth may eliminate concomitant rotation of the skeleton and produce more efficient sutural modifications for subsequent maxillary growth and repositioning. These considerations will be effective in terms of normal maxillary growth direction. Singh and McNamara10 compared Class III and normal mandibular configuration for changes in size using FEM. For changes in shape, mandibular configurations were predominantly isotropic, with the exception of the anterior region in the Class III subjects. Incremental growth differences are consistent and concluded that the absence of physical restraint is associated with mandibular prognathism. Iseri et al11 evaluated the biomechanical effect of rapid maxillary expansion (RME) on the craniofacial complex by using a 3-D FEM of the craniofacial skeleton, based on computer tomography (CT) scans of the skull of a 12-year-old male subject. The CT pictures were digitized and converted to the finite element model. The mechanical response in terms of displacement and stresses was determined by expanding the maxilla upto 5 mm on both sides. High stress levels were observed in the canine and molar regions of the maxilla, lateral wall of the inferior nasal cavity, zygomatic and nasal bones, with the highest stress concentration at the pterygoid plates of the sphenoid bone in the region close to the cranial base. Dermaut et al used a â&#x20AC;&#x2DC;Patronâ&#x20AC;&#x2122; finite element processor and constructed 3-D FEM model of a dog skull to calculate bone displacements under orthopedic loads. 12

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Five different entities were distinguished: Cortical and cancellous bone, teeth, acrylic and sutures. Prior to construction of the FEM, an in vivo study was undertaken using the same dog. The initial orthopedic displacements of the maxilla and bone displacements of the maxilla were calculated and the results were compared with the in vivo measurements. Compared with the initial displacement measured in vivo, the value of the constructed FEM to simulate the orthopedic effect of extraoral force application was high for cervical traction and acceptable for anteriorÂ traction. Jafari et al13 analyzed the stress distribution patterns within the craniofacial complex during rapid maxillary expansion. The 3-D pattern of displacement and stress distribution was then analyzed. Maximum lateral displacement was 5.313 mm at the region of upper central incisors. The inferior parts of the pterygoid plates were also markedly displaced laterally. But there was minimum displacement of the pterygoid plates approximating the cranial base. Maximum forward displacement was 1.077 mm and was seen at the region of the anteroinferior border of the nasal septum. In the vertical plane, the midline structures experienced a downward displacement. The ANS and point A moved downward. The findings of this study provide some explanation of the concept of correlation between the areas of increased cellular activity and the areas of dissipation of heavy orthopedic forces. Therefore, the reason for the occurrence of sensation of pressure at various craniofacial regions, reported by the patients undergoing maxillary expansion could be correlated to areas of high concentration of stresses as seen in the study. Additionally, the expansive forces are not restricted to the intermaxillary suture alone but are also distributed to the sphenoid and zygomatic bones and other associated structures. FEM Studies on Tooth and Periodontium Studies have attempted to quantify periodontal properties during instantaneous tooth movement (Tanne, 1995; Volp et al., 1996).23 These studies have allowed the development of more clinically valid 3-D finite models of the tooth. Bobak et al14 used FEM to analyze theoretically the effects of a transpalatal arch (TPA) on periodontal stresses of molars that were subjected to typical retraction forces. They determined stress patterns 43

Review Article

Figure 3. FEM studies on effect of headgear on the tooth and tooth supporting structures.

Figure 4. FEM studies on stress levels on PDL and alveolar bone with different levels of alveolar bone height.17

and displacements with and without the presence of a TPA. Results suggested that the presence of a TPA has no effect on molar tipping, decreases molar rotations, and affects periodontal stress magnitudes by <1%. Results also suggest an inability of the TPA to modify orthodontic anchorage through modification of periodontal stresses.

occasions and five consistent readings were made this data was used to calculate the physical properties of the PDL. Tooth displacements ranged from 0.012 to 0.133 mm. The maximum strain located at the alveolar bone was 35 times less than that of the PDL (Fig. 4).

Tanne et al15 conducted a study to quantify the magnitude of tooth mobility in adolescents and adults, and to investigate the differences in the biomechanical response of tooth and periodontium to orthodontic forces. By integrating the differences in tooth mobility in both subject groups with analytical tooth displacements, the Youngâ&#x20AC;&#x2122;s modulus of the PDL was demonstrated to be greater in the adults than in the adolescent subjects. The differing biomechanical properties of the PDL in adults were demonstrated to result in almost equivalent or somewhat increased stress levels in the PDL in adult subjects. It suggested that this might produce a reduction in the biological response of the PDL and thus lead to a delay in tooth movement in adults.

FEMs has been applied to the evaluation of orthodontic attachment. Ghosh18 have used 3-D FEM models of ceramic orthodontic bracket designs to determine the stress distribution and likely mode of cohesive failure within the bracket when a full dimension stainless steel arch wire is engaged within the bracket slot.

Jones et al16 in their study developed a 3-D computer model of the movement of the maxillary incisor tooth when subjected to orthodontic load. This was to be used to validate the finite element-based computer model. The design took the form of a prospective experiment at a laboratory at the University of Wales. A laser apparatus, was used to sample tooth movement every 0.01 seconds over a one-minute cycle for 10 healthy volunteers, when a constant load of 0.39N load was applied â&#x20AC;&#x153;this process was repeated on eight 44

FEM Studies on Materials

FEM has been used to simulate en masse anterior teeth retraction in sliding mechanics by Tanaka M (Fig. 6). The degree of labiolingual tipping of the maxillary central incisor was calculated when the retraction force was applied to different heights of a power arm set mesial or distal to the canine. They concluded that the placement of the power arm of an archwire between the lateral incisor and canine enables orthodontists to maintain better control of the anterior teeth in slidingÂ mechanics. Katona and Moore19 have used a 2-D fine element model of the bracket tooth interface to assess the stress distribution in the system when bracket removing forces are applied. 3-D analysis using the FEM has been used to study M/F ratios of four different closing loops by Geramy20 and associates. They compared the forces, moments and moment/force (M/F) ratios of the opus loop, Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article

Figure 5. A FEM model to study and compare ratio constancy of three different loops designs.

Figure 6. 3-D model of the anterior teeth.22

L-loop, T-loop and vertical helical closing loop in a segmented arch (Fig. 5). The highest horizontal and vertical forces were produced by the L-loop with and without preactivation bends and in most cases the lowest forces were produced by the VHC loop. Loops with preactivation bends produced marked changes in the M/F ratio and loops without preactivation bends low, but relatively constant, M/F ratios over the full range of activation.

position and angulation of the miniscrew are changed. A tensile force of 2 N was applied to a miniscrew inserted between the lower first and second molars. The von Mises stresses along the buccal walls of the sockets of the first and second molars were derived following changes in miniscrew position and angulation. Results showed that when the miniscrew was inserted at right angles to the bone and midway between the molars, the stress in the crestal area was 0.093 MPa. This stress increased proportionally in the first molar socket as the miniscrew was moved towards the first molar and declined when the miniscrew was tipped towards the second molar. Stresses also decreased in the crestal area of the second molar as the miniscrew was moved towards the first molar, but increased when it was tipped towards the second molar.

A finite element model of an orthodontic bracket bonded to enamel with glass ionomer cement was developed by Katona et al. The loading on the model simulated tensile loading. The results indicate that peak stress values increase as the load deflection angulation increases. If the tensile load is inadvertently applied entirely on one wing of the bracket, the stress components nearly double in magnitude. Similarly, Rossouw and Tereblanche21 have used a simplified 3-D finite element model to evaluate the stress distribution around orthodontic attachments during debonding. Katona (1997) compared different methods of bracket removal and suggested that different loading methods resulted in significantly different stress patterns. In addition, peak stress concentrations were suggested to be responsible for attachment failure indicating that mean stress values were of little value in quantifying the quality ofÂ attachment. Geramy and associates studied stresses around a miniscrew (3-D analysis with FEM). They analyzed the stresses in the buccal walls of the sockets of lower molars adjacent to a miniscrew under load when the Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Conclusion In future with this proviso, computer models of various types can be used increasingly for fundamental biomechanics research in dentistry. They also provide an ideal â&#x20AC;&#x2DC;test-bedâ&#x20AC;&#x2122; for research and development of new materials for use in mouth. References 1. Cattaneo PM, Dalstra M, Melsen B. The finite element method: a tool to study orthodontic tooth movement. J Dent Res 2005;84(5):428-33. 2. Farah JW, Craig RG. Finite element stress analysis of a restored axisymmetric first molar. J Dent Res 1974;53(4):859-66. 3. Yettram AL, Wright KW, Pickard HM. Finite element stress analysis of crowns of normal and restored teeth. Acta Orthop Scand 1972;3:304-4.

Review Article 4. Halazonetis DJ, Computer experiments using a twodimensional model of tooth support. Am J Orthod Dentofacial Orthop 1996;109(6):598-606.

14. Bobak V, Christiansen RL, Hollister SJ, Kohn DH. Stress related molar response to transpalatal arch: a FEM study. Am J Orthod Dentofacial Orthop 1997;112(5):512-8.

5. McGuinness N, Wilson AN, Jones M, Middleton J, Robertson NR. Stresses induced by edgewise appliances in the periodontal ligament: a finite element study. Angle Orthod 1992;62(1):15-22.

15. Tanne K, Yoshida S, Kawata T, Sasaki A, Knox S, Jones ML. An evaluation of biomechanical response of the tooth and periodontium to orthodontic forces in adolescent and adult subjects. Br J Orthod 1998;25(2):109-15.

6. Tanne K, Koenig HA, Burstone CJ. Moment to force ratio and center of rotation. Am J Orthod Dentofacial Orthop 1998;94(5):426-31. 7. Tanne K, Hiraga J, Sakuda M. Effects of direction of maxillary protraction forces on biomechanical changes in the craniofacial complex. Eur J Orthod 1989;11(4):38291. 8. Tanne K, Kakiuchi K, Hiraga J, Yamagata Y, Sakuda M. Biomechanical effect of anteriorly directed extraoral forces on the cranial complex: a study using FEM method. Am J Orthod Dentofacial Orthop 1989;95(3):200-7. 9. Tanne K, Sakuda M. Biomechanical and clinical changes of craniofacial complex from orthopedic maxillary protraction. Angle Orthod 1991;61(2):145-52. 10. Singh GD, McNamara JA, Lozanoff S. Mandibular morphology in subjects with Class III malocclusions: Finite-element morphometry. Angle Orthod 1998;68(5):409-18. 11. IĹ&#x;eri H, Tekkaya AE, Oztan O, BilgiĂ§ S. Biomechanical effects of rapid maxillary expansion on the craniofacial skeleton, studied by the finite element method. Eur J Orthod 1998;20(4):347-56. 12. Verrue V, Dermaut L, Verhegghe B. Three-dimensional finite element modelling of a dog skull for the simulation of initial orthopaedic displacements. Eur J Orthod 2001;23(5):517-27. 13. Jafari A, Shetty KS, Kumar M. Study of stress-distribution and displacement of various craniofacial structure following application of transverse orthopedic forces: a 3D FEM study. Angle Orthod 2003;73(1):12-20.

16. Jones ML, Hickman J, Middleton J, Knox J, Volp C. A validated finite element method to study orthodontic tooth movement in human subjects. J Orthod 2001;28(1):29-38. 17. Geramy A. Initial stress produced in the periodontal membrane by orthodontic loads in the presence of varying loss of alveolar bone: a three-dimensional finite element analysis. Eur J Orthod 2002;24(1):21-33. 18. Ghosh J, Nanda RS, Duncanson MG Jr, Currier GF. Ceramic bracket design: an analysis using the finite element method. Am J Orthod Dentofacial Orthop 1995;108(6):575-82. 19. Katona TR. The effects of load location and misalignment on shear/peel testing of direct bonded orthodontic brackets: a finite element model. Am J Orthod Dentofacial Orthop 1994;106(4):395-402. 20. Safavi MR, Geramy A, Khezri AK. M/F ratios of four different closing loops: 3D analysis using the finite element method (FEM). Aust Orthod J 2006;22(2): 121-6. 21. Rossouw PE, Treblanche E. Use of finite element analysis in assessing stress distribution during debonding. J Clin Orthod 1995;29(11):713-7. 22. Tominaga JY, Tanaka M, Koga Y, Gonzales C, Kobayashi M, Yoshida N. Optimal loading conditions for controlled movement of anterior teeth in sliding mechanics. Angle Orthod 2009;79(6):1102-7. 23. Andersen KL, Pedersen EH, Melsen B. Material parameters and stress profiles within the periodontal ligament. Am J Orthod Dentofac Orthop 1991;99(5):427-40.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original RESEARCH

Mineral Loss before and after Bleaching and Mineral Uptake on Application of Remineralizing Agent Poornima Jose*, Malathi Suresh*, S Kavitha†, S Mahalaxmi‡

Abstract The use of tooth bleaching agents has increased recently, with carbamide peroxide being most commonly used. Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) is a nanocomplex of calcium, phosphate and hydroxyl ions stabilized by phosphopeptides. This agent is commonly used for the remineralization of enamel lesions. The basis of this in vitro study was to analyze remineralization potential of two remineralizing agents like casein phosphopeptide stabilized amorphous calcium phosphate (CPP-ACP) and amorphous calcium fluoride phosphate (CPP-ACFP) on enamel after bleaching with 10% carbamide peroxide along with the mineral loss and uptake with the help of a X-ray diffractometer (XRD). Key words: Demineralization, remineralization, nanocomplex

he use of tooth bleaching agents has increased recently, with carbamide peroxide (CO[NH2]2. H2O2) being a commonly used bleaching material. The use of carbamide peroxide at 10% was first used by Haywood and Heyman (1989).1 Carbamide peroxide is commonly used at a concentration of 6-35% w/v which in water/saliva produces hydrogen peroxide (H2O2 -2 to 12% w/v) and urea.2,3 Tooth sensitivity is a common side effect of vital tooth bleaching and demineralization of dental structures has been reported due to low pH of some of these materials.4 An in vitro study reported that hydrogen peroxide penetrates enamel and dentin and enters the pulp chamber during bleaching therapy.5 Casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) is a nanocomplex of calcium ions, phosphate ions and hydroxide ions stabilized by casein phosphopeptides. One of the systems developed for remineralization of enamel lesions uses casein phosphopeptide to stabilize calcium and phosphate ions at high concentrations as CPP-ACP and CPP amorphous calcium fluoride phosphate (CPP-ACFP). The CPP allows high concentrations of calcium, phosphate and fluoride ions to be stabilized in a *Postgraduate Student † Professor ‡ Professor and Head Department of Conservative Dentistry and Endodontics SRM Dental College, SRM University, Chennai Address for correspondence Dr Malathi Suresh Old No: 82, New No: 34, Arunachalam Street Chintadripet, Chennai - 600 002 E-mail: malu.dr2008@yahoo.com

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

metastable solution in a form that is bioavailable for the promotion of remineralization.6 Tooth Mousse crème containing 10%, CPP-ACP has been widely used to decrease sensitivity. Aim To analyse the mineral loss on tooth samples after bleaching with 10% carbamide peroxide and the mineral uptake by the tooth on using two remineralizing agents like stabilized amorphous calcium phosphate (CPP-ACP) and amorphous calcium fluoride phosphate (CPP-ACFP). Material and Methods Thirty noncarious, extracted single rooted central incisors were used for the study (n = 30). All the teeth had an average cervicoincisal length of 10.5 mm and mesiodistal diameter of 8.5 mm. The crown portion of the tooth was used and the palatal surface of the tooth was smoothened to give a near flat surface. The initial mineral content of all the teeth were analyzed with the X-ray diffractometer (XRD). Ten specimens served as controls and the remaining 20 were exposed to the bleaching agent, 10% carbamide peroxide for 52 hours at 37°C and the preparations were changed every four hours. The mineral content of all the specimens were again analyzed using the XRD. Now the specimens were randomly divided into two groups of 10 teeth each and the remineralizing agent was applied according to the manufacturer’s instructions. 47

Original research Group I

Tooth Mousse crème was applied, containing 10% CPP-ACP an left for 20 minutes. Group II

Tooth Mousse plus containing CPP-ACFP was applied and left for 20 minutes. The mineral content of all the 20 specimens were analyzed using the XRD. Statistical analysis was done using ANOVA and post-Hoc tests. Results After bleaching with 10% carbamide peroxide the tooth samples showed a decrease in the mineral content. There was complete loss of fluoride and fluorapatite. On application of the remineralizing agent, both Group I and Group II showed an increase in all the minerals analyzed. But on statistical analysis Group II was found to be more statistically significant (p < 0.05). Discussion Tooth enamel is the most highly mineralized body tissue with minerals constituting 96% of the enamel, the rest being water and organic material. The primary mineral component is hydroxyapatite, with the basic formula: Ca10(PO4)6(OH)2. The organic portion of enamel does not contain collagen, as dentin and bone do.7 Tooth discoloration varies in etiology, appearance, localization, severity and adherence to tooth structure. Exposure to high levels of fluoride, tetracycline administration, developmental disorders, trauma and pulpal necrosis are the main causes for intrinsic discoloration. Various bleaching agents like sodium perborate, carbamide peroxide, hydrogen peroxide, etc. are used for the treatment of tooth discoloration. In this study, 10% carbamide peroxide was used as the Control Bleached CPP-ACP Group I CaPO4 8.42% 1.23% 3.81% 3.56% 0 0 Fluoride 5.23% 0 1.23% CaFPO4 4.67% 1.08% 1.23% CaF2 Ca(OH)2 3.41% 2.23% 3.56% 0 1.02% Fluorapatite 6.67%

CPP-ACFP Group II 2.67% 3.82% 2.54% 3.61% 6.89% 4.43%

bleaching agent. Carbamide peroxide is a commonly used tooth bleaching agent at a concentration of 6-35% w/v (H2O2 -2 to 12% w/v) which in water/ saliva produces hydrogen peroxide and urea,3 which in turn breaks down producing water, oxygen, carbon dioxide and ammonia. This results in concomitant slight lowering of pH of the bleaching agent. This reduction in pH would affect the dissolution of the mineral content of enamel. Hydrogen peroxide is a strong oxidant that produce oxygen free radicals and the perhydroxyl ion (HO2– ) to chemically change (bleach) stained organic molecules (chromophores).3 Bleaching results in demineralization, i.e., the calcium/phosphate ratio of dentin is significantly decreased by bleaching with 10% carbamide peroxide. The dissolution of enamel in an acid occurs as a result of the interaction of hydrogen ions and hydroxyapatite:7 Ca10(PO4)6(OH)2 + 8H+

10Ca2+ + 6HPO42- + 2H2O Quantification of the phosphate group in hydroxyapatite therefore seems to be a good indicator of the degree of remineralization of enamel and was thus done in this study.7 In this study, the two remineralizing agents used were, CPP-ACP and CPP-ACFP. According to a study,6 when CPP-ACP and CPP-ACFP were used as remineralizing agents, the highest positive correlation between remineralization rate and ion activity gradient were for the species CaF+ and H2PO4-. The ions CaF+ and H2PO4- are in equilibrium with the neutral ions CaHPO40 and HF0 through the reaction: CaF+ + H2PO4-

CaFH2PO40

CaHPO40 + HF0

Therefore, it was concluded that the neutral ion species CaHPO40 and HF0 had significance in the remineralization of enamel lesions. Both of these species have no charge and therefore their diffusion into the lesion would not be impeded by the charged enamel surface. Remineralization of enamel subsurface lesions involves diffusion of ions through the lesion’s surface layer and Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Original research then deposition of the ions into crystal voids of the demineralized enamel of the lesion. The correlation of the neutral ion CaHPO40 activity gradient with the rate of remineralization suggests that it is the diffusion of ions into the subsurface lesion that is the ratelimiting step in subsurface lesion remineralization as the diffusion of charged ions through a charged surface layer would be impeded relative to the neutral ion.6 The neutral ions, which are in equilibrium with charged ions will dissociate to form charged species (Ca2+ and PO43-) for crystal growth. According to the results of this study, both Group I and Group II showed an increase in the mineral content on application of a remineralizing agent. But when comparing Group I and Group II, Group II showed an increase in the mineral content. This can be attributed to the fact that fluoride is a known promoter of remineralization as it thermodynamically favors crystal growth.8 The presence of fluoride in the CPP-ACFP solutions coupled with the low pH increases the activity of the neutral species HF0. The increased activity of HF0 would allow greater penetration of fluoride into the lesion to accelerate crystal growth6 therefore accounting for the significant difference between CPP-ACP and CPP-ACFP remineralization. The study also showed an increase in the calcium hydroxide and calcium fluoride content on application of CPP-ACFP. According to a study, topical application of fluoride is known to produce a threelayered structure consisting of fluorapatite, calcium fluoride and calcium hydroxide as reaction products.9 Calcium hydroxide is known to have an antimicrobial effect and a potential for inducing remineralization. Therefore, increased amounts of CaF2 and Ca(OH)2 indicates increased remineralization.9

Conclusion Within the limits of this in vitro study, it can be concluded that application of CPP-ACFP as a remineralizing agent is better than CPP-ACP in reducing postbleaching tooth sensitivity. References 1. Haywood VB, Heymann HO. Nightguard vital bleaching. Quintessence Int 1989;20(3):173-6. 2. Joiner A. The bleaching of teeth: a review of literature. J Dent 2006;34(5):412-9. 3. Manton DJ, Bhide R, Hopcraft MS, Reynolds EC. Effect of ozone and Tooth Mousse on the efficacy of peroxide bleaching. Aust Dent J 2008;53(2):128-32. 4. Lewnstein T, Hirschfeld Z, Stabholz A, Rostein I. Effect of hydrogen peroxide and sodium perborate on the microhardness of human enamel and dentin. J Endod 1994;20(2):61-3. 5. Thitinanthapan W, Statmanont P, Vongsavn N. In vitro penetration of the pulp chamber of three brands of carbamide peroxide. J Esthet Dent 1999;11(5):259-64. 6. Cochrane NJ, Saranathan S, Cai F, Cross KJ, Reynolds EC. Enamel subsurface lesion remineralization with casein phosphopeptide stabilized solutions of calcium, phosphate and fluoride. Caries Res 2008;42(2):88-97. 7. Santini A, Pulham CR, Rajab A, Ibbetson R. The effect of 10% carbamide peroxide bleaching agent on the phosphate concentration of tooth enamel assessed by Raman spectroscopy. Dent Traumatol 2008;24(2): 220-3. 8. Ten Cate JM, Van Loveren C. Fluoride mechanisms. Dent Clin North Am 1999;43(4):713-42. 9. Gerth HU, Dammaschke T, Schafer E, Zuchner H. A three layer structure model of fluoridated enamel containing CaF2, Ca(OH)2 and FAp. Dent Mater 2007;23(12):1521-8.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

REVIEW Article

Dental Implants in Children and Adolescents Santhosh Kumari*, Mamta Harilal Nichani**, Vishnu Rekha C†, Vijaya Prabha K**, Hariharan VS**

Abstract Children and adolescents often require prosthodontic rehabilitation for the restoration of edentulous areas which could be due to congenitally missing teeth and teeth lost due to trauma. These children are usually treated with removable prosthesis considering the fact that skeletal and dental growth and development is not completed and this treatment modality can lead to residual alveolar resorption, periodontal problems and increased risk of dental caries. The concern of placing implants in growing children is jaw growth. An osseointegrated implant behaves like ankylosed teeth and fails to move with surrounding structure leading to infraocclusion. When a choice is made to place the implant in growing children it should be closely monitored and implant prosthesis should be designed to accommodate the growth and development. This article is a review on placement of implants in children and effect of growth and development on implants. Key words: Implants in children, growth and development, trauma, osseointegration, ankylosed teeth

sseointegrated implants have been successfully used in dentistry for adults since the discovery of implants by Bränemark in 1969.1 In adults, the success depends on the quality and quantity of bone and proper treatment plan, surgical technique and proper oral hygiene measures. These factors are also equally important in growing children but another critical factor that has to be considered is the ongoing growth and development in children and adolescents.2 Teeth loss due to trauma and congenitally missing teeth are often encountered in young children and removable prosthesis, Maryland bridge or orthodontic movement of teeth to close space are usually the treatment modalities in such patients because jaw 3 growth is not completed. However, these options may lead to increased caries rate, increased residual alveolar resorption and other periodontal complications.4 Implants can be a good alternative because it can prevent residual alveolar resorption. Other factors that favors early placement of implants in children would include excellent local blood supply, positive immunological resistance, uncomplicated osseous 5 healing. When restoring the edentulous space in young children and adolescents using implants, the basic knowledge of growth and development is *PG Student **Senior Lecturer † Reader Dept. of Paedodontics Sree Balaji Dental College and Hospital, Chennai E-mail: ijmdent@gmail.com

essential to assess the implants’ response to craniofacial growth. Implants behave like ankylotic teeth and fail to move together with the surrounding structures leading to infraocclusion of implants and difficulties with prosthesis.3 This article will discuss current status of using implants in growing children and its effect on growth and development. Growth and Development A basic knowledge of facial growth is critical in assessing how an implant may respond in the adolescent. An osseointegrated implant behaves like an ankylosed primary tooth because both lack a periodontal ligament. The periodontal ligament has an important function in allowing teeth to erupt and adapting for dentoalveolar and facial growth, not only vertically but also in anteroposterior and transverse dimensions.6 Early animal studies have shown that osseointegrated implants remain fixed in their initial position and cannot adapt for growth changes.7,8 Growth of the Jawbones Growth is first completed in the transverse plane then in sagittal plane and finally in vertical plane. The growth of mandible is closely associated with general body growth, whereas growth of the maxilla is more associated with the growth of the cranial structures. As a rule of thumb, which applies to both the maxilla and mandible, transverse growth is first completed before the pubertal growth spurt and is followed by Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article growth in length and finally growth in height, which 9 is completed last. Maxillary Growth and Implants Transverse Growth

During early childhood, the transverse growth of the maxilla is influenced by the increasing width of the cranial base. Growth in width of the median palatal suture accelerates at puberty and is the most significant factor in transverse growth of the maxilla. Transverse growth is the earliest of the three-dimensional growth completed in adolescence.2,10 The median suture is critical in normal growth. Voss and Freng11 surgically created submucous midpalatal clefts in growing cats and found a significant decrease in both maxillary and mandibular widths as compared to controls. Freng found that on extirpation of midpalatal suture during growth resulted in a significant decrease in maxillary width, with 52% of the children having dental crossbite.11 Thus, the midpalatal suture is an important growth site that must be allowed to grow undisturbed. Any implant prosthesis must not restrict growth in this important adaptive area.10,12 Implants placed in the central incisor region will result in diastema with the adjacent natural teeth and shift in the midline.10,13 Sagittal Growth

The maxilla usually grows in a downward and forward direction relative to the anterior cranial base. Although the initial growth is related to growth of cranial base, the maxilla shows much greater changes from age 4 to adulthood than does the cranial base.10,13 Maxillary growth occurs as a result of both passive displacement and enlargement. During early childhood, passive growth is a major factor in a maxillary growth but becomes less important as anterior sutures of the cranial base closes. After the age 7, approximately one-third of the maxillary growth is accounted for passive displacement. The other two-third occurs as a result of enlargement of maxilla itself.14 Resorption in anterior region will result in gradual loss of bone in the labial aspect of the implants resulting in labial fenestration and exposure of implants.10 Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Vertical Growth

Vertical growth of the maxilla occurs by sutural lowering i.e., passive displacement of maxilla and apposition on the tooth-borne surfaces of the maxillary alveolus. The orbit enlarges with increasing eye size with compensatory apposition at the floor of the orbits. The nasal floor is lowered by resorption on its nasal surface and by deposition on the palatal and alveolar surface. Hence, as the alveolus increases in height by apposition on its occlusal aspect, it is simultaneously decreased by resorption at the nasal floor. Approximately one-third of the total increase in alveolar height is accounted by nasal resorption. Therefore, observation from dental casts reflects less than two-thirds of the total amount of vertical alveolar growth. Resorptive lowering of the nasal floor is strongly differentiated and is usually greater anteriorly than posteriorly. This differential pattern is a compensation for the rotational displacement of the maxilla in which the posterior segments roll downwards at a greater rate than the anterior segments. Vertical maxillary skeletal growth dramatically affects implants.10,13 To prevent the complication in the vertical growth due to remodeling it is advisable to delay the placement of implant will 18 years or till growth is completed. Mandibular Growth and Implants The timing of mandibular growth is similar to that of maxilla but not identical. The differential growth of mandible converts the convex profile of child into a straight profile in adults.10,12 Transverse Growth

Changes in the width of the mandible are much less than in the maxilla. The increase in the width of the mandible occurs primarily in the posterior region of the mandible. As the mandible increases in length, it also increases in posterior width because of its V-shape. The width in the anterior mandible ceases due to early closure of mandibular symphysis (around 1-year). Thus, mandibular anterior width stabilizes relatively early and increases only slightly by appositional growth, whereas mandibular posterior width increases with the increasing length of the mandibular body.10,14 Implants can be placed in anterior mandibular region at an early age. But implants in mandibular posterior 51

Review Article region of growing children will result in lingual position due to bone remodeling in premolar molar region.10,13

creating a deviation of the erupting adjacent teeth, or were lost because of bone resorption.7

Sagittal Growth

Endosseous Implants in Children and Adolescents with Ectodermal Dysplasia

Changes in arch length in the mandible differ from those in the maxilla. As the permanent incisors erupt, there is generally little or no change in mandibular arch length. Sagittal growth of mandible is due to both endochondral growth and remodeling of bone. The growth of the condyle results in increase in the length of mandible. To accommodate posterior teeth, the body of the mandible increases in length by resorption on anterior aspect of ramus and deposition on the posterior aspect. An implant placed in early age will result in exposure of an implant due to pattern of resorption.14 Vertical Growth

Mandibular growth increases by condylar growth and by bone apposition at dentoalveolar complex. When serial lateral cephalograms are superimposed on the cranial base, the mandible appears to grow downward and forward. Bjork however, using metallic implants as stable landmarks for serial cephalometric superimposition, found that during puberty the mandible does not necessarily grow downward and forward in a linear manner. Instead, the mandible rolls forward, with apposition below the symphysis and resorption below the gonial angle. Thus, during growth, the face and the mandible tend to rotate, with the center of rotation influenced by the direction of condylar growth.15 Animal Studies Animal studies were done by various authors to find out the behavior of implants on growing jaws. Odman et al 19913 developed an animal model to determine whether implants placed in a growing child behave as normally erupting or ankylosed teeth during the dynamic phase of growth. Implants that integrated in the mandible became displaced to stand lingually in the alveolar process; implants placed in the maxilla endedup palatally off the alveolar crest. The implants seemed to retard growth of the alveolar process and changed the eruption path of tooth germs located distal to the inserted implants. Another study by Thilander et al 19927 stated that osseointegrated implants in pigs remained stable in space and either became buried in alveolar bone, 52

Ectodermal dysplasia is an inherited disorder in which at least two structures derived from the ectoderm are abnormal. Kearns et al 199916 did not find evidence of restriction to transverse and sagittal growth due to implant use in children with ectodermal dysplasia. Endosseous implants can be successfully placed and can provide support for prosthetic restoration in patients with hereditary ectodermal dysplasia. However, vertical dentoalveolar growth results in submergence of the implant relative to the adjacent natural dentition when implants are placed adjacent to erupting permanent teeth. Prosthesis remodeling was necessary is some patient secondary to implant submergence. Another study by Bergendal et al 199617 concluded that implants must be placed when growth is almost completed, except for rare cases of total aplasia, as ectodermal dysplasia. Elsewhere, it has been recommended that treatment with implant must be delayed until the age of 1, since an implant placed at age 7 or 8 may not be in a favorable position at age 16.17 Johnson et al 2002 in his analysis of craniofacial development in children with hypohidrotic ectodermal dysplasia with and without endosseous implants concluded that craniofacial morphology did not differ significantly between implant-treated and nontreated ectodermal dysplasia children. This suggested that treatment with intraosseous dental implants, as applied in this population, did not reduce normal craniofacial growth and development.18 Recommendations for Implant Placement Specific recommendations can be made for the placement of dental implants in the growing patient.4 Maxillary Anterior Region

The maxillary anterior region is an important area for consideration because frequent congenital tooth absence and traumatic tooth loss are often encountered in this area. The vertical and anteroposterior growth changes in this area are substantial, and for esthetic and functional reasons implant placement should be delayed until growth is completed in this region. Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article The vertical growth of the maxilla exceeds all other dimensions of growth in this region; therefore, premature implant placement can result in the repetitive need to lengthen the transmucosal implant connection resulting in poor implant-to-prosthesis ratio and the potential for load magnification. Premature placement of an implant near the  midline can create a mesiodistal spatial disharmony secondary-to-median sutural growth, which accelerates at puberty. The placement of implants in the anterior maxillary  region before age 15 in female patients and age 17 in male patients should be attempted only to achieve unique treatment planning goals and with particular emphasis on the determination of skeletal age, informed consent and the possibility of future implant replacement. Maxillary Posterior Region

The extreme variation in vertical and anteroposterior growth is also seen in the posterior maxilla. An important additional growth factor is transverse maxillary growth at the midpalatal suture and in the alveolus. The increase in width at the posterior aspect of the midpalatal suture is approximately three times that seen at the anterior aspect of the midpalatal suture. This variation not only produces heightened transverse growth, but also a rotational growth. All of these variables serve as a cautionary note and reinforce the fact that the more predictable treatment occurs closer to the end of maturation. The severe variability of vertical growth seen in this region has the potential to cause a serious biomechanical load magnification problem because of the increased masticatory force placed on posterior occlusal surfaces. Placement of osseointegrated dental implants in the maxillary posterior quadrant is best delayed until age 15 in females and age 17 in males. Particular care must be exercised when placing implants before skeletal maturity because of the appositional and resorptive pattern of the posterior maxilla. Mandibular Anterior Region

From a standpoint of growth and development, the anterior mandibular region presents the best site for the placement of an osseointegrated implant before skeletal maturation. Although, the mandible presents fewer confounding variables, the closure of the Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

mandibular symphysis suture occurs during the first two years of life. Recommendations have been made to begin treatment in children with ectodermal dysplasia as early as three years of age, creating improvement in facial appearance leading to demonstrable emotional, psychological, phonetic and functional benefits. Mandibular Posterior Region

A large variation in the growth occurs in the posterior mandibular region leading to progressive infraocclusion of the implant, and harms the adjacent teeth. So implant in this region should not be placed until skeletal growth is completed. Conclusion While placing implant for single missing tooth adjacent to permanent teeth, dentoalveolar development occurs around the edentulous space. If an implant is placed before dentoalveolar growth is complete, the implant will become submerged relative to the adjacent teeth because implant behaves like an ankylosed tooth, resulting in poor esthetics and poor implant to crown ratio. To avoid such complication in the growing child, it is recommended not to place implants until two annual cephalograms shows no change in the position of the adjacent teeth.19 Missing single or multiple teeth with adjacent permanent teeth form the most complex group of patients to be treated using implants. In terms of overall diagnosis, they may have some form of non-syndromic partial anodontia or ectodermal dysplasia. In planning implant placement, future dentoalveolar development and the psychological development of the patient needs to be considered.19 In cases of completely edentulous arch, because teeth are not present, one need not to be concerned about dentoalveolar growth. The only concern is the downward and forward growth of the entire mandible. This can result in a jaw size discrepancy due to mandibular rotation, but the implant position will not be adversely affected. Careful consideration must be given to the physical and psychological development of the patient when an implant placement is planned. Patients must understand the oral hygiene requirements and perform them adequately. Oral hygiene is rarely satisfactory in patients younger than seven years old. For these reasons, the placement of implants in patients younger than the age of 7 is not indicated.19,20 On the basis of the studies of jaw growth, it is better to avoid placement of implants posterior to the mandibular 53

Review Article canines. In patients with ectodermal dysplasia, implants have been successfully placed in the maxillary arch and in the mandible anterior to the mental foramen. Extreme caution must be used in placing implants in children because of growth changes of the jaws and the dentition. Whenever possible, implant placement should be delayed until age 15 for girls and 18 for boys. Growing patients treated with dental implants should have adequate follow-up. Further research is needed regarding placing implants in growing children. References 1. Brånemark Pl, Adell R, Breine U, Hansson BO, Lindström J, Ohlsson A. Intra-osseous anchorage of dental prostheses. 1. Experimental studies. Scand J Plast Reconstr Surg 1969;3(2):81-100. 2. Brahim JS. Dental Implants in children. Oral Maxillofacial Surg Clin North Am 2005;17(4):375-81. 3. Lendermann PD, Hassell TM, Heffi AF. Osseointegrated dental implants as alternative therapy to bridge construction or orthodontics in young patients: seven years clinical experience. Pediatr Dent 1993;15(5): 327-33. 4. Cronin RJ Jr, Oesterle LJ. Implant use in growing patients. Treatment planning concerns. Dent Clin North Am 1998;42(1):1-34. 5. Percinoto C, Vieira AE, Barbieri CM, Melhado FL, Moreira KS. Use of dental implants in children: a literature review. Quintessence Int 2001;32(5):381-3. 6. Williams P, Travess H, Sandy J. The use of osseointegrated implants in orthodontic patients: 1. Implants and their use in children. Dent Update 2004;31(5):287-90. 7. Thilander B, Odman J, Grondahl K, Lekholm U. Aspects of osseointegrated implants inserted in growing jaws. A biometric and radiographic study in the young pig. Eur J Orthod 1992;14(2):99-109. 8. Odman J, Grondahl K, Lekholm U, Thilander B. The effect of osseointegrated implants on the dento-alveolar development. A clinical and radiographic study in growing pigs. Eur J Orthod 1991;13(4):279-86.

9. Profit WR, Henry W. Fields contemporary orthodontics. 3rd edition, Mosby 10. Heij DG, Opdebeeck H, van Steenberghe D, Kokich VG, Belser U, Quirynen M. Facial development, continuous tooth eruption, and mesial drift as compromising factors for implant placement. Int J Oral Maxillofac Implants 2006;21(6):867-78. 11. Voss R, Freng A. Growth of the dental arches after ablation of midpalatal suture. A study in domestic cat. J Maxillofac Surg 1982;10(4):259-63. 12. OP Heij DG, Opdebeeck H, van Steenberghe D, Quirynen M. Age as a compromising factor for implant insertion. Periodontol 2000. 2003;33:172-84. 13. Oesterle LJ, Cronin RJ Jr, Ranly DM. Maxillary implants and the growing patient. Int J Oral Maxillofac Implants 1993;8(4):377-87. 14. Cronin RJ Jr, Oesterle LJ, Ranly DM. Mandibular implants and the growing patient. Int J Oral Maxillofac Implant 1994;9(1):55-60. 15. Bjork A. Variations in the growth pattern of the human mandible: longitudinal radiographic study by the implant method. J Dent Res 1963;42:400-11. 16. Kearns G, Sharma A, Perrott D, Schmidt B, Kaban L, Vargervik K. Placement of endosseous implants in children and adolescents with hereditary ectodermal dysplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88(1):5-10. 17. Bergendal B, Bergendal T, Hallonsten AL, Koch G, Kurol J, Kvint S. A multidisciplinary approach to oral rehabilitation with osseointegrated implants in children and adolescents with multiple aplasia. Eur J Orthod 1996;18(2):119-29. 18. Johnson EL, Roberts MW, Guckes AD, Bailey LJ, Phillips CL, Wright JT. Analysis of craniofacial development in children with hypohidrotic ectodermal dysplasia. Am J Med Genet 2002;112(4):327-34. 19. Sharma AB, Vargervik K. Using implants for growing child. J Calif Dent Assoc 2006;34(9):719-34. 20. Sweeney P, Ferguson JW, Heggie AA, Lucas JO. Treatment outcomes for adolescent ectodermal dysplasia patients treated with dental implants. Int J Paediatr Dent 2005;15(4):241-8.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review article

Marfan Syndrome Srisha Basappa*, Aruna Das**, Syed Parveez Ali†

Abstract Marfan’s syndrome is a hereditary connective tissue disorders affecting both genders. Marfan’s syndrome is not life-threatening, they can cause decreased mobility and chronic pain, there by creating significant impact on quality-of-life. If unrecognized, patients may potentially develop aortic rupture or sudden cardiac arrest. Key words: Marfan’s, collagen disorder, joint hyperextensibility

arfan-archad syndrome or archnodactyly, is a hereditary disease, transmitted as autosomal dominant trait.1-3 Marfan syndrome was first described in 1896 by Antoine Bernard Jean Marfan.2 The syndrome occurs 1 in 10,000 individuals and has an equal distribution between the sexes.4 Child of parent with Marfan syndrome has 50% chance of inheriting the disease. It affects multiple organs such as eyes, skeleton, lungs, heart and blood vessels.1,2,4 Etiopathogenesis Basically, it is a connective tissue disease related to defective organization of collagen which is abnormally soluble. Marfan syndrome results from defect in gene on chromosome 15; changes in this gene affect production of fibrillin, a connective tissue protein.1,4-6 Clinical Features  Skeletal: Excessive length of tubular bones resulting in (dolichostenomelia) or disproportionate long and thin extremities and archnodactyly or spidery fingers.1,5,7,8 Dolichostenomelia is defined by an upper segment-to-lower segment ratio (US/LS) of at least 2 SD below the mean, or arm-span-toheight ratio of at least 1.05.8 Upper body segment is shorter than lower and arm span exceeds height by 5 cm or more.9 *Associate Professor, Dept. of Oral Medicine and Radiology Farooqia Dental College and Hospital, Mysore **Professor and Head, Dept. of Oral Medicine and Radiology Dental College, Azamgarh † Senior Lecturer, Dept. of Oral Medicine and Radiology Farooqia Dental College and Hospital, Mysore Address for correspondence Dr Srisha Basappa Associate Professor Dept. of Oral Medicine and Radiology Farooqia Dental College and Hospital Umer Khayam Road, Eidgah, Mysore - 570 021 E-mail: srisha4155@yahoo.com

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010



Craniofacial: Skull and face are long and narrow, ears are large, eyes appear sunken and frontal bossing is seen.1,7 Joint: Hyperextensiblity of joints with habitual dislocations, kyphosis or scoliosis and flat foot.1,3,7,8 Ocular: Bilateral ectopia lentis caused by weakening or rupture of suspensory ligaments, myopia, glaucoma. 1,7-12 Cardiovascular: Aortic aneurysm, aortic regurgitation, valvular defects, enlargement of heart, infective endocarditis.3,7,8,12,13 Skin and integument: Striae gravidarum, lingual hernia.8 Miscellaneous: Dural ectasia and sacral meningocele.8

Oral Manifestations  



Palate: High arched palate, bifid uvula.2,3,7,8 Maxilla and mandible: Malocclusion, multiple odontogenic cysts of maxilla and mandible, mandibular prognathism.3,7,8 Clinical diagnosis: Spider fingers, high arch palate, hyperextensibility of joints.7

Investigations of Marfan Syndrome Aortic Aneurysm 



Chest radiograph shows broadening of upper mediastinum and distortion of aortic knuckle (in 60% of patients). A left-sided pleural effusion is common.12,13 Electrocardiography (ECG): May show left ventricular hypertrophy in patients with hypertension.13 55

Review Article Table 1. Ghent Criteria for Diagnosing Marfan Syndrome8 System

Major

Minor

Family/genetic history

Having a first-degree relative (parent, child or sibling) who meets these diagnostic criteria independently

None

Presence of a mutation in FBN1 known to cause the Marfan syndrome Presence of a haplotype around FBN1, inherited by descent, known to be associated with unequivocally diagnosed Marfan syndrome in the family Skeletal

Presence of at least 4 of the following manifestations: Pectus carinatum

Pectus excavatum of moderate severity joint hypermobility Highly arched palate with crowding of teeth

Pectus excavatum (requiring surgery) Reduced upper-to-lower segment ratio or arm span-to-height ratio greater than 1.05 Wrist and thumb signs

Facial appearance (dolichocephaly, malar hypoplasia, enophthalmos, retrognathia, down-slanting palpebral fissures)

Scoliosis >20째 or spondylolisthesis Reduced extensions at the elbows (<170째) Medial displacement of the medial malleolus causing pes planus Protrusio acetabulare of any degree (ascertained on radiographs)

Ocular

Ectopia lentis (dislocated lens)

Abnormally flat cornea (as measured by keratometry) Increased axial length of globe (as measured by ultrasound)

Cardiovascular

Dilatation of the ascending aorta with or without aortic regurgitation and involving at least the sinuses of Valsalva or dissection of the ascending aorta

Mitral valve prolapse with or without mitral valve regurgitation Dilatation of the main pulmonary artery, in the absence of valvular or peripheral pulmonic stenosis or any other obvious cause in patients age <40 years Calcification of the mitral annulus in patients age <40 years Dilatation of dissection of the descending thoracic or abdominal aorta in patients age <50 years

Pulmonary

None

Spontaneous pneumothorax Apical blebs (ascertained by chest radiography)

Skin and integument

None

Stretch marks not associated with marked weight changes, pregnancy or repetitive stress Recurrent incisional hernias

Dura

Lumbosacral dural ectasia as demonstrated by CT or MRI scans

None

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Review Article 

CT and MRI: Defect early aortic dilatation and can be used to monitor the disease.13

Aortic Regurgitation 

 

Electrocardiography (ECG): Initially normal, later left ventricular hypertrophy and T-wave inversion.13 Chest radiograph: Aortic dilation is seen.13 Echocardiography: Dilated left ventricle and hyperdynamic left ventricle.13

Infective Endocarditis 



Blood culture is advised because it may identify infection and guide antibiotic therapy. ECG is key investigation for detecting and following the progress of vegetations, for assessing valve damage and detecting abscess formation.13 Chest radiograph may show evidence of chest failure and cardiomegaly.13

allows minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of antimicrobial drug to be measured. Plasma antibiotic concentrations 4-8 times of the MIC/MBC will usually eradicate the infection.13 Dental Treatment

Enucleation of entire cyst with vigorous curettage of the cystic wall. 5,7,14 marsupialization reduces size of large cysts before surgical excision.14,15 Peripheral osteotomy of bone cavity can be done to reduce chances of recurrence5,6,14 Chemical cauterization of bony cavity can be done with intraluminar injection of Carnoy’s solution allow freeing cyst from bony wall which in turn allow easier removal of cyst. Large multilocular lesions require en bloc resection followed by bone grafting. Decompression is achieved with the help of polyethylene drainage tube kept in the bony cavity.15

Laboratory Aids

Discussion

Preimplantation and prenatal diagnosis by molecular studies have been accomplished. During the third trimester, diagnosis can be strongly suspected on the basis of ultrasonographic analysis of limb lengths. Some parents may benefit from emotional preparation for the birth of an affected child. Lumbosacral dural sac dimensions can be measured by MRI. Dural ectasia is a good marker for Marfan syndrome.8

There is no specific treatment for Marfan syndrome. A cardiologist, ophthalmologist and orthopedic surgeon should review patients regularly. Early identification of risk factor such as aortic dilation should prevent delayed complications. With early diagnosis and preventive management a person with Marfan syndrome should expert to have similar life expectancy to that of the average person.

Treatment

References

No specific treatment and the prognosis is good.

1. Babic GS, Vujanovic M, Dordevic-Jocic J, Cekic S. Ocular features of Marfan syndrome. Med Bio 2008;15:37-40.

Medical Treatment

2. Goh KL, Hassan Z, Tan CT. Infective endocarditis in Marfan syndrome: a case report. Sing Med J 1986;27(5):446-9.

Patients with scoliosis should be referred to spine deformity expert and surgery is an appropriate option for curves over 45°.12 Patients with excessive kyphosis are referred to spine deformity experts. Spinal fusion is an option for curves over 70° in the thoracic spine and significant deformity of thoracolumbar region. Patients with eye problems such as vision problem should be advised for ophthalmological consultation. Patients with aortic regurgitation must undergo aortic root replacement.13 For aortic aneurysm, β-blockers reduce rate of aortic dilation and risk of rupture. In cases of infective endocarditis, a tooth with periapical abscess should be extracted. Isolation of organism Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

3. Rajendran R. Diseases of bone and joints. In: Shafer’s Textbook of Oral Pathology. 6th edition, Rajendran R, Sivapathasundaram B, (Eds.), Elsevier: New Delhi 2009:696-7. 4. Rangasetty UC, Karnat BM. Clinical signs of Marfan syndrome. Hosp Physician 2006;32-8. 5. Avivi E, Arzi H, Paz L, Caspi I, Chechik A. Skeletal manifestations of Marfan syndrome. Isr Med Assoc J 2008;10(3):186-8. 6. Regezi JA, Sciubba JJ, Jordan RC. Metabolic and genetic diseases. In: Oral Pathology Clinical Pathological Correlations. 5th edition, Elsevier: Noida 2009:351-2.

Review Article 7. Ghom AG. Diseases of bone manifested in jaw. In: Textbook of Oral Medicine. 2nd edition, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi 2010:853.

12. Greager MA, Loscalzo J. Diseases of aorta. In: Harrison’s Principles of Internal Medicine. 17th edition, Fuauci AS et al (Eds.), McGraw-Hill: America 2008:1563-6.

8. Gorlin RJ, Cohen MM, Hennekam RCM. In: Syndromes of Head and Neck. 4th edition, Oxford Publishers Calcutta 2001:327-34.

13. Bloomfeild P, Bradbury A, Grubb NR, Newby DE. Cardiovascular disease. In: Davidson’s Principles and Practice of Medicine. 20th edition, Boon NA, Colledge NR, Walker BR (Eds.), Churchill Livingstone: Philadelphia 2006:519-47.

9. Solomon L, Warwick D, Nayagam S. In: Apleys System of Orthopedics and Fractures. 8th edition, Arnold, Great Britain 2001:151-2. 10. Nahum Y, Spierer A. Ocular features of Marfan syndrome: diagnosis and management. Isr Med Assoc J 2008;10(3):179-81. 11. Ozkan B, Ceviz N, Buyukmali M. Marfan syndrome: Short Report. Tr J Med Sci 1999;29:195-7.

14. Kerr RA, Phelan JA. Benign Lesion of Oral Cavity. In: Burket’s Oral Medicine. 11th edition, Greenberg MS, Glick M, Ship JP (Eds.), BC Decker Inc: New Delhi, 147-8. 15. Ghom AG. Cysts of jaw. In: Textbook of Oral Medicine. 2nd edition, Jaypee Brothers Medical Publishers (P) Ltd: New Delhi 2010:238-41.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

Indian Journal of

Original research

Multidisciplinary Dentistry

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.

Indian Journal of Multidisciplinary Dentistry, Vol. 1, Issue 1, Nov-Dec 2010

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.)_________________

Total number of pages____________________________________

Number of tables________________________________________

Number of figures_______________________________________

Special requests_________________________________________

Suggestions for reviewers (name and postal address)

Indian 1.______________ Foreign 1. _______________ 2.____________________

2._______________

All author’s signatures____________________________________

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

__________________________________________________________

For Editorial Correspondence 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: masthankmk@yahoo.com, ijmdent@gmail.com