Journal of Dental Herald E ISSN : Awaited

P ISSN : Awaited

Affiliated to Indian Dental Association, Jammu Branch

Editorial Board Patron Dr. Mahesh Verma Vice President, Dental Council of India

Editor-in-chief Dr. Bhanu Kotwal

Chief Patron Dr. Dibyendu Mazumder President, Dental Council of India

Editorial Advisor Dr Mark Bartold Editor-Australian Dental Journal, Director-Australian Clinical Dental Research Centre, University of Adelaide, Australia.

Associate Editor Dr. Ritesh Gupta

Assistant Editor Dr. Nanika Mahajan

Editorial Coordinator Dr. Rakesh K. Gupta. H.O.D., Deptt. of Pedodontics, IGGDC, Jammu. Co-Editors Dr. Rajesh Ahal, Dr. Satish Sharma, Dr. Rajiv Mengi, Dr. Arvind Mengi, Dr. Gautam Sharma, Dr. Neetu Gupta

Dr. Vikas Jindal Principal, Himachal Dental College, Sundernagar, HP. Dr. Romesh Singh Principal, Indira Gandhi Govt. Dental College, Jammu. Dr. Vinod Sachdev Principal, ITS Dental College, Muradnagar. Dr. Virender Goyal Professor, Deptt of Pedodontics, Dashmesh Institute of Research and Dental Sciences, Faridkot. Dr. Vivek Hegde Professor, Deptt.of Conservative Dentistry and Endodontics, M. A. Rangoonwala Dental College, Pune. Dr. Manesh Lahori Professor & Head, Deptt. of Prosthodontics, K.D. Dental College & Hospital, Mathura. Dr. Sharath Kumar Shetty Director (PG studies), Professor & HOD, Deptt.of Orthodontics, KVG Dental College, Sulli, Karnatka. Dr. Mahesh Kumar Y. Professor, Deptt of Orthodontics, KVG Dental College, Sulli, Karnatka. Dr. Suvarna Nene B.D.S. D.U. (France)

Dr. Robert L. Ramus DDS Ohio, USA Dr. Souheil R. Hussaini, MS President, Chairman of scientific committee - CDE Implant Dentistry - Study Consortium (ID-SC), Columbia University School of Dentistry, Assistant professor, College of Dentistry, University of Sharjah, UAE.

National Editorial Board Dr. Vimal Sikri Principal, Punjab Govt Dental College, Amritsar Dr. Riyaz Farooq Principal, Govt. Dental College, Srinagar. Dr. Gurkeerat Singh Professor, Deptt.of Orthodontics, SudhaRustagi College of Dental Sciences and Research, Faridabad. Dr. Sridevi Padmanabhan Professor, Deptt.of Orthodontics, Sri Ramachandra Dental College, Chennai. Dr. Sanghmitra Das Gupta Director: CORE; Former Professor & Head. Deptt. of Oral and Maxillofacial Surgery, Vydehi Dental College, Bangalore. Dr. Himanshu Aeran Director PG Studies, Seema Dental College, Rishikesh. Dr. Ankur Rustagi MDS, Oral & Maxillofacial Surgery AIIMS; Senior consultant & Maxillofacial Surgeon. Delhi Heart & lung Hospital, New Delhi. Dr. Manish Khatri Professor& Head, Deptt.of Periodontics, IDST, Modinagar.

International Editorial Board Dr. Ramon J.Baez DDS, MPH Boerne, TX USA Dr. Shiva Mortazavi, DDS, MS, Assistant Professor, Dental School & Research Center, Isfahan University of Medical Sciences Isfahan, Iran. Dr. Mohammad Altamash Dr. Med. Dent. (Germany), FACD (USA),President.Principal, Altamash Institute of Dental Medicine, Karachi. Pakistan.

Dr. Anil Singla Director, Himachal Dental College, Sundernagar, H.P. Dr. Gaurav Gupta Director, Institute of Dental Sciences, Paonta Sahib. Dr. Anil Chandra Professor, Deptt. of Conservative Dentistry and Endodontics, Faculty of Dental Sciences, K.G's medical University, Lucknow. Dr. Ashok Kumar Jena Deptt.of Dental Surgery, AIIMS, Sijua, Dumduma, Bhubaneswar. Dr. Neeraj Mahajan Professor & Head, Deptt.of Pedodontics, Guru Nanak Dev Dental College and Research Institute,Sunam, Punjab. Dr. D. K. Gautam Professor& Head, Deptt. of Periodontics, Himachal Dental College, Sundernagar, H.P. Dr. Ramesh Reddy Professor, Deptt. of Periodontology, Narayana Dental College, ChintareddyPalem, Nellore, A.P. Dr. Vinay Kumar Bhardwaj Assistant Professor, Deptt. of Public Health Dentistry), Govt. Dental College, Shimla.

Dr. Suchetan Pradhan M.D.S. (Prosthodontics) M.Sc. Laser Dentistry (Aachen Univ., Germany), EMDOLA(European Union, Mumbai, India. Dr. Mohammed Mustafa Assistant Professor, Head of Endodontic Division, Coordinator for Quality & Development,College of Dentistry & Hospital, Saudi Arabia.

Executive Committee Dr. K. S. Kotwal Dr. Parveen Lone Dr. Akshay Gupta

Dr. Nikhil Dev Wazir Dr. N. P. Gupta Dr. Reecha Gupta

Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

Dr. Azhar Malik Dr. Sarbjeet Singh Dr. Gautam Mengi

Dr. Rubina Anjum Dr. Satvinder Singh Dr. Chander Joshi

A

Journal of Dental Herald E ISSN : Awaited

P ISSN : Awaited

Affiliated to Indian Dental Association, Jammu Branch Journal of Dental Herald 1st Dental Journal from the State of Jammu & Kashmir, India. General Information Journal of Dental Herald is a peer-reviewed journal published by likeminded well-wishers of Dental fraternity of Jammu through the dais of prestigious Indian Dental Association Jammu Branch. The journal publishes information related to all the fields of Dentistry with emphasis on clinical point of view so as to help the young and budding dentist& to bridge the gap between under graduate & post graduate. The journal is published quarterly in January, April, July and October. Instructions to Authors Manuscripts must be prepared in accordance with "Uniform requirements for Manuscripts submitted to Biomedical Journal" developed by International Committee of Medical Journal Editors (October 2001). The uniform requirements and specific requirement of Journal of Dental Herald summarized below. Before sending a manuscript contributors are requested to check for the latest instructions available. The Editorial Process The manuscripts will be reviewed for possible publication with the understanding that they are being submitted to one journal at a time and have not been published, simultaneously submitted, or already accepted for publication elsewhere. The Editors review all submitted manuscripts initially. Manuscripts with insufficient originality, serious scientific flaws, or absence of importance of message are rejected. The journal will not return the unaccepted manuscripts. Other manuscripts are sent to two or more expert reviewers without revealing the identity of the authors to the reviewers. Within a period of eight to ten weeks, the contributors will be informed about the reviewers' comments and acceptance/rejection of manuscript. Articles accepted would be copy edited for grammar, punctuation, print style, and format. Page proofs will be sent to the first author, which has to be returned within five days. Correction received after that period may not be included. All manuscripts received are duly acknowledged. Types of Manuscripts and word limits Original research articles : Randomized controlled trials, intervention studies, studies of screening and diagnostic test, outcome studies, cost effectiveness analyses, casecontrol series, and surveys with high response rate. Up to 2500 words excluding references and abstract. Short Communication : Up to 1000 words excluding references and abstract. Up to 8 references. A short communication contains only a short report of the case (only pertinent details) and a short discussion and references up to a maximum of 8. Number of figures should be restricted to a maximum of 6. Case Reports : Only New / interesting / very rare cases can be reported. Cases with clinical significance or implications will be given priority, whereas, mere reporting of a rare case may not be considered. Up to 2000 words excluding references and abstract and up to 10 references. Review Articles : Systemic critical assessments of literature and data sources. Up to 3500 words excluding references and abstract. Letter to the Editor : Should be short, decisive observation. They should not be preliminary observations that need a later paper for validation. Up to 400 words and 4 references. Announcements of conferences, meetings, courses, awards, and other items likely to be of interest to the readers should be submitted with the name and address of the person from whom additional information can be obtained. Up to 100 words. Authorship criteria : All persons designated as authors should qualify for authorship, and all those who qualify should be listed. Each author should have participated sufficiently in the work to take public responsibility for appropriate portions of the content. One or more authors should take responsibility for the integrity of the work as a whole, from inception to published article. The name and order of the authors cannot be changed once the article is provisionally accepted. Authorship credit should be based only on : Substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data; Drafting the article or revising it critically for important intellectual content; and Final approval of the version to be published. Conditions 1, 2, and 3 must all be met. Acquisition of funding, the collection of data, or general supervision of the research group, by themselves, do not justify authorship. The order of authorship on the byline should be a joint decision of the co-authors. Authors should be prepared to explain the order in which authors are listed. Once submitted the order cannot be changed without written consent of all the authors. For a study carried out in a single institute, the number of authors should not exceed six. For a case-report and for a review article, the number of authors should not exceed four. For short communication, the number of authors should not be more than three. A justification should be included, if the number of authors exceeds these limits. Only those who have done substantial work in a particular field can write a review article. A short summary of the work done by the authors (s) in the field of review should accompany the manuscript. The journal expects the authors to give post-publication updates on the subject of review. The update should be brief, covering the advances in the field after the publication of article and should be sent as letter to editor, as and when major development occur in the field. Images: Submit good quality color images. Each image should be less than 400 kb in size. Size of the image can Sending the Manuscript to the Journal Articles should be submitted online from http://www.dherald.in or e mailed- [email protected] First Page File: Prepare the title page, covering letter, acknowledgement, etc., using a word processor program. All information, which can reveal your identity, should be here. Do not zip the files. Article file: The main text of the article, beginning from Abstract till References (including tables) should be in this file. Do not include any information such as acknowledgement, your names in page headers, etc., in this file. Do not zip the files. Limit the file size to 400 kb. Do not incorporate images in the file. If the file size is large, graphs can be submitted as images separately without incorporating them in the article file to reduce the size of the file. be reduced by decreasing the actual height and width of the images (keep up to 1024x760 pixels or 5 inches). All image formats (jpeg, tiff, gif, bmp, png, eps, etc.) are acceptable; jpeg is most suitable. Do not zip the files

Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

B

Legends: Legends for the figures/images should be included at the end of the article file.The authors' form and copyright transfer form has to be submitted to the editorial office by post, in original with the signatures of all the authors within two weeks of online submission. Images related to the articles should be sent in a 'compact disc' or as hard copies to the journal office at the time of acceptance of the manuscript. These images should of high resolution and exceptional quality. Editorial office : Dr. Bhanu Kotwal (Editor in Chief) Journal of Dental Herald, 31 B Bakshi Nagar, Jammu (J&K) Tel: 0191-2586421; Cell: +919622322322;[email protected]. For any queries: Dr. Ritesh Gupta (Associate-Editor) Cell: +91-9419143373. Preparation of the Manuscript : The manuscripts should be typed in A4 size (212 × 297 mm) paper, with margins of 25 mm (1 inch) from all the four sides. Use 1.5 spacing throughout. Number pages consecutively, beginning with the title page. The language should be British English. Title Page: The title page should carry: Type of manuscript : The title of the article, which should be concise, but informative; Running title or short title not more than 50 characters; Name of the authors (the way it should appear in the journal), with his or her highest academic degree(s) and institutional affiliation; The name of the depar tment(s) and institution(s) to which the work should be attributed; The name, address, phone numbers, facsimile numbers, and e-mail address of the contributor responsible for correspondence about the manuscript; The total number of pages, total number of photographs and word counts separately for abstract and for the text (excluding the references and abstract). Source(s) of support in the form of grants, equipment, drugs, or all of these; and If the manuscript was presented as part at a meeting, the organization, place, and exact date on which it was read. Abstract Page : The second page should carry the full title of the manuscript and an abstract (of no more than 150 words for case reports, brief reports and 250 words for original articles). The abstract should be structured and state the Context (Background), Aims, Settings and Design, Methods and Material, Statistical analysis used, Results and Conclusions. Below the abstract should provide 3 to 10 key word. Introduction State the purpose of the article and summarize the rationale for the study or observation.Methods Describe the selection of the observational or experimental subjects (patients or laboratory animals, including controls) clearly. Identify the age, sex, and other important characteristics of the subjects. Identify the methods, apparatus (give the manufacturer's name and address in parentheses), and procedures in sufficient detail. Give references to established methods, including statistical methods; provide references and brief descriptions for methods that have been published but are not well known; describe new or substantially modified methods, give reasons for using them, and evaluate their limitations. Identify precisely all drugs and chemicals used, including generic name(s), dose(s), and route(s) of administration. Reports of randomized clinical trials should present information on all major study elements, including the protocol, assignment of interventions (methods of randomization, concealment of allocation to treatment groups), and the method of masking (blinding), based on the CONSORT statement (Moher D, Schulz KF, Altman DG: The CONSORT Statement: Revised Recommendations for Improving the Quality of Reports of Parallel-Group Randomized Trials. Ann Intern Med. 2001;134:657-662, also available at http://www.consort-statement.org/). Authors submitting review manuscripts should include a section describing the methods used for locating, selecting, extracting, and synthesizing data. These methods should also be summarized in the abstract. Ethics When reporting experiments on human subjects, indicate whether the procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional or regional) and with the Helsinki Declaration of 1975, as revised in 2000 (available at http://www.wma.net/e/policy/17c_e.html). Do not use patients' names, initials, or hospital numbers, especially in illustrative material. When reporting experiments on animals, indicate whether the institution's or a national research council's guide for, or any national law on the care and use of laboratory animals was followed. Statistics When possible, quantify findings and present them with appropriate indicators of measurement error or uncertainty (such as confidence intervals). Report losses to observation (such as dropouts from a clinical trial). Put a general description of methods in the Methods section. When data are summarized in the Results section, specify the statistical methods used to analyse them. Avoid non-technical uses of technical terms in statistics, such as 'random' (which implies a randomising device), 'normal', 'significant', 'correlations', and 'sample'. Define statistical terms, abbreviations, and most symbols. Use upper italics (P < 0.05). Results Present the results in logical sequence in the text, tables, and illustrations. Do not repeat in the text all the data in the tables or illustrations; emphasise or summarise only important observations. Discussion Emphasize the new and important aspects of the study and the conclusions that follow from them. Do not repeat in detail data or other material given in the Introduction or the Results section. Include in the Discussion section the implications of the findings and their limitations, including implications for future research. Relate the observations to other relevant studies. In particular, contributors should avoid making statements on economic benefits and costs unless their manuscript includes economic data and analyses. Avoid claiming priority and alluding to work that has not been completed. State new hypotheses when warranted, but clearly label them as such. Recommendations, when appropriate, may be included. Acknowledgments As an appendix to the text, one or more statements should specify 1. Contributions that need acknowledging but do not justify authorship, such as general support by a departmental chair; 2. acknowledgments of technical help; and 3. Acknowledgments of financial and material support, which should specify the nature of the support. This should be the last page of the manuscript. References References should be numbered consecutively in the order in which they are first mentioned in the text (not in alphabetic order). Identify references in text, tables, and legends by Arabic numerals in superscript. References cited only in tables or figure legends should be numbered in accordance with the sequence established by the first identification in the text of the particular table or figure. Use the style of the examples below, which are based on the formats used by the NLM in Index Medicus. The titles of journals should be abbreviated according to the style used in Index Medicus. Use complete name of the journal for non-indexed journals. Avoid using abstracts as references. Information from manuscripts submitted but not accepted should be cited in the text as "unpublished observations" with written permission from the source. Avoid citing a "personal communication" unless it provides essential information not available from a public source, in which case the name of the person and date of communication should be cited in parentheses in the text. For scientific articles, contributors should obtain written permission and confirmation of accuracy from the source of a personal communication. If the number of authors is more than six, list the first six authors followed by et al. Tables Tables should be self-explanatory and should not duplicate textual material. Tables with more than 10 columns and 25 rows are not acceptable. Type or print out each table with double spacing on a separate sheet of paper. If the table must be continued, repeat the title on a second sheet followed by "(contd.)". Number tables, in Arabic numerals, consecutively in the order of their first citation in the text and supply a brief title for each. Place explanatory matter in footnotes, not in the heading. Explain in footnotes all non-standard abbreviations that are used in each table. Obtain permission for all fully borrowed, adapted, and modified tables and provide a credit line in the footnote. For footnotes use the following symbols, in this sequence: *, †, ‡, §, ¦, *,*, ††, ‡‡ Illustrations (Figures) Figures should be numbered consecutively according to the order in which they have been first cited in the text. Symbols, arrows, or letters used in photomicrographs should contrast with the background and should marked neatly with transfer type or by tissue overlay and not by pen. Titles and detailed explanations belong in the legends for illustrations not on the illustrations themselves. When graphs, scatter-grams or histograms are submitted the numerical data on which they are based should also be supplied. The photographs and figures should be trimmed to remove all the unwanted areas. If photographs of people are used, either the subjects must not be identifiable or their pictures must be accompanied by written permission to use the photograph. If a figure has been published, acknowledge the original source and submit written permission from the copyright holder to reproduce the material. A credit line should appear in the legend for figures for such figures. The Journal reserves the right to crop, rotate, reduce, or enlarge the photographs to an acceptable size. Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

C

Article submission Submit the manuscript to [email protected]. Submit good quality color images. Each image should be less than 100 kb in size. Size of the image can be reduced by decreasing the actual height and width of the images (keep up to 400 pixels or 3 inches).\ All image formats (jpeg, tiff, gif, bmp, png, eps, etc.) are acceptable; jpeg is most suitable. The images should be scanned at 72 dpi, size not more than 3x4 inches (or 300x400 pixels), with only the necessary portion of the photographs. Wherever necessary, scan at greyscale (e.g. x-rays, ECGs). For hard copies (to be submitted only after acceptance of the manuscript) Send sharp, glossy, un-mounted, color photographic prints, with height of 4 inches and width of 6 inches. Each figure should have a label pasted (avoid use of liquid gum for pasting) on its back indicating the number of the figure, the running title, top of the figure and the legends of the figure. Do not write the contributor/s' name/s. Do not write on the back of figures, scratch, or mark them by using paper clips. Labels, numbers, and symbols should be clear and of uniform size. The lettering for figures should be large enough to be legible after reduction to fit the width of a printed column. For soft copies (to be submitted only after acceptance of the manuscript) Use a Compact Disc. There should be no other document, file, or material on the disc other than the

images. Label the disc with first authors' name, short title of the article, type of image (eg. Jpeg, tiff), and file name. For online submission (To be launched soon) Submit good quality color images. Each image should be less than 100 kb in size. Size of the image can be reduced by decreasing the actual height and width of the images (keep up to 400 pixels or 3 inches).\ All image formats (jpeg, tiff, gif, bmp, png, eps, etc.) are acceptable; jpeg is most suitable. The images should be scanned at 72 dpi, size not more than 3x4 inches (or 300x400 pixels), with only the necessary portion of the photographs. Wherever necessary, scan at greyscale (e.g. x-rays, ECGs). For hard copies (to be submitted only after acceptance of the manuscript) Send sharp, glossy, un-mounted, colour photographic prints, with height of 4 inches and width of 6 inches. Each figure should have a label pasted (avoid use of liquid gum for pasting) on its back indicating the number of the figure, the running title, top of the figure and the legends of the figure. Do not write the contributor/s' name/s. Do not write on the back of figures, scratch, or mark them by using paper clips. Labels, numbers, and symbols should be clear and of uniform size. The lettering for figures should be large enough to be legible after reduction to fit the width of a printed column. For soft copies (to be submitted only after acceptance of the manuscript) Use a Compact Disc. There should be no other document, file, or material on the disc other than the images. Label the disc with first authors' name, short title of the article, type of image (eg. Jpeg, tiff), and file name. Legends for Illustrations Type or print out legends (maximum 40 words, excluding the credit line) for illustrations using double spacing, with Arabic numerals corresponding to the illustrations. When symbols, arrows, numbers, or letters are used to identify parts of the illustrations, identify and explain each one clearly in the legend. Explain the internal scale and identify the method of staining in photomicrographs. Protection of Patients' Rights to Privacy. Identifying information should not be published in written descriptions, photographs, sonograms, CT scans, etc., and pedigrees unless the information is essential for scientific purposes and the patient (or parent or guardian) gives written informed consent for publication. Informed consent for this purpose requires that the patient be shown the manuscript to be published. When informed consent has been obtained, it should be indicated in the article and copy of the consent should be attached with the covering letter. Sending a revised manuscript While submitting a revised manuscript, contributors are requested to include, along with single copy of the final revised manuscript, a photocopy of the revised manuscript with the changes underlined in red and copy of the comments with the point-to-point clarification to each comment. The manuscript number should be mentioned without fail. The authors' form and copyright transfer form has to be submitted in original with the signatures of all the contributors at the time of submission of revised copy. Article printing charges Free of cost. Copyrights The whole of the literary matter is the copyright of the Editorial Board. The Journal, however, grants to all users a free, irrevocable, worldwide, perpetual right of access to, and a license to copy, use, distribute, perform and display the work (either in pre-print or post-print format) publicly and to make and distribute derivative works in any digital medium for any reasonable non-commercial purpose, subject to proper attribution of authorship and ownership of the rights. The journal also grants the right to make small numbers of printed copies for their personal non-commercial use. The copyright form duly signed by all the authors should be submitted immediately after submitting the manuscript Contributors' Form Manuscript Title _____________________________________ Manuscript Number _____________________________ I / We certify that I/we have participated sufficiently in the intellectual content, conception and design of this work or the analysis and interpretation of the data (when applicable), as well as the writing of the manuscript, to take public responsibility for it and have agreed to have my/our name listed as a contributor. I/we believe the manuscript represents valid work. Neither this manuscript nor one with substantially similar content under my/our authorship has been published or is being considered for publication elsewhere, except as described in the covering letter. I/we certify that all the data collected during the study is presented in this manuscript and no data from the study has been or will be published separately. I/we attest that, if requested by the editors, I/we will provide the data/information or will cooperate fully in obtaining and providing the data/information on which the manuscript is based, for examination by the editors or their assignees. Financial interests, direct or indirect, that exist or may be perceived to exist for individual contributors in connection with the content of this paper have been disclosed in the cover letter. Sources of outside support of the project are named in the cover letter. I/We hereby transfer(s), assign(s), or otherwise convey(s) all copyright ownership, including any and all rights incidental thereto, exclusively to the Journal of Dental Herald, in the event that such work is published by the Journal of Dental Herald. The Journal of Dental Heraldshall own the work, including 1) copyright; 2) the right to grant permission to republish the article in whole or in part, with or without fee; 3) the right to produce preprints or reprints and translate into languages other than English for sale or free distribution; and 4) the right to republish the work in a collection of articles in any other mechanical or electronic format. We give the rights to the corresponding author to make necessary changes as per the request of the journal, do the rest of the correspondence on our behalf and he/she will act as the guarantor for the manuscript on our behalf. All persons who have made substantial contributions to the work reported in the manuscript, but who are not authors, are named in the Acknowledgment and have given me/us their written permission to be named. If I/we do not include an Acknowledgment that means I/we have not received substantial contributions from non-authors and no author has been omitted. Name Signature Date signed 1 ------------- --------------- ------------ 2 ------------- --------------- ------------ 3 ------------- --------------- ------------ (up to three authors for short communication) 4 ------------- --------------- ------------ (up to four authors for case report/review) 5 ------------- --------------- ------------ 6 ------------- ---------------

Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

D

------------ (up to six authors for original studies from single centre) Checklist (to be tick marked, as applicable and one copy attached with the manuscript) Manuscript Title ______________________________________________ Covering letter Signed by all contributors Previous publication / presentations mentioned Source of funding mentioned Conflicts of interest disclosed Authors Middle name initials provided Author for correspondence, with e-mail address provided Number of contributors restricted as per the instructions Identity not revealed in paper except title page (e.g. name of the institute in material and methods, citing previous study as 'our study', names on figure labels, name of institute in photographs, etc.) Presentation and format Double spacing Margins 2.5 cm from all four sides Title page contains all the desired information (vide supra) Running title provided (not more than 50 characters) Abstract page contains the full title of the manuscript Abstract provided (not more than 150 words for case reports and 250 words for original articles) Structured abstract provided for an original article Key words provided (three or more) Key messages provided Introduction of 75-100 words Headings in title case (not ALL CAPITALS) References cited in superscript in the text without brackets References according to the journal's instructions, punctuation marks checked Language and grammar Uniformly British English Abbreviations spelt out in full for the first time Numerals from 1 to 10 spelt out Numerals at the beginning of the sentence spelt out Tables and Figures No repetition of data in tables and graphs and in text Actual numbers from which graphs drawn, provided Figures necessary and of good quality (colour) Table and figure numbers in Arabic letters (not Roman) Labels pasted on back of the photographs (no names written) Figure legends provided (not more than 40 words) Patients' privacy maintained (if not permission taken) Credit note for borrowed figures/tables provided Manuscript provided on a floppy (with single spacing)

Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

E

Editorial

I wish to extend a warm welcome to the readership of Journal of Dental Herald and take this opportunity to extend my gratitude to the authors and anonymous reviewers, all of whom have contributed to the success of the Journal. We are dedicated for the dissemination of high quality research paper in different spare of dentistry and prepare the dental community to face the challenges of the 21st Century. It is also a forum for exchange of information on varied aspects of dentistry. The motive of this journal is to give the readers the best of the quality Original researches, Reviews, Case reports, Newer techniques and above all the latest Book and Product reviews, which would help the readers to keep the pace with the updates. We are also trying to upload the videos of the standard procedure and which will enhance the readers to the know and learn more about dentistry. We, the editorial team will try and focus on the latest updates on researches, reviews, materials and techniques so as to augment the information and to stimulate interest, debate, discussion and interaction among dentists and specialists of all disciplines within the field of dentistry. We will rely on honesty, integrity, strength and ability of our contributors to place the journal among the very best. The editorial policy of the journal will be to disseminate among its readers factual information on research, clinical practice and cases of interests in dentistry.

Dr. Bhanu Kotwal Editor-in-Chief

We wish to express our sincere gratitude to the dedicated editorial board for their efforts and to our contributors. We also want to wish our readers a happy Diwali. I would like to express my recognition for the excellent work and tireless efforts of our team. Awaiting your write-ups for the biggest boom in dentistry. We gladly solicit your valuable contributions and continued support, and I am confident you will take this journal to new heights with a wider coverage and information. I would like to invite your colleagues to step in the laser dentistry world by participating in the 14th diploma module to be held at Rangoonwala Dental College, Pune on August 28th, 29th, 30th, and 31st. Dr. Bhanu Kotwal Editor-in-Chief Journal of Dental Herald E-mail: [email protected]

Journal of Dental Herald. ( Issue:3, Vol.:1, July 2014) All rights are reserved

F

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report

Bilateral And Vertical Mandibular Canine Impaction In Symphysis Region: A Case Report Kaundal Jai Ram1, Chauhan Deepak2, Sharma Kapil Rajeev3, Chauhan Tripti4 1

Assistant professor, Department of Orthodontics, H.P. Government Dental College, Shimla, Himachal Pradesh, India. Senior Lecturer, Department of Pedodontics and preventive dentistry, H.P. Government Dental College, Shimla, Himachal Pradesh, India. 3 Professor and Head. Department of Pedodontics and preventive dentistry H.P. Government dental College and Hospital, Shimla, Himachal Pradesh, India. 4 Assistant Professor, Department of Community Medicine, Indira Gandhi Medical College and Hospital, Shimla, Himachal Pradesh, India. 2

Abstract Retention of a tooth that is unerupted more than a year after the normal age of its eruption is a relatively rare phenomenon, except in the case of the third molars and the upper canines. Here we are reporting a case of 12 year old female patient presenting with bilateral mandibular canine impaction. This rare condition usually requires extraction of the involved tooth because orthodontic forces are seldom successful at erupting these teeth into their proper location. Henceforth, the canines were extracted.

Key Words Retention, phenomenon, Bilateral, Mandibular Canine Impaction

Introduction: Impaction refers to a failure of a tooth to emerge into the dental arch, usually due to either space deficiency or the presence of an entity blocking its path of eruption. Although heredity has long been described as playing a role, many times the aetiology is unknown. Impacted teeth are commonly found in the dental practice and they pose a threat for the maintenance and continuity of dental health. Primarily because of their eruption pattern and sequence, canines are especially prone to impaction and the maxillary canines are affected twenty times more frequently than mandibular canines.[1] Case Report A 12 years old female patient reported to the Department Of Pedodontics And Preventive Dentistry Subsequently Referred To The Department Of Orthodontics with the chief complaint of swelling in her lower front region (Fig.1). Intra-oral clinical examination revealed that she had all her permanent dentition except for the retained deciduous mandibular molars and cupids and had Angle's class II division1 malocclusion with hypoplastic upper right central incisor. The patient was unaware of her prevailing condition. Panoramic radiography revealed over retained deciduous cupids and bilaterally impacted canines lying vertically in the midline at the level of apical 1/3 of the lower incisors. Routine orthodontic diagnostic procedures were carried out including cast analysis, intraoral periapical radiograph, panoramic and lateral cephalogram (Fig.1, 2 & 3). After analysing and joint consultation we reached at a conclusion to extract the impacted canines. Because there are several treatment modalities proposed for impacted mandibular canines including its surgical removal, Quick Response Code

exposure and orthodontic alignment, transplantation and observation. Orthodontic movement of an impacted tooth depends on a

Fig. 1 : Intra oral photograph of the patient showing bulge in the lower anterior region.

Address For Correspondence: Dr. Kaundal Jai Ram Assistant professor, Department of Orthodontics, H.P. Government Dental College, Shimla, Himachal Pradesh, India. Email : [email protected] Fig. 2 : Panoramic radiograph showing bilaterally impacted canines located at the level of apical 1/3 of the lower incisors in vertical position.

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

001

surgical removal of the impacted canines as they were lying just anterior to incisors and signs of cyst or infection were also seen around crowns (Fig. 2). After extraction patient underwent fixed mechanotherapy for correction of her class11 div.1 malocclusion, which showed excellent results at the end of treatment and normal bony healing in pattern (Fig. 4& 5) in the symphysis region.

Fig. 3 : Lateral cephalogram showing impacted canine located in front of the lower incisor.

Fig. 4 : Post treatment Orthopantogram after surgical removal of impacted canines and undergoing fixed mechanotherapy

Fig. 5 : Post treatment lateral cephalogram showing normal healing of bone in symphysis region (two years follow-up)

variety of factors, such as the position of the impacted tooth relative to neighbouring teeth, its angulation, the distance that tooth has to be travelled, and the possible presence of alkalosis.[2] Which does not seem to be practical in this particular case as she has upright incisors and minimal crowding supported extraction of no further permanent tooth other than the impacted canines (Fig.2). Hence we planned for

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Discussion Failure of eruption of the mandibular canine is an unusual event. Mandibular canine impaction is regarded as a much rarer phenomenon and there are limited numbers of studies revealing its frequency of occurrence.[2] The incidence of maxillary canine impaction is in the range of 0.8 to 2.8% and the prevalence is 0.9 to 2.2%. Grover and Lorton found only 11 impacted canines (0.22%) in the mandible in 5000 individuals.[4] Chu et al reported five mandibular impacted canine (0.07%) teeth in 7486 patients.[5] A study by Rohrer examining 3,000 patients radiographically found 62 impacted maxillary canines (2.06%) and only three impacted mandibular canines (0.1%), a 20:1 ratio.[6] In another study by Aydin et al involving 4500 Turkish patients, the incidence of mandibular canine impaction was 0.44%. There are many reasons why canines fail to erupt.[7] Most surgeons agree the reasons may include a suspected pathological condition, infection, interference with prosthetic devices, disturbance of the existing dentition, pain, and ectopic eruption. Many authors have also speculated about the cause of impacted mandibular canines.[8] These causes include inadequate space, supernumerary teeth, premature loss of the deciduous canine, excessive crown length, hereditary factors, functional disturbances of the endocrine glands, tumours, cysts and trauma.[2],[7],[8],[9],[10] Impacted mandibular canines are also more likely to be located on the labial aspect of the dental arch than are maxillary canines and the removal of impacted teeth routinely involves an intraoral surgical approach.[11] But Plumpton suggested that some extractions of the impacted mandibular canine teeth may be done via an extra-oral surgical approach.[12] There are several treatment options proposed for impacted mandibular canines including surgical removal, exposure and orthodontic alignment, transplantation and observation. Some authors believe asymptomatic impacted teeth can be left in place, but in these patients a series of successive radiographs should be taken periodically. Observation of impacted mandibular canines may be indicated in the following circumstances. [ 1 3 ] If a systemic contraindication to a surgery exists or there is a deeply impacted asymptomatic mandibular canine with no associated pathology, particularly in an older patient. Whenever the patient has a satisfactory dental appearance and does not want surgical intervention. If the deciduous canine has a good root length and it is aesthetically acceptable observation of an asymptomatic mandibular canine can be recommended. A large number of completely impacted teeth may be retained when they are asymptomatic.[14] However; Bishara et al. Suggested [15],[16] labial or lingual malpositioning of the impacted tooth and migration of the neighbouring teeth and loss of arch length as a sequelae of canine impaction. Surgical extraction is required in the following situations: Infection particularly with partial eruption resulting in pain and trismus of jaw.

002

? The existence of infection, cyst or tumour related to the

impacted canine.[17] ? The impacted tooth causes the periodontal disturbance of the adjacent teeth.[17] ? Referred pain with neurologic symptoms.[17] ? Crowding of the mandibular arch requiring therapeutic extractions to correct crowded incisor teeth.[3] ? The impacted canine is ankylosed and cannot be transplanted. ? There is evidence of root resorption affecting the adjacent teeth. ? The root of impacted canine is severely dilacerated. ? Severe impaction of canine tooth. ? Patient rejection of orthodontic treatment or transplantation. Conclusion Impaction of the mandibular canine in the symphysis region is a rare phenomenon and early clinical and radiographic examination of a patient is important for treatment planning. Presence of over-retained deciduous canine or missing permanent canine should be evaluated for its presence or absence. An early and timely intervention would lead to better management and hence avoids the potential complications associated with canine impaction. References: 1. Aras MH, Buyukkurt MC, Yolcu Ü, Ertas Ü, Dayi E. Transmigrant maxillary canines. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontology. 2008;105 (3): e48-e52. 2. Rebellato J, Schabel B. Treatment of patient with an impacted transmigrant mandibular canine and a palatally impacted maxillary canine. Angle Orthod 2002;73(3):32836. 3. Camilleri S, Scerri E. Transmigration of mandibular canines – A review of the literature and a report of five cases. Angle Orthod 2003;73:753-62. 4. Grover PS, Lorton L. The incidence of unerupted permanent teeth and related clinical cases. Oral Surg Oral Med Oral Pathol 1985;59:420-25.

5. Chu FCS, Li TKL, Lui VKB, Newsome PRH, Chow RLK, Cheung LK. Prevalence of impacted teeth and associated pathologies – a radiograph study of the Hong Kong Chinese population. Hong Kong Med J 2003;9:158-63. 6. Rohrer A. Displaced and impacted canines. Int J Orthod Oral Surg 1929;15:1003. 7. Wright DM. A case report: Forced eruption of an impacted lower canine in a 48-year-old man. J Am Dent Assoc 1995; 126:1025-27. 8. Milano M, Barrett L, Marshall E. extraction of a horizontally impacted mandibular canine through a genioplasty approach: Report of a case. J Oral Maxillofacial Surg 1996;54:1240-42. 9. Joshi MR. Transmigrant mandibular canines: A record of 28 cases and a retrospective review of the literature. Angle Orthod 2001;71: 12-22. 10. Brezniak N, Ben-Yehuda A, Shapira Y. Unusual mandibular canine transposition: A case report. Am J Orthod Dentofacial Orthop 1993;104:91-94. 11. Fonseca JR. Oral and Maxillofacial Surgery. Phailadelphia : W.B.Saunders, 2002;1:342-71. 12. Plumpton S. The extraction of mandibular teeth via an extra-oral approach. Br J Oral Surg 1966;4:127-31. 13. Yavuz MS, Aras MH, Buyukkurt MC, Tozoglu S. Impacted Mandibular Canines. J Contemp Dent Pract 2007;7(8):078-85. 14. Yamaoka M, Furusawa K, FujimotoK, Uematsu T. Completely impacted teeth in dentate and edentulous jaws. Aust Dent J 1996: 41:169-72. 15. Bishara SE, Kommer DD, McNeil MH, Montagano LN, Oesterle LJ, Youngquist W. Management of impacted canines. Am J Orthod 1976: 69:371-87 16. Bishara SE. Impacted maxillary canines. Am J Orthod Dentofac Orthop 1992: 101:159-71. 17. Alaejos-Algarra C, Berini-Aytes L, Gay-Escoda C. Transmigration of mandibular canines: Report of six cases and review of the literature. Quintessence Int. 1998: 29:395-398.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

003

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report

Non Extraction Treatment Using Different Self Ligation Appliance – A Case Series Gurkeerat Singh1, Naseem Joy Garg2, Amit Dahiya3, Daya Shankar4, Rajeev K Shukla5 1

Professor And Head, Department Of Orthodontics, Sudha Rustagi College Of Dental Sciences And Research, Faridabad, India Senior Lecturer, Department Of Orthodontics, Rajasthan Dental College And Hospital, Jaipur, India 3 Former Postgraduate Student, Department Of Orthodontics, Sudha Rustagi College Of Dental Sciences And Research, Faridabad, India 4 Former Postgraduate Student, Department Of Orthodontics, Sudha Rustagi College Of Dental Sciences And Research, Faridabad, India 5 Associate Professor, Department Of Dentistry, Late Shri B K M Govt. Medical College, Jagdalpur, India 2

Abstract Self-ligation in orthodontics implies that the orthodontic bracket has the ability to engage itself to the archwire and is therefore assumed to reduce friction by eliminating the ligation force. These bracket systems have a mechanical device built into the bracket to close off the edgewise slot. Various clinical researches have shown advantages of self ligation in relation to friction, treatment duration and the level of discomfort. This article consists of four cases treated with different self ligation bracket systems highlighting its application and versatility.

Key Words Non Extraction, Self-ligating brackets, SLBs

Introduction Self-ligating brackets were introduced in this specialty in its first form some decades ago but in the past 2 decades, there has been a boost in the manufacturing and release of self-ligating appliances with active or passive ligation modes. Self-ligating bracket restrains the archwire within the slot by means of a slide or a clip that covers the slot.

A 17-year-old post-pubertal female reported with a complaint of spacing in upper front teeth. She had a Skeletal Class I relation on account of normally positioned maxilla and mandible, vertical growth pattern, dento-alveolar Angle’s Class I molar relation with a labially impacted canine in maxillary arch. She had mild crowding in mandibular arch and non-coincident midlines. (Fig.1)

The self ligation in based on principal of using biologically induced tooth moving forces in each phase of orthodontic treatment. The final position of the teeth after treatment with the self-ligating bracket systems is determined by the balanced interplay between the oral musculature and periodontal tissues and not by heavy orthodontic forces.[1],[2]

On extra-oral examination, patient had apparently symmetrical face with an orthognathic profile. (Fig.2) The space available for impacted canine was only 4mm. Self ligating brackets (American Orthodontics) were bonded with

The most compelling potential advantages attributed to SLBs are a reduction in overall treatment time[3],[4] and less associated subjective discomfort.[5] Other purported improvements include more efficient chairside manipulation[4] and promotion of periodontal health due to poorer biohostability.

Fig : 2

This article consists of four cases treated with different Self ligation systems highlighting its application and versatility in orthodontics. Case 1: Quick Response Code

Fig : 3 Address For Correspondence: Dr. Gurkeerat Singh Professor and Head, Department of Orthodontics, Sudha Rustagi College of Dental Sciences and Research, Faridabad, India

Fig : 4

which arch development occurred, providing sufficient space for the canine to erupt. Disimpaction of canine was completed in 6 months by using series of CuNiTi round archwires:- .013” & .016” and rectangular:- 0.014 x 0.025” CuNiTi , 0.016 x 0.025” CuNiTi. Finishing and detailing was done on 0.019 x 0.025” TMA in both arches. (Fig.3) The active treatment duration was 14 months. This was

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

004

Fig : 7

Fig : 5 Fig : 6

Fig : 10 Fig : 8 Fig : 9

Fig : 11

Fig : 14

Fig : 13 Fig : 12

Fig : 15

followed by a permanent retention using fixed lingual bonded retainers. (Fig.4 & Fig.5) Case 2 A 14-year-old post pubertal female reported with a complaint of irregular upper teeth. She had a Skeletal Class I relation on account of normally positioned maxilla and mandible, horizontal growth pattern, dento-alveolar Angle’s Class I molar relation with mild crowding of 1mm in maxillary arch and 3mm in mandibular arch and increased overbite. (Fig.6 & Fig.7) The Damon Q brackets were bonded and leveling and aligning undertaken with 0.013” CuNiTi in both arches. Finishing and detailing was done using 19x25” TMA in both arches. (Fig.8) The active treatment duration was 11 months. This was followed by a permanent retention using fixed lingual bonded retainers in both arches. The contact area between left maxillary central and lateral incisor still required some finishing but it could not be done as patient had to go abroad. (Fig.9 & Fig.10) Case 3 A 16 year old post-pubertal female reported with complaint of irregular front teeth. She had skeletal Class I jaw base relation with an underlying horizontal growth pattern and Angle’s Class I malocclusion with crowding in both arches, multiple rotations, increased overbite, shifted midlines and carious mandibular first molars. After endodontic treatment, Self ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Fig : 16

ligating brackets(IRIS SL; Orion Orthodontics) were bonded. Bite turbo was used for overbite correction. The active treatment duration was 11 months. This was followed by a permanent retention using fixed lingual bonded retainers in both arches. (Fig.11, Fig.12, Fig.13, Fig.14 & Fig.15) Case 4 A 14-year-old postpubertal female reported with a complaint of irregular upper front teeth. Diagnosis confirmed Skeletal Class I relation on account of normally positioned maxilla and mandible, horizontal growth pattern, dento-alveolar Angle’s Class I molar relation with mild crowding in maxillary arch, increased overbite and posterior crossbite. Damon 3MX was bonded. Arch development corrected the posterior crossbite. The active treatment duration was 15 months. This was followed by a permanent retention using fixed lingual bonded retainers in both arches. (Fig.16, Fig.17, Fig.18, Fig.19 & Fig.20) Discussion This case series shows that self ligation system does have a versatile applicability with its foremost advantage of significant reduction with regard to chair time. Research has shown that in patients with moderate crowding the selfligating group had 2.7 times faster correction[6] with an additional advantageous in that they do not promote poor oral hygiene, as with elastomeric ties, and eliminate any chance of 005

Fig : 17 Fig : 18

Fig : 20

soft tissue laceration to both the patient and the orthodontist from the use of stainless steel tie wires. It is all because of these factors that self ligation is becoming the preferred bracket system in present orthodontic world. References 1. Non extraction treatment approach in adolescents using Damon appliance: Case series; Garg NJ, Singh G, Gupta G, Dahiya A, Gupta A; Dental Practice; May-June 2013; Vol 11(6); 68-71 2. Damon 3MX a Versatile Appliance: Case Series; Dahiya A, Singh G, Garg NJ, Kannan S, Kaul A, Goyalia A; Journal of Orofacial & Health Sciences; January-April, 2013; Vol.

Fig : 19

4(1); 42-46 3. Harradine NW. Self-ligating brackets and treatment efficiency. Clin Orthod Res. 2001;4(4): 220–227. 4. Eberting JJ, Straja SR, Tuncay OC. Treatment time, outcome, and patient satisfaction comparisons of Damon and conventional brackets. Clin Orthod Res. 2001;4: 228–234. 5. Damon DH. The Damon low-friction bracket: a biologically compatible straight-wire system. J Clin Orthod. 1998;32: 670–680. 6. Self-ligating vs conventional brackets in the treatment of mandibular crowding: A prospective clinical trial of treatment duration and dental effects; Pandis N, Polychronopoulou A, Eliades T; Am J Orthod Dentofacial Orthop 2007;132: 208-15

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

006

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report

Hollow Bulb Obturator Prosthesis For Maxillectomy Patient – A Case Report Deept Jain1, Rohan Sikka2, Dhruv Arora3, C. Nisha4, Narendra Kumar5 1

Senior Lecturer, Department Of Periodontics, Institute Of Dental Studies & Technologies Modinagar,Ghaziabad,Uttar Pradesh, India. Senior Lecturer, Department Of Prosthodontics, Institute Of Dental Studies And Technologies Modinagar, Ghaziabad, Uttar Pradesh, India. 3 Senior Lecturer, Department Of Prosthodontics, Institute Of Dental Studies And Technologies Modinagar, Ghaziabad, Uttar Pradesh, India. 4 Senior Leturer, Department Of Prosthodontics, Institute Of Dental Studies And Technologies Modinagar, Ghaziabad, Uttar Pradesh, India. 5 Professsor & Head, Department Of Prosthodontics, Institute Of Dental Studies And Technologies Modinagar, Ghaziabad, Uttar Pradesh, India. 2

Abstract Defect in the maxillae may be due to congenital malformation, traumatic injury or surgical intervention resulting in a communication between the oral and nasal cavities. Several techniques ranging from surgical to prosthetic reconstruction have been advocated for reconstruction of these defects. The use of obturator prosthesis is one of them with emphasis on retention of the prosthesis and comfort of the patient while maintaining a good oral hygine. This clinical report describes the fabrication of maxillary denture with a closed bulb hollow obturator for a patient with a maxillary defect after undergoing surgical procedure.

Key Words Obturator, Maxillae, Prosthesis

Introduction Oral cancer in India constitutes 12% of all the cancers in men & 8% among women. Surgical resection of tumors of the hard palate, maxillary sinus and the buccal mucosa results in the oral cavity, maxillary sinus, nasal cavity and nasopharynx becoming one unified chamber. Prosthetic rehabilitation using maxillary obturator prosthesis is essential for restoring the contours of the resected palate and recreating the functional separation of the oral cavity, sinus and nasal cavities. Prosthetic rehabilitation should be planned prior to surgical resection. Lack of anatomic boundaries between these cavities creates severe disabilities in speech and deglutition. Food bolus escapes from the oral cavity to exit the nares, making adequate oral nutrition difficult. Speech becomes unintelligible due to hyper-nasality, distorting sounds that require impounding of air within the oral cavity. Case Report A 76 year old male patient was referred to department of Periodontics of our dental college, with chief complaint of bad mouth odor and ill fitting feeding plate. Patient was a diagnosed case of carcinoma left maxillary sinus and was operated upon eight months ago. He was given an interim feeding maxillary feeding plate after the surgery to prevent the ingress of food and oral fluids into nasal cavity while eating.. (Fig:A) No facial asymmetry or swelling was detected on extra-oral examination. Regional lymph nodes were soft and not fixed to the underlying structures. Patient was unable to maintain good oral hygine due to ill fitting feeding plate. (Fig:B) On periodontal evaluation it was found that patient had Quick Response Code

heavy deposits of plaque and calculus on existing dentition. Complete oral prophylaxis was done for the patient in multiple appointments keeping in mind the mouth opening of a maxillectomy patient. The patient was the referred to the department of Prosthodontics for further treatment of fabrication of definitive obturator prosthesis. Thorough oral prophylaxis was carried out and an irreversible hydrocolloid (Zelgan, Dentsply Co Ltd) impression (Fig:C) was made with a stock tray (Jabbar Co Ltd). Diagnostic cast was poured in dental stone (Kalstone, Kalabhai Pvt Ltd). Custom tray was used for making a secondary impression for which border molding was done with a medium fusing impression compound and functional impression was made with a silicone material (Silagum, DMG chemicals) The impression was boxed and poured in high strength dental stone (Fig:D) (Kalstone, Kalabhai Pvt Ltd). Unfavourable defect undercut were blocked on the cast with the help of modeling wax (Y Dent Co Ltd). Temporary denture bases were constructed with shellac base plate (Samit Dental Products) on which occlusal rims with modelling wax (Y Dent Co Ltd) were fabricated. (Fig:E) A class I ridge relationship was recorded, the vertical dimensions were kept on the lower side and the plane of occlusion was kept towards maxillary arch.

Fig A

Fig B

Fig C

Fig D

Address For Correspondence: Dr. Deept Jain Department Of Periodontics, Institute Of Dental Studies And Technologies, Modinagar, Ghaziabad, Uttar Pradesh, India E Mail Id : [email protected] Mobile No: 09871048800

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

007

internal surface which is necessary due to the accumulation of deposits from saliva, mucous crusts, and food. Thus, a light weight denture was fabricated for the patient improving oral hygine and quality of life for the patient.

Fig E

Fig F

Fig G

Fig H

Fig I

Fig J

The prosthesis was designed to be in two portions. First portion extended into the defect area while the second portion was the oral palatal plate. The area between the two portions was kept hollow so that the prosthesis was light in weight. Undercuts on the defect were blocked with clay and a wax sheet was adapted to the rest of the defect area. The bulb portion was flasked and packed with heat cured polymethylmethacrylate resin, the palatal plate portion was acrylised separately. The two portions of the interim obturator were joined together using autopolymerising acrylic resin (Fig: F, Fig: G, Fig: H). The obturator was examined for any leakage by immersing it in water. The prosthesis should float if the hermetic seal is maintained. The prosthesis was tried in the patient’s mouth (Fig: I) and minor adjustments were carried out. Occlusion was verified on the non-resected side (Fig: J). Patient was educated regarding insertion & removal of the prosthesis and also motivated regarding the post insertion oral hygine maintenance of the prosthesis. Patient was asked to report for post insertion adjustments at 1 day, 7 days and 30 days. Discussion Defect in the maxillae resulting in a communication between the oral and nasal cavities causes difficulty in swallowing, nasal reflux, unintelligible speech and an unesthetic appearance, adversely affecting the quality of life of the individual. Approximately 6 months after surgery, definitive obturator prosthesis may be fabricated if the patient is comfortable. The weight of prosthesis should be considered with respect to retention and comfort of the patient. The bulb extending into the defect area could be open or closed but usually made hollow. The closed hollow bulb is preferred over open one. Disadvantage for open designs of obturator is that nasal secretions accumulate leading to bad odour and contribute to poor oral hygine and also increase the weight of the prosthesis. If secretions do tend to accumulate, a small diagonal opening may be made between the inferior-lateral walls of the obturator through to the cheek surface for drainage. The other disadvantages of an open type hollow obturator include difficulty in polishing and cleaning the

Summary Rehabilitation of maxillofacial defects is a real challenge, closed bulb hollw obturators helps in feeding besides improving speech and improving psychological well-being of the patient by maintaining lighter weight for the overall prosthesis. References 1. Khandekar SP, Bagdey PS, Tiwari RR. Oral cancer and some epidemiological factors: A hospital based study. Ind J Comm Med Vol. 31, No. 3 (2006-07 - 2006-09) 2. Aramany MA. Basic principles of obturator design for partially edentulous patients. Part I: Classification. J Prosthet Dent 1978; 40: 554. 3. Aramany MA. Basic principles of obturator design for partially edentulous patients. Part II: Design principles. J Prosthet Dent 1978; 40: 656. 4. Key F. Obturator prostheses for hemimaxillectomy patients. J Oral Rehabil 2001; 28:821-29. 5. Shetty V, Gali S, Ravindran S. Light Weight Maxillary complete denture: A case report using a simplified technique with thermocol. J Interdisp Dent 2011; 1:45-48. 6. Beumer J, Curtis TA, Firtell DN. Maxillofacial rehabilitation. St. Louis: Mosby; 1979:188-243. 7. Thota KK, Tella S, Anulekha CKA, Ravuri R. A Prosthodontic Rehabilitation of a Partial Maxillectomy Patient with Hollow Bulb Obturator. Ind J Dent Adv 2010; 2:383-385. 8. Paprocki GJ, Jacob RF, Kramer DC. Seal integrity of hollow-bulb obturators. Int J Prosthodont 1990;3:457-62. 9. Taylor TD, La Velle WE. Dental management and rehabilitation. In: Thawley SE, 10. Panje WR, Batsakis JG, Lindberg RD, editors. Comprehensive management of head and neck tumors. Philadelphia: W.B. Saunders; 1987. p. 596-605. 11. Desjardins RP. Obturator prosthesis design for acquired maxillary defects. J Prosthet Dent 1978;39:424-35. 12. Brown KE. Clinical considerations improving obturator treatment. J Prosthet Dent 1970;24:461-6. 13. Nidiffer TJ, Shipmon TH. The hollow bulb obturator for acquired palatal openings. J Prosthet Dent 1957;7:126-34. 14. Mahdy AS. Processing a hollow obturator. J Prosthet Dent 1969;22:682-6. 15. Palmer B, Coffey KW. Fabrication of the hollow bulb obturator. J Prosthet Dent 1985;53:595-6. 16. Matalon V, LaFuente H. A simplified method for making a hollow obturator. J Prosthet Dent 1976;36:580-2. 17. Bair FM, Hunter NR. The hollow box maxillary obturator. Br Dent J. 1998;184:484–487. 18. Shaker KT. A simplified technique for construction of an interim obturator for a bilateral total maxillectomy defect. Int J Prosthodont. 2000;13:166–168. 19. Wu YL, Schaaf NG. Comparison of weight reduction in different designs of solid and hollow obturator prostheses. J Prosthet Dent. 1989;62:214–217.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

008

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report Surgical Removal Of Palatally Placed Dilacerated Central Incisor. Nivedita Rewal1, Arun Singh Thakur2, Nanika Mahajan3, Ritika Sharma4 1

Assistant Professor, Dept. of Pedodontics and Preventive Dentistry, Himachal Dental College Sundernagar Assistant Professor, Dept. of Public Health Dentistry, Himachal Dental College Sundernagar 3 Registrar, Indira Gandhi Govt Dental College, Jammu 4 DA, Greenwood Dental, Salt Lake City, Utah, USA. 2

Abstract Any trauma that occurs to the primary dentition might result in damage to the underlying developing permanent tooth. The permanent tooth might result in one with enamel hypoplasia or with a dilacerated root.This paper is a report of a 12 year old girl with a dilacerated left central incisor.

Key Words Dilacerated, Trauma, Central Incisor.

Introduction Dilaceration is a developmental disturbance in shape of teeth. It refers to an angulation, or a sharp bend or curve, in the root or crown of a formed tooth. On an average thirty to forty percent of children incur at least oneinjury to the primary teeth and the incidence is notgender related.[1] Dilaceration is one of the causes of central incisor eruption failure and also results in the angulation of the permanent tooth. The condition is due to trauma during the period in which the permanent tooth is forming.It is the close proximity of the developing permanent tooth to the already primary tooth present in the arch which results in such malformations.[2] The case presented in this report is of dilacerated left central incisor. Case Report A 12 year old girl reported to the Department of Pedodontics and Preventive Dentistry, Himachal dental college, Sundernagar with the chief complaint of missing left central incisor (Figure 1). History of the patient as specified by the parent revealed trauma to the primary dentition. An intra oral periapical radiograph was taken to confirm the presence of the central incisor. The tooth was found to be impacted with dilaceration. The position and the diagnosis were confirmed by taking an orthopantograph (Figure 2). The position of the tooth was such that orthodontic extrusion was not possible. Therefore a surgery to remove the dilacerated central incisor was planned. The blood investigations were carried out before the surgery. After obtaining adequate anaesthesia an incision was given and buccal flap was raised (Figure 3). Bone cutting was done and the tooth was removed with utmost care (Figure 4). The follicle of the tooth was

enucleated and curettage was done followed by copious irrigation and a clean cavity was visible thereafter. Sutures were placed at the end of surgery to promote healing (Figure 5). The healing was uneventful and sutures were removed after 1 week. A finger spring appliance was delivered to the patient in order to create space by distalization of the left lateral incisor (Figure 6, 7). After the creation of space to accommodate the left central incisor, giving due consideration to the socioeconomic condition, a removable prosthesis wasdelivered to the patient (Figure 8).

Figure 1 : Preoperative Photograph

Figure 2 : Opg

Figure 3 : Flap Raised Figure 4 : Tooth Removed

Quick Response Code

Address For Correspondence: Dr. Arun Singh Thakur Assistant Professor Department of Public Health Dentistry Himachal Dental College Sundernagar -175002 Himachal Pradesh. Email id: [email protected] Figure 5 : Sutures Placed

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Figure 6 : Appliance Delivered

009

removable prosthesis was delivered to the patient after adequate space was available to accommodate the left central incisor.

Figure 8 : Removable Prosthesis Delivered Figure 7 : Creation Of Space

Discussion Intrusive injuries in the primary dentition result in developmental disturbances in the permanent dentition.Crowndilaceration of permanent teeth occurs in permanent maxillary incisors because of the close proximity of their tooth germs to the primary incisors, which are more susceptible to trauma. Studies have shown that proper crown exposure surgery and orthodontic traction can be used to successfully manage impacted maxillary anterior teeth.[3],[4],[5] Thetreatment options available are surgical exposure with or without orthodontic treatment, removal of dilacerated part of the crown, temporary crown until root formation, semi or permanent restoration and prosthetic or orthodontic space closure after extraction.[6] In the present case report the dilacerated tooth had to be removed as the orthodontic repositioning was not possible. In order to create space between right central and left lateral incisor a finger spring appliance was delivered to the patient. A

References 1. Shafer WG, Maynard KH, Bernet ML. Oral Pathology. W.B. Saunders Co: Philadelphia; 1993. p 40. 2. Sennhenn-Kirchner S, Jacobs HG. Traumatic injuries to the primary dentition and effects on permanent successors – a clinical follow – up study. Dent Traumatol 2006; 22: 237-41. 3. Crawford LB. Impacted maxillary central incisor in mixed dentition treatment. Am J OrthodDentofacOrthop. 1997;112: 1-7. 4. Wasserstein A, Tzur B, Brezniak N. Incomplete canine transposition and maxillary central incisor impaction: A case report. Am J OrthodDentofacialOrthop. 1997;111: 635-639. 5. Kajiyama K. Esthetic management of an unerupted maxillary central incisor with a closed-eruption technique. Am J OrthodDentofacialOrthop.2000;118: 224-228 6. Asokan S, Rayen R, Muthu MS, Sivakumar N. Crown dilaceration of maxillary right permanent central incisor – A case report. J Indian socPedoPrev Dent 2004;22: 197200.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

010

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report

A Technique To Restore Endodontically Treated Posterior Teeth With Customized Split Post And Core: A Case Report Aditi Sharma1, Pallak Arora2 1 2

Department of Prosthodontics, ECHS Hospital Jammu, India Senior Resident Department of Oral Medicine and Maxillofacial Radiology, Kalka Dental College, Meerut, India

Abstract Self-ligation in orthodontics implies that the orthodontic bracket has the ability to engage itself to the archwire and is therefore assumed to reduce friction by eliminating the ligation force. These bracket systems have a mechanical device built into the bracket to close off the edgewise slot. Various clinical researches have shown advantages of self ligation in relation to friction, treatment duration and the level of discomfort. This article consists of four cases treated with different self ligation bracket systems highlighting its application and versatility.

Key Words Endodontically, Split Post, ligation Force

Introduction Posterior teeth carry greater occlusal loads than anterior teeth, and restorations must be planned to protect posterior teeth against fracture. The post, the core, and their luting or bonding agent together form a foundation restoration to support a coronal restoration for the endodonticallytreated tooth.[1] All the changes that accompany root canal therapy influence the selection of restorative materials and procedures for endodontically treated teeth. Important considerations include the following:

Indications for Split Cast Metal Post and Core For multirooted teeth with divergent roots having grossly decayed coronal tooth structure.

? The amount of remaining tooth structure. ? The anatomic position of the tooth. ? The occlusal forces on the tooth. ? The restorative requirement of the tooth. ? The esthetic requirements of the tooth.

Aim The aim of the technique used in this case is to place post and core assembly in endodontically treated molar with almost total coronal destruction which may be salvageable by using multiple post in divergent canals.

Also the endodontically treated posterior teeth are subjected togeather loading because of their closerproximity to the transverse horizontal axis.[2] Careful occlusaladjustment will reduce potentially damaging lateral forcesduring excursive movements. Nevertheless, endodonticallytreated posterior tooth should receive cuspal coverage toprevent biting forces from causing fracture. Possibleexceptions are mandibular premolars and first molars withintact marginal ridges and conservative access cavities notsubjected to excessive occlusal forces. Relatively long postswith a circular crosssection provide good retention andsupport in anterior teeth but should be avoided in posteriorteeth, which often have curved roots and elliptical or ribbon-shaped canals.[3],[4] For these teeth, retention is better providedby two or more relatively short

Case Report A 22 years old femalecame with grossly destructive molar, lower left endodonticallytreated posteriortooth. Patient complained of difficulty in chewing food due to insufficient tooth structure present in relation to the same.On examination, it was revealed insufficient coronal tooth structure in relation to 37 (Figure1 a and b).

Quick Response Code

posts in the divergent canals. Canal configuration aids in making a choice between acustomdesigned post and a prefabricated post.If theselected post closely fits or conforms to the canal shape andsize, it may be a more conservative option because lessdentin removal is required.[8],[9]

To retain a porcelain fused to metal crown alone which was endodontically treated an indirect technique was used for fabrication of cast post and core. Post space preparation was

Address For Correspondence: Dr. Aditi Sharma. Department of Prosthodontics, ECHS Hospital Jammu, India E-mail: [email protected]

Fig : 1a A Female With Insufficient Coronal Tooth I.R.T 37

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Fig : 1b A Female With Insufficient Coronal Tooth I.R.T 37

011

light finger pressure. Rapid seating, excessive cement, and heavy seating pressure can produce high hydraulic pressure inside the root that may be great enough to crack the tooth (Fig.3).

Fig : 2a Master Cast After Final Impression With Post Space.

Fig : 2b Split Post And Core For Mesial And Distal Root.

Fig : 3 Post And Core Cemented With Adequate Amount Of Cement With Mild Finger Pressure.

Fig : 4a Tooth Preparation Done After Cementation. Fig : 4b Crown Cemented After Tooth Preparation

done with a post space drills less than size 3 gate-glidden drill. Method A final impression of the prepared tooth and post space was made using light body and putty. Post space impression was recorded using orthodontic stainless steel wire and light body. Orthodontic wire was measured and adjusted upto the required depth into post space. After adjusting, the wire was later removed andcoated with the light body and again re-inserted into the post spaces till the light body sets. Over this assemblya final impression of tooth and entire arch was made with elastomeric putty impression material. Final impression was removed from the mouth and was thoroughly examined for any error. The impression was later disinfected in the laboratory with 1:213 iodophor and poured with the die material. The impression tray was later removed form the set cast.Split post and core design was panned in the procedure. Separate post was made for the distal root and the mesial root. (Fig. 2a & 2b). Separating media was coated inside the post spaces of 37 over the cast and theseprate wax patterns using inlay waxfor distal and mesial(buccal and lingual) post space was prepared. Once the post space wax pattern has been prepared, additional inlay wax was used to make core. This entire assembly was later sent to laboratory for spruing, investing and casting with the base metal alloy. After finishing the casting both posts with a metal core has been adjusted inside the primary(distal) and secondary(mesial) canal one by one. An adequate amount of cement was placed on the post and core restoration, which was then slowly seated into the tooth with

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Finally, the tooth preparation was done to receive a crown.The "margins" of the crown preparation are usually prepared slightly below the gum line, and on tooth structure, rather than on the core material. The prepared part of the tooth above the gum which includes both tooth structure and core (filling) material is called the preparation (Fig 4a). And finally the PFM crown was cemented over the final preparation (Fig 4b). Discussion A pulpless tooth has commonly lost substantial toothstructure as a result of previous restorations, dental caries,and the access preparation for endodontic therapy.Consequently, a pulpless tooth requires a restoration thatconserves and protects the remaining tooth structure. It hasbeen reported that a large number of endodontically treatedteeth are restored to their original function with the use ofintraradicular devices.[2] These devices vary from a conventionalcustom cast post and core to one-visit techniques, usingcommercially available prefabricated post systems.Markus Balkenhol et al in their longitudinal studyconcluded that post and cores customfabricated using astandardized fabrication technique has a good long-termprognosis. Posts and cores are commonly required withpulpless teeth. Custom-cast posts and cores are generallyrecommended for posterior as well as anterior teeth withgrossly decayed crown structure.[3],[4] The cast post and core iscustom fitted to the prepared root canal space and designedto resist torsional forces. Morgano SM, Heydeche G, MentinAG quoted custom-fabricated, cast post and cores are stillregarded as the established technique or gold standard forrestoring extensively damaged teeth.[5] The presence of a split for the post system reducesinsertion and cementation stresses for this post system.[6] Thesplit may act as a vent for release of hydrostatic pressureduring cementation of the post into the canal and minimizesstresses during cementation. Ash M, Smith CT stated thatcanal configuration aids in making a choice between acustom-designed post and a prefabricated post. If theselected post closely fits or conforms to the canal shape andsize, it may be a more conservative option because lessdentin removal is required, thus enhancing fractureresistance of the tooth, as well as retention of the post.[7],[8] Theprimary reason for using a post is to retain the core thatsubstitutes the missing coronal tooth structure. Therefore,the post head design is an important factor. The post headshould provide adequate retention and resistance todisplacement of the core material.[10] Studies have reportedthat prefabricated metal posts with direct cores made of glass-ionomer, composite, or amalgam are less reliable than aone-piece cast post and core because of the interface betweenthe post and the core. Conclusion Not every tooth with a root canal needs a post, but every tooth with a root canal needs a core! The goal of restoration of endodontically treated teeth is to retain natural teeth with maximum function and esthetics and it 012

also replaces missing tooth structure, maintains function and esthetics, and protects against fracture and infection.Successful endodontic debridement and apical sealing are essential underpinnings for the restoration of the non-vital tooth. Looking at the condition of the tooth, one can see that without the core (filling) portion of the preparation, there would not be much tooth left above the gum line to retain the crown. Even a tooth that is largely intact after the root canal treatment has a hole leading into the pulp chamber to allow access for the root canal procedure. This needs to be filled before doing the crown preparation. Otherwise, the empty space inside the preparation would leave the tooth weak and prone to breaking off after the crown is placed. In this case report there is a different path of insertion forboth the posts. Seating the post first in the distal canal isbeing followed by the seating the post in the mesialcanal of the mandibular molar. Simplified design and easeof fabrication are the major advantages of this case report.The technique can be accomplished in any dental clinicwithout using any complicated equipments.

2. Lakshaykumar et al. International journal of Prosthodontics and Restorative Dentistry, January march 2012; 2(1):16-18. 3. Rosenstiel, Land, Fujimoto. Contemporaray fixed Prosthodontics 3rd edition 2001; 272-312. 4. Shillinburg, Hobo S. Fundamental of fixed Prosthodontics (3rd edition) Chicago. Quintessence 1997. 5. Goerig AC. Munenighoff LA. Management of endodontically treated tooth. Part II: technique. J PProsthet Dent 1983; 49:491-97. 6. Morgano SM, Milot P. Clinical success of cast metal posts and core. J Prosthet Dent 1993;70:11-16. 7. Brett I etal. Comparison of photoelstic stress for a split shank threaded posts. J Prosthet Dent 1994;3:53-55. 8. Barban DJ. The restoration of endodontically treated teeth: An update. J Prosthet Dent 1988;59:553-58. 9. Lewis R, Smith BG. A clinical survey of failed post retained crowns. Br Dent J 1988;165:95-97. 10. Sorenson JA etal. Effect of post adaptation on fracture resistance of endodontically treated tooth. J Prosthet Dent 1990;64:419-24.

References: 1. Devendrakumar et al. Journal of Orofacial Research, April june2012; 2(2):95-98. Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

013

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

Case Report

A Rare Presentation Of Bilateral Mesiodens And Its Management In A 6 Year Old Child – A Case Report Jingarwar MM1, Bajwa Nk2, Pathak A.3 1 2 3

Post Graduate Student, Department Of Pedodontics, Govt. Dental College & Hospital, Patiala. Punjab Mds, Dept. Of Pedodontics, Govt. Dental College & Hospital, Patiala. Punjab Mds, Professor And Head Of Department Of Pedodontics, Govt. Dental College & Hospital, Patiala. Punjab

Abstract Mesiodens refers to supernumerary tooth present in midline between the central incisors. Mesiodens is the most common supernumerary teeth, occurring in 0.15% to 1.9% of the population.It is associated withdisturbances in tooth eruption, midline diastema, axialrotation, inclination of erupted permanent incisors orcomplications such as resorption of adjacent teeth anddevelopment of dentigerous cysts. It is therefore important for the clinician to diagnose amesiodens early in development to allow for optimal yet minimal treatment.Early diagnosis allows the most appropriate treatment, often reducing the extentof surgery, orthodontic treatment and possible complications. This paper reports the presence and describes the management of bilateral mesiodens in a 6 year old child.

Key Words bilateral mesiodens, child patient, supernumerary

Introduction A supernumerary tooth is a developmental anomaly of number characterized by the presence of tooth in addition to the normal series. The first report of a supernumerary tooth appeared between AD 23 and 79[1].The term mesiodens refers to a supernumerary tooth present in the premaxilla between the two central incisors. Mesiodens are more common in permanent than in primary dentition. The incidence of occurrence of mesiodens is 0- 1.9% for deciduous teeth and 0.15-3.8% for permanent teeth with male to female occurrence ratio of 2:1[2]. It is associated with disturbances in tooth eruption, midline diastema, axial rotation or inclination of erupted permanent incisors or complications such as resorption of adjacent teeth and development of dentigerous cysts[3],[4]. Case Report A 6 year old male patient visited the Department of Pediatric and Preventive Dentistry, Government Dental College and Hospital Patiala, with a chief complaint of an extra tooth in upper front region of jaw. On careful clinical examination,bilateral mesiodens were seen in maxillary anterior region palatal to 11 and 21. Intraoral periapical radiograph of maxillary anterior region confirmed the presence of bilateral mesiodens. In addition, the periapical view showed deviation in path of eruption of 11 due to the presence ofmesiodens. out of two one mesiodens was erupted fully in oral cavity and only tip of other was visible.Extraction was planned for the mesiodens teeth one by one. Under

adequate local anesthesia,mesiodens tooth which was fully erupted in oral cavity was extracted. After a week, second mesiodens tooth was extracted by raising a full thickness mucoperiosteal palatal flap. Post extraction hemostasis was ensured and the patient was given post operative instructions.Antibioticsand analgesic medication was prescribed. Patient was recalled after 7 days. Satisfactory healing of the extraction wounds was noted. Patient was kept on recall at intervals of 1 month. At the 6 month recall visit, path of eruption of incisor was observed to be normal on an intra oral periapical view.

Figure 1 : Preoperative Photograph

Figure 2 : Tip Of Mesiodense

Figure 4 : Extracted Mesiodense

Quick Response Code

Address For Correspondence: Dr. Jingarwar MM., Department of Pedodontics & Preventive Dentistry, Govt. Dental college and hospital, Patiala Email ID [email protected] Mob:- 9108699365070

Figure 3 : Iopa Showing Is Visible Bilateral Mesiodense

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Figure 5 : Surgically Extracted Mesiodense

014

Discussion Mesiodens can be classified according to their morphology (conical,tuberculate, or molariform)[7]. In the present case, the bilateral mesiodens presentbetween the permanent maxillary central incisorswere conical in shape. No familial tendencyfor occurrence of supernumerary teeth was observed. The present case is raredue to the presence of bilateral mesiodens betweenthe permanent maxillary central incisors as an isolated trait i.e. without thepresence of any other supernumerary teeth or related syndrome. Various theories exist explaining the formation of different types of supernumerary teeth. One theory suggests that the supernumerary tooth is created as a result of dichotomy of the permanent tooth bud. Another theory, well supported in the literature, is the hyperactivity theory, which suggests that supernumerary teeth are formed as a result of local, independent, conditioned hyperactivity of the dental lamina[5]. Heredity may also play a role in the occurrence of this anomaly [6] . There is no consensus on the literature about the best time for mesiodens removal. Studies have shown that the removal of a mesiodens during the early mixed dentition stage allows normal eruptive forces to promote spontaneous eruption of the impacted tooth after 6 to 24 months. Some authors recommend postponement of surgical intervention until the age of 8–10 years, when apex of the permanent central incisor is almost mature. However, thelater the extraction of the mesiodens, the greater the chance that the permanent tooth either will not spontaneously erupt or will have a deviated path of eruption. Unfortunately, by this time the forces that cause normal eruption of the incisors are diminished, and surgical exposure and subsequent orthodontic treatment are more frequently required. Also, space loss and a midline shift of the central incisors may have already occurred by this age, since the lateral incisors will have erupted and may have drifted mesially into the central space. Thus, a significant delay in

treatment may create the need for more complex surgical and orthodontic management[8]. Hence, in this case, immediate surgical removal of the mesiodens teeth was the preferred treatment option to facilitate spontaneous eruption of the permanent central incisor. References 1. Maya C, Ashok Kumar BR. Familial Occurrence of mesiodens with unusual findings: Case report. Quintessence Int 1998;29:49-51. 2. Prabhu NT, Rebecca J, Munshi AK. Mesiodens in theprimary dentition: A case report. J Indian Soc PedoPrev Dent 1998;16:93-95. 3. Von Arx T Anterior maxillary supernumerary teeth: a clinical and radiographic study. Aust Dent J 1992; 37:189195. 4. Gündüz K, Çelenk P, Zengin Z and Sümer P.Mesiodens: a radiographic study in children J Oral Sci2008; 50(3): 287291. 5. Liu JF. Characteristics of premaxillary supernumerary teeth: A survey of 112 cases. ASDC J Dent Child 1995;62:262-265. 6. Ersin N K, Candan U, Alpoz A R, Akav C. Mesiodens in primary, mixed and permanent dentitions: A clinical and radiographic study. J Clin Pediatr Dent 2004;28:295-298. 7. Russell K A, Folwarczna M A. Mesiodens- diagnosis and management of a common supernumerary tooth. J Can Dent Assoc 2003;69:362-366. 8. Gurgel CV, Soares Cota AL, Kobayashi TY, Silva SMB, Machado MAAM, Rios D, Garib DG, Oliveira TM. Bilateral Mesiodens in Monozygotic Twins: 3D Diagnostic and Management. Case reports in dentistry 2013, article ID- 193614.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

015

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Surmounting The Endodontic Biofilms : The Nano Way S. Sai Kalyan1, Girish Parmar2, Rita Chandki3 1 2 3

Assistant Professor, Department Of Conservative Dentistry And Endodontics, Rural Dental College, Loni,Maharashtra, India. Dean, Government Dental College And Hospital, Ahmedabad,Gujarat Assistant Professor, Department Of Conservative Dentistry And Endodontics, Sri Aurobindo College Of Dentistry And Pg Institute, Indore.

Abstract The world of dentistry is continuously evolving and Endodontics is no exception. Last decade has been a landmark as there have been amazing changes in the area of Endodontics, leading to a dramatic shift from routinely practiced mechanical therapy to a more scientific and biological approach. Irrigation plays a central role in the successful endodontic treatment. The ubiquitous presence of microbial strains capable of forming biofilms with inherent resistance properties is a compelling force behind research for a solution better than over-saturation of disinfectants and antimicrobials. With the increased understanding of Endodontic disease as biofilm induced infection and hence in relentless pursuit of complete disinfection, newer irrigating agents and techniques are being constantly developed. In recent times, the use of nanotechnology has become an effective weapon in the armory for biofilm reduction. The possibilities are infinite and coveting. The technological innovation in the science of irrigation may one day take us from disinfection to sterilization. This review paper focuses on the concept of Endodontic disease as a ‘biofilm mediated infection’ and potential role of Nanotechnology in combating these stubborn biofilms, all to enhance the overall success of Endodontic treatment.

Key Words Microbial Biofilms, Nanobiosystems, Endodontic Irrigation, Silver Nanoparticle.

Introduction Chemomechanical preparation has been considered to play the central role in endodontic treatment.[1] Despite the myriad of technological advancements made over the decades, all parts of the root canal system are not amenable to mechanical cleaning. It has been proved that bacteria might penetrate dentinal tubules to depths of 200 mm or more.[2],[3] Complete uniform enlargement of a root canal by 200 mm is not achieved with any contemporary instrument; this appears to be an insurmountable intent for any mechanical canal preparation technique.[4] Given that the current instrumentation techniques alone are unable to render root canals bacteria-free[5], a chemical irrigant is considered a necessary adjunct to assist in reducing the bacterial load and their toxic by-products. In relentless pursuit of complete disinfection, A plethora of irrigants have been developed with distinct biological and mechanical properties but till date, none of the irrigants is considered ideal for complete elimination of bacteria and its byproducts from the root canal system without having any cytotoxic effects on the adjacent vital tissues. In recent times, the use of nanotechnology has become an effective weapon in the armory for biofilm reduction. The possibilities are infinite and coveting. The technological innovation in the science of irrigation may one day take us from disinfection to sterilization. This review article discusses Endodontic disease as a ‘biofilm mediated infection’ and potential role of Nanotechnology in combating these stubborn biofilms, all to Quick Response Code

Address For Correspondence: Dr. S.Sai Kalyan, Assistant Professor, Department Of Conservative Dentistry And Endodontics, Rural Dental College, Loni,Maharashtra, India. e-mail: [email protected] Tel: +91-9890785288

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

enhance the overall success of Endodontic treatment. Biofilms: The Paradox Biofilms are nothing new. Bacterial cells have been growing in the form of biofilms for billions of years, as a part of their gimmick to colonize the pugnacious environment. Centuries ago, Antonie van Leeuwenhoek was the first to observe what he called “animalcules” swarming on living and dead matter. But it was in 2002, when Donland and Costerton[6] provided the most salient description on biofilms. They described biofilm as “a microbially derived sessile community characterized by cells that are irreversibly attached to a substratum or interface or each other, embedded in a matrix of extracellular polymeric substances that they have produced, and exhibit an altered phenotype with respect to growth rate and gene transcription”. A biofilm is essentially a community of microflora networked within an exopolysaccharide (EPS) matrix with a distinct architecture. In addition to the EPS, it also contains proteins, nucleic acids,peptidoglycan, lipids, phospholipids, and other cell components.[7], [8] In most biofilms, while the bacterial populations account for less than 10% of the dry mass,the EPS matrixcan account for over 90%.[9] This overproduction of EPS architecture aids in both structural and protective functions. It forms channels to facilitate the exchange of nutrients, enzymes, metabolites, and disposal of waste products within and outside of the biofilm matrix.[10], [11] This architecture is essential in terms of supporting the needs of amulti-cellular biofilm, allowingfor each individual cell’s requirements to be met in order to sustain viability. As a result of these characteristics, the EPS matrix confers properties in biofilm-associated communities which are different from their planktonic counterparts. Ultrastructurally biofilms form tower- or mushroom-shaped microcolonies with interspersed channels that are separate from the external environment and through which fluids move by convection.[12]

016

The formation and properties of biofilms depends on several factors such as: characteristics of the microbial species and strains; composition and roughness of the surface material where the microorganisms attach; composition, pH, temperature and ionic strength of the liquid and hydrodynamics of the fluid.[13] The bioilm mode of growth confers following properties[14],[15],[16],[17] to the bacteria when compared to that in planktonic state: (i) allows for the growth of a more diverse microbiota; (ii) increased metabolic diversity and efficiency due to food chains/webs and enzymatic co-operation to degrade complex nutrients; (iii) ability to overcome host defenses, antimicrobial agents, and environmental stresses; (iv) facilitated genetic exchanges, including genes encoding antibiotic resistance and virulence factors; (v) facilitated quorum sensing ( Intraspecies communication between the members of the biofilm), which can influence survival and virulence; (vi) enhanced pathogenicity, especially due to synergism between different bacterial species in a mixed community. It should also be noted that bacteria living in biofilms present a different pattern of gene expression. Proteomic techniques or DNA arrays have clearly demonstrated that genes expressed by cells organized in biofilms differed by 20–70% from those expressed by the same cells growing in planktonic cultures.[19],[20],[21],[22] The major challenge of biofilm removal is addressing their increased resistance to disinfection. Biofilms can be between 100-1000 times more resistant to antibiotics and disinfecting agents than planktonic cells.[22], [23] Research has identified the influence of several different innate biofilm factors affecting antibiotic resistance; [14],[24],[25],[26],[27] First, the biofilm matrix may act as a diffusion barrier, preventing antibiotics from reaching their targets. Second, establishment of microenvironments within biofilms, such as reduced oxygen zones may slow down bacterial growth. Third, formation of persistor cells with inherent antibiotic resistance. Finally, several resistance genes have been identified that are specifically regulated within biofilms. Persister cells have been proposed as an additional innate mechanism for biofilm antibiotic resistance.[28] In the persister theory, a small subpopulation of bacteria, whether in biofilms or planktonic culture, differentiates into dormant, spore-like cells that survive after extreme antibiotic treatment. Differentiation into this dormant state has been hypothesized to be the result of phenotypic variation rather than a stable genetic change.[29] However, none of these phenomena can adequately account for every aspect of the biofilm resistance phenotype and the exact mechanism of biofilm resistance still remains to be elusive. Endodontic disease as a ‘Biofilm mediated infection’ Biofilms have been implicated in various aspects of science. But it was Nair in 1987 who first introduced the concept of biofilm in endodontics[30]. Using transmission electron microscopy (TEM),he found that even after instrumentation, irrigation, and obturation in a single visit endodontic treatment, microorganisms were found in the form of biofilms in untouched areas in the main canal, isthmuses, and accessory canals in 14 of the 16 endodontically treated teeth.[5] Since then, various studies have shown that Apical ramifications, lateral canals and isthmuses connecting main root canal harbor ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

bacterial cells frequently organized in biofilm like structure. [31] From the panorama of the "single-pathogen" concept, apical periodontitis can be considered as of no specific microbial etiology. However, based on the "community-as-pathogen" concept, it can be speculated that some bacterial communities are more related to certain forms of the disease than others. [32], [33]

Riccuci and Siquiera revealed revealed a very high prevalence of bacterial biofilm in the apical root canals of both untreated and treated teeth with apical periodontitis. [34] The bacteria present within the dentinal tubules are not accessible to the currently used irrigants , medicaments, and sealers because of their limited ability of penetration into the dentinal tubules. [35],[36] Hence, the endodontic community is continuously striving to develop techniques to conquer these bacterial biofilms. Nanotechnology in combating Biofilms Nanotechnology can be defined as the engineering and utilization of material, structures, devices and systems at the atomic, molecular and macromolecular scale. The term nanotechnology was coined by Norino Taniguchi in 1974.[37] Nanomaterials and nanostructures have nanoscale dimensions roughly between 1 and 100 nm and frequently exhibit novel and significantly physical, chemical and biological changed proprieties and functions resulting from their small structures[38], [39]. They are excellentadsorbents, catalysts, and sensors due to their large specific surface area and high reactivity.[40] Some of these nanomaterials are engineered to perform specific tasks, being able even to respond to outside signals by changing their structure and properties. For this, they are label as “smart” materials.[41] The field that applies this technology and particles to understand and transform biosystems can be defined as nanobiotechnology.[38] The physical properties of a particle vary dramatically as a function of size, composition and coatings[42] and can be very different from bulk material.[43] Overall, all different types of nanomaterials can be generated by either top down synthesis,where they are created by the formation of atoms from the bulk material, starting with a bulk solid and decomposing it, i.e. lithography, etching, milling, etc, or by a bottom up synthesis, in which n NPs are formed by the reaction and nucleation of smaller molecular components.[44] Recently, the biosynthesis of nanoparticles, combining the science of nanotechnology and biotechnology has received increasing attention due to a growing need to develop environmentally benign technologies in material synthesis.[45] The biological synthesis of silver nanoparticles uses harmless, eco-friendly reducing agents and the stabilization of nanoparticle structure is due to the presence of the proteins in the environment eliminating the additional step of using stabilizers as in chemical synthesis. Moreover, biological synthesis is ecofriendly and allows ease of bulk synthesis.[46] Silver Nanoparticles Ag NPs are one of the best studied nanoparticles due to their antimicrobial action. Silver is a rare chemical element (67th in abundance among the elements) with an atomic weight of 47.The mode of action of Ag NPs is still not well understood, however the antimicrobial activity of Ag NPs has often been attributed to the release of Ag ions, independently of the high reactivity and size of the particle.[47] It is well known that silver ions interact with thiol groups inactivating respiratory enzymes and proteins; they disrupt DNA replication and affect 017

the structure and permeability of the cell membrane.[48], [49] Silver diamine fluoride was evaluated as an antibacterial agent against E.faecalis biofilms, and it was concluded that it can be used as an effective antimicrobial root canal irrigant or interappointment dressing, especially in areas where potential discoloration of dentin by metallic silver is not an issue.[50] Zinc oxide Nanoparticles: Kishen et al[51] demonstrated that root canal surfaces treated with cationic antibacterial nanoparticulates such as zinc oxide alone and a combination of zinc oxide and chitosan nanoparticulates are able to significantly reduce E.feacalis adherence to dentin. In theory, such surface treatment could prevent bacterial recolonization and biofilm formation in vivo. Antimicrobial activity of polycationic CS-np and ZnO-np can be explained on the basis of the the electrostatic attraction of these particles with the negatively charged bacterial cell, which could alter the cell wall permeability, resulting in leakage of the components of cell and ultimately the death of the cell.[52], [53] Bioactive glasses of silica have been shown to possess antimicrobial activity through the release of ionic alkaline species over time. Reduction of particles to nano size allows for active exchange surface of glass and surrounding liquid, and thereby increased ionic release into suspension and enhanced antimicrobial efficacy.[54] Recently, polymer-based nanoparticles have been used in Photodynamic therapy for photosensitizer delivery and release systems. Engineered biodegradable polymericnanoparticles like Poly lactic-co-glycolic acid (PLGA)[55] have been used as a drug delivery system for photosensitizers. They have been approved by Food and drug administration[56],[57]. Encapsulation within PLGA results in a loss of their phototoxicity.[57] On incubation into target cells, they show a time-dependent release of the photosensitizer resulting in an activatable PDT nanoagent.[58] Conclusion: Introducing this biofilm concept to endodontic microbiology is a major step forward in our understanding of root canal infections, especially those of the persistent kind, because microorganisms growingin biofilms are better protected from adverse environmental changesand other antimicrobial agents.[59],[60] Evidence already exists showing that biofilms of oral bacteria are highly resistant to chlorhexidine, amine fluoride, amoxycillin, doxycycline,and metronidazole than planktonic cells[61], [62] Implementing the “biofilm concept” to the endodontic microflora implies that the efforts should not be directed to specific individual organisms, but to a group of well-adapted organisms which are more resistant to a plethora of antimicrobial agents. In non surgical endodontic treatment, these nanoparticulates could be successfully delivered into the anatomical complexities of root canal system. References: 1. Goldman LB, Goldman M, Kronman JH, Lin PS. The efficacy of several irrigating solutions for endodontics: a scanning electron microscopic study. Oral Surg Oral Med Oral Pathol 1981: 52: 197–204. 2. Haapasalo M, Ørstavik D. In vitro infection and disinfection of dentinal tubules. J Dent Res 1987; 66: 1375–1379. 3. Love RM, Jenkinson HF. Invasion of dentinal tubules by oral bacteria. Crit Rev Oral Biol Med 2002; 13: 171–183. 4. Paqué F, Ganahl D, Peters OA. Effects of root canal ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

preparation on apical geometry assessed by microcomputed tomography. J Endod 2009: 35: 1056– 1059. 5. Nair et al. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005; 99: 231-52. 6. Rodney M. Donlan1 and J. William Costerton, Bio¬films: Survival Mechanisms of Clinically Relevant Microorganisms CLINICAL MICROBIOLOGY RE¬VIEWS, Apr. 2002, p. 167-193. 7. Sutherland, I.W. The biofilm matrix--an immobilized but dynamic microbial environment. Trends in microbiology 2001; 9: 222-227. 8. Vu, B., Chen, M., Crawford, R.J., Ivanova, E.P. Bacterial extracellular polysaccharides involved in biofilm formation. Molecules (Basel, Switzerland) 2009; 14: 2535-2554. 9. Flemming HC, Wingender J. The biofilm matrix. Nat Rev Microbiol 2010: 8: 623–633 10. Cuthbertson, L., Mainprize, I.L., Naismith, J.H., Whitfield, C. Pivotal roles of the outer membrane polysaccharide export and polysaccharide copolymerase protein families in export of extracellular polysaccharides in gram-negative bacteria. Microbiology and molecular biology reviews 2009; 73: 155-177. 11. Stoodley, P., Sauer, K., Davies, D.G., Costerton, J.W. Biofilms as complex differentiated communities. Annual Review of Microbiology 2002; 56: 187-209. 12. Lawrence JR, Korber DR, Hoyle BD, Costerton JW, Caldwell DE. Optical sectioning of microbial biofilms. J Bacteriol 1991; 173: 6558–67. 13. Melo, L. F. (2003). Biofilm formation and its role in fixed film processes. In: The Handbook of Water and Wastewater Microbiology. London, UK, Academic Presspp. 337-349. 14. Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002: 15: 167–193. 15. Socransky SS, Haffajee AD. Dental biofilms: difficult therapeutic targets. Periodontol 2000 2002: 28: 12–55. 16. Hall-Stoodley L, Costerton JW, Stoodley P. Bacterial biofilms: from the natural environment to infectious diseases. Nat Rev Microbiol 2004: 2: 95–108. 17. Marsh PD. Dental plaque: biological significance of a biofilm and community life-style. J Clin Periodontol 2005: 32(Suppl 6): 7–15. 18. Marsh PD. Are dental diseases examples of ecological catastrophes? Microbiology 2003; 149: 279–294. 19. Sauer K, Camper AK, Ehrlich GD, Costerton JW,Davies DG. Pseudomonas aeruginosa displays multiple phenotypes during development as a biofilm. J Bacteriol 2002; 184: 1140–1154. 20. Oosthuizen MC, Steyn B, Theron J, Cosette P, Lindsay D, Von Holy A, Brozel VS. Proteomic analysis reveals differential protein expression by Bacillus cereus during biofilm formation. Appl Environ Microbiol 2002; 68:2770–2780. 21. Beloin C, Valle J, Latour-Lambert P, Faure P, Kzreminski M, Balestrino D, Haagensen JA, Molin S, Prensier G, Arbeille B, Ghigo JM. Global impact of mature biofilm lifestyle on Escherichia coli K-12 gene expression.Mol Microbiol 2004: 51: 659–674. 22. Smith, K., Hunter, I.S. Efficacy of common hospital biocides with biofilms of multi-drug resistant clinical isolates. Journal of medical microbiology 2008; 57: 966973. 23. Stewart, P.S., Costerton, J.W. Antibiotic resistance of 018

bacteria in biofilms. 2001; 358: 135-138. 24. Costerton JW, Stewart PS, Greenberg EP. Bacterial biofilms: a common cause of persistent infections. Science 1999; 284:1318–1322. 25. Dunne WM Jr. Bacterial adhesion: seen any good biofilms lately? Clin Microbiol Rev 2002; 15:155–166 26. Mah TF, O’Toole GA. Mechanisms of biofilm resistance to antimicrobial agents. Trends Microbiol 2001; 9: 34–39. 27. Patel R. Biofilms and antimicrobial resistance. Clin Orthop Relat Res 2005:41–47. 28. Lewis K. Persister cells and the riddle of biofilm survival. Biochemistry (Mosc) 2005; 70: 267–274. 29. Keren I, Kaldalu N, Spoering A, Wang Y, Lewis K (2004a) Persister cells and tolerance to antimicrobials. FEMS Microbiol Lett 230:13–18. 30. Nair PN. Light and electron microscopic studies on root canal flora and periapical lesions. J Endod 1987; 13: 29-39. 31. Riccuci D, Siquira JF. Fate of the tissue in lateral canals and apical ramifications in response to pathologic conditions and treatment procedures. J Endod. 2010 Jan; 36(1): 1-15 32. Siqueira JF Jr, Rôças IN, Rosado AS. Investigation of bacterial communities associated with asymptomatic and symptomatic endodontic infections by denaturing gradient gel electrophoresis fingerprinting approach. Oral Microbiol Immunol 2004; 19: 363-370. 33. Sakamoto M, Rôças IN, Siqueira JF Jr, Benno Y. Molecular analysis of bacteria in asymptomatic and symptomatic endodontic infections. Oral Microbiol Immunol 2006; 21: 112-122. 34. Riccucui D, Siquiera J. Biofilms and Apical Periodontitis: Study of prevalence and association with clinical and histopathologic findings. J Endod. 2010 Aug; 36(8):127788. 35. Peters OA, Scho¨ nenberger K, Laib A. Effects of four Ni–Ti preparation techniques on root canal geometry assessed by micro computed tomography. Int Endod J 2001; 34:221–30. 36. Salzgeber RM, Brilliant JD. An in vivo evaluation of the penetration of an irrigating solution in root canals. J Endod 1977; 3: 394–8. 37. Taniguchi N (1974) Proceedings of International Conference on Precision Engineering (ICPE), Tokyo, Japan. 38. Roco, M. C. "Nanotechnology: convergence with modern biology and medicine." Current Opinion in Biotechnology 2003; 14(3): 337-346. 39. Theron, J., J. A. Walker and T. E. Cloete "Nanotechnology and water treatment: applications and emerging opportunities." CriticalReviews in Microbiology 2008; 34(1): 43-69. 40. Li, Q., S. Mahendra, D. Y. Lyon, L. Brunet, M. V. Liga, D. Li and P. J. J. Alvarez. Antimicrobial nanomaterials for water disinfection and microbial control: potential applications and implications. Water Research 2008; 42(18): 4591-4602. 41. Ratner, M. and D. Ratner (2003). Nanotechnology: a gentle introduction to the next big idea. New Jersey, Prentice Hall PTR pp. 42. Handy R.D., von der Kammer F., Lead J.R., Hassellov M., Owen R. & Crane M. The ecotoxicology and chemistry of manufactured nanoparticles. Ecotoxicology. 2008;17: 287-314. 43. Madden A.S. & Hochella M.F. A test of geochemical reactivity as a function of mineral size: Manganese

oxidation promoted by hematite nanoparticles. Geochim. Cosmochim. Acta 2005; 69: 389-398. 44. Ju-Nam Y. & Lead J.R. Manufactured nanoparticles: An overview of their chemistry, interactions and potential environmental implications. Sci. Total Environ. 2008; 400: 396- 414. 45. Kalishwaralal K, Deepak V, Ramkumarpandian S, Nellaiah H, Sangiliyandi G. Extracellular biosynthesis of silver nanoparticles by the culture supernatant of Bacillus licheniformis. Mater Lett 2008; 62: 4411–3. 46. M. Rai and N. Duran (eds.), Metal Nanoparticles in Microbiology, DOI 10.1007/978-3-642-18312-6_2, # Springer-Verlag Berlin Heidelberg 2011 47. Lok C.N., Ho C.M., Chen R., He Q.Y., Yu W.Y., Sun H., Tam P.K.H., Chiu J.F. & Che C.M. Silver nanoparticles: partial oxidation and antibacterial activities. Journal of Biological Inorganic Chemistry 2007; 12: 527-534. 48. Silver S. Bacterial silver resistance: molecular biology and uses and misuses of silver compounds. Fems Microbiology Reviews 2003; 27: 341-353. 49. Feng Q.L., Wu J., Chen G.Q., Cui F.Z., Kim T.N. & Kim J.O. A mechanistic study of the antibacterial effect of silver ions on Escherichia coli and Staphylococcus aureus. Journal of Biomedical Materials Research 2000; 52: 662668. 50. Hiraishi N, Yiu CK, King NM, Tagami J, Tay FR. Antimicrobial efficacy of 3.8% silver diamine fluoride and its effect on root dentin. J Endod 2010; 36: 1026–9. 51. Kishen A, Shi Z, Shrestha A, Neoh KG. An investigation on the antibacterial and antibiofilm efficacy of cationic nanoparticulates for root canal disinfection. J Endod. 2008 Dec; 34(12):1515-20. 52. Jung BO, Kim CH, Choi KS, Lee YM, Kim JJ. Preparation of amphiphilic Chitosan and their antimicrobial activities. J Appl Polym Sci 1999; 72: 1713–9. 53. Rabea EI, Badawy MET, Stevens CV, Smagghe M, Steurbaut W. Chitosan as antimicrobial agent: applications and mode of action. Biomacromolecules 2003; 4:1457–65. 54. Waltimo T, Brunner TJ, Vollenweider M, Stark WJ, Zhender M. Antimicrobial effect of nanoactive biometric glass 45S5. J dent Res 2007; 86: 754-757. 55. Koo YEL, Fan W, Hah H, et al. Photonic explorers based on multifunctional nanoplatforms for biosensing and photodynamic therapy. Appl Opt 2007; 46: 1924–30. 56. Langer R. Drug delivery and targeting. Nature 1998; 392: 5–10. 57. Konan YN, Berton M, Gurny R, et al. Enhanced photodynamic activity of mesotetra(4-hydroxyphenyl) porphyrin by incorporation into sub-200 nm nanoparticles. Eur J Pharm Sci 2003;18:241–9. 58. McCarthy JR, Perez JM, Bru¨ ckner C, et al. Polymeric nanoparticle preparation that eradicates tumors. Nano Lett 2005; 5: 2552–6. 59. Gilbert P, Das J, Foley I. Biofilm susceptibility to antimicrobials. Adv Dent Res 1997; 11: 160 –7. 60. Brown MR, Gilbert P. Sensitivity of biofilms to antimicrobial agents. J Appl Bacteriol 1993; 74 Suppl:87S–97S. 61. Larsen T. Susceptibility of Porphyromonas gingivalis in biofilms to amoxicillin, doxycycline and metronidazole. Oral Microbiol Immunol 2002; 17: 267–71. 62. Shani S, Friedman M, Steinberg D. The anticariogenic effect of amine fluorides on Streptococcus sobrinus and glucosyltransferase in biofilms. Caries Res 2000; 34:260 –7.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

019

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review

Recent Trends In Endodontic Therapy, Regenerative Endodontics And Tissue Engineering : A Review Neeraj Mahajan1, Utkarsh Passi2 1 2

Proffessor And Head, Deptt Of Pediatric &preventive Dentistry, Gnddc Sunam PG Student, Deptt Of Pediatric &preventive Dentistry, Gnddc Sunam

Abstract One of the challenges in endodontics is the treatment and management of an immature tooth with a necrotic pulp. Traditional treatment approaches include creation of a hard barrier which root canal filling material can be obturated against. This root end closure procedure is called apexification. These traditional techniques leave the roots with thin dentin walls and short overall root length, leaving the tooth more susceptible to failure due to root fracture Regenerative endodontics is a contemporary approach to addressing this problem.This procedure uses tissue engineering principles in facilitating the continued growth and development of the pulp-dentin complex. Inother words, this procedure, allows for continued root development,thicker dentin walls, longer root length, and a closed apex,thus reducingthe risk of fracture during tooth function.

Key Words Stem Cells, Scaffold, Revascularization

Introduction Tissue engineering is the norm of the day and man is striving to play god .The amalgamation of bioengineering and medicine has resulted in the emergence of a new field known as tissue engineering. The term "Tissue engineering" was coined by Langer and Vacanti in 1993 to describe the process by which the tissues and organs are generated by cell transplantation with or without a scaffold.[2] Tissue engineering is the restoration of lost tissuefunction through the delivery of synthetic or natural tissue constructs in the laboratory. It is also developingnew frontiers in dentistry known as regenerative dentistry[1]. Emphasis is on the formation of lost dentinal tissues and restoration of pulp function Regenerative endodontic procedures can be defined as biologically based procedures designed to replace damaged structures, including dentin and root structures, as well as cells of the pulp-dentin complex[4]. The objectives of regenerative endodontic procedures are to regenerate pulp-like tissue, ideally, the pulp-dentin complex; regenerate damaged coronal dentin, such as following a carious exposure; and regenerate resorbed root, cervical or apical dentin. Regenerative dental procedures had been performed at around 1952, when Dr. B. W. Hermann reported on the application of Ca(OH) in a case report of vital pulp amputation[4] In dentistry potential for successful pulp regeneration therapies is increasing due to accumulated knowledge of stem cells, especially dental pulp stem cells. Undifferentiated mesenchymal cells within the dental pulp can differentiate into odontoblasts and secrete reparative dentin. These cells within the pulp also have the potential to Quick Response Code

Address For Correspondence: Dr. Neeraj Mahajan Proffessor And Head, Deptt Of Pediatric & preventive Dentistry, Gnddc Sunam Email Id : [email protected] Contact no. : 09814366829

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

differentiate into other cell types, including fibroblasts, to repair the damaged soft pulp tissue.The ability to stimulate the stem cell differentiate into odontoblasts-like cells, rather than fibroblasts, is critical in dentin repair. Although pulp regeneration and revascularization is not essential, due to the fact that the pulpless tooth can survive for a long time after a successful endodontic treatment, maintaining the vitality of dental pulp provides many benefits like maintaining the capacity for limited dentin regeneration. Retaining the structural integrity of treated tooth, Maintaining the vital pulp also helps reduce the occurrence of apical periodontitis by blocking bacterial infections and in terms of aesthetics, endodontic therapy can often result in discoloration of the tooth crown, mainly due to staining from endodontic filling material. In the future, the scope of regenerative endodontics may be increased to include the replacement of periapical tissues, periodontal ligaments, gingiva, and even whole teeth. Regenerative endodontics comprises research in adult stem cells, growth factors, organ-tissue culture, and tissue engineering material. Concepts of Tissue Engineering: Tissue Engineering Triad Tissue engineering is the employment of biological therapeutic strategies which are aimed at the replacement, repair, maintenance and/or the enhancement of tissue function. Tissue engineering is generally considered to consist of three key elements 1. Stem cells/progenitor cells 2. Scaffolds or extra cellular matrix 3. Signaling molecules. Stem Cells Stem cells are considered to be the most valuable cells for regenerative medicine. Research on stem cells is providing advanced knowledge about how an organism develops from a single cell, and how healthy cells replace damaged ones in

020

adult organisms. Stem cells have the ability to continuously divide to either replicate themselves (self replication), or produce specialized cells that can differentiate into various other types of cells or tissues (multilineage differentiation) Types of stem cells :1) Early embryonic stem cells 2) Blastocyst embryonic stem cells 3) Fetal stem cells 4) Umbilical cord stem cells 5) Adult stem cells Generally adult stem cells or postnatal stem cells have been found in almost all body tissues, including dental tissues .The identification of these dental stem cells provides better understanding of the biology of the pulp and periodontal ligament tissues, and their regenerative potential after tissue damage Scaffolds The basic role of scaffolds in tissue engineering is to act as carriers for cells, to maintain the space and to create an environment in which the cells can proliferate, and produce the desired tissue matrix. Ideal requirements of a scaffold[10]:(a) Should be porous to allow placement of cells and growth factors. (b) Should allow effective transport of nutrients, oxygen, and waste. (c) Should be biodegradable, leaving no toxic byproducts. (d) Should be replaced by regenerative tissue while retaining the shape and form of the final tissue structure. (e) Should be biocompatible. (f) Should have adequate physical and mechanical strength. Types of Scaffold a) Biological/natural Scaffolds These consist of natural polymers such as collagen and glycosaminoglycan, which offer good biocompatibility and bioactivity. Collagen is the major component of the extracellular matrix and provides great tensile strength to tissues. As a scaffold, collagen allows easy placement of cells and growth factors and allows replacement with natural tissues after undergoing degradation[14]. However, it has been reported that pulp cells in collagen matrices undergo marked contraction, which might affect pulp tissue regeneration . b) Artificial Scaffolds These are synthetic polymers with controlled physicochemical features such as degradation rate, microstructure, and mechanical strength[15], for example: • Polylactic acid (PLA), polyglycolic acid (PGA), and their copolymers, poly lactic-co-glycolic acid (PLGA). • Synthetic hydrogels include polyethylene glycol (PEG)based polymers. • Scaffolds modified with cell surface adhesion peptides, such as arginine, glycine, and aspartic acid (RGD) to improve cell adhesion and matrix synthesis within the three-dimensional network. [13] • Scaffolds containing inorganic compounds such ashydroxyapatite (HA), tricalcium phosphate (TCP) and calcium polyphosphate (CPP), which are used to enhance bone conductivity , and have proved to be very effective for ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

•

tissue engineering of DPSCs. [12] Micro-cavity-filled scaffolds to enhance cell adhesion.

Scaffolds for Tissue Engineering: Cumulative reports have shown that pulp cells can be isolated, multiplied in culture, and seeded onto a matrix scaffold where the cultured cells form a new tissue similar to that of the native pulp.[10] These findings have suggested the possibility of generating pulp and dentin in pulpless canals. However, when implanting cells/scaffolds into root canals that have a blood supply only from the apical end, enhanced vascularization is needed in order to support the vitality of the implanted cells in the scaffold. This can be optimized with the addition of growth factors such as VEGF and/or platelet-derived growth factor or, further, with the addition of endothelial cells.[9] Through the use of computer-aided design and three-dimensional printing technologies, scaffolds can be fabricated into precise geometries with a wide range of bioactive surfaces. Such scaffolds have the potential to provide environments conducive to the growth of specific cell types. Signaling Molecules These are the molecules that transmit signals between cells,functioning as stimulators/inhibitors of growth, as well as the modulators of differentiation. These consist of growth factors (PDGF, TGF), differentiation factors (BMPs) and stimulating factors.Morphogens such as BMPs can induce DPSCs to differentiate into odontoblast-like cells. Mouse dental papilla cells transfected with growth/differentiation factor 11 (Gdf) [11] were demonstrated to express dentin sialoprotein (DSP)[5]; Osteo-dentin formation during pulpal wound healing was observed in dog teeth in vivo after Gdf [11] electroporation. The same group also used Gdf[11] ultrasoundmediated gene delivery using microbubbles, demonstrating complete reparative dentin formation in animal model in vivo. The effectiveness of this kind of in vivo gene therapy highly depends on the vitality of the remaining dental pulp cells. Ex vivo gene therapy, involving the transfer of in vitro transfected cells back in vivo, may provide a better solution Regenerative Strategies for Dental Pulp There aredifferent approaches for revascularization and regeneration of dental pulp. These approaches are :? Root canal revascularization via blood clotting, ? Postnatal stem cell therapy ? Pulp implantation, ? Scaffold implantation, ? Injectable scaffold delivery, ? Three-dimensional cell printing, ? Gene delivery. Root canal revascularization Necrosis of immature tooth with open apex wouldrender the tooth weak and prone to fracture. Idealtreatment would be to induce the root completion followedby restoration. Revascularization method assumes thatonce root canal space had been disinfected and the formation of blood clot is initiated by over instrumentationresults in fibrin matrix formation that traps cells that arecapable of initiating new tissue formation. It has beensuggested that these cells originates from local tissuesadjacent to the apex of root but not from systemiccirculation.Theseundifterentiatedmesenchymal cells arederived from SCAP's and difterentiates into 021

primaryodontoblasts to complete root formation. Other possiblemechanism of root development can be attributed to stemcells from periodontal ligament.It was demonstrated that the regenerated tissue does not, histologically resemble to the pulp but it consists of tissuesresembling cementum, periodontium and bone[2] Scaffold implantation It involves positioning of cells in scaffold and inserting the assembly in the disinfected pulp space. A scaffold should contain growth factors to aid proliferation and differentiation, leading to improved and faster tissue development [2]. Injectable scaffold delivery Root canal have varied three dimensional anatomy and a rigid scaffold may not occupy all the canal space. So cells are injected with liquid scaffold which enables them to reach all the area of canal anatomy. An example of injectable scaffold is hydrogel.Three dimensional cell printing One of the major disadvantages of the previously mentioned methods includes aberrant histology of formed pulp. Three dimensional cell printing enables precisespatial arrangement of the cells in predetermined position and the resultant tissue would mimic the natural tissue.[2] Gene therapy Gene therapy includes modification or alteration of gene to regulate the cellular processes and responses and to utilize it for therapeutic benefit. Vector is used for this alteration which can be viral or non-viral. The transfected gene can stimulate immune response, modify cellular information, or developmental programme or produce a therapeutic protein with specific function. One use of gene therapy would be to deliver mineralizing genes into pulp to promote tissue mineralization. However FDA approval for gene therapy was withdrawn, in 2003 when a 9 year old boy receiving gene therapy was found to have developed tumours in difterent parts of his body[2] Future Scope The scope for regenerative endodontics includes research on the the ability to stem cells to trigger regeneration hard tissues of the tooth, vitalization of a nonvitalpulp, replacement of periapical tissues and peridontal ligaments .The ability to generate biological tooth substitutes from autologous human tissues would be a valuable clinical tool[1]. The future for regenerative and tissue-engineering applications to dentistry is of enormous prospective,capable of bringing quantum advances in treatment for our patients. Till date the design of suitable growth factor delivery system meeting all requirements and mimicking a natural biological environment still remains as one of the most important subjects in tissue engineering [1] Conclusion: One of the challenges in endodontics is the treatment and management of an immature tooth with a necrotic pulp Regenerative endodontics is a contemporary approach to addressing this problem. This procedure uses tissue engineering principles in facilitating the continued growth and development of the pulp-dentin complex. In other words, when you have a case with an immature apex and necrotic pulp, regenerative endodontics allows for continued root

development, thicker dentin walls, longer root length, and a closed apex, thus reducing the risk of fracture during tooth function.Success is dependent on the activity of a newly identified population of stem cells, the so-called stem cells from apical papilla (SCAP) , a hidden treasure with enormous potential for tissue regeneration and bioroot engineering Bioengineering has a tremendous potential in dentistry. Researchers continue to optimize scaffolds that may encourage revascularization of the pulp space, and to explore the options of seeding cell populations into the properly sterilized pulp spaces of immature teeth .Dentistry’s call for action has never been louder as we seek effective, biologically based treatments for our pediatric patients. References 1. Kundabala M. Parolia A RegernativeEndodontics: A review 2. Ghazanfaruddin M Tissue Engineering And Regenerative Endodontics -A Review; doi:10.5368/aedj.2012.4:4.4.3 3. Hargreaves KM, Law AS. Regenerative Endodontics. Chapter 16. Pathways of the Pulp 10th ed. Eds, Hargreaves KM, Cohen S. Mosby Elsevier, St Louis, MO, 2011: 60219. 4. Murray PE, Garcia-Godoy F, Hargreaves KM: Regenerative endodontics: a review of current status and a call for action. J Endod 2007; 33: 5. Nakashima M, Mizunuma K, Murakami T Etal. Induction of dental pulp stem cell differentiation into odontoblasts by electroporation-mediated gene delivery of growth/differentiation factor 11 (Gdf11).Gene Therapy. 2002;9(12):814–818. 6. Brazelton TR, Blau HM. Optimizing techniques for tracking transplanted stem cells in vivo. Stem cells 2005; 23:1251-65. 7. Huang GTJ, Sonoyama W, Liu Y, Liu H, Wang S, Shi S. The hidden treasure in apical papilla: the potential role in pulp/dentin regeneration and bioroot engineering. J Endod 2008; 34:645-51. 8. Lieberman J, Trowbridge H. Apical closure of non vital permanent incisor teeth 9. Glickman GN, Koch KA.21st-century endodontics. Journal of the American Dental Association.2000;131(supplement 6):39S–46S. 10. CS. Young, S. Terada, J. Vacanti P etal.. Tissue engineering of complex tooth structures on biodegradable polymer scaffolds. J Dent Res81(10):695-700, 2002 11. Smith AJ. Vitality of the dentin-pulp complex in health and disease: growth factors as key mediators. J Dent Educ 2003; 67:678-689. 12. Wang FM, Qiu K, Hu T, etal. Biodegradable porous calcium polyphosphate scaffolds for the three-dimensional culture of dental pulp cells. IntEndod J.2006; 39:477-483. 13. Burdick JA, Anseth KS, Photoencapsulation of osteoblasts in injectable RGD-modified PEG hydrogels for bone tissue engineering. Biomaterials 2002;23:4315-4323. 14. Feng Z, Yamato M, Akutsu T, etal. Investigation on the mechanical properties of contracted collagen gels as a scaffold for tissue engineering. Artif Organs 2003; 27: 8491. 15. Sharma B, Elisseeff JH. Engineering structurally organized cartilage and bone tissues. Ann Biomed Eng 2004;32:148-159.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

022

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review

Influence Of Fixed Orthodontic Appliances On Periodontal Status In Young Adults Pradeep Kumar1, Priyanka Aggarwal2, Shradha Sethi3, Geetanjali Sikka4 1

Reader, Department of Periodontontology and Oral Implantology, Rajasthan Dental College & Hospital, Jaipur Post graduate student, Department of Periodontontology and Oral Implantology, Rajasthan Dental College & Hospital, Jaipur Senior Lecturer, Department of Periodontontology and Oral Implantology, Rajasthan Dental College & Hospital, Jaipur 4 Senior Lecturer, Department of Periodontontology and Oral Implant;ology, SGT Gurgaon. 2

3

Abstract In the present review emphasis has been made on influence of orthodontic appliances on periodontal health, such as the effects of orthodontic fixed attachments on periodontal status and microflora found around the gingival margins. Plaque accumulation and subsequent gingivitis, enamel demineralisation, microbial infection etc, are some of the common problem associated with fixed orthodontic appliances. Maintenance of oral hygiene is one of the control measures for small relaxation from unfavourable effect. Supporting evidence given by different authors and dentist also discussed in this review.

Key Words Orthodontic Appliances, Periodontal Status, Plaque, Enamel Demineralisation, Oral Hygiene

Introduction Most commonly three groups are suggested for orthodontic treatment first one is, people with defects in the jaw and/or face as well as children with a handicap; second is, younger children requiring interceptive treatment to prevent malocclusion or to create optimal conditions for normal occlusal development or preventing traumatic tooth damage and last one is, teenagers with severe malocclusions that may negatively influence psychosocial well-being or oral function. Future dental problems can be eliminated with orthodontic treatment problems including the problem of abnormal wear. Treatment can be ease to maintain good oral hygiene and minimise decay and future periodontal problems. In addition, orthodontics can provide a pleasant smile, which may enhance one’s self-image. Orthodontic treatment not only improves periodontal health in these circumstances, but it may hold some potential for harm to the periodontal tissues. Maintenance of oral hygiene is during treatment is one of the important factor which can protect from plaque accumulation and subsequent inflammation in patient. Orthodontic bands placed sub-gingivally may encroach on alveolar bone. Soft- or hard-tissue defects may be present in extraction sites. Therefore, both positive and negative periodontal outcomes seem possible after orthodontic therapy. Oral hygiene: One of the important environmental factors affecting periodontal status Orthodontic appliances covered greater tooth area and also complex in nature which in turn makes it difficult to maintain oral hygiene. Maintaining oral hygiene during orthodontic Quick Response Code

Address For Correspondence: Dr. Priyanka Aggarwal Post Graduate Student, Department of Periodontontology and Oral Implantology, Rajasthan Dental College & Hospital, Jaipur Email: [email protected]

treatment will help in good gingival health, which reflects in final orthodontic treatment outcome. Importance of oral hygiene in orthodontic patients is always intensified to prevent any further periodontal disease. In case of negligence of oral hygiene maintenance, plaque accumulation on orthodontic appliance components leads destruction of periodontal tissues[1]. Poor maintenance of oral hygiene is due to either lack of knowledge or negligence by patients themselves. Patients are not given with proper instructions; (Alexander, 1991; Alstad and Zachrisson, 1979) may be one big reason for patient’s noncompliance.[2],[3] However, despite receiving appropriate instructions, many individuals fail to follow instructions; also many of them lack knowledge on maintenance. It is important to motivate them to compile the instructions and maintain oral health. It is always needed to assess the knowledge of orthodontic patients on gingival health.[4] Plaque related gingivitis: Orthodontic treatment may be result into both negative and positive consequence, regarding the periodontal tissues, which may be sometimes very significant in increasing the periodontal health status, and sometimes a harmful procedure which can be followed by several types of periodontal complications, such as gingival recessions, bone dehiscence, gingival invaginations and/or the formation of gingival pockets. Mostly young patients are referred for orthodontic treatment and they often suffer from plaque related gingivitis.[5] Gingivitis is an inflammation of the gums surrounding teeth. Gingivitis is one of many periodontal diseases that affect the health of the periodontium[6]. Periodontal diseases are often classified according to their severity. They range from mild gingivitis; to more severe periodontitis[7]. It is well known the presence of bands, brackets, wires and

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

023

other orthodontic attachments make the patient’s teeth highly susceptibility to plaque accumulation.[8] Many dentists are reluctant to refer adult patients for orthodontic treatment if they have suffered, or are suffering from, obvious signs of periodontal disease such as chronic periodontitis.[3] Obvious signs of periodontal disease in adults are a hindrance to being referred for orthodontic treatment. Almost every fixed orthodontic patient develops gingival disease at some time during treatment.[9] Gingival enlargement and inflammation are often transient and can be easily resolves within weeks of rebonding. Contemporary bonded orthodontic appliances cause less gingivitis than banded appliances.[10] Adolescents have certainly been shown to suffer worse gingivitis than adults during orthodontic treatment.[11] Primary aim before any orthodontic intervention should be to stabilize the periodontal condition.[12] Stable gingival health status throughout the orthodontic treatment would deliver accurate treatment result. Delivering proper instructions on gingival health maintenance to orthodontic patients plays vital role in this aspect. Motivating and making them to practice oral hygiene measures in young age groups will certainly enhance the levels of oral hygiene standards (Polson et al., 1988).[12],[13] Many patients do not exactly know how to maintain high oral hygiene standards which may be conducive to excellent orthodontic treatment outcomes.[14] Proper brushing is ideal for good gingival health, while prolong brushing may distort the gingival tissues. Wasting diseases like abrasion are mainly caused by improper brushing. On awareness of gingival health, comparatively very few are having awareness while most of them are not aware of that.[4] Enamel Demineralization Enamel demineralization is one of the undesirable complications associated with orthodontic fixed appliance therapy. Several studies have reported a significant increase in the prevalence and severity of demineralization after orthodontic therapy compared with controls, and the overall prevalence amongst orthodontic patients ranges from 2 to 96 percent.[15],[16],[17] The Subsurface demineralization can be marked as an opaque white appearance of the enamel lesion which is mainly due to the increase in porosity and consequential changes in the optical properties of the enamel.[18] Demineralization during orthodontic treatment, like its more common counterpart, the smooth surface proximal carious lesion, can be considered a dietary carbohydrate- and salivamodified bacterial infectious disease.[19]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Dietary carbohydrate-induced enrichment of the plaque microbiota with organisms such as Streptococcus mutans and lactobacilli which in turn cause an increase in the pH lowering potential of dental plaque. The shift in the plaque proportions of these organisms is related in part to their high tolerance of acidic environments.[18] Dental plaque and subsequent biological determinants influence the development of a carious lesion is complex. The introduction of fixed appliances into the oral environment appears to alter the ecology, introducing yet another variable into the system. Insertion of fixed orthodontic appliances creates stagnation areas. The irregular surfaces of brackets and bands provides some protection from physical forces (movement of food and the oral musculature) and reduces access by saliva, encouraging a lowering of plaque pH in the presence of carbohydrates. Plaque accumulation is accelerated. Plaque not only provides a source of acid production in the presence of fermentable substrates, but also acts as a physical barrier which limits the diffusion of acid away from the enamel surface, and prevents remineralization by calcium and phosphate ions from the saliva. These changes in the local environment favour colonization of aciduric bacteria, resulting in a rise in the levels of Streptococcus mutans and lactobacilli.[20] The type and frequency of carbohydrate consumption also influences plaque microbiology. Overall, an increase in cariespromoting bacteria and plaque during orthodontic treatment will promote demineralization. On the other hand, resting salivary flow rate increases during fixed appliance therapy.[21] Since salivary pH and buffer capacity increase with salivary flow rate (Andersson et al., 1974)[22], these changes may counteract the tendency for demineralization to occur. This may explain why in some patients there is little demineralization around orthodontic appliances despite moderate plaque scores. In these individuals, the balance between periods of enamel dissolution and repair favours remineralization. While it is difficult to predict those patients who will experience demineralization during treatment, there is some evidence that at least 50 per cent of patients undergoing orthodontic treatment are relatively resistant to demineralization, even when no supplemental fluoride programme is followed.[23] Nevertheless, an assessment of susceptibility prior to orthodontic treatment seems sensible. Microbial Factors Large numbers of lactobacilli are present in advanced carious lesions, where they play a significant role in the further development of the carious lesion. Like Streptococcus mutans, they are both aciduric and acidogenic. Although lactobacilli may not be important in the initiation of caries, their presence in large numbers indicates that the necessary conditions for producing dental caries do exist.[24] The insertion of fixed orthodontic appliances results in new retention sites in the mouth. Several studies have shown an increased proliferation of Streptococcus mutans and Lactobacillus sp in patients undergoing fixed appliance 024

therapy[20],[25],[26]. Both the number of orthodontic attachments and the duration of treatment may influence this process.[26] Mucogingival Considerations during Treatment An adequate amount of attached gingiva is very essential for gingival health[27] and, therefore, to allow appliances (functional or orthopedic) to deliver orthodontic treatment without causing periodontal complications. With labial bodily movement, incisors showed apical displacement of the gingival margin.[28] Loss of connective tissue occurred where inflammation was present.[29] Therefore, if the tooth movement is expected to result in a reduction of soft tissue thickness and an alveolar bone dehiscence may have occurred in the presence of inflammation, gingival recession is a risk.[30] Trossello and Gianelly found in their retrospective study of orthodontically treated adults, a low prevalence of mucogingival defects (5%).[31] Other clinical studies (Coatoam et al., 1981[30]; Dorfman,1978[28]) have shown that a narrow band of gingiva is capable of withstanding the stress caused by orthodontic forces. Results from an experimental study (Wennstrom et al., 1987) indicate that as long as the tooth is moved within the envelope of the alveolar process, the risk of harmful side-effects on the marginal soft tissue is minimal.[32] Thin, delicate tissue is far more prone to exhibit recession during orthodontic treatment than in normal or thick tissue. If a minimal zone of attached gingiva or thin tissue exists, a free gingival graft that enhances the type of tissue around the tooth helps control inflammation. This should be done before any orthodontic movement is begun.[33],[34],[35] Tooth extraction is considered a frequently needed procedure when planning most orthodontic treatments, especially those which aim at correcting the insufficient space disorders in the upper and the lower jaws and/or some other aesthetic and occlusal problems. The first premolars - and sometimes the second premolars - in either the upper or the lower jaw are usually the first choice when extraction becomes a part of the whole orthodontic treatment plan. Gingival invaginations are defined as superficial changes in the shape of gingiva which arise after moving the teeth orthodontically in order to close the spaces resulted from extraction procedures.[36] Gingival invaginations were noted in 35% of cases after orthodontic space closure procedures.[37] They vary from slight fissures located in the keratinized gingiva to deep gaps crossing the interdental papilla buccally or lingually through the alveolar bone deeply.[38],[39] Histological and histo-chemical specimens taken from sites of gingival invagination showed hypertrophy in the epithelial and the connective tissues, and sometimes, loss of gingival collagen.[37],[40] The real reason for gingival invaginations is still unknown. One expected reason could be the break-up of the continuity of the fiber models within the gingiva, and also the movement of the root.[41] However, other studies suggest the gingival peeling as a reason for such changes.[42] Since gingival invaginations may offer good sites in which dental plaque can be easily embedded, researchers considered these changes in the gingiva as risk factors for the periodontal tissue disorders during orthodontic treatment.[43] The gingival recession has been shown to be a common adverse effect during and/or after the orthodontic treatment.

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

This effect has been noted more frequently while using buccal orthodontic movements.[32] If teeth that have thin tissue are going to be moved lingually, there is a potential for the tissue to move coronally and become thicker.[44] If no orthodontic treatment is planned for children adolescents, areas of thin gingival tissues should be monitored only periodically as the width of the attached gingiva generally increases with normal growth from the mixed to the permanent dentition.[45] It has been shown that most cases of gingival recession which occur during an orthodontic treatment occurred in the regions of the anterior upper and lower teeth.[46],[47] An expected relationship could be established between (Tipping) orthodontic movements and gingival recession. However, this relationship is still, to date, controversial. In a study of Batenhorst[48], gingival recessions and bone dehiscences after orthodontic tipping of the lower incisors in monkeys had been recorded. In other studies, no real cases of gingival recession or mucogingival defects had been recorded after orthodontic tipping of the incisors.[49] Aspects in Periodontic-Orthodontic Interrelationships Generally, the main reasons routinely cited to justify the provision of orthodontic treatment are improvement of facial and dental aesthetics and of dental health and function. However, association between malocclusions and periodontal condition is still controversial. Ngom and co-workers [50] found significant correlations between malocclusions and periodontal condition and suggested that malocclusions are risk markers for periodontal diseases. However, a real inference about a cause/effect relationship between malocclusions and periodontal condition in this study was not possible. A review of the literature conducted by Van Gastel[51] showed contradictory findings on the impact of malocclusion and orthodontic appliances on periodontal health, since only a few studies reported attachment loss during orthodontic treatment. It has been suggested that this contradiction may be partly due to the selection of materials and differences in the research methods employed. However, our previous studies showed that orthodontic treatment in general does not have any negative effects on the periodontal tissues when a high level of oral hygiene is maintained.[52] In a review, Chang et al. (1997)[18] discussed about the aetiology of enamel demineralization during fixed orthodontic treatment and its sequelae. A summary is given of the various methods available to assess the risk of demineralization prior to active treatment. According to this review, the best preventive strategy would appear to be an assessment of risk factors prior to banding, coupled with fluoride rinses, regular reinforcement of oral hygiene, and dietary advice throughout the course of treatment. Actually, between the year 1964 and 2007, sufficient studies had been conducted in terms of orthodontic treatment and possible related periodontal changes. Thus, it sounds plausible to extract evidence-based conclusions from those studies by means of systematic reviews. According to Dr Jabur (2008) placement of orthodontic appliances creates a favourable environment for the accumulation of microbiota. Patients need to understand and be aware of the implications for their oral health, when accept recommended orthodontic treatment.

025

On the other hand, accepting appliance orthodontic therapy has important implications for patients’ home care. In 2008, Bollen[53] conducted two systematic reviews to address the following questions: does a malocclusion affect periodontal health, and does orthodontic treatment affect periodontal health. The first review found a correlation between the presence of a malocclusion and periodontal disease. Subjects with greater malocclusion have more severe periodontal disease. The second review identified an absence of reliable evidence on the effects of orthodontic treatment of periodontal health. The existing low-quality evidence suggests that orthodontic therapy results in small detrimental effects to the periodontium. It has been suggested that the results of both reviews do not warrant recommendation for orthodontic treatment to prevent future periodontal problems, except for specific unusual malocclusions. Another systematic review of controlled evidence related to the same last author[54] suggested that orthodontic therapy was associated with 0.03 millimeters of gingival recession, 0.13 mm of alveolar bone loss and 0.23 mm of increased pocket depth when compared with no treatment, and it was concluded that the effects of orthodontic therapy on gingivitis and attachment loss were inconsistent across studies. According to these recent reviews, it could be concluded that an absence of reliable evidence for the positive effects of orthodontic therapy on patients periodontal status seems to be indicated.[55] On the other side, it seems that there still are studies that give the orthodontic treatment positive points regarding periodontal health. Gray and McIntyre [56] conducted a systematic literature review to determine the effectiveness of orthodontic oral health promotion (OHP) upon gingival health, and it has been found that an OHP program for patients undergoing fixed appliance orthodontic treatment produces a short-term reduction (up to 5 months) in plaque and improvement in gingival health. A recent study of Thornberg and co-workers[57] aimed to document and investigate changes in periodontal pathogen levels before, during, and after orthodontic treatment in adolescents, eight pathogens were examined; Actinobacillus actinomycetemcomitans (AA), Porphyromonas gingivalis (PG), Prevotella intermedia (PI), Tannerella forsythia (TF), Eikenella corrodens (EC), Fusobacterium nucleatum(FN), Treponema denticola (TD), and Campylobacter rectus (CR). It has been shown that for six (PI, TF, EC, FN, TD, CR) of the eight pathogens, the percentages of subjects with high pathogen counts increased significantly after six months of fixed appliance treatment, but these returned to pretreatment levels by 12 months of orthodontic treatment. No pathogen level was significantly higher after 12 months of orthodontic treatment, and orthodontic treatment was found to be significantly protective for half of the pathogens (EC, FN, TD, and CR) post-treatment. It was concluded that orthodontic treatment with fixed appliances does not increase the risk of high levels of these periodontal pathogens. The existing evidence, in general, does not seem to support the claim that orthodontic therapy results in overall improvement in periodontal health. ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

References: 1. Kitada and de Toledo. Increase in detectable opportunistic bacteria in the oral cavity of orthodontic patients. International Journal of Dental Hygiene 2009; Volume 7, Issue 2, pages 121–125 2. Alstad S, Zachrisson BU. Longitudinal study of periodontal condition associated with orthodontic treatment in adolescents. Am J Orthod 1979; 76(3): 277286 3. Nomaan Nasir, Sarah Ali, Ulfat Bashir, Atta Ullah. Effect of orthodontic treatment on periodontal tissue. Pakistan Oral & Dental Journal Vol 31, No. 1 (June 2011) 4. Dr. Elanchezhiyan, Dr.Raja. Awareness on gingival health among orthodontic correction seeking individual. JIADS VOL -1 Issue 3 July - September,2010 |20 5. Derrick Willmot. Orthodontic treatment and the compromised periodontal patient. Eur J Dent. 2008 January; 2: 1–2. 6. Stuteville OH. Injuries caused by orthodontic appliances and methods of preventing these injuries. JADA 1937;24:1494–507. 7. Skillen WG. Krivanek FJ. Effects of orthodontic appliances on gingival tissues. Northw Uni Bull 1938;38:18–22. 8. Imtiaz Ahmed, Saif ul Haque, Rozina Nazir. Periodontal status of first molars during orthodontic treatment. J Ayub Med Coll Abbottabad 2011;23(1) 55-57 9. Boyd RL, Baumrind S. Periodontal implications of orthodontic treatment in adults with reduced or normal periodontal tissue versus those of adolescents. Angle Orthod 1992. 42;62: 117-26 10. Zachrisson S, Zachrisson BU. Gingival conditions associated with orthodontic treatment. Angle Orthod 1972; 42: 26-34. 11. Hamp SE, Lundstrom F, Nyman S. Periodontal conditions in adolescents subjected to multiband orthodontic treatment with controlled oral hygiene. Eur J Orthod 1982; 4(2): 77-86 12. Boyd RL, Murray P, Robertson PB. Effects of rotary toothbrush versus manual tooth brush on periodontal status during orthodontic treatment. Am J Orthod Dentofac Orthop 1989; 96: 342-347 13. Eliasson LA, Hugoson A, Kurol J, Siwe H. The effects of orthodontic treatment on periodontal tissues in patients with reduced periodontal support. Eur J Orthod 1982; 4:1-9 14. Steffensen B, Storey AT. Orthodontic intrusive forces in the treatment of periodontally compromised incisors: a case report. Int J Perio Rest Dent 1993; 13: 433-441 15. Mizrahi E. Enamel demineralisation following orthodontic treatment. Am J Orthod Dentofac Orthop 1982;82:62-7. 16. Gorelick L, Geiger AM, Gwinnett AJ. Incidence of white spot formation after bonding and banding. Am J O rthod 1982;81:93-8. 17. Mitchell L. Decalcification during orthodontic treatment with fixed appliances – an overview. Br J Orthod 1992;19:199-205. 18. H. S. Chang, L. J. Walsh, T. J. Freer. Enamel demineralization during orthodontic treatment. Aetiology and prevention. Australian Dental Journal 1997;42:(5):322-7 19. Newbrun E. Cariology. 3rd edn. Chicago: Quintessence, 1989:29-61. 026

20. LundstrÖm F, Krasse B. Streptococcus mutans and lactobacilli frequency in orthodontic patients; the effect of chlorhexidine treatments. Eur J Orthod 1987;9:109-16. 21. Forsberg CM, Oliveby A, Lagerl¨of F. Saliva ry clearance of sugar before and after insertion of fixed orthodontic appliances. Am J Orthod Dentofac Orthop 1992;102:52730. 22. Andersson R, Arvidsson E, Crossner CG, Holm AK, Mansson B, Grahnen H. The flow rate, pH and buffer effect of mixed saliva in children. J Int Assoc Dent Child 1974;5:5-12. 23. Gorelick L, Geiger AM, Gwinnett AJ. Incidence of white spot formation after bonding and banding. Am J O rthod 1982;81:93-8. 24. van Houte J. Bacterial specificity in the etiology of dental caries. Int Dent J 1980;30:305-26. 25. Rosenbloom RG, Tinanoff N. Salivary Streptococcus mutans levels in patients before, during, and after orthodontic treatment. Am J Orthod Dentofac Orthop 1991;100:35-7. 26. Scheie AA, Arneberg P, Krogstad O. Effect of orthodontic treatment on prevalence of Streptococcus mutans in plaque and saliva. Scand J Dent Res 1984;92:211-7. 27. Lang NP, Loe H. The relationship between the width of keratinized gingiva and gingival health. J Periodontol. 1972;43:623–7 28. Dorfman HS. Mucogingival changes resulting from mandibular incisor tooth movement. Am J Orthod 1978;74:286-97. 29. Wennstrom J, Lindhe J, Nyman S. Role of keratinized gingiva for gingival health.Clinical and histologic study of normal and regenerated gingival tissue in dogs. J Clin Periodontol. 1981;8:311–28 30. Coatoam GW, Behrents RG, Bissada NF. The width of keratinized gingiva during orthodontic treatment: Its significance and impact on periodontal status. J Periodontol 1981;52:307-13. 31. Trossello VK, Gianelly AA. Orthodontic treatment and periodontal status. J Periodontol. 1979;50:665–71 32. Wennstrom JL, Lindhe J, Sinclair F, Thilander B. Some periodontal tissue reactions to orthodontic tooth movement in monkeys. J Clin Periodontol.1987;14:121–9. 33. Foushee DG, Moriarty JD, Simpson DM. Effects of mandibular orthognathic treatment on mucogingival tissues. J Periodontol. 1985;56:727–33 34. Maynard JG. The rationale for mucogingival therapy in the child and adolescent. Int J Periodontics Restorative Dent. 1987;7:36–51. [ 35. Steiner GG, Pearson JK, Ainamo J. Changes of the marginal periodontium as a result of labial tooth movement in monkeys. J Periodontol. 1981;52:314–20. 36. Edwards JG. The prevention of relapse in extraction cases. Am J Orthod.1971;60:128–44. 37. Kurol J, Ronnerman A, Heyden G. Long-term gingival conditions after orthodontic closure of extraction sites: Histological and histochemical studies. Eur J Orthod. 1982;4:87–92 38. Rivera Circuns AL, Tulloch JF. Gingival invagination in extraction sites of orthodontic patients: Their incidence, effects on periodontal health, and orthodontic treatment. Am J Orthod. 1983;83:469–76. 39. Wehrbein H, Bauer W, Diedrich PR. Gingival invagination

area after space closure: A histologic study. Am J Orthod Dentofacial Orthop. 1995;108:593–8. 40. Ronnerman A, Thilander B, Heyden G. Gingival tissue reactions to orthodontic closure of extraction sites: Histologic and histochemical studies. Am J Orthod. 1980;77:620–5. 41. Atherton JD. The gingival response to orthodontic tooth movement. Am J Orthod. 1970;58:179–86. 42. Robertson PB, Schultz LD, Levy BM. Occurrence and distribution of interdental gingival clefts following orthodontic movement into bicuspid extraction sites. J Periodontol. 1977;48:232–5 43. Helm S, Petersen PE. Causal relation between malocclusion and periodontal health. Acta Odontol Scand. 1989;47:223–8. 44. Boyd RL. Mucogingival considerations and their relationship to orthodontics. J Periodontol. 1978;49:67–76 45. Sperry TP, Speidel TM, Isaacson RJ, Worms FW. The role of dental compensations in the orthodontic treatment of mandibular prognathism. Angle Orthod. 1977;47:293–9. 46. Sadowsky C, BeGole EA. Long-term effects of orthodontic treatment on periodontal health. Am J Orthod. 1981;80:156–72. 47. Polson AM, Reed BE. Long-term effect of orthodontic treatment on crestal alveolar bone levels. J Periodontol. 1984;55:28–34. 48. Batenhorst KF, Bowers GM, Williams JE., Jr Tissue changes resulting from facial tipping and extrusion of incisors in monkeys. J Periodontol. 1974;45:660–8 49. Allais D, Melsen B. Does labial movement of lower incisors influence the level of the gingival margin? A casecontrol study of adult orthodontic patients.Eur J Orthod. 2003;25:343–52. 50. Ngom PI, Benoist HM, Thiam F, Diagne F, Diallo PD. Influence of orthodontic anomalies on periodontal condition. Odontostomatol Trop.2007;301:9–16. 51. van Gastel J, Quirynen M, Teughels W, Carels C. The relationships between malocclusion, fixed orthodontic appliances and periodontal disease: A review of the literature. Aust Orthod J. 2007;23:121–9. 52. Dannan A, Darwish MA, Sawan MN. How do the periodontal tissues react during the orthodontic alignment and leveling phase? Virtual J Orthod.2008;8:1–7. 53. Bollen AM. Effects of malocclusions and orthodontics on periodontal health: Evidence from a systematic review. J Dent Educ. 2008;72:912–8. 54. Bollen AM, Cunha-Cruz J, Bakko DW, Huang GJ, Hujoel PP. The effects of orthodontic therapy on periodontal health: A systematic review of controlled evidence. J Am Dent Assoc. 2008;139:413–22. 55. Chung MH, Henwood RW. Inconclusive evidence of the effects of orthodontic therapy on periodontal health. J Am Dent Assoc. 2009;140:575–6. 56. Gray D, McIntyre G. Does oral health promotion influence the oral hygiene and gingival health of patients undergoing fixed appliance orthodontic treatment? A systematic literature review. J Orthod. 2008;35:262–9. 57. Thornberg MJ, Riolo CS, Bayirli B, Riolo ML, Van Tubergen EA, Kulbersh R. Periodontal pathogen levels in adolescents before, during, and after fixed orthodontic appliance therapy. Am J Orthod Dentofacial Orthop.2009;135:95–8.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

027

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Lemon Grass Oil For Improvement Of Oral Health Vinesh Kamath K1, Vidya Rekha Kamath2, Indranil Sarkar3 1 2 3

Senior Lecturer, Dept Of Periodontics, Coorg Institute Of Dental Sciences, Virajpet Lecturer, General Surgery, Coorg Institute Of Dental Sciences, Virajpet Pg Student, Dept Of Periodontics, Coorg Institute Of Dental Sciences, Virajpet

Abstract Harnessing Mother Nature’s bountiful remedies for rejuvenation has been in vogue since time immemorial. Lemon grass oil - a touchstone promising to offer myriad of possibilities in providing the healing touch is emerging as an alternative treatment option for periodontal diseases. It possesses anti-inflammatory, anti-oxidant, anti-microbial and wound healing properties. Antioxidants are those substances which when present in minimum quantities prevents the oxidation of a substrate. Recently, there has been a considerable interest in finding natural antioxidants from plants. Natural antioxidants are presumed to be safe and are seen as more desirable than their synthetic counter parts. Plants possess enzymatic systems that protect them against H2O2 and other harmful reactive oxygen species and also superoxide scavenging property. Reductionin the bacterial load, decrease in inflammation and reduction of the oxidative stress will bring about the overall healthof the tissues. Based on above propertiesthis article apprises lemongrass oil mouthwash can be used as an adjunct along with the nonsurgical therapy.

Key Words Lemon Grass, Harnessing Mother, Rejuvenation, Antioxidants.

Introduction Essential oil is a concentrated volatile liquid containing hydrophobic components. They are used medicinally to treat fungal and bacterial infections. They are used as mouth washes to treat plaque gingivitis to maintain inter dental hygiene preprocedural rinsing for controlling infection and for maintaining the implant.[1] Lemon Grass Oil Lemon grass [Figure 1] belongs to the family Poaceace and genus Cymbopogon. Common names: lemon grass, barbed wire grass, citronella grass, Tanglad, Hierba luisa. Scientific name: Cymbopogon nardus, Citratus Distribution: India, Tropical Asia and Africa. Botanical description ? Tropical grass ? Grow in dense clumps ? Up to 6 ft. in height ? and 4 ft. in width ? Short rhizome.[2] Active Ingredients ? Citronellol ? Geraniol Medicinal uses ? To treat rheumatism Quick Response Code

Figure 1: Lemon grass plant and its essential oil in a clear glass vial (http:// en.wikipedia.org/wiki/Cymbopogon)

Address For Correspondence: Dr. Priyanka Aggarwal Post Graduate Student, Department of Periodontontology and Oral Implantology, Rajasthan Dental College & Hospital, Jaipur Email: [email protected]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

[3]

? To treat periodontitis ? To treat hyper cholesterolemia[4] ? To treat hypertension ? As an anti-oxidant.[5]

Anti-bacterial activity A research conducted by Saddiq and Khayyat showed that citral epoxide, which is an active ingredient of lemon grass oil have high activity against the growth of bacteria than fungi and also showed that it effectively inhibits methicillin resistant species of Staphylococcus aureus.[2] Another research conducted by Naik et al. showed that lemon grass oil is effective against Gram-positive bacteria than Gram-negative bacteria even at low concentration. It also showed that it is effective in treating many species of drug resistant bacteria.[6] In the oral cavity Gram-positive bacteria is predominant over Gram-negative bacteria. Hence, lemon grass oil can be used as a mouth wash to prevent bacterial accumulation, which in turn can prevent dental caries. Lemon grass was found effective against all the test organisms except Pseudomonas aeruginosa. Chemical composition and antibacterial activity of aqueous extract of Cymbopogon citratus leaves were studied. Antimicrobial activities of aqueous and ethanol extract of C. citratus was compared against certain bacteria by disc diffusion method. In accordance with the nutrient and chemical contents determined, C. citrates leaves are safe and effective as a therapeutic agent in traditional therapies and also as dietary supplements.[7] In management of periodontitis Periodontitis is an inflammatory condition caused due to oxidative stress along with microbial toxins. It is characterized by inflamed tissue with or without bleeding around the teeth and there will be loosening of the collagen fibers around the teeth leading to super infections followed by mobility of the teeth. Lemon grass oil have anti-oxidant properties, which

028

helps in prevention and treatment of periodontitis hence by increasing the level of thiol anti-oxidants and also by reducing the bacterial load showed in a study conducted by Anand et al.[3] Another study by Rabbani et al. showed that the antioxidant action can be responsible for the anticlastogenic effect of citral against nickel chloride.[8] Anti-plaque activity Plaque, which is also known as biofilm produced by bacterial toxins is adherent to tooth surfaces and may lead to gingivitis. Plaque will get trapped in inter dental spaces and accumulate bacteria in them and induces an inflammatory reaction in the gingiva. Hence, ultimately it will lead to gingivitis which on further progression leads to periodontitis. Lemon grass oil can be used as an adjunct in mouth washes in order to prevent plaque formation and also to remove the plaque. Thereby it will inhibit the caries formation. A study published in the journal of ethno pharmacology proved that essential oil of lemon grass is effective in busting through the tough biofilm that Candida hides behind[3] and hence it can be used as a mouth wash and toothpaste to remove biofilm, which ultimately forms plaque.[9] Anti-candida activity A study done by American Association of Microbiology confirmed that lemon grass showed 100% toxicity against fungal growth. The essential oil of lemon grass 1000 ppm inhibited fungal growth completely.[10] Hence, lemon grass oil can be used in the treatment of oral candidiasis. A randomized controlled trial was done to analyze the use of lemon grass essential oil in the treatment of oral thrush in a human immunodeficiency virus (HIV)-positive population. Though the patient population was small, the use of lemon juice and lemon grass for the treatment of oral candidiasis in an HIV population was validated.[11] Few references says that citral acts as a fungicidal agent because it is able to form a charge transfer complex with an electron donor of fungal cells, resulting in fungal death.[12] The results demonstrated the potentiality of using the lemon grass oil instead of the citral in pharmaceuticals preparations, because of its similar anti-fungal activity, the minor cost and toxicity.[13] According to a study by Tyagi and Malik on minimum inhibitory concentration of different essential oils in the liquid phase, assayed through agar plate dilution, broth dilution and 96-well micro plate dilution method and vapor phase activity evaluated through disc volatilization method proved that lemon grass essential oil is highly effective in the vapor phaseagainst Candida albicans, leading to deleterious morphological changes in cellular structures and cell surface alterations.[14] Conclusion Hence, these researches concluded that lemon grass oil has anti-bacterial, anti-fungal, anti-oxidant, anti-proliferative, anti-viral and anti-inflammatory properties, which hints that it can be used to treat various diseases in human. The extract can be used as a mouth rinse or tooth paste or medicament to treat

various dental issues. Further researches should be done in lemon grass oil in relation with oral cavity for the prevention and treatment of various dental diseases. References 1. Yengopal V. Essential oils: Some lesser known uses and properties for improved oral health. J Minimum Interv Dent 2009;2:190-6. 2. Saddiq AA, Khayyat SA. Chemical and antimicrobial studies of monoterpene; citral. Pestic Biochem Physiol 2010;98:89-93. 3. Anand M, Goyal R, Bhat GS, Kamath S, Aggarwal M, Bhandarkar MA, et al. Antioxidant property of a novel lemongrass oil mouth wash: an experimental study. Rec Res Sci Technol 2011;3:14-8. 4. Shah G, Shri R, Panchal V, Sharma N, Singh B, Mann AS. Scientific basis for the therapeutic use of Cymbopogon citratus, stapf (Lemon grass). J Adv Pharm Technol Res 2011;2:3-8. 5. Cheel J, Theoduloz C, Rodríguez J, Schmeda-Hirschmann G. Free radical scavengers and antioxidants from lemongrass (Cymbopogon citratus (DC.) Stapf.). J Agric Food Chem 2005;53:2511-7. 6. Naik I, Fomda BA, Bhat JA. On antibacterial activity of lemongrass (cymbopogon citratus) oil against some selected pathogenic bacteria. Asian Pac J Trop Med 2010;3:535-8. 7. Oloyede OI. Chemical profile and antimicrobial activity of Cymbopogon citratus leaves. J Nat Prod 2009;2:98-103. 8. Rabbani SI, Devi K, Khanam S, Zahra N. Citral, a component of lemongrass oil inhibits the clastogenic effect of nickel chloride in mouse micronucleus test system. Pak J Pharm Sci 2006;19:108-13. 9. Edris AE. Pharmaceutical and therapeutic potentials of essential oils and their individual volatile constituents: A review. Phytother Res 2007;21:308-23. 10. Tyagi AK, Malik A. Liquid and vapour-phase antifungal activities of selected essential oils against Candida albicans: Microscopic observations and chemical characterization of Cymbopogoncitratus. BMC Complement Altern Med 2010;10:65. 11. Wright SC, Maree JE, Sibanyoni M. Treatment of oral thrush in HIV/AIDS patients with lemon juice and lemon grass (Cymbopogon citratus) and gentian violet. Phytomedicine 2009;16:118-24. 12. Mishra AK, Dubey NK. Evaluation of some essential oils for their toxicity against fungi causing deterioration of stored food commodities. Appl Environ Microbiol 1994;60:1101-5. 13. Kurita N, Miyaji M, Kurane R, Takahara Y. Antifungal activity of components of essential oils. Agric Biol Chem 1981;45:945-52. 14. Silva Cde B, Guterres SS, Weisheimer V, Schapoval EE. Antifungal activity of the lemongrass oil and citral against Candida spp. Braz J Infect Dis 2008;12:63-6.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

029

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Bone Grafts In Periodontal Surgery . A Review Abhishek Kandwal1, Jigyasa Bhardwaj2, Sunny3, Mannu Batra4 1

Assistant Professor, Dept. Of Periodontics, Himalayan Institute Of Medical Sciences, Dehradun Private Practitioner, Dehradun Senior Lecturer, Dept. Of Periodontics & Oral Implantology, Uttaranchal Dental And Medical Research Institute Dehradun 4 Assistant Professor, Dept Of Public Health Dentistry , Teerhankar Mahaveer Dental College And Research Center Moradabad 2

3

Abstract Periodontal disease is one of the most prevalent afflictions worldwide. The most serious consequence is the loss of the periodontal support structure, which includes cementum, the periodontal ligament, and alveolar bone. Conventional periodontal treatments, such as root planing, gingival curettage, and scaling, are highly effective at repairing disease-related defects and halting the progression of periodontitis. These are important steps; however, the conventional therapies do relatively little to prompt the regeneration of lost periodontal support structure. In fact, studies indicate that they typically result in the development of a long junctional epithelium between the root surface and gingival connective tissue rather than the regrowth of tissue that restores the architecture and function. Thus, more effective techniques that predictably promote the body's natural ability to regenerate its lost periodontal tissues, particularly alveolar bone still need to be developed. Bone grafting is the most common form of regenerative therapy today and is usually essential for restoring all types of periodontal supporting tissue. To date, histologic evidence in humans indicates that bone grafting is the only treatment that leads to regeneration of bone, cementum, and a functionally oriented new periodontal ligament coronal to the base of a previous osseous defect.

Key Words Periodontal Disease, Bone Grafts, Cementum

Classification Of Bone Grafts Human bone ? Autogenous grafts (autografts) Extraoral Intraoral ? Allogenic grafts (allografts) Fresh frozen bone Freeze-dried bone allografts Demineralized freeze-dried bone allografts Bone substitutes ? Xenogeneic grafts (xenografts) Bovine-derived hydroxyapatite Coralline calcium carbonate ? Alloplastic grafts (alloplasts) Polymers Bioceramics Tricalcium phosphate Hydroxyapatite - dense, nonporous, nonresorbable; porous, nonresorbable hydroxyapatite derived at , low temperature (xenograft) resorbable Bioactive glasses The Indications For Osseous Grafts: 1) Deep Intraosseous Defects - The deeper the defect, the greater amount of bone fill that can be expected; at the same

Quick Response Code

Address For Correspondence: Dr. Abhishek Kandwal Assistant Professor Periodontics , Oral Implantology & Oncodontics Dept Of Dental Surgery Himalayan Institute Of Medical Sciences Dehradun 248001

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

time, the residual defect may be significant. It is the opinion of many clinicians that the greater the number of osseous walls and the greater the support and containment for the graft material, the greater will be the bone fill. The degree of regeneration in an osseous defect of a given volume and morphology varies directly with the adequacy of the soft tissue cover and with the surface area of the vascularized bony walls lining the defect; it varies inversely with the root surface area. Therefore, a three-wall defect should heal with more bone fill than a two-wall or a one-wall lesion, and a one-wall defect should heal better than a furcation defect. Furthermore, intraosseous defects caused by periodontal abscesses or pulpal pathosis will respond favorably with bone fill without a graft, following appropriate emergency or endodontic therapy. 2) Tooth Retention - The use of bone grafts may restore functional stability to such a degree as to obviate the need for extraction. 3) Support for Critical Teeth - Teeth severely weakened by loss of alveolar support can benefit from the use of osseous grafts. This may be the case for an abutment tooth or those teeth that are critical for the preservation of arch integrity. 4) Bone Defects Associated With Juvenile Periodontitis These extensive lesions have been reported to respond very favorably to osseous grafting, especially when grafting is combined with an antibiotic, such as tetracycline. 5) Esthetics (Shallow Intraosseous Defects) - The resection of shallow intraosseous defects in the anterior region of the mouth by osteoplasty/ostectomy followed by an apically positioned flap to eliminate the periodontal pocket will result in gingival recession and a long clinical crown. This may be esthetically unacceptable. The use of osseous grafts to reconstruct bone architecture allows placement of the gingival margin as close as possible to its original position. Successful healing will result in minimal apical displacement of the gingival margin.

030

6) Furcation Defects - This indication applies mainly to class II furcation defects. Bone grafts, especially if used in conjunction with guided tissue regeneration, have proven to be the therapeutic modality of choice for treating this type of lesion. Clinical Objectives Of Bone Grafting For Periodontal Regeneration: The objectives of bone grafting procedures for patients with periodontitis are as follows: (1) Probing depth reduction (2) Clinical attachment gain (3) Bone fill of the osseous defect (4) Regeneration of new bone, cementum, and periodontal ligament

4.

5.

6.

Ideal Characteristics Of A Bone Graft: ? Nontoxic ? Nonantigenic ? Resistant to infection ? No root resorption or ankylosis ? Strong and resilient ? Easily adaptable ? Readily and sufficiently available ? Minimal surgical procedure ? Stimulates new attachment

Advantages Of Bone Grafts 1. Regeneration of the attachment apparatus is possible. Reconstruction of lost bone, cementum, and periodontal ligament has been adequately documented with autogenous and allogeneic graft materials. 2. By reconstructing the periodontium, it is possible to reverse the disease process. 3. Increased tooth support, improved function, and enhanced esthetics are concomitant results of successful bone graft therapy. 4. Bone grafts have application for all categories of intraosseous defects and certain furcation defects. This is in contrast to other forms of regenerative therapy. 5. Idealistic therapeutic objectives may be achievable. With the advent of growth factors to augment the osteogenic potential of current or future graft materials, complete disease reversal is a realistic goal. Disadvantages Of Bone Grafts: 1. Bone graft therapy involves additional treatment time. Because of graft procurement and/or preparation, as well as placement, the time allotted to the surgical procedure must be lengthened. For the clinician inexperienced in regenerative periodontal therapy, the learning curve and the subsequent increase in treatment time will be significant. 2. Autografts require the removal of host donor tissue. Unless bone can be removed from within the primary surgical site, a secondary surgical site, either extraoral or intraoral, is necessary. The risks of any surgical procedure will apply here as well. In addition, the quantity of intraoral bone to fill multiple or deep defects is often lacking. Root resorption and ankylosis are problems encountered only with fresh iliac cancellous bone and marrow. 3. The availability and added expense of bone allografts are ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

7.

8.

ongoing problems. Patients and clinicians fears of disease transfer can be ameliorated by reference to the scientific literature. Additional postoperative care is often necessary with bone graft therapy. This can range from technical problems to management of soft tissue defects associated with wound healing. Bone grafts take a long time to heal. As much as a 2-year postoperative interval may be necessary before there is final radiographic resolution of the defect. Although most patients can receive restorative care 6 months following treatment, partial bone fill or delayed healing may delay needed restorative care. Bone graft therapy is not routinely predictable in the hands of all practitioners. Bone grafts are highly successful for those practitioners who have taken the time and effort to master this technique-sensitive therapy. Bone graft adds greater expense to the therapy. Economic considerations involve the cost of procurement or of the material itself, additional surgical treatment time, and postoperative maintenance treatment. Multistep therapy is sometimes necessary, either to regraft residual osseous defects, where additional bone fill is possible and feasible, or to eliminate the residual osseous defect by resection.

Requirements For A Successful Graft The most important surgical considerations in performing bone grafts for periodontal regeneration are as follows: Patient Selection Attention to patient selection is particularly important in the use and success of regenerative procedures, particularly bone grafts. The patient must demonstrate a high level of motivation and ability to remove plaque effectively on a daily basis. The patient must also show a commitment to keeping the often lengthy and rigorous appointments necessary for periodontal maintenance. During these, baseline records and a plaque index assessment help to determine the patient's progress. Other factors that must be considered are the patient's health, emotional status, habits (particularly smoking), and the ability to tolerate lengthy dental appointments. If any of these are unfavorable, bone grafts may be contraindicated. Material Selection Matching the contours of a defect to appropriate treatment is also clearly important for any regenerative or augmentation treatment. For instance, the more walls of bone that are present in the defect site, the better a graft's chance for success. Many failures are due to the selection of a treatment for a defect that will not respond well to the procedure. In general, the larger the defect, the more important it is to use autogenous bone, which provides the maximal levels of both cellularity and structure on which new bone can form. Whether an autograft or allograft is used, cancellous bone is favored over cortical bone for various reasons. In cancellous grafts, revascularization is more rapid and thus likely to preserve more osteogenic cells. The more dense cortical bone, however, is slowly revascularized and experiences a much faster rate of resorption. In addition, bone formation depends on an ample blood supply and mechanical support.

031

Proper Flap Reflection and Wound Stability Full-thickness flaps are generally recommended to provide access to periodontal defect sites. Internally beveled scalloped incisions with full gingival retention should be used so that the site can be completely closed when the surgery is concluded. Vertical releasing incisions should be used as necessary to allow access to the defect. Improper flap design can result in compromised blood supply to an underlying graft. As an alternative to the traditional approach of positioning the flap margin so it directly approximates the healing area, a coronally positioned flap procedure, which positions the flap margin away from the critical healing area and coronal to the cementoenamel junction, has been shown to provide better regenerative results for class II and class III furcation defects. Crown-attached sutures have also been shown to stabilize the flap margin better and prevent it from receding. Revascularization The underlying bone that receives the graft material must exhibit several marrow spaces and a good blood supply because prompt revascularization is crucial to ensure the survival of undifferentiated mesenchymal cells and osteoblasts at the site. For the largest number of osteocytes in graft material to survive and provide osteogenesis, early vascularization of the graft is crucial. If the host site is lined with cortical bone, this must be penetrated with a round bur to open into the underlying marrow, thus allowing progenitor cells and blood vessels to migrate into the area. Passanezi et al in 1989 noted that the narrower the distance between the bony walls and from the bone walls to the root, the more predictably the graft will take. Root Debridement Root debridement is a crucial step in grafting procedures. Both ultrasonic and hand instruments are generally used to ensure that all hard and soft deposits and any altered cementum are completely removed from the root surface. Rotary instruments and fiberoptic light sources may also enhance debridement. Postsurgical care Antibiotics are prescribed to suppress plaque accumulation for the first 10 days after surgery or until the patient can adequately control plaque in the area.This is critical for proper wound repair. It is important to emphasize during each recall visit the need for the patient to maintain scrupulous oral hygiene habits,including antibacterial rinses. During recall visits, plaque control should be continually monitored, and scaling and prophylaxis are performed as well as occlusion and healing assessment. Conclusion Although complete periodontal regeneration is unpredictable with any regenerative therapy currently used, periodontal bone grafts show strong potential. A large body of clinical evidence clearly indicates that grafts consistently lead to better bone fill than nongrafted controls. As more is learned about the biologic process of periodontal regeneration, new graft materials are expected to make the task of periodontal regeneration even more predictable. References

1. Constantino PD, Freidman CD. Synthetic bone graft substitutes. Otolaryngol. Clin. North Am. 1994; 27: 1037–73. 2. Cypher TJ, Grossman JP. Biological principles of bone graft healing. J. Foot Ankle Surg. 1996; 35: 413–17. 3. Triffitt JT. The stem cell of the osteoblast. In: Bilizekian J, Raisz L, Rodou G (eds) Principles of Bone Biology. San Diego, CA: Academic, 1996; 39–50. 4. Kurz LT, Garfin SR, Booth JR. Harvesting autogenous iliac bone grafts: A review of complications and techniques Spine 1989; 14: 1324–31. 5. Fernyhough JC, Schimandle JJ, Weigel MC. Chronic donor site pain complicating bone graft harvesting from the posterior iliac crest for spinal fusion. Spine 1992; 17: 1474–80. 6. Mankin HJ, Gebhardt MC. Long term results of allograft replacement in the management of bone tumours. Clin. Orthop. 1996; 324: 86–97. 7. Simonds RJ, Holmberg SD, Hurwitz RL et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ and tissue donor. N. Engl. J. Med. 1992; 326: 726–32. 8. Sanan A, Haines SJ. Repairing holes in the head: A history of cranioplasty. Neurosurgery 1997; 40: 588–603. 9. Hench LL, Wilson J. Surface active biomaterials. Science 1984; 226: 630–6. 10. Gross V, Brandes J. The ultrastructure of the interface between a glass ceramic and bone.J. Biomed. Mater. Res. 1981; 15: 291–305. 11. Kinnunen I, Aitasalo K, Pollonen M, Varpula M. Reconstruction of orbital floor fractures using bioactive glass. J. Craniomaxillofac.Surg. 2000; 28: 229–34. 12. Peltola M, Suonpaa J, Aitasalo K et al. Experimental follow-up model for clinical frontal sinus obliteration with bioactive glass. ActaOtolaryngol. Suppl. 2000; 543: 167–9. 13. Oonishi H, Kushitani S, Yasukawa E et al. Particulate bioglass compared with hydroxyapatite as a bone graft substitute. Clin. Orthop. 1997; 334: 316–25. 14. Schrooten J, Helsen JA. Adhesion of bioactive glass coating to Ti6A14V oral implants.Biomaterials 2000; 21: 1461–9. 15. Thompson ID, Hench LL. Mechanical properties of bioactive glasses, glass-ceramics and composites.Proc. Inst. Mech. Eng. 1998; 212: 127–36. 16. Xu X, Huang Z, Wang C. Clinical study of bioactive glass ceramics as orbital implants. Hunan I Ko Ta HsuehHsuehPao 1997; 22: 440–2. 17. Wittwer C, Devlin AJ, Hatton PV, Brook IM. The release of serum proteins and dye from glass ionomer and acrylic cements: A pilot study. J. Mater. Sci. 1994; 5: 711–14. 18. Heimke G. Aluminium oxide. In: Williams D (ed.) Concise Encyclopaedia of Medical and Dental Materials. Oxford: Pergamon,1990; 28–34. 19. Peltier LF, Bickel EY. The use of plaster of Paris to fill defects in bone.Ann. Surg. 1957; 146: 61. 20. Coetzee AS. Regeneration of bone in the presence of calcium sulphate.Arch. Otolaryngol. 1980; 106: 405–9. 21. Klawitter JJ, Bawell JG. An evaluation of bone ingrowth into porous high density polyethylene. J. Biomed. Mater. Res. 1976; 10:311.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

032

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review

Direct Metal Laser Sintering – A Digital Alternative To Conventional Casting Monica Sharma1, Nikita Singh2, Bhavna Sharma3, Arvind Sharma4, Sonali Razdan5 1

Deppt Of Prosthodontics, Post Graduate Student, Bhojia Dental College Deppt Of Prosthodontics, Post Graduate Student, Bhojia Dental College Deppt Of Prosthodontics, Post Graduate Student, Bhojia Dental College 4 Deppt Of Prosthodontics, Post Graduate Student, Bhojia Dental College 5 Deppt Of Prosthodontics, Post Graduate Student, Bhojia Dental College 2

3

Abstract \Laser sintering is a relatively new method compared to conventional casting procedure.Direct metal laser-sintering (DMLS) is a well-known method for e-Manufacturing, the fast, flexible and cost-effective production directly from 3D CAD data.The DMLS method is a newly introduced technique for producing metal FDPs and is currently being introduced widely in clinical practice; however, research on its clinical utility compared to traditional methods is limited.

Key Words Laser Sintering, Casting, CAD, Crown Bridge

Introduction Casting metals by lost-wax process has been recognized in industry and the arts for many years.No record exists to indicate exactly when and where this type of casting procedure was first developed. All that is known is that somewhere along the line - it may have been in ancient China/Egypt-someone conceived the idea of making a wax replica of an item to cast, surrounding this replica with an investment material, letting this harden, then melting wax and burning out the wax to produce an intricate and accurate mold was conceived. The next step involved is melting the metal and pouring it into the cavity.[1] In dentistry lost wax technique has become a common practice after it was introduced by William H. Taggart in 1907. Casting is a technique-sensitive method, requiring qualified technicians, control of the wax pattern fabrication and investing procedure, and careful attention during the casting process.[2] In recent years casting technology is undergoing a radical shift due to industrialization. Digitalized technologies are been employed for the production of metallic structures, mainly in prosthetic dentistry. These technologies can be classified as based on subtractive manufacturing, such as the milling of premanufactured materials assisted by computer-aided design/computer-aided manufacturing (CAD/CAM) systems[3],[4],[5],[6] or on additive manufacturing, such as the recently developed laser sintering technology.[7],[8],[9],[10] Laser-Sintering was first introduced by Deckard and Beaman. Laser sintering isbasically manufacturing of solid parts by solidifying powderlikematerials layer-by-layer by exposing the surface of a powder bed with a laser or otherenergy beam. Direct Metal Laser-Sintering (DMLS) is a Quick Response Code

Address For Correspondence: Dr. Monica Sharma Deppt Of Prosthodontics, Post Graduate Student Bhojia Dental College And Hospital, Bhud, Nalagarh Mail Id : [email protected]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

type of laser-sintering using a metal powder so that metal parts are produced directly in the building process.[11] DMLS requires basically three inputs: material, energy source,CAD model. The material used is specially developed powder blend containing a range of alloying elements with the particle size of 3-14 µm. A special version of CoCr superalloy developed by EOS CobaltChrome SP1 and later modified to SP2 is available which is used exclusively for metal-ceramic restorations. The energy source is a laser beam (Yb-fibre or CO2) of 200W power which fuses thepowder layers of metal of 20µm thickness. The data from the CAD model guides layering process to fabricate the shape of the restorations. These layers correspond to the virtual cross-sections from the CAD model. The standard data interface between CAD software and the machine is the STL (Standard Tessellation Language) file format. The STL file creation process mainly converts the continuous geometry in the CAD file into a header, small triangles, or coordinates triplet list of x, y, and z coordinates and the normal vector to the triangles. The smaller the triangles the closer they are to reality.[12] The CAD process of producing copings by DMLS technique is carried by scanning the impression or the poured cast using the optical scanner. The crown/bridge is designed over this digitilised cast using CAD software. This data is then sent to production centre which are usually the remote laboratories equipped with DMLS machines. The machine converts the CAD software into STL file which helps in carrying out laser sintering of Co-Cr powder, layer by layer of thickness 20 µm in an inert atmosphere. After a layer is built, the building platform is lowered and a new layer of powder is applied. The procedure is carried out until the desired shape of the coping is obtained.Upto 90-120 units of crown/bridge can be obtained per run of the machine. A total of 450 units in 24 hours fully automated and of high accuracy. Discussion Direct metal laser-sintering (DMLS) is a well-known method for e-Manufacturing, the fast, flexible and cost-effective production directly from 3D CAD data. Advantages of the DMLS system include easy fabrication of complicated shapes, 033

operation of an automatic system, and short working time due to elimination of the procedures of fabricating a wax pattern, investing, burning, and casting works. While the traditional casting method using the lost wax method might waste metal in spruing and other procedures, the DMLS system could reduce metal waste by selectively shooting the required amount.[13] As the machine can create hundreds of units at a time, the cost of each one is relatively reduced. In addition, parts produced have consistent quality and excellent mechanical properties. The DMLS copings are densely sintered upto density 99.9% with practically no voids. Resulting in increased strength and accuracy of the restorations. They also have finer grain size than the cast or wrought materials. This is generally attributed to the very rapid resolidification due to almost instantaneous removal of heat input once the scanning laser spot has moved on and the rapid conduction of heat out of the melted zone into the surrounding solid metal and/or powder bed.[11] The DMLS method is a newly introduced technique for producing metal FDPs and is currently being introduced widely in clinical practice; however, research on its clinical utility compared to traditional methods is limited. The first clinical study to compare the marginal and internal fit of metal ceramic crowns fabricated using laser sintering process and the influence of ceramic firing on the marginal and internal accuracy of these crowns using two different alloys was carried out by Quante. et al.[7] For the total 28 restoration, the mean marginal discrepancy and internal gap were found to be clinically acceptable.Ucar et al.[10] carried an in vitro and reported no differ-ences for the internal gap width of lasersintered and cast Co-Cr conventional crowns. Where as Ortorp et al.[14] recorded lower discrepancies forlaser-sintered Co–Cr than for cast Co–Cr in the construction ofthree-unit, conventional fixed restorations. Akova et al.[9] compared shear bond strengths of cast Ni-Cr and Co-Cr alloys and a laser-sintered Co-Cr alloy to dental porcelain. The authors reported that the bond strengths were not significantly different and that the laser-sintering technique for the Co-Cr alloy appeared promising for dental applications.Tara et al.[15] carried out an in vivo study in which they placed 64 single crowns fabricated by laser sintering technology in 39 patients and found that there was no chipping of the veneering ceramic during an observation period of 47 months. Jabbari et al. recently found that there are differences in microstructural and hardness properties among the Co–Cr dental alloys fabricated via conventional casting, milling and selective laser melting, therefore he concluded that further differences in their clinical behavior may be anticipated.[16] Conclusion Laser sintering is a relatively new method compared to conventional casting procedure. The accuracy of CAD/CAM prosthetic frameworks may rely on the precision of the scanner that reads the abutments, on the ways in which the software can transform the scanning data into a 3D model on the computer, and on the accuracy of the machine that uses CAM to produce objects from the CAD data. Therefore, CAD/CAM techniques could minimize some of the risk factors related to casting procedures, as proven in the DLMS group, where few critical manual steps are present. The proper use of the DMLS technology may result in the most predictable fabrication method under the tested experimental conditions. However,

clinical implementation of the DMLS system seems to require further investigation, because studies of restoration longevity are scarce. References 1. Asgar K. Casting metals in dentistry: past--present--future. Adv Dent Res. 1988 Aug;2(1):33-43. 2. Bhaskaran E, Azhagarasan NS, Miglani S, Gajapathi B.Comparative Evaluation of Marginal and Internal Gap of Co–Cr Copings Fabricated from Conventional Wax Pattern, 3D Printed Resin Pattern and DMLS Tech: An In Vitro Study. J Indian Prosthodont Soc 2013; 13(3): 189195. 3. Van Noort R. The future of dental devices is digital. DentMater 2012;28:3–12. 4. Willer J, Rossbach A, Weber HP. Computer-assisted milling ofdental restorations using a new CAD/CAM data acquisitionsystem. J Prosthet Dent 1998;80:346–53. 5. Miyazaki T, Hotta Y. CAD/CAM systems available for thefabrication of crown and bridge restorations. Aust Dent J2011;56(Suppl. 1):97–106. 6. Witkowski S, Komine F, Gerds T. Marginal accuracy oftitanium copings fabricated by casting and CAD/CAMtechniques. J Prosthet Dent 2006;96:47–52. 7. Quante K, Ludwig K, Kern M. Marginal and internal fit ofmetal–ceramic crowns fabricated with a new laser meltingtechnology. Dent Mater 2008;24:1311–5. 8. Traini T, Mangano C, Sammons RL, Mangano F, Macchi A,Piattelli A. Direct laser metal sintering as a new approach tofabrication of an isoelastic functionally graded material formanufacture of porous titanium dental implants. DentMater 2008;24:1525–33. 9. Akova T, Ucar Y, Tukay A, Balkaya MC, Brantley WA.Comparison of the bond strength of laser-sintered and castbase metal dental alloys to porcelain. Dent Mater2008;24:1400–4. 10. Ucar Y, Akova T, Akyil MS, Brantley WA. Internal fitevaluation of crowns prepared using a new dental crownfabrication technique: laser-sintered Co–Cr crowns. JProsthet Dent 2009;102:253–9. 11. Shellabear, M. and O. Nyrhila. “DMLS – Development History and State of the Art”. Presented at LANE 2004 conference. Erlangen, Germany. Sept. 21-24, 2004. 12. Kaufui V. Wong, Aldo Hernandez. 2012. A Review of Additive Manufacturing. Mechanical Engineering 2012, 1-10. 13. Kim KB, Kim WC, Kim HY, Kim JH. An evaluation of marginal fit of three-unit fixed dental prostheses fabricated by direct metal laser sintering system. Dent Mater 2013;29(7):e91-6. 14. Ortorp OA, Jonsson D, Mouhsen A, Von Steyern PV. The fit of cobalt–chromium three-unit fixed dental prostheses fabricated with four different techniques: A comparative in vitro study. Dent Mater 2011;27:356-363. 15. Abou Tara M, Eschbach S, Bohlsen F, Kern M. Clinical outcome of metal-ceramic crowns fabricated with lasersintering technology. Int J Prosthodont. 2011 JanFeb;24(1):46-8. 16. Al Jabbari YS, Koutsoukis T, Barmpagadaki X, Zinelis S. Metallurgical and interfacial characterization of PFM CoCr dental alloys fabricated via casting, milling or selective laser melting. Dent Mater. 2014 Apr;30(4):e79-88.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

034

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Regenerative Endodontics – A Review Siddharth Bisht1, Amarjit Singh Chadda2, Manoj Rawat3 1 2 3

Senior Lecturer, Deptt Of Conservative Dentistry, Uttrakhand Dental College, Dehradoon Lecturer, Department Of Prosthodontics And Crown & Bridge, G.D.C Shimla Himachal Pradesh, India. Private Practioner, Shimla

Abstract While the regeneration of a lost tissue is known to mankind for several years. The modern concept of medicine emphasizes on prevention and reversal of diseases. The growing understanding of biological concepts in the regeneration of oral/dental tissues coupled with experiments on stem cells is likely to result in a paradigm shift in the therapeutic armamentarium of dental and oral diseases culminating in an intense search for "biological solutions to biological problems”. Regenerative endodontic procedures can be defined as biologically based procedures designed to replace damaged structures, including dentin and root structures, as well as cells of the pulp-dentin complex. Regenerative endodontics comprises researchin adult stem cells, growth factors, organ-tissue culture, and tissue engineering materials and often these disciplines are combined, rather than used individually to create regenerative therapies.

Key Words Regenerative Endodontics, Regenerative medicine, Tissue Engineering, Regenerative approaches, Stem Cell Banking.

Introduction While the regeneration of a lost tissue is known to mankind for several years, it is only in the recent past that research on regenerative medicine/dentistry has gained momentum and eluded the dramatic yet scientific advancements in the field of molecular biology. The growing understanding of biological concepts in the regeneration of oral/dental tissues coupled with experiments on stem cells is likely to result in a paradigm shift in the therapeutic armamentarium of dental and oral diseases culminating in an intense search for “BIOLOGICAL SOLUTIONS TO BIOLOGICAL PROBLEMS”. Stem cell and tissue engineering research and therapies, for example, have not only attracted mass media attention, provoked philosophical and bioethical debates but also entered the political arena. Regenerative endodontic procedures can be defined as, “Biological procedures designed to replace damaged structures, including dentin and root structures, as well as cells of the pulp-dentin complex.”[1] Although case reportsprimarily involve treating the immature permanent tooth, it isquite possible that knowledge gained from this clinical applicationwill have value in developing regenerative endodonticprocedures for the fully developed permanent tooth.[2] In short,the question is no longer “Can Regenerative Endodontic ProceduresBe Successfull?”[2] General Idea Of Regenerative Medicine The basis for regenerative medicine is the utilization of tissue engineering therapies. Probably the first definition of tissue Quick Response Code

Address For Correspondence: Dr. Amarjit Singh Chadda Lecturer, Department Of Prosthodontics And Crown & Bridge, G.D.C Shimla Himachal Pradesh, India. Mobile: 09418064299 Email – [email protected]

engineering was by Langer and Vacanti who stated, It was “an interdisciplinary field that applies the principles of engineering and life sciences toward the development of biological substitutes that restore, maintain, or improve tissue function”.[3] Tissue engineering and regenerative medicine seek to replacelost or damaged tissues due to any reason, and this needs three major ingredients which are:1- Morphogenic signals such as growth factors and differentiation factors, these factors play an important role in the multiplication and differentiation of stem cells into the specifically needed type of cells.[4] 2- Responding stem cells which are originally harvested from the patient and preserved under good conditions to maintain their special ability to differentiate into a wide range of cells. 3- Scaffold of extra cellular matrix, which provide these cells with the e n v i r o n m e n t whichmould to grow into what we want them to become and function. The principles of regenerative medicine can be applied to endodontic tissue

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Morphogenic Signals

Stem Cells

Scaffold

035

engineering. Regenerative endodontics comprises research in adult stem cells, growth factors, organ-tissue culture, and tissue engineering materials.[1] Root Canal Revascularization

Regenerative Approaches In Endodontics We have identified several major areas of research that might have application in the development of regenerative endodontic techniques[5]. These techniques are:-

Stem Cell Therapy

Pulp Implantation

(a) Root canal revascularization via blood clotting, (b) Postnatal stem cell therapy, (c) Pulp implantation, (d) Scaffold implantation, (e) Injectable scaffold delivery, (f) Three-dimensional cell printing, (g) Gene delivery system 1) Root canal revascularization via blood clotting : The canal was disinfected without mechanical instrumentation but with copious irrigation with 5.25% sodium hypochlorite and the use of a mixture of ciprofloxacin, metronidazole, and minocycline. A blood clot was produced to the level of the cemento-enamel junction to provide a scaffold for the ingrowth of new tissue followed by a double seal of mineral trioxide aggregate in the cervical area and a bonded resin coronal restoration above it.Several case reports have documentedthe revascularization of the necrotic root canal systems by disinfection, followed byestablishing bleeding into the canal system via over instrumentation.[6] 2) Post natal stem cell therapy: The term stem cell was proposed for scientific use by Russian histologist Alexander Maksimov in1908.[7] In the year 2003 Dr. Songtao Shi a paediatric dentist discovered baby tooth stem cells by using the deciduous teeth of his six year old daughter, he was luckily able to isolate,grow and preserve these stem cells’ regenerative ability, and named them as SHED (Stem cells from Human Exfoliated Deciduous teeth).[8] Stem cells are defined by having two major properties: - They are capable of self-renewal - They divide, some daughter cells give rise to cells that eventually differentiate. To date, four types of human dental stem cells have been isolated and characterized: (i) (ii) (iii) (iv)

dental pulp stem cells (DPSCs)[9], stem cells from exfoliated deciduous teeth (SHED)[8] stem cells from apical papilla (SCAP)[10], periodontal ligament stem cells (PDLSCs)[11].

Utilization of stem cells to regenerate the lost tissues may, thereby, reverse tissues to their normal state. The simplest method to administer the cells of appropriate regenerative potential is to inject the post natal stem cells into the disinfect root canal systems after the apex is opened. The post natal stem cells can be derived from multiple tissues including skin,

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Injectable Scaffold Delivery

Three Dimensional Cell Printing

Scaffold Implantation

Gene Therapy

buccal mucosa, fat and bone.[12] Postnatal stem cell source capable of differentiating into the diverse cell population found in adult pulp (e.g., fibroblasts, endothelial cells, odontoblasts). Application of the cells together with a fibrin clot or other scaffold material would help to position and maintain cell localization. In general, scaffolds, cells, and bioactive signalling molecules are needed to induce stem cell differentiation into a dental tissue type. 3) Pulp implantation: In pulp implantation, the cultured pulp tissue is transplanted into cleaned and shaped root canal systems. The pulp tissue is grown in sheets in vitro on biodegradable polymer nanofibers or on sheets of extracellular matrix proteins such as collagen I or fibronectin.[13] The source of pulp tissue may be a purified pulp stem cell line that is disease or pathogen-free, or is created from cells taken from a biopsy, that has been grown in the laboratory.The limitation of this technique is that specialized procedures may be required to ensure that the cells properly adhere to the root canal walls. 4) Scaffold implantation: Pulp stem cells must be organized into a three-dimensional structure that can support cell organization and vascularization. This can be accomplished by 036

using a porous polymer scaffold which is seeded with pulp stem cells.[14] Rania M.El-Backly etal concluded that using a PLGA (polylactic-co-glycolic acid) scaffold with specially designed characteristics may act as a suitable matrix to support dental pulp stem cells and their differentiation to form an organised dentine/pulp-like tissue.[15] Another research believed that platelet-rich plasma (PRP) satisfies many of tissue regeneration criteria as it is autologous, fairly easy to prepare in a dental setting, rich in growth factors, degrades over time, and forms a 3-dimensional fibrin matrix. 5) Injectable scaffold delivery: Tissue engineered pulp tissue is seeded into the soft three-dimensional scaffold matrix, such as a polymer hydrogel. Hydrogels are injectable scaffolds that can be delivered by syringe[16], they have the potential to be noninvasive and are easy to deliver into the root canal systems. Theoritically, the hydrogel may promote pulp regeneration by providing a substrate for cell proliferation and differentiation into an organized tissue structure. 6) Three dimensional cell printing: The three dimensional cell printing technique can be used to precisely position cells and this method has the potential to create tissue constructs that mimic the natural tooth pulp tissue structure.[17] The ideal positioning of cells in a tissue engineering construct would include placing odontoblastoid cells around the periphery to maintain and repair dentin, with fibroblasts in the pulp core supporting a network of vascular and nerve cells. 7) Gene therapy: Gene therapy has been recently used as a means of delivering genes for growth factors, morphogens, transcription factors and extracellular matrix molecules locally to the somatic cells of individuals, with resulting therapeutic effect.[18] The gene can stimulate or induce a natural biological process by expressing the molecules which are involved in the regenerative response for the tissue of interest. One use of gene delivery in endodontics would be to deliver mineralizing genes into the pulp tissues to promote tissue mineralization. Collectively, there has been a tremendous increase in our clinicaltools (ie, materials, instruments, and medications) and knowledgefrom the trauma and tissue engineering fields during thelast decade.But every method has some merits and demerits.Root canal revascularization is simple to perform, low chances of pathogen transmission but major limitation is concentration and composition of cells trapped in the fibrin clot is unpredictable and these can be overcomed by stem cell therapy in which predictable cells are easy to deliver but stem cell therapy donot produce new functional pulp as cells have low survival rate and position of cells is difficult to control.[19] Pulp implantation has definite advantage over stem cell therapy in which sheet of cells can be easily grown but small constructs are possible due to low vascularity.[20] In scaffold implantation structure support cell organization[21] but the cells have low survival. The other method 3- D cell printing in which multiple cell types can be precisely positioned[22] but they must be engineered to fit root canal. This limitation is subsided by injectable scaffolds which provide subsititute for extra cellular matrix[23] but low cell survival is the problem. These tissue engineering methods have low cell survival which can be overcome by gene therapy which donot require stem cells but the main drawback is that the process is not easy to ©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

control.Current concept mainly focus on methods permittingthe delivery of known cells, signaling molecules, and a scaffold such as PRP (Platelet rich plasma) into the apical 1–2 mm of a root canal system and then “backfilling” the root canal system with a solution of PRP and signaling molecules[24]. There is significant amount of debate among researchers about the ethical concern of tissue engineering therapies involved in Regenerative Endodontic procedures. Various ethical question which comes on mind are- should the tissue source be another person or can animal tissue can be used?, should the donor be payed for the tissue sample?, should fetal tissue be used as cell culture? Conclusion Regenerative endodontic methods have the potential for regenerating both pulp and dentin tissues and therefore may offer an alternative method to save teeth that may have compromised structural integrity. Several developmental issues have been described to accomplish endodontic regeneration. The success of regenerative endodontic therapy is dependent on the ability of researchers to create a technique that will allow clinicians to create a functional pulp tissue within cleaned and shaped root canal systems. The source of pulp tissue may be from root canal revascularization, stem-cell therapy and pulp implantation.Stem Cell Banking is proving a new concept of preservation of stem cells and it is critical for both research and clinical application of stem-cell based therapies. Stem cell banks opened in North India are LucknowSanjay Gandhi PGIMS, Delhi- Army R and R Hospital, Maulana Azad Medical College. In our opinion, the path to the future should focus ontranslational research models that simulate likely clinical procedures and designed to regenerate a functional pulp-dentin. Hence tissue-engineering studies are needed to help make regenerative endodontics a reality. Bibliography 1. Murray PE, Garcia-Godoy F, Hargreaves KM. Regenerative endodontics: A review of current status and a call for action. J Endod 2007;33:377-90. 2. Kenneth M. Hargreaves. Regeneration Potential of the Young Permanent Tooth: What Does the Future Hold? Pediatric Dentistry May / Jun 2008; 30: 3. 3. Langer R, Vacanti JP. Tissue engineering. Science 1993;260:920–6. 4. Nakashima M, Mizunuma K, Murakami T, et al. Induction of dental pulp stem cell differentiation into odontoblasts by electroporation-mediated gene delivery of growth/differentiation factor 11 (Gdf11). Gene Ther. 2002 Jun;9(12):814-8. 5. Darnell Kaigler and David Mooney. Tissue engineering’s impact on dentistry. J Dent edu.2001; 65, 5:456-462. 6. Banchs F, Trope M. Revascularization of immature permanent teeth with apical periodontitis: new treatment protocol. J Endod 2004; 30:196-2000. 7. Becker Aj, MccullochEa, Till Je. Cytological demonstration of the clonal nature of spleen colonies derived from transplanted mouse marrow cells. Nature. 1963 FebV2;197:452-4. 8. Miura M, Gronthos S, Zhao M, et al. SHED: stem cells from human exfoliated deciduous teeth. ProcNatlAcadSci U S A. 2003 May13;100(10):5807-12. 037

9. Gronthos S, Mankani M, Brahim J, et al. Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo. ProcNatlAcadSci U S A 2000;97:13625-30 10. Sonoyama W, Liu Y, Yamaza T, et al. Characterization of the apical papilla and itsresiding stem cells from human immature permanent teeth: A pilot study. J Endod 2008;34:166-71. 11. Seo BM, Miura M, Gronthos S, et al. Investigation of multipotent postnatal stem cells from human periodontal ligament. Lancet 2004;364:149-55. 12. Kindler V. Postnatal stem cell survival: does the niche, a rare harbor where to resist the ebb tide of differentiation, also provide lineage-specific instructions? J Leukoc Biol 2005;78:836–44. 13. Venugopal J, Ramakrishna S. Application of polymer nanofibers in biomedicine and biotechnology. ApplBiochemBiotechnol 2005; 125:147-58. 14. N a k a s h i m a M . T i s s u e e n g i n e e r i n g i n endodontics.AustEndod J 2005; 31:111-3. 15. Rania M. El-Backly, Regeneration of dentine/pulp-like tissue using a dental pulp stem cell/poly(lactic-coglycolic) acid scaffold construct in New Zealand white rabbits, AustEndod J 2008; 34: 52–67. 16. Trojani C, Weiss P, Michiels J F et al. Three dimensional culture and differentiation ofhuman osteogenic cells in an i n j e c t a b l e hydroxypropylmethylcellulosehydrogel.Biomaterials 2005; 26:509-17. 17. Dusseiller MR, Schlaepfer D, Koch M. An inverted micro

contact printing method on topographically structured polystyrene chips for aryed micro-3-D culturing of single cells.Biomaterials 2005; 26:5917-25. 18. Nakashima M, Reddi AH. The application of bone morphogenic proteins to dental tissue engineering. Natural biotech2003; 21:1025-32. 19. Brazelton TR, Blau HM. Optimizing techniques for tracking transplanted stem cells in vivo. Stem Cells 2005;23:1251– 65. 20. Helmlinger G, Yuan F, Dellian M, et al. Interstitial pH and pO2 gradients in solid tumors in vivo: high-resolution measurements reveal a lack of correlation. Nat Med 1997;3:177– 82. 21. Van Amerongen MJ, Harmsen MC, Petersen AH, et al. The enzymatic degradation of scaffolds and their replacement by vascularized extracellular matrix in the murine myocardium. Biomaterials 2006;27:2247–57. 22. Barron JA, Krizman DB, Ringeisen BR. Laser printing of single cells: statistical analysis, cell viability, and stress. Ann Biomed Engl 2005;33:121–30. 23. Alhadlaq A, Mao JJ. Tissue-engineered osteochondral constructs in the shape of an articular condyle. J Bone Joint Surg Am 2005;87:936–44. 24. Anitua E, Sanchez M, Nurden AT, et al. New insights into and novel applications for platelet-rich fibrin therapies. Trends Biotechnol 2006; 24:227–34.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

038

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Probiotics Parul Agrawal1, Srinivasa T. S.2, Pravesh Goyal3, Meghna Dewan4 1

Post Graduate Student, Department of Periodontology, Rungta College of Dental Sciences and Research, Bhilai, Chhattisgarh, India. Associate Professor, Department of Periodontology, Rungta College of Dental Sciences and Research, Bhilai, Chhattisgarh, India. Post Graduate Student, Department of Conservative dentistry and endodontics, Darshan Dental College and Hospital, Loyara, Udaipur, Rajasthan India. 4 Post Graduate Student, Department of Periodontology, Himachal Dental College, SunderNagar 2

3

Abstract Probiotics are health-beneficial bacteria which have only recently been introduced in dentistry after years of successful use in mainly gastrointestinal disorders. Probiotics favor the growth of beneficial bacteria over that of harmful ones and commonly consumed as part of fermented foods with specially added active live cultures such as in yogurt or as dietary supplements. Probiotic therapy could be considered as a means of inhibiting oral biofilm development, together with dental caries, represent a major part of the global burden of oral diseases. The application of probiotic strategies may, in near future provide an end to many infections occurring in oral cavity. This article summarizes the currently available data on their mechanism of action, potential benefits for oral health and also about the risks associated.

Key Words Probiotics, Periodontal Disease, Microbial Balance

Introduction: Bacteriotherapy or the use of harmless bacteria to displace pathogenic organisms is a promising way of combating infections. Probiotic, a Greek word meaning “towards life,” is a food product containing bacteria, which exerts desirable influences on the host by balancing his/her digestive microbial flora.[1] In 1907 Eli Metchnikoff was the first to state that lactic acidproducing strain Lactobacillus bulgaricus (contained in Bulgarian yoghurt) is able to displace pathological intestinal microbiota. He suggested that the dependence of the intestinal microbes on food makes it possible to adopt measures to modify the flora in our bodies and to replace the harmful microbes by useful microbes.[2] In 1965 Lilley and Stillwell initially proposed the term "Probiotic", as opposed to "antibiotic" as a substances produced by microorganisms which promote the growth of other microorganisms.[3] In 1989 Fuller, emphasized the importance of living cells in probiotics and defined probiotics as 'A live microbial feed supplement which beneficially affects the host animal by improving its intestinal microbial balance'.[2] In 1984 Hull et al introduced first probiotic species in research as Lactobacillus acidophilus followed by Bifidobacteriumbifidum by Holcombh et al. in 1991.[4] In 1994, the World Health Organization deemed probiotics to be the next-most important immune defense system when commonly prescribed antibiotics are rendered useless by antibiotic resistance. These incidences paved way for a new concept of probiotics in medicine and dentistry.[5] The term replacement therapy (also called bacteriotherapy or bacterial interference is sometimes used interchangeably with Quick Response Code

Address For Correspondence: Dr. Parul Agrawal Post Graduate Student, Department Of Periodontology, Rungta College Of Dental Sciences And Research, Bhilai, Chhattisgarh, India. Email: [email protected]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

probiotics but it has following differences: (Table 1) Selection Criteria For Probiotics: They should be non-toxic and non-pathogenic to the host, able to withstand the acidity of the GIT, enhancement of the nonspecific and specific immune response of the host, able to replace and reinstate the intestinal microflora, have a good shelf life, adhesion and colonization in the human body; adhesion may increase the retention time of a probiotic and place bacteria and host surfaces.[6],[7] Sources Of Probiotics: There are a number of different organisms that can be classified as probiotics. The most common probiotic strains belong to the genera streptococci,Lactobacillus and Bifidobacterium. Following are themicro-organisms currently used as probiotics: Lactobacillus species from which probiotic strains included are L. acidophilus, L. casei, L. rhamnosus, L. johnsonii, L. gasseriandL. reuteri.Bifidobacteriumstrains include B. bifidum, B. breve, B. longumand B. infantis.Streptococcus species include S. Lactis, S. cremoris, S. diacetylactis, Escherichia coli, Fusobacterium species, Enterococcus species include E. fecalis, E. faecium, Yeasts and Moulds.[8] The most common probi¬otic carrying food is yogurt; cheese, fermented and unfermented milks, juices, smoothies, cereal, nutrition bars, and infant/toddler formula all are food vehicles for probiotic delivery. Probiotics areavailable as foods, dietary supplements, medical foods, and drugscomposed of concentrated, dried microbes packaged into capsules, tablets or sachets.[9] Mechanism Of Action: Several mechanisms have been proposed to explain how probiotics work. The mechanisms of probiotics in the gastrointestinal tract can be divided into three main categories.[10] 1. Metabolic effects 2. Normalisation of the intestinal microbial flora 039

3. Immune modulation By microbial adhesion to the target tissue, the probiotics compete with the pathogenic microbes on adhesion sites and nutrients. Once adhered, they secrete several antimicrobial substances such as bacteriocins, hydrogen peroxide and organic acids. The later can further lower the pH so that the plaque bacteria cannot form dental plaque and calculus that causes periodontal disease. The oxidation-reduction potential is alteredand adversely affects the pathogenic microbes and facilitates their elimination. Antioxidants prevent plaque formation by neutralizing the free electrons that are needed for the mineral formation. In addition, probiotics can stimulate the non-specific immunity and modulate the cellular and humoral immune response. In the oral cavity, probiotics are able to form a biofilm that lines and hence protects the oral mucosa or tooth surface from the invading bacteria. In addition probiotics compete with cariogenic bacteria, periodontal pathogens, and bacteria associated with halitosis (Table 1), (Table 2).[11],[12],[13] Probiotics And General Health: A number of probiotic induced benefits on the generalhealth have been proposed, such as reduced susceptibilityto infections, reduction of allergies and lactose intolerance,as well as lowered blood pressure and serum cholesterolvalues, relief of enzymatic maldigestion, for application in oral health in dental caries, periodontal disease and halitosis.[14],[15] Probiotics and dental caries: Probiotic bacteria need to adhere to the oral mucosa anddental tissues as part of the biofilm and compete with thegrowth of dental pathogens.Comelli et al. examined 23micro organisms used in the dairy industry for potentialprobiotic properties with respect to the prevention of dentalcaries. They showed that two S. thermophilus species and twoL lactis species were able to adhere to hydroxyapatite. So such a property in a nonpathogenicdairy bacterial strain might prove beneficial in modulatingthe establishment of cariogenic dental plaque.[16] Probiotics and Periodontal Disease The use of antibiotics or antiseptics, either locally or systemically, does not really improve the long-term effect of periodontal therapy.[17] Probiotics might not only suppress the emergence of endogenous pathogens or prevent the superinfection with exogenous pathogens, they might also protect us through the promotion of a beneficial host response (Table 3).[18],[19] In 1954, a beneficial effect of lactic acid bacteria on inflammatory infections of the oral mucosa was reported. The use of a Russian probiotic preparation called Acilact, a five live lyophilized lactic acid bacteria, with or without Bifidobacterium is claimed to improve both clinical and microbiological parameters in patients with gingivitis and mild periodontitis.[2] Twetman et al.[20] used L. reutericontaining chewing gum in 42 healthy patients and assessed its effects on crevicular fluid volume, cytokine (interleukin-1β, interleukin-6, interleukin10, and TNF-α) levels, and bleeding on probing. Crevicular fluid volume, as well as TNF-α and interleukin-8 levels, and bleeding were significantly reduced. The regular (three times daily for eight weeks) intake of tablets containing Lactobacillus salivarius (L.salivarius) resulted in benefits in terms of pocket probing depth and plaque index in individuals at high risk of periodontal disease (smokers) compared to a placebo control group.[21]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

Table 2 : Possible Probiotic Activities In The Oral Cavity

Table 3 : Treatment Strategies Possible For Probiotics To Affect Periodontal Health

Probiotics in prevention of halitosis: Halitosis is believed to affect a large proportion of the population and is caused by a number of volatiles, which originate from the oro-pharynx or from expired alveolar air. A diverse consortium of bacteria has been found to contribute to the problem, including Fusobacteriumnucleatum, P. gingivalis, P. intermedia and Treponemadenticola. Oral microorganisms, present on the tongue, are the primary cause

040

of halitosis, current treatments focus on the use of chemical or physical antibacterial regimes to reduce the numbers of these bacteria but most of these treatments exhibit only a temporary effect and are associated with undesirable side-effects when used over a long period of time. To prevent the regrowth of odor-causing organisms, pre-emptive colonization of the oral cavity with probiotics might have a potential application as adjuncts for both the treatment and prevention of halitosis.[2] A study by Kang et al.[22] reported the ability of various strains of Weissellacibaria (W. Cibaria) to decrease the production of volatile sulphur compounds by Fusobacteriumnucleatum (F. Nucleatum). Various probiotic products are marketed for both mouth and gut associated halitosis, although their efficacy demands more clinical studies. Safety Issues In Probiotic Use Safety is the state of being certain that adverse effects will notbe caused by an agent under any defined conditions. The issue of safety for any product is arguablyparamount during pregnancy and in newborn babies.[23] Probiotic species such as Lactobacillus acidophilus have beensafely used for more than 70 years.Most probiotic bacteria are weakly proteolytic and, for example, Lactobacillus bulgaricus, was shown to be incapable of degrading some host tissue components. However, there have been some cases of bacteraemia and fungaemia associated with probiotic use, although these have been in subjects who are immunocompromised, or who suffer from chronic disease.[24] Some more side effects by its usage like systemic infections, metabolic and enzymatic effects, immunological effects. Studies have shown that to be able to exert probiotic properties in the oral cavity it is essentialfor the micro-organisms to resist the oral environmental conditions and defense mechanisms, adhere to the saliva coated surfaces, colonize and grow in the mouth, inhibit oral pathogens andbe safe for the host.[25] Conclusion The use of probiotics is an interesting emerging and not to be neglected field in general and oral healthcare. However, great care is still warranted because it is uncertain that there is not a window of infectivity, either naturally occurring in a growing child or induced by antibiotics, antiseptics, immune suppression or mechanical removal of the indigenous oral microbiota, in which a patient can become permanently colonized. Even without a permanent colonization, it can be anticipated that the repeated daily use of probiotic products over a long period of time will support an increased level of lactic acid bacteria in the oral cavity. Additionally, it should be noted that manufacturers of probiotic foods can sometimes add a lot of sugar to their product to improve the taste. This, as such, can confer an oral health risk. Refernces 1. Poureslami H, Pishbin L,Eslaminejad Z, Moqadam FJ, Farokhi MR. The Effects of a Dairy Probiotic Product, Espar, on Salivary Calcium and Mutans Streptococci..J Dent Res Dent Clin Dent Prospect 2013;7:147-151. 2. TeughelsW, Essche MV, Sliepen I, Quirynen M. Probiotics and oral healthcare. Periodontology 2000 2008;48:111–147. 3. Magnusson I, Lindhe J, Yoneyama T, Liljenberg B. Recolonization of a subgingivalmicrobiota following scaling in deep pockets. J ClinPeriodontol 1984: 11: 193–207.

4. Gupta G. Probiotics and periodontal health. J Med Life. 2011; 4: 387–394. 5. Manisha N, Prajapathi JB. Role of probiotic cultures and fermented milk in combating blood cholesterol. . Indian J Microbial. 2001;41:75–86. 6. Chitra N, Thomas KE, Viswaja K. Probiotics in dentistry. Advanced Biotech 2011;10;3-5. 7. Prabhu P, Srinivas R, Srinivasa TS. Probiotics for Prevention IJCD 2012;3;68-72. 8. Agarwal E, Bajaj P, Guruprasad CN, Naik S, Pradeep AR. Probiotics: A novel step towards oral health. AOSR 2011;1:108-115. 9. Probiotics: Their Potential to Impact Human Health. Council for agricultural science and technology 2007;36:1-19. 10. Stamatova I, Meurman JH. Probiotics: Health benefits in the mouth. Am J Dent 2009;22:329-338. 11. Haukioja A. Probiotics and Oral Health. Eur J Dent 2010;4: 348-55. 12. Çaglar E, Kargul B, Tanboga I. Bacteriotherapy and probiotics´ role on oral health. Oral Diseases 2005;11: 1317. 13. Meurman JH. Probiotics: do they have a role in oral medicine and dentistry? Eur J Oral Sci 2005; 113: 188–196. 14. Reid G, Jass J, Sebulsky MT, McCormick JK. Potential uses of probiotics in clinical practice. ClinMicrobiol Rev 2003;16:658-72. 15. Chinnappa A, Konde H, Konde S, Raj S, Beena JP. Probiotics for future caries control: A short-term clinical study. Indian Journal of Dental Research 2013; 24;547549. 16. Comelli EM, Guggenheim B, Stingele F, Neeser JR. Selection of dairy bacterial strains as probiotics for oral health. Eur J Oral Sci 2002;110:218-24. 17. Quirynen M, Teughels W, De Soete M, van Steenberghe D. Topical antiseptics and antibiotics in the initial therapy of chronic adult periodontitis: microbiological aspects. Periodontol 2000 2002: 28: 72–90. 18. Roberts FA, Darveau RP. Beneficial bacteria of the periodontium. Periodontol 2000 2002: 30: 40–50. 19. Stamatova I,MeurmanJH . Probiotics and periodontal disease Periodontology 2000 2009;51:141–151. 20. Twetman S, Derawi B, Keller M, Ekstrand K, YucelLindberg T, Stecksen-Blicks C. Short-term effect of chewing gums containing probiotic Lactobacillus reuteri on the levels of inflammatory mediators in gingival crevicular fluid. ActaOdontolScand 2009;67: 19-24. 21. Shimauchi H, Mayanagi G, Nakaya S, Minamibuchi M, Ito Y, Yamaki K, et al. Improvement of periodontal condition by probiotics with Lactobacillus salivarius WB21: a randomized, double-blind, placebo-controlled study. J ClinPeriodontol 2008;35: 897–905. 22. Kang MS, Kim BG, Chung J, Lee HC, Oh JS. Inhibitory effect of Weissellacibaria isolates on the production of volatile sulphur compounds. J ClinPeriodontol 2006;33: 226-32. 23. Reid G. Safe and efficacious probiotics: what are they? Trends in Microbiology 2006;14():348-52. 24. Husni RN, Gordon SM, Washington JA, Longworth DL. Lactobacillus bacteremia and endocarditis: review of 45 cases. Clin Infect Dis 1997;25: 1048-55. 25. Gupta V, Gupta B. Probiotics and Periodontal Disease: A Current Update.Johcd 2010;4(Spl):35-37.

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

041

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Various Modalities Towards Nicotine De-addiction : A Review Srivastava R1, Biharim2, Jyoti B3, Gupta A4 1

Rahul Srivastava, Senior Lecturer, Deptt Of Oral Medicine And Radiology, Rama Dental College Hospital And Research Centre, Kanpur, Uttar Pradesh Manoramabihari, Professor, Physiology, Cm Medical College, Durg, Chattisgarh Bhuvanjyoti, Dental Surgeon And Consultant-oral Medicine And Radiology, Ranchi Institute Of Neuro-psychiatry And Allied Sciences, Ranchi, Jharkhand 4 Anuj Gupta, Intern, Dept Of Oral Medicine And Radiology, Rama Dental College Hospital And Research Centre, Kanpur, Uttar Pradesh 2

3

Abstract Nicotine replacement therapy involves the use of products that provide low doses of nicotine but do not contain the toxins found in smoke. The goal of therapy is to relieve cravings for nicotine and ease the symptoms when someone stops using cigarettes and smokeless tobacco. Because of nicotine habituation and/or addiction, “breaking the habit” may be accomplished by substituting other sources for nicotine needs.Quitting all types of tobacco use greatly reduces the risk for oral cancer. The best prevention is to avoidtobacco use altogether. This review highlights the role of nicotine replacement therapy in the cessation of tobacco.

Key Words Addiction, Habit, Nicotine Replacement Therapy, Toxins

Introduction Tobacco smoke is a toxic mix of more than 7,000 chemicals. Many are poisons. When these chemicals get deep into the body’s tissues, they cause damage. Body must fight to heal the damage each time an individual smokes. Over the time, the damage can lead to disease.[1] Tobacco products including cigarettes, cigars, chewing tobacco, snuff, and loose pipe tobacco contain the dried, processed leaves of the tobacco plant Nicotianarusticaor Nicotianatabacum. All forms of tobacco contain nicotine, an extremely addictive drug that can act as both a central nervous system stimulant and depressant.In addition to nicotine, tobacco contains thousands of other chemicals and additives to enhance the effects and flavor of the tobacco.[2] Nicotine is a tertiary amine composed of a pyridine and apyrrolidine ring. Nicotine binds to acetylcholine receptors atganglia and neuromuscular junctions and in the brain. Inits non-ionized form, nicotine freely permeates membranes, including thebuccal mucosa and the blood-brain barrier. As a weak base, nicotine is lessionized and penetrates membranes more easily in alkaline solutions. Chewingtobacco and snuff, as well as nicotine gum, are buffered to an alkalinepH to facilitate absorption of nicotine.Nicotine is absorbed more slowly from smokeless tobacco (ST) than from tobacco smoke,but peak venous levels are similar. Whereas, blood levels ofnicotine fall rapidly after smoking, the concentration plateau during andafter smokeless tobacco(ST) use is consistent with continued absorption even after the tobacco isremoved from the mouth.[3] One person dies prematurelyevery six seconds due to addiction to tobacco. One in two long-term smokers—largelyin low- and middleincome countries —will die fromtobacco addiction.This epidemic reflects the highlyaddictive nature of tobacco, and

Quick Response Code

Address For Correspondence: Dr. Srivastava R Senior Lecturer, Deptt Of Oral Medicine And Radiology, Rama Dental College Hospital And Research Centre, Kanpur, Uttar Pradesh

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

specifically of nicotine,its principal addicting component.[4], [5] Bidis have higher nicotine concentrations (21.2 mg/g) than filtered (16.3 mg/g) and unfiltered (13.5 mg/g) cigarettes. [6] Nicotine content in cigars depends upon their size. Commonly cigars contain5 to 17 g of tobacco which contains from 10 mg to more than 300 mg ofnicotine.[7],[8] Most of the cigars have no filters and take an houror more to smoke.In the cases of smokingcigarette nicotine reaches to the brain in as little as seven seconds after inhalation.[9] Typical cigarette contains approximately 0.5 to 1.0 g oftobacco and, on average, 10 mg of nicotine.A typical smoker smokes a cigarette in 10 puffs and within 5 minutes with absorption of 1 to 2 mg of nicotine, butabsorption can range from 0.5 to 3 mg.[10],[11],[12],[13] The levelof nicotine in the blood decreases by one half after asmoker stops smoking for that length of time.[13] About 3–4 g of tobacco is used in a pipe having a clay bowl filled with tobacco,with smoke inhaled through a stem. An average 20 gram of tobacco is used in typical waterpipe (hookah).Moist snuff contains nicotine ranged from 3.4 mg/g to11.5mg/g. The highest concentrations of nicotine is in dry snuff, which contains an average of 16.8 mg/g.[14] Addiction Addiction is defined by the World Health Organization as “repeated use of a psychoactivesubstance or substances, to the extent that the user is: ? Periodically or chronically intoxicated, ? Shows a compulsion to take the preferred substance(s), ? Has great difficulty in voluntarily ceasing or modifying substance use, ? Exhibits determination to obtain psychoactive substances by almost any means, and ? Tolerance is prominent and a withdrawal syndrome frequently occurs when substanceuse is interrupted.”[15] As nicotine is absorbed, it enters the bloodstream where it circulates throughout the body and travels to the brain where it crosses the blood-brain barrier. Once in the brain, it binds to and activates receptors called the cholinergic receptors.These

042

cholinergic receptors are present in the brain as well as in other areas such as the muscles, heart, adrenal glands and other vital organs. Normally, these receptors are activated by the neurotransmitter acetylcholine which is produced at nerve endings in the brain and in the nerves of the peripheral nervous system.Since nicotine has a similar structure to acetylcholine, it can activate the cholinergic receptors. However, unlike acetylcholine, nicotine enters the brain and disrupts its normal functioning.[16] A person can become addicted to nicotine even after just a few uses because the brain adjusts itself and develops a level of nicotine tolerance that the addict must reach in order to maintain the feeling of comfort. Once this comfort level has been established, a lack of nicotine in the brain will cause uncomfortable withdrawal symptoms in the user. These withdrawal symptoms can make the user edgy and irritable, and using tobacco while in this state will have a sedative effect on the user.It is important to note that smoking, whether it is called “social smoking” or simply trying a cigarette, can easily lead to an addiction.[17] Nicotine Replacement Therapy NRT is an abbreviation for nicotine replacement therapy.Nicotine replacement therapy is sometimes called therapeuticnicotine, medicinal nicotine, or nicotine reduction therapy. Nicotinereplacement therapy (NRT) describes a group of products delivering nicotine that are licensed for the relief of withdrawal as an aid to smoking cessation.[18],[19] Quitting the tobacco habit is notoriously difficult and eventhe best strategies are rather ineffective (US DHHS, 1988). Themost effective current methods for quitting are behaviorbased,and they place considerable demands on the time of healthpersonnel. For these reasons, it is worthwhile to seek a pharmacologicalaid for tobacco use cessation.The only drug treatment readily available for those who wishto quit using to b acco is n ico tin e r ep lacemen t th er ap y. Th is approachfollows, logically enough, from the widely held view that habitual tobaccouse is a form of nicotine dependence.[20] Nicotine replacement is a way to get nicotine without the other harmful chemicals intobacco.The Food and Drug Administration (FDA) has approved these NRT products as effectiveaids for helping people to quit smoking. None of these products has been FDA-approvedspecifically to help people quit smokeless tobacco. Studies are still being done, but manyare reporting success using these methods: Nicotine gum Nicotine patch Nicotine lozenges Nicotine inhaler Nicotine nasal spray [21] Nicotine Gums Nicotine gums were the first pharmacologicalintervention in the form of NRT approved by theFDA way back in the year 1984.Boyle et al in the year1992 conducted a study to evaluate the efficacy of nicotine gum for smokeless tobacco cessation.Randomized, double-blind, placebocontrolledtrial was conducted to evaluate the 2mg of nicotine gum vs.placebo in 100 patients.The main outcome was quitrates at the end of 6 weeks.[22] Nicotine gum comes in 2 strengths. If person smokes 25 or more ciga¬rettes per day, advise him to use 4 mg strength. If person smokes fewer than 25 cigarettes per day, advise him to use 2 mg strength.Table 1 shows how much nicotine gumbeused during the weeks after quitting smoking.There is a certain way to chew and park nicotine gum. This method helps body absorb the nicotine and lessen side

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

effects. Parking means putting the gum between your cheek and gum and holding it there. There are following steps to chewing the nicotine gum: 1. Warm the gum in the mouth for 1 to 2 minutes. 2. Chew slowly until the feeling of a slight tingling or peppery taste which takes about 15 chews to have these feelings. 3. Then stop chewing. Place (park) the gum betweencheek and gums. 4. In about a minute, the taste or tingling will go away. Chew and park the gum again. Put the gum in a different spot in mouth every time of park. This will help to keep person from getting mouth ulcers. Try to avoid chewing in areas of mouth that have fillings or crowns. 5. Continue to chew and park for about 30 minutes. At this point, most of the nicotine is gone from the gum. Now rinse mouth with water or mouthwash.[23] Nicotine Patch Nicotine patches can help people quit smokingwhen they are used with a program tohelp change their behaviour. After wearing a patch, the nicotine passesthrough the skin and into the bloodstream. In the bloodstream, it replaces some ofthe nicotine. The patch puts less nicotine in the blood than cigarette smoking. But the nicotinein the blood is still high enough to decreasecravings and withdrawal symptoms (such as irritability, frustration, anger, anxiety, difficulty concentrating, and restlessness). Sticking withthe patch will increase the chances of success. Nicotine patches are available as brand names Nicoderm CQ (original and clear) and Nicotrol. Nicoderm CQ and store brand patchescome in three strengths. The strengths are 21 milligrams perday (Step 1), 14 milligrams per day (Step 2),and 7 milligrams per day (Step 3).If person smokes more than 10 cigarettes perday, start with Step 1 (21mg). Use Step 1for 6 weeks. Then switch to Step 2 (14mg)and use it for 2 weeks. Then switch againto Step 3 (7mg) and use it for another2 weeks.If person smoking fewer than 10 cigarettes perday, start with Step 2 (14mg). Use Step 2for 6 weeks. Then switch to Step 3 (7mg)and use it for 2 weeks.NicodermCQ patches can be worn for 16 to 24 hours a day. Nicotrol skin patches come in 3 strengths aswell. The strengths reflect how much nicotinethe patch gives in 16 hours: 15 mg, 10 mg,and 5 mg.Nicotrol patches are worn while personis awake for16 hours each day.Start with the 15 mg patch and use it for6 weeks.After week 6, step down to the 10 mg patch anduse it for 2 weeks.Then step down again to the 5 mg patch and useit for 2 weeks.[24] Nicotine Lozenges Nicotine lozenges are a safe method to reduce cravings for cigaretteswhen used as directed. They have been approved by the Federal DrugAdministration (FDA) to be sold over-thecounter (without aprescription).Lozengesare characterized by a number of advantages, suchas fewer potential oral health limitations (e.g. dentalworks or temporomandibular joint pain), better socialacceptance (e.g. at workplaces), and greater ease of use asthey do not require chewing.[25],[26] If person smokes first cigarette within 30 minutes of waking up, use 4mg lozenge. If person smokes first cigarette more than 30 minutes after waking up, use 2mg lozenge.There are following steps for using lozenges: 043

1. Do not eat or drink 15 minutes before using lozenge (food or drink can impair the absorption of nicotine). If person have eaten within 15 minutes, advise him to rinse his mouth with waterbefore using the lozenge. 2. Use the lozenge on a fixed schedule: 1 piece every 1-2 hours. 3. Place the lozenge inmouth and allow lozenge to dissolve slowly (about 20-30 minutes). Do not chew or swallowlozenge. 4. The person may feel a warm or tingling sensation. 5. To improve the chances of quitting, use at least 9 lozenges per day for the first 6 weeks if person is not using other nicotine medication. 6. After a month or two of not smoking, start to slowly cut down the number of lozenges per day: 1 lozenge per day, every 4-7 days.[25] Nicotine Inhaler Nicotine inhaler is used as part of a plan to help in quitting the smoking by acting as a replacement for the nicotine in cigarettes.[27] Nicotine inhaler is inhaled in to the mouth. Nicotine inhaler releases specific amounts of nicotine that is absorbed through the cheeks inside the mouth and the upper throat.[28] The first published study of inhaled nicotine used a pressurized metered-dose inhaler (pMDI) to deliver a dose of 53 mg per puff (two puffs every 30 s), compared with a nonnicotine aerosol, lettuce cigarette, and tobacco cigarette, and determined that the cardiovascular effects of these aerosols were caused by nicotine rather than throat irritation (Herxheimer et al., 1967).[29] Nicotrol® Inhaler and Nicorette® inhalers are available in the market. These Nicotine inhalators contain a mouthpiece with a replaceable nicotine cartridge. Person inhales through the mouthpiece in the same way as smoking a cigarette. This causes the nicotine in the cartridge to vaporise and it is then absorbed through the mucous membranes in the mouth, rather than travelling into the lungs. The inhaler can be useful for people who miss the physical act of smoking, or need to do something with their hands when quitting. Insert the cartridge in the inhalator and then inhale through the mouthpiece in the same way as smoking a cigarette. This causes the nicotine in the cartridge to vaporize and it is then absorbed through the mucous membranes in the mouth as it inhale. Person will get less amount of nicotine from each puff on the inhalator than person would from a puff on a cigarette, so person may need to inhale from the inhalator more often than he would with a cigarette to get the same amount of nicotine. Cartridges that last twice as long are now available for Nicorette inhalators. Each new 15mg cartridge lasts for about 40 minutes of intense use before it will need replacing. ? Do not use more than six 15mg cartridges per day. ? Nicotine inhaler should be avoided in cases of cardiovascular disease, recent history of heart attack or stroke, diabetes, peptic ulcer, gastritis, oesophagitis, asthma. Do not consume acidic beverages (e.g. coffee, tea, soft drinks, alcohol or citrus juices) while using the inhaler; they may interfere with the delivery of nicotine. Use the inhaler at room temperature; cold temperatures may reduce the amount of nicotine that is delivered. Store the inhaler at room temperature in a closed container away from heat and humidity.[30],[31]

Nicotine Nasal Spray Nicotine nasal spray is a safe method to reduce cravings for cigarettes when used as directed. It has been approved by theFederal Drug Administration (FDA) to be sold only with a prescription.[32] The nicotine nasal spray is the strongest form of nicotine replacement therapy, which is particularly useful and effective for highly dependent heavy smokers who cannot give up by any other means.Nasal spray is more effective is because of its fast action. Once the nicotine has been administered, it enters the bloodstream and reaches the brain within 10 minute. Other methods take much longer. This method also most realistically mimics the fast "hit" obtained when smoking a cigarette. This makes it much easier to control and satisfy cravings if they suddenly arise. One dose with this form of NRT is two sprays, one into each nostril. Each spray is the equivalent of 0.5 mg of nicotine; so one spray into each nostril gives a total amount of 1 mg of nicotine, which is about the same amount of nicotine received upon smoking one cigarette. As the nicotine is administered into each nostril, it is inhaled and rapidly absorbed into the bloodstream through the lining of the nose. This is the fastest way that nicotine can enter the bloodstream. As the nicotine reaches the brain, the user receives nicotine "rush" that is very similar to the rush obtained from smoking a cigarette.[33] There are following steps to use nicotine spray: Tilt the head back slightly. ? Hold breath and spray once in each side of nose. Put the tip in to the nose and point the tip to the outer side of nostril and spray once in each nostril. Breathe outthrough the mouth and don’t sniff or breathe in whilespraying. Wait 2-3 minutes before blowing thenose. ? The spray may irritate the nose at first but this should get better as individual keep using it. ? Use as initial dose of 1-2 doses per hour, minimum 8 doses per day and maximum 40 doses per day. Don’t use more than 5 doses per hour ? After 6-8 weeks start to cut down following the scheduleas per advise of health provider.[32] Nicotine nasal spray is available as brand name of NICORETTE® thatcontainsNicotine 10 mg/ml. Each spray of 50 µl delivers 0.5 mg nicotine.[34] Advantages ofNicotine Nasal Spray The fast hit of nicotine helps to control the cravings quicker and more effectively. The dose is controlled rather than a steady supply. It is possibly the most effective form of NRT. It has proved successful with high nicotine dependency smokers.[33] Disadvantages ofNicotine Nasal Spray Side effects with the nasal spray than with any other form of NRT. It can be quite inconvenient having to carry a nasal spray around. It is not very discreet to use. It is more addictive than the other forms of NRT. The side effects may be uncomfortable and difficult to ignore. In heavy smokers, it may be difficult to control the number of doses taken.[33] There are following side effects of nicotine nasal spray: Watering eyes and runny nose Burning sensation in the nose

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

044

Irritated Throat Sneezing and coughing [32] Limitations of Current Nicotine Replacement Therapy Long-term quit rates are low. Only 10% of smokers who try to quit remain abstinent after 12 months.NRTs may have side effects that limit their use, such as local irritation, nausea/vomiting, coughing, hiccup, dyspepsia, and sleep disturbances.Current NRTs are not very rewarding. Therefore, smokers rarely use them regularly enough to quit smoking.NRT does not control urges to smoke in response to condi¬tioned cues, such as advertising.NRTs cannot always be used in the situations in which smokers feel the strongest urges to smoke.NRT administration routes are embarrassing or unappealing to some smokers.NRT does not fully suppress weight gain after cessation of smoking.[29] Conclusion Tobacco has been used in India for centuries. More than 4,000 different chemicals have been found in tobacco and tobacco smoke. More than 60 of these chemicals are known to cause cancer (carcinogens). Nicotine is a drug found in tobacco. It is highlyaddictive – as addictive as heroin or cocaine.The slower release of nicotine from NRT makes it much less addictive.Public health messages andhealth-care professionals should encourage the smokers as well as tobacco chewers to quit and suggest the nicotine replacement therapy as an option for effective treatment. References 1. Benjamin RM. U.S. Department of Health and Human Services. A Report of the Surgeon General: How Tobacco Smoke Causes Disease: What It Means to You. U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office o n S m o k i n g a n d H e a l t h , 2 0 1 0 . Av a i l a b l e from:http://www.cdc.gov/tobacco/data_statistics/sgr/201 0/consumer_booklet/pdfs/consumer.pdf 2. Cigarettes and Other Tobacco Products. NIDA InfoFacts. Retrieved November 8, 2006. Available from http://www.drugabuse.gov/Infofacts/Tobacco.html. 3. Benowitz NL.Pharmacology of Smokeless Tobacco Use:Nicotine Addiction and Nicotine–Related Health Consequences. Smoking and Tobacco Control Monograph No. 2.p.219-28. Available from: http://cancercontrol. cancer.gov/brp/tcrb/monographs/2/m2_4.pdf 4. Jha P et al. Tobacco addiction. In: Jamison DT et al., eds. Disease control priorities in developing countries 2nd ed. New York, NY, Oxford University Press, 2006.p.869–86. 5. WHO report on the global tobacco epidemic: implementing smoke-free environments, Geneva, World Health Organization, 2009. Available from: http://whqlibdoc.who.int/publications/2009/9789241563 918_eng_full.pdf 6. Malson JL, Sims K, Murty R, Pickworth WB. Comparison of the nicotine content of tobacco used in bidis and conventional cigarettes. Tob Control. 2001;10:181–3. 7. Burns DM. Cigar smoking: overview and current state of the science. In: National Cancer Institute, Cigars: health effects andtrends. Bethesda, MD, National Cancer Institute, 1998:1–20 (Smoking and Tobacco Control M o n o g r a p h 9 ) . Av a i l a b l e f r o m : h t t p : / / cancercontrol.cancer.gov / Brp / tcrb / monographs / 9 / m9_1. pdf 8. Henningfield JE, Fant RV, Radzius A, Frost S. Nicotine

concentration, smoke pH and whole tobacco aqueous pH of some cigar brands and types popular in the United States. Nicotine Tob Res. 1999 Jun;1(2):163-8. 9. Maisto SA, Galizio M, Connors GJ, eds. Drug use and abuse, 4th ed.Belmont, CA, Wadsworth/Thompson Learning, 2004. 10. Royal College of Physicians. Harm reduction in nicotine addiction: helping people who can’t quit. A report by the Tobacco Advisory Group of theRoyal College of Physicians. London: RCP, 2007. Available from: http://www.tobaccoprogram.org/pdf/4fc74817-64c54105-951e-38239b09c5db.pdf 11. Nicotine addiction. Bethesda, MD, National Institute on Drug Abuse, 2001, rev. 2006 . Available from: http:// www. drug abuse.gov / PDF / RR Tobacco.pdf. 12. Karan LD, Dani JA, Benowitz NL. The pharmacology of nicotine dependence. In: Principles of addiction medicine, 3rd ed. Washington, DC, American Society of Addiction Medicine, 2003:225–48. 13. Lynch B, Bonnie RJ, eds. Growing up tobacco free: preventing nicotine addiction in children and youths. Institute of Medicine Committee on Preventing Nicotine Addiction on Children and Youths. Washington,DC, National Academy Press, 1994. 14. Centers for Disease Control and Prevention. Determination of nicotine, pH, and moisture content of six US commercial moist snuff products— Florida, JanuaryFebruary 1999. Morbidity and Mortality Weekly Report, 1999, 48:398–401. 15. Management of Substance Abuse. WHO Lexicon of a l c o h o l a n d d r u g t e r m s . Av a i l a b l e f r o m : http://whqlibdoc.who.int/publications/9241544686.pdf?u a=1 16. Mandal A. Nicotine- What is Nicotine? Available from: http://www.news-medical.net/health/Nicotine-What-isNicotine .aspx 17. Research Report Series: Tobacco Addiction. NIDA. Retrieved November 8, 2006. Available from: http://www.drugabuse.gov/researchreports/nicotine/nicoti ne.html. 18. McNeill A, Foulds J, Bates C. Regulation of nicotine replacement therapies (NRT): a critique of current practice. Addiction 2001; 96 (12):1757–68. 19. Tackling tobacco. Action on smoking and disadvantage. Nicotine Replacement Frequently Asked Questions. Available from: http://askthequestion.com.au/wp-content/ uploads / 2011/11/CAN-3373-Nicotine-ReplacementTherapy-FAQs-1-Sep-2010.pdf 20. Clarke PBS.Recent Advances in UnderstandingThe Actions of Nicotine in the Central Nervous System.Smoking and Tobacco Control Monograph No. 2. p. 229-38. 21. American cancer society Guide to Quitting Smokeless Tobacco. Available from: http://www.cancer.org / acs / groups /cid / documents/webcontent/acspc-035551pdf.pdf 22. Aggarwal A, Jain M, Bhatia MS .Pharmacotherapy for smokeless tobacco use:A Review.Delhi Psychiatry Journal 2008; 11(2):163-73. 23. Nicotine Gum.University of Pittsburgh Medical Center P i t t s b u r g h , PA , U S A . Av a i l a b l e f r o m : https://medicine.mc.vanderbilt.edu/sites/default/files/ima ges/housestaff/nicotinegum.pdf 24. Nicotine Skin Patches University of Pittsburgh Medical Center Pittsburgh, PA, USA. Available from:

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

045

https://medicine.mc.vanderbilt.edu/sites/default/files/ima ges/housestaff/nicotine_patches.pdf 25. What you should know about the nicotine lozenge. Available from: http://www.acbhcs.org / tobacco / docs / Nicotine_Lozenge.pdf. 26. Dautzenberg B, Nides M, Kienzler JL,Callens A. Pharmacokinetics, safety and efficacy from randomized controlled trials of 1 and 2 mg nicotine bitartrate lozenges (Nicotinell®) BMC Clinical Pharmacology 2007;7:11. 27. Capital Health Regional Pharmacy Services. Nicotine inhaler. Prepared by: Regional Pharmacy Services, University of Alberta Hospital (Tara Spencer, Pharmacy Student) Last revised: July 18/05. Available from: http://www.capitalhealth.ca/NR/rdonlyres/eh7d4ctgfgodn cri3seo7z4we5oljlkc6z2bg6e5louh24wqziammd3odayoz 4s7tc6mbali5omt3usq4n27h4bmkmf/PatientInfoSheetNi cotineInhaler.pdf 28. Nicotine Replacement Therapy (NRT). Available from: http://www.northeastern.edu/uhcs/PDF/Nicotine%20Rep lacement%20Therapy.pdf 29. Caldwell B,Sumner W, Crane J.A Systematic Review of Nicotine by Inhalation: Is There a Role for the Inhaled

Route?Nicotine Tob Res 2012; 14(10):1127-39 30. N i c o r e t t e I n h a l a t o r . A v a i l a b l e f r o m : http://www.netdoctor.co.uk / smoking-cessation / medicines / nicorette-inhalator. html 31. What you need to know about…Prescription Medication: Nicotine Inhaler (Nicotrol® Inhaler). Available from: http://www.tcyh.org /smoking /downloads /rha /Nicotine_Inhaler.pdf 32. What you should know about the nicotine nasal spray. Available from: http:// www.acbhcs.org / tobacco / docs / Nicotine_Nasal_Spray.pdf 33. Guide to the nicotine nasal spray including possible side effects and how it works. Available from: http:// www . help with smoking.com/nicotine-replacement/nicotinenasal-spray .php. 34. Electronic Medicines Compendium. SPC: Nicorette Nasal Spray 2009b.[online]. Available at: http:// www .medicines. org.uk / EMC / medicine / 20679 / SPC / Nicorette + Nasal + Spray / # PRODUCTINFO

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

046

Journal of Dental Herald

Journal of Dental Herald

www.dherald.in

(July 2014) Issue:3, Vol.:1 E ISSN No. : 2348 – 1331 P ISSN No. : 2348 – 134X

A Review Tobaccouse And Its Impact On Periodontal Health Raghav Sharma1 1

House Surgeon , Indira Gandhi Govt Dental College, Jammu

Abstract It is a well established fact that tobacco smoking has a devastating effect on the health & well being of society . This article reviews the effects of tobacco on periodontal status & therapy as well as the potential mechanisms for the adverse effects of tobacco on periodontium. Approximately half of periodontitis cases have been attributed to either current or former smoking . The study of relationship between periodontal disease & smoking has received increased attention during the last few years . Tobacco smoking has wide spread systemic effects, many of which may provide mechanisms for the increased susceptibility to periodontitis & the poorer response to treatment as upto 90% of refractory periodontitis patients are smokers . There is evidence that smoking has negative effect on host response but an encouraging finding is that periodontal disease progression slows in patients who quit smoking & they have a similar response to periodontal therapy as non-smokers. These facts should be considered by clinicians during treatment planning & should be shared with patientswho use tobacco products.

Key Words Tobacco, smoking, Periodontitis, Risk factors, Adverse effects.

Introduction : With the modernisationof man , his needs whether biological, social or economical has also increased. Man is constantly running after them & failure to meet his needs and desires make him feel frustrated , filled with anger & under immense stress. To free himself from all his fears &stresses , modern man is falling prey to habits of addiction, most commonly smoking . Smoking has long been linked to a variety of medical problems like cancer, low birth weight, pulmonary & cardiovascular diseases[1]. However , in the past two decades there has been an increasing awareness of the effect of tobacco use on the prevalence & severity of periodontal diseases[2]. History : Tobacco is a plant whose history traces back to about 6000 B.C. when it was believed that it began growing in the north &south America. When Columbus came to America, he met some natives who inhaled smoke from leaves through a long wooden tube which they called ‘tobago or tobaca’ . From this came the name applied to the plant. Soon after this sailors brought tobacco to Europe. The generic nameNicotinaTobaccum was named after the French ambassador to Portugal, “ Jean Nicot “ who introduced tobacco into the French court in 1560. Prevalence : ? The prevalence of smoking is higher in males (31%) than in females (25%) . ? In Indian society, more than 5,500 adolescents are taking to tobacco everyday & there are estimated 10 lakh deaths annually in India because of tobacco. [ A study by centre for global health research, university of Toronto, in 2008.] ? In India, highest rate of smoking is seen in Mizoram where approximately 85% of men& 65% of women smoke. This Quick Response Code

Address For Correspondence: Dr. Raghav Sharma, House Surgeon , Indira Gandhi Govt Dental College, Jammu Email: [email protected]

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

is followed by West Bengal where 71% of people use tobacco & its related products. ? Incidence is also rising in females due to high amount of emotional stress. ? It is more common among low income adults than in medium or high class. ? The prevalence also increases with decreasing years of education. ? 72% tobacco users in India are bidi smokers, 12.5% are cigarette smokers, while 16% use smokeless tobacco. Toxins Present In Cigarette Smoke : More than 4000 substances are present in Cigarette smoke, these include• Carcinogens : 1) Tar ( aggregate of particulate matter in cigarette smoke after subtracting nicotine & moisture ) 2) NNN-> N-Nitroso Nor Nicotine with tumor initiating properties. 3) Polycyclic aromatic hydrocarbons. 4) Benzopyrene- cause irritation & tumor promotion. 5) Trace metals- Nickel,Arsenic,Polonium. 6) Nitrosamine. 7) Hydrazine. • Co-carcinogens: 1) Phenol 2) Cresol • Addicting Agents : 1) Nicotine • Others : 1) carbon monoxide: impairs oxygen carrying capacity of RBC’s by forming carboxyhaemoglobin. 2) oxidesof nitrogen: cause toxic damage to oral & respiratory epithelium, are ciliotoxins . Effect Of Smoking On Periodontium : 1) On Gingival Tissues : • Smokers present with lower levels of gingival inflammation to a specific level of plaque than nonsmokers[3]. • Smokers also exhibit less bleeding on probing as compared to non-smokers[4].

047

•

Also, smoking causes extrinsic stains on tooth which act as nidus for plaque retention leading to gingival diseases.

2) On Periodontal Tissues: • Smoking increases the prevalence & severity of periodontal destruction. • Tomar & Asma[5], in a study concluded that approximately half of periodontitis cases were attributable to either current smoking or former smoking. • As compared to non-smokers, current smokers were about four times , while former smokers were 1.68 times more likely to have periodontitis. • The rate of bone loss in smokers was almost four times greater than that of non-smokers[6]. • Despite similar plaque levels, smokers have deeper probing depths & attachment loss[7] . • The generalized form of aggressive periodontitis is more associated with smoking than the localized form of aggressive periodontitis[8]. • Compared to non-smokers, smokers have a high prevalence of furcation involvement. Effect Of Other Forms Of Tobacco On Periodontal Status : ? Unlike cigarette smokers, who experience widespread

periodontal destruction, the oral effects of smokeless tobacco are localized to the site of placement. The primary periodontal alteration in smokeless tobacco users is localized gingival recession & white mucosal lesions. ? The majority of the white mucosal lesions regress when the smokeless tobacco habit is discontinued,with in six weeks of tobacco cessation. Response To Periodontal Therapy In Smokers ? Smoking impairs the response to periodontal therapy with

significantly less improvement in clinical parameters among smokers than non-smokers . Numerous studies have found that upto 90% of refractory periodontitis patients are smokers[9]. ? Numerous studies have shown that smoking compromises attachment gain outcomes following non-surgical therapy & also has a negative impact on regenerative therapy, including osseous grafting, Guided tissue regeneration or a combination of these treatments. ? Some clinicians believe that smoking is a relative contraindication to dental implant therapy since implant failure rates were more than twice as high in smokers as reported by Bain & Moy[10]. Effect Of Smoking On Etiology & Pathogenesis Of Periodontal Disease : Microbial Effects: Smoking increases the colonization of periodontal pathogens in periodontal pockets. Smoking also alters the quality of flora favoring more of anaerobic species. Physiological Effects : In smokers , there is less pronounced inflammation in response to infection, less GCF flow & less bleeding on probing . There is less subgingival temperature & less oxygen tension in the gingiva of smokers. Effect On Host Response : Smoking impairs the function of Neutrophils which are the first line of defence against bacterial infection. Neutrophils in smokers have shown decreased chemotaxis[11], phagocytosis

& adherence. Smoking also decreases serum IgG concentrations, thereby affecting another protective host mechanism. Smoking has also been shown to inhibit fibroblast attachment & proliferation. These effects could impact wound healing & periodontitis progression . Smoking Cessation & Its Impact On Periodontal Status : The periodontal status of former smokers ranks between current smokers & non-smokers[12] . This suggests that while smoking cessation doesnot reverse the past effects of smoking, the deterioration doesnot continue after cessation. It is also encouraging to note that former smokers respond to periodontal therapy in a manner similar to non-smokers[13]. Conclusion : Cigarette smoking is a major risk factor & smokers are a high risk group for periodontitis .It is very difficult to treat them with conventional therapy as they respond only partially to such therapies .Given the overwhelming evidence of the negative impact of tobacco on periodontal status & response to periodontal therapy, the American Academy of Periodontology’s parameters of care 14 recommends tobacco cessation therapy for the periodontal patient when appropriate . So, counseling for smoking prevention should be included in the protocol for managing patients with periodontal disease . However, the motivation towards a positive change should be achieved by each individual “ after all whose life is it any way “ References : 1. Wald NJ, HackshawAK .Cigarette smoking : an epidemiological overview, Br Med Bull 1996; 52:3-11 2. Haber J, Wattes J, Crowley M, Mandell R, Joslipura K, Kent RL. Evidence for cigarette smoking as a major risk factor for periodontitis. J periodontol 1993;64:16-23. 3. Tonetti MS. Cigarette smoking & periodontal diseases. Etiology & management of disease. Ann periodontol 1998;3:88-101. 4. Clarke NG, Shepherd BC, Hirish RS. The effects of intra arterial epinephrine & nicotine on gingival circulation. Oral Surg Med Oral Path 1981;52:577-82. 5. Tomal SL, Asma S. Smoking – attributable periodontitis in the United states. Findings from NHANES III . National h e a l t h & n u t r i t i o n e x a m i n a t i o n s u r v e y. J Periodontol2000;71:743-51 6. Bergstrom J, Eliason S, Dock J. A 10-year prospective study of tobacco smoking & periodontal health. J Periodontol 1997,24:102-9 7. Linden GJ, Mullally BH. Cigarette smoking & periodontal destruction in young adults. J Periodontol 1994;65:718-23 8. Mullally BH, Breen B, Linden GJ . Smoking & patterns of bone loss in early onset periodontitis. J. periodontal 1999; 70: 394-401. 9. MacFarlene GD, Herzberg MC, Wolff LF, Hardie NA. Refractory periodontitis associated with abnormal PMN leucocyte phagocytosis &cigarette smoking. J. periodontal 1992;63:908-13. 10. Bain CA,Moy PK. The association betweenthe failure of dental implants & cigarette smoking. Int. J oral maxillofacImplants, 1993;8:609-15 11. Kraal JH, Kenney EB. The response of PMN leucocytes to chemotactic stimulation, for smokers & non-smokers. J periodontol Res 1979;14:383-9. 12. Haber J, Kent RL. Cigarette smoking in periodontal practice. J periodontal 1992;63:100-6. 13. Grossi SG, Zambon J, Machtei EE, et al. Effects of smoking & smoking cessation on healing after mechanical periodontal therapy. J Am Dent Assoc 1997;128:599-607. 14. American Academy of periodontology, parameters of care, J periodontol 2000;71: i-ii , 847-83

Source of Support : Nill, Conflict of Interest : None declared

©Journal of Dental Herald (July 2014 Issue:3, Vol.:1).

048