Journal of International Dental and Medical Research

Journal of International Dental and Medical Research Editor list of 2009

ISSN: 1309-100X

Assoc. Prof. Dr. Izzet YAVUZ Editor-in-Chief and General Director Assist. Prof. Dr. Ozkan ADIGUZEL Associate Editor and Director Prof. Dr. M. Zulkuf AKDAG, Prof. Dr. Sinerik N. AYRAPETYAN Associate Editor for Biomedical research Assoc. Prof. Dr. Refik ULKU Associate Editor for Medicine Assist. Prof. Dr. Filiz ACUN KAYA Associate Editor for Dentistry Advisory Board Betul KARGUL (TURKEY) Ferranti WONG (UNITED KINGDOM) Filiz ACUN KAYA (TURKEY) Gauri LELE (INDIA) Gulten UNLU (TURKEY) Jalen Devecioglu KAMA (TURKEY) Moschos A. PAPADOPOULOS (GREECE) Nik Noriah Nik HUSSEIN (MALAYSIA) Sabiha Zelal ULKU (TURKEY) Sadullah KAYA (TURKEY) Editorial Board Xiong-Li YANG (CHINA) Zurab KOMETIANI (GEORGIA) Gajanan Kiran KULKARNI (CANADA) Mehmet Zulkuf AKDAG (TURKEY) Yuri LIMANSKI (UKRAINE) Gulten UNLU (TURKEY) Nik Noriah Nik HUSSEIN (MALAYSIA) Rafat Ali SIDDIQUI (PAKISTAN) Jalen DEVECIOGLU KAMA (TURKEY) Ferranti WONG (UNITED KINGDOM) Betul KARGUL (TURKEY) Susumu TEREKAWA (JAPAN) Nihal HAMAMCI (TURKEY) Moschos A. PAPADOPOULOS (GREECE) Izzet YAVUZ (TURKEY) Halimah AWANG (MALAYSIA) Serdar ERDINE (TURKEY) Margaret TZAPHLIDOU (GREECE) Ozkan ADIGUZEL (TURKEY) Muhammad FAHIM (INDIA) Smaragda KAVADIA (GREECE) Sabiha Zelal ULKU (TURKEY) Abdel Fattah BADAWI (EGYPT) Sossani SIDIROPOULOU (GREECE) Emin Caner TUMEN (TURKEY) Mostaphazadeh AMROLLAH (IRAN) Medi GANIBEGOVIC (BOSNIA and HERZEGOVINA) Filiz Acun KAYA (TURKEY) Stephen D. SMITH (UNITED STATES OF AMERICA) Guvenc BASARAN (TURKEY)

Sinerik N. AYRAPETYAN (ARMENIA) Suleyman DASDAG (TURKEY) Gauri LELE (INDIA) Ali GUR (TURKEY) Refik ULKU (TURKEY) Shailesh LELE (INDIA) Murat AKKUS (TURKEY) Fadel M. ALI (EGYPT) Alpaslan TUZCU (TURKEY) Igor BELYAEV (SWEDEN) Sedat AKDENIZ (TURKEY) KING Nigel MARTYN (HONG KONG SAR, P R CHINA) Muzeyyen YILDIRIM (TURKEY) Christine Bettina STAUDT (SWITZERLAND) Senay ARIKAN (TURKEY) Karla PADILLA (MEXICO) Eylem OZDEMIR (TURKEY) Selahattin TEKES (TURKEY) Claudia DELLAVIA ( ITALY ) Feriha CAGLAYAN (TURKEY) Marco MONTANARI (ITALY) Aziz YASAN (TURKEY) Filippo BATTELLI (ITALY) Ugur KEKLIKCI (TURKEY) Ali Al-ZAAG (IRAQ) Zeki AKKUS (TURKEY) Benik HARUTUNYAN (ARMENIA) Sadullah KAYA (TURKEY) Guliz Nigar GUNCU (TURKEY) Nurten ERDAL (TURKEY)

*Formerly the Name of “Journal of International Dental and Medical Research” was “International Dental and Medical Disorders”.

Journal of International Dental and Medical Research Table of Contents

ISSN: 1309-100X

2009 Volume 2 - Number 2

DENTISTRY Mental Foramen / Canal / and Mental Block Anesthesia Mokhalad F. ALMUDARES, Marwan M. AL-SEGHAIRI Pages 37-39 The Prevelance and Etiology of Dental Trauma Among 5-72 Months Preschool Children in South-Eastern Anatolia, Turkey.

Emin Caner TUMEN, Ozkan ADIGUZEL, Sadullah KAYA, Ersin UYSAL, Izzet YAVUZ, Fatma ATAKUL Pages 40-44 Talon Cusp: A Literature Review and 3 Case Reports Senem YIGIT OZER Pages 45-49 A Diagnosis and Treatment of the Multiple Compound Odontoma in Mandibula Behiye SEZGIN BOLGUL, Belgin GORGUN, Torun OZER, Sema CELENK, Buket AYNA, Fatma ATAKUL Pages 50-52 The Effects of Ectodermal Dysplasia on Periodontal Tissues Tuba TALO, Filiz ACUN KAYA Pages 53-57 MEDICINE Primary Yolk Sac Tumor in the Thoracic Wall: Case Report Alper AVCI, Refik ULKU, Serdar ONAT, Cemal OZCELIK Pages 58-60 BIOMEDICAL RESEAERCH Effect of Extremely Low Frequency Magnetic Fields in Safety Standards on Structure of Acidophilic and Basophilic Cells in Anterior Pituitary Gland of Rats: an Experimental Study Mehmet Zulkuf AKDAG, Suleyman DASDAG, M.Aydin KETANI, Hakan SAGSOZ Pages 61-66

Journal Of International Dental And Medical Research ISSN: 1309-100X http://www.ektodermaldisplazi.com/journal.htm

Mental Block Anesthesia Mokhalad F. Almudares, and Marwan M. Al-Seghairi

Mental Foramen / Canal / and Mental Block Anesthesia Mokhalad F. Almudares1*, Marwan M. Al-Seghairi2 1. Mokhalad F. Almudares*; BDS, PhD.; Associate Prof. Faculty of Dentistry, Ajman University of Science & technology, UAE. 2. Marwan M. Al-Seghairi**; DDS. GP; Faculty of Dentistry, Ajman University of Science & technology, UAE.

Abstract Fifty Chinese skulls were used in our study thirty one of their mandibles showed mental canals of various length and width extend from the mental foramen outward and the inferior dental canal inward.

Also, the opening of the mental foramen is mostly directed upward and posteriorly.

This will affect mental block anesthesia. If the insertion technique of the injecting needle into the mental foramen is not done properly, the anesthetic solution will not flow into the canal. Even the mental nerve is anesthetized and the lip numbs, but there will be no block anesthesia to the continuation of the inferior dental nerve.

This will make confusion when the patient feels numbness of the lower lip whereas there is no nerve block which supplies the premolars and the anterior teeth. Palpation the foramen is not always possible because the opening is oblique and directed posterior-superiorly as reported in most studies.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 37-39) Keywords: Mental canal, mental foramina, mental block anesthesia.

Received date: 25 July 2009 Introduction The locations of the mental foramen were defined by many studies1-11. Its location can vary from the mandibular canine to the first molar12.

This foramen is contained entirely within the buccal cortical plate of the mandibular bone1, 2. The accurate identification of the mental foramen is important for both diagnosis and block mental anesthesia in oral surgery. The radiographic appearance of the mental foramen may misdiagnosis as radiolucent lesion in the periapical area of the mandibular premolars teeth.

The presence of mental canal and its dimension is the purpose of this work. Therefore the mental foramen is defined as an opening in the lateral surface of the mandible at the outer end of the mental canal

Accept date: 13 August 2009 The reamer was inserted into the canals while the rubber stopper marks the outer opening of the canal. The measurements of the canals were marked from the tip of the reamer to stopper (Fig. 1, 2, and 3); the way of measuring the length and the width is illustrated in fig.2.

Digital periapical radiograph and computer for analysis and interpretations of the radiographs were used. Periapical film folder was used to obtain proper angulations to have more accurate dimensions.

The entire periapical radiograph must follow these criteria: 1- High quality with respect to angulations and contrast 2- The film must be free from any radiolucent or radio-opaque lesion 3- Shouldn't show radiographic exposure inaccuracy or artifacts.

Material and Methods Fifty Chinese Skulls were used for this study.

A fine reamer and a rubber stopper with central hole through it the reamer passed was to measure the depth of the mental canal. *Corresponding author: Associate Prof. Mokhalad F. Almudares Faculty of Dentistry, Ajman University of Science & technology, UAE E-mail: mukhallad7@yahoo.com

Volume 2 ∙ Number ∙ 1 ∙ 2009

Panoramic radiographs (OPG) to the out patients in the faculty of the dentistry at Ajman University of Science and Technology to evaluate the location of the mental foramen were taken. Also, the patients were examined to finding out the possibility of palpating the foramen.

Results The digital radiographs of the fifty mandibles concerning the presence of mental canal and the locations of the mental foramen reveal the following findings (Tab. 1) Page 37

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1- 6% of foramina anterior to the first premolar; none of them shows canal 2- 80% of foramina between the two premolars; 62.5% of them have canals 3- 14% of foramina posterior to the second premolar; 85.7% of the have canals.

4- Out of fifty cases 31 show mental canals, whereas 19 cases didn't show canals, but only a mental foramen directly comes out of the inferior dental canal. The range of the length is 1.8 to 4.4 mm, and width 1.4 to 3.5 mm (Fig. 2).

Fig.2 Showing measurements of length and width of mental canal.

Mental Block Anesthesia Mokhalad F. Almudares, and Marwan M. Al-Seghairi

the directions of the openings of the mental foramina.

This study clearly demonstrates the presence of mental canal, and the digital periapical radiograph and computer analysis interprets various dimensions of the mental canal, which is between the mental foramen externally and the inferior dental canal internally (Fig. 1, 2).

From these finding mental block anesthesia needs direct injection of anesthetic into the mental foramen/canal/ to block the continuation of the inferior dental nerve to its end. Failure to achieve this then anesthetic solution will not flow into the mental canal especially when the foramen is directed upward and posteriorly.

Fig. 3 No mental canal are illustrated.

Discussion The locations of the mental foramen were defined by many studies1-12. Our results conformed these locations of the foramen; our examination of fifty dry Chinese skulls showed (80%) of the mental foramen were between the premolars; this is in consistent with previous studies. While (6%) of the foramen were found anterior the first premolar and (14%) posterior to the second molar. Beside this the opening of mental foramen showed various directions, but mostly upward and posteriorly as reported1.

Our observation of the Chinese skulls agrees with pervious studies of the locations and Volume 2 ∙ Number ∙ 1 ∙ 2009

Tab. 1 shows: various locations of mental foramen, and presence of mental canals in 31/50 Chinese mandibles.

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Mental Block Anesthesia Mokhalad F. Almudares, and Marwan M. Al-Seghairi

Then there will no block anesthesia to the continuation of the inferior dental nerve, but only anesthesis the mental nerve outer to its exist from the mental foramen, This will make confusion when the patient feels numbness of the lower lip whereas there is no nerve block which supply the premolars and the anterior teeth.

Conclusions This study showed the presence of different lengths of mental canal in about two third of the Chinese mandible and the presence of mental foramen anterior to the first premolar, between the premolars and posterior to the second premolar teeth. This variation has to be consideration in the mental block anesthesia. Therefore the mental foramen is an opening in the lateral surface of the mandible at the outer end of the mental canal.

References 1- Sina Haghanifar, Mehrak Rokouei; Radiograph evaluation of the mental foramen in a selected Iranian opulation. ; 2009 J Original Research, Vol 20, Issue 2, Page 150-152.

2- Moiseiwtsch JR. Position of the mental foramen in a North American,white population. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:457-60.

3- Fishel D, Buchner A, Hershkowith A, Kaffe I;. Roentgenologic study of the mental foramen. Oral Surg Oral Med Oral Pathol 1976;41:682-6.

4- Olasoji HO, Tahir A, Ekanem AU, Abubakar AA. Radiographic and anatomic locations of mental foramen in northern Nigerian adults.

Niger Postgard Med J 2004; 11:230-3.

5- Phillips JL,Weller RN, Kulild JC. The mental foramen: Part1.

Size,orientation and positional relationship to the mandibular second premolar. J Endod 1990;16:221-3.

6- Ngeow WC, Yuzawati Y. The location of the mental foramen in a selected Malay population. J Oral Sci 2003; 45: 171-5.

7- Yosue T, Brooks SL. The appearance of mental foramina on panoramic radiographs. Evaluation of patients. Oral Surg Oral Med Oral Pathol 1989;68:360-4.

8- Yosue T, Brooks SL. The appearance of mental foramina on panoramic and periapical radiographs. II.Experimental evaluation.

Oral Surg Oral Med Oral Patho 1989; 68:488- 92.

9- Shankland WE 2nd. The position of the mental foramen in Asian Indians. J Oral Implantol 1994;20:118-23.

10- Mwaniki DL, Hassanali J. The position of mandibular and mental foramina in Kenyan African mandibles. East Afr Med J 1992; 69:210-3.

11- Al Jasser NM, Nwoku AL. Radiographic study of the mental foramen in a selected Saudi population. Dentomaxillofac Radiol 1998; 27: 341-3.

12- Greenstein G. Tarnow D; J. Periodontol, 2006 Dec; 77(12): 193343.

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Traumatized anterior primary teeth Emin Caner Tumen et al.

The Prevelance and Etiology of Dental Trauma Among 5-72 Months Preschool Children in South-Eastern Anatolia, Turkey.

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Emin Caner TUMEN , Ozkan ADIGUZEL , Sadullah KAYA , Ersin UYSAL , Izzet YAVUZ , Fatma ATAKUL 1

Assist. Prof., DDS PhD, Dicle University, Faculty of Dentistry Department of Pedodontics Diyarbakir/TURKEY. Assist. Prof., DDS PhD, Dicle University, Faculty of Dentistry Department of Operative Dentistry Diyarbakir/TURKEY. Assist. Prof., DDS PhD, Dicle University, Faculty of Dentistry Department of Operative Dentistry Diyarbakir/TURKEY. 4 Assist. Prof., DDS PhD, Dicle University, Diyarbakır Vocational High School, Department of Technique Programs Diyarbakir/TURKEY. 5 Assoc. Prof., DDS PhD, Dicle University, Faculty of Dentistry Department of Pedodontics Diyarbakir/TURKEY. 6 Professor and Chair, DDS PhD, Dicle University, Faculty of Dentistry Department of Pedodontics Diyarbakir/TURKEY. 2 3

Abstract The main objective of this study was to assess the epidemiology of traumatic dental injuries to the primary teeth in children from 5 to 72 months, all atendees in 11 public nursery schools in South-Eastern Anatolia, Turkey.

A total of 657 children (346 boys and 311 girls) of both sexes participated in the study. Traumatic dental injuries were classified according to the modified classification proposed by Ellis. An interview was carried out by two trained and calibrated examiners, and clinical oral examinations included distribution of dental injuries by age and sex, etiology of dental trauma, prevelance of affected teeth and type of damage.

All results were analyzed using the Statistical Package for Social Sciences (SPSS) software, version 15.0. The prevalence of traumatic dental injuries was 5.02%. There was greater involvement of boys (78.8%), of children aged 37–48 months (63.63%) and of the maxillary central incisors (92.68%).

Falls were more often the etiology for dental injuries (66.7%). Most children with a traumatic dental injuries experienced traumatic injuries to one tooth (3.81%), while 1.21% had two traumatized teeth and 94.9% had no traumatic dental injuries. The most common crown fracture was in enamel only (65.9%), followed by discoloration teeth (14.6%).

The prevalence of dental injuries in Turkish preschool children was very low. The present study findings emphasize the importance of encouraging parents to visit the dentist with their child at an early stage. Moreover, traumatic dental injury is widespread in the population; it has both physical and psychological effects, it is treatable; and, most importantly, it is preventable.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 40-44) Keywords: Epidemiology, dental injuries, preschool children, trauma, anterior primary teeth.

Received date: 14 March 2009 Introduction Epidemiologic studies have focused on the investigation of the prevelance or incidence of dental injury. The prevelance of dental trauma in preschool children is a continuing clinical and dental public health problem1, 2.

An oral traumatic injury can frequently lead to tooth lesions, affecting both supporting dental structures and hard tissues3. Moreover the dental *Corresponding author: Assist.Prof.Emin Caner TUMEN, Dicle University Faculty of Dentistry Department of Pedodontics Diyarbakir/TURKEY Phone: + 90. 412. 2488101/3406 Fax: + 90. 412. 2488100 E-mail: emin.caner@isnet.net.tr

Volume 2 ∙ Number ∙ 2 ∙ 2009

Accept date: 14 June 2009 injuries represent serious problems affecting children physically, esthetically and psychologically, and traumatic injuries to the primary teeth can affect the development and eruption of the permanent teeth, but more attention has been given to injuries of permanent teeth than primary teeth4-8. Despite the importance of these problems, there are few reports available on the epidemiology of injuries to the teeth of children in developing countries. Also, the causes of dental injuries have rarely been studied in cross-sectional surveys including both developing and developed countries2.

The prevelance of dental trauma in various epidemiological studies has been found to differ considerably9-11. This variation may be caused by a number of factors such as differences in data collection method, sample selection and the place where the study was conducted12.

Nevertheless, few studies are available about the prevalence of traumatic injury to the Page 40

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primary dentition in children aged 5–72 months.

The literature report that children aged 3-4 years have a higher incidence of trauma, with no difference between boys and girls13. The most frequent cause is a fall against a hard object12,14-16.

The maxillary central incisors were the most vulnerable to injury. Single tooth injury was predominant in all age groups13,15.

Because of the presence of so little information on the prevalence and etiology of traumatic dental injuries in 5-72 months Turkish preschool children the main objective of this study was to assess the epidemiology of traumatic dental injuries to the primary teeth of preschool children in South-Eastern Anatolia, Turkey.

Material-Methods A cross-sectional survey was carried out in South-Eastern Anatolia, Turkey in 2007-2008. The study involved 657 children 5-72 months of age attending 11 urban public nursery schools. The schools showed great similarity in their environment (child care, medical care and diet). A total of 346 boys and 311 girls were examined. Of these children, 7 were at the age of 5-12 months; 35 at 13-24 months; 194 at 25-36 months; 181 at 37-48 months; 197 at 49-60 months, and 43 at 61-72 months, respectively.

A sample of 30 children was used to train the examiners (ECT, ÖA) and test the feasibility of the dental examinations. No changes were made to the methodology previously proposed. Ethical clearance was obtained from the Ethical Committee of the Faculty of dentistry, University of Dicle.

Local authorities (Health Council and The Education Council) provided the necessary information for the construction of a sample frame.

The following information was obtained: name of all nursery schools in Diyarbakır, their addresses and total number of children (679) in each nursery school by age. A letter was sent to the parents of the all children explaining the aim, characteristics and importance of the study, and asking for their participation. Negative consent was accepted without any prejudice being attached to the children who had opted not to participate. Of these 679 children all attending nursery schools; 22 of them were excluded because of their parents’ being unwilling to participate in the study.

All dental examinations were carried out by two dentist (ECT, ÖA) who participated in a training and calibration exercise for the criteria used to identify dental injuries. The dental examination for traumatic dental injuries included only maxillary and mandibular primary incisors. The criteria used to Volume 2 ∙ Number ∙ 2 ∙ 2009

Traumatized anterior primary teeth Emin Caner Tumen et al.

assess traumatic dental injuries were derived from a modified version of Ellis’ classification17.

It included fracture of the crown involving the enamel only, fracture of the crown involving enamel and dentin, fracture of the crown involving the pulp, tooth missing due to trauma. In addition to those criteria the presence of tooth discoloration was recorded. Pulp involvement was assessed through the presence of discoloration and presence of fistulous tract without signs of caries. Root fractures and pulp status recorded in Ellis’ classification were not recorded in this study because dental radiographs or pulp tests are not appropriate for epidemiological surveys.

The children were examined in a chair at nursery schools during class hours in predetermined order in a private room under natural light. Some of these parents sometimes helped to hold very young children. Gauze squares, cotton buds and sterile sets of plane mouth mirrors, periodontal probes were packed in sufficient quantities for each day. The examiners wore new gloves for each clinical examination. Data were collected through clinical oral examinations.

All results were analyzed using the Statistical Package for Social Sciences (SPSS) software, version 15.0 and the Medcalc version 9.4.2.0. Data analysis included descriptive statistics (frequency, distribution). Statistical significance for the association between the occurrence of traumatic dental injuries and distribution of dental injuries by age and sex, etiology of dental trauma, prevelance of affected teeth and type of damage was determined using chi-square and Fisher’s exact tests. The level of significance was set at 5%.

Results The prevalence of traumatic injuries in primary incisors was 5.02% : 7.5% in boys and 2.3% in girls. The difference was statistically significant (P = 0.0037). Aged 37-48 months experienced more trauma (63.63%), with the male sex predominating all of the groups; the difference was statistically significant (P< 0.01) (Tab. 1).

There were no significant differences in the prevalence of traumatic dental injuries between boys and girls in all specimens (P> 0.05). Besides boys suffered more traumatic injuries than girls and when each age was analyzed separately, there was statistically significant difference between both sexes (P=0.0015). Of a total of 657 children, 25 had suffered one tooth traumatic injuries (3.81%), eight had suffered two teeth traumatic injuries (1.21%) and 624 had no traumatic dental injuries (94.98%).

The differences were statistically significant (P < 0.05) (Tab. 1).

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Traumatized anterior primary teeth Emin Caner Tumen et al.

maxillary primary right central incisor showed the highest percentage of injured teeth when only one tooth was involved (41.46%), followed by the maxillary primary left central incisor (14.63%).

The most common crown fracture was in enamel only (65.9%), followed by discoloration teeth (14.6%). Crown fracture of enamel and dentin following trauma occurred in 12.2% of those with traumatic dental injuries. The prevelance of fracture of the crown involving the pulp, missing teeth due to trauma and presence of fistulous tract without signs of caries were similar with 2.43% (Tab. 4). In this distribution, there were no significant differences between boys and girls (P> 0.05).

Tab. 1 Prevalence and distribution of dental injuries in the primary dentition, by age in months and sex Diyarbakır, Turkey (n =657) *X2= 9.512 The main causes of tooth injury were falls (66.7%), collisions with objects (24.2%), sports (6.1%) and traffic accidents (3 %) (Tab. 2).

Tab. 2 Etiology of dental traumas in preschool children.

When the etiology was analyzed by gender, falls, and collisions with objects were the most frequent causes of tooth injuries in boys and girls.

The group of teeth most affected was maxillary incisors (97.56%), with the central incisors being the most frequently involved (92.68%) (Table 3).

Tab. 3 Prevalence of affected.

The maxillary arch was the most affected (97.56%), the difference was statistically significant between the right and the left side (P= 0.0139). The Volume 2 ∙ Number ∙ 2 ∙ 2009

Tab. 4 Distribution of affected teeth in relation to different types of dental injuries, Diyarbakır, Turkey (n =41).

Discussion The present study provides information on the etiology and prevelance of dental trauma among Turkish preschool children aged 5-72 months. The findings of this research extend and corroborate earlier findings4,7,18-21 regarding certain epidemiological characteristics of traumatic dental injuries present in preschool children. The present research showed that according to gender, boys had more injuries in all groups. Many other authors also reported a similar pattern22-25.

According to retrospective and prospective studies reported in the literature, the prevalence of traumatic injuries involving the primary dentition ranged from 4% to 37%4,26-32. With increased knowledge of possible sequelae to traumatized teeth, dentists can understand better how to treat these teeth and how to deal with potential complications. Careful attention should be paid when comparing studies dealing with the prevelance and distribution of different types of injury involving the primary dentition because it varies according to the place where the study is conducted, the type of study applied, and the classification used to categorize the injuries5,6,9,33,34.

The prevalence of traumatic dental injuries may have increased with age. This is due to its cumulative effect. In a Swedish study oral injuries Page 42

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were most frequent during the first 10 years of life, decreasing gradually with age and were very uncommon after the age of 30, whereas non-oral injuries were seen most frequently in adolescents and occurred throughout life35.

Several studies have demonstrated that the majority of traumatic dental injuries occur during childhood. The literature reports that the highest incidence of dental trauma is observed in children aged 12-36 months because the child is in the process of gaining mobility and independence, yet lacks full coordination5,9.

The first peak in traumatic dental injuries appears at 2–4 years of age. By the age of 7 years, 28% of the girls and 32% of the boys have suffered a traumatic dental injuries to the primary dentition.

Furthermore the parents’ anxiety in seeking dental care is higher in very young children, even after small traumatic accidents, which can affect the incidence in this age group11.

However, in retrospective studies, it has been stated that more traumatic dental injuries are recorded in older children probably because the register of injuries to hard tissues is usually cumulative36,37. This is in agreement with this investigation data, where the group aged from 37 to 48 months was the most affected by trauma, without gender difference.

The number, location, type and severity of dental injuries per person differ according to their age and the cause of the damage9. The majority of studies found that trauma to primary teeth usually involved a single tooth, and rarely more than two teeth18,28,36,38,39. In this study, it was observed that the majority of the affected preschool children (60.97%) had one traumatized tooth, while 19.51% had two damaged teeth. No child had more than two damaged teeth. This proportion is similar to that reported in the literature13,15,16,40. The explanation for the difference in numbers of teeth involved in the traumatic episodes may be the individual characteristics of the children and the varied methodologies of the studies.

The etiology of the dental injuries of the group studied was basically a fall (66.7%), in agreement with other studies12,14. The high incidence of these falls is explained by the developing motor coordination at the age of the study population4,25,40.

The anterior teeth are the most commonly traumatized. The maxillary central incisors are generally more proclined than the mandibular centrals and tend to be the first to receive a direct blow producing a fracture. In addition, the maxilla is fixed to the skull which makes it rigid, while the mandibula, being a flexible part, tends to reduce the Volume 2 ∙ Number ∙ 2 ∙ 2009

Traumatized anterior primary teeth Emin Caner Tumen et al.

impact forces directed on the mandibular anterior teeth by movement41. In the present study, the maxillary central incisors were the teeth most affected (92.68%), and these findings are very similar to those reported by other authors13,15,2225,40,42-44 .

Fractures of crowns involving the enamel only were the most common type of injury in the group studied. This finding corroborates previous researchers18,38,39,41,45. In other published studies, crown fractures were also the most common type of injury, with prevalences ranging from 63.8% to 90% of trauma involving primary teeth19,21,36,46.

In the present research, enamel fractures dominate (65.9%) followed by discoloration (14.6%) and enamel–dentin fracture (12.2%). The highest number of crown fractures observed (77.0%) was also found in other retrospective studies conducted in preschool children13,16,44. However, in previous investigations22,24, it has been reported that the most common injuries were luxations.

Conclusions The prevalence of dental injuries in Turkish preschool children was very low. The present study findings emphasize the importance of encouraging parents to visit the dentist with their child at an early stage. Moreover, traumatic dental injury is widespread in the population; it has both physical and psychological effects, it is treatable; and, most importantly, it is preventable. In order to reduce the frequency of traumatic dental injuries in preschool children and to avoid its financial consequences, there is a great need for more efforts and health promotion policies to encourage preventive strategies.

In addition, preventive educational program should be instituted in Turkey, directed at parents and preschool teachers to inform them about the importance of traumatic dental injuries and the benefit of immediate attendance for dental treatment.

With the help of this educational program sequelae of traumatic dental injuries would be also minimized considerably.

Acknowledgements: The authors thank, the local authorities (Health Council and The Education Council), nursery school directors and teachers, children and families from Diyarbakır-Turkey, for their support and contributes in this study.

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2. Marcenes W, Al BN, Tayfour D, Issa S. Epidemiology traumatic dental injuries to the permanent incisors of 9–12- year-old schoolchildren in Damascus, Syria. Dent Traumatol 1999;15: 117–23.

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7. Perez R, Berkowitz R, Mellveen E, Forrester D. Dental trauma. in children: a survey. Endod Dent Traumatol 1991; 7: 212-3.

8. Von Arx T. Develomental of permanent teeth following trauma to primary dentition. Aust Dent J 1993; 38: 1–10.

9. Bastone EB, Freer TJ, McNamara JR. Epidemiology of dental trauma: a review of the literature. Aust Dent J 2000; 45: 2–9.

10. Sanchez AV, Garcia-Godoy F. Traumatic dental injuries in 3- to 13year-old boys in Monterrey, Mexico. Endod Dent Traumatol 1990;6: 63– 5.

11. Wilson CFG. Management of trauma to primary and developing teeth. Dent Clin North Am 1995; 39: 133–67.

12. Andreasen JO, Andreasen FM. Textbook and color atlas of traumatic injuries to the teeth. 3rd edn. Copenhagen: Munksgaard; 1994. p. 771.

13. Kramer PF, Zembruski C, Ferreira SH, Feldres CA. Traumatic dental injuries in Brazilian preschool children. Dent Traumatol 2003;19: 299–303.

14. Soporowski NJ, Allred EN, Needleman HL. Luxation injuries of primary anterior teeth – prognosis and related correlates. Pediatr Dent 1994;16: 96–101.

15. Caldas AF Jr, Burgos MEA. A retrospective study of traumatic dental injuries in a Brazilian dental trauma clinic. Dent Traumatol 2001; 17: 250–3.

16. Altay N, Gungor HC. A retrospective study of dental alveolar injuries in Ankara. Turkey. Dent Traumatol 2001; 17: 201–4.

17. Ellis, RG. The classification and treatment of injuries to the teeth of children, 3rd edn. Chicago: The Year Book Publishers, 1952.

18. Ferguson FS, Ripa LW. Prevalence and type of traumatic. injuries to the anterior teeth of preschool children. J Pedod. 1979; 4: 3–8.

19. Garcia-Godoy F, Morban-Laucer F, Corominas R, Franjul RA, Noyola M. Traumatic dental injuries in preschoolchildren from Santo Domingo. Community Dent Oral Epidemiol 1983; 11:127–30.

20. Bijella MFTB, Yared FNFG, Bijella, VT, Lopes ES. Ocurrence of primary incisor traumatism in Brazilian children: a house-by house survey. J Dent Child 1990; 21: 424 -7.

21. Otuyemi OD, Segun-Ojo IO, Adegboye AA. Traumatic anterior dental injuries in Nigerian preschool children. East Afr Med J 1996; 73: 604–6.

22. Onetto JE, Flores MT, Garbanino ML. Dental trauma in children and adolescents in Valparaiso, Chile. Endod Dent Traumatol 1994;10: 223– 7.

23. Garcia-Godoy F, Morban-Laucer F, Corominas R, Franjul RA, Noyola M. Traumatic dental injuries in schoolchildren in Santo Domingo.

Community Dent Oral Epidemiol 1985;13: 177–9.

24. Cardoso M, Rocha MJC. Traumatized primary teeth in children assisted at the Federal University of Santa Catarina – Brazil. Dent Traumatol 2002;18: 129–33.

25. Kargul B, Caglar E, Tanbuga I. Dental trauma in Turkish children, Istanbul. Dent Traumatol 2003;19:72–5.

26. Fried I, Erickson P: Anterior tooth trauma in the primary dentition: incidence, classification, treatment methods, and sequelae: a review of the literature. J Dent Child 1995; July-August: 256-61.

27. Rodríguez JG. Traumatic anterior dental injuries in Cuban preschool children. Dent Traumatol 2007; 23: 241-42.

28. Carvalho JC, Vinker F, Declerck D. Malocclusion, dental injuries and dental anomalies in the primary dentition of Belgian children. Int J Paediatr Dent 1998; 8: 137-41.

29. Jones ML, Mourino AP, Bowden TA. Evaluation of occlusion,

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Traumatized anterior primary teeth Emin Caner Tumen et al.

trauma, and dental anomalies in African-American children of metropolitan Headstart programs. J Clin Pediatr Dent 1993;18: 51–4.

30. Holm A-K, Arvidsson S: Oral health in preschool Swedish children.

Odontologica Revy 1974; 25: 1-9.

31. Wilson S, Smith GA, Preisch J, Casamassimo PS. Epidemiology of dental trauma treated in an urban pediatric emergency department.

Pediatr Emerg Care 1997;13: 12–5.

32. Zerman N, Cavalleri G. Traumatic injuries to permanent incisors.

Endod Dent Traumatol 1993;9: 61–4.

33. Sanchez JR, Sanchez R, Garcia-Godoy F. Traumatic injuries of the anterior teeth in preschool children. Acta Odontol Pediatr 1981; 2: 1723.

34. Oikarinen K, Kassila O. Causes and types of traumatic tooth injuries in a public health. dental clinic. Endod Dent Traumatol 1987; 3: 172-7.

35. Eilert-Petersson E, Schelp L. An epidemiological study of bicyclerelated injuries. Accid Anal Prev 1997;29: 363–72.

36. Mestrinho HD, Bezerra ACB, Carvalho JC. Traumatic dental injuries in Brazilian pre- school children. Braz Dent J 1998;9: 101–4.

37. Forsberg CM, Tedestam G. Traumatic injuries to the teeth in Swedish children living in an urban area. Swed Dent J 1990; 14: 115– 22.

38. Zadik D. A survey of traumatized primary anterior teeth in Jerusalem preschool children. Community Dent Oral Epidemiol 1976;4: 149–51.

39. Hargreaves JA, Cleaton-Jones PE, Roberts GJ, Williams S, Matejka JM. Trauma to primary teeth of South African pre-school children.

Endod Dent Traumatol 1999;15: 73–6.

40. Segura JJ, Poyato M. Tooth crown fracture in 3 years old Andalucia children. J Dent Child 2003;70: 55–7.

41. Baghdady VS, Ghose LJ, Enke H. Traumatic anterior teeth in Iraqi and Sudanese children – a comparative study. J Dent Res 1981;60: 677–80.

42. Garcia-Godoy F, Garcia-Godoy FM. Primary teeth traumatic injuries at a private pediatric dental center. Endod Dent Traumatol 1987;8: 213– 4.

43. Rav JJ. Dental injuries in Copenhagen school children, school years 1967–72. Community Dent Oral Epidemiol 1974;2: 231–45.

44. Cunha RF, Pugliesi DMC, Viera AEM. Oral trauma in Brazilian patients age 0–3 years. Dent Traumatol 2001;17: 210–2.

45. Andreasen JO, Andreasen FM. Textbook and atlas of traumatic dental injuries to the teeth. Copenhagen: Munksgaard, 2001.

46. Yagot KH, Nazhat NY, Kuder AS. Traumatic dental injuries in nursery schoolchildren from Baghdad, Iraq. Community Dent Oral Epidemiol 1988;16: 292–3.

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Talon Cusp Senem YIGIT OZER

Talon Cusp: A Literature Review and 3 Case Reports

Senem YIGIT OZER1* 1

Assistant Professor, DDs, PhD. Department of Operative Dentistry and Endodontics, Faculty of Dentistry, Dicle University, Diyarbakir, TURKEY.

Abstract Talon cusp is an uncommon anomaly seen both in primary and permanent dentition. In most instances they are associated with other clinical problems such as occlusal interferences, poor esthetics and caries susceptibility. Management of such problems requires a detailed knowledge of the clinical entity as well as the problems associated with it. This paper presents three different cases of Talon cusps, discusses possible etiology and treatment techniques.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 45-49) Keywords: Review, Talon cusp, Treatment,Type.

Received date: 10 May 2009 Introduction Talon Cusp (TC) was first recognized by Mitchell in 1892 and is a rare anomaly of the teeth.

It mostly resembles an eagle's talon in shape, usually arising from the lingual surface of primary or permanent anterior teeth1-6. In canines and incisors, it originates usually in the palatal cingulum as a tubercle projecting from the palatal surface and the anomaly can be rarely detected on the labial surface of the tooth7,8.

The anomalous TC is composed of normal enamel and dentin with varying extensions of pulp tissue. Shay9 reported that pulp tissue can extend to the center of the tubercle and, once fractured, the pulp is exposed. TC occurs more frequently in permanent than in the primary dentition. A review of the literature shows that 75% of the cases exhibited TC in their permanent dentition and 25% of the cases in the primary dentition10. TC is more frequently seen in maxilla than the mandible.The maxillary lateral incisors are the most involved (67%) teeth followed by the central incisors (24%) and canines (9%)11.

Although the exact etiology of the anomaly has not been well defined, it is suggested the TC has a multifactorial etiology combining both genetics and environmental factors10,12. Most of the authors consider that, as with other dental abnormalities, TC *Corresponding author: Assist. Prof. Dr. Senem YIGIT OZER Dicle University, Faculty of Dentistry, Department of Operative Dentistry and Endodontics, 21280 Diyarbakir, TURKEY GSM: +905324760051 E-mail: senemygt@hotmail.com

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Accept date: 05 July 2009 occurs during the morphodifferentiation stage of odontogenesis. Developmentally, they may be a result of an outfolding of the enamel organ or hyperproductivity of the dental lamina12-16.

Hattab et al.10,11 described a classification system for these anomalous cusps, on the basis of the degree of cusp formation and extension: Type 1 (Talon) is the structure that projects from the palatal surface of the tooth and extends at least one half the distance from the cementoenamel junction to the incisal edge.

Type 2 (Semitalon) is the additional cusp with a length of 1 mm or more, but extending less than one half the distance from the cementoenamel junction to the incisal edge.

Type 3 (Trace talon) is an enlarged and prominent cingulum.

When TC interferes with the normal occlusion, the premature contact caused by the anomalous cusp can generate occlusal trauma and reversible acute apical periodontitis of the opposing tooth and itself. In these cases an occlusal adjustment by grinding the palatal cusp must be performed, with the possibility of exposure of the dentin-pulp complex and, consequently, pulp necrosis17-19.

Other clinical problems attributed to TC include poor aesthetics, caries, displacement of tooth, periodontal problems, irritation of the tongue and accidental cusp fracture causing pulpal exposure. Clinical management of this anomaly can be very different depending on the size and shape of the affected tooth and on the problems caused by this enlarged cusp13-15,20,21.

This paper present 3 cases of TC, varying with different types (Type 1,2 and 3), discusses possible etiology and draws attention to possible complications associated with this anomaly.

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CASE REPORT Case 1: Type 1, Talon A 8 year old female patient was referred to Dicle University, Faculty of Dentistry, Department of Orthodontics. She had referred to her family dentist with complaint of pain during chewing. Dentist had tried to extract the tooth but due to problems on analgesia, he was unable to finish the process. The edge of the anomaly had broken during the procedure and patient was guided to a specialist by those explained means. Her medical history was non-contributory. No other family members had similar dental anomaly.

Clinical examination revealed Class 1 dental malocclusion in mixed dentition. The maxillary permanent left central incisor was on vestibuloposition and has affected the occlusal relationship anteriorly. Central incisor had a cusplike lingual projection, sizing 5,1X3,1 mm in length and width which extended almost from the cervical third of the crown to the incisal edge (Fig. 1).

Talon Cusp Senem YIGIT OZER

bur followed by fluoride (Denti-Care, Medicom, NY) application and sealent (Ultraseal XT TM S.Jordan,UT) placement on each visit (Fig. 3). ,

Fig. 2. No evidence of associated pathosis was found and apexification was not completed.

Fig. 1. Cusp-like lingual projection, sizing 5,1X3,1 mm in length and width.

Cusp was seperated from rest of crown by noncarious developmental grooves. Clinically, the tooth was asymptomatic and responded normally to pulp vitality tests. Radiographically, no evidence of associated pathosis was found and apexification was not completed (Fig. 2).

It revealed a V-shaped radiopaque cusp like structure with a pulpal extension with it. On the basis of its characteristic features, a diagnosis of TC, Type 1 was made. Because the cusp have effect on the occlusal interference and cause occlusal trauma, a selective cuspal grinding was planned to preserve the tooth vitality and remain apexification.

The treatment lasted 6 months, selective grinding was performed with pear shaped diamond Volume 2 ∙ Number ∙ 2 ∙ 2009

Fig. 3. Grinding level of talon cusp in one session.

Case 2: Type 2, Semitalon A 40 year old female patient was referred to Dicle University, Faculty of Dentistry, Department of Operative Dentistry and Endodontics. She had tooth decay on maxillary posterior teeth and she was suffering from pain during cold applications. Her medical history was non-contributory. Clinical examination revealed Class 1 dental occlusion and a TC was identified by coincidince. Her maxillary permanent right lateral incisor was on vestibuloposition, having no occlusal contact with its antogonist.

Clinical examination showed no signs of occlusal trauma, carries and pathological change.

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The cusp size was extending less than one half the distance from the cementoenamel junction to the incisal edge (Fig. 4).

Talon Cusp Senem YIGIT OZER

On the basis of its characteristic features, a diagnosis of TC, Type 2 was made. Since she had no complaint about the affected tooth, a gradual reduction of the TC was planned for treatment. The treatment lasted 2 months, selective grinding was performed with pear shaped diamond bur followed by fluoride application and sealent (Ultraseal XT TM placement on each visit to ,,S.Jordan,UT) preserve tooth vitality (Fig. 6).

Fig. 4. The cusp size was extending less than one half the distance from the cementoenamel junction to the incisal edge.

Clinically, the tooth was asymptomatic and responded normally to pulp vitality tests.

Radiographically, no evidence of associated pathosis was found and it revealed a V-shaped radiopaque cusp like structure without a pulpal extension (Fig. 5).

Fig. 5. Radiograph revealed a V-shaped radiopaque cusp like structure without a pulpal extension.

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Fig. 6. Level of grinding in the last session.

Case 3:Type 3, Trace talon A 17 year old male patient was referred to Dicle University, Faculty of Dentistry, Department of Orthodontics. He was suffering from esthetics and he had Class 1 occlusion with moderate crowding anteriorly.

Clinical examination revealed TCs bilaterally on maxillary permanent right and left lateral incisors.

He also had dens evagination on maxillary permanent right first premolar (Fig 7).

Fig. 7. Talon cusps Type 3 are seen on maxillary permanent right and left lateral incisors. Note the “dens evagination” on maxillary permanent right first premolar.

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His occlusion was within normal limits and he had no history of occlusal trauma. TCs were enlarged and viewed as prominent cingulums.

Clinically, teeth were asymptomatic and responded normal to pulp vitality tests.

Radiographically, there were resorption areas apically around maxillary right/ left central/ lateral incisors (Fig. 8,9).

Talon Cusp Senem YIGIT OZER

Laterals revealed a V-shaped radiopaque cusp like structure. On the basis of characteristic features, a diagnosis of TC, Type 3 was made.

Prophylactically, cusps were grinded in the same treatment prothocol to prevent malocclusion during orthodontic movement. Orthodontic force applied to central and lateral incisors was reduced to prevent resorption by the orthodontist.

Discussion

Fig. 8. Detected resorption areas around maxillary permanet right central and lateral incisors.

Fig. 9.Resorption areas are well defined on maxillary permanenet left central and lateral insicors due to orthodontic movement.

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TC originates during the morphodifferentiation stage of dental development, but the exact etiology and genesis are unknown. Reports on TCs in family members22,23, twins24, offspring from consanguineous marriages10,12,17 and in some genetic syndromes 25-28 support genetic etiology of the condition. The anomaly appears to be more prevalent in patients with Rubinstein-Taybi syndrome, Mohr syndrome and Sturge-Weber syndrome. Various dental abnormalities in association with TC have been reported like peg shaped lateral incisors, impacted mesiodens, complex odontoma, supernumerary teeth, megadont, dens invaginatus, shovel shaped maxilla incisors, bifid cingula, exaggerated cusps of carabelli 3,10,22,29,30.

The common problems associated with TCs are: a) Caries susceptibility b) Occlusal interferences c) Compromised esthetics 3,10,22,31.

Within the limitations of these problems, conservative treatment techniques can be applied.

The groove between the cusp and the tooth should be prophylactically sealed to prevent decaying32. Deep developmental grooves should be cleaned of debris and plaque, and prophylactically sealed with fissure sealant or treated with excavation and filling in case of caries.

Occlusal interference should be eliminated through gradual occlusal reduction over a period of months to avoid a pulpal exposure, and the tooth surface should be treated with a desensitizing agent3,10,32.

Whenever there is occlusal interference, it can lead to rotation or displacement of the tooth or opposing tooth.

If esthetics is effected due to a TC sequential grinding or complete excision of the cusp followed by therapeutic endodontic procedure should be done. However Fabra Campos has reported increased chances of endodontic failure in a case with a palatal gingival groove in maxillary lateral incisor with a TC33.

Radiographically, the TC is seen as a radiopaque structure, in which the enamel, dentin and occasionally the pulp can be seen. Typically the cusp resembles a V-shaped structure superimposed Page 48

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over the normal image of the crown 10,11. A definitive diagnosis of a TC cannot be made based only on the radiographic findings alone because a TC on an unerupted tooth may be radiographically misinterpreted as a supernumerary tooth, compound odontoma or dens in dente29,30.

In case of finding a TC, taking of an orthopantomogram is recommended for exclusion of association with other abnormalities.

Conclusions Early diagnosis and treatment are needed to avoid possible complications. Procedures briefly told here can be manipulated for the treatment of TC if they are causing trauma and esthetic problems: 1- Selective cuspal grinding of accessory cusp over a 6-8 week interval with applivation of flouride as a desensitizing agent, so that it will avoid possibility of pulpal exposure and helps in reparative dentin formation.

2- If the affected tooth is immature and if there is pulpal pressure, complete reduction of cusp can be a choice for treatment.

3- Root canal treatment should be done if complete cuspal reduction is considered.

References 1. Mitchell WH. Case report. Dental Cosmos 1892;34: 1036.

2. Mellor JK, Ripa LW. Talon cusp: a clinically significant anomaly. Oral Surg Oral Med Oral Pathol 1970;29:225-8.

3. Mader CL. Talon cusp. J Am Dent Assoc 1981;103: 244-6.

4. Salama FS, Hanes CM, Hanes PJ, Ready MA. Talon cusp: a review and two case reports on supernumerary primary and permanent teeth.

ASDC J Dent Child 1990;57: 147-9.

5. Lomali G, Hazar S, Altinbulak H. Talon cusp: Report of five cases.

Quintes Int 1994;25: 431-3.

6. Dankner E, Harari D, Rotstein I. Dens evaginatus of anterior teeth.Literature review and radiographic survey of 15,000 teeth. Oral Surg Oral Med Oral Pathol 1996;81: 472-6.

7. Jowharji N, Noonan RG, Tylka JA. An unusual case of dental anomaly: a ‘facial’ talon cusp. ASDC J Dent Child 1992;59:156-8.

8. Abbott PV. Labial and palatal ‘talon cusps’ on the same tooth. A case report. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:72630.

9. ShayJC. Dens evaginatus. A case report of a successful treatment. J Endod 1984;7:324-6.

10. Hattab FN,Yassin OM, Al Nimri KS. Talon cusp in permanent dentition associated with other dental anomalies: review of literature and reports of seven cases. ASDC J Dent Child 1996;63:368-76.

11. Hattab FN, Yassin OM, Al Nimri KS. Talon cusp-clinical significance and management: case reports. Quintess Int 1995;26:115-20.

12. Al-Omari, Hattab FN, Darwazeh MG, Dummer PM. Clinical problems associated with unusal cases of talon cusp. Int Endod J 1999; 21:183-90.

13. Güngör HC, Altay N, Kaymaz FF. Pulpal tissue in bilateral talon cusps of primary central incisors. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:231–5.

14. McNamara T, Haeussler AM, Keane J. Facial talon cusp. Int J Paediatr Dent 1997;7:255–8.

15. Segura-Egea JJ, Jime´nez-Rubio A, Velasco-Ortega E, Rı´osSantos JV. Talon cusp causing occlusal trauma and acute apical

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Talon Cusp Senem YIGIT OZER

periodontitis: report of a case. Dent Traumatol 2003;19:55–9.

16. Hattab FZ, Hazza AM. An unusual case of talon cusp on geminated tooth. J Can Dent Assoc 2001;67:263–6.

17. Segura JJ, Jime´nez-Rubio A. Talon cusp affecting permanent maxillary lateral incisors in 2 family members. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:90–2.

18. Soares AB, De Araujo JJ, De Sousa MG, Veronezi MC. Bilateral talon cusp: case report. Quintess Int 2001;32:283–6.

19. Ferraz JAB, Carvalho JRJr, Saquy PC, Pecora JD, Sousa- Neto MD. Dental anomaly: dens evaginatus (talon cusp). Braz Dent J 2001;12:132-4.

20. De Sousa SMG, Tavano SMR, Bramante CM. Unusual case of bilateral talon cusp associated with dens evaginatus. Int Endod J 1999;32:494–8.

21. Hattab FZ, Yassin OM, Sasa IS. Oral manifestations of Ellis-van Creveld syndrome: report of two siblings with unusual dental anomalies.

J Clin Pediatr Dent 1998;22:159–65.

22. Davis PJ, Brook AH. The presentation of talon cusp: diagnosis, clinical features, associations and possible aetiology. Br Dent J. 1986;160:84-8.

23. Meon R. Talon cusp in two siblings. N Z Dent J. 1990;86:42-4.

24. Liu JF, Chen LR. Talon cusp affecting the primary maxillary central incisors in two sets of female twins: report of two cases. Pediatr Dent.

1995;17:362-4.

25. Gardner DG, Girgis SS. Talon cusps: A dental anomaly in the Rubinstein-Taybi syndrome. Oral Surg 1979;47:519-21.

26. Hennekam RC, Van Doorne JM. Oral aspects of Rubinstein-Taybi syndrome. Am J Med Genet Suppl. 1990;6:42-7.

27. Goldstein E, Medina JL. Mohr syndrome or oral-facial-digital II: report of two cases. J Am Dent Assoc. 1974;89:377-82.

28. Tsutsumi T, Oguchi H. Labial talon cusp in a child with incontinentia pigmenti achromians: case report. Pediatr Dent. 1991;13:236-7.

29. Natkin E, Pitts DL, Worthington P. A case of talon cusp associated with other odontogenic abnormalities. J Endod 1983;9:491-5.

30. Lehl GK. Talon cusp associated with other dental anomalies - A case report. J Ind Soc Pedo Prev Dent 1999;17:13-4.

31. Hsu Chin-Ying S, Girija V, Fei YJ. Bilateral Talon Cusps in Primary Teeth: Clinical significance and treatment. J Dent Child 2001;68:23943.

32. Myers CL. Treatment of a talon-cusp incisor: report of a case. J Dent Child 1980;47:43-5.

33. Fabra-Campos H. Failure of endodontic treatment due to a palatal gingival groove in a maxillary lateral incisor with talon cusp. J Endod 1990;16:342-5.

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Multiple Compound Odontoma Behiye SEZGIN BOLGUL et al.

A Diagnosis and Treatment of the Multiple Compound Odontoma in Mandibula Behiye SEZGIN BOLGUL*1, Belgin GORGUN2, Torun OZER3, Sema CELENK4, Buket AYNA5, Fatma ATAKUL6 1

Assist.Prof., DDs. PhD. Dicle University Dental Faculty Department of Pedodontics Diyarbakir-Turkey.

Prof., DDs. PhD. Dicle University Dental Faculty Oral and Maxillofacial Surgery Diyarbakir-Turkey.

3 Assoc.Prof., DDs. PhD. Dicle University Dental Faculty Department of Orthodontics Diyarbakir-Turkey.

4 Assoc.Prof., DDs. PhD. Dicle University Dental Faculty Department of Pedodontics Diyarbakir-Turkey.

5 Assist.Prof., DDs. PhD. Dicle University Dental Faculty Department of Pedodontics Diyarbakir-Turkey.

6 Prof., DDs.PhD. Dicle University Dental Faculty Department of Pedodontics Diyarbakir-Turkey.

2

Abstract Odontomas are classified as odontogenic tumours: however, they are thought to be developmental anomalies in which all dental tissues are represented. Compound odontomas are the most common type of odontogenic tumours and generally they are asymptomatic. The occurence of odontoma in the primary dentition is also uncommon.

This paper, describes a case of compound odontomas diagnosed in 9 years old male child who presented to the Dicle University Dental Faculty Pediatric clinic complaining about unerupted teeth.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 50-52) Keywords: Odontoma, diagnosis, pediatric dentistry.

Received date: 14 February 2009 Introduction Odontomas are considered to be developmental anomalies resulting from the growth of completely differentiated epithelial and mesenchymal cels that give rise to ameloblasts and odontoblasts. These tumors are basically formed of enamel and dentin but they can also have variables amounts of cement and pulp tissue.1 Traditionally, odontomas have been classified as benign odontogenic tumors and are subdivided into complex or compound odontomas morphologically.2 These odontogenic tumors can be found anywhere in the dental arches. The majority of odontomas which are located in the anterior region of the maxilla are compound, while the great majority of odontomas located in the posterior areas, especially in the mandible, are complex odontomas.1,3,4 The etiology of the odontoma is unknown.5 In general they are asymptomatic, have slow growth1, and seldom exceed the size of a tooth, but when large can cause expansion of the cortical *Corresponding author: Behiye SEZGİN BOLGÜL Assist.Prof., DDs. PhD. Dicle University Dental Faculty Department of Pedodontics Diyarbakır-Turkey.

E-mail: behiyebolgul@hotmail.com

Volume 2 ∙ Number ∙ 2 ∙ 2009

Accept date: 08 June 2009 bone. Odontomas occur more often in the permanent dentition and are very rarely associated with the primary teeth.1,6 Radiographic aspects of odontoma are characteristic. The compound odontoma shows calcified structures resembling teeth in the center of a well-defined radiolucent lesion. A developing odontoma can be discovered by routine radiography however, the degree of calcification of odontoma in the primary dentition is sometimes less than is seen in relation to permanent teeth, and radiographic features are therefore more weakly radioopaque. It is important therefore, to examine the radiographs carefully.5,7 Odontomas are treated by conservative surgical removal and there is little probability of recurrence.1,8 When the odontomas are associated with unerupted teeth , orthodontic traction of the impacted tooth soon after removal of the lesion may be needed, especially if it is not diagnosed and treated early.3,9 CASE REPORT 9 year old boy came to Dicle University Dental Faculty department of Prdodontics with the complaint of a retantive deciduous tooth and delay of eruption. After a careful examination and anemnesis no history of a trauma was obtained. In his family history, no hypodonti or impacted tooth was reported.

On the left side of his mandible central and Page 50

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Multiple Compound Odontoma Behiye SEZGIN BOLGUL et al.

lateral deciduous incisors were retentive and canine were impacted. No carious lesions were obtained.

In the clinical examination no labial or lingual position of the tooth was determined. There were a lot of radioopaque structures in incisor and canine region in periapical and panaromic radiographs. (Fig. 1) the positions of permanent lateral and canine tooth was affected by the lesion.

Fig. 3 Small tooth like calcified pieces excavated.

Discussion

Fig. 1 Radiographic view.

After a multidisciplinary team study of a pedodontist, oral surgeon and an orthodontist surgery was planned. Without any premedication surgery was done. Small tooth like calcified pieces were excavated from the lesion region. (Fig. 2,3)

Fig. 2 Small tooth like calcified pieces.

A compound type odontoma containing enamel and dentine was reported in the pathology results. No cement was obtained.

For the guidence of eruption patient was taken into a routine appointment schedule. Surgical orthodontic treatment is planned, if needed.

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In the management of eruption disturbances in the primary dentition early recognition and diagnosis as well as proper step of treatment and careful following up are very important.

An impacted tooth is one in which eruption into a normal functional position is obstructed by some physical barrier.10 Impaction of the primary teeth is uncommon. Factors contributing to impaction include developmental anomalies such as malposition, dilaceration, ankylosis, tumors, odontoma, dentigerous cysts, presence of supernumerary teeth and systemic-genetic interrelation such as cleidocranial dysostosis and hypopituitarism.10,11 Impaction of an anterior primary tooth is very rare. When it occurs it is most often associated with the presence of a supernumerary tooth or odontoma.12 However, there have been many studies in which odontomas caused various disturbances to tooth eruption.4,7,9,13-16 Many times, odontoma may cause disturbances in the eruption of teeth such as impaction, delayed eruption or retention of primary teeth.11 The most frequent cause of discovery of an odontoma is impaction of the permanent teeth with or without persistence of the primary teeth or, less frequently, symptomless swelling or accidental radiographic finding.4 Thus it is very important for paediatric dentists to understand the clinical features of odontoma in children.

Many studies have reported that odontoma occurs most frequently during the first two decades of life.2,4,13,17-21 Katz reported that odontomas were most commonly removed from the 11-15-year-old age group.13 Tomizawa and Otsuka reported that 50% were in the first decade of life in 39 cases.22 In the present study, the case was 9-year-old.

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As for location, in the incidence of odontomas in the maxilla was 50.9-59.3% .17-20 In studies by Regezi 18 and Kaugars20 the most common location was the anterior portion (incisor and canine region) of the maxilla followed by the anterior portion of the mandible. The canines, followed by upper central incisors and third molars, are the most frequent teeth impacted by odontomas.13 Tomizawa and Otsuka observed that the most common location was the anterior region of the maxilla.22 Kaugars reported that the percentage of odontomas in the molar region gradually increased with each successive decade of life.20 Katz also reported that odontomas were apparently age and location related. Those from incisor locations were diagnosed and treated at an earlier age than those from the canine or third molar regions and reported that odontomas rarely involved the primary dentition and found only five of 396 odontomas patients.13 In the present case, odontoma is placed in left mandibular anterior region. Left mandibular deciduous canine teeth did not erupted. Mandibular left deciduous incisors were retentive. Mandibular left permanent incisors and canine tooth were affected by odontoma. Therefore the present case is very rare.

The treatment advocated for odontomas in both primary and permanent dentition is their surgical removal and there is little probability of recurrence. Ameloblastic fibroodontomas and odontoameloblastomas show a great resemblance to common odontomas, especially in the radiographic examination. Therefore, it has been suggested that all specimens should be sent to an oral pathologist for microscopic examination.5,8

8.

9.

10.

11.

12.

13.

14.

15.

16.

17.

18.

19.

20.

21.

22.

Multiple Compound Odontoma Behiye SEZGIN BOLGUL et al.

M. Compound Odontomes associated with impacted maxillary primary central incisors: report of two cases. International Journal of Paediatric Dentistry 1995; 4:251-256.

Areal-Lopez L, Silvestre DF, Gil LJ: Compound Odontoma Erupting in the mouth: 4 year follow-up of a clinical case. J Oral Pathol 1992; 21:285-88.

Oliver RG, Hodges CGL. Delayed Eruption of a Maxillary central incisor associated with an odontome: report of case. ASDC J Dent Child 1988; 55:368-71.

Motokawa W, Braham RL, Morris ME, Tanaka M. Surgical Exposure and orthodontic alignment of an unerupted primary maxillary second molar impacted by an odontoma and a dentigerous cyst: a case report. Quintessence International 1990; 21(2): 159-162.

Snawder KD. Delayed eruption of the anterior primary teeth and their management: report of a case. Journal of Dentistry for Children 1974; 41(5):52-54.

Brunetto AR, Turley PK, Brunetto AP, Regattieri LR, Nicolau GV. Impaction of a primary maxillary canine by an odontoma: surgical and orthodontic management. Pediatric Dentistry 1991; 13(5); 301302.

Katz RW. An analysis of compound and complex odontomas.

Journal of Dentistry for Children 1989; 56: 445-449.

Morning P. Impacted teeth in relation to odontomas. Int J Oral Surg 1980; 9:81-91.

Kaihara Y, Sasaki N, Morimoto H, Nagasaka N. A case of odontoma that caused delayed eruption of mandibular first permanent molar. Pediatric Dental Journal 2000; 10: 129-132.

Yeung KH, Cheung RCT, Tsang MMH. Compound odontoma associated with an unerupted and dilacerated maxillary primary central incisor in a young patient. Int J Padiatric Dentistry 2003; 13: 208-212.

Owens BM, Schuman NJ, Mincer HH, Turner JE, Oliver FM. Dental odontomas. A retrospective study of 104 cases. J Clin Paediatric Dent 1997; 21:261-264.

Regezi JA, Kerr DA, Courtney R. Odontogenic tumours: analysis of 706 cases. J Oral Surg 1978; 36: 771-778.

Tretti EF, Miller AS, Peezick B. Odontomas: an analysis of 167 cases. Journal of Pedodontics 1984; 8: 282-284.

Kaugars GE, Miller ME, Abbey LM. Odontomas. Oral Surg Oral Med Oral Pathol 1989; 67:172-176.

Higuchi Y, Tashiro H, Nakamuro N, adachi M, Oka m. Clinical tudy of the odontogenic tumors. Japanese J Oral Maxillofacial Surg 1990; 36: 1699-1706.

Tomizawa M, Otsuka Y, Noda t. Clinical observations of odontomas in Japanese children: 39 cases including one recurrent case. Int J Paediatric Dent 2005; 15(1) 37-43.

Conclusions The result of pathology reports indicated that this present case is compound composite odontoma.

References 1. Neville BW, Damm DD, Allen CM, Bouquot JE. Oral and maxillofacial pathology. Philadelphia: Saunders,1995; 531-33.

2. Kramer IRH, Pindborg JJ, Shear M. World Health Organization International Histological Classification of Tumours-Histological Typing of Odontogenic Tumours, 2nd edn. Berlin Heidelberg: Springer-Verlag,1992; 16-21.

3. Bengston AL, Bengston NG, Benassi LRDC. Odontomas em pacientes pediatricos. Revista de Odontopediatria 1993; 2:25-33.

4. Budnick SD. Compound and complex odontomas. Oral Surg Oral Med Oral Path 1976;42:501-506.

5. Shafer WG, Hine MK, Levy BM: A textbook of oral pathology, 4th Ed. Philedelphia: Saunders, 1983; 308-11.

6. Cawson RA, Binnie WH, Eveson JW: Color Atlas of Oral Disease.

Clinical and Pathological Correlations. Hong Kong: Mosby-Wolfe, 1993; 6-19.

7. Haishima K, Haishima H, Yamada Y, Tomizawa W, Noda T, Suzuki

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Ectodermal Dysplasia and Periodontal Tissues Tuba TALO and Filiz ACUN KAYA

The Effects of Ectodermal Dysplasia on Periodontal Tissues Tuba TALO1*, Filiz ACUN KAYA1 1. Dicle University, Faculty of Dentistry, Department of Periodontology, Diyarbakir / Turkey.

Abstract Ectodermal dysplasia (ED) is a heterogeneous group of disorders characterized by developmental dystrophies of ectodermal structures. ED may effect only ectodermal tissues, or may be associated with anomalies of other organs and systems. It is generally classified into three subgroups; anhidrotik (EDA), hypohidrotik (HED) and hidrotik.

All the ED appear to be genetic in etiology. However, only a small number of ED genes has been genetically mapped or cloned.

Missing teeth or delay in teething often starts to worry the parents and leads to the diagnosis of ED in the second year of life. The most important cause of periodontal problems of ED patients is the decreased level of saliva secretion. Excellent oral hygiene is crucial for the successful treatment of these patients.

By this review we aimed to determine the probable relations between periodontal diseases and ED. (Journal of International Dental and Medical Research 2009; 2: (2), pp. 53-57) Keywords: Ectodermal dysplasia, Christ-Siemens Tourine syndrome, anodontia, hypohidrosis.

Received date: 10 june 2008 Introduction Ectodermal dysplasia (ED) is a heterogeneous group of disorders characterized by developmental dystrophies of ectodermal structures.

Ectodermal dysplasia MAY Effect only ectodermal tissues, or may be associated with anomalies of other organs and systems1.

Although ed ıs classıfıed differently, it is generally classified into three subgroups; anhidrotik (EDA), hypohidrotik (HED) and hidrotik2.

EDA is a rare, hereditary disease that has an autosomal recessive mode of inheritance. it is characterized by partial and complete abscence of sweat and sebasseous glands, females are effected more than males2.

HED is usually inherited as an autosomal recessive genetic trait; the disorder is fully expressed in males only. HED patients exhibit

*Corresponding author: Dt Tuba TALO YILDIRIM, Research Assistant Dicle University, Faculty Of Dentistry, Department of Periodontology, 21280 Diyarbakır, TURKEY. Tel: +90 412 248 81 01-3430 Fax: +90 412 248 81 00 E-mail: dt_talo@hotmail.com

Volume 2 ∙ Number ∙ 2 ∙ 2009

Accept date: 02 January 2009 clinical signs AS; hypotrichosis, onychodysplasia, hypodontia or anodontia. Hypohidrotic ectodermal dysplasia is characterized with sparse hair, inability to sweat due to lack of sweat and sebasseous glands. The lack of sweat glands may lead to hyperthermia, followed by brain damage or death in early infancy if unrecognized3,4.

Hidrotic ectodrrmal dysplasia is characterizeted normal sweat glands and craniofacial structures. But others findings are similar to hypohidrotic or anhidtotic type. Autosomal dominant type ectodermal dysplasia fist described by weech. This type patient have normal hair and eyebrow and missing teeth (anodontia,hypodontia) nail dystrophy5.

About 160 clinically and genetically distinct hereditery ectodermal dysplasia types have been catalogued, only a few have been diagnosed at the molecular level1.

Except the clasification above there are a lot of clafications about ED. Lamartine (2003) classified ED into four subgroups according to the functions of the genes discovered: cell-cell communication and signalling, cell adhesion, regulation of transcription, and development6.

Witkop’s classification is composed of7,8: Type I: The most common and best characterised of these conditions is X-linked hypohidrotic ectodermal dysplasia.

Type II: Tooth and nail syndrome (Witkop sydrome) is AN autosomal dominant type of ED characterized Page 53

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by missing teeth and poorly formed nails.

Type III: X-linked autosomal dominant especially this case have normal tooth abnormal hair and nails.

Ectodermal disorders is clasificationed four major group by Freire –Maia8,9: a) Hypohydrosis: Hypoplasia and aplasia of salivary and sebasseous glands b) Hypotrichosis: Thin and sparse hair, absence of eyebrow and eyelashes. c) Hypodontia: Anodontia or most common oligodontia d) Onychodysplasia: Abnormalites and nail dystrophy Several cases of EDs involving at least two of the ectodermal appendages of hair, nails and teeth have been reported in the literature.

Diagnosis Criteria This X-linked recessive disorder affects males and is inherited through female carriers. The diagnostic tool is the typical clinical physionomy.

The most characteristic findings in mEn are the reduced number and abnormal shape of teeth. The delay in teethening is often the first step in diagnosis. The men have an easily recognizable facIes also referred to as an old man facies. Same infants have a premature look with scaling of the skin. This can also form a clue to the diagnosis. The number of sweat glands is reduced and both scalp and body hair are sparse, with lack of eyebrows and eyelashes. The clinical findings in carrier females are the same as those in affected males. One third of carriers appears healthy, another third of them show mild symptoms, and the last third exhibits significant symptoms, but often milder than the affected males10.

Prenatal diagnosis of EDA has occasionally been reported. The diagnosis has been made on fetal skin biopsy, obtained by fetoscopy by 20 weeks gestation, after determination of the sex of the fetus. By histological analysis they demonstrate complete lack of or reduction in the number of polisebaceous follicles and lack of sweat glands primordia in multiple skin biopsis. The interpretation of the biopsy may be difficult. If one does not appreciate the normal regional variability of the distribution of skin appendages of fetal skin which sweat gland primordia only begin to develop at around 20 weeks of gestation. This procedure is complicated and implies a consirederable risk to the pregnancy. The use of linked markers on DNA from chorionic villi has greatly improved the safety of prenatal diognosis of X-linked ED. The new method of prenatal diagnosis has major advantages as well Volume 2 ∙ Number ∙ 2 ∙ 2009

Ectodermal Dysplasia and Periodontal Tissues Tuba TALO and Filiz ACUN KAYA

as disadvantages. It is technically simpler and may present a lover risk to the pregnancy than fetoscopy and multiple skin biopsies11.

Differential Diagnosis The differential diagnostic problem is the distinction of autosomal recessive form of HED from EDA. Anhidrotic form is considerably less common than HED. The clinical features are quite similar in both conditions but due to the different mode of inheritance HED affects both males and females and the heterozygotes have no signs at all. For adequate genetic counseling it is thus important to recognize HED heterozygotes by dental examination and sweat tests12.

Epidemiplogy The prevalence of EDA is unknown; however the incidence in male is estimated at 1 in 100000 births although the condition is usually overlooked in infants. This X-linked recessive disorder affects males and is inherited through female carriers.This carriers–incidence is probably 17,3 in 100000 women13.

Ethiology and Genetics All the ectodermal dysplasias appear to be genetic in etiology. However, only a small number of ED genes has been genetically mapped or cloned.

The gene associated with HED has been identified, and several splice forms of this gene exists. In situ hybridization revealed that the gene was expressed in the hair follicles and epidermis of adult skin.The discoveries of disease genes and the identification of mutations in patients represent A great progress in biomedical science14,15.

The recent studies TNF ligand and receptor have developmental regulatory role and are tightly associated with epithelial-mesenchymal interactions and signaling pathways that regulate ectodermal appendage formation and organogenesis during the initiation of development11.

Clinical Features Ectodermal dysplasia is characterized by triad of signs: 1) Sparse hair (atrichosis or hypotrichosis) 2) Abnormal or missing teeth (anodontia or hypodontia) 3) Inability to sweat due to lack of sweat glands (anhidrosis or hypohidrosis) Most patients with ectodermal dysplasia have a normal life expectancy and normal Page 54

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intelligence. However, the lack of sweat glands may lead to hyperthermia, followed by brain damage or death in early infancy if unrecognized. Thus, an early diagnosis is important11,16,17.

Craniofacial Structures Considering how much osseous and dental tissue is missing, these patients have surprisingly normal facial structures. Clinically, this patients have skeletal abnormalities; the forehead appears square, with frontal bossing. There is a prominent supra orbital ridge. The nose has a depressed nasal bridge and is called a saddle nose. The midface is depressed and hypoplastic. The cheekbones are high and broad, although they appear flat and the lips everted and protuberant18,19.

Hair, Nails, Skin and Skintags Abnormalities of hair are present in all affected individuals. Most individuals have sparse, fine, slowly growing scalp hair. Sparse eyebrows and eyelashes are always found. However, bread and moustache hair are normal2,11,14,16,17.

Nail problems occur more frequently in older individuals. About half of the affected individuals exhibit mild fingernail abnormalities and nail dystrophy. Slow nail growth and split nails are most often reported findings. Toenails were generally normal. The nail beds are more susceptible to progressive injury with age2,11,14,16.

Most individuals repot dry skin. Affected individuals have a smooth, almost velvety skin texture. The skin of patients also seems to be thinner than expected for age11,14,20.

Almost all affected relatives have decreased sweating, and many show heat intolerance. Some individuals only sweat in certain areas on their body.

Because of the reduced number of sweat glands, there is a danger of hyperthermia. The hyperthermia may also lead to brain damage. Episodes of hyperpyrexia and severe respiratory infections are life threatening components in EDA11,14,20,22.

Oral Structures Missing teeth or delay in teething often starts to worry the parents and leads to the diagnosis of ED in the second year of life. A dentist should not hesitate to radiographically examine a patient whose teeth have not erupted by the appropriate age in order to exclude ED2,14.

Mostly There is hypodontia which is known as one of the major factors of ectodermal dysplasia.

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Ectodermal Dysplasia and Periodontal Tissues Tuba TALO and Filiz ACUN KAYA

In severe cases no teeth may form. More often most of the deciduous form but there are few or no permanent teeth. The teeth are usually peg shaped conical, which give an undesirable appearance. The enamel layer is thin. Enemal is rarely hypoplastic.

The outer and inner enamel epithelium can not be observed in the buds from the HED fetus, but is clearly seen in the normal fetus11,23.

Taurodontism frequently on the second deciduous molars, is a common feature. Not only the shape is abnormal, but also the number. A severe hypodontia is a universal feature among affected individuals. There are generally more teeth in the maxilla than in the mandibula. Most often the lower incisors and premolars are missing, followed by the upper premolars and incisors11,16.

All affected individuals had sagittally underdeveloped maxillary retrusion and vertical dentoalveolar development are related to severe hypodontia.this patients had deep palatinal arch2,21.

Also the HED oral mucosa differed from the normal specimen. The inner epithelial lining in the lower lip seemed to be intact in both the HED fetus and the specimen. In contrast, the epithelium in the palate was found to be separated from the underlying mesenchymal tissue in the HED fetus15.

Many patients complain of dry mucous membranes in mouth and nose. Reduced salivary secretion has been spotted in some EDA patients.

Autopsy has also shown absence of mucous glands in the pharynx, larynx, trachea and bronchiI. This is in agreement with the susceptibility to respiratory infections. Analysis of the saliva has revealed a reduced buffer capacity and an increased number of bacterial cultures. Most affected individuals were susceptible to dental carries11,23-28.

Saliva, consisting of 99% water and 1% organic and inorganic components, has several important functions in the oral cavity. One of them is to modulate the oral microflora by favoring the attachment and proliferation of certain microorganisms and promoting the clearance of others. Saliva also protects the oral tissues from desiccation and exogenous insult from acids and degradative enzymes. Lactoferrin binds iron, which is an important nutrient factor for many microbial species. It also displays bacteriostatic and/or bactericidal activity towards several microbial species. Lactoferrin has been found in increased concentrations in hyposalivation. A high lactoferrin concentration in saliva can result from damage to the salivary glands, gingival inflammation or leakage of serum through inflamed mucosal membranes29.

ED patients has reduced salivary secretion.

Decreased salivary flow and alterations in salivary composition cause a clinically oral imbalance Page 55

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manifested by increased caries incidence, susceptibility to oral candidiasis, xerostomia, difficulties with speech, mastication and swallowing, altered taste perception and halitosis. It has been mentioned that dentures may not be suitable for patients with hyposalivation; however, dentures could be the only restorative choice. The tongue adheres to and dislodges the denture, causing decreased retention of partial and totally removable prosthesis and resulting in abrasions, sore spots, ulceration and irritation, all unpleasant and painful experiences for the patient. A constant feeling of dry mouth is very uncomfortable and annoying. There are no universally accepted methods for the treatment of dry mouth. The aim is to relieve oral discomfort and to keep the mouth moist. A simple method is the use of water followed by saline solutions, tea and water with sodium bicarbonate.

Medication capable of stimulating the salivary glands may be prescribed for certain individuals.

With the diminished salivary output xenogenic patients are more prone to caries, and therefore diligent oral hygiene and regular dental care are essential. Antibacterial mouthwashes such as 0.12% chlorhexidine are useful to inhibit the development of dental plaque and gingivitis since patients with xerostomia tend to have a greater susceptibility. The use of topical fluorides should be based on the severity of the patient’s condition as well as individual caries risk. Biotene is available as a sugar-free chewing gum,an alcohol-free mouthwash and a toothpaste, while Oralbalance is available as a moisturizing gel. Multiple co-factors such as hydrogen peroxide and halides, enable the efficiency of the anti-microbial activity. The patients dont use alcohol caffein, cigarette and should use vitamin C23-28.

The Effects of Ectodermal Dysplasia on Periodontal Tissues The most important cause of periodontal problems of ED patients is the decreased level of saliva secretion. Saliva is an important defence factor for oral cavity. If the saliva secretion decreases, bacterial plaque and food accumulation occurs easily. Also the oxygen contain of saliva protects oral cavity against anaerob bacterial proliferation, caries and halithosis. In addition, saliva proteins and electrolytes inhibit bacterial proliferation and buffer oral acid formation. Because of all these factors, individuals become prone to periodontal diseases. Also these individuals, mobile prosthethic restoration usement become harder.

Because saliva lubricates and protects oral mucosa, also increases holding capacity23-29.

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Ectodermal Dysplasia and Periodontal Tissues Tuba TALO and Filiz ACUN KAYA

Treatment Children with ED present many and different clinical problems from early childhood though adolescence. Clinical manifestations of HED also cause considerable social problems in affected patients. Dental treatments of the clinical traits of HED can have a profound impact on these patients.

The ability to look and feel like their pers is imperative for the psychological development of these patients2,14.

All patients should be referred for management of the oral manifestations of their HED. The aim of treatment is to determine the amount of support to patients affected by HED such as restoring missing teeth, establishing normal vertical dimensions and providing support for the facial soft tissues. Conventional prosthodontic treatment (complete dentures, overdentures or a combination of fixed and removable partial dentures) is hard because of the anatomic abnormalities of existing teeth and alveolar ridges. The conically shaped teeth and ‘knife edge’ alveolar ridges result in poor retention and instability of prostheses. There is usually a need to remake dentures in young patients as they grow16,22.

Conclusions In conclusion, when confronted with multiple dental agenesys, the clinician should look for an association of ED signs, because ED may also be detected. The major goal of dental management is to provide the patient with optimal aesthetics and function so that the patient could develop physically, emotionally, and socially like other healthy individuals. Dental management allows these patients preventive and supportive aesthetic activity, and as a result avoids social problems associated with partial or full dentures, particularly in young people.

Excellent oral hygiene is crucial for the successful treatment of these patients. Patients should use daily topical fluoride for prophylaxis against new caries attacks early placement of partial or full dentures is commonly recommended from the age of two or three years onward. The denture must be periodically modified as alveolar growth, erupting teeth and rotational jaw growth change both the alveolar,occlusal and basal dimensions. They have also a limited retention and stability. For this reason, in young children we prefer a treatment with crowns and bridge.

It is commonly agreed that osseo-integrated implants should be not placed before cessation of growth. Even in young adults, alveolar growth can Page 56

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be remarkable. Impaired salivary secretion rates constitute an increased risk for dental diseases, namely caries. The fragile oral mucosa may affect the clinical situation as well as possibilities to wear removable prostheses.

Ectodermal Dysplasia and Periodontal Tissues Tuba TALO and Filiz ACUN KAYA

28. Singh Rashmi, Gauri S Lele. Hypohidrotic Ectodermal Dysplasia: A Case Report.

International Dental & Medical Disorders. 2008; 1: 11-14.

29. Almstahl A, Wikström M, Groenink J. Lactoferrin, Amylase And Mucin MUC5B And Their Relation To The Oral Microflora İn Hyposalivation Of Different Origins. Oral Microbiol Immunol 2001: 16: 345–352.

References 1. Pinherio M, Freire-Maia N. Ectodermal displasias: A Clinical Classification and A Causal Review. Am J Med Genet 1994; 53:153– 162.

2. Köymen G, Karaçay Ş, Başak F, Akbulut E,Altun C Ektodermal Displazi Olgusunda Kombine Dişsel Tedavi gülhane Tıp Dergisi 2003; 45 (1) : 79-81.

3. Gürbüz A, Uludağ B, Tulga F: Bir Olgu Nedeniyle Ektodermal Displazi Ve Protetik Yaklaşım, A.Ü. Dişhek Fak Derg 1990; 17(2) : 2714.

4. Nigiz R, Zengingül AÝ: Ektodermal Displazili Bir Hastan ın Prot etik Rehabilitasyonu, D.Ü. Dişhek Fak Derg 1996; 7(1,2,3): 18-22.

5. Murdoch-Kinch CA, Miles DA, and Poon CK: Hypodontia And Nail Dysplasia Syndrome, Oral Surg Oral Med Oral Pathol 1993; 75:403-6.

6. Lamartine J. Towards A New Classification Of Ectodermal Dysplasia.

Clin Exp Dermatol 2003;28:351–354.

7. Redpath TH, Winter GB: Automosal Dominant Ectodermal Dysplasia With Significant Dental Effects, Br Dent J 1966; 126:123-8.

8. Freirmnin N: Ectodermal Dysplasias, Hum Hered 1971; 21:309.

9. Pişkin T, Günday M, Akan D, Reşmor A: Diş-Tırnak Sendromlu (Hidrotik Ektodermal Displazi) Ve Protetik Rehabilitasyonu, Oral 1985; 3(3):12-5.

10. Sofaer J.A : A Dental Approach To Carrier Screening İn X-Linked Hypohidrotic Ecdodermal Dysplasia. J. Med. Genet 1981;18:459-460.

11. Wackens G,Anhidrotik Ektodermal Displazi, Orphanet Encyclopedia 2004 Eylül.

12. Munoz F, Lestringant G, Sybert V, et al. Definitive Evidence For An Autosomal Recessive Form Of Hypohidrotik Ectodermal Dysplasia Clinically İndistinguishable From The More Common X-Linked Disorder.

Am. J. Hum. Genet 1997; 61:94-100.

13. Bergendal B, Koch G,Kurol J,Wanndahl G, Consensus Conference On Ectodermal Dysplasia With Special Reference To Dental Treatment .

The Institute For Postgraduate Dental Education, Jönköping, Sweden 1998.

14. Yıldırım M, Baysal V, Çandır Ö, Anhıdrotıc Ectodermal Dysplasia (Case Report) T Klin Tıp Bilimleri 2000; 20:366-368.

15. H Nordgarden, I Reintoft, D Nolting, B Fischer-Hansen, I Kjær. Oral And Maxillofacial Pathology Craniofacial Tissues Including Tooth Buds In Fetal Hypohidrotic Ectodermal Dysplasia Oral Diseases 2001; 7, 163–170.

16. Altun S, Altun Ş, Yavuz İ, Agüloğlu S, Ectodermal Dysplasia: Report Of 3 Cases T Klin Tıp Bilimleri 2001, 7:154-160.

17. M. Tariq, M. S. Chishti, G. Ali and W. Ahmad A Novel Locus for Ectodermal Dysplasia of Hairs, Nails and Teeth Type Maps to Chromosome 18q22.1–22.3 Annals of Human Genetics 2008; 72,19–25.

18. Hasanreisoğlu U, ArasÞ, Sakaoğlu F, Tulga F: Hidrotik Ve Anhidrotik Ektodermal Displazinin Protetik Rehabilitasyonu: 6 Olgu Nedeniyle, A.Ü. Dişhek Fak Derg 1987;14(3):337-44.

19. Winstanley RB: Prosthodontic Treatment Of Patients With Hypodontia, J Prosthet Dent1984;52: 687-91.

20. Akarsu S, et al., Hipohidrotik Ektodermal Displazi Tanılı Dört Olgu Sunumu: Christ-Siemens-Touraine Sendromu Fırat Tıp Dergisi 2007;12(4): 315-31.

21. Yavuz I, et al. Ectodermal Dysplasia: Retrospective Study Of Fifteen Cases.Archives Of Medical Research 37 2006; 403–409.

21. www.hekimim.com (last reach date: 25 April 2009).

22. www.dentartist.com (last reach date: 12 May 2009).

23. www.bilgipano.com (last reach date: 05 May 2009).

24. www.sağlıkkutuphanesi.com.

25. Balci Gokcen, Baskan Sabiha Zelal, Akdeniz Sedat. Ectodermal Dysplasia: Report of Four Cases and Review of Literature. International Dental & Medical Disorders. 2008; 1: 56-59.

26. Adiguzel Ozkan , Kaya Sadullah, Yavuz Izzet, Atakul Fatma. Oral Findings of Ectodermal Dysplasia and Literature Review. International Dental & Medical Disorders. 2008; 1: 43-49.

27. Yavuz Izzet et al. Ectodermal Dysplasia: Clinical Diagnosis.

International Dental & Medical Disorders; 2008; 1: 1-10.

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Yolk Sac Tumor in the Thoracic Wall Alper AVCI and Refik ULKU

Primary Yolk Sac Tumor in the Thoracic Wall: Case Report Alper AVCI1*, Refik ULKU2, Serdar ONAT3, Cemal OZCELIK4 1

MD Dicle University Medical School, Department of Thoracic Surgery, 21280 Diyarbakir / TURKEY. Assoc.Prof.Dr. Dicle University Medical School, Department of Thoracic Surgery, 21280 Diyarbakir / TURKEY. Assist.Prof.Dr. Dicle University Medical School, Department of Thoracic Surgery, 21280 Diyarbakir / TURKEY. 4 Prof.Dr. Dicle University Medical School, Department of Thoracic Surgery, 21280 Diyarbakir / TURKEY. 2 3

Abstract Malignant extragonadal germ cell tumors primary to the thoracic wall are quite uncommon lesions, but pure yolk sac tumor is even more exceptional. This is believed to be the first reported case of yolk sac tumor of the chest wall. A 33-year-old female patient with a primary extragonadal giant yolk sac tumor presenting with thoracic wall mass, complaint of back pain.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 58-60) Keywords: Yolk sac tumor, thoracic wall, spinal cord compression, surgery.

Received date: 25 April 2009

Accept date: 15 July 2009

Introduction

symptom of back pain. She had been aware of mass for 3 months. She had been misdiagnosed as Yolk-sac tomur mimics the yolk sac of the skin infection and discharced home with medical embryo, and the presence of alpha fetoprotein in treatment by local hospital. She was hospitalized for the tumor cells is highly characteristic(1). chest wall mass found in right and back. Complete Extragonadal germ cell tumors are rare lesions and blood counting values were in normal limits. Blood are mainly located in the retroperitoneal, biochemistry values were also in normal limits, mediastinal, pineal and presacral regions(2). The except ALP: 430 U/L, ALT: 118 U/L, AST: 96 U/L, primary location of non-metastatic germ cell tumors and GGT (533 U/L). Tumor markers were; Beta of the chest is the anterior mediastinal compartment. hCG: 0.1 ng/ml, CA125: 18.62 ng/ml, CA19-9: 66.3 Germ cell tumor arising from chest wall is one of the ng/ml, CA15-3: 25.27 ng/ml, CEA: 3.42 ng/ml. rarest conditions in human. The prognosis and Thorax computed tomography (CT), and Abdominal management of patients with Germ cell tumors ultrasonography (USG) were obtained. Thorax CT (GCTs) depends on the tumor histology and site of showed the mass; 105x64 mm dimensioned, origin(3). Most of the tumors of the chest wall paravertebral localicated in right-down hemithorax, adjacent ribs and muscles, presented with a nonpainful mass. With continued invasioned growth and tumor involvement of surrounding tissue, destructioned T8 vertebral corpus. And another 67x62 mm dimensioned mass in liver (Fig. 1). pain invariably occurs.

There is no reported case about primary yolk sac tumor in chest wall in the review of the English literature. We would like to emphasize; yolk sac tumor could be found in chest wall, as our patient.

Case A 33-year-old woman admitted to our hospital with palpable chest wall mass and *Corresponding author: Alper Avci, MD. Dicle University Medical School, Department of Thoracic Surgery, 21280 Diyarbakir / TURKEY Tel: +90 412 2488001 Fax: +90 412 2488440 E-mail: dr.avci@yahoo.com

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Fig. 1 Chest Computed Tomography of admitting.

Abdominal USG showed 69x63 mm dimensioned, right lobe superior segment Page 58

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(subsegment 5) localicated, solide mass, other abdominal organs were normal. Open biopsy for thoracic wall mass was done under local anesthesia and reported tumoral tissue with necrosis. Than dynamic abdominal CT obtained. It showed liver mass had been bloodstained peripherally before, centrally later, and diagnosed giant hemangioma firstly, other abdominal organs, especially genital organs were normal. Thoracic magnetic resonans imagination (MRI) showed; spinalis cord was compressed by the mass but there was no invasion.

The mass and adjacent invasioned tissues were extracted with operation. Resection distances were 4 cm in superior, inferior, and lateral dimentions. Resection included vertebral invasioned body, and because of the medulla spinalis, resection distances was less than 0.3 cm in medial dimention. Surgical resection, and appropriate reconstruction of large chest wall defect were done.

Post-op chest tube daily draniage was more than 400 cc for 10 days period. Therefore it, upper diafragmatic chest tube was not be ended. Skin necrosis in the operation area was seen at the 12 th day. Debridment operations were done in operation room for twice. Acinotobacter baumannii bacterial infection was defined into operation area. Antibiotics were used for infection for 20 days. Than chest tube was ended.

Muscle and skin replacement operations were done for the large skin and muscular defect.

The metilymetacrilate reconstruction prosthesis was removed in the same operation.

Sense and motor deficit were occured at the 29th day after operation. Thoracolomber MRI showed; right paravertebral 120x75 mm dimensioned mass, compression of spinal cord, methastasis in T8 vertebral corpus, and compression fracture in T9 vertebral body. Alpha fetoproein was more than 1210 ng/ml, AST: 209 U/L, and ALT: 446 U/L at the post-op 35th day.

Pathological diagnosing of the thoracic wall mass was Yolk sac tumor. It was diagnosed by alpha fetoprotein immunhistochemical painting (Fig. 2).

Adjuvant chemotheraphy was planned for patient. The first cure of cisplatin, etoposit, and bleomycin was done at the 41st day after oparation.

Sense and motor deficits were still continued. Alpha feto protein level was still more than 1210 ng/ml after fırst chemotheraphy cure. Patient was discharged with planning second cure of chemotheraphy at the 48th day.

After the second cure of chemotheraphy thorax and abdominal CT were obtained. These scannings showed multipl metastasis in lungs and liver, and abdominal effusion. And no decreasing at Volume 2 ∙ Number ∙ 2 ∙ 2009

Yolk Sac Tumor in the Thoracic Wall Alper AVCI and Refik ULKU

the level of alpha feto protein.

Fig. 2 Tumor cells with alpha fetoprotein painting.

Discussion Primary chest wall tumors are rare; of these, soft tissue tumors account for roughly 50%. Surgical resection is the most effective treatment for the vast majority of chest wall tumors. Keys to successful management include accurate diagnosis, wide surgical resection, and appropriate reconstruction of large chest wall defect(4). A diagnosis of a malignant extragonadal germ cell tumour can be established if the criteria laid by Einhorn(5) are fulfilled. They include absence of a detectable (including stigmata of burnt-out lesion) or subsequent appearance of a gonadal tumour and absence of nodal metastases in the para-aortic and iliac regions. With these stringent criteria, the thoracic wall emerges as an extremely uncommon site for such tumors. In an early study by Holt et al(6), 20 teratomatous tumours were found to involve the thoracic region. Seven among these were excluded because of probable mediastinal location. Thirteen had primary pulmonary location and five of these were malignant. There has been no reported thoracic wall primary yolk sac tumor case. Recognising such thoracic wall tumors in patients is important because these tumors are sensitive to chemotherapy with increased patient survival.

We do not have the alpha feto protein level at the time of admitting. Because we did not think the thoracic wall mass could be a yolk sac tumor.

Preoperatif pathological diagnosing was necrosis with tumor tissue. The operation and mass exicision was performed in accordig to this diagnosis. In spite of two chemotheraphy cure, multıpl metastasis were seen, and alpha feto protein level was stil more than 1200. Can it shows that primary thoracic wall yolk sac tumor is resistant for chemotheraphy?

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Yolk Sac Tumor in the Thoracic Wall Alper AVCI and Refik ULKU

Conclusion As a result we would like to emphasize that extragonadal germ cell tumors can be find in the thoracic wall rarely. But it should be thought while pre operation period.

References 1. Abdel Rahman AR, Ebied EN, Nouh MA, Gal AA, Mansour KA. Primary yolk sac tumor of the lung. Ann Thorac Surg. 2009; 87: 1925-6.

2. Vaideeswar P, Deshpande JR, Jambhekar NA. Primary pleuropulmonary malignant germ cell tumours. J Postgrad Med 2002;48:29-31.

3. Fauci A.S., Braunwald AB, Isselbacher KJ, et al. Harrison’s principles of internal medıcıne, 16 th edıtıon, page 553. McGraw-hill medical publishing division.1998. International edition.

4. Shields TW, LoCicero J, Ponn RB, Rusch VW. Genral Thoracic Surgery. 6th edition, page 710. Lippincott Williams&Wilkins. 2005.

Philadelphia.

5. Einhorn LH. Extragonadal germ cell tumors. In: Einhorn LH, editor.

Testicular tumors. New York: Masson Publishing; 1980:185-204.

6. Holt S, Deverall PB, Boddy JE. A teratoma of the lung containing thymic tissue. J Pathol 1978;126: 85-9.

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Journal Of International Dental And Medical Research ISSN 1309-100X Effect of ELF-MF Exposure on Anterior Pituitary of Rats http://www.ektodermaldisplazi.com/journal.htm M.Zulkuf Akdag, Suleyman Dasdag, M.Aydin KETANI, Hakan SAGSOZ

Effect of Extremely Low Frequency Magnetic Fields in Safety Standards on Structure of Acidophilic and Basophilic Cells in Anterior Pituitary Gland of Rats: an Experimental Study Mehmet Zulkuf AKDAG1*, Suleyman DASDAG1, M.Aydin KETANI2, Hakan SAGSOZ2 1 Department of Biophysics, Medical Faculty of Dicle University, Diyarbakir-TURKEY. 2 Department of Histology and Embriyology, Veterinary Faculty of Dicle University, Diyarbakir-TURKEY.

Abstract After discovery of magnetite in the brain of several mammalian species including humans, it was suggested that the human brain is sensitive to magnetic fields. The present study investigated the effect of 100 µT and 500 µT extremely low frequency magnetic fields (ELF-MF), established guidelines by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) for public and occupational magnetic field exposure limits at 50 Hz, on acidophilic and basophilic cells in the anterior pituitary gland of rats. 30 adult male Sprague Dawley rats were separated into three groups in this study (sham group: 10 and two study groups: 20). Rats in the study (experimental) groups separated equally into two groups that is 100 µT and 500 µT exposure groups. First experimental group rats exposed to 100 µT while second experimental group exposed to 500 µT ELF-MF for 2 hours per day (7 days in a week) during 10 months.

For the sham group, the same experimental procedure was applied to the rats (2 hours / day / 7 days in a week for 10 months) except ELF-MF exposure. After ELF-MF and sham exposure, the pituitary gland were removed totally to examine the structure of acidophlic and basophilic cells in the anterior pituitary gland of rats as histomorphometric and histochemical. Affinity against dye in acidophilic and basophilic cells of first experimental groups’ rat was found lower than sham group. It means that degranulation may occur in sitoplasmic granuls of these cells. Disappearing in the affinity of Periodic Acid-Shchiff (PAS)Orange-G in acidophilic and basophilic cells of second exposure group has been indicating high disappearing of granuls in these cells. No significant differences were found between sham and exposure groups in terms of the number of acidophilic and basophilic cells in the anterior pituitary gland (p>0.05).

Although degranulation observed in acidophilic cells, the results were not found to be significant between experimental groups (p>0,05). However, degranulated basophilic cells were found significant between experimental groups (p<0,05). In conclusion, it was suggested that long-term ELF-MF exposure, which are the limits for public environmental and occupational magnetic field exposure guidelines, can affect affinity of PAS-Orange G in acidophilic and basophilic cells of the anterior pituitary gland in rats.

(Journal of International Dental and Medical Research 2009; 2: (2), pp. 61-66) Keywords: ELF Magnetic field, anterior pituitary gland, acidophil cells, basophil cells.

Received date: 21 April 2009 Introduction The possible association between exposure of humans to extremely low frequency magnetic fields (ELF-MF) and adverse health effects has attracted a great deal of scientific attention. Relation to the mammalian nervous system, exposure to 50/60 Hz electromagnetic fields (EMFs) has been *Corresponding author: Dr. Mehmet Zulkuf Akdag Department of Biophysics, Medical Faculty of Dicle University, 21280, Diyarbakir-TURKEY Tlf: +90-412-2488001 Fax : +90-412-2488440 E-mail: akdag@dicle.edu.tr , mzakdag@gmail.com

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Accept date: 09 July 2009 implicated in a wide spectrum of effects1. Poole et al. reported an increased incidence of headaches and depression for individuals residing near 2 transmission lines in humans . In animal studies, alterations in central neurotransmitter turnover and pineal function have been observed after 60 Hz MF exposure. 3,4 These reports suggest that neural cells may be capable of transducing power line frequency EMFs into physiological responses5. Whether or not long-term ELF-MF exposure can increase risk for the adverse health outcomes is a central issue in the study of possible ELF-MF health effects.

It was reported that MF exposure can give rise to changes in neuroendocrine system function in a mammalian laboratory model6. Suppression of melatonin in the blood and pineal of the rat or hamster after magnetic field exposure have been reported by several studies7-10.

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The anterior pituitary gland regulates the activity of the thyroid, adrenals, and reproductive gland11. Among other hormones it produces growth hormone, prolactin, thyrotropin, and corticotrophin.

The pituitary also secretes endorphins that act on the nervous system to reduce sensitivity to pain11,12.

The production and secretion of pituitary hormones can be influenced by factors such as emotions and seasonal changes. To accomplish this, the hypothalamus conveys information sensed by the brain to the pituitary11,12. All these features make the pituitary gland a suitable system to study the biological impact of non-ionising radiation11.

Several organizations have established guidelines for public and occupational exposures to power frequency MF. At 50 Hz, magnetic field exposure limits have been set at 100 µT for public exposure and 500 µT for occupational exposure by the International Commission on Non-Ionizing Radiation Protection (ICNIRP)13. Thus, we chose 100 and 500 µT, with the idea that it is a more accurate reflection of the actual values in daily life.

The aim of the study was to ivestigate the effect of long term 100 and 500 µT ELF magnetic field exposure on acidophilic and basophilic structure of the anterior pituitary gland in rats.

MATERIALS and METHODS Subjects and Animal Care The experiments were performed on 30 male Sprague-Dawley rats obtained from Medical Science Application and Research Center of Dicle University, aged 4 months at the beginning of the study, weighing 300- 390g, and fed with standard pelleted food (TAVAS Inc. Adana, Turkey). The animals were kept in 14/10h light/dark environment at constant temperature of 22 ± 3°C, 45 ± 10% humidity. This protocol was approved by the local ethics committee.

Rats were separated into three groups in this study (sham group: 10 and two study groups: 20).

Rats in the experimental groups separated equally into two groups that is 100 µT and 500 µT exposure groups. First experimental group rats exposed to 100 µT while second experimental group exposed to 500 µT extremely low frequency (ELF) magnetic field for 2 hours per day (7 days in a week) during 10 months in a plexiglas cage. For the sham group, the same experimental procedure was applied to the rats (2 hours / day / 7 days in a week for 10 months) except ELF-MF exposure.

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Magnetic field generation and exposure of rat to magnetic field The MF was generated in a device designed by us that had one pair of Helmholtz coils of 25 cm in diameter in a Faraday cage (130×65×80 cm) that earthed shielding against the electric component.

This magnet was constructed by winding 225 turns of insulated soft copper wire with a diameter of 1.0mm. Coils were placed horizontally as facing one another. The distance between coils was 25 cm. An AC current produced by an AC power supply (DAYM, Turkey) was passed through the device.

The current in the wires of the energized exposure coil was 0.12 A for 100 µT and 0.50 A for 500 µT, which resulted 50 Hz MF. The MF intensities were measured once per week as 100 µT and 500 µT in different 15 points of methacrylate cage by using digital teslameter (Phywe, 209101074, Göttingen, Germany) to ensure homogeneity of the field during the course of the experiment. Magnetic field measurements showed that, at the conditions of the experiment, the magnetic field exposure system produced a stable flux density of 100 µT, 500µT and stable frequency of 50 Hz with neglible harmonics and no transients.

The 50 Hz stray fields in the sham-exposure system were 0,1 µT. The static earth magnetic field was measured with a Bell 7030 Gauss/Teslameter (F.W. Bell, Inc., Orlando, FL). The component parallel to the exposure field was 14 µT and the component perpendicular to the exposed field was 34 µT. All field measurements were performed by persons not involved in the animal experiments. Observers were not aware of which group of rats was ELF Magnetic Field-or sham-exposed, i.e. the whole study was done blind. No temperature differences were observed between exposure and sham coils during the exposure.

The first and second experimental groups were exposed to 100 µT and 500 µT ELF MF during 10 months, 2 h a day respectively. Third group was sham that were treated like experimental group except ELF-MF exposure (corresponding to first and second groups, respectively) in methacrylate boxes.

The rats were free in methacrylate cage inside the coils. After ten months of MF exposure, the study was terminated. Immediately after the last exposure, blood of the animals was collected by cardiac puncture under ketamine anesthesia (100 mg/kg, intramuscularly) to kill rats and pituitary gland of the rat was removed for histopathological evaluation.

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Journal Of International Dental And Medical Research ISSN 1309-100X Effect of ELF-MF Exposure on Anterior Pituitary of Rats http://www.ektodermaldisplazi.com/journal.htm M.Zulkuf Akdag, Suleyman Dasdag, M.Aydin KETANI, Hakan SAGSOZ

Histological procedure Pituitary glands taken from the rats were fixed respectively in formaldehyde (10%) for histological assessment. After routine histological processing, the tissues were embedded in paraffin, sectioned, and stained with PAS-orange G. The histochemical stains used for specific chemical groups, such as the Periodic Acid-Shchiff (PAS) reaction for carbohydrates of glycoproteins14.

Histological assessments were performed with a light microscope (Nikon eclipsse-400, colpix4500), which has digital camera atachment. In histological evaluations, It was examined the structure of acidophil and basophil cells that were pars distalis of the anterior pituitary gland. Both normal and degranulated forms of acidophil and basophil cell were performed with an object lens40 in 1 mm2 field.

It was determined statisticaly significant alteration between exposure groups by counting degranulated cells.

in sham groups’ rats. Acidophilic cells (→), Basophilic cells (*), sinusoid (s). (PAS-Orange G, ×40).

Histochemical staining of acidophilic and basophilic cells in the first experimental group was significantly found different than sham group.

Affinity against dye in acidophilic and basophilic cells of first experimental groups’ rat was found lower than sham group. It means that degranulation may occur in sitoplasmic granuls of these cells ( Fig. 2).

Statistical Analysis Data were analyzed by Kruskal–Wallis oneway analysis of variance ANOVA on ranks and post-hoc tests using Tukey and LSD and using Mann-Whitney U test. All hypothesis tests used a criterion level of α = 0.05.

Results Polygonal and round shaped acidophilic and basophilic cells were observed around of sinusoids of the anterior pituitary gland in sham group. In this group, It was examined granuls, which were stoplasm of acidophilic and basophilic cells, stained clearly with PAS-orange G. We observed that acidophilic cells were high affinity against PASorange G stains, stained as orange-G positive and basophilic cells was PAS positive (Fig. 1).

Fig. 2 The appearance of the anterior pituitary gland in first experimental groups’ rats. Acidophilic cells (→), Basophilic cells (*), sinusoid (s), capiller (k).

(PAS-Orange G, ×40) On the other hand, shrinking in sinusoids and disordering in cell arrangement was also observed in the first exposure group.

Disappearing in the affinity of PAS-OrangeG in acidophilic and basophilic cells of second exposure group has been indicating high disappearing of granuls in these cells (Fig. 3).

Fig. 3 The appearance of the anterior pituitary gland in second experimental groups’ rats. Acidophilic cells (→) , Basophilic cells (*), sinusoid (s), capiller (k). (PAS-Orange G, ×40)

Fig. 1 The appearance of the anterior pituitary gland Volume 2 ∙ Number ∙ 2 ∙ 2009

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Journal Of International Dental And Medical Research ISSN 1309-100X Effect of ELF-MF Exposure on Anterior Pituitary of Rats http://www.ektodermaldisplazi.com/journal.htm M.Zulkuf Akdag, Suleyman Dasdag, M.Aydin KETANI, Hakan SAGSOZ

group were more affected than first experimental group. No granuls observed in the sitoplasm of the second exposure group. However, restricted sinusoids and only nucleus were observed in the sitoplasm of the second exposure group. The numbers of asidophilic and basophilic cells in the anterior pituitary gland were presented in the table 1.

No significant differences were found between sham and exposure groups in terms of the number of acidophilic and basophilic cells in the anterior pituitary gland (p>0.05). Although degranulation observed acidophilic cells, the results were not found to be significant between exposure groups (p>0,05). By the way, degranulated basophilic cells were found significant between exposure the groups (p<0,05) (Tab. 1).

Tab. 1 The counts and degranulation situation of basophilic and acidophilic cells of pars distalis in the anterior pituitary gland. a P<0.05 as compare to exposure groups by Mann-Whitney-U test.

Discussion The brain and central nervous system are considered to be among the most likely sites of interaction between biological systems and powerfrequency fields.15 Although the mechanisms of the influence of these fields on nervous tissue remain mostly unknown, studies in relation to the effect of ELF-MF on brain and nervous system have been continuing to explain interaction mechanisms.

Barbier et al. studied the effect of exposure of single rat pituitary cells to 50 Hz sine wave magnetic fields of various strengths on the intracellular free Ca2+concentration16. They have concluded that a 50 Hz, 50 µT magnetic field can markedly affect endocrine cell physiological processes16. Espinar et al. showed that static magnetic field can induce irreversible developmental effects on the processes of cell migration and differentiation of the chick cerebellar cortex17. Wilson et al. investigated the effects of 60 Hz magnetic field exposure on the pineal and hypothalamic-pituitary-gonadal axis in the Siberian hamster18. They indicate that both one-time and Volume 2 ∙ Number ∙ 2 ∙ 2009

repeated exposure to a 0.1 mT, 60 Hz MF can give rise to neuroendocrine responses in the Siberian hamster18. Boland et al. have shown that neither continuous nor intermittent EMF exposure is able to modify cell death of cultured hipocampal cells19.

Jelenkovic et al. investigated the possible effect of ELF-MF (50 Hz, 0,5 mT) on the brain of adult male Wistar rats following a 7-day exposure20. According to their results, they indicate that a 7-day exposure to extremely low-frequency magnetic field can be harmful to the brain, especially to the basal forebrain and frontal cortex due to development of lipid peroxidation20. Zecca et al. investigated the biological effects of prolonged exposure to ELF electromagnetic fields in rats21. In their study, groups of adult male Sprague Dawley rats were exposed for 8 months to electromagnetic fields (EMF) of two different field strength combinations: 5µT - 1kV/m and 100µT - 5kV/m21. According to their findings, they suggested that EMF may cause alteration of some brain functions21. It has been reported that prolonged exposure of extremely low frequency electromagnetic radiation attenuates the circadian nocturnal rise of melatonin in the pineal gland22,23. Canedo et al. showed that short MF exposures had a long term effect on cerebral cortex 5-HT and no long term effect on the pineal gland levels of 5-HT, a precursor of melatonin24. Cook et al. suggests that weak magnetic fields can affect the infiltration of immunologically responsive cells and the presence of mast cells in brain parenchyma25.

Lisi et al. showed that exposure to 50 Hz ELF-EMF is responsible for the premature differentiation in pituitary corticotrope-derived AtT20 D 16 V cells11.

In a toxicological studies, some authors investigated the effects of magnetic field on brain tissue. For instance, In a recent study, Kim et al investigateted the effect of 20 kHz triangular magnetic field on Sprague-Dawley rats.

They found no histopathological alterations on rats’ brain tissue after exposure to 20 kHz triangular magnetic field26.

Robertson et al. investigated potential health effects of 10 kHz magnetic fields on mice in a toxicological study. However, they found no pathology in brain of mice after magnetic field exposure27.

In the present study, the results describes the effect of long-term ELF-MF exposure on acidophilic and basophlic cells in the anterior pituitary gland in rats. It was determined doseresponse interaction in relation to histopathologic alterations in acidophilic and basophilic cells. The results indicate that long-term 100 and 500 µT magnetic field exposure can affect affinity of PASOrange G in acidophilic and basophilic cells. It was also observed that 500 µT magnetic field was effective dose that affect affinity of PAS-Orange-G Page 64

Journal Of International Dental And Medical Research ISSN 1309-100X Effect of ELF-MF Exposure on Anterior Pituitary of Rats http://www.ektodermaldisplazi.com/journal.htm M.Zulkuf Akdag, Suleyman Dasdag, M.Aydin KETANI, Hakan SAGSOZ

and granuls of cytoplasm in acidophilic and basophilic cells. However, acidophilic and basophilic cell counts were not alter after long-term 100 and 500 µT magnetic field exposure.

There are many studies in relation to the effect of ELF-MF on brain and electrophysiological interaction. However, no studies have been reported in the literature considering the effects of ELF-MF on acidophilic and basophilic cells of rat anterior pituitary gland. Therefore, we couldn’t compare the results of the present study with other studies.

Although acidophilic cells secretes GH and prolactin hormones, basophilic cells secretes FSH, LH, TSH and ACTH hormones.28 In the present study, it was determined significant difference in degranulated basophilic cells of rats that exposed to 100 and 500 µT ELF-MF (p<0,05). Degranulation in basophilic cells may cause deficiency in FSH, LH, TSH and ACTH hormones. This deficiency may cause functional disturbance in target organs depending on hormonal alterations.

Conclusions In conclusion, it was suggested that longterm ELF-MF exposure, which are the limits for public environmental and occupational magnetic field exposure guidelines, can affect affinity of PASOrange G in acidophilic and basophilic cells of the anterior pituitary gland in rats. It was also determined that 500 µT magnetic field was effective dose that affect affinity of PAS-Orange-G and granuls of stoplasm in acidophilic and basophilic cells. A detailed and molecular studies must be carried out to explain interaction mechanisms between ELF-MF and nervous system especially in relation to acidophilic and basophilic cells in the anterior pituitary gland.

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