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ISSN 2218-0885

International Arab Journal of Dentistry ‫المجلة العربية الدولية لطب االسنان‬

Revue arabe internationale de dentisterie

Vol. 5 – Issue 2


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ISSN 2218-0885

International Arab Journal of Dentistry ‫اﻟﻤﺠﻠﺔ اﻟﻌﺮﺑﻴﺔ اﻟﺪوﻟﻴﺔ ﻟﻄﺐ اﻻﺳﻨﺎن‬

Revue arabe internationale de dentisterie

Vol. 5 – Issue 2

The International Arab Journal of Dentistry (IAJD) is a specialized, and refereed journal that is published quarterly in French and English. IAJD is the official journal of the Society of Arab Dental Faculties (SARDF) and is published by the Faculty of Dental Medicine - Saint-Joseph University of Beirut.

Université Saint-Joseph 2014 - International Arab Journal of Dentistry - www.iajd.org Society of Arab dental Faculties - www.sardf.org Published by Facuty of Dental Medicine, USJ All rights reserved For any information concerning the IAJD, please contact us by e-mail :

info@iajd.org or fmd@usj.edu.lb


AUTHOR GUIDELINES Submission Manuscripts should be submitted by one of the authors of the manuscript through the online Submission System. Regardless of the source of the word-processing tool, only electronic PDF (.pdf) or Word (.doc, .docx, .rtf) files can be submitted through the MTS with priority for PDF file. There is no page limit. The attached file should not exceed 12Mb for low speed connection, and 32 Mb for high speed connection. Only online submissions are accepted to facilitate rapid publication and minimize administrative costs. Submissions by anyone other than one of the authors will not be accepted. The submitting author takes responsibility for the paper during submission and peer review. If for some technical reason submission through the MTS is not possible, the author can contact info@iajd.org for support.The attached file should be scanned with an antivirus software before submitting. Terms of Submission Papers must be submitted on the understanding that they have not been published elsewhere (except in the form of an abstract or as part of a published lecture, review, or thesis) and are not currently under consideration by another journal published by Hindawi or any other publisher. The submitting author is responsible for ensuring that the article’s publication has been approved by all the other coauthors. It is also the authors’ responsibility to ensure that the articles emanating from a particular institution are submitted with the approval of the necessary institution. Only an acknowledgment from the editorial office officially establishes the date of receipt. Further correspondence and proofs will be sent to the author(s) before publication unless otherwise indicated. It is a condition of submission of a paper that the authors permit editing of the paper for readability. All enquiries concerning the publication of accepted papers should be addressed to info@iajd.org. Peer Review All manuscripts are subject to peer review and are expected to meet standards of academic excellence. Submissions will be considered by an editor and—if not rejected right away—by peer-reviewers, whose identities will remain anonymous to the authors. Units of Measurement Units of measurement should be presented simply and concisely using System International (SI) units. Title and Authorship Information The following information should be included: t 1BQFSUJUMF t 'VMMBVUIPSOBNFTonly in the submission form and not in the manuscript

www.iajd.org t 'VMMJOTUJUVUJPOBMNBJMJOHBEESFTTFT t&NBJMBEESFTTFT Abstract The manuscript should contain an abstract. The abstract should be self-contained and citation-free and should not exceed 150 words. Introduction This section should be succinct, with no subheadings. Acknowledgments All acknowledgments (if any) should be included at the very end of the paper before the references and may include supporting grants, presentations, and so forth. References Authors are responsible for ensuring that the information in each reference is complete and accurate. All references must be numbered consecutively and citations of references in text should be identified using numbers in square brackets (e.g., “as discussed by Smith [9]”; “as discussed elsewhere [9, 10]”). All references should be cited within the text; otherwise, these references will be automatically removed. Proofs Corrected proofs must be returned to the publisher within 2-3 days of receipt. The publisher will do everything possible to ensure prompt publication. It will therefore be appreciated if the manuscripts and figures conform from the outset to the style of the journal. Copyright Open access authors retain the copyrights of their papers, and all open access articles are distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution and reproduction in any medium, provided that the original work is properly cited. The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations. While the advice and information in this journal are believed to be true and accurate on the date of its going to press, neither the authors, the editors, nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.

Statements and opinions expressed in the articles and communications herein are those of the author(s) and not necessarily those of the editor or the publisher. Professional qualifications stated in each article are provided by authors. The editor and the publisher disclaim any responsibility or liability for such material and do not guarantee, warrant or endorse any product or service advertised in this publication nor do they guarantee any claim made by the manufacturer on such product or services.


COMITÉ DE RÉDACTION - EDITORIAL BOARD Rédacteur en chef – Editor-in-Chief Prof. Edgard NEHMÉ Faculty of Dental Medicine, Saint-Joseph University, Lebanon

Comité exécutif de l’association des facultés dentaires arabes - Officers Society of Arab Dental Faculties

Rédacteur en chef adjoint - Associate Editor

Prof. Nada BOU-ABBOUD NAAMAN, General Secretary, Dean Faculty of Dental Medicine, Saint-Joseph University, Lebanon

Dr. Hiam WEHBÉ Faculty of Dental Medicine, Saint-Joseph University, Lebanon

Prof. Ihab ABDEL MOHAMMAD HAMMAD, Dean Faculty of Dental Medicine, University of Alexandria, Egypt

Comité de Direction – Editorial Advisory Board Ass. Prof. Roula ABIAD Prof. Nabih BADAWI Ass. Prof. Antoine BERBERI Dr. Pascale HABRE HALLAGE Ass. Prof. Jeanine HOYEK GEBEILY Ass. Prof. Alfred NAAMAN Ass. Prof. Balsam NOUEIRY Dr. Ziad NOUJEIM Prof. Issam OSMAN Prof. Khaldoun RIFAI Prof. Lucette SEGAAN

Prof. Elham ABU ALHAIJA, Dean Faculty of Dentistry, Jordan University of Science and Technology, Jordan Prof. Jawad BEHBEHANI, Dean Faculty of Dental Medicine, Kuwait University, Kuwait Prof. Amal AL-WAZZANI, Dean Faculty of Dental Medicine, Hassan 2 University, Morocco Prof. Razan KHATTAB, Dean Faculty of Dental Medicine, University of Damascus, Syria Prof. Antoine KHOURY, telltale & treasurer, Saint-Joseph University, Lebanon

COMITÉ DE LECTURE – SCIENTIFIC BOARD Prof. Raad Mehieddine Helmi, Iraq Dr. Nadim Mokbel, Lebanon Ass. Prof. Alfred Naaman, Lebanon Prof. Nada Naaman, Lebanon Prof. Balsam Noueiry, Lebanon Dr. Ziad Noujeim, Lebanon Prof. Issam Osman, Lebanon Prof. Lamia Oualha, Tunisia Prof. Herve Reychler, Belgium Dr. Faouzi Riachi, Lebanon Prof. Sana Rida, Morocco Prof. Khaldoun Rifai, Lebanon Prof. Nouhad Rizk, Lebanon Prof. Joseph Sader, Lebanon Prof. Fayez Saleh, Lebanon Prof. Elizabeth Sarkis, Syria Prof. Lucette Segaan, Lebanon Dr. Bassel Tarkaji, Syria Prof. Georges Tawil, Lebanon Prof. Abed Yakan, Syria Prof. Nadia Ahmad Yehia, Sudan Dr. Ronald Younes, Lebanon Prof. Mohamed Youssef, Syria Ass. Prof. Carina Zogheib, Lebanon

Ass. Prof. Khansa Ababneh, Jordan Prof. Nabil Abdel Fattah, Iraq Prof. Maha Abdel Salam, Egypt Ass. Prof. Roula Abiad, Lebanon Prof. Elham Abu Alhaija, Jordan Prof. Salem Abu Fanas, UAE Prof. Hani Amin, Egypt Ass. Prof. Ola Al- Batayneh, Jordan Prof. Fouad Al-Belassi, Egypt Prof. Fahed Al-Harbi, KSA Prof. Abadi Al-Kadi, Egypt Dr. Qasem Al- Omari, Kuwait Prof. Abdallah Al-Shammari, KSA Prof. Khaled Al-Wazzan, KSA Prof. Amal Al-Wazzani, Maroc Prof. Athanasios Athanasiou, Greece Prof. Fouad Ayoub, Lebanon Prof. Nabih Badawi, Lebanon Prof. Zaid Baqaeen, Jordan Prof. Nayla Bassil- Nassif, Lebanon Prof. Jawad Behbehani, Kuwait Prof. Joseph Bou Serhal, Lebanon Ass. Prof. Antoine Berberi, Lebanon Ass. Prof. Paul Boulos, Lebanon Dr. Diego Capri, Italy

Dr. Robert Cavezian, France Prof. Nada Chedid, Lebanon Dr. Maroun Dagher, Lebanon Dr. Maha Daou, Lebanon Prof. Azmi Darwazeh, Jordan Prof. Mounir Doumit, Lebanon Miss Lea El Korh, Lebanon Prof. Kifah El-Jemaani, Jordan Prof. Rabab el-Sabbagh, Syria Dr. Amine El Zoghbi, Lebanon Dr. Pascale Habre- Hallage, Lebanon Prof. Ahmad Hamdan, Jordan Prof. Ihab Abdel Mohammad Hammad, Egypt Dr. Louis Hardane, Lebanon Prof. Raed Moheiddine Helmi, Iraq Ass. Prof. Jeanine Hoyek Gebeily, Lebanon Prof. Mohammad Mazen Kabbani, Syria Dr. Tarek Itani, Lebanon Prof. Imad Keaid, Syria Prof. Carlos Khairallah, Lebanon Prof. Razan Khattab, Syria Dr. Roland Kmeid, Lebanon Prof. Ammar Laika, Syria Ass. Prof. Nada Mchayleh, Lebanon Prof. Ahmed Medra, Egypt

Secrétaire de rédaction – Editing Secretary

Conception et mise en page – Design and Layout

Impression et diffusion – Printing and Promotion

Miss Mireille Abdallah Faculty of Dental Medicine, Saint-Joseph University, Lebanon

Alarm sarl, Beirut, Lebanon

Dental News group, Beirut, Lebanon

mireille.abdallah@usj.edu.lb


EDITORIAL Pr. Edgard Nehmé Editeur

Chers Lecteurs, Chers Confrères, Le 24 décembre 2013 nous recevions de la très respectable Organisation Mondiale de la Santé - Bureau Régional de la Méditerranée Orientale – la notification relative à la sélection de l’IAJD parmi les sources de données de l’Index Medicus pour la Méditerranée Orientale (IMEMR). La banque de donnée complète de l’IMEMR est disponible sur le réseau Internet ; elle est régulièrement mise à jour et elle peut être consultée sur le lien : http://www.emro.who.int/information-resources/publications/. Toutefois, l’annuaire de l’IMEMR est également disponible sur le lien : http://www.emro.who.int/information-resources/imemr-journals-directory/. Quels sont les critères de sélection des revues dans l’Index de l’IMEMR ? Nous les rapportons ici intégralement : La couverture géographique de l'IMEMR est la Région de la Méditerranée orientale de l'OMS. La région couvre 23 pays: Afghanistan, Bahreïn, Djibouti, Égypte, République islamique d'Iran, Iraq, Jordanie, Koweït, Liban, Libye, Maroc, Pakistan, Territoire palestinien occupé, le Qatar, l'Arabie Saoudite, la Somalie, le Soudan du Sud, Soudan, Syrie République arabe syrienne, Tunisie, Emirats arabes unis et le Yémen. Les domaines couverts : Les sujets traités comprennent tous les sujets de santé publique, de la médecine et de toutes ses sous-spécialités, la santé environnementale, la dentisterie, la pharmacie, les soins infirmiers, la gestion de la santé et de l'administration et des sciences vétérinaires. Les magazines qui sont purement commerciales ou bulletins de commerce et des nouvelles générales et des bulletins qui n'ont pas de contenu scientifique et technique ne sont pas inclus dans l'Index. CONTENU ET LE TYPE DE MATÉRIAUX

La valeur scientifique et l'examen par les pairs sont les facteurs les plus importants dans le choix d'un journal à l’index. La qualité : les revues sélectionnées doivent être objectives, crédibles et de contenu de haute qualité.


La couverture linguistique : L’IMEMR contient des revues médicales en anglais, arabe, farsi, français et ourdou. Résumés en anglais : les Journaux sélectionnés doivent comprendre un résumé en anglais. Publication régulière : les revues sélectionnées devraient être publiées sur une base régulière. L’IAJD a donc pleinement rempli et honoré les critères de l’indexation ; elle est désormais intégrée à la liste des revues scientifiques de l’IMEMR. Le nombre total de publications produites par le Bureau régional en 2013 était de 78 ainsi reparties : arabe (23), anglais (38), français (17). Le nombre total de revues qui ont été indexées dans l'Index Medicus pour la Région de la Méditerranée orientale est de 572. En plaçant la revue à un niveau d’indexation régional, un nouveau pas est franchi et nous nous en réjouissons. C’est par notre détermination à tous, par les encouragements qui nous parviennent des Doyens-membres de l’Association des facultés dentaires arabes, mais encore et surtout par la qualité de vos travaux et publications que vous viserons toujours plus loin, plus haut. La parution de ce numéro coïncide avec la tenue des XIe Journées Odontologiques de la faculté de médecine dentaire de l’université Saint-Joseph de Beyrouth. Tout comme nous souhaitons plein succès à cet événement international et régional, nous saisissons l’occasion pour inviter les Doyens des facultés-membres de l’Association à nous communiquer leurs activités scientifiques de manière à pouvoir les diffuser dans nos pages. Nous sommes enfin très honorés de lire dans ce numéro l’éditorial réservé à notre invité le Doyen de la faculté dentaire arabe de Beyrouth et nous le remercions chaleureusement d’avoir gentiment répondu à notre invitation. Nous lui souhaitons ainsi qu’à la très respectable institution qu’il représente davantage de succès et de réalisations.


EDITORIAL Pr. Edgard NehmĂŠ Editeur

Dear readers, Dear fellows, On December 24th, 2013 we received from the very respectable World Health Organization Regional Office for the Eastern Mediterranean - the announcement of the selection of the IAJD among data sources of the Index Medicus for the Eastern Mediterranean (IMEMR ). The comprehensive database of IMEMR is available on the Internet; it is regularly updated and can be found on the link : http://www.emro.who.int/information-resources/publications/. However, the IMEMR directory is also available on the link: http://www.emro.who.int/information-resources/imemr-journals-directory/. What is the IMEMR and what are the criteria for selecting journals in the Index IMEMR? We report them here in entirely: “The Index Medicus for the Eastern Mediterranean Region (IMEMR) provides health care professionals and researchers from the Region with access to health and biomedical information and increases the visibility of their work at national, regional and international level. CRITERIA FOR SELECTION OF JOURNALS FOR THE INDEX

Geographic coverage: Geographic coverage of the IMEMR is the WHO Eastern Mediterranean Region. The Region covers 23 countries: Afghanistan, Bahrain, Djibouti, Egypt, Islamic Republic of Iran, Iraq, Jordan, Kuwait, Lebanon, Libya, Morocco, Pakistan, occupied Palestinian territory, Qatar, Saudi Arabia, Somalia, South Sudan, Sudan, Syrian Arab Republic, Tunisia, United Arab Emirates and Yemen. Subject coverage: Subject coverage includes all public health topics, medicine and all its subspecialties, environmental health, dentistry, pharmaceutical, nursing, health management and administration and veterinary sciences. Magazines that are purely commercial or for trade and general news bulletins and newsletters which lack scientific and technical content are not included in the Index.


Content and type of materials: Scientific value and peer review are the most important considerations in selecting a journal to index. Quality: Selected journals should be objective, credible and of high-quality content. Language coverage: The IMEMR contains medical journals in Arabic, English, Farsi, French and Urdu. English abstracts: Selected journals should contain abstracts in English. Regular publishing: Selected journals should be published on a regular basis. The IAJD has fully completed and honoured the criteria for selection; Your Journal is now integrated to the list of scientific journals of the IMEMR. The total number of publications produced by the Regional Office in 2013 was 78 and distributed: Arabic (23), English (38) and French (17). The total number of journals that have been indexed in Index Medicus for the Eastern Mediterranean Region is 572�. By placing the journal at a regional level of indexing, a new step has been taken and we rejoice. This is through our commitment to all of, by the encouragement we receive of Deans member of the Arab Association of Dental Schools, but also and especially by the quality of your work and papers, we are aiming even further and higher. The publication of this issue coincides with holding the Eleventh Odontological Meeting of the Faculty of Dental Medicine at Saint-Joseph University of Beirut. Just as we wish success to this international and regional event, we take this opportunity to invite the Deans member of the Association to notify us directly of their scientific activities so as to disseminate them in our pages. Finally, we are honored to read in this issue the Editorial written by our Guest, the Dean of the Faculty of Dentistry at Beirut Arab University - whom we gratefully acknowledge for accepting our invitation. We wish him and the very respectable institution he represents more success and achievements.


EDITORIAL GUEST Prof. Essam Osman Vice President for Medical Sciences Dean, Faculty of Dentistry Beirut Arab University, Beirut, Lebanon

“We are what we repeatedly do. Excellence, therefore, is not an act, but a habit.� Aristotle said that very long ago, but as educators wandering in the vast fields of dentistry, we are still implementing this constantly. There is no single thing a person can do to reach excellence; it is in fact the product of constant trials, embarking on a quest to reach out to the best of us. Concerning Dentistry, excellence is a necessity not an option. To reach it, we need a habit and not an act, and this habit may be encapsulated in two simple ideas that summarize all the required attributes of a qualified ethical dentist; these are education and research. This entails the restriction of the practice to only those who are competent enough, through an elaborate educational system which trains the young dentist to become a critical thinker, a problem-based learner, and an evidence-based practitioner. Here, at Beirut Arab University, we are an example of that, adapting the most recent trends in educational reform worldwide, and providing the most advanced technologies to offer our students and researchers the chance to innovate and push dentistry another step forward towards excellence. We are doing our job to reach excellence, and the International Arab Journal of Dentistry as a journal are also taking part in this quest; in fact, a large number of people are involved in this, even though they might not be aware of it. As an educational institution, we are the basis to attaining excellence. But we are definitely not alone. Every person working in this field is considered a soldier in this battlefield fighting dental diseases. When will we announce the victory? Probably never, because as human beings we don't accept things the way they are and we are persistently looking to become better.


«Nous sommes ce que nous faisons à plusieurs reprises. L'Excellence donc n'est pas un acte, mais une habitude.’’ Aristote a émis cette réflexion depuis longtemps, mais en tant qu’éducateurs qui sont sans cesse confrontés aux vastes domaines de la dentisterie, nous essayons d’appliquer cette pensée en permanence. On ne peut pas atteindre l'excellence dès la première fois, c’est en fait le produit d'essais constants ; il s’agit de se lancer dans une quête permanente pour atteindre le meilleur qui est en nous. En ce qui concerne la dentisterie, l'excellence est une nécessité et non une option. Pour y parvenir, nous avons besoin d'une habitude et non pas d’un acte, et cette habitude peut être résumée en deux idées simples qui réunissent tous les attributs nécessaires d'un dentiste qualifié et soucieux de son éthique : l'éducation et la recherche. Réduire la pratique seulement à ceux qui sont suffisamment compétents, à travers un système éducatif élaboré, approfondi, qui forme le jeune dentiste à devenir un penseur critique, un apprenant par problème, et un praticien qui se fonde sur des preuves. Ici, à l'Université Arabe de Beyrouth, nous ne sommes qu’un exemple: en adoptant les tendances les plus récentes en matière de réforme de l'éducation dans le monde entier, et en utilisant les technologies les plus avancées pour offrir à nos étudiants et chercheurs, la chance d'innover, et pousser la dentisterie un autre pas en avant vers l'excellence. Nous faisons notre travail pour atteindre l'excellence, et la revue arabe internationale de dentisterie participe également à cette quête; en fait, beaucoup de gens sont impliqués dans ce domaine même s’ils ne se rendent pas compte. Nous, en tant qu'institution éducative, pouvons former les fondements pour atteindre l'excellence. Mais nous ne sommes certainement pas les seuls. Toute personne travaillant dans ce domaine est considérée comme un soldat dans ce champ de bataille, la lutte contre les maladies dentaires. Quand allons-nous annoncer la victoire? Probablement jamais, parce que nous les êtres humains n'acceptons pas les choses comme elles sont et nous sommes constamment à la recherche du meilleur.


SOMMAIRE | TABLE OF CONTENTS 51 51

ARTICLE SCIENTIFIQUE / SCIENTIFIC ARTICLE Orthodontie / Orthondontics Periodontal health status of Saudi patients undergoing orthodontic treatment Azzam Al-Jundi

59

Pédodontie / Pedodontics Prevalence of hypodontia in permanent dentition in a sample of Sudanese university students Amal Abu Affan / Abeer Serour

65 65

REVUE DE LA LITTÉRATURE / LITTERATURE REVIEW Prothèses Fixées / Fixed Prostheses Self-adhesive cements and all ceramic crowns: A review Foudda Homsy / Elie Daou / Maha Ghotmi / Mireille Rahi

74

Médecine Orale /Oral Medicine L’halitose : origine, classification et traitement Guenane Yamina / Adel Ayat / Hayet Lazili / Badia Saari

79 79

CAS CLINIQUE / CASE REPORT Médecine Orale /Oral Medicine Carcinome épidermoïde: à propos de deux cas Chirine Chammas / Nadia Skandri / Dolly Roukoz

85

Médecine Orale /Oral Medicine Oral tertiary syphilis – A case report 'HHSD06$QLWD%DODQ6XQLO6%LÀ-R\


51

ARTICLE SCIENTIFIQUE / SCIENTIFIC ARTICLE

Introduction

Orthodontie / Orthodontics

PERIODONTAL HEALTH STATUS OF SAUDI PATIENTS UNDERGOING ORTHODONTIC TREATMENT Azzam Al-Jundi * Abstract The growing awareness about dental aesthetics and functionality in the general population has led to more and more people seeking orthodontic treatment. The patient’s ability to achieve and maintain good overall oral hygiene and prevent periodontal disease is fundamental while undergoing orthodontic treatment. This study was done to evaluate the periodontal health status of Saudi patients scheduled for fixed orthodontic treatment. Fifty patients (12-26 years old) were selected from orthodontic clinics of King Abdul-Aziz Medical City of National Guard, Riyadh, Saudi Arabia. The periodontal health status of the patients was evaluated using the plaque index (PI), the orthodontic plaque index (OPI) and the gingival bleeding index (GBI). These indices were determined prior to the placement of fixed appliances, after 6 months and after 12 months of the beginning of the orthodontic treatment. Results showed that PI and OPI were high with mean scores of 65.24 ± 16.43 for PI and 53.56 ± 8.74 for OPI, while the average GBI scored a much lower value of 19.14 ± 7.95. After 6 months of treatment, the probing pocket depth at the first molars was 1.5-2.0 mm. In some severe cases it exceeded 3mm. After 12 months of treatment, the probing pocket depth was greater than that observed at 6 months and it mostly fell in the range of 2.0-2.5mm. No significant differences were observed between male and female patients for the PI (p=0.925) and for OPI (p=0.072); However, a significant difference was observed for the GBI (p=0.033). Thus it was concluded that plaque deposition during orthodontic treatment can promote periodontal inflammation and destruction. Oral hygiene measures, patient education and motivation can help maintain oral hygiene and minimize the hazardous effects of orthodontic treatment on periodontal tissues. Keywords: Plaque index - bleeding index - probing pocket depth – gingivitis - oral hygiene - fixed orthodontics.

Résumé La prise de conscience sur l’esthétique et la fonction dentaire dans la population générale a poussé de plus en plus les gens à demander un traitement orthodontique. Lors d’un traitement orthodontique, la capacité du patient à maintenir une bonne hygiène bucco-dentaire et à prévenir les maladies parodontales est fondamentale. Cette étude a été réalisée pour évaluer l'état de santé parodontale des patients saoudiens subissant un traitement orthodontique fixé. Cinquante patients (12 - 26 ans) ont été sélectionnés à partir des cliniques d'orthodontie de la Cité Médicale de la Garde Nationale du roi Abdul -Aziz, Riyad, Arabie Saoudite. L’examen parodontal a été effectué avant, après 6 mois et après 12 mois du début du traitement. L'état de santé parodontale des patients a été évalué en utilisant l'indice de plaque, l'indice de plaque d'orthodontie et l'indice gingival de saignement. Les résultats ont montré que l'indice de plaque et l'indice de plaque orthodontique sont élevés avec des scores moyens respectifs de 65,24 ± 16,43 et 53,56 ± 8,74. Seul l'indice de saignement gingival était plus faible, avec une valeur de 19.14 ± 7.95. Après 6 mois de traitement, la profondeur de poche au niveau des premières molaires était de 1,5 -2 mm. Dans certains cas graves, elle a dépassé les 3 mm. Après 12 mois de traitement, la profondeur de poche était supérieure à celle observée à 6 mois avec des valeurs de 2-2,5 mm. Aucune différence significative n'a été observée entre les hommes et les femmes pour l’indice de plaque (p = 0,925) et pour l'indice de plaque orthodontique (p = 0,072). Cependant, une différence significative a été observée pour l'indice de saignement gingival (p = 0,033). En conclusion, la déposition de plaque au cours du traitement orthodontique a entrainé une destruction du parodonte. Un détartrage régulier des dents couplé à la motivation du patient permettent de maintenir une bonne hygiène bucco-dentaire et de minimiser les effets néfastes du traitement orthodontique sur les tissus parodontaux. Mots-clés : indice de plaque – indice de saignement – gingivite – hygiène orale – orthodontie.

* BDS, MSsD, PhD College of Dentistry King Saud bin Abdul Aziz University for Health Sciences, Riyadh, Saudi Arabia azjundi@hotmail.com


52

IAJD Vol. 5 – Issue 2

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Introduction Periodontal disease is one of the major problem and concern during orthodontic treatment. Periodontal disease is not a single pathologic entity but comprises a number of inflammatory and degenerative processes of the supporting periodontal structures [1, 2]. The most important etiological factor of periodontal disease is plaque deposition around gingival margin [3, 4]. The accumulation of plaque can cause gingival redness, bleeding, edema, changes in gingival morphology, reduced tissue adaptation to the teeth, an increase in the flow of gingival crevicular fluid and other clinical signs of inflammation. It is well established that the patients who undergo orthodontic treatment have a high susceptibility to plaque accumulation on their teeth because of the presence of bands, brackets, wires and other orthodontic attachment [5]. The elements of fixed orthodontic appliance can change the biological balance in the oral cavity [6] (Fig. 1). An important rational in performing orthodontic treatment is to promote the health of the periodontium, thereby enhancing longevity of the dentition [8, 9]. Orthodontic treatment is a doubleaction procedure 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, namely gingival recession, bone dehiscence, gingival invaginations and/or the formation of gingival pockets [10]. Thus orthodontic treatment can be referred to as a twoedge sword. The positive effects of orthodontic treatment on patient’s appearance and self-esteem are easy to envision [11]. Past studies have shown that orthodontic treatment can positively affect the periodontal health; however,

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(streptococcus mutans, Lactobacilli) ph calcium phosphate

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Demineralization of the tooth surface

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recent reviews didn’t show reliable evidence on the positive effects of orthodontic therapy on patients’ periodontal status [12]. Periodontic-orthodontic interrelationships are still controversial. However, a standard language between the periodontist and the orthodontist must always be established to improve the outcomes of the whole treatment [12]. Therefore, it is essential to emphasize oral hygiene instructions and to maintain high standards of oral hygiene for patients undergoing orthodontic treatment [13]. The aim of the present study was to evaluate the periodontal health status in patients scheduled for orthodontic therapy with fixed appliances.

Materials and Methods The sample in the present study consisted of 50 orthodontic patients attending the orthodontic clinic in King Abdul-Aziz Medical City of National Guard, Riyadh, Saudi Arabia. Saudis patients, between 12 and 26 years old, and requiring full-mouth fixed orthodontic treatment were included in the study. All maxillary and mandibular teeth should be present, exempt of caries, extensive fillings or

crowns. Also, the initial probing pocket depth on all first molars should not exceed 1.5mm. Patients who received orthodontic treatment or need treatment with removable appliances, have a history of taking antibiotics for the last three months and smoking habits or suffering from any systemic disease, generalized periodontal problems, cyst, clefts, or congenital malformation were excluded from the study. All patients were treated with preadjusted fixed appliances, with 0.022˝ x 0.028˝ slot brackets (MBT prescription, American Orthodontics, Sheboygan, WI, USA). Fixed appliances were placed on the buccal surfaces of teeth according to the specific needs for tooth movements and alignments either buccally, lingually, gingivally or occlusally. Brackets were placed in the centre of the middle third of the crown along the long axis of the tooth, bearing in mind the level and the contour of the gingival margins. The study did not obtain any confidential demographic information such as income or education level. Before starting the study, the objectives of the research were explained to the patients and their parents; a consent form was signed.


53 Orthodontie / Orthodontics Maxillary Cervical

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Central

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3x

Occlusal/Incisal

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Tooth number

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3

4

5

6

7

Mandibular Occlusal/Incisal

S

1x

Central

S

3x

Cervical

S

2x

Sub-Total OPI= Sum Total – Number of Teeth x 6 Table 1: Orthodontic plaque index (OPI) form. The number of stained sites is added and the total is multiplied by the corresponding factor.

Patients were strictly advised with oral hygiene measures before and during the entire course of the treatment. Clinical examination was conducted by one examiner (A.A) in the orthodontic clinic at King Abdul-Aziz Medical City, Riyadh, SA. The instruments used in the clinical examination were: - Plane dental mirror. - Michigan periodontal probe. - Metallic ruler with an accuracy of 1.0 mm. The following periodontal parameters were assessed for each participant: - O‘Leary plaque index (PI). - Orthodontic plaque index (OPI). - Gingival bleeding index (GBI). - Pocket depth (PD). To determine the O’Leary plaque index [14], plaque is disclosed with a chewable tablets and its amount estimated. To determine an individual’s score, the examiner multiplies the number of surfaces with plaque by 100 and divides that by the number of tooth surfaces examined (WHO, 2011) [15]. The orthodontic plaque index [16] was used to evaluate plaque level in the areas cervical to the bracket base and mesial and distal to the brac-

ket body considered the most critical zones of plaque accumulation. OPI was calculated using the formula shown in table 1. The factor used was: 1 for occlusalincisal; 2 for cervical and 3 for central. OPI was scored as: Good: 0-25 points. Average: 26-50 points. Poor: > 50 points. For the gingival bleeding index [17], all four surfaces of each tooth were assessed to determine whether probing elicited bleeding or not. The severity of gingivitis was expressed as a percentage calculated as follows: The pocket depth in the present study was probed using the Michigan periodontal probe. Probing was performed by inserting the probe gently into the gingival sulcus until the base of the pocket was reached. Pocket depth was assessed as the distance (mm) from the gingival margin to the bottom of the pocket. The probe was stepped around the tooth at about 1mm increments. The probe was kept as close as possible to axial direction of the tooth while the tip maintained in contact with the root surface. Probing was done on 6 points of each first molar, i.e, buccal, mesio-

buccal, disto-buccal, lingual, mesiolingual and disto-lingual. Periodontium was also evaluated and categorized into thick or thin on a site level. This evaluation was based on the transparency of the periodontal probe through the gingival margin while probing the sulcus at the midfacial aspect of both central maxillary incisors [18]. If the outline of the underlying periodontal probe could be seen through the gingiva, it was categorized as thin (score: 0); if not, it was categorized as thick (score: 1) [18]. Calculus deposits were removed prior to measuring pocket depths. Hand scaling was performed by examiner (A.A) in order to have a clean area while probing pocket depth. Examiner calibration Ten of the participants were examined on two occasions within one week interval by the same examiner (A.A) using the three indices (PI, GBI and OPI) to establish intra-examiner reliability. The kappa test was used to analyze the intra-examiner reliability and scored 70.4% for GBI, 78.7% for PI and 80% for OPI. For measurements made on a continuous scale such as pocket depth in millimeters, Pearson’s correlation


54

IAJD Vol. 5 – Issue 2

$UWLFOHVFLHQWLÀTXH_6FLHQWLÀF$UWLFOH Min.

Max.

Mean

PI

27.8

95.6

65.24 ± 16.43

GBI

5.2

43.8

19.14 ± 7.95

OPI

36.7

73.3

53,56 ± 8.74

Table 2: Mean values of PI, GBI and OPI obtained throughout the study.

test and paired t-test were used to evaluate the probing pocket depth at 240 registration points of both jaws. Paired t-test showed no statistically significant differences between the readings (p< 0.05) and the Pearson correlation test showed that the two readings were highly correlated. Statistical Analysis Mean, standard deviations and range for quantitative variables were computed using SPSS software for windows, version 15. One-way analysis of variance (ANOVA) was used to determine any significant difference at the 5% significance level (p< 0.05).

Results The study was performed with 50 patients (32 males (64%) and 18 females (36%)) undergoing fixed orthodontic treatment. Their age ranged between 12-26 years (mean age = 17.44 ± 3.073 years). The clinical examination of their periodontal status showed that the mean value of the PI was 65.24 ±16.43 while the GBI was 19.14 ± 7.95; the OPI was 53.56 ± 8.74 (Table 2). The patients were analyzed on the basis of the pocket depth on six different surfaces of the first molars. Table 3 presents the pocket depth probing at the first molars of the patients 6 months after the beginning of the orthodontic treatment. After 6 months of treatment, the probing pocket depth at the first molars was 1.5-2.0 mm. In some severe cases it exceeded 3mm.

Table 4 shows data of patients at 12 months of treatment. Pocket depth values were greater than those obtained at 6 months; values fell mostly in the range of 2.0-2.5mm. No significant difference was observed between male and female patients for PI (p=0.925) and for OPI (p=0.072). However, a significant difference was observed for the GBI (p=0.033) (Table5). When studying the correlation between the indices, we found no significant correlation between the OPI and the GBI (p=0.99) (Table 6).

Discussion The results of the current study showed a marked change in periodontal status after placement of fixed appliances. Similar results were reported by Naranjo et al.[19] who found that the placement of fixed appliances promoted the accumulation of the biofilm at the retentive sites and modified the ecological environment. The marked increase in plaque and gingival indices reflected the increase in bleeding and periodontal inflammation [19]. Dental plaque is the primary etiologic factor in gingivitis [20]; the plaque index and orthodontic plaque index were high in general, with a mean value of 65.24 for PI and 53.56 for OPI, respectively. This finding is in agreement with the previous studies reporting an increase in tooth surfaces displaying visible plaque following the placement of orthodontic appliances [21 -23]. This observation is due to the increase in plaque retentive areas and the inability of the patient to perform adequate oral hygiene [24].

The mean value of GBI was 19.14, which is considered reasonable. This result could possibly be due to the fact that 32% of the patients visited the hygienist during their orthodontic therapy. The values of the probing pocket depth increased with time. Similar age group has been studied by Zachirson et al. [25] with the data collected at pretreatment, 1 and 2 months after the beginning of the treatment showing an increase in pocket depth values after 2 months. The presence of fixed appliances with banded molars influences inflammation which is clearly related to the increase in pocket depth [26]. Pocket depth values obtained in our study were slightly higher than those reported by Kobayashi [27] because of many factors like oral hygiene measures, band positioning and over hanging materials. Inter-dental areas are especially more periodontally affected in orthodontic patients, as suggested by Baer et al. [28]. This increase reflects the accumulation of dental plaque on these surfaces and the difficulty for patients to maintain those areas free of plaque [28, 29]. In our study, the pocket depth increased significantly on mesial and distal sites. Zachrisson et al. [30] reported an increase in probing depth, gingival bleeding and a slight loss of attachment around teeth of patients who underwent orthodontic treatment with fixed appliances. In their study, the maximal record of probing depth was 2.34mm after 6 months (lower jawmesial sites), whereas in our study, the maximum recorded pocket depth


55 Orthodontie / Orthodontics

Tooth number

Probing site

16

26

36

46

Pocket depth values (mm) 1

1.5

2

2.5

3

3.5

Buccal

5

23

22

0

0

0

Mesio-buccal

7

20

17

6

0

0

Disto-buccal

7

15

19

7

2

0

Lingual

11

24

12

3

0

0

Mesio-lingual

3

20

19

6

2

0

Disto-lingual

6

16

16

10

2

0

Buccal

10

17

20

3

0

0

Mesio-buccal

5

20

15

10

0

0

Disto-buccal

7

15

14

11

3

0

Lingual

13

23

10

4

0

0

Mesio-lingual

8

17

17

8

0

0

Disto-lingual

8

22

14

6

0

0

Buccal

10

17

19

4

0

0

Mesio-buccal

5

24

14

7

0

0

Disto-buccal

8

16

18

5

3

0

Lingual

15

17

16

2

0

0

Mesio-lingual

5

23

18

4

0

0

Disto-lingual

8

15

22

5

0

0

Buccal

10

18

20

2

0

0

Mesio-buccal

6

18

13

11

2

0

Disto-buccal

8

15

12

12

3

0

Lingual

11

19

18

2

0

0

Mesio-lingual

5

23

16

6

0

0

Disto-lingual

6

19

18

5

2

0

Table 3: Prevalence of the different values of probing pocket depth at WKHVL[VLWHVDURXQGHDFKĂ&#x20AC;UVWPRODUVL[PRQWKVDIWHUWKHEHJLQQLQJ of the treatment.


56

IAJD Vol. 5 â&#x20AC;&#x201C; Issue 2

$UWLFOHVFLHQWLĂ&#x20AC;TXH_6FLHQWLĂ&#x20AC;F$UWLFOH

Tooth number

Probing site

16

26

36

46

Pocket depth values (mm) 1

1.5

2

2.5

3

3.5

Buccal

0

7

35

8

0

0

Mesio-buccal

0

4

29

17

0

0

Disto-buccal

0

5

20

23

2

0

Lingual

0

7

23

20

0

0

Mesio-lingual

0

6

16

21

7

0

Disto-lingual

0

5

23

16

6

0

Buccal

0

5

22

23

0

0

Mesio-buccal

0

7

25

18

0

0

Disto-buccal

0

4

20

26

0

0

Lingual

0

5

25

20

0

0

Mesio-lingual

0

6

21

23

0

0

Disto-lingual

0

5

19

26

0

0

Buccal

0

3

25

23

0

0

Mesio-buccal

0

4

21

25

0

0

Disto-buccal

0

2

15

25

8

0

Lingual

0

13

25

12

0

0

Mesio-lingual

0

6

31

13

0

0

Disto-lingual

0

6

28

16

0

0

Buccal

0

7

29

12

2

0

Mesio-buccal

0

5

17

26

1

1

Disto-buccal

0

7

17

21

5

0

Lingual

0

9

29

12

0

0

Mesio-lingual

0

10

26

12

2

0

Disto-lingual

0

6

27

16

1

0

Table 4: Prevalence of the different values of probing pocket depth DWWKHVL[VLWHVDURXQGHDFKĂ&#x20AC;UVWPRODUWZHOYHPRQWKVDIWHUWKH beginning of the treatment.


57 Orthodontie / Orthodontics Index

Sex

N

Mean

STD. DEV.

P Value

PI

M

32

65.4

16.76

0.925*

F

18

64.94

16.3

NS

M

32

20.78

8.49

0.33**

F

18

16.22

6.08

S

M

32

55.3

8.1

0.072*

F

18

50.46

9.2

NS

GBI

OPI

Table 5: Relationship between indices and gender. 161RWVWDWLVWLFDOO\VLJQLÀFDQW 66WDWLVWLFDOO\VLJQLÀFDQW

Index

OPI

GBI

Correlation

OPI

GBI

Pearson correlation

1.000

0.238

Sig. (2-tailled)

0.99

N

50

50

Pearson correlation

0.236

1.000

Sig. (2-tailled)

0.99

N

50

50

Table 6: Correlation between OPI and GBI.

after 6 months was 3mm. The scores remained almost unchanged after 12 months of treatment; only a slight increase of 0.5mm in some cases and sites was observed. These differences between the results obtained after 6 and 12 months don’t reflect any destructive disease that may have affected the periodontal tissues. Periodontal status in patients undergoing orthodontic treatment should be monitored carefully. Removable and fixed orthodontic appliances impede correct periodontal hygiene, resulting in more plaque accumulation, inflammation and bleeding. Therefore, appropriate oral hygiene methods and instruments should be used to control plaque. Powered and interdental toothbrushes, special types of floss and the use of mouthwashes have shown improved plaque control in orthodontic patients [31].

Conclusion Within the limitations of the present study, we found that during the orthodontic treatment, the plaque accumulation promoted by the fixed appliances was increased; this was reflected by a raise of the PI, OPI, GBI and the probing depth. Further histological studies are still needed in order to reveal the exact tissue alterations that might take place during the different phases of orthodontic treatments.


58

IAJD Vol. 5 â&#x20AC;&#x201C; Issue 2

$UWLFOHVFLHQWLĂ&#x20AC;TXH_6FLHQWLĂ&#x20AC;F$UWLFOH

References 1. Carranza FA, Newman MG, Glickmanâ&#x20AC;&#x2122;s I, Clinical Periodontology. 8th ed. Philadelphia, W.B. Sanders Co. 1996; ch1,4:pp12-16, 218-232. 2. El-Mangoury NH, Soheir Gaafar M, Yahiya Mostafa A. Mandibular anterior crowding and periodontal disease. Angle Orthod 1987;Jan:33-38.

19. Naranjo AA, Trivino ML, Jaramillo A, Betancourth M, Botero JE. Changes in the subgingival microbiata and periodontal parameters before and 3 months after bracket placement. Am J Orthod Dentofacial Orthop 2006;130:275 e17-22. 20. LĂśe H, Theilade E, Jensen SB. Experimental gingivitis in man. J Periodontal 1965;36:177-87.

3. Brandtzaeg P. Local factors of resistance in the gingival area. J Periodontal Res 1966;1:19â&#x20AC;&#x201C;42.

21. Buckley L. The relationship between malocclusion and periodontal disease. J Periodontol 1972;43(7):415-7.

4. Boyd YD, Baumrind S. Periodontal considerations in the use of bonds or bands on molars in adolescents and adults. Angle Orthod 1992;62:117â&#x20AC;&#x201C;26.

22. Geiger AM, Wasserman BH, Turgeon LR. Relationship of occlusion and periodontal disease. Part VIII. Relationship of crowding and spacing to periodontal destruction and gingival LQĂ DPPDWLRQ-3HULRGRQWDO  

5. 0DQVFKRW $ 2UWKRGRQWLFV DQG LQDGHTXDWH RUDO K\JLHQH compliance as a combined cause of localized gingival recession: a case report. Quintessence Int 1991;22(11):865-70. 6. *ZLQQHWW$-&KHHQ5)3ODTXHGLVWULEXWLRQRQERQGHGEUDFNHWV â&#x20AC;&#x201C; Scanning Microscope Study. Am J Orthod Dentofac Orthop 1979;75 (6):667-677. 7. MadlĂŠna M (2012). The importance and possibilities of proper oral hygiene in orthodontic patients. Orthodontics - Basic Aspects and Clinical Considerations, Prof. FaridBourzgui (Ed.), ISBN: 978-953-51-0143-7, InTech, DOI: 10.5772/30939. Available from:http://www.intechopen.com/books/orthodontics-basicaspects-and-clinical-considerations/the-importance-andpossibilities-of-proper-oral-hygiene-in-orthodontic-patients. 8. /XVWHUPDQ ($ &OLQLFDO VLJQLĂ&#x20AC;FDQFH RI SHULRGRQWLF RUWKRGRQWLF interrelationships. N. Y. State Dent J 1974;40:147â&#x20AC;&#x201C;156. 9. Kessler M. Interrelationships between orthodontic periodontics. Am J Orthod 1976;70:154â&#x20AC;&#x201C;177.

and

10. Artun J, Urbye KS. The effect of orthodontic treatment on periodontal bone support in patients with advanced loss of marginal periodontium. Am J Orthod Dentofacial Orthop 1998;93:143-8.

23. /XQGVWU|P ) +DPS 6( 1\PDQ 6 6\VWHPDWLF SODTXH FRQWURO in children undergoing long-term orthodontic treatment. Eur J Orthod 1979;2(1):27-39. 24. Hamp SE, LundstrĂśm F, Nyman S. Periodontal conditions in adolescents subjected to multiband orthodontic treatment with controlled oral hygiene. Eur J Orthod 1982;4(2):77-86. 25. Zachrisson BU, Alnaes L. Periodontal condition in orthodontically treated and untreated individuals. Loss of attachment, gingival pocket depth and clinical crown height. The Angle Orthodontist 1973;43(4):402-11. 26. Di Murro C, Paolantonio M, Petti S, Tomassini E, Festata F, Grippaudo C et al. The clinical and microbiological evaluation RI WKH HIĂ&#x20AC;FDF\ RI RUDO LUULWDWLRQ RQ WKH SHULRGRQWDO WLVVXHV RI SDWLHQWV ZHDULQJ Ă&#x20AC;[HG RUWKRGRQWLF DSSOLDQFHV 0LQHUYD Stomatologica 1992;41:499-506. 27. Kobayashi Ly, Ash MM Jr. A clinical evaluation of an electric toothbrush used by orthodontic patients. Angle Orthod 1964;34:209-19. 28. Baer PN, Coccaro PJ. Gingival enlargement coincident with orthodontic therapy. J Periodontol 1964;35:436-9.

11. Bollen AM. Effect of malocclusions and orthodontics on periodontal health: Evidence from a systematic review. J Dent Educ 2008;72(8):912-8.

29. Nunn ME. Understanding the etiology of periodontitis: An overview of periodontal risk factors. Periodontal 2000 2003;32:11-23.

12. Danann A. An update on periodontic â&#x20AC;&#x201C; orthodontic interrelationships. J Indian Soc Periodontol 2010;14(1):66-71.

30. Zachrisson S, Zachrisson BU. Gingival condition associated with orthodontic treatment. Angle Orthod 1972;42(1):26-34.

13. =KDR+;LH<0HQJ+(IIHFWRIĂ&#x20AC;[HGDSSOLDQFHRQSHULRGRQWDO status of patients with maloclusion. Zhonghua Kou Qiang Yi Xue Za Zhi 2000;35(4):286-8.

31. Diedrich P, Rudzki-Janson I, Wehrbein H, Fritz U. Effect of orthodontics bands on marginal periodontal tissues. A histological study on two human species. J Orofac Orthop 2001;62:146-56.

14. 2¡/HDU\7-'UDNH5%1D\ORU-(7KHSODTXHFRQWUROUHFRUG- Periodontol 1972;43(1):38. 15. :+22UDO+HDOWK&RXQWU\$UHDSURĂ&#x20AC;OHSURJUDP -XO\  7KH SODTXH FRQWURO UHFRUG 2¡/HDU\ 7 'UDNH 5 7D\ORU   August 23, 2011. Available from: http://www.mah.se/capp/ PHWKRGVBDQGBLQGLFHVRUDOK\JLHQHLQGLFHVSODTXH FRQWUROB record. 16. Heintze SD, Jost-Brinkmann PG, Finke C, Miethke RR. OrthoSODTXH LQGH[ ,Q RUDO KHDOWK IRU WKH RUWKRGRQWLF SDWLHQW Chicago: Quintessence: 1999; pp.67-70. 17. Ainamo J, Bay I. Problems and proposals for recording gingivitis DQGSODTXH,QW'HQW-   18. Kan J, Rungcharassaeng K, Umezu K, Kois J. Dimensions of peri-implant mucosa: an evaluation of maxillary anterior single implants in humans. J Periodontol 2003;74(4):557-562.


59

ARTICLE SCIENTIFIQUE / SCIENTIFIC ARTICLE

Introduction

Pédodontie / Pedodontics

PREVALENCE OF HYPODONTIA IN PERMANENT DENTITION IN A SAMPLE OF SUDANESE UNIVERSITY STUDENTS Amal Abu Affan* | Abeer Serour** Abstract The congenital absence of one or more permanent teeth is a common dental anomaly. It can seriously affect a young person, both physically and emotionally, particularly when the missing tooth is located in the anterior region of the maxillary dental arch. The aim of the present descriptive cross-sectional study was to evaluate the prevalence of hypodontia of the permanent dentition and to determine the most common congenitally missing permanent teeth in a sample of 2401 Sudanese university students. A total of 100 congenitally missing teeth were observed in 64 students (7 males and 57 females); the overall prevalence of hypodontia in permanent dentition was 2.66% (2.69% in males, 2.66% in females). Hypodontia was more prevalent in the mandible (61%) than in the maxilla (39%) and in the left side of the jaws (55%) than in the right side (45%). The most common congenitally missing permanent tooth was the mandibular lateral incisor (23%), followed by the maxillary lateral incisor (19%), the mandibular 2nd premolar (18%) and the maxillary 2nd premolar (17%). The present study results give a clue of the magnitude of the problem. However, strong conclusion cannot be drawn since the sample studied is not representative to the whole Sudanese community. Further studies are required with a large sample collected from the different provinces of the Sudan.

Résumé L’absence congénitale d’une ou de plusieurs dents permanentes est une anomalie dentaire commune. Elle peut gravement affecter un adolescent, à la fois esthétiquement et émotionnellement, en particulier lorsqu’il s’agit d’une dent antérieure. Le but de cette étude descriptive transversale était d’évaluer la prévalence de l’hypodontie de la dentition permanente dans un échantillon de 2401 étudiants soudanais et de déterminer les dents les plus incriminées. Un total de 100 dents congénitalement absentes a été observé chez 64 étudiants (57 femmes et 7 hommes). La prévalence globale de l’hypodontie de la dentition permanente était de 2,66 % (2,69% chez les hommes et 2,66% chez les femmes). L’hypodontie était plus fréquente à la mandibule (61 %) et dans la partie gauche de la mâchoire (55%). L’incisive mandibulaire latérale (23%) était la dent la plus fréquemment absente, suivie par l’incisive latérale maxillaire (19%), la 2ème prémolaire inférieure (18%) et la 2ème prémolaire maxillaire (17%). Les résultats de la présente étude donnent une idée de la fréquence de cette anomalie. Cependant, une conclusion ne peut être tirée puisque l’échantillon étudié n’est pas représentatif de l’ensemble de la communauté soudanaise. Des études épidémiologiques avec des échantillons plus larges menées dans les différentes provinces du Soudan sont nécessaires; elles permettront une meilleure appréciation de cette anomalie.

Keywords: Hypodontia – congenitally missing tooth – permanent dentition.

Mots- clés: hypodontie - absence congénitale de dent – dentition permanente.

* Associate Professor Head Dept of Orthodontic, Pedodontic and Preventive dentistry, University of Khartoum, Sudan amalabuaffan@yahoo.com

** BDS, MSc in Orthodontics,

Head Dept of Orthodontic clinic, Military Dental Hospital, Khartoum, Sudan


60

IAJD Vol. 5 – Issue 2

$UWLFOHVFLHQWLÀTXH_6FLHQWLÀF$UWLFOH

Introduction Congenitally missing teeth is the most common developmental dental anomalies in humans [1]. Many terms were used to describe this phenomenon: oligodontia, anodontia, aplasia of teeth, absence of teeth, agenesis of teeth and lack of teeth; however, hypodontia is the most frequently used. The term hypodontia is used when one to six teeth (excluding the third molars) are missing; oligodontia refers to the situation when more than six teeth (excluding the third molars) are missing. Anodontia denotes the complete absence of teeth. Anodontia and oligodontia are rarely used [2, 3]. Hypodontia can occur in an isolated mode, caused by local factors that can disrupt the normal development of the permanent dentition. These factors include early irradiation of the tooth germ, hormonal and metabolic influences, trauma, and osteomyelitis. Hypodontia can also occur as a symptom of more generalized systemic conditions such as ectodermal dysplasia, cleft lip and palate, Down syndrome, ….[3]. Although tooth agenesis is caused by environmental factors in the majority of cases, hypodontia has a genetic basis. A familial hypodontia is an autosomal dominant inheritance with incomplete penetrance and variable expressivity. An autosomal recessive mode of inheritance is also possible [4-5]. In general, if one or few teeth are missing, the absent tooth will be the most distal tooth of any given type, i.e., lateral incisors, second premolars and third molars. Whereas congenitally missing canine is an unusual condition [2]. The prevalence of hypodontia in the permanent dentition ranged between 4 to 11.3% depending on the investigated populations and the samples ‘size [6-24]. It was found to be more frequent among females than males [11-14]. The most commonly missing teeth were the mandibular second premolars [6, 8, 18-21, 23, 24] and the maxillary

lateral incisors [9, 11, 12, 14, 17]. The missing teeth were more often absent on the maxillary arch than on the mandibular arch [9] and on the right side than on the left side within the dental arch [17]. The congenital absence of teeth can seriously affect a young person, both physically and emotionally particularly when the missing tooth is located in the anterior region of the mouth [1]. Early detection of hypodontia may allow a more favorable prognosis and minimal functional, esthetical and psychological complications [25]. The treatment options available for cases with congenitally missing teeth are the maintenance of the primary teeth, orthodontic space closure, space maintenance, restoration with adhesive or fixed denture, tooth transplantation, dental implant or orthodontics space redistribution to facilitate the prosthetic treatment [26]. Patients with congenitally missing teeth present a clinical challenge to the general dental practitioners and the orthodontists alike. Successful management of these patients necessitates a multidisciplinary approach (orthodontics, restorative dentistry, oral surgery) [27- 29]. No study has been yet conducted to assess the prevalence of hypodontia in Sudan. The aim of the present study was to create baseline information by evaluating the prevalence of hypodontia of the permanent dentition in a sample of a Sudanese’s university students.

Materials and Methods A descriptive cross-sectional study was carried out in the medical campus at the University of Khartoum, Sudan, during the period ranging from February 2012 to December 2012. Ethical approval was obtained from the research committee at the Faculty of Dentistry; written consent was obtained from each medical student participating in the study. The students who are Sudanese and with no history of orthodontic treat-

ment, extractions or previous tooth loss caused by trauma or periodontal problem were selected according to a random stratified sampling technique with probability proportional to size. The total number of students in the medical campus at the University of Khartoum was obtained from the students’ affairs office. The initial screenings for the selected students were carried out in the day light. The permanent teeth were considered to be congenitally missing if they didn’t erupt, were not radiographically assessed and were not previously extracted. All students with missing permanent teeth or retained deciduous teeth were referred to the orthodontic department for further investigations: personal data and history, clinical examination and radiographic investigation. Orthopantomograms or periapical x-rays were taken for every student by a well-trained technician at the Department of Radiology, Faculty of Dentistry, University of Khartoum, Sudan. The panoramic radiographs were taken using Cranex 3+ Cephalostat (Orion corporation soredex™) using extraoral films (Kodak MXG green sensitive). Students were positioned properly using the headpositioning devices and light beam marker positioning guides. The teeth were positioned to lie within the focal trough [30].

Statistical analysis The statistical package for social sciences (SPSS) computer program -version 15- was used for statistical analysis; chi-square test was used for data analysis. The level of significance was at p<0.05.

Results 2401 medical students (260 males and 2141 females) participated in the present study. Ninety-eight out of 2401 students had unerupted permanent teeth. Radiographic investigations


61 PĂŠdodontie / Pedodontics

Fig. 1: Distribution of congenitally missing permanent teeth in the maxilla and mandible.

Fig. 2: Distribution of congenitally missing permanent teeth in the left and right sides.

Congenitally missing teeth

Fig. 3: Percentage of students with hypodontia.

Maxillary arch

Mandibular arch

Females

Males

Total

Females

Males

Total

Right central incisor

0

0

0

4

1

5

Left central incisor

0

0

0

2

1

3

Right lateral incisor

10

0

10

7

1

8

Left lateral incisor

9

0

9

14

1

15

Left canine

0

0

0

1

0

1

Right 1st premolar

1

0

1

3

0

3

Left 1st premolar

2

0

2

7

0

7

Right 2nd premolar

8

1

9

6

3

9

Left 2nd premolar

8

0

8

5

4

9

Right 1st molar

0

0

0

1

1

Table1: Distribution of congenitally missing permanent teeth in the maxillary and mandibular arches.

0


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IAJD Vol. 5 – Issue 2

$UWLFOHVFLHQWLÀTXH_6FLHQWLÀF$UWLFOH Authors

Country

Sample size

Prevalence

Most common congenitally missing teeth

González-Allo et al. [6]

Portugal

2888

6.1%

Mandibular 2nd premolar

Mammon [7]7

Jordan

3660

8.85%

Young Ho [8]

Korea

3055 9-30yrs

11.3%

Mandibular 2nd premolar

Vahid-Dastjerdi et al. [9]

Iran

1751

9.1%

Maxillary lateral incisor

Tallón-Walton et al. [10]

Spain

1518

9.48%

Celikoglu et al. [11]

Turkey

3341

4.6%

Maxillary lateral incisor

Gomes et al. [12]

Brazil

1049

6.3%

Maxillary lateral incisor

Al-Ajwadi [13]

,UDT

389

Sisman et al. [14]

Turkey

2413

7.54%

Maxillary lateral incisor

Albashaireh & Khader [15]

Jordan

1045

5.5%

Mandibular 2nd premolar

Goren et al. [16]

Israel

226

5.3%

Maxillary lateral incisor

Fekonja [17]

Slovenia

212

11.3%

Maxillary lateral incisor

Polder et al. [18] (Meta-analysis)

Upper lateral incisor Mandibular 2nd premolar

Males 4.6% 5.5%

-Europe -Australia -North America

Females 6.3% 7.6%

3.2%

4.0%

Goya et al. [19]

Japan

2072

9.4%

Mandibular 2nd premolar

Ng’ang’a et al. [20]

Kenya

615

6.3%

Mandibular 2nd premolar

Al-Emran [21]

Saudi Arabia

500

4%

Mandibular 2nd premolar

Davis [22]

China

1093

6.9%

Mandibular incisor

Rølling [23]

Denmark

3325

7.8%

Mandibular 2nd premolar

Magnússon [24]

Iceland

1116

6.7%

Mandibular 2nd premolar

Abu Affan & Serour

Sudan

2401

2.66%

Mandibular lateral incisor

Table 2: Prevalence of hypodontia of permanent dentition in previous studies.

were carried out for 85 students; four students dropped out from the study. The results showed that 64 students (7 males, 57 females) out of 2401 had hypodontia (2.66%). 21 students (0.87%) had impacted permanent teeth. Male to female ratio with hypodontia was 1:8.3 although the incidence of hypodontia was found more or less the same in males (2.69%) and in females (2.66%). No statisti-

cally significant difference was noted between gender (p>0.05). A total of a one hundred congenitally missing teeth were found among the 64 students; 13 teeth in males and 87 teeth in females. Congenitally missing permanent teeth were more frequent in the mandible (61%) than in the maxilla (39%) (Fig.1). Moreover, hypodontia was more frequent in the left side (55%) than in the right side

(45%) of the maxillary and mandibular arches (Fig. 2). The majority of the students had one congenitally missing permanent tooth (tooth #36) (56.25%), followed by two congenitally missing permanent teeth (tooth #23) (35.94%). Two students (3%) had three congenitally missing permanent teeth. More than three missing teeth were observed among three students (4.6%). When


63 Pédodontie / Pedodontics the percentage of students with hypodontia was compared to the number of missing permanent teeth, a statistically significant difference was noted, indicating that hypodontia with one or two missing teeth is more common than multiple missing teeth (p<0.05). The most common congenitally missing permanent tooth was the mandibular lateral incisor (23%), followed by the maxillary lateral incisor (19%), the mandibular second premolar (18%) and the maxillary second premolar (17%) (Table 1). The results in the present study showed that 74% of the second premolar hypodontia was associated with retention of the deciduous second molar. Also, 5% of retained deciduous incisors were correlated with the absence of their permanent counterpart. When the deciduous canine was retained, the permanent canine was often present and impacted.

Discussion Although the percentage of dental anomalies has been reported in many countries, there has been no data published among Sudanese population about the prevalence of hypodontia in the permanent dentition. The present study aimed to determine the overall prevalence of hypodontia in a sample of Sudanese medical students at Khartoum University. The prevalence of hypodontia ranged between 4% and 11.3% [6-24]. However, in the present study, the overall prevalence of hypodontia was found to be 2.66%. The observed discordance can be attributed to the genetic and racial differences as well as to the sample size of the examined group. In the literature, the lowest percentages of hypodontia were reported by Al-Emran [21] in a sample of 500 Saudis male children (4%) and by Celikoglu et al. [11] who examined Turkish orthodontic patients (4.6%). A high prevalence of hypodontia was found in the mandibular arch compared to the maxillary arch; this was in contrast to the findings of Vahid-

Dastjerdi et al. [9] who obtained a higher prevalence of hypodontia in the maxillary arch among Iranian orthodontic patients. The prevalence of hypodontia in the left side of the jaw was found to be more frequent than hypodontia in the right side in our study. However, Fekonja [17] reported a higher prevalence on the right side of the jaw among 212 orthodontically treated children. This variation may be attributed to the study sample size and the racial background. No gender dimorphism in the prevalence of hypodontia was reported among different populations. Although there was a difference in the sample size between males and females in the present study, this prevalence wasn’t statistically different. These findings coincide with those of previous studies [6, 7, 9, 12, 15]. However others [11, 13, 18, 19, 22, 23] recorded a high prevalence of hypodontia among females. On the other hand Ng’ang’a et al. reported that in Kenyan population hypodontia was more predominant among males than females [20]. In the present study, the percentage of congenitally missing one or two permanent teeth was reported among 90% of the Sudanese students (56% missing one single tooth and 34% missing two teeth). In Slovenia, comparative results (87.7%) were reported by Fekonja [17] among treated children sample. However, a higher prevalence for two- teeth hypodontia (58.5%) was observed compared to one-tooth hypodontia (29.2%). None of the participants in the present study showed oligodontia. According to Celikoglu [11], the prevalence of oligodontia in Turkish population was 0.3% and 0.16% among Danish school students [23]. Previous published results revealed that the most common congenitally missing teeth were either the maxillary lateral incisor [12, 14, 16, 17], the mandibular second premolar [15, 19, 20, 23, 24] or the mandibular incisor [20]. In contrast, the present results showed that the most common

congenitally missing tooth was the mandibular lateral incisor, followed by the maxillary lateral incisor and the maxillary and mandibular second premolars. This difference can be related to ethnic and racial differences in the studied populations.

Conclusion Although this study was carried out in a randomly selected sample of Sudanese university students, the results reflect the importance of the problem. However, the sample size was small and not representative of the entire Sudanese population. That’s why the obtained results cannot be generalized. Additional studies including larger, representative samples specifying most tribes of Sudanese population are necessary to determine the overall prevalence of hypodontia of permanent dentition among Sudanese population.


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IAJD Vol. 5 â&#x20AC;&#x201C; Issue 2

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References 1. 9DOOH $/ /RUHQ]RQL )& 0DUWLQV /0 9DOOH &90 +HQULTXHV JFC, Almeida ALPF et al. A multidisciplinary approach for the management of hypodontia: Case report. J Appl Oral Sci 2011;19:544-48. 2. 3URIĂ&#x20AC;W : )LHOGV + 6DYHU ' &RQWHPSRUDU\ 2UWKRGRQWLFV WK Edition St Louis; Mosby 2007;135-6,467-71. 3. Larmour C, Mossey P, Thind B, Forgie A, Stirrups D. Hypodontia: A retrospective review of prevalence and etiology. Part I. Quintessence Int 2005;36(4):263-70. 4. $KPDG:%UDQFROLQL9XO)DL\D]0)/DP+XO+DTXH6+DLGHU M, et al. A locus for autosomal recessive hypodontia with DVVRFLDWHG GHQWDO DQRPDOLHV PDSV WR FKURPRVRPH T Am J Hum Genet 1998;62:987â&#x20AC;&#x201C;91. 5. Pirinen S, Kentala A, Nieminen P, Varilo T, Thesleff I, Arte S. Recessively inherited lower incisor hypodontia. J Med Genet 2001;38:551â&#x20AC;&#x201C;6. 6. GonzĂĄlez-Allo A, Campoy MD, Moreira J, et al. Tooth agenesis in a Portuguese population. Int Orthod 2012 Jun 10(2):198-210. 7. Mamoon M. Dental anomalies in children in North Jordan. Pakistan Oral & Dental J 2011;31(2):309-13. 8. Young Ho K. Investigation of hypodontia as clinically related dental anomaly: Prevalence and characteristics. ISRN Dentistry 2010;(2011):246135.

16. Goren S, Tsoizner R, Dinbar A, Levin L, Brezniak N. Prevalence of congenitally missing teeth in Israeli recruits. Refuat Hapeh Vehashinayim 2005;22(2):49-53. 17. Fekonja F. Hypodontia in orthodontically treated children. Euro J Orthod 2005;27(5):457-60. 18. Polder BJ, Vant Hof MA, Van der Linden FPGM, KuijpersJagtman J. More women in Europe and Australia have dental agenesis than their counterparts in North America. EvidenceBased Dentistry 2005;6(1):22â&#x20AC;&#x201C;3. 19. Goya HA, Tanaka S, Maeda T, Akimoto Y. An orthopantomographic study of hypodontia in permanent teeth of Japanese pediatric patients. J Oral Sc 2008;50(2):143-50. 20. Ngâ&#x20AC;&#x2122;angâ&#x20AC;&#x2122;a RN, Ngâ&#x20AC;&#x2122;angâ&#x20AC;&#x2122;a PM. Hypodontia of permanent teeth in a Kenyan population. East African Medical Journal 2001;78(4):200â&#x20AC;&#x201C;203. 21. Al-Emran S. Prevalence of hypodontia and developmental malformation of permanent teeth in Saudi Arabian schoolchildren. Br J Orthod 1990;17(2):115-18. 22. Davis P. Hypodontia and hyperdontia of permanent teeth in Hong Kong school children. Community Dent Oral Epidemiol 1987;15:218-20. 23. Rolling S. Hypodontia of permanent teeth in schoolchildren. Scand J Dent Res 1980;88(5):365-9.

Danish

9. Vahid-Dastjerdi E, Borzabadi-Farahani A, Mahdian M, Amini N. Non-syndromic hypodontia in an Iranian orthodontic population. J Oral Sc 2010;52(3):455-61.

24. Magnusson TE. Prevalence of hypodontia and malformations of permanent teeth in Iceland. Community Dent Oral Epidemiol 1977;5:173â&#x20AC;&#x201C;8.

10. TallĂłn-Walton V, Nieminen P, Arte S, Carvalho-Lobato P, UstrellTorrent J, Manzanares-CĂŠspedes C. An epidemiological study of dental agenesis in a primary health area in Spain: Estimated prevalence and associated factors. Med Oral Patol Oral Cir Bucal 2010;15(4):e569-74.

25. Popa M, Dinu S, Bratu E. Interceptive treatment in hypodontia. Jurnalul Pediatrului 2010;10:43-46.

11. Celikoglu M, Kazanci F, Miloglu O, Oztek O, Kamak H, Ceylan , )UHTXHQF\ DQG FKDUDFWHULVWLFV RI WRRWK DJHQHVLV DPRQJ DQ orthodontic patient population. Med Oral Patol Oral Cir Bucal 2010;15:797-801. 12. Gomes RR, Calaça da Fonseca JA, Paula LM, Faber J, Acevedo AC. Prevalence of hypodontia in orthodontic patients in Brasilia, Brazil. European Journal of Orthodontics 2009;32(2010):302â&#x20AC;&#x201C;6. 13. Al-Ajwadi S. An orthopantomographic study of hypodontia in SHUPDQHQWWHHWKRI,UDTLSDWLHQWV0'-   14. Sisman Y, Uysal T, Gelgor IE. Hypodontia. Does the prevalence and distribution pattern differ in orthodontic patients? European Journal of Dentistry 2007;1(3):167-73. 15. Albashaireh Z, Khader Y. The prevalence and pattern of hypodontia of the permanent teeth and crown size and shape deformity affecting upper lateral incisors in a sample of Jordanian dental patients. Community Dent Health 2006;23(4):239-43.

26. Hobson RS, Carter NE, Gillgrass TJ, Jepson NJ, Meechan JG, Nohl F, Nunn JH. The Interdisciplinary management of hypodontia the relationship between an interdisciplinary team and general dental practitioner. Br Dent J 2003;194(9):479-82. 27. Lazzara R et al. Retrospective multicenter analysis of 3i HQGRVVHRXVGHQWDOLPSODQWVSODFHGRYHUDĂ&#x20AC;YH\HDUSHULRG&OLQ Oral Implant Res1996;7(1) :76-84. 28. .LU]LRĂšOX = 6HQWXW 7. 2]D\ (UWÂ UN 26 .DUD\LOPD] + &OLQLFDO features of hypodontia and associated dental anomalies: a retrospective study. Oral Diseases 2005;11:399â&#x20AC;&#x201C;404. 29. Ting-Ling C. Prosthodontic treatment of hypodontia. Cda. Journal 2006;34(9):727-33.

patients

with


REVUE DE LA LITTÉRATURE / LITERATURE REVIEW

Prothèses Fixées / )L[HG3URVWKRGRQWLFV

SELF-ADHESIVE CEMENTS AND ALL CERAMIC CROWNS: A REVIEW Foudda Homsy * | Elie Daou ** | Maha Ghotmi *** | Mireille Rahi *** Abstract Adhesive bonding techniques and modern all-ceramic systems offer a wide range of highly esthetic treatment options. The inherent brittleness of some ceramic materials and certain clinical situations require resin bonding of the restoration to the tooth for long-term clinical success. A surface pretreatment of the ceramic and the tooth is necessary to obtain a good adhesion. The clinician faces many problems when luting restorations such as the choice of the appropriate agent depending on the restoration material, the technique sensitivity and the necessity of applying different luting materials. To overcome some of the disadvantages of the conventional and resin cements, self-adhesive cements were introduced to the market. They do not require any pretreatment of the tooth surface and their application is accomplished in a single clinical step. A wide literature review was conducted, through a MEDLINE search. Articles that treat self-adhesives properties were selected. According to in vitro studies, self-adhesive cement adhesion to dentin and to all-ceramic materials is satisfactory and comparable to other multistep resin cements. Randomized clinical trials and long-term in vitro studies are necessary prior to any recommendation regarding their use. Keywords: Self-adhesive cement - bonding all-ceramic restoration - resin cement.

Résumé Les techniques de collage et les systèmes d’adhésifs modernes offrent un large éventail d’options de traitements esthétiques. Dans certaines situations cliniques, la fragilité inhérente à certains matériaux en céramique exige le collage de la restauration à la dent à l’aide d’un ciment à base de résine pour une meilleure pérennité. Un traitement préalable de la surface de la céramique et de celle de la dent est nécessaire pour obtenir une bonne adhérence. Le clinicien est confronté à de nombreux problèmes lors du collage des restaurations tels que le choix de l’agent approprié en fonction du matériau de restauration et la nécessité de procéder souvent par étapes. Pour pallier à certains inconvénients des ciments conventionnels, des ciments auto-adhésifs ont été introduits sur le marché. Ces derniers ne nécessitent pas un traitement préalable de la surface dentaire et ils sont appliqués en une seule étape. Une revue de la littérature a été réalisée par une recherche sur MEDLINE. Les articles qui traitent des ciments auto- adhésifs ont été sélectionnés. Selon les études obtenues, l’adhésion du ciment auto-adhésif à la dentine et aux restaurations en céramique est satisfaisante et comparable aux autres ciments en résine conventionnels. Des essais cliniques randomisés et de long-terme sont nécessaires avant toute recommandation concernant l’utilisation des ciments auto-adhésifs. Mots-clés: ciment auto-adhésif - ciment à base de résine.

* BDS, DESS Dpt of Prosthodontics Dental Faculty, Lebanese University, Lebanon loubab3@hotmail.com

** DESS,

Chef de Clinique, Dpt of Prosthodontics Dental Faculty, Lebanese University, Lebanon

*** BDS, DESS

Dpt of Prosthodontics Dental Faculty, Lebanese University, Lebanon

**** BDS, DUA,

DUB in Prosthodontics


66

IAJD Vol. 5 – Issue 2

5HYXHGHODOLWWpUDWXUH_/LWHUDWXUH5HYLHZ

Introduction To fulfill patients’ expectations, dental biomaterials must have a highly aesthetic appearance comparable to that of natural teeth as well as good mechanical properties [1]. This explains the professionals’ growing interest for all-ceramic restorations [1, 2]. On the other hand, successful bonding of the luting material to both the restorative material and the tooth structure is imperative for the retention and longevity of the restoration [3]. Obtaining adhesion between a luting agent and a ceramic surface requires surface pretreatment [4, 5] such as etching, priming and bonding [6-9]. Until recently, resin cements were divided into two subgroups according to the adhesive system used to prepare the tooth prior to cementation. One group utilizes etch-and-rinse adhesive systems (example: RelyX™ ARC, 3M ESPE, St. Paul, Minn). The second group uses self-etch primer (example: Panavia™ F, Kuraray Medical Inc, Tokyo, Japan) [10, 11]. Multistep luting materials make the procedure technique-sensitive [11]. In-vitro studies on the shear bond, the microtensile bond and the long-term durability of the resin cement on the tooth substrate and the ceramic restoration demonstrated that the bond strength was impaired when the surface treatment was insufficient [12-50]. Bonding to traditional silica-based ceramics is a predictable procedure yielding durable results when fabricants ’guidelines are respected [51-63]. However, the composition and physical properties of high-strength ceramic materials, such as aluminum oxide (Al2O3) [64-72] and zirconium oxide (ZrO2) ceramics [73-76] differ substantially from silica-based ceramics and require alternative bonding techniques to achieve a strong and durable resin bond [28, 29, 54, 61]. An ideal dental adhesive must be biocompatible and resistant to microleakage [2, 12]. The cement should also provide a durable bond between

dissimilar materials, possess favorable compressive and tensile strengths, have sufficient fracture toughness to prevent dislodgment as a result of interfacial or cohesive failures [13, 14], be able to wet the tooth and the restoration surfaces, exhibit adequate film thickness and viscosity to ensure complete seating [12-15], exhibit minimal solubility in the oral cavity [13, 14, 16] and demonstrate adequate working and setting times [12-15]. The dental adhesive should also enhance the fracture resistance of the full-ceramic crowns [2, 13, 17] and ensure adequate marginal adaptation [18]. Resin cements are composites that consist of a resin matrix, eg bis-GMA or urethane dimethacrylate, and a filler of fine inorganic particles. Bonding of resin-based composite materials to tooth hard tissues has been simplified recently [11]. Even though enamel and dentin bonding has progressed from the first to the current seventh-generation adhesives, bonding to dentin remains less predictable than bonding to enamel [19-21]. All luting agents required the application of one of these adhesive systems to prepare the tooth prior to cementation [6, 19, 22, 23]. This multistep procedure and the performance of the etch-and-rinse or self-etch adhesive itself can influence the bonding effectiveness [11, 24]. To overcome some of the shortcomings of both conventional and resin cements, resin-based self-adhesive cements were introduced in 2002 as a new subgroup of resin cements. The goal was to present the favorable characteristics of different classes (total etch, self-etch) in a single product [10]. This new category of cements does not require any surface treatment of the teeth or restorations and provides effective bond strength [3, 8, 13, 26, 27]. Self-adhesive cements aim to combine the favorable properties of conventional (zinc phosphate, glass ionomers and polycarboxylate cements) and resin luting agents [10, 16]. In fact, it is reported that selfadhesive resin cements provide the

equivalent bond strength of conventional resin cements to dentin [19, 23], gold alloy and glass ceramics [34] and zirconia [35, 36]. Attar et al. [38] demonstrated that resin-based cements that rely on the application of etch-and-rinse adhesive systems have greater flexural strength than conventional resin cements; different studies found lower bond strengths [11, 23]. Due to its simplified application technique, the first self-adhesive cement introduced to the market (RelyX™ Unicem; 3M ESPE, St. Paul, Minn) rapidly gained popularity among clinicians [11]. Thus, several brands developed self-adhesive cements (RelyX™ Unicem; RelyX™ U100; 3M ESPE, St. Paul, Minn; SmartCem® 2 Dentsply Caulk, Milford; G-Cem™, GC America, Inc, Alsip, Ill; Maxcem Elite™ (Kerr Corp, Orange, Calif) ; SeT (SDI Ltd, Bayswater, Australia); SACH, SAC-A (Kuraray Medical, Tokyo,…) (Table 1). Regarding their composition, self-adhesive cements are based on phosphoric-acid methacrylates that demineralize and infiltrate the tooth substrate, resulting in micromechanical retention. Secondary reactions have been suggested to provide chemical adhesion to hydroxyapatite [10, 32]. The basic inorganic fillers are able to undergo a cement reaction with the phosphoric-acid methacrylates. The dominant setting reaction starts with free radical polymerization, which can be initiated either by light or by a redox system (dual-curing composite materials) [3, 32]. The purpose of this literature review is to evaluate the reliability of self-adhesive luting agents when used with all-ceramic crowns and compare them to the conventional etch-andrinse and self-etching luting agents.

Materials and Methods A broad systematic search of English dental litterature was initiated. Keywords or phrases included: silica-based ceramics, aluminum oxide ceramics, zirconium oxide cera-


67 Prothèses Fixées / )L[HG3URVWKRGRQWLFV mics, dental cements, composite resin cements, adhesives, total-etch adhesives, self-etch adhesives, self-adhesives, RelyX™ Unicem, BisCem®, Breeze™, G-Cem®, Maxcem Elite™, Monocem®, Clearfil, Embrace, Multilink® Sprint, SmartCem®, SeT and iCEM®. Peer-reviewed articles published in English between 1976 and 2010 were identified through a MEDLINE search (Pubmed and Elsevier) as well as a hand search of relevant textbooks and annual publications.

Results Of the retrieved articles, articles on the bonding to silica-based ceramics [22, 44, 76], on the bonding to aluminium oxide ceramics [34, 58, 76] and on the bonding to zirconium oxide ceramics [30, 34-36, 72] were selected. Additional references were included to accompany statements of facts [1, 21, 23-71, 73-76]. RelyX™ Unicem was the most thoroughly investigated self-adhesive while one article investigated other currently marketed self-adhesive cements. Two main subjects were treated: bonding to tooth structure and bonding to ceramics. Bonding to tooth structure Dental cement acts as a barrier against microbial leakage, sealing the interface between the tooth and the restoration [16, 33]. This attachment may be mechanical, chemical, or a combination of both [15, 34]. Research has also shown that leakage may occur even with successful bonding, or that shrinkage may cause cohesive fracture of tooth structure although the bond is preserved [36]. However, it is well established that the cementing agent used for bonding influence microleakage [35]. Enamel and dentin are dissimilar in composition and structure. The resin tags mainly determine the adhesive performance of the enamel bond [37] and the penetration of the resin

cement in the microporosities forms a well-accepted micromechanical bond [20, 38]. The bond between the cementing agent and the dentinal hard tissue is compromised by the tubular microstructure, the higher content of organic material, and the intrinsic humidity of the dentinal substrate [28]. Finish lines placed below the cemento-enamel junction result in a significant loss of adhesion [40], since cementum cannot be infiltrated by resin to the same extent as the dentin [41]. The favorable bond strength observed for RelyX™ Unicem has been attributed to the micromechanical retention and chemical interaction between monomer acidic phosphate groups and dentin/enamel hydroxyapatite [9, 19, 31, 35, 42, 43]. The smear layer is partially removed or incorporated by acidic monomers that promote micromechanical retention to the tooth structure [19]. The quality of the dentin-adhesivecement interface is closely related to the extension of monomers infiltration into the demineralized collagen network [46] and to their ability to chemically interact with dentin hydroxyapatite [24, 31]. Despite the low initial pH of RelyX™ Unicem (pH<2 in the first minute, according to the manufacturer), almost no demineralization and no true hybrid layer formation was observed on the dentin surface [19, 27, 31]. It was found that RelyX™ Unicem applied to fractured dentin only interacts very superficially without any evidence of a smear layer or resin tags (irregular interaction zone ranging from nearly 0 to 2μm [21]). This may explain the low bond strengths recorded [19, 47] and the high number of adhesive failures for the self-adhesive materials [24, 31]. This finding might be attributed to the high cement viscosity, which hinders the wetting and infiltrating of the dentin surface by the luting agent [19]. The multifunctional monomers having acidic phosphate groups are supposedly capable of demineralizing

and infiltrating the substrate simultaneously [10]. According to the manufacturers, the self-etching capacity is attributed to the presence of different monomers in the luting agent formulation, such as the hydrophilic monomer 4-MET in SmartCem® and methacrylated phosphoric esters in SeT [11]. An increase in pH from 1 to 7 is observed as a consequence of the reaction between phosphate groups and both alkaline filler particles and hydroxyapatite from enamel and dentin, to neutralize resin acidity [13, 22]. Han et al. [13] reported low pH values for G-Cem™, Maxcem Elite™, SmartCem® and RelyX™ Unicem a few seconds after manipulation. However, after 48 hours, only RelyX™ Unicem presented a neutral pH (pH=7.0). Unlike conventional cements, resin materials designed for adhesive use are anhydrous and have silanized, unreactive fillers [32]. The pH neutralization results in water formation and a more hydrophilic cement, which enhances the cement’s wetting ability on the dentin surface and the cement tolerance to water. Water is crucial for self-adhesive luting agents to release hydrogen ions required for smear layer demineralization [20] and is also reused in the reaction between multifunctional acidic phosphate monomers and alkaline filler particles. Shear bond strength of RelyX™ Unicem to enamel was evaluated prior to and after thermocycling [3]. Before thermocycling, this cement produced bond strength of 14.5 MPa, which was significantly lower than the bond strengths of other resin luting systems investigated, which range between 17 and 32 MPa. Moreover, its shear bond strength to enamel was significantly lower after thermocycling, in contrast to other resin cements that were not influenced by the same aging condition [3]. The author concluded that RelyX™ Unicem might not be the ideal material for luting if a considerable enamel surface area is present [3] and is contraindicated for veneers. Similar results in terms of enamel bond strengths were reported in


68

IAJD Vol. 5 â&#x20AC;&#x201C; Issue 2

5HYXHGHODOLWWpUDWXUH_/LWHUDWXUH5HYLHZ Product

Delivery system

BisCemÂŽ (Bisco; Schaumburg, IL, USA)

Paste/paste dual syringe; direct dispensing through a mixing tip

Breezeâ&#x201E;˘ (Pentron Clinical Technologies, Wallingford, CT,USA)

Working/setting time

Shades

Composition

1min/6min at 22ÂşC

Translucent 2SDTXH

Bis (hydroxyethyl methacrylate) phosphate (base), tetraethylene glycol dimethacrylate, dental glass

Paste/paste dual syringe; direct dispensing through a mixing tip

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Clearfil SA (Kuraray, Tokyo, Japan; SL)

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1min/5min

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Bis-GMA, TEGDMA, MDP, barium glass, silica, sodium fluoride

Embrace WetBond resin cement (Pulpdent; Watertown, MA, USA)

Automix or standard syringe packaging

Completely autocures in 7min

One shade

Di-, tri-, and multi-functional acrylate monomers into a hydrophilic, resin acid-integrating network (RAIN).

2min/4min

A2, AO3, Translucent, BO1

Powder: fluoroaluminosilicate glass, initiator, pigment. /LTXLG0HWSKRVSKRULFDFLGHVWHUPRQRPHU water, UDMA, dimethacrylate, silica powder, initiator, stabilizer

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No information available GPDM (glycerol dimethacrylate dihydrogen phosphate), comonomers (mono,di, and tri-functional methacrylate monomers), proprietary self-curing UHGR[DFWLYDWRUSKRWRLQLWLDWRU FDPSKRUTXLQRQH  stabilizer, barium glass fillers, fluoroaluminosilicate glass filler, fumed silica (filler load 67%wt, particle size 3.6Îźm

Maxcem Elite â&#x201E;˘(Kerr; Orange, CA, USA)

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Monocemâ&#x201E;˘ (Shofu Dental; San Marcos, CA, USA)

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A1 A2 Universal Translucent :KLWHRSDTXH $2SDTXH

Powder: glass fillers, silica, calcium hydroxide, self-curing initiators, pigments, ligth-curing initiators. /LTXLGPHWKDFU\ODWHGSKRVSKRULFHVWHUV dimethacrylates, acetate, stabilizers, self-curing initiatirs, ligth-curing initiators

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Capsules

5min

Translucent, A1, A2, OA3 :KLWHRSDTXH

UDMA, phosphate, fluoroaluminosilicate glass, silica Urethane dimethacrylate; di- and tri-methacrylate resins; phosphoric acid modified acrylate resin; barium boron fluoroaluminosilicate glass; organic SHUR[LGHLQLWLDWRUFDPSKRUTXLQRQHSKRWRLQLWLDtor; phosphene oxide photoinitiator; accelerators; butylated hydroxy toluene; UV stabilizer; titanium dioxide; iron oxide; hydrophobic amorphous silicon dioxide

Dimethacrylates, ytterbium trifluoride, co-polymer, glass filler, silicon dioxide, adhesive monomer initiators, stabilizers and pigments

SmartCemÂŽ (DentsplyCaulk- Germany)

SpeedCEMâ&#x201E;˘ (Ivoclar, Vivadent)

Dual-barreled syringe

2min/6min

Translucent Light Medium Dark 2SDTXH

Double syringe

Working time: self 100 â&#x20AC;&#x201C; 140s, dual100 â&#x20AC;&#x201C; 140s Setting time: (37 °C) self150 â&#x20AC;&#x201C; 220s, dual150 â&#x20AC;&#x201C; 220s

Transparent 2SDTXH Yellow

Table 1: Characteristics of self-adhesive cements of different brands.


69 Prothèses Fixées / )L[HG3URVWKRGRQWLFV microtensile bond strength investigations. Enamel microtensile bond strengths of RelyX™ Unicem ranged between 10.7 MPa [27] and 19.6 MPa [19] and were significantly lower than the bond strengths of the self-etching cement Panavia™ F 2.0 and other resin cements which ranged between 25 and 49 MPa [19, 27]. The majority of the results obtained are consistent and demonstrate that in contrast to enamel adhesion, RelyX™ Unicem performs comparably to other multistep systems on coronal dentin. Comparable bond strength with Panavia™ F was obtained [3, 19, 27]. In contrast to the positive effect observed on enamel, de Munck Jan [19] found that acid etching was detrimental to RelyX™ Unicem dentin adhesion. However, in a recent study, Pavan et al. [16] proposed, as for glass ionomer materials, that the use of polyacrylic acid (Ketac Conditioner; 3M ESPE, Seefeld, Germany) might have enhanced the dentin bond strength of self-adhesive cement [16]. In terms of marginal adaptation, Frankenberger and al. [49] reported that RelyX™ Unicem offers a tight seal at dentin margins, while self-adhesive cements cannot compete with cements which utilize etch-and-rinse adhesives in terms of bonding performance [49]. On the other hand, it should be noted that with the latest generation of dental adhesives, in pull and shear testing adhesion, values are so high that fracturing no longer occurs at the interface (adhesive failure), but directly in dentin (cohesive failure) [32]. Bonding to ceramics Ceramics fall into three main categories that differ by their composition and their physical properties: silicabased ceramics, aluminium oxidebased ceramics and zirconium oxidebased ceramics. The ability of the combination of resin cement/adhesive system to adhere to dental ceramics depends on the microstructure of the esthetic restoration and the applied surface treatment [9].

Silica-based ceramics Silica-based ceramics, such as feldspathic porcelain (Vita Mark II, VITA Zahnfabrik, Bad Sackingen, Germany) and glass ceramic Empress, Empress II and Emax (Ivoclar, Vivadent, Schaan, Liechtenstein) [50] are used to veneer metal frameworks or high-strength ceramic copings for all-ceramic restorations. In spite of the inherent brittleness and limited flexural strength of silica-based ceramics, final adhesive cementation with composite increases the fracture resistance of the ceramic restoration and the abutment tooth [50]. Surface preparation of ceramic material is important for a strong resin bond [51]. To achieve this bond, the porcelain surface may be chemically or mechanically modified to promote surface roughness and/or reactivity of the porcelain to the luting agent [52]. Several authors have described various surface treatment procedures to allow adhesion of all-ceramic restorations [22, 28, 52-56]. Bonding to silicatebased ceramics is usually obtained by two simultaneous mechanisms: 1) micromechanical retention provided by acid-etching of the ceramic surface, and 2) chemical coupling by the application of a silane coupling agent [50, 53, 54, 57-59]. The hydrofluoric (HF) acid reacts with the glassy matrix that contains silica, dissolving the surface to the depth of a few micrometers [53]. This glassy matrix is selectively removed and the crystalline structure is exposed [54]. The silane coupling agent presents bifunctional characteristics, promoting a chemical interaction between the silica in the glass phase of ceramics and the methacrylate groups of the resin through siloxane bonds [53, 60, 61]. It has been demonstrated that silane primers may confer a resistance to the degradation of the ceramic-resin bond exposed to moisture and intraoral thermal changes [62]. Etching and silanization increase the surface energy and the wettability of the ceramic substrate, which decrease

the contact angle between the ceramic surface and the resin cement [53, 54]. Several studies have demonstrated that RelyX™ Unicem can achieve high or comparable bond strength to other investigated cements without any pretreatment steps such as etching, priming or bonding [53, 63]. However, other studies observed higher shear bond strength values after etching with HF acid and silanized [22, 28, 50, 53]. In a study of Kumbuloglu et al. [55], RelyX™ Unicem showed lower shear bond strengths than the other resin cements investigated, but no pretreatment of the ceramic surface was performed. In the study of Reich et al., only the RelyX™ Unicem, in contrast to Variolink (Ivoclar, Vivadent) and Calibra (DeTrey Dentsply, Konstanz, Germany), was able to survive the whole thermocycling procedure in the case of no pretreatment. This indicates that besides mechanical interlocking, additional bonding mechanisms with RelyX™ Unicem to the ceramic surface are possible. The specific phosphoric acid methacrylates have the ability to provide physical interactions with the ceramic surface and are able to provide strong hydrogen bonding with hydroxyl groups present on the ceramic surface [22]. An increase in the bond strength after pretreatment with hydrofluoric acid and silane was also observed [22]. This is in agreement with the study of Piwowarczyk [28] who reported that, in comparison with 10 cements from different classes, only RelyX™ Unicem exhibited high shear bond strength after 14 days of water storage followed by thermal cycling. In the same study, it was reported that the light polymerization of the self-adhesive resin cements enhances shear-bond strength in comparison to autopolymerization [28]. Aluminium oxide ceramics The aluminium oxide serves as reinforcement of the glassy matrix [50]. In general, ceramics containing less than 15% silica are not regarded as silica-based or silicate ceramics [50]. Glass-infiltrated aluminium oxide


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IAJD Vol. 5 – Issue 2

5HYXHGHODOLWWpUDWXUH_/LWHUDWXUH5HYLHZ ceramic (In-Ceram, Vita Zahnfabrik, Bad Sackingen, Germany) and denselysintered high-purity aluminium oxide ceramic (Procera® All-Ceram, Nobel Biocare, Goteborg, Sweden) are widely used representatives of this group. Glass-infiltrated aluminium oxide ceramic In-Ceram is made of a high-content aluminium oxide opaque core that is glass-infiltrated to achieve its final strength [50, 66]. Because of its low silica content, neither acid etching nor adding a silane resulted in an adequate resin bond to the alumina-based In-Ceram ceramic [58, 62]. However, other authors recommended a surface treatment of etching and/or sandblasting followed by silanization [68, 69]. Silanization of glass-infiltrated aluminium oxide ceramic does not provide a chemical bond but may have a rewetting effect on air-particle-abraded alumina surfaces [50]. Air abrasion with Al2O3 abrasive particles is effective and practical for creating a roughened surface for aluminium oxide ceramics [58]. Silica coating with silanization can increase the bond strength significantly compared to that of airborne-particle abrasion alone [67]. The adhesive functional phosphate monomer 10-methacryloloxydecyl dihydrogen phosphate (MDP) chemically bonds to metal oxides such as aluminium and zirconium oxides [50, 70]. These results are confirmed by Baldissara who revealed that MDP-based resin cement with sandblasting with Al2O3 particles and bis-GMA-based resin cement with tribochemical silica coating were the best luting protocols for the alumina ceramic [71]. Procera All-Ceram Procera uses a high-purity aluminium oxide ceramic with an aluminium oxide content of 99.9%. Borges et al. [70] showed that the ceramic surface of densely sintered alumina was not etched by hydrofluoric acid because it does not contain a silica phase [70].

Other authors confirmed this result [50, 59]. Airborne particle abrasion with a micro-etcher (50μm Al2O3) is necessary to create porosities which improve microretention of the luting agents by interlocking [58, 70, 72]. Borges et al. [70] found in his study that airborneparticle abrasion of the material with 50μm aluminium oxide caused flattening of the alumina rather than creating microretentive features. SEM revealed only an irregular surface texture [70]. Hummel [72] reported that the phosphate monomer containing composite resin Panavia™21 showed the highest bond strength to sandblasted Procera which did not decrease significantly over storage time. The same study revealed that the use of Variolink II after priming the sandblasted ceramic showed high bond strength. The silane might increase the wettability, which allows flow of the bonding resins into the undercuts and porosities [72]. Blixt et al. [50] found tribochemical surface treatment with the Rocatec™ system (to bis-GMA based resin cement) to be superior to other treatments; however, this study was limited to short-term observations [50]. Piwowarczyk et al. [28] demonstrated that among 12 cementing agents, only RelyX™ Unicem and Panavia™ F exhibited strong bond strengths to airborne particle-abraded pure aluminum oxide ceramic after 14 days of water storage followed by thermal cycling. Zirconium oxide ceramics Polycristalline ZrO2 is typically used in a tetragonal crystalline phase [73]. A number of zirconia-oxide ceramic systems have been recently introduced, such as Cercon® (Dentsply, Amherst, N.Y.), DCS® system (DCS® Dental AG, Allschwil, Switzerland), Lava™ (3M ESPE) and Procera allZirkon (NobelBiocare, Goteborg, Sweden). Each of the commercial zirconia systems has unique material properties due to the specific fabrication process, creating a unique intaglio surface that influences bonding beha-

vior [73]. Full coverage zirconium oxide may not require adhesive cementation [73]; however, some authors concluded that adhesive cementation is preferable for ensuring better retention, marginal adaptation and fracture resistance of the restoration and the abutment tooth [75]. Neither the application of HF acid nor the silanization resulted in a satisfactory resin bond to zirconia [63] because of the high crystalline content and the limited vitreous phase (below 1%) of this high strength core ceramic [73, 75]. Conventional silanes are not as effective on zirconia as on silicabased ceramics. Airborne particle abrasion with Al2O3 abrasive particles has proven to be effective [50, 56]. It increases surface energy and, therefore, wettability [56]. It has been reported that the 10-MDP (10-methacryloxydecyl dihydrogen phosphate) containing luting system (Clearfil™ Esthetic cement) seems to be the most suitable to bond zirconia ceramic surfaces and it does not require any pretreatment of the ceramic surface before luting [75]. The adhesive potential of MDP to zirconia may depend on the presence of a passive coating of zirconium oxide on the ceramic surface. Chemical reactions involving the hydroxyl groups of the layer and the phosphate ester monomers of the MDP may occur at the interfacial level [76]. Therefore, the MDP containing self-adhesive resin cement Clearfil SA luting (Kuraray, Tokyo, Japan) is more suitable to bond the zirconia surface than other selfadhesive resin cements when no pretreatment of the ceramic was done [76]. Blatz [74] found that the application of a MDP-containing bonding/ silane coupling agent is the key factor for a reliable resin bond to airborne particle-abraded Procera AllZirkon (NobelBiocare, Goteborg, Sweden) and is not influenced by the resin luting agent used. Jie Lin [76] found that silica coating and tribochemical treatment improved the bond strength of the self-adhesive cements (RelyX™ Unicem, Maxcem Elite™, Smartcem®,


71 Prothèses FixĂŠes / )L[HG3URVWKRGRQWLFV Breezeâ&#x201E;˘, Biscemâ&#x201E;˘, Clearfil SA) to zirconia compared to untreated ceramic. Furthermore, De Oyague [75] found that RelyXâ&#x201E;˘ Unicem bonded to zirconia, regardless of the ceramic surface treatment and without additional coupling agent application. According to Kumbuloglu [56], RelyXâ&#x201E;˘ Unicem showed higher bond strength than the Panaviaâ&#x201E;˘ F in both water-storage and thermocycling when used with a zirconium oxide (DCS Dental AG) [56]. Panaviaâ&#x201E;˘ F and RelyXâ&#x201E;˘ Unicem contain phosphoric-acid methacrylates that provide a strong physical interaction, such as hydrogen bonding, with the air abraded ceramic surface [28].

Conclusion Based on the published articles, RelyXâ&#x201E;˘ Unicem - the most investigated self-adhesive cement- proved to be satisfactory and comparable to other multistep resin cements. However, RelyXâ&#x201E;˘ Unicem bonding performance was found to be better on dentin than on enamel. On the other hand, this product can bond to the silica-based ceramics, aluminium oxide ceramics, zirconium oxide ceramics regardless of the ceramic treatment. Self-adhesive cements seem to be promising in indirect restorative procedures because they offer a simplified technique, reduce the occurrence of postoperative sensitivity and are suitable for a wide range of applications. Prospective, long-term studies are necessary to evaluate self-adhesives introduced in the market prior to making any general recommendation regarding their use.

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5HYXHGHODOLWWpUDWXUH_/LWHUDWXUH5HYLHZ 20. Knobloch Lisa A, Azer S, Johnston w, Clelland N, Kerby R. Bond strengths of one- and two-step self-etch adhesive systems. J Prosthet Dent 2007;97:216-22.

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22. Reich SM, Frankenberger R, Zajc D. Effect of surface treatment on the shear bond strength of three resin cements to a machinable feldspatic ceramic. J Biomed Mater Res Appl Biomater 2005;74:740-6. 23. Hikita K, De Munck J, Ikeda T, van Landuyt K, Maida T. Bonding effectiveness of adhesive luting agents to enamel and dentin. Dent Mater 2007;23:71-80. 24. Yoshida Y, Nagakane K, Fukuda R, Nakayama Y, Okazaki M, Shintani H. Comparative study on adhesive performance of functional monomers. J Den Res 2004;83:454-8. 25. Van Meerbeek B, Yoshida Y, Inoue S, Vargas M, Vijay P, Van Landuyt K et al. Adhesion to enamel and dentin: current status and future challenges. Oper Dent 2003;28:215-235. 26. Behr M, Rosentritt M, Regnet T, Lang R, Handel G. Marginal adaptation in dentin of a self-adhesive universal resin cement compared with well-tried systems. Dent Mater 2004;20:191-7. 27. Goracci C, Curry A, Cantoro A, Papachini F, Tay FR, ferrari M. Microtensile bond strength and interfacial properties of selfetching and self-adhesive resin cements used to lute composite onlays under different seating forces. J Adhes Dent 2006;8:32735. 28. Piwowarczyk A, Lauer H-C, Sorensen J. In vitro shear bond VWUHQJWKRIFHPHQWLJDJHQWVWRĂ&#x20AC;[HGSURVWKRGRQWLFUHVWRUDWLYH materials. J Prosthet Dent 2004;92:265-73. 29. Palacios RP, Johnson GH, Philips KM, Raigrodski AJ. Retention of zirconium oxide ceramic crowns with three types of cement. J Prosthet Dent 2006;96:104-14. 30. Attar N, Tam L, Mc Comb D. Mechanical and physical properties of contemporary dental luting agents. J Prosthet Dent 2003;89:127-34.

40. Peumans M, Van Meerbeek B, Lambrechts P. Porcelain veneers: a review of the literature. J Dent 2000;28:163-77. 41. Federlin M, Schmidt S, Hiller KA, Thonnemann B, Schmalz G. 3DUWLDO FHUDPLF FURZQV LQĂ XHQFH RI SUHSDUDWLRQ GHVLJQ DQG luting material on internal adaptation. Oper Dent 2004;29:56070. 42. Schenke F, Hiller K, Schmalz G, Federlin M. Marginal integrity of partial ceramic crowns within dentin with different luting WHFKQLTXHVDQGPDWHULDOV2SHU'HQW 43. Ibarra G, Johnson G, Geurtsen W, Vargas MA. Microleakage of porcelain veneer restorations bonded to enamel and dentin with a new self-adhesive resin-based dental cement. J Den Res 2007;23:218-25. 44. Zicari F, Couthino E, De Munck J, Poitevin A, Scotti R, Naert , HW DO %RQGLQJ HIIHFWLYHQHVV DQG VHDOLQJ DELOLW\ RI Ă&#x20AC;EHUSRVW bonding. Dent Mater 2008;24:967-77. 45. Mazitelli C, Monticelli F, Osorio R, Casucci A, Toledano M, Ferrari M. Effect of simulated pulpal pressure on self-adhesive cements bonding to dentin. Dent Mater 2008;24:1156-63. 46. Hashimoto M, De Monk J, Ito S, Sano H, Kaga M , Ogushi H, et al. In vitro effect of nanoleakage expression on resin-dentin bond-strengths analyzed by microtensile bond test, SEM/EDX and TEM. Biomaterials 2004;25:5565-74. 47. Goracci C, Sadek F, Fabianelli A, Tay FR, Ferrari M. Evaluation of WKHDGKHVLRQRIĂ&#x20AC;EHUSRVWVWRLQWUDUDGLFXODUGHQWLQ2SHU'HQW 2005;30:627-35. 48. Wang VJ, Chen Y, Yip KH, Smales RJ, Meng QF, Chen L. Effect RI WZR Ă&#x20AC;EHU SRVW W\SHV DQG WZR OXWLQJ FHPHQW V\VWHPV RQ regional post retention using the push-out test. Dent Mater 2008;24:372-7.

31. Gerth H, Zuchner H, Schafer E. Chemical analysis and bonding UHDFWLRQRI5HO\;Â&#x152;8QLFHPDQG%LĂ&#x20AC;[FRPSRVLWHVDFRPSDUDWLYH study. Dent Mater 2006;22:934-941.

49. Frankenberger R, Lohbauer U, Schaible RB, Nikolaenko SA, 1DXPDQQ0/XWLQJRIFHUDPLFLQOD\VLQYLWUR0DUJLQDOTXDOLW\ of self-etch and etch-and-rinse adhesives versus self-etch cements. Dent Mater 2008;24:185-191.

32. Technical data sheet: Expertise RelyXâ&#x201E;˘ Unicem (3M ESPE), S.G., 2002.

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51. Kamada K, Yoshida K, Atsuta M. Effect of ceramic surface treatments on the bond of four resin luting agents to a ceramic material. J Prosthet Dent 1998;79:508-13.

34. Bergenholtz G. Evidence for bacterial causation of adverse pulpal responses in resin-based dental restorations. Crit Rev Oral Biol Med, 2000;11:467-80. 35. Piwowarczyk A, L.H-C, Sorensen John A. Microleakage of various cementing agents for full cast crowns. Dent Mater 2005;21:445-453. 36. Bouillaget S, Gysi P, Wataha JC. Future directions in bonding resins to the dentine-pulp complex. Journal of Oral Rehabilitation 2004;31:385-392. 37. Heng-Liang L, Chun-Li L, Ming-Tsung S, Yen-Hsiang C. Numerical investigation of macro- and micro-mechanics of a ceramic veneer bonded with various cement thicknesses using WKHW\SLFDODQGVXEPRGHOLQJĂ&#x20AC;QLWHHOHPHQWDSSURDFKHV-'HQW 2009;37:141-148.

52. Ayad M, Fahmi N, Rosenstiel S. Effect of surface treatment on roughness and bond strength of a heat-pressed ceramic. J prosthet dent 2008;99:123-130. 53. 3LVDQL3URHQFD - (UKDUGW * 9DODQGUR ) ,QĂ XHQFH RI FHUDPLF surface conditioning and resin cements on microtensile bond strength to a glass ceramic. J Prosthet Dent 2006;96:412-7. 54. Chaiyabutor Y, Mc Gowan S, Phillips K, Giordano R. The effect RIK\GURĂ XRULFDFLGVXUIDFHWUHDWPHQWDQGERQGVWUHQJWKRID zirconia veneering ceramic. J Prosthet Dent 2008;100:194-202. 55. Kumbuloglu O, Lassila LVJ, User A, Toksavul S, Vallittu P.K. Shear bond strength of composite resin cements to lithium disilicate ceramics. J Oral Rehab 2005;32:128-133.


73 Prothèses FixĂŠes / )L[HG3URVWKRGRQWLFV 56. Kumbuloglu O, Lassila LVJ, User A, Vallitu PK. Bonding of resin composite luting cements to zirconia oxide by two air-particle abrasion methods. Oper Dent 2006;31(2):248-255. 57. $GGLVRQ 2 0DUTXLV 3 )OHPLQJ * 5HVLQ VWUHQJWKHQLQJ RI dental ceramics- the impact of surface texture and silane. J Dent 2007;35:416-424. 58. Blatz M, Sadan A, Arch G, Lang B. In vitro evaluation of longterm bonding of Procera Allceram alumina restorations with a PRGLĂ&#x20AC;HGUHVLQOXWLQJDJHQW-3URVWKHW'HQW 59. Kato H, Matsumura H, Tanaka T, Atsuta M. Bond strength and durability of porcelain bonding systems. J prosthet Dent 1996;75:163-8. 60. Matinlinna J, Vallittu P. Silane based concepts on bonding resin composite to metals. The Journal of Contemporary Dental Practice 2007;8(2):1-8. 61. Bottino M, Valandro LF, Scotti R, Buso L. Effect of surface treatments on the resin bond to zirconium-based ceramic. Int J Prosthodont 2005;18:60-65. 62. 2ZHQ$0DUTXLV30)OHPLQJ*$GKHVLYHOXWLQJRIDOOFHUDPLF restorations- The impact of cementation variables and shortterm water storage on the strength of a feldspathic dental ceramic. J Adhes Dent 2008;10:285-294. 63. 7HFKQLFDOSURGXFWSURĂ&#x20AC;OH0(63(5HO\;8QLFHP6HOI$GKHVLYH Universal Resin Cement. 64. Trajtenberg CP, Caram SJ, Kiat-amnuay S. Microleakage of AllCeramic Crowns using self-etching luting agents. Oper Dent 2008;33(4):392-399. 65. Ferrari M. Marginal integrity of ceramic inlays luted with a selfcuring resin system. Dent Mater 2003;19(4):270-276. 66. Al-Wahadani A, Hussey D, Grey N, Hatamieh M. Fracture resistance of aluminium oxide and lithium disilicate-based crowns using different luting cements: an in vitro study. The Journal of Contemporary Dental Practice 2009;10(2):51-58. 67. .HUQ 0 7KRPSVRQ 3 %RQGLQJ WR JODVV LQĂ&#x20AC;OWUDWHG DOXPLQD ceramic: Adhesive methods and their durability. J Prosthet Dent 1995;73:240-9. 68. Begazo C, de Boer H, Kleverlaan C, Van Waas M, Feilzer A. Shear bond strength of different types of luting cements to an aluminium oxide-reinforced glass ceramic core material. Dent Mater 2004;20:901-907. 69. Madani M, Chu F, McDonald A, Smales R. Effects of surface treatments on shear bond strengths between a resin cement and an alumina core. J Prosthet Dent 2000;83:644-7. 70. Borges G, De Goes MF, Platt J, Moore K, Hueb de Menezes F, Vedovato E. Extrusion shear strength between an aluminabased ceramic and three different cements. J Prosthet Dent 2007;98:208-215. 71. Baldissara P, Valandro LF, Monaco C, Ferrari M, Bottino MA, 6FRWWL 5 )DWLJXH UHVLVWDQFH RI WKH ERQG RI D JODVVLQĂ&#x20AC;OWUDWHG alumina ceramic to human dentin. J Adhes Dent 2006;8(2):97104. 72. Hummel M, Kern M. Durability of the resin bond strength to the alumina ceramic Procera. Dent Mater 2004:20;498-508. 73. %ODW]0*&KLFKHV+6DGDQ$,QĂ XHQFHRIVXUIDFHWUHDWPHQW and simulated aging on bond strengths of luting agents to zirconia. Quintessence Int 2007;38:745-753.

74. Blatz M, Sadan A, Martin J, Lang B. In vitro evaluation of shear bond strengths of resin to densely-sintered high-purity zirconium-oxide ceramic after long-term storage and thermal cycling. J Prosthet Dent 2004;91:356-62. 75. De Oyague R, Monticelli F, Toledano M, Osorio E, Ferrari M, 2VRULR 5 ,QĂ XHQFH RI VXUIDFH WUHDWPHQWV DQG UHVLQ FHPHQW selection on bonding to densely-sintered zirconium-oxide ceramic. Dent Mater 2009;25:172-179. 76. Lin J, Shinya A, Gomi H, Shinya A. Effect of self-adhesive resin cement and tribochemical treatment on bond strength to zirconia. Int J Oral Sci 2010;2(1):28â&#x20AC;&#x201C;34.


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IAJD Vol. 5 – Issue 2

REVUE DE LA LITTÉRATURE $UWLFOHVFLHQWLÀTXH_6FLHQWLÀF$UWLFOH

/ LITERATURE REVIEW

Médecine Orale / 2UDO0HGLFLQH

L’HALITOSE : ORIGINE, CLASSIFICATION ET TRAITEMENT Guenane Yamina* | Adel Ayat** | Hayet Lazili*** | Badia Saari****

Résumé Bien qu’il s’agisse d’un problème de santé relativement mineur, la mauvaise haleine peut être une source de détresse et un réel handicap social et/ou psychologique. Les causes retenues sont d’origine bucco-dentaire dans 85 % des cas. Toutefois, l’origine de l’halitose est également à rechercher dans les domaines otorhino-laryngologique, gastro-intestinal, pulmonaire, respiratoire, métabolique et hormonal, ou liée à certains médicaments. De ce fait, la prise en charge de cette pathologie est pluridisciplinaire. Mots- clés : mauvaise haleine – halitophobie - hygiène buccale.

* Professeur en pathologie bucco-dentaire CHU Mustapha Pasha; AlgerAlgerie

** DDM,

Service de médecine dentaire; hôpital militaire régional universitaire de Constantine; Algérie adel.rida@gmail.com

Abstract Although it is a relatively minor health problem, bad breath can be a source of distress and social or psychological handicap. The identified causes are of dental origin in 85% of the cases. However, the origin of halitosis is also sought for in ear, nose and throat (ENT), gastrointestinal, pulmonary, respiratory, metabolic and hormonal systems or related to medication. Therefore, this pathology requires a multidisciplinary approach. Keywords: Halitosis – halitophobia - oral hygiene.

*** DDM,

Service de médecine dentaire; hôpital central de l'armée; Alger; Algérie

**** Professeur en pathologie

bucco-dentaire; Service de pathologie bucco-dentaire, CHU Mustapha Pasha; Alger; Algérie


75 Médecine Orale / 2UDO0HGLFLQH

Introduction Le paraître et les rapports sociaux occupent une place prépondérante dans notre société. La mauvaise haleine est souvent une entrave évidente et majeure au bien-être de la personne. Cette affection désignée sous le terme d’« halitose » est définie comme étant une odeur désagréable qui émane de la bouche lors de l'expiration ou simplement lors de l'ouverture buccale [1]. L’halitose peut être temporaire ou chronique [2], subjective (perçue uniquement par la personne elle-même) ou objective (perçue par l’examinateur) [3, 4]. Cette affection présente à la fois deux aspects : -Un aspect pathologique qui peut révéler des maladies buccales ou systémiques parfois graves. -Un aspect social à l’origine d’un handicap socio-psychologique par la création d’une barrière, un isolement social et/ou des échecs sentimentaux. L’halitose à travers le temps L’halitose est connue et documentée depuis les temps anciens (la préoccupation vis-à-vis de l’haleine est très ancienne). Hippocrate a décrit un lien entre les maladies parodontales et l’halitose [5] et a insisté sur la valeur diagnostique de ces odeurs [6]. Le plus surprenant est la dimension religieuse que revêt cette affection puisqu’on retrouve des références d’origine grecque, romaine, chrétienne et islamiste. Dans le contrat de mariage traditionnel, la ketuba, des manuscrits stipulent qu’un mariage peut être légalement rompu si l’un des partenaires dégage de mauvaises odeurs [4]. Au fil des temps, cette préoccupation s’est accrue et aujourd’hui elle fait partie au même titre que la coiffure et l’habillement «des éléments de l’image de soi ». Le problème d’halitose a été envisagé pour la première fois dans la littérature médicale dans les années 1930s. Entre les années 1940s et

1950s, Brening [7], Fosnick et coll. [5] ont mis au point un instrument appelé osmoscope, qui a permis de mesurer les sources de mauvaises odeurs. Ils ont démontré que le problème pouvait être physiologique ou pathologique et l’implication de facteurs buccaux est soupçonnée. En 1964, Tonzetich et Richter [8] ont identifié les composés sulfurés volatiles (CSV) responsables de l’halitose. Prévalence de l’halitose Les informations concernant la prévalence de l’halitose sont peu abondantes, particulièrement par défaut d’études épidémiologiques et de critères standards pouvant être adoptés pour apprécier ou définir l’halitose [6]. L’incidence et la sévérité de la mauvaise haleine sont pratiquement les mêmes chez les femmes et les hommes [9]. Cependant, un nombre plus élevé de femmes consulte pour le traitement. Cela pourrait s’expliquer par le fait que les femmes sont généralement plus soucieuses de leur santé et de leur apparence [10]. En outre, l’observation de différents groupes d’âge a révélé une augmentation significative, liée à l’âge, des valeurs moyennes de CSV responsables de la mauvaise haleine [10]. Etiopathogénie Parmi les composants chimiques volatiles à l’origine de la majeure partie de la mauvaise haleine, on trouve différentes catégories [11] : - Les composés sulfurés volatiles. - Les diamines. - Les composés aromatiques volatiles. - Les acides organiques. - Les composés azotés. - Les alcools et autres composés. Les CSV représentent la majeure partie des gaz malodorants responsables de l’halitose. Ils sont constitués essentiellement de méthyl-mercaptan, sulfure d’hydrogène, diméthyle-sulfures…. [12]. Ces composés font suite à la dégradation par les bactéries du biofilm (anaérobies Gram-négatifs), des protéines et des acides gras libres

des cellules épithéliales desquamées ou/et des résidus alimentaires, en présence de conditions physico-chimiques favorisantes (xérostomie, milieu pauvre en oxygène, apport nutritif riche en protéines,…). Les diamines, telles que la cadavérine et la putrescine, seraient également à l’origine de la mauvaise haleine. Elles ont toutes deux une odeur de chair en décomposition comme leur nom l’indique [5]. Classification de l’halitose Lorsqu’un patient se plaint d’halitose, il est important de savoir de quel type d’halitose il s’agit. Pour cela, une classification a été établie [13]. L’halitose peut être subdivisée en trois catégories : -L’halitose vraie. -La pseudo-halitose. -L’halitophobie. Halitose vraie Le problème est réel, il peut être mesuré à l’aide de différents outils de mesure. Cette catégorie englobe l’halitose physiologique, qui est en général une mauvaise haleine transitoire (souvent le matin au réveil ou après avoir consommé certains aliments [5] ; et l’halitose pathologique qui elle, est plutôt permanente. L’halitose physiologique Les mauvaises odeurs proviennent de processus de putréfaction à l’intérieur de la cavité orale. Aucun trouble spécifique ou pathologie qui auraient pu provoquer cette halitose ne peut être identifié. Dans ce cadre, on cite : – L’halitose transitoire occasionnelle qui apparaît communément après ingestion de certains aliments, le jeûne, le réveil. – L’halitose du matin, appelée encore «haleine du réveil», due à la disparition nocturne des mouvements de mastication et à la diminution du flux salivaire, la fermeture buccale permettant la création de conditions d’anaérobiose. Cette odeur est atténuée par les repas qui favorisent le nettoyage des surfaces dentaires.


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5HYXHGHODOLWWpUDWXUH_/LWHUDWXUH5HYLHZ – L’haleine de la faim, comme celle du jeûne et des régimes amaigrissants, qui correspond à la consommation d’acides gras par l’organisme. Le métabolisme de ces substances va libérer des produits volatiles qui vont s’éliminer du sang par la voie pulmonaire. – Avec l’âge, l’haleine acquiert une odeur plus spécifique qui peut être plus ou moins déplaisante selon que l’on se trouve en présence d’un terrain de pathologie parodontale ou souvent de pathologie générale. – Chez la femme enceinte, les troubles du transit, les renvois fréquents liés à la compression, la grande vulnérabilité des tissus mous buccaux du fait de l’imprégnation hormonale pendant cet état gestationnel vont libérer des produits volatiles malodorants [4]. – L’halitose nutritionnelle est perçue lors de l’ingestion de certains aliments tels que les aliments aillés (ail, oignon, poireau, ciboulette….) ou de certains médicaments. Des substances chimiques (des huiles volatiles) passent dans le sang puis atteignent les poumons. A l’expiration, ils induisent une odeur désagréable. – Le tabac et l’alcool affectent l’odeur de l’haleine par modification du pH et de la flore salivaire. L’halitose pathologique persistante L’halitose est dite pathologique quand elle devient chronique et qu’elle persiste malgré une bonne hygiène buccodentaire. Son origine peut être buccale ou reliée à une condition médicale générale. L’halitose pathologique d’origine buccale est provoquée par un trouble, une pathologie ou un dysfonctionnement des tissus oraux : caries, obturations défaillantes, aphtes ou ulcération des muqueuses, péricoronarite des dents de sagesse et maladies parodontales. L’halitose provenant de l’enduit lingual et modifiée par une pathologie (parodontopathie, xérostomie) est incluse dans cette subdivision. Différentes études ont établi que la

langue était le premier «réservoir » de bactéries de la cavité buccale [14]. Ceci est en rapport avec la morphologie de la face dorsale de la langue, très irrégulière, qui comporte de multiples fissures et anfractuosités. Ces fissures et cryptes sont des pièges favorables à la rétention de débris et peuvent créer un environnement où les micro-organismes sont bien protégés de l’action d’évacuation de la salive [15]. Les CSV ont été retrouvés en nombre accru dans les poches parodontales. Ces produits sont hautement toxiques pour les tissus, même à de très faibles concentrations. Par conséquent, ils peuvent jouer un rôle dans la pathogenèse des conditions inflammatoires affectant le parodonte, comme dans la parodontite [16]. Présents dans la salive, ils augmentent en cas d’inflammation gingivale et diminuent par contre une fois l’inflammation réduite [17]. L’halitose pathologique d’origine extra-buccale est associée à des problèmes systémiques [18]. La respiration buccale, le stress, les changements hormonaux, certaines maladies et/ou médicaments induisent une sécheresse de la bouche. La diminution du flux salivaire entraîne la manifestation de l’halitose. Parmi les maladies générales, on cite : – Le diabète, à l’origine d’une odeur d’acétone [19]. – Les maladies broncho-pulmonaires [20]. – Un écoulement nasal postérieur, signe d’une sinusite aiguë et les anomalies structurelles des sinus [21, 22]. – L’insuffisance rénale: haleine dont l’odeur ressemble à celle de l’urine (odeur ammoniacale) [23]. – L’insuffisance hépatique qui donne une haleine fétide. – Certaines affections hématologiques. – L’inflammation de l’amygdale [24]. – Certains cancers, notamment de l’œsophage et de l'estomac [25].

Pseudo-halitose Aucune mauvaise odeur notable n’est perçue par les autres, bien que le patient se plaigne obstinément de sa présence [13, 5]. La maladie est améliorée par des conseils (en utilisant des supports papiers, la sensibilisation, des explications des résultats d’examen) et par des mesures d’hygiène orale simples. Halitophobie L’halitose est décrite par le malade, mais non objectivable par l’entourage ou par le praticien [26, 27]. Il s’agit de l’halitose psychogène (sensation obsessionnelle d’avoir une mauvaise haleine). Diagnostic de l’halitose Le diagnostic est essentiellement clinique; il repose sur la perception de la mauvaise haleine pendant que le patient parle. Au cours de l’interrogatoire qui sera mené sans port de masque, il sera intéressant de noter les antécédents médicaux et chirurgicaux, les habitudes alimentaires et le mode d’évolution de l’halitose (intermittent ou continu). La cavité buccale sera ensuite soigneusement examinée. Après cette étape, il peut être nécessaire de faire examiner le pharynx et les fosses nasales par un oto-rhino-laryngologue. Si après toutes ces investigations aucune cause locale ou loco-régionale n’a pu être mise en évidence, le patient sera adressé à un médecin interniste pour la recherche de causes générales. Les tests diagnostiques de l’halitose nécessitent un appareillage complexe. Cependant, il existe un test simple qui permet de confirmer l’origine locale buccale ou générale de l’affection [6]: 1) On demande au patient de souffler à travers les narines en maintenant la bouche et les lèvres fermées. Si l’odeur apparaît, il s’agit d’une cause générale. 2) On lui demande ensuite de pincer le nez et de fermer la bouche, de rester quelques secondes en apnée puis d’ouvrir la bouche sans respirer.


77 Médecine Orale / 2UDO0HGLFLQH Si la mauvaise odeur apparaît, il s’agit d’une cause buccodentaire. Traitement de l’halitose Un traitement sera mis en oeuvre toutes les fois où une cause précise est identifiée. Il s’agira soit de soins bucco-dentaires, oto-rhino-laryngologiques. psychiatriques ou de traitement des différentes affections générales [28]. Lorsqu’aucune cause évidente n’a pu être identifiée ou que l’affection causale identifiée ne peut être définitivement éliminée, un traitement symptomatique sera mis en route pour apporter un soulagement au patient. Une bonne hygiène alimentaire et le maintien d’une santé buccodentaire correcte constituent d’excellents moyens de prévention de l’halitose. La bonne hygiène alimentaire sousentend avoir une alimentation équilibrée (sans excès de graisse, de féculents, de produits odoriférants comme l’ail, l’oignon et les régimes riches en protéines) et boire beaucoup d’eau. La bonne santé buccodentaire quant à elle prend en compte [28] : -Le brossage des dents avec une brosse souple au moins deux fois par jour (matin et soir après les repas). -L’utilisation d’accessoires comme le fil dentaire, les brossettes inter-dentaires et surtout le gratte langue ou une brosse aux poils très souples. Le brossage de la langue réduit l’émission de CSV et son effet dure jusqu’à 7 heures. La technique consiste à enlever la pellicule blanche visible sur le dos de la langue. La tête de la brosse à dents peut être immergée dans un bain de bouche. Le brossage doit être effectué en sortant la langue au maximum et en brossant à partir du V lingual vers la partie antérieure de la langue ; -L’utilisation des bains de bouche avec des produits sans alcool, afin d’éviter le desséchement des muqueuses. Les pastilles à sucer et le chewinggum permettent de masquer sur une courte période la mauvaise haleine.

– La réduction de la consommation d’alcool et de café et l’arrêt du tabac. – Des visites régulières chez le dentiste.

Conclusion « Halitose » est le terme scientifique désignant la mauvaise haleine, ou l'émission par le souffle d’odeurs désagréables qu’elles soient d’origine buccale ou nasale. Cette halitose a le plus souvent une étiologie buccale, ce qui place le chirurgien-dentiste comme acteur principal de la prise en charge. La prise en charge de ce trouble comprend des traitements préventifs, curatifs et palliatifs mis en place par le chirurgien-dentiste, mais aussi l’implication de l’équipe pluridisciplinaire constituée du médecin traitant, de l’ORL et du psychologue/psychiatre. Le maintien d’une bonne santé bucco-dentaire demeure un excellent moyen de prévention de l’halitose.


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RĂŠfĂŠrences 1. Mel Rosenberg et Van Steenberghe d. Bad breath: A multidisciplinary approach. Leuven university press ed 1996. 2. Ordre des HygiĂŠnistes Dentaires du QuĂŠbec. Halitose PDXYDLVH KDOHLQH  >OH  KWWSZZZRKGTFRP SantĂŠ/ Problèmes Buccodentaires/Halitose.aspx]. 3. Di Constanzo V et Di Constanzo J. Lâ&#x20AC;&#x2122;halitose ou mauvaise haleine chez lâ&#x20AC;&#x2122;enfant. J Pediatr PuĂŠriculture 2001;14(2):67-76. 4. Davarpanah M, De Corbière S, Caraman M, Abdul-Sater S. Lâ&#x20AC;&#x2122;halitose. Une approche pluridisciplinaire. MĂŠmento ed. CdP 2006;11. 5. Sanz M, RoldĂĄn S, Herrera D. Les principes fondamentaux de lâ&#x20AC;&#x2122;halitose. J Contemp Dent Pract 2001 Nov;(2)4:01-17. 6. Iwakura M, Yasuno Y, Shimura M, Sakamoto S. Clinical characteristics of halitosis: differences in two patient groups with primary and secondary complaints of halitosis. J Dent Res 1994;73(9):1568-74. 7. Brening RH, Sulser GF, Fosdick LS. The determination of halitosis by use of the osmoscope and the cryoscopic method. J Dent Res 1939;18(2):127-132. 8. Tonzetich J, Richter VJ. Evaluation of volatile odoriferous components of saliva. Arch Oral Biol 1964;9:39-46. 9. Newman MG. The role of periodontitis in oral malodour: Clinical perspectives. In van Steenberghe D, Rosenberg M, eds. Bad Breath: A multidisciplinary approach. Leuven: Leuven University Press, 1996. 10. Miyazaki H, Sakao S, Katoh Y, Takehara T. Correlation between volatile sulphur compounds and certain oral health measurements in the general population. J Periodontol 1995;66(8):679-84. 11. Velde S, Quirynen M, Van Hee P, Van Steenberghe D. Halitosis associated volatiles in breath of healthy subjects. J Chromatogr B Analyt Technol Biomed Life Sci.2007;853(12):54-61. 12. Cabrol J. Halitose et pathologie gĂŠnĂŠrale. Thèse chir dent Lille, 1986. 13. <DHJDNL . &RLO -0 ([DPLQDWLRQ FODVVLĂ&#x20AC;FDWLRQ DQG WUHDWPHQW of halitosis: clinical perspectives. J Can Dent Assoc 2000;66(5):257-61. 14. Goldberg S, Kozlovsky A, Gordon D, Gelernter I, Sintov A, Rosenberg M. Cadaverine as a putative component of oral malodor. J Dent Res 1994 Jun;73(6):1168-72. 15. De Boever H, Loesche WJ. Assessing the contribution of DQDHURELFPLFURĂ RUDRIWKHWRQJXHWRRUDOPDORGRU-$P'HQW Assoc 1995;126(10):1384-1393. 16. Gilmore E L, Bhaskar S N: Effect of tongue brushing on bacteria DQGSODTXHIRUPHGLQYLWUR-3HULRGRQWRO² 17. Reingewirtz Y. Halitose et parodontite; revue de littĂŠrature. Journal de parodontologie & dâ&#x20AC;&#x2122;implantologie orale 1999;18:2735. 18. Carmona T, Limeres Posse, Diz DP, Fernandez FJ, Garcia V. Extra oral aetiology of halitosis. Med-Oral 2001;6(1):40-47. 19. Soell M, Millauskaite A, Hassan M, HaĂŻkel Y, Selimovic D. Diabète et santĂŠ bucco-dentaire. MĂŠdecine des maladies 0pWDEROLTXHV   20. François M. Pathologie des voies aĂŠriennes supĂŠrieures. 3pGLDWULH  (GLWLRQV 6FLHQWLĂ&#x20AC;TXHV HW 0pGLFDOHV (OVHYLHU SAS. p. 1-10.

21. Mogica Mogica JD, Canseco Gonzalez C, Gonzalez Escamilla JA, Gonzalez Diaz SN, Galindo Rodriguez G. Chronic rhinosinusitis: predominant symptoms in children under 14 years of age who were seen at the Regional Center for the Prevention and Treatment of Allergic Diseases. Rev Alerg Mex 1996;43:16-18. 22. Robertson J, Friedman E, Rubin B. Nasal and sinus disease in F\VWLFĂ&#x20AC;EURVLV3DHGLDWULF5HVSLUDWRU\5HYLHZV 23. )DZ]L 5 HW DO ,QVXIĂ&#x20AC;VDQFH UpQDOH FKURQLTXH HW RGRQWRORJLH SpGLDWULTXH-2GRQWRVWRPDWRO3HGLDWU   24. Dulguerov P, Landis B et Giger R. Abcès pĂŠriamygdalien: mise au point. Revue MĂŠdicale Suisse 2004 [http://revue.medhyg.ch/ article.php3?sid=24113]. 25. Duvillard C et Romanet P. Tumeurs bĂŠnignes du pharynx. Otorhino-laryngologie 2008, Encycl. MĂŠd Chir (Elsevier Masson SAS, Paris), pp. 1-7. 26. Porter SR, Scully C. Oral malodour (halitosis). BMJ 2006;333:632635. 27. Yaegaki K, Qian W, Murata T, et al. Oral malodorous compound causes apoptosis and genomic DNA damage in human gingival Ă&#x20AC;EUREODVWV-3HULRGRQWDO5HV   28. Akaa A, Diakite K. Lâ&#x20AC;&#x2122;halitose: donnĂŠes actuelles et prise en FKDUJHGXSDWLHQW0pGHFLQHG¡$IULTXH1RLUH   583.


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CAS CLINIQUE / CASE REPORT

Introduction

Médecine Orale2UDO0HGLFLQH

LE CARCINOME ÉPIDERMOÏDE : A PROPOS DE DEUX CAS Chirine Chammas* | Nadia Skandri** | Dolly Roukoz*** Résumé Le carcinome épidermoïde représente plus de 90% des tumeurs malignes de la cavité buccale. Ce type de cancer peut se présenter sous différents aspects cliniques et dans diverses localisations. Seul un dépistage précoce peut contribuer à améliorer son pronostic. La responsabilité du dentiste est capitale dès qu’il s’agit de dépister et/ou de diagnostiquer ce type de lésions dans les meilleurs délais, le patient pouvant ainsi bénéficier d’un traitement rapide et adapté, et surtout d’un meilleur pronostic. Nous allons présenter deux cas de carcinome épidermoïde diagnostiqués précocement. Le premier, au niveau du bord latéral de la face ventrale de la langue, le second au niveau de la muqueuse jugale évoluant sur un lichen plan réticulaire et érosif. Mots-clés : carcinome épidermoïde – tumeur maligne – pronostic.

* DCD, DU de Pathologie et Diagnostic Oraux Dpt de Pathologie et Diagnostic Oraux Faculté de Médecine Dentaire, Université Libanaise drchirinechammas@hotmail.com

** DCD, DEMS en pathologie

buccale, Faculté de Médecine Dentaire, Université Libanaise

Abstract Squamous cell carcinoma accounts for over 90% of malignant tumors of the oral cavity. This type of cancer can be present in different clinical aspects and in various locations. Only early diagnosis can improve prognosis. The responsibility of the dentist is crucial when it comes to detecting and / or diagnosing such lesions promptly, the patient may benefit from a quick and appropriate treatment, and especially a better prognosis. We present two cases of squamous cell carcinoma diagnosed at early stages. The first, at the lateral edge of the ventral surface of the tongue, the second at the buccal mucosa evolving on reticular and erosive lichen planus. Keywords : Squamous cell carcinoma – malignant tumour – prognosis.

*** DCD, DU de Pathologie et

Diagnostic Oraux Dpt de Pathologie et Diagnostic Oraux Faculté de Médecine Dentaire, Université Libanaise


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Introduction Le carcinome épidermoïde ou carcinome spinocellulaire ou malpighien est la tumeur maligne le plus souvent observée dans la cavité buccale. Il représente plus de 90 % de tous les cancers buccaux [1-5] et touche deux à trois fois plus d’hommes que de femmes [1-4]. La majorité des cas sont découverts chez des personnes âgées de plus de 45 ans, bien qu’un nombre croissant de cancers de la cavité buccale, entre 4% et 6%, soit maintenant diagnostiqué chez des adultes de moins de 40 ans [1–6]. Le carcinome épidermoïde de la cavité buccale peut se présenter sous divers aspects cliniques, telles une érythroplasie, une érythroleucoplasie, une ulcération chronique, une masse bourgeonnante ou une lésion endophytique. Les lésions bourgeonnantes ou végétantes ont un meilleur pronostic que les lésions infiltrantes et surtout ulcérantes [7, 8]. Les lésions débutantes sont souvent discrètes et totalement asymptomatiques. En revanche, les lésions avancées sont typiquement indurées et peuvent être associées à une douleur importante. A ce stade, ces carcinomes deviennent faciles à détecter dès lors qu’ils deviennent symptomatiques [9]. Les sites de prédilection du carcinome épidermoïde sont la langue, le plancher buccal, le palais mou, l’oropharynx et le complexe gencive-crête alvéolaire, particulièrement dans la région mandibulaire [1, 4, 9–11]. Les facteurs favorisants sont multiples; on parle de facteurs extrinsèques tels que le tabac et l’alcool et intrinsèques tels que les facteurs héréditaires [3]. L’association alcool et tabac paraît être un facteur de risque signifiant [1, 3, 9, 11]. Il est intéressant de signaler que les altérations histologiques typiques du carcinome épidermoïde n’ont pas pu être mises en rapport avec l’action carcinogénique de l’alcool ou du tabac [1]. Le carcinome de la langue représente un peu plus de la moitié de tous les cancers de la cavité buccale. Il a

tendance à toucher plus particulièrement la partie postéro-latérale, mais peut aussi affecter la face antéro-latérale ou ventrale et, plus rarement, la face dorsale; l’atteinte de la face dorsale médiane est exceptionnelle. Ce carcinome, tout comme celui du plancher buccal, tend à métastaser rapidement. Les lésions débutantes peuvent être confondues avec un processus bénin et sont souvent très peu douloureuses [3, 12] voire même asymptomatiques [9, 13]. Ainsi, les patients peuvent présenter un petit foyer de kératose anodin, un érythème atypique ou une ulcération superficielle d’allure traumatique. Les lésions plus avancées infiltrent ou déforment la surface de la langue, prenant habituellement la forme d’une masse bourgeonnante indurée, ulcérée ou nécrosée, entremêlée de foyers leucoplasiques ou érythroplasiques. Ces lésions peuvent aussi saigner facilement. Le carcinome de la langue a souvent tendance à envahir le plancher buccal, voire la loge amygdalienne et le palais mou, lorsqu’il se développe dans la région postéro-latérale. Les cancers de la région postérieure de la langue peuvent entraîner une odynophagie, une dysphagie, des troubles de l’élocution et de la mastication, une otalgie réflexe ainsi qu’une paresthésie linguale [4, 12]. Le carcinome du plancher buccal constitue la deuxième localisation du carcinome épidermoïde. D’après Marx [13], il représente 15 à 20% des cas. Il se présente cliniquement sous forme d’une lésion exophytique ou infiltrante ayant la capacité de métastaser à distance. Il est habituellement situé sur la ligne médiane, à proximité du frein lingual. Il a souvent tendance à envahir la face ventrale de la langue et la face linguale de la mandibule, ce qui rend le traitement plus complexe. La partie postérieure du plancher buccal est un site plus rarement affecté [3, 4, 12, 13]. Dans le carcinome épidermoïde du plancher buccal la symptomatologie n’est pas en rapport avec la sévérité de la lésion ce qui explique que les lésions sont extrêmement étendues

dès la première consultation [4, 10, 13]. La muqueuse jugale et le palais dur sont les moins affectés. Le carcinome de la muqueuse jugale prend généralement la forme d’une lésion exophytique indurée, partiellement ulcérée, qui comporte couramment une composante leucoplasique ou érythroplasique. Le carcinome du palais dur, quant à lui, est une lésion souvent extensive, indurée et ulcérée qu’il faut distinguer des autres processus malins qui peuvent affecter le palais tels le carcinome muco-épidermoïde, le carcinome adénoïde kystique, l’adénocarcinome polymorphe de bas grade, la tumeur mixte maligne et l’adénocarcinome à cellules acinaires [3, 4, 6].

Cas cliniques Deux cas de carcinome épidermoïde sont présentés: le premier au niveau de la face latérale et ventrale de la langue et le second au niveau de la muqueuse jugale. Premier cas Une patiente de 74 ans est référée au département de Pathologie et de Diagnostic Oraux pour une gêne au niveau de la langue à la mastication. Une thyroïdectomie a été réalisée en 1990 et des examens sanguins annuels sont entrepris pour le suivi du taux de TSH et T3 (le dernier en date remonte à septembre 2008). Depuis, elle est sous Eltroxin® (1 cp le matin), Indéral® (1 cp matin et soir) et Lexotanil® (1 cp le soir). Rien n’est signalé à l’examen exobuccal. L’inspection buccale a montré une tuméfaction du bord latéral gauche de la langue (Fig. 1) s’étendant à la face dorsale et à la face ventrale (Fig. 2) «criblée» par deux ulcérations: – la première, au niveau du bord latéral de la langue, de forme arrondie, de 1,5 cm de diamètre, avec des bords surélevés irréguliers, un fond bourgeonnant saignant au moindre contact, à base indurée à la palpation,


81 Médecine Orale / 2UDO0HGLFLQH

A B

Fig. 1: vue du bord latéral gauche de la langue (A et B : ulcérations). Fig. 2: vue de la face dorsale de la langue.

)LJDHWEWUDYpHVHWOREXOHVGHFHOOXOHVpSLGHUPRwGHVTXLLQÀOWUHQWOHFKRULRQ

s’étendant approximativement 1 cm au-delà de sa limite clinique (Fig 1; A). – la deuxième, au niveau de la face ventrale, en arrière de la première, de forme ovalaire, le grand axe mesurant 2 cm et le petit axe mesurant 1,5 cm, à bords nets et irréguliers, un fond plat, jaunâtre et nécrotique et une base ferme à la palpation (Fig. 1; B). Les signes cliniques font craindre volontiers la présence d’une lésion maligne, en l’occurrence un carcinome épidermoïde. Une biopsie incisionelle a été pratiquée pour un examen anatomopathologique.

Fig. 4: glossectomie partielle.

Fig. 5: cicatrice du curage ganglionnaire cervical et submandibulaire.

L’examen macroscopique de la pièce excisée a montré «un fragment beige-grisâtre irrégulier de 2.5x0.8x0.6 cm. L’examen microscopique a montré une prolifération néoplasique constituée par des cellules épidermoïdes moyennement différenciées. Ces cellules dessinent des travées et des lobules qui infiltrent le chorion. Des images de kératinisation sont notées. Le stroma est inflammatoire» (Figs. 3a et 3b). Le diagnostic définitif était un carcinome spino-cellulaire moyennement différencié, infiltrant.

La patiente a été orientée vers un centre hospitalier spécialisé. Un bilan médical pré-chirurgical a été alors réalisé comportant: - Un CT scan de la face et du cou qui a révélé quelques nodules lymphatiques inférieurs à 6 millimètres au niveau des régions latéro-cervicale et submandibulaire. - Une formule et numération sanguine, une radiographie du thorax et une échographie abdominale qui n’ont révélé aucun indice ou déviation en faveur d’une pathologie bénigne ou maligne.


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&DVFOLQLTXH_&DVHUHSRUW

Fig. 6: vue de de la muqueuse jugale gauche : lésions exophytiques papillomateuses.

Fig. 8: cicatrice après curage ganglionnaire cervical.

Le traitement a consisté en une glossectomie partielle (Fig. 4) englobant la lésion et une marge approximative d’un centimètre de tissu sain avec un curage ganglionnaire submandibulaire et cervical (Fig. 5). L’examen microscopique des nodules lymphatiques a confirmé l’absence de cellules atypiques. Une chimiothérapie et/ou une radiothérapie n’ont pas été envisagées compte tenu de l’absence d’infiltration des nodules lymphatiques. L’excision totale de la tumeur a été réalisée. La glossectomie partielle a altéré la phonation. Un suivi régulier mensuel durant les 3 premiers mois et trimestriel durant 2 ans a été recommandé. Second cas Une patiente de 71 ans est référée au département de Pathologie et de Diagnostic Oraux pour une sensation de brûlure au niveau de la muqueuse jugale gauche.

)LJYXHGHODPXTXHXVHMXJDOH droite:lichen plan érosif et réticulaire.

Fig. 9 : travées de cellules épidermoïdes LQÀOWUDQWOHFKRULRQ

Fig. 10: cellules épidermoïdes moyennement différenciées.

La patiente est épileptique depuis près de 28 ans et traitée actuellement par Topamax® 100 mg (1cp et demi matin et soir), Tegretol® 400 mg (1cp matin, midi et soir) et Gardenal® (1cp le soir). Une chirurgie de prolapsus rectal a été réalisée en 2005. Elle présente une hypertriglycéridémie traitée par Lipanthyl® (1cp à midi). La patiente, tabagique, est considérée à 40 paquets-année (40 PA). Dans les antécédents oraux, on a noté la survenue depuis 3 ans d’un lichen plan réticulaire et érosif bilatéral de la muqueuse jugale, alors confirmé par l’examen anatomopathologique du matériel prélevé par biopsie. Cet examen n’avait pas montré d’atypies cellulaires. La patiente avait depuis, omis de respecter les consignes de compliance et de suivi réglementaires. L’examen exobuccal a révélé des nodules lymphatiques submandibulaires gauches de consistance molle,

infracentimètriques, sensibles à la palpation. L’examen endobuccal a montré de multiples lésions exophytiques papillomateuses de forme et de taille irrégulières s’étendant sur toute la muqueuse jugale gauche jusqu’au fond du vestibule mandibulaire. Ces lésions étaient séparées par des cratères assez profonds; le contour était mal défini; la couleur était rose pâle à certains endroits et rougeâtre à d’autres. A la palpation, ces lésions avaient une consistance ferme et une base indurée plus large que la lésion clinique (Fig. 6). Notre diagnostic provisoire était un carcinome épidermoïde. Au niveau de la muqueuse jugale droite, des zones érosives et des lignes blanches réticulaires sont notées (Fig. 7). Cet aspect des lésions est en faveur d’un lichen plan érosif et réticulaire. Aucune lésion cutanée n’a été mise en évidence lors de l’examen exobuccal et de l’interrogatoire.


83 Médecine Orale / 2UDO0HGLFLQH Une biopsie incisionnelle a été pratiquée au niveau de la muqueuse jugale gauche. L’examen anatomopathologique a confirmé le diagnostic de carcinome épidermoïde moyennement différencié et infiltrant. La patiente a été orientée vers un centre spécialisé d’oncologie pour sa prise en charge. Le bilan médical pré-chirurgical n’a signalé aucune déviation de la normale. Il a comporté: – une formule et numération sanguine; – un CT scan de la face et du cou; – une radiographie thoracique; – une échographie abdominale. Une excision des lésions de la muqueuse jugale gauche a été alors pratiquée avec une marge de sécurité d’un centimètre tout autour de la lésion. De même, un curage ganglionnaire cervical a été réalisé avec une excision de la glande submandibulaire (Fig. 8) et un comblement de la perte de substance par un greffon libre de peau de la région inguinale. L’examen anatomopathologique a montré que « les limites analysées étaient dépourvues de prolifération carcinomateuse infiltrante (Figs. 9, 10). La lésion présentait des aspects hétérogènes; elle est tantôt papillomateuse régulière tantôt papillomateuse présentant des atypies architecturales et cytonucléaires plus rarement devenant carcinomateuse épidermoïde infiltrante s’accompagnant d’un abondant infiltrat inflammatoire avec exocytose dans l’épithélium de revêtement. Il n’a pas été retrouvé d’image d’engainement péri-nerveux ni d’embols carcinomateux. Les différents ganglions, au nombre de 23, qui ont été analysés étaient indemnes d’une atypie cellulaire». Le diagnostic définitif était une lésion papillomateuse diffuse avec dégénérescence carcinomateuse épidermoïde infiltrante multifocale avec des limites chirurgicales saines et sans métastase carcinomateuse. Le traitement a consisté en une exérèse large dont la seule consé-

quence a été une limitation de l’ouverture buccale, séquelle fonctionnelle et transitoire d’une durée de 6 mois, alors que la phonation, la déglutition et la mastication n’ont pas été altérées. L’excision chirurgicale complète et l’absence d’infiltration nodulaire n’ont pas rendu nécessaire le recours à une chimiothérapie et/ou une radiothérapie adjuvante. Le même protocole de suivi (mensuel durant les 3 premiers mois et trimestriel durant 2 ans) a été aussi recommandé.

Discussion Le carcinome épidermoïde de la cavité buccale est deux à trois fois plus fréquent chez l’homme que chez la femme [3]. Les deux cas présentés étaient de sexe féminin. Une augmentation du risque d’atteinte du sexe féminin durant la dernière décennie par le carcinome épidermoïde est décrite dans la littérature [1, 7]. Les deux patientes ont plus de 70 ans. La survenue d’un carcinome épidermoïde a lieu au-delà de 45 ans. Chez la femme, le taux d’incidence augmente nettement à partir de 60 ans pour atteindre un maximum à 85 ans. La mortalité suit la même évolution que l’incidence avec l’âge [1]. Dans la littérature, le tabac augmente le risque du cancer de 2 à 4 fois, et quand il est associé à l’alcool, le risque devient 15 fois plus élevé [9, 10]. Dans le premier cas, la patiente n’a jamais fumé alors que dans le second la patiente, tabagique, est considérée à 40 paquets-année (40 PA) ce qui est en soi un facteur carcinogène majeur. Les sites de prédilection du carcinome épidermoïde sont la langue, le plancher buccal, le palais mou, l’oropharynx et le complexe gencive-crête alvéolaire, particulièrement la région mandibulaire [4, 6]. Le site dans le premier cas est la langue et dans le second, la muqueuse jugale gauche. Les carcinomes épidermoïdes peuvent être primaires ou développés en deuxième intention sur une lésion potentiellement maligne tels que la leucoplasie inhomogène, l’érythropla-

sie, le lichen plan érosif ou atrophique, … [1,6, 13]. Dans le premier cas il s’agit, très probablement, d’un carcinome épidermoïde primaire caractérisé par la présence d’une ulcération avec des bords surélevés irréguliers, un fond bourgeonnant saignant au moindre contact et une base indurée plus large que la lésion clinique. Alors que dans le deuxième cas, le carcinome s’est développé sur un lichen plan évoluant depuis 3 ans avec des lésions exophytiques papillomateuses de taille et de forme irrégulières et une base indurée plus large. La classification T.N.M. (sigle anglais de Tumor, Node, Metastasis) permet d’établir le bilan de la maladie cancéreuse et de guider le choix des diverses modalités thérapeutiques. Le traitement des carcinomes au stade I (T1 N0 M0) et au stade II (T2 N0 M0) est chirurgical puisque la taille de la lésion permet une excision totale; le bilan élimine la présence d’autres lésions primaires ou métastatiques et l’examen microscopique des ganglions sentinelles montre l’absence des cellules atypiques. La radiothérapie et la chimiothérapie sont alors écartées. Celles-ci sont des thérapies adjuvantes au traitement chirurgical dans le stade III (T3 N0 M0, tout T N1 M0) et le stade IV (tout T N2 M0, tout T N3 M0, tout T ou N M1) et palliatives dans les cas des carcinomes inopérables [3, 13]. Dans le premier cas, le carcinome est au stade I (T1 N0 M0). Le traitement, une glossectomie partielle, a altéré la phonation. Dans le second cas, le carcinome est au stade III (T3 N0 M0) et l’examen microscopique des 23 ganglions excisés a montré l’absence d’atypie cellulaire ce qui a écarté le recours à des thérapies adjuvantes. L’exérèse large n’a engendré que la limitation de l’ouverture buccale comme séquelle fonctionnelle transitoire pour 6 mois approximativement alors que la phonation, la déglutition et la mastication n’ont pas été altérées. Dans les deux cas la perte de substance a été limitée aux tissus mous sans altérations de l’esthétique à


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&DVFOLQLTXH_&DVHUHSRUW lâ&#x20AC;&#x2122;exception des cicatrices du curage ganglionnaire. Le siège du carcinome ĂŠpidermoĂŻde est un ĂŠlĂŠment primordial quant aux consĂŠquences fonctionnelles et esthĂŠtiques postchirurgicales des traitements. Lâ&#x20AC;&#x2122;option thĂŠrapeutique sâ&#x20AC;&#x2122;est donc limitĂŠe exclusivement au traitement chirurgical. Les ĂŠtudes menĂŠes par Allisson [14] et Barrelier et coll. [7] ont montrĂŠ que le principal facteur dĂŠterminant des taux de survie est le stade de la maladie au moment du dĂŠpistage. Entre 1992 et 1998, les taux de survie Ă cinq ans des patients atteints de carcinomes de la bouche et du pharynx se situaient Ă  82% dans le cas dâ&#x20AC;&#x2122;une lĂŠsion localisĂŠe au stade I ou II; Ă  47% si la maladie ĂŠtait au stade III et avait touchĂŠ les territoires avoisinants, par exemple un cancer qui envahit les ganglions lymphatiques cervicaux; et Ă  23%, si elle est au stade IV avec des mĂŠtastases Ă  distance [7, 14]. Les chances de guĂŠrison sont quatre fois plus grandes si lâ&#x20AC;&#x2122;on dĂŠcouvre le carcinome au stade I ou II, et les sĂŠquelles beaucoup moins importantes. Il est malheureusement regrettable que la plupart des cancers buccaux ne sont dĂŠtectĂŠs que tardivement après ĂŞtre devenus symptomatiques [9, 10].

Conclusion Le dentiste a un rĂ´le primordial dans le dĂŠpistage prĂŠcoce du carcinome ĂŠpidermoĂŻde de la cavitĂŠ buccale ce qui rend le traitement moins mutilant et par la suite le pronostic plus favorable [4, 15]. Le dentiste doit donc intĂŠgrer dans sa pratique le dĂŠpistage systĂŠmatique des lĂŠsions orales, en lâ&#x20AC;&#x2122;occurrence celles Ă caractère prĂŠ-malin ou malin. Une familiarisation du dentiste avec les signes cliniques pĂŠjoratifs dâ&#x20AC;&#x2122;un processus malin (dĂŠveloppĂŠs plus haut) et les diffĂŠrents aspects cliniques du carcinome ĂŠpidermoĂŻde, et des cancers en gĂŠnĂŠral, est indispensable pour mener Ă  bien cette tâche.

RĂŠfĂŠrences 1. Barthelemy I, Sannajust JP, Revol P, MondiĂŠ JM. Cancers de OD FDYLWp EXFFDOH 3UpDPEXOH pSLGpPLRORJLH pWXGH FOLQLTXH Encycl MĂŠd Chir; Elsevier SAS, Paris, Stomatologie, 22-063-A10, 2005. 2. /DORQGH%/¡H[DPHQFOLQLTXHGHODERXFKHOHPHLOOHXUPR\HQ de dĂŠtecter le cancer buccal. Journal dentaire du QuĂŠbec 2004;SupplĂŠment:12-15. 3. 1HYLOOH%'DPP'$OOHQ&%RXTXRW-2UDODQG0D[LOORIDFLDO Pathology, 2nd edition. Philadelphia, W.B. Saunders; 2002. 4. 3pUXVVH 5 /HV PDQLIHVWDWLRQV FOLQLTXHV GX FDQFHU EXFFDO Journal dentaire du QuĂŠbec 2004;SupplĂŠment:16-21. 5. Szpirglas H, Guilbert F. Cancers de la cavitĂŠ buccale. PrĂŠambule. Encycl MĂŠd Chir, (Elsevier SAS, Paris), (Stomatologie, 22-063-A05), 1996 3p. 6. Regezi JA, Sciubba JJ, Jordan RC. Oral pathology: Clinical pathologic correlations, 5th edition. St Louis: Saunders Elsevier. 2008. 7. Barrelier P, Granon C. Ă&#x2030;pidĂŠmiologie des cancers de la cavitĂŠ buccale. Encycl MĂŠd Chir (Elsevier SAS, Paris), (Stomatologie, 22-063-B-10), 1997:10p. 8. Samson J, Duran D, Carrel JP. LĂŠsions prĂŠcancĂŠreuses et prĂŠcurseurs des carcinomes ĂŠpidermoĂŻdes de la cavitĂŠ buccale. RĂŠal Clin 1999;10(3):373-387. 9. Mashberg A, Samit A. Early diagnosis of asymptomatic oral DQG RURSKDU\QJHDO VTXDPRXV FDQFHUV &$ &DQFHU - &OLQ 1995;45(6):328-351. 10. Bouletreau P, Froget N, Gleizal A, Breton P. Affections du plancher de la bouche. EMC, Stomatologie, 2005 ;22-056-A-10, 11p. 11. Scully, Crispian (2008). Oral and maxillofacial medicine: the basis of diagnosis and treatment (2nd ed.). Edinburgh: Churchill Livingstone. pp. 201â&#x20AC;&#x201C;203. 12. Laskaris G. Atlas des maladies buccales. Paris: Flammarion. 2ème ĂŠdition, 1994. pp: 230. 13. Marx R, Stern D. Oral and Maxillofacial Pathology: A rationale for diagnosis and treatment. Second edition, Quintessence Publishing Co, Inc. 2012. 14. Allison P. Ă&#x2030;pidĂŠmiologie et ĂŠtiologie des cancers de la bouche et du pharynx, au Canada et au QuĂŠbec. Journal dentaire du QuĂŠbec 2004; SupplĂŠment: 6-11. 15. Boisvert P. Parler du cancer buccal : une approche adaptĂŠe aux besoins dâ&#x20AC;&#x2122;information des patients. Journal dentaire du QuĂŠbec 2004;SupplĂŠment:26-27.


CAS CLINIQUE / CASE REPORT

Médecine Orale2UDO0HGLFLQH

ORAL TERTIARY SYPHILIS : A CASE REPORT

'HHSD06 _$QLWD%DODQ _6XQLO6 _%LÀ-R\

Abstract Currently, tertiary syphilis is very rarely seen. This paper describes a case of benign tertiary syphilis. The lesion appears as a solitary hypertrophic lesion on the dorsum of the tongue. The oral aspects of tertiary syphilis and the importance of considering this pathologic entity in the differential diagnosis of oral lesions are highlighted.

Résumé Actuellement, la syphilis tertiaire est très rarement observée. Cet article décrit un cas de syphilis tertiaire bénin. La lésion apparaît comme une lésion hypertrophique solitaire sur le dos de la langue. Les caractères oraux de la syphilis tertiaire et l’importance d’envisager cette entité pathologique dans le diagnostic différentiel des lésions buccales sont mis en évidence.

Keywords: Spirochetes – Treponema pallidum - tertiary syphilis.

Mots-clés : spirochètes – Tréponème pallidum – syphillis tertiaire.

* Prof. Head Dept of Oral Medicine, Azeezia College of Dental Sciences and Research, Kollam, Kerala, India docdeepams@yahoo.co.in

** Prof.

Head Dept of Oral Medicine & Radiology Governmental Dental College, Calicut, Kerala, India

*** Prof.

Dept of Oral & Maxillofacial Pathology, Azeezia College of Dental Sciences and Research, India

**** Ex PG Student

Dept of Dermatology, Medical College, Trivandrum, India


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Introduction Syphilis is a sexually transmitted disease (STD) produced by Treponema pallidum, a microaerophilic spirochete which mainly infects humans [1]. This infection can also be transmitted in utero, and rarely by blood transfusion or non-sexual contact [2]. Syphilis has two main clinical stages: early and late. Early or infectious syphilis (recently acquired, or of less than two years’ duration) is the more contagious stage, and includes the primary and secondary forms and the early latent period [3]. In tertiary syphilis, which is extremely rare, manifestations may take up to 10 years to appear and then present themselves as benign tertiary (gummatous lesions), cardiovascular syphilis, or neurosyphilis [4]. Fortunately, manifestations of tertiary syphilis have become rare due to the development of programs that control sexually transmitted diseases and the inadvertent therapy with antibiotics administered for other pathologic conditions. In this report, we describe a case of benign tertiary syphilis represented by a solitary lesion of the tongue.

Case Presentation A 65-year-old lady was referred to the Department of Oral Medicine & Radiology for the evaluation of a solitary painless ulcer on the dorsum of tongue from the Department of Venerology, Medical College, Trivandrum, Kerala. Her medical history was uneventful. She had increased salivation for the past 5 years. Her husband died 17 years ago. She had 4 healthy children. The clinical examination didn’t reveal any active skin or genital lesion. She had a solitary painless, 2x2cm well-defined ulcer in the middle of dorsum of tongue (Fig. 1) with a pale granulation tissue at the base. There was no fluid exudation on pressure.

Fig 1: Clinical photograph showing ulcer on the dorsum of tongue.

Fig. 2: Photomicrograph showing nonVSHFLÀFLQÁDPPDWLRQRIWKHFRQQHFWLYH tissue, H& E section, 10X.

Cervical and generalized lymphadenopathy was not detected. Subsequent hematological, serological and histopathological investigations were carried out. Hematological examinations were within normal limits. Blood serologic tests for syphilis (STS) showed positivity in 1 of 32 dilutions. Treponema pallidum haemagglutination (TPHA) test was positive; hepatitis B surface antigen (HBsAg) and the enzyme-linked immunosorbent assay (ELISA) were negative. Histopathological examination revealed only a chronic nonspecific inflammation (Fig. 2). Based on the results of serological examination, the patient was diagnosed as having a gummatous ulcer on the tongue and was put on penicillin therapy as intramuscular injection – PP 12 lakh units- daily for 12 consecutive days. A resolution of the lesion was noticed 2 weeks after the initiation of the penicillin therapy and blood STS became non-reactive after 3 months.

incubation period of up to 90 days, a chancre develops at the site of inoculation. These ulcers may be solitary or multiple, and generally heal spontaneously without treatment within 3–8 weeks. Syphilis gives rise to a wide spectrum of orofacial manifestations [5-7]. However the exclusive oral localization, not associated with general manifestations, is uncommon [8]. The various orofacial manifestations of the different stages of syphilis are shown in table 1 [9]. Gummas tend to arise on the hard palate and tongue; although very rare, they may occur on the soft palate, lower alveolus and parotid gland. The signs and symptoms of primary and secondary syphilis resolve spontaneously. Patients enter then the latent stage of infection [10, 11]. Manifestations of tertiary syphilis may appear after several years of non-treatment with cardiovascular and neurologic involvements including severe manifestation of general paresis and aneurysm of aorta. Benign tertiary syphilis is characterized by the tissue immunological reaction that leads to a specific lesion designed as gumma. These lesions are destructive granulomatous inflammation that may develop in any organ [4]. In the present case, the lesion observed on the dorsal surface of the tongue was a “gummatous inflammation” of tertiary syphilis. Conclusive diagnosis of syphilis infection is based on confirmation of

Discussion Infective syphilis is caused by the spirochete Treponema pallidum. Transmission occurs via close contact with an infected lesion, which usually occurs on the genitals. Following contact, Treponema pallidum penetrates the genital or oral mucosa, multiplies at this site of entry, and systemically spreads via the lymphatics and blood. After an average


87 Médecine Orale / 2UDO0HGLFLQH Stage of disease

Orofacial manifestations

Primary

Chancre Non-tender cervical lymphadenopathy

Secondary

Mucous patch ‘Rubbery’ cervical lymphadenopathy Maculopapular eruptions Moth-eaten alopecia Syphilitic leukoedema - patches of hypopigmentation Condylomata lata

Tertiary

Gumma (palate and tongue) Osteomyelitis Atrophic and interstitial glossitis Syphilitic leukoplakia Syphilitic sialadenitis Trigeminal neuropathy (Hitzig’s Syndrome) Argyll-Robertson pupil

Congenital Syphilis

Moon’s / Mulberry molars Hutchinson’s incisors Facial deformity - High arched or gothic palate - Maxillary hypoplasia “Bulldog” jaw - Saddle shaped deformity of nose - Frontal bossing Mucous patches Rhagades (scars radiating from lips) Cranial neuropathies

Table 1: The orofacial manifestations RIGLIIHUHQWVWDJHVRIV\SKLOLV>@

the clinical signs and symptoms with laboratory tests [11]. Treponema pallidum can be identified in lesions by dark field microscopy or direct immunofluorescence, but usually serological confirmation is necessary [12]. The diagnostic serologic tests for syphilis include tests that detect antibodies to non-specific treponemal antigens - the Rapid Plasma Reagin (RPR), Venereal Disease Research Laboratory tests (VDRL) and tests that detect antibodies specific to Treponema pallidum – the Treponema pallidum hameagglutination assay (TPHA) and fluorescent treponema antibodies absorbed assay (FTA-Abs). The non-specific antibody tests are inexpensive, rapid screening tools and markers of disease activity. The specific tests are more sensitive than the non-specific assay. FTA-Abs detects antibodies to Treponema pallidum in the early stages of infection [12, 13]. In the secondary stage, microorganisms may be detected by special silver impregnation techniques and direct fluorescent antibody testing.

Meyer and Shklar reported the features of primary and secondary syphilis to be essentially non-specific and the tertiary lesion to be the most obviously granulomatous and populated by Langhans-type giant cells [14]. The histo-pathologic features in the primary lesions consist of an ulcerated epithelium. The underlying connective tissue may show moderate vascularity with intense chronic inflammatory cell infiltration, predominantly lymphocytes and plasma cells with perivascular pattern. In secondary syphilis, the features include hyperplastic epithelium and the connective tissue shows perivascular infiltration with chronic inflammatory cells. In tertiary lesions, ulcerated epithelium with inflammation of connective tissue and foci of granulomatous inflammation with histiocytes and giant cells are noticed [14-16]. Features of c/c granulomatous inflammation without significant necrosis are typical of early nodular lesions of tertiary syphilis and the sparse numbers of plasma cells

can mask the diagnosis [17]. Tertiary lesions are only sparsely populated with spirochetes [18]. Easy, consistent and reliable identification of Treponema pallidum, however remains problematic.

Conclusion Syphilis is an infectious disease presenting stages associated with specific oral lesions. Therefore, health professionals should be familiar with the different syphilis oral manifestations at each stage and be prepared to refer any suspected patient for further evaluation.


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References 1. Palacios MuĂąoz R, De la Fuente Aguado J, Murillas Angoiti J, Nogueira Coito JM, Santos GonzĂĄlez J. On behalf of the AIDS Study Group (Grupo de Estudio del Sida [GeSIDA]). Syphilis and HIV infection. Enferm Infecc Microbiol Clin 2006;24:34-9. 2. Goh BT. Syphilis in adults. Sex Transm Infect 2005;81:448â&#x20AC;&#x201C;52. 3. Cawson RA, Odell EW. Cawsonâ&#x20AC;&#x2122;s essentials of oral pathology and oral medicine. 8th ed. Philadelphia: Churchill Livingstone Elsevier; 2008. 4. +RRN('0DUUD&0$FTXLUHGV\SKLOLVLQDGXOWV1(QJO-0HG 1992;326:1060-1069. 5. Aloi F. Lip syphilitic chancre in a child. Pediatr Dermatol 1987;4:63. 6. Bhatt AP. Case of the mouth. Primary chancre of the lower lip. J Indian Dent Assoc 1986;58:1. 7. Hart G. Syphilis tests in diagnostic and therapeutic decision making. Ann Inter Med 1986;104:368-376. 8. $TXLOLQD & 9LUDEHQ 5 'HQLV 3 6HFRQGDU\ V\SKLOLV VLPXODWLQJ oral hairy leukoplakia. J Am Acad Dermatol 2003 Oct;49(4):74951. 9. Carlesimo M, Palese E, Mari E et al. Isolated oral erosions: an unusual manifestation of secondary syphilis. Dermatology. Online Journal 2008;14(2):23. 10. Anderson J, Mindel A, Towei SJ, Williams P. Primary & secondary syphilis, 20 yearsâ&#x20AC;&#x2122; experience. Diagnosis, treatment and follow-up. Genitourin Medm 1989;65:239-243. 11. Hutchinson CM, Hook EW. Syphilis in adults. Med Clin North Am 1990;74:1389-1416. 12. Alam F, Argiriadou AS, Hodgson TA, kumur N and Porter SR. Primary syphilis remains a cause of oral ulceration. British Dent J 2000;189:352-354. 13. Young H. Syphilis serology. Dermatologic clinics 1998;16: 691698. 14. 0H\HU6KNODU*7KHRUDOPDQLIHVWDWLRQVRIDFTXLUHGV\SKLOLV Oral Surg Oral Med Oral Patho 1967;23:45-57. 15. Little JW. Syphilis: an update. Oral Surg Oral Med Oral Path Oral Radiol Endo 2005;100:3-9. 16. Montone KT. Infectious diseases of head and neck. A review. Am J Clin Pathol 2007;128:35-67. 17. Mckee P. Infections diseases in skin pathology. Edinburgh: Churchill Livingstone, 1997;549-54. 18. Siegel MA. Syphilis and gonorrhea. Dent Clin North Am 1996;40:369-83.


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