balkan journal of stomatology - balkan stomatological society

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141TUPNBUPMPHJDBM!!TPDJFUZForthcoming Meeting16 th Congress of the Balkan Stomatological Society28 April - 1 May, 2011, Bucharest, RomaniaBALKAN STOMATOLOGICAL SOCIETY&ROMANIAN DELEGATION OF THE BaSSInvite you cordially to Bucharest on the occasion of the16 th Congress of the Balkan Stomatological SocietyPresident of the CongressProf. Norina FornaDear colleagues and friends,On behalf of the Local Organizing Committee, it gives me great pleasure to invite you for the 16 th Balkan StomatologicalSociety Congress (BaSS) to be held in Bucharest, Romania, in April 2011. This event will be organized by the Romaniadelegation of the BaSS with the support of the Romanian Society of Oral Rehabilitation (ASSRO), The Romania DentalCouncil (CMDR) and Romanian Association of Oral Implantology and Biomaterials (SRIOB), under the theme “Updatein dental medicine”.The success of the Annual Bass Congress underlines the crucial role of the scientifi c programme’s quality. In recent yearswe have not only seen an increase in the number of participants but also the growth and development of what is now anoutstanding scientifi c programme with continuing efforts to elevate Balkan stomatology to a higher level. This certainlycould not have been achieved without your valuable support at the BASS congresses and for that we are extremelygrateful.As the Local Organizing Committee, we hope that, in addition to intellectual and professional growth, we can also provideyou with a relaxing and enjoyable social experience. The capital of Romania is an attractive tourist destination, whichoffers the opportunity to all of you to pay a visit to the numerous historical sites and enjoy the extraordinary Romanianscenery.We look forward to seeing you all in Bucharest.Kind regardsProfessor Norina FornaPresident of the CongressCo-Organizer:Eurolink Medical CongressesStr. Carpaţi nr. 2, Iaşi, 700729, Româniaemail: eurolink@eurolink-tours.co.ukwww.eurolink-tours.co.uk

BALKAN JOURNALOF STOMATOLOGYOfficial publication of the BALKAN STOMATOLOGICAL SOCIETYVolume 15 No 1 March 2011ISSN 1107 - 1141

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141TUPNBUPMPHJDBM!!TPDJFUZEditor-in-ChiefLjubomir TODOROVIĆ, DDS, MSc, PhDFaculty of DentistryUniversity of BelgradeDr Subotića 811000 BelgradeSerbiaEditorial boardALBANIARuzhdie QAFMOLLA - EditorEmil KUVARATIBesnik GAVAZIBOSNIA AND HERZEGOVINAMaida GANIBEGOVIĆ - EditorNaida HADŽIABDIĆMihael STANOJEVIĆAddress:Dental University ClinicTirana, AlbaniaAddress:Faculty of DentistryBolnička 4a71000 Sarajevo, BIHBULGARIANikolai POPOV - EditorAddress:Nikola ATANASSOVFaculty of DentistryNikolai SHARKOV G. Sofiiski str. 11431 Sofia, BulgariaFYROMJulijana GJORGOVA - EditorAna STAVREVSKALjuben GUGUČEVSKIAddress:Faculty of DentistryVodnjanska 17, SkopjeRepublika MakedonijaGREECEAnastasios MARKOPOULOS - Editor Address:Haralambos PETRIDISAristotle UniversityLambros ZOULOUMISDental SchoolThessaloniki, GreeceROMANIAAlexandru-Andrei ILIESCU - Editor Address:Victor NAMIGEANFaculty of DentistryCinel MALITA Calea Plevnei 19, sect. 170754 Bucuresti, RomaniaSERBIAVojislav LEKOVIĆ - Editor Address:Slavoljub ŽIVKOVIĆFaculty of DentistryZoran STAJČIĆ Dr Subotića 811000 Beograd, SerbiaTURKEYEnder KAZAZOGLU - EditorPinar KURSOGLUArzu CIVELEKCYPRUSGeorge PANTELAS - EditorHuseyn BIÇAKAikaterine KOSTEAAddress:Yeditepe UniversityFaculty of DentistryBagdat Cad. No 238Göztepe 81006Istanbul, TurkeyAddress:Gen. Hospital NicosiaNo 10 Pallados St.Nicosia, CyprusInternational Editorial (Advisory) BoardChristoph HÄMMERLE - Switzerland George SANDOR - CanadaBarrie KENNEY - USA Ario SANTINI - Great BritainPredrag Charles LEKIC - Canada Riita SUURONEN - FinlandKyösti OIKARINEN - Finland Michael WEINLAENDER - AustriaBALKAN STOMATOLOGICAL SOCIETYTUPNBUPMPHJDBM!!TPDJFUZCouncil:President:Past President:President Elect:Vice President:Secretary General:Treasurer:Editor-in-Chief:Prof. P. KoidisProf. A. IliescuProf. H. BostanciProf. N. SharkovProf. A.L. PissiotisDr. E. HassapisProf. Lj.TodorovićMembers: R. QafmollaP. KongoM. GanibegovićS. KostadinovićA. FilchevD. Stancheva ZaburkovaM. CarčevA. MinovskaT. LambrianidisS. DalambirasA. AdžićM. DjuričkovićN. FornaA. BucurD. StamenkovićM. BarjaktarevićE. KazazogluM. AkkayaG. PantelasS. SolyaliThe whole issue is available on-line at the web address of the BaSS (www.e-bass.org)

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYVOLUME 15 NUMBER 1 March 2011 PAGES 1-56ContentsOP T. Zarra Comparative Study of Calcium Hydroxide Extrusion with 5T. Lambrianidis Different Techniques of Intra-Canal PlacementE. KostiOP V. Biočanin Efficacy of Computer-Controlled Articaine Delivery for 11M. Milić Supplemental Intraoral AnaesthesiaD. BrajkovićB. BrkovićD. StojićLj. TodorovićOP D. Sapourides Caries Experience among Greek Pomak Children Living in 15V. Topitsoglou Rural North-Eastern Greece. A Cross-Sectional StudyS. MuronidisN. KotsanosOP A. Dimkov Effects of Orbit Sugar-free Chewing Gum for Kids in Overall and 24N. Panovski Cariogenic Salivary Microflora ReductionE. GjorgievskaOP E. Zabokova-Bilbilova Fluoride Released from Orthodontic Bonding Material: 31A. Sotirovska-Ivkovska An In Vitro EvaluationI. GjorgovskiOP N. Topouzelis Variation of Skeletal Cephalometric Variables in 35A. Zafiriadis Class II Division 2 Patients with AgeH. MarkovitsiOP M. Popovska Clinical Oral Manifestation in Gastrointestinal Disorders 41B. StavrovaA. Atanasovska-StojanovskaP. MisevskaS. StrezovskaL. KanurkovaJ. Gjurcheski

CR M. Lazaridou Recurrent Atypical Fibroxanthoma in a Patient with Scleroderma: 48L. Zouloumis Report of a CaseK. KontosA. NikolaidouK. VachtsevanosCR A. Ntomouchtsis Unusual Penetrating Metallic Foreign Bodies Injured 52D. Maggoudi Maxillofacial and Orbital Region with Minimal DamageH. PanidouA. KondylidouK. Antoniades

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYComparative Study of Calcium Hydroxide Extrusionwith Different Techniques of Intra-Canal PlacementSUMMARYIntroduction: To investigate Ca(OH) 2 extrusion from the apicalforamen in relation to the placement mode.Methods: 200 teeth, prepared with ProTaper files with and withoutapical patency, were divided in Groups A and B respectively, and filled withCa(OH) 2 at 1 and 3 mm short of working length, using K-files manually andwith mechanical spiral techniques (Pastinject/Lentulo) at 500 and 700rpm.Extrusion was graded as present/absent. Experimental categories werecompared using Fisher’s exact test.Results: Extrusion was observed only in teeth with patency. Therewas no extrusion with K-files in all cases and with Pastinject andLentulo inserted at 3 mm short of working length. Speed elevation did notsignificantly increase the extrusion cases.Conclusions: K-files tend to be safer than mechanical techniques.Pastinject and Lentulo at 3 mm short of working length prevented Ca(OH) 2extrusion. Raising speed from 500 to 700 rpm did not significantly increasethe extrusion risk.Keywords: Calcium Hydroxide; K-files; Lentulo; Pastinject; Patency; Rotation SpeedT. Zarra, T. Lambrianidis, E. KostiAristotle University of ThessalonikiDental School, Department of EndodonticsThessaloniki, GreeceORIGINAL PAPER (OP)Balk J Stom, 2011; 15:5-10IntroductionCalcium hydroxide Ca(OH) 2 is widely used as anintra-canal medicament. A homogenous and sufficient inlength, obturation of the root canal space with Ca(OH) 2 isessential in order to benefit from the paste’s antimicrobialeffect.Several techniques and specialized instruments forintra-canal placement of Ca(OH) 2 have been advocated.These can be divided into 3 main categories: (a) spiraltechniques, performed with hand endodontic instruments,most commonly with K-files rotated counterclockwise,or by mechanically rotating instruments used in variousspeeds ranging from as low as 150rpm for Nickel-Titanium instruments, 500rpm to 1000 rpm for theLentulo paste carrier and the Pastinject (MicroMega,Besancon, France), moderate speed (5,000rpm) for theGutta-Condensor (Maillefer, Ballaigues, Switzerland)to even higher speed (10,000 rpm) for the McSpaddencompactor (Ransom and Randolph, Toledo, Ohio);(b) ultrasonic techniques using specifically designedinstruments mounted on an ultrasonic generator, such asK-type ultrasonic files and the Meca-Shaper (Maillefer,Ballaigues, Switzerland); and (c) injection techniques,such as the Messing Root Canal Gun (Dentsply Maillefer,Ballaigues, Switzerland), the Calasept injection system(Scania Dental AB, Sweden) and the Ultracal syringesystem (Ultradent, South Jordan, UT, USA). Theselast techniques use a syringe and a needle to insertthe Ca(OH) 2 into the prepared root canals. Althoughcommonly the above techniques are used separately,a combination has also been proposed 34 . Followingplacement of the paste, condensation can be achieved withfiles, absorbent paper points and manual pluggers.The effectiveness of current techniques forCa(OH) 2 filling of the root canal space varies. Deveauxet al 7 showed that Pastinject and Lentulo provideda better filling in single-rooted teeth compared toGutta-Condensor, Meca-Shaper and K-type ultrasonicfile. Estrela et al 8 concluded that K-files rotatedcounterclockwise, combined with the use of absorbentpaper points and pluggers, achieve better quality of fillingwith less empty spaces in all thirds of the root canalcompared to Mc Spadden compactors, Lentulo spirals

6 Theodora Zarra et al. Balk J Stom, Vol 15, 2011and syringes 8 . When the Pastinject and the Lentulo weredirectly compared, Pastinject proved to be more effectivefor placement of Ca(OH) 2 7,22 . Similarly, when comparingLentulo to an injection technique, the Lentulo provideda denser and up to the desired length filling of the rootcanal 30 . However, it has been suggested that if straight orslightly curved root canals are prepared up to at least size50, high quality Ca(OH) 2 fillings can be achieved with asyringe 32 . There is discrepancy in the literature regardingthe effectiveness of different techniques. However, thereis a consensus that better filling of the root canal spacewith Ca(OH) 2 is achieved in root canals that have beenadequately instrumented, when compared to those thathave been only minimally prepared as is often a caseduring an emergency appointment 31,32,34 .During root canal treatment, Ca(OH) 2 dressingmaterial might unintentionally escape through the rootapex into the periapical tissues 4,6,35,21 . Although theeffectiveness of various techniques in filling the root canalspace has been widely studied 7,8,30-32 , there are no reportsin the literature on the effectiveness of those techniquesin preventing extrusion into the periapical tissues. Onlyin a pilot study on plastic blocks 34 , extrusion was notedin cases of patent blocks with the carrier placed at theworking length and therefore, in the main study, this wasprevented and thus not studied by placing tape where thecanal exited the plastic block. The aim of this study wasto investigate the frequency of extrusion of Ca(OH) 2 fromthe apical foramen in relation to the technique of intracanalplacement, the distance from the apical foramen androtation speed.Materials and Methods200 freshly extracted, fully formed human permanentsingle-rooted teeth obtained from a pool of teethwere studied. Calculus and conjunctive deposits wereremoved and teeth were kept in 10% formalin until use.2 radiographs were taken, 1 from the buccal and 1 fromthe proximal side of the tooth to verify the existenceof a single non-calcified root canal with a curvature of0-10 0 according to Schneider 28 . Once the access cavitywas prepared, the working length was establishedradiographically at a distance of 1 mm from theradiographic terminus. The teeth were divided in 2 groups:Group A: The root canals were instrumented withthe ProTaper rotary files (Dentsply, Tulsa Dental, Tulsa,OK, USA) according to the manufacturer’s instructions,starting with file S1 up to file F3. Between each file,the root canal was irrigated with 2.5% NaOCl using a27-gauge needle (Ultradent Products INC, South Jordan,UT, USA) placed passively in the canal at 2-3mm shortof the working length, and a #10 K-file was placed intothe root canal and advanced until the tip of the file passed1mm from the apical foramen to maintain the patency ofthe apical constriction.Group B: The instrumentation procedure wasidentical to that of group A but patency file was not used.After instrumentation, the root canals were driedwith paper points and the teeth were adjusted to holescreated through the rubber stoppers of vials and weresecured in place using sticky wax. The vials were handheld.The operator was shielded from seeing the root apexduring the filling procedure by a rubber dam that coveredthe vial.Pure Ca(OH) 2 powder (Merck K GaA, Darmstadt,Germany) was moistened with saline and mixed to arelatively thick paste (corresponding to a toothpasteconsistency). Then, the specimens of each group wererandomly divided into 10 experimental groups comprising10 teeth each. The groups are presented in table 1.The entire length of a size # 30 Lentulo spiral(Maillefer, Ballaigues, Switzerland) and a size #30Pastinject (MicroMega, Besancon, France) file werecoated with the paste, introduced in the canal at 1 and 3mm short of the working length and then rotated at 500and 700 rpm using a handpiece mounted on a speedand torque control machine (X-Smart, Dentsply, TulsaDental, Tulsa, OK, USA). A size #30 K-file (Maillefer,Ballaigues, Switzerland) was coated with Ca(OH) 2and introduced into the canal at 1 and 3 mm short ofthe working length with a counterclockwise rotationresulting in 20 subgroups (Tab. 1). For all 3 techniquesof placement, the paste was condensed with a size #10plugger (Maillefer, Ballaigues, Switzerland), then driedand compacted with the blunt end of a paper point andthe procedure was repeated for a total of 3 times for eachtooth.When the intra-canal placement of Ca(OH) 2 wascompleted, the tooth-rubber stopper unit was removedfrom the mouth of the vial and the root ends were viewedunder a microscope (OPMI, Carl Zeiss Surgical Inc,Dublin, CA, USA) at x 4.5 magnification. The extrusionof Ca(OH) 2 was recorded as either present or absentby 2 examiners masked on the group and techniqueexamined. Any amount of Ca(OH) 2 that past the apicalforamen was considered extrusion (Fig. 1a and 1b.).Only if the 2 examiners agreed upon their answer, theanswer considered valid. In case of disagreement, a thirdexaminer was consulted. Cases in which there was noconsensus were excluded from the study.Fisher’s exact test was used to compare theexperimental categories, with the level of significanceset at p

Balk J Stom, Vol 15, 2011 Calcium Hydroxide Extrusion during Intra-canal Placement 7Table 1. 20 experimental sub-groups and the extrusion of Ca(OH) 2 in relation to the method of intra-canal placement, distance fromthe apical foramen and rotation speed (rpm).Group Technique Length Rotation speed (rpm) ExtrusionYes (N)No (N)LENTULO (N=40)-1mm-1mm500700-3mm 500 0 1001109A (N=100) With patencyB (N=100) Without patencyPASTINJECT (N=40)K-FILE (N=20)LENTULO (N=40)PASTINJECT (N=40)K-FILE (N=20)-3mm 700 0 10-1mm 500 3 7-1mm 700 4 6-3mm 500 0 10-3mm 700 0 10-1mm - 0 10-3mm - 0 10-1mm 500 0 10-1mm 700 0 10-3mm 500 0 10-3mm 700 0 10-1mm 500 0 10-1mm 700 0 10-3mm 500 0 10-3mm 700 0 10-1mm - 0 10-3mm - 0 10Figure 1. Figure 1.

8 Theodora Zarra et al. Balk J Stom, Vol 15, 2011ResultsThe number of teeth with extruded Ca(OH) 2 in eachgroup is shown in table 1. Patency of the apical foramensignificantly increased Ca(OH) 2 extrusion. In groupA, K-files used for intra-canal placement of Ca(OH) 2prevented extrusion; there were 8 cases of extrusionwhen mechanical spiral techniques were used; however,there was no statistically significant difference. Insertionof the paste carriers at 3 mm short of the working lengthconstricted the paste inside the root canal more efficientlycompared to insertion at 1mm short of the working length,but the difference between them was not statisticallysignificant. At 500 rpm and at 1 mm short of the workinglength, Pastinject caused extrusion of Ca(OH) 2 in 3 out of10 teeth, but the difference was not statistically significantwhen compared to the Lentulo technique, where noextrusion was detected. Elevating the speed from 500to 700 rpm did not lead to significantly more cases ofextrusion for either Lentulo or Pastinject, although therewas a tendency (4 out of 10 cases) for extrusion whenusing Pastinject at 700 rpm and at 1 mm short of theworking length.DiscussionAlthough it is suggested that the deliberate extrusionof Ca(OH) 2 into the periradicular tissues may have adirect effect on inflamed tissue and epithelial cysticlinings and potentially favour periapical healing andencourage osseous repair 35 , it is not widely recommended.Extensive extrusion of Ca(OH) 2 into the periapicaltissues did not appear to compromise ultimate periapicalhealing 4,6,21 ; however, in the majority of cases, it seemedto delay it. Moreover, there are reports of immediate flareup induced by extrusion 6 . Cases with complete healingof the pre-existing periapical lesion even after 3 21 or 4years 16 with incomplete resorption of the extruded pastecontaining BaSO 4 (used to enhance its radiopacity) havealso been reported.The use of Ca(OH) 2 as an intracanal medicament hasbeen linked with a number of severe side effects. Therehave been case reports with necrosis of the gingiva andmucosa due to its alkalinity 3 , severe tissue necrosis afterintra-arterial injection 29 , orbital pain and headache 36 ,severe facial ischemia 18 , mental or inferior alveolarnerve paraesthesia after penetration of the materialinto the mandibular canal 1,24,27 , formation of antrolithsfollowing its extrusion into the antrum 10,12 and foreignbody granuloma in the nearby gingival tissues 15 . Inmice, inflammatory responses were reported followinginoculation of various Ca(OH) 2 pastes into subcutaneoustissue. The severity of the response varied by the pastetype used 5,20 .In our study, extrusion of Ca(OH) 2 was recordedas either present or absent. Similarly, previous studieson the extrusion of gutta-percha used the presence andabsence of extrusion as a criterion to evaluate the safetyof filling techniques in obturating the root canals 25 . Thepositive/negative criterion is not sensitive enough todistinguish among techniques. However, the consistencyof the extruded calcium hydroxide and its contact withthe root surface does not allow measurements as in thecases of debris or irrigant extrusion studied extensively inthe literature 14,17 . The techniques investigated are amongthe most widely recommended for intra-canal calciumhydroxide placement in clinical practice and they havebeen thoroughly investigated for their efficacy 7,8,22,30-32,34 .Thus, it was thought unnecessary to study their fillingefficacy. Therefore, this study presents only results of theextrusion of the material, regardless quality of the fillingof the root canal in each case, as extrusion in clinicalpractice is not related to the quality of the filling.In the present study, extrusion of Ca(OH) 2 wasonly recorded in teeth where patency was preserved.Establishing patency of the apical foramen during rootcanal instrumentation to effectively prevent blockagesand loss of working length has been proposed 2,9,11 .Patency facilitates removal of debris from the entireroot canal space, especially in teeth with necrotic pulptissue and bacteria load 13 and improves tactile senseduring apical shaping and thus reduces the chances ofcanal transportation and ledge formation 2 . However, theconcept of apical patency is considered controversial dueto the differences in the amount of the extruded materialfound in cases with and without patency filing 2,19,33 . Inthis study, a #10 K-file was used as patency file as it wasfound that more material was extruded apically whendiameter of the apical patency increased 33 .A wide range of rotation speeds have been usedduring the spiral filling techniques, ranging from 150 upto 10,000 rpm 7,8,22,23,30-32,34 . In the present study, elevatingrotation speed from 500 to 700 rpm resulted in morecases of Ca(OH) 2 extrusion in teeth with patent apicalconstriction, but the difference did not reach statisticalsignificance.In previous studies on the effectiveness of intracanalplacement techniques of Ca(OH) 2 7,8,30-32,34 , thepaste carrier was introduced in the root canal at 0 to3 mm short of the working length. The most effectivedelivery of Ca(OH) 2 was achieved when the paste carrierswere introduced to working length 31 . In the other cases,some distance of Ca(OH) 2 from the working length wasobserved 22 . In the present study, the extrusion of Ca(OH) 2from the apical foramen was recorded when the carrierwas introduced at 1 and 3 mm short of the working length.The results of this study demonstrated that the distanceof 3 mm short of the working length was safe to preventextrusion, even in teeth with patency and at 700 rpm

Balk J Stom, Vol 15, 2011 Calcium Hydroxide Extrusion during Intra-canal Placement 9rotation speed with any of the paste delivering techniquesevaluated.Our observations need to be interpreted withcaution as ex-vivo experimentation cannot be regardedas directly representative of the clinical situation. Tissuepressure and resistance by the periapical tissues in the invivo conditions may reduce the occurrence and extent ofperiapical extrusion of calcium hydroxide, although theexact effect of this variable is difficult to determine 36 .There is a need for more comparative studies on theefficiency of the various Ca(OH) 2 delivering techniques infilling the root canal space in order to educate the clinicianhow to maximize the antimicrobial properties of Ca(OH) 2 ,while avoiding the adverse effects caused by its extrusioninto the periapical tissues.References1. Ahlgren FK, Johannesen AC, Hellem S. Displaced calciumhydroxide paste causing inferior alveolar nerve paresthesia:Report of a case. Oral Surg Oral Mede Oral Pathol OralRadiol Endod, 2003; 96:734-737.2. Buchanan LS. Management of the curved root canals. JCalif Dent Assoc, 1989; 17:18-27.3. De Bruyne MAA, De Moor RJG, Raes FM. Necrosis of thegingival caused by calcium hydroxide: a case report. IntEndod J, 2000; 33:67-71.4. De Moor RJ, De Witte AM. Periapical lesions accidentallyfilled with calcium hydroxide. Int Endod J, 2002; 35:946-958.5. De Moraes Costa MT, De Oliveira SHP, Gomes-FilhoJE. Mechanism of calcium hydroxide-induced neutrophilmigration into air-pounch cavity. Oral Surg Oral Med OralPathol Oral Radiol Endod, 2008; 105:814-821.6. De Witte A, De Bruyne M, De Moor R. Accidental extrusionof calcium hydroxide based pastes into periapical lesions.Rev Belge Med Dent, 2003; 58 49-63.7. Deveaux E, Dufour D, Boniface B. Five methods of calciumhydroxide intracanal placement. An in vitro evaluation.Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2000;89:349-3558. Estrela C, Mamede Neto I, Lopes HP, Estrela CRA, PecoraJD. Root canal filling with calcium hydroxide usingdifferent techniques. Braz Dent J, 2002; 13:53-56.9. Fava L. Acute apical periodontitis: incidence of postoperativepain using two different root canal dressings. IntEndod J, 1998; 31:343-347.10. Fava LRG. Calcium hydroxide paste in the maxillary sinus:a case report. Int Endod J, 1993; 26:306-310.11. Goldberg F, Massone EJ. Patency file and apicaltransportation: an in vitro study. J Endod, 2002; 28:310-311.12. Güneri P, Kaya A, Calişkan K. Antroliths. Survey of theliterature and report of a case. Oral Surg Oral Med OralPathol Oral Radiol Endod, 2005; 99:517-521.13. Gutierrez JH, Brizuela C, Villota E. Human teeth withperiapical pathosis after overinstrumentation and overfillingof the root canals: a scanning electron microscopic study. IntEndod J, 1999; 32:40-48.14. Hülsmann MJ, Peters O, Dummer PM. Mechanicalpreparation of root canals: Shaping goals, techniques andmeans. Endodontic Topics, 2005; 10:30-76.15. Kim JW, Cho KM, Park SH, Song SG, Park MS, Jung HR,et al. Overfilling of calcium hydroxide-based paste CalcipexII produced a foreign body granuloma without acuteinflammatory reaction. Oral Surg Oral Med Oral PatholOral Radiol Endod, 2009; 107:e73-e76.16. Lambrianidis T. Risk management in root canal treatment.1 st ed, Thessaloniki: University Studio Press: 2001; pp 254-255.17. Lambrianidis T, Tosounidou E, Tzoanopoulou M. The effectof maintaining apical patency on periapical extrusion. JEndod, 2001; 27:696-698.18. Lingren P, Eriksson KF, Ringberg A. Severe facial ischemiaafter endodontic treatment. J Oral and Maxillofac Surg,2002; 60:576-579.19. Lomcali G, Sen BH, Cankaya H. Scanning electronmicroscopic observations of apical root surfaces of teethwith apical periodontitis. Endod Dent Traumatol, 1996;12:70-76.20. Nelson Filho P, Silva LA, Leonerdo MR, Utrilla L,Figueiredo F. Connective tissue responses to calcium-basedroot canal medicaments. Int Endod J, 1999; 32:303-311.21. Orucoglu H, Cobankara F. Effect of unintentionallyextruded calcium hydroxide paste including barium sulfateas a radiopaquing agent in treatment of teeth with periapicallesions: Report of a case. J Endod, 2008; 34:888-891.22. Oztan MD, Akman A, Dalat D. Intracanal placement ofcalcium hydroxide: A comparison of two different mixturesand carriers. Oral Surg Oral Med Oral Pathol Oral RadiolEndod, 2002; 94:93-97.23. Peters CI, Koka RS, Highsmith S, Peters OA. Calciumhydroxide dressings using different preparation andapplication modes: density and dissolution by simulatedtissue pressure. Int Endod J, 2005; 38:889-895.24. Poveda R, Bagan JV, Fernandez MD, Sanchis JM. Mentalnerve paresthesia associated with endodontic paste withinthe mandibular canal: report of a case. Oral Surg Oral MedOral Pathol Oral Radiol Endod, 2006; 102:e46-e49.25. Robinson MJ, McDonald NJ, Mullally PJ. Apical extrusionof thermoplasticized obturating material in canalsinstrumented with Profile 0.06 or Profile GT. J Endod,2004; 30:418-421.26. Salzgeber RM, Brilliant JS. An in vivo evaluation of thepenetration of an irrigating solution in root canals. J Endod,1977; 22:394-398.27. Scanaro A, di Carlo F, Quaranta A, Piatelli A. Injury of theinferior alveolar nerve after overfilling of the root canal withendodontic cement: A case report. Oral Surg Oral Med OralPathol Oral Radiol Endod, 2007; 104:e56-e59.28. Schneider SW. A comparison of canal preparations instraight and curved root canals. Oral Surg, 1971; 32:271-275.29. Sharma S, Hackett R, Webb R, Macpherson D, Wilson A.Severe tissue necrosis following intra-arterial injection ofendodontic calcium hydroxide: a case series. Oral Surg OralMed Oral Pathol Oral Radiol Endod, 2008; 105:666-669.30. Sigurdsson A, Stancill R, Madison S. Intracanal placementof Ca(OH) 2 : A comparison of techniques. J Endod, 1992;18:367-370.

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYEfficacy of Computer-Controlled Articaine Delivery forSupplemental Intraoral AnaesthesiaSUMMARYObjective. The aim of this study was to investigate quality and safetyof supplemental intraoral anesthesia - periodontal ligament anaesthesia(PDL) and intraseptal anaesthesia (ISA) after computer-controlled articainedelivery.Method. 54 ASA I volunteers randomly divided into 2 groupsparticipated in this study. 0.4 ml of 4% articaine with 1:100.000 epinephrinewere randomly administered with computer-controlled local anaestheticdelivery system on the mesial and distal side of maxillary lateral incisor forISA or PDL. An electric pulp tester was used to test the pulpal anaesthesia, in2-minute cycles for 60 minutes. Anaesthesia was considered successful when2 or more consecutive no-response at 80 readings were obtained. Soft-tissueanaesthesia was measured by pin-prick test.Results. Success rates for ISA and PDL were 77.8% and 55.6%respectively, but difference was not statistically significant (p>0.05). Durationof complete pulpal anaesthesia was significantly longer (p

12 Vladimir Biočanin et al. Balk J Stom, Vol 15, 2011tissue resistance 7 . CCLADS provides less painfulinjections than traditional system 19,22 . Likewise, thissystem enables clinicians to perform easier, faster,more reliable and less painful dental anaesthesia andis better accepted by patients than standard method ofinjection 4 . Traditionally, PDL and ISA have been usedwith a conventional or high pressure syringe 10,11,12with the possibility to change parameters of thecardiovascular function 3,15 . However, Nusstein et al 13reported that PDL used with CCLADS did not causeneither significant nor clinically meaningful increasein heart rate. Evaluation of the anaesthetic parametersshowed that duration of complete pulpal anaesthesiausing CCLADS with PDL was about 30 minutes incomparison with conventional pressure syringe whereduration was 10-15 minutes 2,8,9 .The aim of this study was to investigate quality andsafety of the intraoral supplemental anaesthesia (PDLand ISA) after computer-controlled articaine delivery(CCArtD).Method54 randomly selected ASA I volunteers participatedin this study. All patients were informed of the goalsof the study and signed a written consent. The studywas approved by the Etical Committee of the Faculty ofDentistry, University of Belgrade. Persons were randomlydivided into 2 groups: (1) the 1 st group (27 volunteers)undergone the ISA; (2) the 2 nd group (27 volunteers)undergone the PDL. The tested tooth was upper lateralincisor. Previous clinical examination indicated that allthe tested teeth were free of caries, large restorations orperiodontal disease, and none had a history of trauma orsensitivity.The local anaesthetic injected was 4% articaine with1:100 000 epinephrine (Septanest ®, Septodont, France).The total dose of anaesthetic solution was 0.4 ml pertooth, both for ISA and PDL. Time of local anaestheticadministering, 0.2 ml mesially and 0.2 ml distally, wasapproximatelly 80 seconds (40 seconds at each side).Anaesthetic solution was injected with computercontrolledlocal anaesthetic delivery system (Anaeject®,Septodont, France) with constant pressure and speed,approximately 0.005 ml per second.The site of needle insertion for ISA was 2-3 mmabove the tip of interdental papilla, with 90° angulation ofthe needle to the surface of the papilla, until contact withthe bone. Blanching of the gingiva overlying bone wasindicator that the anaesthetic solution had been properlydeposited. The site of needle insertion for PDL was theregion of gingival sulcus at 30° to the tooth long axis atbucomesial and bucodistal aspect of the rooth. We used a30G short needle (Septodont®, Dental Needle, France),both for ISA and PDL.Duration and success of pulpal anaesthesia of theupper lateral incisor were evaluated using tooth vitalitytester (Vitality Scanner Model 2006®, Sybron Endo).Fluoride gel (Fluorogal forte®, Galenika, Beograd)was used as an electrolyte between the pulp tester probeand the tooth. Before the injections were given, theexperimental tooth and control contralateral canine weretested 3 times by means of a Vitality Scanner, Model2006, to record baseline vitality. After administeringanaesthesia, electrical stimulation was repeated every2 min until the reading became lower than 80 (max).Duration of complete pulpal anaesthesia was periodbetween the first and the last 80 readings on electricalpulp tester. Anaesthesia was considered successful when2 or more consecutive no response at 80 readings wereobtained.Soft tissue anaesthesia was measured as absenceof pain when pin-prick test was used in the region ofthe attached gingiva. The width of the anaesthetic field,expressed in millimetres, was measured 5 min after thelocal anaesthetic injection by flexible ruler and pinpricktesting in the region of the attached gingiva and oralmucosa. We used 27 gauge needle (MonoJect®, DentalNeedle, Mansfield, USA) for pin prick testing. Pinpricktesting was done directly until contact with the periosteumoccured, immediately after the end of injection, every5 min during the first 20 min, and after that every 2 minuntil patient felt blunt pain.Patients were followed for 5 days to record anylocal postoperative side-effects, such as postoperativesensitivity to bite, papillary necrosis, postoperative pain orswelling.Statistical analysis was performed by using statisticalsoftware SPSS, version 10.0. The results were analysed byunpaired t-test (2-tailed), Man-Whitney non-parametrictest and χ² test.ResultsThere were no statistical significant differences(p>0.05) between the groups in respect to the successrate of pulpal anaesthesia achieved by both techniques;ISA being slightly more successful (77.8%) than PDL(55.6%).Significantly wider area of the anesthetized attachedgingiva and oral mucosa at the buccal aspect of the toothwere obtained by ISA in comparison with PDL (Tab. 1).Duration of complete pulpal anaesthesia (Tab.2) was significantly longer with ISA than with PDL(p

Balk J Stom, Vol 15, 2011 Computer-Controlled Articaine Anesthesia 13ISAPDLpTable 1. Width of the anaesthetized field obtained by theemployed techniquesAnaesthetized area (mean ± SD)Attached gingiva (mm)20.33 ± 11.097.15 ± 7.81p

14 Vladimir Biočanin et al. Balk J Stom, Vol 15, 201111. Malamed SF. Supplemental injection techniques. In:Malamed SF (ed). Handbook of local anesthesia. 5th ed. St.Louis: Mosby, 2004; pp 255-261.12. Meechan JG. Intraligamentary anaesthesia. Review. J Dent,1992; 20:325-332.13. Nusstein J, Berlin J, Reader A, Beck M, Weaver JM.Comparison of injection pain, heart rate increase, andpostinjection pain of articaine and lidocaine in a primaryintraligamentary injection administered with a computercontrolledlocal anesthetic delivery system. Anesth Prog,2004; 51(4):126-133.14. Oertel R, Rahn R, Kirch W. Clinical pharmacokinetics ofarticaine. Clin Pharmacokinet, 1997; 33:417-425.15. Pashley D H. Systemic effects of intraligamental injections.J Endod, 1986; 12(10):501-504.16. Raymond SA, Steffensen SC, Gugino LD, Strichartz GR.The role of length of nerve exposed to local anesthetics inimpulse blocking action. Anesth Analg, 1989; 68:563-570.17. Roahen JO, Marshall J. The effects of periodontal ligamentinjection on pulpal and periodontal tissues. J Endod, 1990;16(1):28-33.18. Saadoun AP, Malamed SF. Intraseptal anesthesia inperiodontal surgery. JADA, 1985; 111:249-256.19. Sumer M, Misir F, Koyuturk E. Comparison of the wandwith a conventional technique. Oral Surg Oral Med OralPathol Oral Radiol Endod, 2006; 101:e106-e109.20. White JJ, Reader A, Beck M, Meyers WJ. The periodontalligament injection: a comparison of the efficacy inhuman maxillary and mandibular teeth. J Endod, 1988;14(10):508-514.21. Woodmansey K. Intraseptal anesthesia: a review of arelevant injection technique. Gen Dent, 2005; 53(6):418-420.22. Yeniseu M. Comparison of the pain levels of computercontrolledand conventional anesthesia techniquesin prosthodontic treatment. J Appl Oral Sci, 2009;17(5):414-420.Correspondence and request for offprints to:Dr. Vladimir BiočaninUniversity of Belgrade, Faculty of DentistryClinic of Oral SurgeryBelgrade, Serbiae-mail: vladimirbiocanin@gmail.com

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYCaries Experience among Greek Pomak ChildrenLiving in Rural North-Eastern Greece.A Cross-Sectional StudySUMMARYPomaks are a cultural and religious minority living in a rural area ofNortheastern Greece, with several factors predisposing them to a very highcaries risk. The main aim of the study was to assess caries prevalence ofPomak schoolchildren. A cross-sectional survey was carried out on a total of700 children 6-12 years old, visually examined in the classroom according toWHO criteria. Generalized Linear Models (GLMs) with Poisson distributionwith over dispersion and Binomial models were preferred (SPSS v16).The SiC DMFT index was 5.64 (SD = 1.86) in 12-year-old Pomaks, whilethe mean DMFT was 3.85 (95%CI: 3.13; 4.56), almost twice the nationalaverage for Greece (2.05, SD 2.50). The proportion of children with severecaries (DMFT≥4) was about 70% at the age of 12. Similarly increasedvalues were found in 6-year-olds [dmft =5.49 (95%CI: 4.46; 6.51) andSiC dmft = 10.48 (SD 2.74)]. Cavity-free children varied by age between 17%for younger children and 3% for older ones. Despite the high dt and thesteeply rising DT values with age, Care indices were extremely low.In conclusion, Pomak schoolchildren have the worst caries indices inGreece, somewhat similar to the values found in urban children 30 years,ago. Thus, oral health promotion policies, using the whole populationapproach strategy, need to be particularly targeted on the Pomak villages.Keywords: Caries Prevalence; Children; Cross-Sectional; Rural;Poisson distribution; PomaksD. Sapourides 1 , V. Topitsoglou 2 , S. Muronidis 3 ,N. Kotsanos 1Aristotle University of Thessaloniki1 School of Dentistry Department of PaediatricDentistry2 School of Dentistry, Department of PreventiveDentistry, Periodontology and Implant Biology3 School of Mathematics, Section of Statistics andOperations ResearchThessaloniki, GreeceORIGINAL PAPER (OP)Balk J Stom, 2011; 15:15-23IntroductionAccording to the results of a recent Greek nationalsurvey of oral health status 25 , the caries experience ofchildren and adolescents in Greece has significantlydeclined in the last 30 years. For example, the DMFTindex for 12 year olds has decreased from 4.30 to 2.05.These favorable data, however, mainly reflect cariesdecline in the urban population.Certain parameters e.g. residential area, age,education level and socio-economic status have an impacton caries scores, as previously reported for variouscountries 2,13,20,23,26,27 and specifically for Greece 6,8,25 .Additionally, some striking differences have been reportedin the oral health of children of ethnic minorities. Mostnotable inequalities were noted in Australia, whereindigenous 5-6 year-old children experienced from 2 to4 times higher caries scores than their non-indigenouscounterparts 10,19 . It is well documented that, in general,oral health in industrialized countries is associated withimproved living conditions and various social factors, oralhygiene, regular use of fluoride and implementation ofpublic health policies 1,28 . However, preventive strategiesmay be relatively ineffective, and oral health related needssignificantly greater, among poor and disadvantagedgroups within these communities 26 .The dental care system in Greece is largely basedon the private sector and utilization of dental servicesis highly dependent on family income 16 . Primary carefor children, however, including the implementation oforal health educational programs, is to a large extentdelivered at Public Dental Health centres. In some areasthat are remote and isolated areas, or where centres arelacking or difficult to access, high caries scores havebeen recorded, especially for primary teeth 18 . Western

16 Balk D. J Stom, Sapourides Vol 15, et 2011 al. Caries Experience among Rural Greek Balk J Pomak Stom, Children Vol 15, 2011 16Thrace, the Northeastern region of mainland Greece, ishomeland to about 36.000 Pomaks, who live in raciallyautonomous communities, mainly in a deprived highlandrural area close to the border with Bulgaria. The villagesconstitute culturally unique Islamic communities,speaking a language with Slavic roots and receivingeducation in Greek, with Turkish as a foreign language 33 .Educational levels tend to be low, as a considerableproportion of children, especially girls, receive onlyelementary education. Transport to urban/semi-urbanplaces is complicated, especially during adverse weatherconditions, because of the topography and harsh landscapeof the highland villages.There is only limited information available on theoral health status of the Pomak child population and thelast national oral health survey 25 did not contain any suchdata. Consequently, the main aim of the present study wasto assess prevalence and treatment needs for caries and,secondly, to record obvious orthodontic problems in thePomak child population of primary school age.MethodsThis cross-sectional study was conducted withinthe frames of social and health interests for the mainlandborder territories of the local Contingent of the HellenicArmed Forces, the Health Section of which acted asthe ethics committee. Invitation for schoolchildren toparticipate in this oral examination was extended toparents orally by informed school authorities.Population SampleOut of the existing 50 Pomak villages, 37 had a stateelementary school with a total student population of 1,430.13 schools were selected on the basis of geographicaluniform distribution and population size, and all theirstudents were included in the study. The great variabilityof student numbers prevented a perfect factorial design.All children present at school on the examination day wereexamined, comprising a total of 700 children (46% malesand 54% females) aged between 6 and 12 years (Tab. 1).Exact ages were calculated according to the formula: (dateof examination - date of birth) / 365.The vast majority of Pomak families have lowincomestatus derived from agricultural work, cattleraisingor manual work. The natural fluoride content ofwater in the whole region is so low as to be negligible,except for one village called Μeses Τhermes with 0.65ppm F and only 4 child inhabitants 34 . There were no dataon fluoride toothpaste consumption.Table 1. Number of students (total n = 700) examined accordingto age, gender and number of inhabitants in their residenceVariablesAge (years)Sample distributionn (%)6 74 (10.6)7 148 (21.1)8 134 (19.1)9 131 (18.7)10 84 (12.0)11 96 (13.7)12 33 (4.7)GenderMale 321 (45.9)Female 379 (54.1)Residence (population size)

Balk J Stom, Vol 15, 2011 Caries Experience among Rural Greek Pomak Children 17Statistical AnalysisIn comparing caries levels with non-normaldistribution, the Generalized Linear Models (GLMs)with Poisson distribution with over dispersion waspreferred 11,19 . In addition, Binomial models were set upto model the dichotomous outcomes. Data processing wasperformed with SPSS software program (v16, Chicago,IL, USA). The alpha level in all tests was set at 0.05.The dependent variables (responses) were: themagnitude of indices DMFT with 13 levels (0-12)and dmft with 20 levels (0-19), the presence of caries2 levels (Yes, No) and the presence of Orthodonticproblem (Yes, No). The independent variables (factors)were Age: 7 levels (6-12 year old), Residence accordingto population size: 3 levels (

18 D. Sapourides et al. Balk J Stom, Vol 15, 2011respectively) confirming the statistical analysis that “Age”plays an important role in the recognition of orthodonticproblems (Model-5).The DMFT was higher in girls (1.82, 95%CI: 1.63;2.01) than in boys (1.52, 95%CI: 1.32; 1.71), especiallyat ages older than 7, and as it was found in Model-1, thefactor “gender” statistically significantly affected themagnitude of DMFT. On the other hand, dmft was lowerin girls (3.40 CI: 95%, 3.07; 3.72) than in boys (3.84 CI:95%, 3.45; 4.23), but here the factor “gender” did notsignificantly affect the magnitude of dmft (Model-2). Inboys, as well as in girls, there were no differences in thepercentage of caries free children (%DMFT+dmft = 0)and of Care indices (FT/DMFT% and ft/dmft%).Table 2. Analysis of variance (ANOVA) using generalized linear models (n = 700)Type III analysis Factors Degrees of freedom (df) SignificanceModel-1 Gender 1 0.000(influence on DMFT)Age 6 0.000Residence 2 0.003Age * Residence 12 0.008Goodness of fit Deviance Value =1007.137, df=678, Value/df =1.485Excluded stepwiseFactor Orthodontic problem and all the 2-way interactions of Orthod- problem & Gender p>0.05)Model-2 Gender 1 0.354(influence on dmft)Age 6 0.000Residence 2 0.126Orthodontic problem 1 0.848Goodness of fit Deviance Value =602.651, df=689, Value/df =0.875Excluded stepwiseAll the 2-way interactions (p>0.05)Model-3 Gender 1 0.001(influence onDMFT≠0 or =0, Yes/No)Residence 2 0.000Orthodontic problem 1 0.007Goodness of fit Deviance Value =11.651, df=7, Value/df =1.664Excluded stepwiseFactor Age and all the 2-way interactions (p>0.05)Model-4 Gender 1 0.568(influence ondmft≠0 or =0, Yes/No)Age 6 0.000Residence 2 0.955Goodness of fit Deviance Value =40.421, df=32, Value/df =1.263Excluded stepwiseFactor Orthodontic problem and all the 2-way interactions (p>0.05)Model-5 Age 6 0.001(influence onOrthod. problem, Yes/No)Residence 2 0.017Goodness of fit Deviance Value =40.421, df=32, Value/df =1.263Excluded stepwiseFactor Gender and all the 2-way interactions (p>0.05)

Balk J Stom, Vol 15, 2011 Caries Experience among Rural Greek Pomak Children 19Table 3. Permanent dentition: Mean DMFT and its components per variable testedVariablesAge (years)DMFTMean (95% CI)DTMean (95% CI)MTMean (95% CI)FTMean (95% CI)6 0.46 (0.24;0.68) 0.46 (0.24;0.68) 0.01 (0.00;0.03) 0.07 (0.01;0.13)7 0.66 (0.48;0.83) 0.57 (0.41;0.74) 0.01 (0.00;0.03) 0.07 (0.01;0.13)8 0.99 (0.79;1.20) 0.91 (0.72;1.10) 0.01 (0.00;0.02) 0.07 (0.01;0.14)9 1.87 (1.60;2.14) 1.61 (1.35;1.88) 0.07 (0.02;0.12) 0.19 (0.10;0.28)10 2.50 (2.13;2.87) 2.26 (1.90;2.62) 0.12 (-0.03;0.27) 0.12 (0.03;0.21)11 3.45 (3.01;3.88) 2.88 (2.43;3.32) 0.28 (0.16;0.40) 0.29 (0.14;0.45)12 3.85 (3.13;4.56) 3.27 (2.66;3.89) 0.27 (-0.01;0.56) 0.30 (0.06;0.55)GenderMale 1.52 (1.32;1.71) 1.35 (1.16;1.54) 0.06 (0.03;0.10) 0.11 (0.06;0.15)Female 1.82 (1.63;2.01) 1.56 (1.39;1.74) 0.10 (0.05;0.15) 0.16 (0.10;0.21)Residence (population size)

20 D. Sapourides et al. Balk J Stom, Vol 15, 2011Figure 1. Mean caries indices (DMFT, dmft) and the respectiveSignificant Caries indices (SiC) for ages 6-12Figure 2. Permanent dentition. Percentage of children distributed in 3groups according to the magnitude of their DMFT index, per ageFigure 3. Primary dentition. Percentage of children distributed in 3groups according to the magnitude of their dmft index, per ageDiscussionThis survey documents the markedly low levelof dental health of Greek Pomak children living inremote communities in a deprived highland regionof Northeastern Greece. Apart from the unfavourableeducational, socioeconomic and geographical parametersalready described, dietary or cultural factors mayexacerbate the problem. Pomaks are Muslims and the dietof some Muslim populations is reported to be rich in sugarproducts 7,17,24 . Additionally, a study among rural Muslimwomen in Israel reported that 60% of all postpartumwomen gave sugar water during the first week of life 3and another in the USA described that Islamic women arerecommended to breast feed their offspring for 2 years,if possible 30 . Both these practices, in the absence of oralhygiene and any fluoride exposure (i.e. through toothpasteor drinking water) may be reasons for early childhoodcaries 35,36 , affecting the caries status of the present studypopulation.The caries experience of 12-year-old Pomakschoolchildren (DMFT = 3.85, SD ± 2.02) of the presentstudy was much higher than that of Christian Orthodoxchildren of the same age from either the greater ruralThrace area, recorded ten years earlier (DMFT = 2.51,SD ± 1.96) 12,34 , or from the nearby rural lowland county(DMFT = 1.81, SD ± 2,12) 9 and the national rural average(DMFT = 2.23) 25 .The average 6-year-old Pomak had 6 carious teeth,5.5 primary and 0.5 permanent teeth. The presence ofsevere caries (dmft≥4) by age 7 in 71% of the Pomaksis disappointing and indicative of a very early onset ofthe disease, and this is not related to population sizeof community of residence (Model-2). By the ages of8, 9 and 10, about half of children had 1 to 3 cariouspermanent teeth. Furthermore, it is alarming that onethird of the 6-year-olds had almost twice the mean valuefor that age (SiC dmft =10.48 SD ± 2.74). Such a severecarious status vindicates the adequacy of visual toothexamination.Differences of at least this magnitude in cariousindices have relatively recently been reported in Australia.Indigenous 5 to 6-year-olds from South Australia had onaverage 3.2 carious primary teeth, while the equivalentAustralian mean was 1.44 10 . Even more strikingly,indigenous children from a Northern Territory ofAustralia at age 5 years had almost 4 times the dmft andat age 10 years had almost 5 times the DMFT of theirnon-indigenous counterparts 15 . The authors considered itmore appropriate that, from a health policy perspective,correcting this inequality would require a public healthand clinical effort aimed at the indigenous children as awhole.It can be seen in table 2 that factor Age wassignificant for the magnitude of DMFT (Model-1), butit did not have any significant influence on whether achild did or did not have caries (Model-3). Subsequently,it shows that children who have caries activity acquiremore and more affected teeth, as time (in this instance“Age”) has a cumulative effect 21 . For this reason it is clearwhy it is necessary to use statistical models that studythe outcome of caries experience as a binary variable incombination with models that study the complete DMFTor dmft scale as a whole.

Balk J Stom, Vol 15, 2011 Caries Experience among Rural Greek Pomak Children 21The next striking consequence of the high cariesindices is the very high level of treatment need, as DT andDMFT or dt and dmft differed very little (Tabs. 3 and 4).While the national 25 mean Care index for permanent teethin 12-year-old children was 55.3% and in the greater ruralThrace 47.5%, Pomak 12-year olds had a mere 7.9%.Regarding the quarter of 11 to 12-year-old Pomakchildren with orthodontic problems, none were currentlyundergoing treatment. This somewhat low prevalenceof malocclusion can be explained mainly by the fact thatantero-posterior molar relationship was not recorded.Mesial drift, as a result of frequent space loss due tothe extensive carious lesions of primary molars makesdiagnosis of true Class II malocclusions difficult in fieldstudies where such high caries indices are prevalent.However, similar malocclusion figures, and even lower,have been recorded, e.g. in India in 12-15 year olds usingthe DAI index 31 .In general, children residing in rural areas of the USAtended to have less access to, and utilization of dental carecompared to children residing in urban areas 37 . In Greece,utilization of private dental services is highly dependenton family income 39 and, as a result, children from moredeprived areas have a significantly lower mean Careindex 16 . This situation probably also affects Pomaks whocould, however, visit the Public Health Centre, locatedin the largest village of our study area, or the dentaldepartments of the civic or military hospitals, locatedat a distance of 20-50 km away in the province capitaland receive basic treatment for free. However, access tohealth care except for an urban-rural dimension seemsto have one of cultural/religious isolation. The minimaldental care of Pomaks is characterized by a problemorienteddental visiting pattern similar to that reported forthe remote lands of Australia 29 , containing elements of avisible appearance visiting pattern reported for cariousteeth of Mexican immigrants’ children in a small UScity 14 .According to the proposals made by Bratthall 5 , theSiC index for 12-year-olds should be less than 3 by theyear 2015 and Pomak 12-year-olds had almost double thatfigure (SiC DMFT =5.64, SD ± 1.86). To achieve this goalin time needs careful planning by both the health and thetransport authorities. A person’s environment is the mostimportant caries-promoting factor and, fortunately, thefactor more amenable to change than, for example, geneticfactors. Facilitating the transportation of the children toPublic Health Centre, providing oral health educationand specific target treatment measures (e.g. fluoridetreatment and placement of fissure sealants on everyposterior erupting tooth) together with regular recalls,are among measures necessary to be taken for timelyimprovements. In this, the Muslim culture (tradition, diet,rules and habits) of our study area is worth additionalconsideration. Oral health education especially forgirls, who frequently become mothers at an early age 33 ,could significantly increase brushing with fluoridatedtoothpaste for themselves and their children.This studyidentified one pocket of rural Greek population - of adiverse religious and cultural background - exhibitingextreme caries indices and care needs, as it has beenreported for non-immigrant small population sectionselsewhere 15 . Inequalities in oral health care constitute anethical problem and these reports increase awareness forthe underprivileged in the making of political decisionsfor planning oral care 29 . Furthermore to alleviatingdental pain and discomfort for these children, a particularcountry’s attempt to improve caries indices of childpopulation is benefited when preventing dental disease inhigh-risk groups 32 .Possible limitations of the present study could bethose related to the adopted field study examinationprotocol. Recording dental plaque deposits, periodontalstatus, oral hygiene and dietary habits would allow betterclinical view of the oral situation of those children.Further studies could also investigate and compare theoral health status of Pomak children residing in evengreater numbers in neighbouring communities in Bulgaria.ConclusionsIt is remarkable that Pomak schoolchildren have thehighest caries indices in Greece today, and these indicesare similar to the values found in urban locations inGreece 30 years ago. Health promotion policies, usingthe whole population approach strategy, as opposedto high-risk, need to be particularly targeted on thisgeographically and socially isolated community ofPomaks.Acknowledgements. This survey was performed whilethe prime author was serving his duty in the HellenicArmed Forces as a dental officer. The authors wish tothank Prof. I. Antoniou of the School of Mathematics,Aristotle University of Thessaloniki, for supportinginterdepartmental cooperation and Ch. Chatzipolichronis,DDS and K. Manthos, DDS for assistance during clinicalexaminations.References1. Aleksejūnienė J, Holst D, Balciūnienė I. Factors influencingthe caries decline in Lithuanian adolescents - trends in theperiod 1993-2001. Eur J Oral Sci, 2004; 112:3-7.2. Al-Malik MI, Holt RD, Bedi R. Prevalence and patterns ofcaries, rampant caries, and oral health in two- to five-year-oldchildren in Saudi Arabia. J Dent Child, 2003; 70:235-242.

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Community Dental Health, 2006;23:140-146.9. Demertzi-Economidou A, Topitsoglou V. Longitudinalstudy with 8-years follow up of caries incidence among128 children from Nestos county, Prefecture of Kavala,Greece, during the school years 1992-1993 to 1999-2000.Pedodontia, 2002; 16: 82-90. (in Greek, English summary)10. Endean C, Roberts-Thomson K, Wooley S. Anangu oralhealth: the status of the Indigenous population of theAnangu Pitjantjatjara lands. Aust J Rural Health, 2008;12:99-103.11. Fabien V, Obry-Musset AM, Hedelin G, Cahen PM. Useof the generalised linear model with Poisson distributionto compare caries indices. Community Dent Health, 1999;16:93-96.12. Heliadou Ch, Topitsoglou V, Valtzidou A, PapadopoulouA, Papaioannou I. Prevalence and distribution of cariesin children 6 to 11 years olds in an area of Thrace. Stoma,1999; 27:169-175. (in Greek, English summary)13. Holst D. Causes and prevention of dental caries: aperspective on cases and incidence. Oral Health Prev Dent,2005; 3:9-14.14. Horton S, Barker JC. Rural Mexican immigrant parents’interpretation of children’s dental symptoms and decisions toseek treatment. Community Dent Health, 2009; 26:216-221.15. Jamieson LM, Armfield JM, Roberts-Thomson KF. Oralhealth inequalities among indigenous and nonindigenouschildren in the Northern Territory of Australia. CommunityDent Oral Epidemiol, 2006; 34:267-276.16. Kalyvas DI, Taylor CM, Michas V, Lygidakis NA. Dentalhealth of 5-year-old children and parents’ perceptionsfor oral health in the prefectures of Athens and Piraeus inthe Attica County of Greece. Int J Paediatr Dent, 2006;16:352-357.17. Karaagaoglu N, Yucecan S. Some behavioural changesobserved among fasting subjects, their nutritional habitsand energy expenditure in Ramadan. Int J Food Sci Nutr,2000; 51:125 -134.18. Kostopoulou M, Topitsoglou V, Makris G. Caries prevalenceand treatment needs of child population on island of Symiin Dodecanese Archipelago, Greece. Pedodontia, 1996;10:132-136. (in Greek, English summary)19. Lewsey JD, Gilthorpe MS, Bulman JS, Bedi R. Ismodelling dental caries a ‘normal’ thing to do?Community Dent Health, 2000; 17:212-217.20. Marthaler TM, O’Mullane DM, Vrbic V. Theprevalence of dental caries in Europe 1990-1995.ORCA Saturday afternoon symposium 1995. CariesRes, 1996; 30:237-255.21. Mejare I, Mjör IA. Prognosis for caries and restorations.In: Fejerskov O, Kidd E (Eds). Dental Caries. The Diseaseand its clinical management. Blackwell, Munksgaard,2003; pp 295-301.22. National Statistical Service of Greece, Athens, 2001. Citedat www.statistics.gr (in Greek)23. Oliveira AF, Chaves AM, Rosenblatt A. The influence ofenamel defects on the development of early childhoodcaries in a population with low socioeconomic status: alongitudinal study. Caries Res, 2006; 40:296-302.24. Olmez S, Uzamis M, Erdem G. Association betweenearly childhood caries and clinical, microbiological, oralhygiene and dietary variables in rural Turkish children.Turk J Pediatr, 2003; 45:231-236.25. Oulis C, Theodorou M, Mastrogiannakis T, Mamai-Chomata H, Polychronopoulou A, Athanasoulis T.Oral health status and treatment needs of the Hellenicpopulation - A pathfinder survey - proposals forimprovement. Hellenic Stomatol Review, 2009; 53:97-120.(in Greek, English summary)26. Peters DH, Garg A, Bloom G, Walker DG, BriegerWR, Rahman MH. Poverty and access to health carein developing countries. Ann N Y Acad Sci, 2008;1136:161-171.27. Petersen PE. Sociobehavioural risk factors in dentalcaries-international perspectives. Community Dent OralEpidemiol, 2005; 33:274-279.28. Petersen PE. Inequalities in oral health. The social contextfor oral health. In: Pine C, Harris R (Eds). CommunityOral Health. 2 nd ed. Quintessence Publishing Co. Ltd,2007; pp 31-58.29. Schwarz E. Access to oral health care - an Australianperspective. Community Dent Oral Epidemiol, 2006;34:225-231.30. Shaikh U, Ahmed O. Islam and infant feeding. BreastfeedMed, 2006; 1:164-167.31. Shivakumar KM, Chandu GN, Subba Reddy VV, ShafiullaMD. Prevalence of malocclusion and orthodontictreatment needs among middle and high school children ofDavangere city, India by using Dental Aesthetic Index. JIndian Soc Pedod Prev Dent, 2009; 27:211-218.32. Swedberg Y, Fredén H, Norén JG. Caries extreme groupsamong adolescents, leaving organised dental care inGöteborg, Sweden. Swed Dent J, 1997; 21:221-226.33. Theocharidis P. Pomaks - the Muslims of Rodopi.History, origin, language, religion, traditions. CulturalCentre of Thrace, Xanthi, 1995. (in Greek)34. Topitsoglou V. Fluoride chart of Greece and Cyprus.Natural fluoride content of drinking water. Monograph,Thessaloniki, 2004. (in Greek)35. Vadiakas G. Case definition, aetiology and risk assessmentof early childhood caries (ECC): a revisited review. EurArch Paediatr Dent, 2008; 9:114-125.

Balk J Stom, Vol 15, 2011 Caries Experience among Rural Greek Pomak Children 2336. Valaitis R, Hesch R, Passarelli C, Sheehan D, SintonJ. A systematic review of the relationship betweenbreastfeeding and early childhood caries. Can J PublicHealth, 2000; 91:411-417.37. Vargas CM, Ronzio CR, Hayes KL. Oral health status ofchildren and adolescents by rural residence, United States. JRural Health, 2003; 19:260-268.38. World Health Organization. Oral health surveys - Basicmethods. 4 th ed. Geneva: WHO, 1997.39. Zavras D, Economou C, Kyriopoulos J. Factors influencingdental utilization in Greece. Community Dental Health,2004; 21:181-188.Correspondence and request for offprints to:Dr. Nikolaos KotsanosAristotle University of Thessaloniki, School of DentistryDepartment of Paediatric Dentistry541 24, Thessaloniki, GreeceE-mail: kotsanos@dent.auth.gr

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYEffects of Orbit Sugar-free Chewing Gum for Kids inOverall and Cariogenic Salivary Microflora ReductionSUMMARYThe effects of Orbit sugar-free chewing gum in plaque acid attackneutralisation, food debris removal, and saliva secretion rate stimulation,have already been clinically proven. Sugar alcohols, which have sincerecently been considered to have a direct impact on bacterial cells, areamong the ingredients of this chewing gum. The objective of this study wasto gain knowledge of the effects of Orbit sugar free chewing gum for kidswith calcium addition in overall salivary flora reduction, and particularlyin the reduction of the cariogenic oral microorganisms, as direct factorsleading to dental decay.The research included a group of 24 healthy schoolchildren of bothgender at the age between 8 and 13. All participants had good oral health,similar hygiene and diet regimens, and similar DMF indices. In order toobtain higher precision and accuracy, the same group was also used as acontrol group, so that saliva samples were taken twice: once before and once20 minutes after Orbit chewing gum had been chewed. The microbiologicalanalyses were performed at the Institute of Microbiology and Parasitologyof Skopje Medical Faculty. The counts of Streptococcus mutans (SM) andLactobacillus species (LB) were determined by commercially available CRTbacteria strips, whereas the total count of saliva microbials was determinedby standard microbiological methods.Significant reductions in salivary SM and LB levels, and declines in thetotal count of aerobe and anaerobe bacteria, and Candida albicans as well,were observed in all cases.Keywords: Chewing Gum; Cariogenic Microorganisms; Salivary Microorganisms;Streptococcus mutans; Lactobacillus speciesAleksandar Dimkov 1 , Nikola Panovski 2 ,Elizabeta Gjorgievska 11 Faculty of Dental MedicineDepartment of Paediatric Dentistry2 Medical FacultyInstitute of Microbiology and ParasitologySkopje, FYROMORIGINAL PAPER (OP)Balk J Stom, 2011; 15:24-30IntroductionThe fact that microorganisms are one of the mostessential factors in dental disease etiology arousesthe question of how to eliminate or reduce them tominimal values. Because of that, the major prerequisiteis typological and numerical verification of themicroorganisms. On the other hand, the key factor of the“struggle” against them is proper maintenance of oralhygiene.In spite of a considerable number of substancesand methods for oral hygiene, since recently sugar-freechewing gums have gained strong influence, particularlyamong the young population. Sugar-free chewing gum hasa positive benefit for dental health by increasing salivaryflow during chewing, which helps to dilute and neutraliseplaque acidity. There is general scientific agreement nowthat chewing sugar-free gum, amongst other things, canhelp to protect teeth against decay.Over the last 25 years there has been considerableclinical research into the effect of salivary stimulation andthe role of saliva in oral health. Clinical evidence suggeststhat sugar-free gum not only will not decay teeth, but thatit will reduce the acidic effects caused by other foods, ifchewed after meals and snacks.Both the chewing action and the taste of sugar-freegum stimulate the production of extra saliva by up to10 times the normal rate. Stimulation of salivary flowchanges its composition and increase concentration ofbicarbonate, which enhance its ability to neutralise plaque

Balk J Stom, Vol 15, 2011 Effects of Sugarfree Chewing Gum on Salivary Microflora 25acid. Also, as salivary flow increases, the availability ofminerals is increased, helping to repair early tooth decay.There are many indications that dissolved calciumcan inhibit demineralisation of the enamel, servingas a substrate for remineralisation of the teeth. Mostchildren love sweets and are very fond of eating betweenmeals. Because after each snack or drink that is rich incarbohydrates the pH of the plaque rapidly becomesacid. This has the effect of drawing off calcium ions andother mineral ions from the tooth enamel (Fig. 1). If suchdemineralisation happens repeatedly in the course of aday, or if it lasts for an extended period, than caries candevelop. This process can happen very quickly in childrenbecause the enamel cap of a milk tooth is only half asthick as that of permanent teeth. For this reason children’steeth need special protection.Figure 1. The way of remineralization after the use of Orbit chewing gumPatients with dry mouth are more susceptible to toothdecay as their flow rate, pH level and buffering capacity islowered. Patients are often recommended to chew sugarfreegum to relieve the symptoms of dry mouth and also tohelp encourage the function of the salivary gland.Wrigley’s Orbit sugar-free chewing gums havebecome the first products given recognition by the WorldDental Federation for providing a significant contributionto oral health. Sugar-free chewing gums consist mainly ofsugar alcohols, which are a combination of hexitols andpentitols. Xylitol and Sorbitol are the most frequent sugaralcohols, whereas Manitol is less frequent. Sugar alcohols,primarily Sorbitol and Xylitol, have a direct effect on thebacterial cell. The ways of action of polyols on bacterialsare illustrated in figure 2.After the uptake of Xylitol, the substance isphosphorylated to Xylitol-5-P. Since most cells lackxylitol-5-P dehydrogenase, it results in its intra-cellularaccumulation. Dephosphorilation of X-5-P takes placeeventually and Xylitol is then emitted from the bacteria.The consequence of the cycle is a futile PEP/energy -consumption leading to an inhibition of the glycolysisand none acid attack on the enamel. The bacterial uptakeof the hexitols results in a phosphorylation to sorbitol-6-Pand mannitol-6-P. 2 separate dehydrogenases transformthe phosphorelated hexitols to fructose-6-P, whichparticipates in glycolysis. Ethanol, formic and lactic acidsare the end products in sorbitol and mannitol metabolism.Orbit sugar-free chewing gums are the most popularchewing gums in FYROM, which was proven by theresults of the poll conducted in 2002, according to which75% of the participants use Orbit chewing gum at leastonce a day (Figs. 3 and 4).GTF – GlycosyltransferasePMF – ProtonmotiveforcePTS – Phosphotransferase systemG-6-P – Glucose-6-PhosphateF-6-P – Fructose-6-PhosphateF-1,6P2 – Fructose 1, 6-bisphosphate3-PGA – 3-PhosphoglyceraldehydeDHAP – Dihydroxyacetonephosphate3 PG – 3-Phosphoglycerate2 PG – 2-PhosphoglyceratePEP – PhosphoenolpyruvatePYR – PyruvateE1 – Enzyme 1HPr – Histidine protein heat resistantE2 – Enzyme 2Figure 2. Ways of action of polyols

26 Aleksandar Dimkov et al. Balk J Stom, Vol 15, 2011Figure 3. Frequency of use of chewing gums among participantsFigure 4. Kind of chewing gum used by participantsThere are various types of Orbit chewing gums,differing from each other as follows:--The type of the sugar alcohols and their proportion;--Addition of mineral ions (e.g. calcium) to enhance theeffects of remineralisation;--Addition of sodium carbonate to maintain teethwhiteness by activating the natural protectivemechanisms of the saliva;--Addition of different aromas;--Menthol additions for stronger mouth freshness.In our investigation we used Orbit sugar-free chewinggum for kids because it contains both xylitol and sorbitolsugar alcohols, as well as calcium, and is produced in oneof 2 fruit flavours that makes it more attractive to kids. Byinvestigating the effects of Orbit sugar-free chewing gumon cariogenic microorganisms and on the whole numberof salivary micro-flora, we wanted to see whether we canadd yet another benefit of Orbit sugar-free chewing gum tothe already well-known benefits mentioned earlier in thistext. The aim of this study was: (1) to estimate the salivarylevels of Streptococcus mutans (SM) and Lactobacillusspecies (LB) before and after chewing Orbit sugar-freechewing gum for kids with calcium; (2) to compare thenumber of whole salivary flora by saliva analyses beforeand after chewing Orbit sugar-free chewing gum for kidswith calcium.Materials and MethodsThe group consisted of 24 healthy schoolchildrenaged 9-13 of both gender. The participants had good oralhealth, similar hygiene and normal dietary regimen andsimilar DMF indices. In order to obtain higher precisionand accuracy, the same group was used as a controlgroup, too. Saliva samples were taken before, and 20minutes after, chewing Orbit gum, early in the morning,after at least 12 hours without oral hygiene. The studysubjects were selected at the Faculty of Stomatology,Department of Pediatric Dentistry - Skopje. Themicrobiological analyses were carried out at the Instituteof Microbiology and Parasitology, Medical Faculty inSkopje.In our study we used the Orbit sugar-free chewinggum for kids with calcium (Wrigley, USA). Itsingredients are:--Xylitol--Sorbitol--Manitol--Acesuflam--Aspartam--Calcium Lactate--Gum base--FlavorsCollecting Saliva SamplesPatients refrained from oral hygiene for at least 12hours before the treatment.First saliva sample was taken without any prior foodconsumption, mouth rinsing or saliva stimulation.Chewing the Orbit sugar free chewing gum for kidswith Calcium (Wrigley, USA), for approximately 20minutes.After chewing gum has been chewed, the mouth wasrinsed with 200 ml of water for about 15 sec.The second saliva sample was taken following a 20min. intermission.Quantitative Evaluation of SM, LB andTotal Number of Salivary MicroorganismsIn order to determine the total number of salivarymicroorganisms, saliva samples were taken by spittingapproximately 3-5 ml. of saliva before and after chewingthe Orbit sugar-free chewing gum for kids with calciuminto special sterile containers made particularly for thispurpose (Fig. 5). The specimens used to determine thecounts of SM and LB in the saliva were taken with CRTbacteria-commercially available strips (Ivoclar-Vivadent,Schaan, Liechtenstein). These strips have selective

Balk J Stom, Vol 15, 2011 Effects of Sugarfree Chewing Gum on Salivary Microflora 27Figure 5. Sterile containers for determining the total numberof salivary microorganismsculture media for determination of the SM count in salivaor plaque on the blue agar surface and for determinationof the LB count in saliva on the bright agar surface.The first step of the procedure was to remove the agarcarrier from the test vial. After that, a NaHCO 3 -tabletwas placed at the bottom of the vial. The protective foilswere carefully removed from 2 agar surfaces, taking carenot to touch the agar. Both agar surfaces are thoroughlymoistened with saliva using a pipette, allowing theexcess saliva to drip off. Finally, the agar carrier was slidback into the vial, the vial was closed tightly and it wasthen sent to the Institute of Microbiology (Fig. 6).Figure 6. Procedure for determining SM and LBMicrobiological Processing of SamplesPlanting was performed simultaneously withsampling. After an incubation period of 48 hours at35-37 0 C, the grown colonies (colony forming units- CFU) were counted, provided their number wassmall, or were compared with the chart supplied by themanufacturer when their number was excessive, and werethen interpreted as 10,000; 10,000-100,000; 100,000-1,000,000 and > 1,000,000 CFUs. The SM colonies weretranslucent on the blue agar surface, while LB colonieswere grey-white on the green agar surface. By countingthe colonies only the approximate number of bacteriacould be determined, because of the notion that 1 bacterialcell causes the growth of 1 colony, and is thus beingdesignated as “a colony forming unit (CFU)” (Fig. 7).After drying up, strips can be stored in a refrigerator at2-8 0 C, where, being protected from light and temperaturefluctuations, they can last for years, and be used forcomparison purposes at any time.

28 Aleksandar Dimkov et al. Balk J Stom, Vol 15, 2011Figure 7. Colony forming units-CFU for SM and LB (standard according to manufacturer's instructions)Figure 8. Growth density sectors

Balk J Stom, Vol 15, 2011 Effects of Sugarfree Chewing Gum on Salivary Microflora 29Semi quantitative determination of whole salivarymicrobial counts was performed with a 4 mm diametercalibrated eza. On each of the 3 bases, 50 salivamicroliters were spread in the usual manner (routineprocessing). In order to obtain isolated colonies bydilution, the material was transplanted up to the half of thePetry dish (sector 1) on 3 sectors of the Petry dish (Fig. 8).Then the eza was sterilized by heating, and the materialsfrom the 2 lines of sector 1 were transplanted onto thequarter in the lower side of the Petry dish (sector 2). Atthe end, the eza was again sterilized by heating and thematerial from the last 2 lines of sector 2 was transplantedonto the last quarter of the Petry dish (sector 3).The results were read out in a semi quantitative way,i.e. the density of growth was marked with the capitalsA, B and C. The capital A was used to mark the growthdensity in the first sector, B was used for the secondsector and C for the third one. The sector marked withA presented a sector with such high density of growthof colonies that they could not be counted (A > 100colonies within the sector), B - a growth of 20 to 100Table 1. Growth density of salivary aerobic and anaerobicbacteria before and after use of Orbit sugar-free chewing gumfor kids with calciumGrowth densityAerobicAnaerobicBefore After Before AfterAAA 4 / 2 /+ + AAV 9 4 4 /AAS 1 3 1 /AVV 1 1 1 /+AVS 5 10 11 9AVO 4 2 1 1ASO / 3 3 8VVO / 1 1 5+ - VSO / / / 1OOO / / / /c2 – p > 0,05(p = 0,09)c2 – p < 0,05(p = 0,0047)colonies, C - 5 to 20, and 0 - 0 to 5 colonies. With theaim to present the results in a more convenient way, wehave split the growth density sectors in accordance withthe number of colonies into high growth density sectors(AAA, AAB, and AAC), medium growth density sectors(ABB, ABC, ABO, and ACO), and into sectors of low orno growth density (BBO, BCO, and OOO). The sectors ofthe first group were labelled with ++, those of the secondgroup with +, and the sectors of the third group with +-.ResultsThe results of this investigation are presented intables 1-3 and diagram 1. As it can be seen, the effectsof chewing a sugar-free chewing gum with calcium weremore pronounced on the counts of anaerobic bacteria andCandida albicans than on the aerobic bacteria (Tab. 1 andDiagram 1). The effect of chewing was more pronouncedon SM than on LB (Tabs. 3 and 4).Diagram 1. CFU in subjects with isolated Candida albicans before andafter use of Orbit sugar-free chewing gum for kids with calcium161412108642040150 1 0 1 04071 2 0I II III IV V VI VIINumber Broj na of kolonii coloniesbefore predBroj na koloniiNumber of coloniesafterpoTable 2. Number of subjects with CFU (colony forming units)of SM and LB in 1 ml saliva before and after use of sugar-freechewing gum with calciumStreptococcusmutans CFU/mlLactobacillusspecies CFU/mlBefore After Before AfterWithout growth (3) 4 (2) /102-3 3 5 5 5103-4 2 2 1 5104-5 1 5 2 4105-6 9 5 4 8106-7 6 / 10 /N 21 21 22 22Table 3. Effects of sugar-free chewing gum with calcium on thereduction of cariogenic salivary micro flora counts (number ofsubjects with logarithmic reduction factor - log RF)log RFStreptococcusmutans0 2 61 10 122 5 43 2 /³ 4 2 /N 21 22Lactobacillusspecies

30 Aleksandar Dimkov et al. Balk J Stom, Vol 15, 2011DiscussionUsing the semi quantitative determination methodfor total microbial salivary counts 6 , aerobic and anaerobicmicroorganisms were separately processed. Therehas been a redistribution of the counts of aerobic andanaerobic microorganism colonies from sectors with highand medium growth density (++ and +) before chewing,to sectors with low or without any growth density(sectors + and + -) after chewing. However, statisticalanalysis (χ 2 test) has shown no statistical significance inthe case of aerobic microorganisms after chewing Orbitchewing gum (p = 0.09). Statistical analysis conductedfor anaerobic microorganisms have shown significantreduction after chewing Orbit chewing gum (p = 0.0047).However, when one considers duration of chewing, whichwas limited to 20 minutes, it becomes apparent that thedecrease in growth density after chewing Orbit sugar-freegum depends to a certain extent also on the mechanicalfunction of the saliva during mastication.Orbit sugar-free chewing gum performed veryeffectively in the reduction of Candida albicans yeastscolonies. Namely, only 1 of 7 participants, in which a totalof 34 colonies had been isolated before chewing Orbitchewing gum, exhibited a growth density of only 1 colonyafter chewing. The total number of colonies was reducedby 34 times on the average.Over the last few years, numerous studies havebeen aimed toward research of the influence of the use ofsugar-free chewing gum in dental caries prevention. Byreducing the principal amount of cariogenic micro-flora,mainly the salivary SM, the incorporation of bacteria intothe plaque is avoided, and their fermentable properties atlow pH-values are suppressed as well, which prevents thestart of the demineralisation process. In our investigationwe obtained a significant difference in the number ofcariogenic microorganisms’ colonies before and afterchewing Orbit sugar-free chewing gum. The reduction washigher in SM than in LB counts, expressed by the numberof subjects with logarithmic reduction factor of cariogenicmicro-flora. The number of subjects with log RF = 0for SM was 2, while it was 6 for LB. 2 subjects had alogarithmic reduction factor of 4 (log RF ≥ 4) for SM, andthere were no subjects with this reduction factor for LB.At the end of the discussion, we would like to emphasizethat until now no research of the effects of Orbit sugar-freechewing gum on the bacterial cell have been carried out,so that the results that were discussed can be consideredas the results of a pioneer experiment in this direction.However, considering the action of sugar alcohols reportedin literature, we can conclude that our results are inaccordance with the research of Birkhed 1 , Edgar 3 , Edgarand Gedds 4 , Mäkinen et al 5 and Szöke et al 7 .ConclusionSignificant reductions in salivary MS and LB levels,and declines in the total count of aerobe and anaerobebacteria and Candida albicans as well, were observed inall cases. Therefore, we can conclude that Orbit sugar-freechewing gum influenced very effectively in the reductionof cariogenic microorganisms.References1. Birkhed D. Cariologic aspects of xylitol and its use inchewing gum: a review. Acta Odontol Scand, 1994;52(2):116-127.2. Dawes C, MacPherson LMD. Effects of nine differentchewing - gums and lozenges on salivary flow rate and pH.Caries Res, 1992; 24:176-182.3. Edgar WM. Sugar substitutes, chewing gum and dentalcaries: a review. Brit Dent J, 1998; 184(1):29-32.4. Edgar WM, Gedds DAM. Chewing gum and dental health: areview. Brit Dent J, 1990: 173-177.5. Mäkinen KK, Soderling E, Isokangas P, Tenovuo J, TieksoJ. Oral biochemical status and depression of Streptococcusmutans in children during 24- to 36-month use of xylitolchewing gum. Caries Res, 1989; 23(4):261-267.6. Panovski N. Ispituvawe na faktorite odgovorni zaopstanokot na medicinski zna~ajnite soevi na nesporogeniteanaerobni bakterii “in vitro” (PhD Thesis). Skopje:Univerzitet “Sv. Kiril i Metodij”, Medical Faculty, 1990. (inMacedonian)7. Szöke J, Bánóczu J, Proskin HM. Effect of after-mealsucrose-free gum-chewing on clinical caries. J Dent Res,2001; 80(8):1725-1729.Correspondence and request for offprints to:Dr. Aleksandar DimkovBul. Partizanski odredi 8/37Skopje, FYR MacedoniaE-mail: adimkov@mail.net.mk

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYFluoride Released from Orthodontic Bonding Material:An In Vitro EvaluationSUMMARYEnamel demineralization is an undesirable but common complicationof orthodontic fixed appliances therapy. The purpose of this study was to testlong-term benefits of resin-modified glass ionomer cement (GC Fuji Ortho TMLC) for the prevention of demineralization in patients receiving orthodontictreatment with fixed bonded appliances.90 healthy extracted premolars without any clinical signs ofdecalcification were selected. All teeth were cleaned and cut in half buccolinguallywith a diamond disc. Thus, the control and test specimens wereobtained from the same teeth. Orthodontic brackets were bonded with aresin-modified glass ionomer cement. The teeth were divided in 3 groupsaccording to the period of monitoring (1, 3 and 6 months). They were storedin artificial saliva until analyzing. Determination of the fluoride in enamelwas done by spectrophotometer.The amount of fluoride in enamel 1 month after the bracketsapplication was significantly higher, after 3 months it was even higher,and after 6 months it was still statistically significantly higher compared toinitial values, but lower than the previous 2 time intervals (and remainedon a constant level). The results of this in vitro study clearly indicate thatfluoride-releasing material used in fixed orthodontic treatment inhibitsdemineralization of enamel around orthodontic appliances.Keywords: Enamel; Brackets; Glass-ionomer Cements; Demineralization; RemineralizationEfka Zabokova-Bilbilova 1 ,A. Sotirovska-Ivkovska 1 , Icko Gjorgovski 21 Department of Paediatric DentistrySchool of Dentistry2 Faculty of Natural Sciences and MathematicsSts. Cyril and Methodius UniversitySkopje, FYROMORIGINAL PAPER (OP)Balk J Stom, 2011; 15:31-34IntroductionOrthodontists are still challenged by an “oldproblem” in their practices: enamel demineralizationaround orthodontic appliances. Patients undergoingorthodontic therapy are exposed to a higher risk of enameldemineralization 1 . Appliances are directly attached to toothsurface, increasing the difficulty of achieving adequateoral hygiene. Some of commonly used accessories,such as hooks, posts, elastic chains and springs, can alsoundermine dental bio-film removal. Thus, the incidenceof white spot lesions can be significantly higher amongorthodontic patients with poor oral hygiene 8 .Enamel demineralization is an undesirable butcommon complication of orthodontic fixed appliancestherapy. Several studies have reported a significantincrease in the prevalence and severity of demineralizationafter orthodontic therapy compared with controls, and theoverall prevalence amongst orthodontic patients rangesfrom 2 to 96% 17,19 . The teeth most commonly affected aremolars, maxillary lateral incisors, mandibular canines andpremolars 15 .The potential risk of enamel surface decalcificationduring orthodontic treatment can be reduced by usingglass ionomer cements (GIC) for bonding the brackets 2-4 .GIC have been showed to consistently release fluorideover time. They also have ability to take up and re-releasefluoride after application of a topical fluorides source.Although the property of fluoride releasing would appearto make GIC an ideal bonding agent for orthodonticbrackets, the adequacy of strength for successfulclinical bonding 9,12,24 is less. Recently, Fuji Ortho TMLC developed the GIC for bonding brackets to teeth.The manufacturer claims it can be applied in a wet fieldand is not as technique-sensitive as composite resins.

32 Efka Zabokova-Bilbilova et al. Balk J Stom, Vol 15, 2011Specifically, it requires no etching of the enamel surfaceand should be applied in wet environment. Anotherattribute of glass ionomers is that they release fluoride,which is known to reduce the incidence of caries 13,22 . Theprocess of fluoride release is by way of polyacid attackon the alumino-silicate glass. As the glass network breaksdown, the Al 3+ , Ca 2+ , and F - ions are released 21 .The capacity of glass ionomers to absorb fluoridefrom rinses and tooth paste in essence allows the glassionomer to reconstitute itself and continuously releasefluoride. This should aid in the decreased incidence ofdecalcification and unsightly white spots around thebrackets. The advantages proposed to be gained by theoperator and patients are substantial. If all these factorswere true for the new Fuji Ortho TM LC product, it wouldbe more beneficial clinically than composite resin alone.Because of these possible improvements over compositeresin, a test of Fuji Ortho TM LC effectiveness in loweringbracket failure rate and incidence of decalcificationseemed in order 5,10 .Cook 6 compared the in vivo bond strength of GICKetac (ESPE Premier Denbol Products), with a compositeresin bonding agent. The result of his evaluation indicatedthat the bond strength of that GIC was not nearly asgood as that of the composite resin. Cook stated thatthorough drying of the teeth before GIC use was notnecessary, but that cotton rolls should be used to isolatethe field of operation. He also suggested that the surfaceof the teeth to be bonded should be wiped off beforebracket placement and stressed that acid etching was notnecessary. The 40 cases studied showed a 12% failurerate, which is considered too great for routine orthodonticpractice.Fajen et al 11 evaluated the bond strength of 3different GIC against a composite resin in vitro, andlike Cook, found the bond strength of the GIC to be“significantly less”. The fluoride release is a result of2 processes: the short-term release is associated witha leakage of relatively loosely bound fluoride fromthe cement matrix. The long-term release is a result ofdiffusion controlled phenomena where the concentrationgradient is the moving force for the release.The purpose of this study was to test the long-termbenefits of resin-modified GIC (GC Fuji Ortho TM LC)for prevention of demineralization in patients receivingorthodontic treatment with fixed bonded appliances.Material and MethodIn this study, 90 healthy extracted premolars withoutany clinical signs of decalcification were selected. Allteeth were cleaned and cut in half bucco-lingually witha diamond disc. Thus, the control and test specimenswere obtained from the same teeth. Orthodontic bracketswere bonded with GC Fuji Ortho TM LC, resin-modifiedGIC. The teeth were divided in 3 groups according tothe period of monitoring (1, 3 and 6 months). Theywere stored in artificial saliva (20 mmol/l NaHCO 3 , 3mmol/l NaH 2 PO 4 and 1 mmol/l CaCl 2 , neutral pH) untilanalyzing. Determination of the fluoride in enamel wasdone by spectrophotometer. Determination started withdistillation, and then 50ml of the distillate was mixedwith 10ml SPADNS and acidic circonyl. The absorbancewas read on the spectrophotometer. Than the results werecalculated by the formula: F ppm= 50A/V, where A is ppmof fluoride measured by the spectrophotometer, and V mlof the sample.For statistical evaluation, a one-way analysis ofvariance (ANOVA) was initially used to see if there was asignificant difference between groups.ResultsTable 1 shows the value of F in enamel in theexperimental group of teeth 1 month after brackets werebonded. Average value of F in the examined group ofteeth was 844,044 ppm, and in the control group of teeththe average value of F was 614,230 ppm. For this timeperiod, a statistically significant difference was foundbetween values of F in the examined groups of teeth.Table 1. Values of F (ppm) in enamel 1 month after bondingbracketsgroup N X¯ SD t ptest 30 844,044 314,130control 30 614,230 177,1593,490 0,00085*Table 2. Values of F (ppm) in enamel 3 months after bondingbracketsgroup n X¯ SD t ptest 30 946,260 449,995control 30 684,072 370,8222,462 0,01672*Table 2 shows the values of F in enamel in the groupof examined and control teeth 3 months after bonding ofbrackets. Again, a statistically significant difference of thevalues was found (946,260 ppm and 684,072 ppm of F inthe examined and control group of teeth, respectively).

Balk J Stom, Vol 15, 2011 Fluoride Released from Orthodontic Bonding Material 33Values of the F in enamel of the examined andcontrol group of teeth 6 months after bonding bracketsare presented in table 3. The result was similar tothe previous. After treatment of 1, 3 and 6 months,statistically significant difference occurred in the averagevalues of fluoride in enamel between the experimental andcontrol groups. The differences were greater after 1 monthand smaller after 6 months (Tab. 4).Table 3. Values of F (ppm) in enamel 6 months after bondingbracketsgroup n X¯ SD t ptest 30 557,398 198,477control 30 454,539 185,1172,076 0,04438*Table 4. Comparative display of F values in enamel at the testand control groupgroupntame/monthstest 30 844,044 314,130X¯ SD t p1 3,490 0,00085*control 30 614,230 177,159test 30 946,260 449,9953 2,462 0,01672*control 30 684,072 370,822test 30 557,398 198,4776 2,076 0,04438*control 30 454,539 185,117DiscussionAfter completing the fixed orthodontic treatment,and as a reason that ideal oral hygiene usually is notachieved, demineralised zones are spotted. They are morenoticed in the gingival part of labial surface of the teeth,where plaque accumulation is significantly higher. Suchdemineralised zone appears as early as 4 weeks afterorthodontic brackets and bands placement. It is knownthat these demineralised zones are able to remineraliseand to restore the damaged apatite crystals. The processof remineralisation in the oral cavity is favoured byfluoride. This effect is one of the reasons why applicationof fluoride is recommended every time to prevent,neutralise or restore demineralised enamel (with goodoral hygiene). Its crystals are larger than the original ones,which is linked to the reducing possibility of dissolving.This explains the positive cariostatic effect of materialscontaining fluoride used for bonding the brackets 18,20 .Around some brackets bonded with such materials, dueto the released fluoride, a weaker demineralization ofenamel appears than in cases where they are bonded withmaterials which do not release fluoride 7,16 .Results of this study clearly show that the content offluoride in enamel significantly increased after applicationof GIC containing fluoride. Thus, the amount of fluoridein enamel before fixing the brackets was 614,230 ppm;after 1 month of their bonding, the amount of fluoridein enamel was 844,044 ppm, which is statisticallysignificantly higher of the initial coverage of fluoride inenamel. After 3 months, the value of fluoride in enamel inthe examined group was even higher (946,260 ppm). After6 months decrease the amount of fluoride (557,398 ppm)was noticed, although still significantly higher comparedto the control group.In our study enamel demineralization in vitro wasinhibited to a certain degree. Similar prevention ofdecalcification was reported by many authors for otherfluoride-releasing materials 14,23 . Besides the positiveimpact on local fluoride-released cement used for bondingthe brackets in inhibiting demineralisation of the enamelaround orthodontic brackets and bands, the release offluoride from GICs provides continuous presence of lowconcentrations of fluoride in the oral medium, which alsoinfluence with inhibition on demineralised enamel aroundorthodontic brackets and bands.ConclusionsThe fluorides contribute to inhibition ofdemineralization process around the brackets andbands during fixed orthodontic treatment. The amountof fluoride in enamel after 1 month after the bracketsapplication was significantly higher, after 3 months itwas higher, and after 6 months it was still statisticallysignificantly higher compared to initial values; yet it isstill lower than the previous 2 time intervals (and remainson a constant level).The results of this in vitro study clearly indicate thatfluoride-releasing materials used in fixed orthodontictreatment inhibit demineralization of enamel aroundorthodontic appliances.References1. Artun J, Brobakken BO. Prevalence of caries white spotsafter orthodontic treatment with multibonded appliances.Eur J Orthod, 1986; 8:229-234.

34 Efka Zabokova-Bilbilova et al. Balk J Stom, Vol 15, 20112. Basdra EK, Huber H, Komposch G. Fluoride released fromorthodontic bonding agents alters the enamel surface andinhibits enamel demineralization in vitro. Am J OrthodDentofacial Orthop, 1996; 109:466-472.3. Bishara SE, Gordon VV, Von Wald L, Jakobsen JR. Shearbond strength of composite glass ionomer, and acidicprimer adhesive systems. Am J Orthod Dentofacial Orthop,1999; 115:24-28.4. Bishara SE, Olsen ME, Damon P, Jakobsen JR. Evaluationof a new light-cured orthodontic bonding adhesive. Am JOrthod Dentofacial Orthop, 1998; 114:80-87.5. Bishara SE, Saliman M, Lafton J, Warren J. Share bondstrength of a new fluoride release glas-ionomer adhesive.Angle Orthod, 2007; 78 (1):125-128.6. Cook PA, Youngson CC. An in vitro study of the bondstrength of glass ionomer cement in the direct bonding oforthodontic brackets. British J Orthod, 1988; 15:247-253.7. Corry A, Millett DT, Creanor SL, Foye RH, GilmourWH. Effect of fluoride exposure on cariostatic potentialof orthodontic bonding agents: an in vitro evaluation. JOrthod, 2003; 30(4):323-329.8. Chang HS, Walsh LJ, Freer TJ. Enamel demineralizationduring orthodontic treatment. Aetiology and prevention.Aust Dent J, 1997; 42(5):322-327.9. Charles C. Bonding orthodontic brackets with glassionomercement. Biomaterials, 1998; 19:589-591.10. Chung CH, Cuozzo PT, Mante FK. Shear bond strengthof a resin-reinforced glass ionomer cement: an in vitrocomparative study. Am J Orthod Dentofacial Orthop, 1999;115:52-54.11. Fajen VB, Duncanson MG, Nanda RS, Currier GF,Angolkar PV. An in vitro evaluation of bond strength ofthree glass ionomer cements. Am J Orthod DentofacialOrthop, 1990; 97:316-322.12. Featherstone JD. The science and practice of cariesprevention. JADA, 2000; 131:887-899.13. Featherstone JD, Glena R, Sharaiti M, Shields CP.Dependence of in vitro demineralization of apatite andremineralization of dental enamel on fluoride concentration.J Dent Res, 1990; 69:620-625.14. Fricker JP. A new self-curing resin modified glass-ionomercement for direct bonding of orthodontic brackets in vivo.Am J Orthod Dentofacial Orthop, 1998; 113:384-386.15. Gorelick L, Geiger AM, Gwinnett AJ. Incidence of whitespot formation after bonding and banding. Am J Orthod,1982; 81(2):93-98.16. Lippitz SJ, Staley RN, Jakobson JR. In vitro study of24-hour and 30-day bond strengths of three resin-glassionomer cements used to bond orthodontic brackets. Am JOrthod Dentofacial Orthop, 1998; 113:620-624.17. Mizrahi E. Enamel demineralization following orthodontictreatment. Am J Ortod, 1982; 82(1):62-67.18. Mellberg JR. Remineralization. A status report. Part III. AmJ Dent, 1988; 1:85-89.19. Ögaard B, Rolla G, Arends J, ten Cate JM. Orthodonticappliances and enamel demineralization. Part 2: Preventionand treatment of lesions. Am J Orthod Dentofacial Orthop,1988; 94:123-128.20. Robinson C, Shore RC, Brookes SJ, Strafford S, Wood SR,Kirkham J. The Chemistry of Enamel Caries. Crit Rev OralBiol Med, 2000; 11(4):481-495.21. Trimpeneers LM, Dermault LR. A clinical evaluation ofthe effectiveness of a fluoride-releasing visible lightactivatedbonding system to reduce demineralization aroundorthodontic brackets. Am J Orthod Dentofacial Orthop,1996; 110(2):218-222.22. Underwood ML, Rawls HR, Zimmerman BF. Clinicalevaluation of a fluoride-exchanging resin as an orthodonticadhesive. Am J Orthod Dentofacial Orthop, 1989; 96:93-99.23. Vorhies AB, Donly KJ, Staley RN, Wefel JS. Enameldemineralization adjacent to orthodontic brackets bondedwith hybrid glass ionomer cements: an in vitro study. Am JOrtod Dentofacial Orthop, 1998; 114(6):668-674.24. White LW. Glass ionomer cement. J Clin Orthod, 1986;20:387-391.Correspondence and request for offprints to:Efka Zabokova-Bilbilova, DDS, PHDDepartment of Paediatric DentistrySchool of DentistryVodnjanska 171000 Skopje, FYR Macedoniae-mail: efka_zabokova@hotmail.com

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYVariation of Skeletal Cephalometric Variables inClass II Division 2 Patients with AgeSUMMARYApart from the dental and maxillofacial features, an importantconsideration in the treatment of Angle Class II division 2 malocclusions isfacial growth, particularly if the case requires not only tooth movement butchanging maxillo-mandibular relation as well. The purpose of this studywas to determine the effect of chronological age on certain skeletal featuresof Angle Class II division 2 patients. The material of the study included96 lateral cephalometric X-rays of patients with Angle Class II division 2malocclusion, ranging in age from 7 to 35 years; on each cephalometricimaging, 8 cephalometric measurements were performed. Statistical dataprocessing included analyses of 1 variable and correlation of 2 variables.In patients with Angle Class II division 2 malocclusion the facialprofile was convex and did not change significantly with age, theanteroposterior position of the chin in the children’s group approximated‘normal’, while there was a tendency for mandibular retrusion among adultpatients. Mandibular morphology changed and became more “square”among older patients.Key words: Class II/2; Skeletal Features; Cephalometric Analysis; AgeNikolaos Topouzelis, Andreas Zafiriadis,Helen MarkovitsiAristotle University of ThessalonikiDental School, Department of OrthodonticsThessaloniki, GreeceORIGINAL PAPER (OP)Balk J Stom, 2011; 15:35-40IntroductionDuring growth and in the period between deciduousand permanent dentition, the features of Angle Class IIdivision 2 malocclusion exacerbate due to increasingincisor over-occlusion, which leads to differential growthbetween the maxilla and the mandible, and consequently,to maxillary protrusion 1 . There was a view that AngleClass II division 2 malocclusion exacerbates with time notdue to a change in the growth pattern but due to increasinganterior rotation of the mandible, which results from theparticular effect of the masseter muscles 2 .Under conditions of normal mandibular growthand development, one would expect a lower incidenceof mandibular retrusion among adults, as compared tominors. However, this is not so in cases of Angle ClassII division 2 malocclusion, probably due to palatalinclination of maxillary incisors and increased incisoroverjet, which result in stunting mandibular growth 3 . Thisfinding is confirmed by observation that in these cases,mandibular alveolar development, as assessed by theS-N-B angle, was more restricted than the development ofosseous base of the mandible, as assessed by the S-N-Pogangle 1,4,5 .The range of views related to dental, skeletal andfacial features of Angle Class II division 2 malocclusionmake it necessary to further study such cases and followtheir particular development through time, which isimportant not only for clinical orthodontists’ needs, butalso for accurate determination of the case description. Theaim of the study was: (a) to examine possible differencesof skeletal cephalometric measurements among 3 agegroups of Angle Class II division 2 malocclusion patients,and (b) to investigate possible correlations betweenpatients’ age and those cephalometric measurementsexamined.Subjects and MethodsResearch material included 96 lateral cephalometricX-rays of Angle Class II division 2 malocclusion patientswho had never had any type of orthodontic treatment.Their selection was based on the basis of dental occlusion

36 Nikolaos Topouzelis et al. Balk J Stom, Vol 15, 2011relations and patients’ ages, out of a total number of 174cases of Angle Class II division 2 malocclusion patientswho asked for orthodontic treatment. The X-rays ofpatients selected were divided into 3 groups.The first group, “a children group”, included 33X-rays. 13 patients were boys and 20 were girls. Theirmean age was 9.5 years; the youngest was 7 and the oldest11 years old. Their dentition was mixed and there wasno case of having lost a deciduous tooth early or missingsome permanent tooth.The second group, “an adolescent group”, included31 X-rays. 13 patients were boys and 18 were girls. Theirmean age was 14 years; the youngest was 13 and the oldest15.5 years old. Their dentition was permanent and therewas no tooth missing in any of the cases.The third group, “an adults group” included 32X-rays. 11 patients were men and 21 women. Their meanage was 21 years; the youngest was 17 and the oldest 35years old. Their dentition was permanent and there was notooth missing in any of the cases.Cephalometric VariablesOn every lateral cephalometric X-ray, 8 cephalometricmeasurements were performed, concerning bothsagittal and vertical dimensions of the facial skeletalstructures. Cephalometric measurements used were thefollowing (Figs. 1 and 2): (1) Facial angle (Po-Or/Na-Pog);(2) Facial Axis Angle (Pt-Gn/Ba-Na); (3) MandibularPlane Angle (Po-Or/Go-Me); (4) Mandibular Arc Angle(Dc-Xi-Pm); (5) Facial Convexity (AàNa-Pog); (6)Mandibular Corpus Axis (XiàPm); (7) Cranial Base Length(BaàNa); and (8) Anterior Cranial Base Length (CCàNa).Method ErrorIn order to determine the experimental methoderror for each variable used, 20 X-rays were selected atrandom. These were traced and re-measured by the sameresearcher 20 days after their initial analysis. T-test wasused to determine method error; the significance level wasa=0.05. No statistically significant differences were foundfor the 8 variables used in the 2 measurements performed.Statistical AnalysisData processing included analyses of 1 variable andcorrelations of 2 variables. All continuous variables werechecked using the Kolmogorov-Smirnov test. The resultswere analyzed with ANOVA and the Duncan test, whereasPearson’s correlation coefficient was used to determinewhether there was a statistically significant correlationbetween age and other quantitative variables or not.ResultsDescriptive statistics for 8 cephalometricmeasurements used concerned both sagittal and verticaldimensions of facial skeletal structures are presented inTables 1 to 8. ANOVA showed that there was no statisticallysignificant difference in the mean values of facial angle(Tab. 1), facial axis angle (Tab. 2) or facial convexity (Tab.5) in the 3 age groups. In the adult group, the mean valuepresented statistically significant differences (p

Balk J Stom, Vol 15, 2011 Cephalometric Variables in Class II Division 2 Patients 37Figure 2. A. Facial Convexity (AàNa-Pog), B. Mandibular Corpus Axis (XiàPm),C. Cranial Base Length (BaàNa), D. Anterior Cranial Base Length (CCàNa)Table 1. Statistical parameters of Po-Or/Na-Pog AngleAge group N Mean Value Standard deviation Minimum value Maximum7 - 11 33 86.5 2.8 81 9113 - 15 31 87.5 3.2 80 9317 - 35 32 88.4 3.8 79 95F = 2.960p = 0.057NSTable 2. Statistical parameters of Pt-Gn/Ba-Na AngleAge group N Mean Value Standard deviation Minimum value Maximum7 – 11 33 89.7 3.1 82 9513 – 15 31 89.7 4.5 80 9817 – 35 32 91.5 4.2 83 100F = 2.193p = 0.117NSTable 3. Statistical parameters of Po-Or/Go-Me AngleAge groupNMean ValueSub-groupsStandard deviation Minimum value Maximum7 – 11 33 20.9 (1) 4.2 13 3013 – 15 31 20.8 (1) 5.6 8 3217 – 35 32 16.8 (2) 6.9 2 30ANOVA (1) (2) Mean value differences appeared in 2 sub-groups (Duncan test)F = 5.549p = 0.005

38 Nikolaos Topouzelis et al. Balk J Stom, Vol 15, 2011Table 6. Statistical parameters of Mandibular corpus axis XiàPmAge group NMean ValueSub-groupsStandard deviation Minimum value Maximum7 – 11 33 64.3 (1) 3.6 58 7313 – 15 31 69.1 (2) 3.5 60 7517 – 35 32 71.9 (3) 5.7 59 88ANOVA (1) (2) (3) Mean value differences appeared in 3 sub-groups (Duncan test)F = 24.636p = 0.000

Balk J Stom, Vol 15, 2011 Cephalometric Variables in Class II Division 2 Patients 39X-ray imaging, cephalometric X-rays should also berestricted to those absolutely necessary and performedonly for diagnostic purposes 6 . Therefore, when toomany X-ray examinations are performed on the sameperson for research purposes, this is criticized due to theincreased radiation the person is exposed to, which isunacceptable 7 . This ethical reasoning has meant fewerX-ray examinations for research purposes, which resultedin avoiding longitudinal growth assessment and repeatedX-ray imaging of the same person.This paper aimed at studying Angle Class II division2 malocclusion cases and determining the improvementor exacerbation of facial skeletal structure relationshipsat various ages. Due to ethical considerations mentionedabove, the material of the study comprised initial lateralcephalometric X-rays of cases with Angle Class IIdivision 2 malocclusion who asked for treatment; thesepatients ranged in age from 7 to 35 years.Initially, 8 cephalometric measurements wereperformed to determine Angle Class II division 2malocclusion in 3 patient groups - a children’s group, anadolescents’ group and an adults’ group - and differenceswere later identified among these 3 groups. Furthermore,it was investigated whether these measurements areaffected by age in all the patients examined.Facial angle, which determines chin position alongthe anterior-posterior axis, was used to assess the positionof the mandible along the sagittal axis. Facial angle(Po-Or/Na-Pog) showed no significant increase in theadolescents’ and adults’ groups, although it was found toincrease with patient’s age. Facial angle increase with agewas attributed mainly to the significant increase of thelength of the mandibular corpus axis. Values found forthe facial angle indicate a “normal” mandibular positionof the mandible in children. On the contrary, there is atendency for slight mandibular retrusion among adults 8 ,which seems to agree with similar findings by numerousauthors 9-12 . Besides, the difference in mandibular positionbetween children and adult patients tends to support theview that Angle Class II division 2 malocclusion is nota primary skeletal syndrome, but a deformation, whichnumerous authors attribute mainly to the pronouncedpalatal inclination of maxillary central incisors, whichresults in stunting mandibular growth 3,13-15 .Mandibular corpus axis length (Xi àPm) appearedsignificantly increased in adults as compared to thatof children and adolescents. Furthermore, all patientsexamined showed significant differences since this lengthincreased with patient age.Skeletal facial convexity was found increased in all3 groups examined. Furthermore, it was not significantlydifferent in all the groups and showed no negativecorrelation with age, although it appeared decreased in theadolescents’ and adults’ groups. Skeletal facial convexitydevelopment is caused by the significant increase foundin mandibular corpus axis length and cranial base lengthwith age, in particular, the increased anterior cranial baselength. Cranial base length (BaàNa) presented significantincrease among adolescents and adults as compared to thechildren’s group, while the difference between adolescentsand adults was not significant. On the contrary, cranialbase length showed a particularly significant positivecorrelation with age, which was expected.Anterior cranial base (CCàNa) was found to besignificantly longer among the adults’ group as comparedto that of the children, while it was not different in theadolescents’ group when compared to the other 2 groups.Similar to “normal” individuals, all patients examinedshowed positive correlation of anterior cranial base lengthwith age.The face, in all 3 groups of patients examined,showed a “normal” direction of increase, since meanvalues of facial angle (Pt-Gn/Ba-Na) in minors andadolescents showed no difference from what wasproposed as “normal” 8,16,17 . Facial angle did not showsignificant differences among all groups examined, norany correlation with age. Brezniak et al 18 used Downs’axis and Ricketts’ facial axis, and found that Angle ClassII division 2 malocclusion patients presented a morehorizontal type of increase in comparison to “normal”individuals.Mandibular angle (Po-Or/Go-Me) and mandibulararc angle (Dc-Xi-Pm) mean values measured supportthe view that patients with Angle Class II division 2malocclusion tend to have a “strong” and “square”mandible with a “strong” muscular system, a smallmandibular angle and a large mandibular arc angle 12,18,19 .Mandibular angle mean values in children andadolescents showed no differences, while in the groupof adult patients this angle was significantly lower thanin the other 2 groups. In all the patients examined, themandibular angle presented a statistically significantdifference, since it reduced with age. The reduction ofmandibular angle with age might be due to the anteriormandibular rotation during its growth 11,20,21 , a fact whichmainly appears in cases with insufficient incisor support 20 .Mandibular arc angle increases with normal growthas a result of increased adaptive changes occurringin the mandible 8 . In the children’s and adolescents’groups, it showed no significant difference, while it wassignificantly increased in adult patients in comparisonto the other 2 groups. In all the patients examined,mandibular arc angle showed particularly significantdifferences with growth since it increased with age.Assessment of findings of this research has led to theconclusion that in patients with Angle Class II division2 malocclusion facial profile was convex and did notsignificantly change with age, while anteroposteriorposition of the mandible showed significant differences inthe 3 groups examined: in the children’s group it might beconsidered “normal”, while among adolescent and adultpatients it showed a tendency for retrusion. Mandibular

40 Nikolaos Topouzelis et al. Balk J Stom, Vol 15, 2011corpus axis presented significant differences in length,since it grew with age. As for mandibular morphology,this was found to significantly change with age andbecome more “square” in older patients. The direction offacial growth was found to be within normal range andshowed no difference at the various ages.In patients with Angle Class II division 2malocclusion, who are still growing, exacerbation of theanteroposterior position and morphology of the mandibleneed to be taken into consideration so that necessarymechanisms may be activated in good time to inhibit thestunting of mandibular growth in the anteroposterior andvertical directions. This view is compatible with mostclinicians’ views, which support that, when a patient whois still growing is developing an Angle Class II division 2malocclusion, this would not be corrected by mandibulargrowth without any intervention 15,22,25 .ConclusionsThe cephalometric study and assessment of findingsof this study suggest that:1) Anteroposterior chin position in childrenapproximated “normal”, while adult patients showed atendency for retrusion;2) Facial profile was convex and showed no significantdifferences among the groups of children, adolescentsand adults and no change with age;3) Mandibular morphology was found to varysignificantly at various ages: it changed and becamemore “square” with age;4) During orthodontic treatment of patients with AngleClass II division 2 malocclusion, it is necessary toconsider and activate in time those mechanismsthat inhibit the stunting of mandibular growth in theanteroposterior and vertical dimensions.References1. Korkhaus G. Über den Aufbau des Gesichtschadels beimDeckbiss. Fortschritte der Kieferorthopädie, 1953; 14:162-171. (in German)2. Maj G, Lucchese F. The mandible in Class II, Division 2.Angle Orthod, 1982; 52:288-292.3. Pancherz H, Zieber K, Hoyer B. Cephalometriccharacteristics of Class II division 1 and Class II division2 malocclusion: a comparative study in children. AngleOrthod, 1997; 67:111-120.4. Hausser E. Zur Atiologie und Genese des Deckbisses.Fortschritte der Kieferorthopädie, 1953; 14:154-161. (inGerman)5. Arvystas M. Non extraction treatment of severe Class IIdivision 2 malocclusions Part 1. Am J Orthod DentofacOrthop, 1990; 97:510-521.6. Indication and frequency of X-ray in connection withorthodontic treatment. Statement by the DeutscheGesellschaft für Kieferothopädie. J Orofac Orthop, 1997;58:286-287.7. Melsen B, Baumrind S. Clinical research applicationsof cephalometry. In: Athanasiou AE (ed). OrthodonticCephalometry. London: Mosby-Wolfe, 1998; pp 181-202.8. Ricketts R, Roth R, Chaconas S, Schulhof R, Engel G.Orthodontic diagnosis and planning. Vol 1. USA: RockyMountain Data Systems, 1982.9. Demisch A, Ingervall B, Thuer U. Mandibular displacementin Angle Class II division 2 malocclusion. Am J OrthodDentofac Orthop, 1992; 102:509-518.10. Binda S, Kuijpers-Jagtmann A, Maertens J, Van Hof M.A log term cephalometric evaluation of treated Class IIdivision 2 malocclusions. Eur J Orthod, 1994; 16:301-308.11. Karlsen A. Craniofacial characteristics in children withAngle Class II division 2 malocclusion combined withextreme deep bite. Angle Orthod, 1994; 64:123-130.12. Pancherz H, Zieber K. Dentoskeletal morphology inchildren with Deckbiss. J Orofac Orthop, 1998; 59:274-285.13. Godiawala R, Joshi M. A cephalometric comparisonbetween Class II, Division 2 malocclusion and normalocclusion. Angle Orthod, 1974; 44:262-267.14. Zieber K, Pancherz H. Cephalometric characteristics of ClassII, division 2 malocclusions. Eur J Orthod, 1995; 17:462.15. You Ζ, Fishman S, Rosenblum R, Subtelny D. Dentoalveolarchanges related to mandibular forward growth in untreatedClass II persons. Am J Orthod Dentofac Orthop, 2001;120:598-607.16. Langlade M. Diagnostic. Editeur Paris: Orthodontiquemaloine SA, 1981.17. Slavicek R, Schadlbauer E. Etude et comparison de valeurscephalometriques regionales en Autriche et en Allemagne.Rev Orthop Dentofac, 1982; 16:417-471. (in French)18. Brezniak N, Arad A, Heller M, Dinbar A, Dinte A,Wasserstein A. Pathognomonic cephalometric characteristicsof Angle Class II Division 2 malocclusion. Angle Orthod,2002; 72:251-257.19. Houston W. A cephalometric analysis of Angle Class IIdivision 2 in the mixed dentition. Dental Practice, 1967;17:372-376.20. Bjork A. Prediction of mandibular growth rotation. Am JOrthod Dentofac Orthop, 1988; 55:585-599.21. Björk A, Skieller V. Normal and abnormal growth ofthe mandible. A synthesis of longitudinal cephalometricimplant studies over a period of 25 years. Eur J Orthod,1983; 5:1-46.22. Subtelny J. To treat or not to treat. Int Dent J, 1973;23:292-303.23. Bishara S, Hoppens B, Jacksen J, Kohout F. Changes in themolar relationship between the deciduous and permanentdentitions: a longitudinal study. Am J Orthod DentofacOrthop, 1988; 93:19-28.Correspondence and request for offprints to:Nikolaos Topouzelis, Associate ProfessorAristotle University of ThessalonikiDental School, Department of OrthodonticsGR-54124 Thessaloniki, GreeceE-mail: ntopouz@dent.auth.gr

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYClinical Oral Manifestation inGastrointestinal DisordersSUMMARYAim: to evidence extraoral and intraoral, subjective and objective,symptoms by patients with Crohn’s disease and ulcerative colitis, dependingof the disease’s phase.Material and Method: to realize the established aim, 12 patients(8 with Crohn’s disease and 4 with ulcerative colitis) were followed at theClinic for gastrointestinal diseases. All patients went through exceptionalanamnesis and clinical control (inspection and palpation). All examineeswere examined in both phases - exacerbation and reemission.Results: As extraoral symptoms, arthralgia, sarcoidosis,thrombophlebitis, anaemia, oedema of the face and mouth were pointed out.The anaemia is mostly present in patients with Crohn’s disease (63%) andulcerative colitis (75%). After that, on the patients oedema of the mouth isevidenced in 38% of patients with Crohn’s disease and 25% of patients withulcerative colitis. From the subjective symptoms, symptoms such as illness,firing/fry, and glow were indicated; at the phase of exacerbation, thesesymptoms were indicated by all 8 patients with Crohn’s disease. Also by allpatients with clinical diagnosis of ulcerative colitis, illness was present andonly 3 out of 4 had an indication of firing and glow. From intraoral dentalsymptoms in both diseases, aphtous stomatitis and glositis were often present.In the exacerbation phase, in patients with Crohn’s disease, aphtous stomatiitswas always present, and glositis in 88% of patients. In the remission phases,the subjective dental symptoms evidently decreased. Considering ulcerativecolitis, the findings were identical, aphtous stomatitis and glositis werepresent in all 4 examinees. Piostomatis vegetans was present by 63% ofpatients with Crohn’s disease, and of patients with ulcerative colitis.Conclusion: the profound clinical manifestation in examinees in theexacerbation phase is due to pathogenetical activities in the gastrointestinaltract. The oral cavity as a beginning part of the gastrointestinal tract, asimilar histological changes and disruptions are shown. For that reason, themost important role of the dentist is to diagnose gastrointestinal disruptions.Keyword: Crohn’s disease; Colitis, ulcerative; Gastrointestinal DisruptionsM. Popovska 1 , B. Stavrova 1 ,A. Atanasovska-Stojanovska 1 , P. Misevska 3 ,S. Strezovska 4 , L. Kanurkova 2 , J. Gjurcheski 11 Faculty of DentistryDepartment of Periodontology and Oral Pathology2 Faculty of DentistryDepartment of Orthodontics3 Faculty of MedicineDepartment of Gastroenterohepatology4 Dental Office IdadijaSkopje, FYROMORIGINAL PAPER (OP)Balk J Stom, 2011; 15:41-47IntroductionDentists and gastroenterohepatologysts put their effortand attention for diagnosis and treatment of certain diseasesof digestive system. Contrary to gastroenterohepatologysts,dentists take care of the oral cavity as the initial part ofdigestive system. Although, each one is diagnosing andthreat different pathology, their points of view and focusescorrelate very often in the clinical practice. Digestivesystem is a long muscular tube which initial part is the oralcavity, through which food and secretions are transmittedtoward rectum. Histological analogy, familiarity andcorrelation of oral cavity and other parts of the digestivesystem determinate certain gastrointestinal disorders togive repercussions in the oral cavity.Having that in mind, dentists should recognize,diagnose and treat oral lesions and infections that are

42 M. Popovska et al. Balk J Stom, Vol 15, 2011related with digestive diseases. In fact, the role of thedentist is quite heterogeneous: from disease detectionwhich is not diagnosed yet, to adjusting dental treatmentwith medical treatment that impacts oral health.Gastrointestinal diseases that mostly affect oralcavity are: ulcerative colitis and Crohn’s disease.There are many articles in medical and dental literaturethat describe extra abdominal and oral expression ofCrohn’s disease and ulcerative colitis. Well-knownand in practice often found oral expressions in relationwith inflammation of the large intestine are: vegetativepyostomatitis, aphthous ulcers, cobbled look oforal epithelium, epithelium shrinks granulomatousinflammation of small salivary glands, candidiasis andangular cheilitis 2,4- 6,8,12,14,18 .Ficcara at al 6 were examining the connectionbetween Crohn’s disease and vegetative pyostomatitisof oral mucosa, which is the marker of intestinalinflammation. The authors describe a 45-year-old womanwith diarrhoea present around 6 months and persistentpainful oral ulceration. The tongue was striated and inthe area of oral commisurrae pustules were present fromwhich Staphylococcus simulans was isolated.It is well known that changes in the oral cavity mayappear year or more before the first signs of inflammationin the bowel has been registered 4,15 . However, Crohn’sdisease and ulcerative colitis are of special interest todentist due to accompanying changes in the mouth and theinfluence of the medical therapy over the dentist treatment.Clinical course of these diseases is characterizedby episodes of acute attacks (phases of exacerbation)and phases of remission. This results in patient’s longtime suffering due to difficulties and slow treatment.Nowadays, dental literature presents data that indicatethe presence of antimicrobial proteins in saliva, as wellas bacterial and fungal infection in patients with Crohn’sdisease and ulcerative colitis having oral changes 1,9,13,16,17 .The aim of the study was to find out extra abdominalchanges in patients with Crohn’s disease and ulcerativecolitis and to evidence subjective symptoms and objectivechanges in the oral cavity in both stages of the diseases(exacerbation and remission), as well as to register intraoralsimilarities and differences in patient with these 2 diseases.Material and MethodFor realization of the established aim, 12 patients (8with Crohn’s disease and 4 with ulcerative colitis) werefollowed at the Clinic for gastrointestinal diseases (Facultyof Medicine) and the Department of periodontology and oraldisease (Faculty of Dentistry) in Skopje. Exceptional medicalhistory data (epidemiological characteristics of the disease -gender, age, duration of disease) and subjective symptoms(pain, glow, burning) were collected from all the patients.With clinical evaluation we noted extraoral andintraoral symptoms. Extraoral signs were: arthralgia,sarcoidosis, thrombophlebitis, anaemia, face oedema,lips swelling. Intraoral signs were: aphthous stomatitis,vegetative pyostomatitis, deep linear ulceration, angularcheilitis, indurative polypoid formation, glossitis, palemucosa, oral hairy leukoplakia. All examinees wereexamined in both phases of exacerbation and reemission.ResultsThe results of our research are presented in tablesand charts. Charts 1 and 2 present gender and age ofpatients with Crohn’s disease and ulcerative colitis. Of thetotal number of patient suffering from Crohn’s disease,50% were women and 50% were men. 1 male patient(25%) had ulcerative colitis and 3 women (75%). Bothdiseases were found in population older than 20 years,mostly at the age 31-50 years.Table 1 presents extraoral characteristics ofpatients with Crohn’s disease and ulcerative colitis inphases of exacerbation and remission. In the phase ofexacerbation, in patients with Crohn’s disease anaemiawas most frequent, in 5 of 8 patients (63%). In the phaseof remission, anaemia was present only in 2 of 8 patientsin phase of exacerbation or remission. In patients withulcerative colitis, in the phase of exacerbation, anaemiawas also the most frequent (3 out of 4 patients) and otherconditions (arthralgia, sarcoidosis, thrombophlebitis lipoedema) were less frequent. Some intraoral consequencesof the anaemia in patients with Crohn’s disease andulcerative colitis are presented in figures 1 and 2.Subjective symptoms (pain, burning and glowing)in patient with Crohn’s disease and ulcerative colitis, inboth phases of the diseases (exacerbation and remission)are presented in table 2. In the phase of exacerbation, all8 patients with Crohn’s disease (100%) had subjectivehardship of pain and burning; however, in the phaseof remission, only 2 of these patients (25%) felt pain inthe oral cavity, while one patient (13%) felt burning. Inthe phase of exacerbation, all 4 patients with ulcerativecolitis had subjective hardship of pain, while burning waspresent in 3 patients (75%). In the phase of remission,subjective hardship was less prominent.Intraoral characteristics among patients with Crohn’sdisease and ulcerative colitis, in phases of exacerbationand remission are presented in table 3. Among intraoralsigns, we have noticed aphthous stomatitis, Pyostomatitisvegetans, indurated polypoid formation, deep linearulcers, pale mucosa, oral hairy leukoplakia, glossitis, andangular cheilitis. Some of these signs are presented infigures 3-6.Charts 3 and 4 present a comparative view ofintraoral signs among patients with Crohn’s disease andulcerative colitis in both phases of the diseases.

Balk J Stom, Vol 15, 2011 Oral Manifestations in Gastrointestinal Disorders 43ABChart 1. Gender distribution of patient with: (A) Crohn’s disease and(B) ulcerative colitisChart 2. represents age distribution of patient with : A)Morbus CrohnB) Colitis ulcerativeTable 1. Extraoral characteristics of patients with Crohn’sdisease and ulcerative colitis in phases of exacerbationand remissionExtraoral characteristicsPhase ofexacerbationCrohn’sdisease (n=8)Ulcerativecolitis (n=4)n =12 number % number %Arthralgia 2 25 1 25Sarcoidosis 1 13 1 25Thrombophlebitis 1 13 1 25Anaemia 5 63 3 75Facial oedema 0 0 0 0Lips oedema 3 38 1 25AArthralgia 1 13 1 25Phase ofremissionSarcoidosis 1 13 0 0Thrombophlebitis 1 13 0 0Anaemia 2 25 1 25Facial oedema 0 0 0 0Lips oedema 2 25 1 25BFigure1. Oedema of the lip in the patient with:(A) ulcerative colitis, and (B) Crohn's diseaseABFigure 2. Consequences of anaemia present in patients with Crohn's disease:(A) angular cheilitis; (B) cheilitis exfoliativa

44 M. Popovska et al. Balk J Stom, Vol 15, 2011Table 2. Subjective symptoms in patients with Crohn’s disease and ulcerative colitis inphases of exacerbation and remissionSubjective symptoms Crohn’s disease Ulcerative colitisnumber % number %Phase of exacerbationPhase of remissionpain 8 100 4 100fry and glow 8 100 3 75pain 2 25 1 25fry and glow 1 13 1 25Table 3. Intraoral signs of Crohn’s disease and ulcerative colitis inboth phases of the disease (in patients with oral symptoms)Phases of thediseaseIntraoral signs Crohn’s disease Ulcerative colitisnumber % number %Aphthous stomatitis 8 100 4 100Pyostomatitis vegetans 5 63 2 50Indurated pylipoid formation 2 25 1 25ExacerbationDeep linear ulcers 2 25 2 50Angular cheilitis 4 50 2 50Pale mucosa 2 25 2 50Glossitis 7 88 4 100Oral chairy leukoplakia 1 13 1 25Aphthous stomatitis 3 38 1 25Pyostomatitis vegetans 2 25 2 50Indurated pylipoid formation 1 13 1 25RemissionDeep linear ulcers 1 13 1 25Angular cheilitis 2 25 1 25Pale mucosa 2 25 2 50Glossitis 2 25 1 25Oral chairy leukoplakia 1 13 1 25

Balk J Stom, Vol 15, 2011 Oral Manifestations in Gastrointestinal Disorders 45Figure 3. Cobbled look of the buccal mucosa in patient withCrohn’s diseaseAFigure 4. Pyostomatitis vegetans in patients with Crohn's diseaseBFigure 6. Aphthous stomatitis in patient with ulcerative colitis:(A) buccal mucosa; (B) apex of the tongueFigure 5. Hyperemia in oral epithelium in the patient withulcerative colitisChart 3. Comparison of intraoral characteristics among Morbus Crohnin a phase of exacerbation and remissionChart 4. Comparison of intraoral characteristics among Colitisulcerative in a phase of exacerbation and remission

46 M. Popovska et al. Balk J Stom, Vol 15, 2011DiscussionUlcerative colitis and Crohn’s disease are 2 of themost frequent intestine irritations in the group of idiopathicinflammations. Ulcerative colitis affects mucosa andsubmucosa of the large intestine and Crohn’s disease isactually regional enteritis, inflammatory condition thataffects all layers of the intestine. Nevertheless, these2 diseases share many common features, including anunknown etiology and not so clear pathogenesis. Bothdiseases are of crucial interest to dentist because of theassociated changes in the mouth and the consequencesarising from therapy (especially the use of corticosteroids).Therefore, many editorials in medical and dental literatureare devoted to extra-abdominal and oral signs of intestineinflammation 1,7,18 , or to oral cavity findings 9,10 .From epidemiological aspects of view, both diseasesdemonstrate 3 well-known peaks of incidence. The first,which is the highest, in the period between 20 and 24years of age, the second between 40 and 44 years of age,and the third between 60 and 64 year. After 60 years ofage, the incidence of ulcerative colitis far exceeds theincidence of Crohn’s disease 4 . Women from England andNorthern Europe have 30% higher risk for developmentof ulcerative colitis and Crohn’s disease. They often affectwhites and Jewish people, particularly those originatingfrom Central Europe: Russia and Poland.Our results are somehow contradictory to thefindings obtained from the literature: the biggest incidencewas registered in the period between 30 and 50 years ofage. This study went through the subjective and objectiveextraoral and intraoral changes in phase of exacerbationand remission. In phase of exacerbation, of the extraoralfindings found in patients with ulcerative colitis andCrohn’s disease, anaemia was dominantly present. Webelieve that pernicious anaemia arises as a result of bloodand iron loss, which is more emphasized in the activephase of both diseases. Inflammatory bowel mucosacan distort absorption of vital nutrients, such as Ca, Fe,or folates, which are absorbed in the small intestine.Therefore, the reduced absorption due to inflammationresults in lack of the previously mentioned nutrients,which is more noticeable in patients with Crohn’s diseasethan in patients with ulcerative colitis. Diarrhoea is amajor cause for dysfunctional balance of electrolytes andlow level of albumin. Lack of iron and folates reflectthe occurrence of anaemia. In the phase of remissionsymptoms are less prominent. Anaemia is also presentas a main extraoral symptom, but only in the half of therespondents. The applied treatment corrects abdominalfindings and decreases the number of patients withanaemia, which explains the obtained findings of ourstudy. Concerning other extraoral signs, oedema of lipswas noticed more often in patients with ulcerative colitis,which was also noticed by Ming 14 and Yamada 10 .Among intraoral objective findings in patients withulcerative colitis in the phase of exacerbation, aphthousstomatitis was the most prominent symptom, followed byglossitis, pyostomatitis vegetans and angular cheilitis. Wepresume that aphthae are the consequence of the lack of iron,folic acid, Vitamin B 12 , intestinal absorption dysfunctionand loss of blood. Aphthae were still present, althoughin a smaller number, even in the phase of remission of thedisease. We believe that their persistence is due to the effectof the applied therapy (treatment with sulfasalizine, salofalkand other drugs results in occurrence of new ulcers orlonger persistence of already existing aphthae - these drugsare excreted through saliva and they irritate oral mucosa).The new eruptions in these patients are often a forerunnerof a new surge of the disease. Question which needs to beanswered is the following: are aphthae a typical sing of thedisease, disease forerunner, only a random clinical finding,or the consequence of the present anaemia?By frequency of presence, at these patients intraoralPyostomatitis vegetans (deep proliferative lesions) ispresent. Their appearance in the oral cavity is related tothe impact of circulating human immune complexes,whose creation shall encourage the intestine antigen ordamaged lining of the colon. The other very often presentsign of the Crohn’s is a cobbled mucous look 21 . Thismorphological change is a reflection of granulomatouschanges that represent the main reason of Crohn’s disease.The consequences of dysfunctional absorption are visiblethrough other present signs: pale mucosa, angular cheilitisand glossitis. These signs are more prominent amongundiagnosed cases, in the acute phase of the disease, orwhen the disease is poorly controlled.In a phase of remission, intraoral clinical signs inpatients with Crohn’s disease could still be present, but ina fewer number of patients. We believe that the improvedabsorption in the intestine has a positive effect on thepatients’ oral status.Subjective symptoms in a phase of exacerbation,as pain, burning and glowing, are due to the presence oferoded or ulcerated areas. In the phase of remission, thereis a gradual normalization of the regulatory mechanismsand a decrease of subjective symptoms in patients withulcerative colitis and Crohn’s disease.Finally, it might be concluded that clinical symptomsamong most of the respondents in the phase of exacerbationwhere the consequence of the events in the gastrointestinaltract. The oral cavity, as mirror of general health statusof each individual, especially reflects disorders of thedigestive system. Therefore, the important role of thedentist is to recognize oral changes, diagnose them andtreat the consequences of ulcerative colitis and Crohn’sdisease. From this point of view, the inter-departmentalclinical and technical cooperation with the colleaguesfrom gastroenteropatology departments is of particularimportance. We hope that it would facilitate treatment andincrease the quality of life of this category of patients.

Balk J Stom, Vol 15, 2011 Oral Manifestations in Gastrointestinal Disorders 47References1. Calobrisi SD, Mutasim DF, McDonald JS. Pyostomatitisvegetans associated with ulcerative colitis: temporaryclearance with fluocinonide gel and complete remissionafter colectomy. Oral Surg Oral Med Oral Pathol OralRadiol Endod, 1995; 79:452-454.2. Chan SWY, Scully C, Prime SS, et al. Pyostomatitisvegetans: oral manifestation of ulcerative colitis. Oral SurgOral Med Oral Pathol, 1991; 72:689-692.3. Bevenius J. Caries risk in patients with Crohn’s disease: apilot study. Oral Surg Oral Med Oral Pathol, 1988; 65:304-307.4. Greenberg MS, Glick M. Burketova oralna medicina,dijagnoza i lečenje. Zagreb: Medicinska naklada. 2006. (inCroat)5. Ghandorour K, Moneim I. Oral Crohn’s disease with lateintestinal manifestations. Oral Surg Oral Med Oral Pathol,1991; 72:565-567.6. Ficarra G, Cicchi P, Amorosi A, et al. Oral Crohn’s diseaseand pyostomatitis vegetans: an unusual association. OralSurg Oral Med Oral Pathol, 1993; 75:220-224.7. Halme L, Meurman JH, Laine P, et al. Oral findings inpatients with active or inactive Crohn’s disease. Oral SurgOral Med Oral Pathol, 1993; 76:175-181.8. Hansen LS, Silverman SJ, Daniels TE. The differentialdiagnosis of pyostomatitis vegetans and its relation tobowel disease. Oral Surg Oral Med Oral Pathol, 1983;55:363-373.9. Healy CM, Farthing PM, Williams DM, et al. Pyostomatitisvegetans and associated systemic disease: a review andtwo case reports. Oral Surg Oral Med Oral Pathol, 1994;78:323-328.10. Yamada T (ed). Textbook of gastroenterology. Philadelphia:JB Lippincott, 1995.11. Kano Y, Shiohara T, Yagita A, et al. Erythema nodosum,lichen planus and lichen nitidus in Crohn’s disease reportof a case and analysis of T-cell receptor V gene expressionin the cutaneous and intestinal lesions. Dermatology, 1995;190:59-63.12. Malins TJ, Wilson A, Ward-Booth RP. Recurrent buccalspace abscesses: a complication of Crohn’s disease. OralSurg Oral Med Oral Pathol, 1991; 72:19-21.13. Meurmen JH, Halme L, Laine P, et al. Gingival and dentalstatus salivary acidogenetic bacteria, and yeast counts ofpatients with active or inactive Crohn’s disease. Oral SurgOral Med Oral Pathol, 1994; 77:465-468.14. Ming SC, Goldman H (eds). Pathology of thegastrointestinal tract. 2 nd ed. Baltimore: Williams andWilkins, 1998.15. Plauth M, Jeness J, Meyle J. Oral manifestations of Crohn’sdisease: an analysis of 79 cases. J Clin Gastroenterol,1991; 13:29-37.16. Rooney TP. Dental caries prevalence in patients withCrohn’s disease. Oral Surg Oral Med Oral Pathol, 1984;57:623-624.17. Schnitt SJ, Antonioli DA, Jaffe B, et al. Granulomatousinflammation of minor salivary gland ducts: a new oralmanifestation of Crohn’s disease. Hum Pathol, 1987;18:405-407.18. Siegel MA. Oral manifestations of gastrointestinal disease:diagnosis and treatment. In: Bayless TM (ed). Currenttherapy in gastroenterology and liver disease. Burlington(Can): BC Decker, 1989; pp 1-5.19. Sundh B, Emilson CG. Salivary and microbial conditionsand dental health in patients with Crohn’s disease: a 3-yearstudy. Oral Surg Oral Med Oral Pathol, 1989; 67:286-290.20. Sundh B, Johansson I, Emilson GC, et al. Salivaryantimicrobial proteins in patients with Crohn’s disease.Oral Surg Oral Med Oral Pathol, 1993; 76:564-569.21. Ward CS, Dunphy EP, Jagoe WS, et al. Crohn’s diseaselimited to the mouth and anus. J Clin Gastroenterol, 1985;7:516-521.Correspondence and request for offprints to:Mirjana PopovskaVodnjanska 171000 SkopjeFYR MacedoniaE-mail: popovskam2002@yahoo.com

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYRecurrent Atypical Fibroxanthoma in a Patient withScleroderma: Report of a CaseSUMMARYAtypical fibroxanthoma is an uncommon mesenchymal tumour, whichusually has a benign clinical course and an excellent prognosis. Treatmentof choice is wide surgical incision since the possibility of recurrence ishighly correlated to positive tumour margins.We report a case of atypical fibroxanthoma in a female patientsuffering from scleroderma. Despite the aggressive treatment, the tumourrecurred several times. This is the first documented case of atypicalfibroxanthoma occurring a patient with a collagen disorder.Keywords: Fibroxanthoma, atypical; SclerodermaMaria Lazaridou 1 , Lambros Zouloumis 1 ,Konstantinos Kontos 1 , Anastasia Nikolaidou 2 ,Konstantinos Vachtsevanos 21 Aristotle University of Thessaloniki, Greece2 Theageneio Hospital, Thessaloniki, GreeceCASE REPORT (CR)Balk J Stom, 2011; 15:48-51Atypical fibroxanthoma is an uncommon, cutaneousmesenchymal tumour. It usually appears as a solitarynodule or ulcerous nodule on sun-damaged skin of theelderly people. Histologically, an anaplastic activitywith marked cytological atypia, increased number ofmitotic figures and presence of multinucleated giant cellsbelies its usually benign clinical course and excellentprognosis 1,2 .Atypical fibroxanthoma is regarded as a superficial, lessaggressive counterpart of malignant fibrous histiocytoma.These 2 tumours are histologically indistinguishable buttheir clinical presentation differs 3,4 . Atypical fibroxanthomaarises superficially; it is usually confined in the dermis of theactinically damaged skin of the head and neck of the elderly,whereas malignant fibrous histiocytoma arises in deep softtissues of the extremities and in the retro-peritoneum ofyounger people 3 . Moreover, atypical fibroxanthoma hasalmost always a benign clinical course, unlike malignantfibrous histiocytoma, which is characterized by a highincidence of metastasis and a high recurrence rate 1 .The treatment of choice of atypical fibroxanthoma iswide surgical excision, since the possibility of recurrenceis highly correlated to positive tumour margins 5 . Wereport a case of atypical fibroxanthoma in a female patientwho suffered from scleroderma. To our knowledge, thisis the first documented case of atypical fibroxanthomareported in a patient with a collagen disorder.Case ReportA 57-year-old Caucasian woman presented to ourdepartment of Oral and Maxillofacial Surgery with an8-month history of a painless ulcerative pre-auriculartumour measuring 3x3cm. She reported the appearanceof a small nodule 8 months ago which had grownrapidly and become ulcerated. The lesion was fragileand asymptomatic, but due to its cosmetic appearancethe patient had to cover it with a piece of gauze. Therest of the examination was unremarkable with nopalpable cervical adenopathy. The chest film was freeof metastatic lesions, although there was an extendedpulmonary fibrosis due to scleroderma. The patient had asmaller lesion resected from the same area one year ago.The histological examination of this tumour revealed akeratoacanthoma.The patient suffered from scleroderma diagnosed 10years ago, being controlled with Prezolon 5 mg (1x3) andCyclophosphamide 50 mg (1x3). Despite the aggressiveimmunosuppressive therapy, she had developedpulmonary hypertension due to the disease, but she hadno gastrointestinal symptoms. Her medical history alsorevealed moderate hypertension and coronal disease.A punch biopsy of the pre-auricular tumour wasperformed and the patient was initially treated withradiotherapy due to her compromised medical status. Theradiotherapy started immediately because the tumour was

Balk J Stom, Vol 15, 2011 Fibroxanthoma in a Patient with Scleroderma 49growing fast and was clinically diagnosed as a squamouscell carcinoma.The biopsy showed an atypical spindle cellneoplasm, which did not stain with cytokeratin, S-100protein, HMB-45, MelanA and SMA. The tumour washistologically characterized as sarcoma. Radiotherapywas subsequently abandoned. Under general anesthesiaa wide excision of the tumour was performed. Part ofthe superficial temporal fascia and part of the zygomaticarch were also excised (Figs. 1 and 2). The defect wascovered with free skin grafts because the duration of thesurgery should be kept to a minimum due to compromisedmedical status of the patient.The biopsy specimen demonstrated a wellcircumscribed,non-encapsulated tumour localized in thedermis, contiguous with the ulcerated epidermis. The cellswere large, pleomorphic, longitudinal and spindle-shapedwith an abundant eosinophilic cytoplasm and frequentmitotic figures (Fig. 3). The margins of the specimen werenot infiltrated and the nearest distance from the marginsof the tumour was 1cm. Immunohistochemical stainingof proliferative cells was strongly positive for vimentin,S-100 (Fig. 4) and CD68, but much more weakly positivefor cytokeratin 8/18 and smooth muscle actin (SMA).Tumour cells did not show any reactivity with HMB45, MelanA, KerAE1/AE3, Ker LMW, KerHMW,Ker7, Ker20, EMA and CD34. The diagnosis of atypicalfibroxanthoma was established.2 months later the patient presented to ourdepartment with 2 nodules located at the margins of theskin graft. Excision of one nodule under local anesthesiawas performed. The histological examination of thespecimen revealed a recurrence of the primary tumour.The next month the patient underwent a wide excisionof the nodules under general anesthesia and the defectwas again reconstructed with free skin grafts (Figs. 5and 6). Once again biopsy was indicative of an atypicalfibroxanthoma. The patient has been closely followed for18 months and she has shown no evidence of a recurrenceor distant metastasis. The patient eventually died from thesystemic disease.Figure 1. The patient after the wide removal of the lesion. Part of thezygomatic arch was also excised since the initial diagnosis of thelesion was sarcomaFigure 3. Biopsy of the tumour shows atypical fibroxanthoma abuttingthe epidermis (H&E, orig. magn. x 10)Figure 2. The excised specimen. The appearance of the lesion is similarto the appearance of a squamous cell carcinomaFigure 4. Positive staining of the tumour cells with S-100 protein(orig. magn. x10)

50 Maria Lazaridou et al. Balk J Stom, Vol 15, 2011Figure 5. Recurrence of the tumour can be seen in the periphery of theskin graftFigure 6. The operative field following the wide excision of the tumour.A skin graft was again used for the reconstruction of the defectDiscussionAtypical fibroxanthoma was first reported by Helwigin 1963 6 . He described a solitary spindle cell neoplasmarising on the sun damaged skin of an elderly patient.Atypical fibroxanthoma begins as a small, firmand solitary nodule, which may be ulcerated (36%) orbleeding (26%) 7 . It usually grows rapidly, but remainsasymptomatic. Some nodules have a pigmentedappearance due to hemosiderin deposits. In this case,differential diagnosis from melanomas may be difficult.Atypical fibroxanthoma usually appears on the head andneck of elderly people with a mean age of 71-86 years 5 ,and less often on the trunk and extremities of youngerpeople. Very rarely it can affect the eye 8 . Our patient was57 years old and presented with a large painless ulcer onthe pre-auricular region.The pathogenesis of atypical fibroxanthoma is stillunknown, although many predisposing factors havebeen reported. Ultraviolet radiation seems to play amajor role by inducing p53 mutations at dipyrimidinesites 9 . Other predisposing factors include trauma,burns, radiotherapy, post-cardiac and post-renaltransplantation and immunosuppressive therapy 10,11 .A high incidence of cutaneous malignancies has beenreported in transplant recipients, which is attributed tothe need of lifelong maintenance immunosuppressivetherapy 12 . Immunosuppressive therapy impairs the tumoursurveillance mechanism of lymphocytes, disrupting thebalance between tumourigenesis and tumourilysis 13 .Immunosuppressive therapy and perhaps the initialradiation therapy may have contributed to the presence ofmultiple recurrences in our patient despite wide surgicalexcision.The diagnosis of atypical fibroxanthoma is basedon histological examination and immunohistochemistry,since its clinical course and appearance leads to avariety of preoperative diagnosis, such as squamous cellcarcinoma, basal cell carcinoma, pyogenic granuloma,melanoma, dermatosarcoma, cutaneous lymphoma andmalignant fibrous histiocytoma 5,10 .Immunohistochemical studies are helpful inestablishing the diagnosis and in differentiating atypicalfibroxanthoma from other cutaneous malignancies.Atypical fibroxanthoma stains positively with vimentinonly, and shows variable reaction with a1-antitrypsin,factor XII and smooth muscle actin (SMA) 13,14 .Squamous and spindle cell carcinoma stain positivelywith cytokeratin and epithelial membrane antigen,whereas atypical fibroxanthoma does not stain with thesemarkers 15 . Moreover, atypical fibroxanthoma does notstain with S-100 protein and HMB-45, which are usuallypositive in melanomas 16 . However, the absence of positivereaction with these markers can not confirm the diagnosisof atypical fibroxanthoma, because in some cases spindlecell carcinomas may not stain with cytokeratin andmelanomas may not stain with S-100 protein 5 . In our case,the tumour stained with vimentin and there was a mildreactivity with SMA, which has been reported before 5 .Interestingly, in our case, there was a strong reactionwith S-100 protein, which has not been reported before.It seems that reactivity with S-100 protein cannot excludethe diagnosis of atypical fibroxanthoma.Immunohistochemical studies are also used in orderto differentiate atypical fibroxanthoma from its malignantcounterpart, namely malignant fibrous histiocytoma.LN-2 is a 35kDa protein mainly expressed on the nuclearmembrane of B-lymphocytes. This protein has beenconsistently identified in malignant fibrous histiocytomasbut not in atypical fibroxanthomas 17 . It seems that LN-2 isa reliable marker in distinguishing between the 2 lesions.

Balk J Stom, Vol 15, 2011 Fibroxanthoma in a Patient with Scleroderma 51The treatment of choice is wide surgical excisionwith at least 1 cm margin 18 . We absolutely agree withGonzalez-Garcia et al 5 that curettage and cryosurgery arenever indicated since they can lead to a remarkably higherrecurrence rate. Mohs microsurgery is a conservativeapproach that should only be reserved for tumoursadjacent to important anatomic structures. Radiotherapyis advocated by some authors, but some others suggestthat following radiotherapy the tumour may show a moreaggressive clinical course 7,19 . We chose to treat our patientwith wide surgical excision despite her compromisedmedical status.Atypical fibroxanthomas are known to recur in about12% of cases 20 , with a mean time of 2 years betweensurgery and recurrence. Recurrences are usually aconsequence of inadequate surgical margins 7,21 . However,multiple recurrences occurred in our patient despite thewide excision of the primary tumour, suggesting thatimmunosuppressive therapy and radiotherapy might alsoplay an important role in clinical course of the tumour.The existence of occasional recurrences advocates for aclose follow-up of the patient, at least for the first 2 yearsfollowing surgery.Although extremely uncommon, metastatic spreadhas been described by some authors 6,22 . Metastasis isusually associated with large tumours with deep vascularinvasion and with immunocompromised hosts. Accordingto Helwig 6 , metastasis usually occurs within 12 to 18months. Metastasis from atypical fibroxanthoma is notalways fatal, since surgical control or even cure may alsohappen.References1. Fretzin DF, Helwig EB. Atypical fibroxanthoma of the skin:A clinicopathologic study of 140 cases. Cancer, 1973;31:1541-1552.2. Kroe DJ, Pitcock JA. Atypical fibroxanthoma of the skin:Report of ten cases. Am J Clin Pathol, 1969; 51(4):487-492.3. Weiss SW, Enzinger FM. Malignant fibrous histiocytoma: Ananalysis of 200 cases. Cancer, 1978; 41:2250-2266.4. Kempson RL, Kryiakos M. Fibroxanthosarcoma of the softtissues: A type of malignant fibrous histiocytoma. Cancer,1972; 29:971-976.5. Gonzalez-Garcia R, Nam-Cha SH, Munoz-Guerra MF, Sastre-Perez J, Rodriguez-Campo FJ, Naval-Gias L. Atypicalfibroxanthoma of the head and neck: Report of 5 cases. JOral Maxillofac Surg, 2007; 65:526-531.6. Helwig EB. Tumor Seminar. Tex State J Med, 1963; 59:664-667.7. Starink T, Hausman R, Van Delden L, Neering H. Atypicalfibroxanthoma of the skin. Presentation of 5 cases andreview of the literature. Br J Dermatol, 1977; 97:167-177.8. Engelbrecht NE, Ford JG, White WL, Yeatts RP. Combinedintraepithelial squamous neoplasia and atypicalfibroxanthoma of the cornea and limbus. Am J Opthalmol,2000; 129:94-96.9. Dei Tos AP, Maestro R, Doglioni C, Gasparotto D, BoiocchiM, Laurino L, et al. Ultra-violet-induced p53 mutationsinatypical fibroxanthoma. Am J Pathol, 1994; 145:11-17.10. Ferri E, Iaderosa GA, Armato E. Atypical fibroxanthoma ofthe external ear in a cardiac transplant recipient: Case reportand the causal role of the immunosuppressive therapy. AurisNasus Larynx, 2008; 35:260-263.11. Kanitakis J, Euvrard S, Montazeri A, Garnier JL, Faure M,Claudy A. Atypical fibroxanthoma in a renal graft recipient.J Am Acad Dermatol, 1996; 35:262-264.12. Veness MJ. Aggressive skin cancer in a cardiac transplantrecipient. Australia Radiol, 1997; 41(4):363-366.13. Longacre TA, Smoller BR, Rouse RV. Atypicalfibroxanthoma. Multiple histologic profiles. Am J SurgPathol, 1993; 17:1199.14. Kindblom LC, Jabobsen GK, Jacobsen M.Immunohistochemical investigations of tumors of supposedfibroplastic histiocytic origin. Hum Pathol, 1982; 13:834-840.15. Rice CD, Gross DJ, Dinehart SM, Brown HH. Atypicalfibroxanthoma of the eyelid and cheek. Arch Ophthalmol,1991; 109:922-923.16. Weiss SW, Langloss JM, Enzinger FM. Value of S-100protein in the diagnosis of soft tissue tumors with particularreference to benign and malignant Schwann cell tumors.Lab Invest, 1983; 49:299-308.17. Lazova R, Moynes R, May D, Scott G. LN-2: A marker todistinguish atypical fibroxanthoma from malignant fibroushistiocytoma. Cancer, 1997; 79:2115-2124.18. Stadler FJ, Scott GA, Brown MD. Malignant fibrous tumors.Semin Cutan Med Surg, 1998; 17:141-152.19. Fish FS. Soft tissue sarcomas in dermatology. DermatolSurg, 1996; 22:268.20. Davis JL, Randle HW, Zalla MJ, Roenigk RK, BrodlandDG. Comparison of Mohs micrographic surgery and wideexcision for the treatment of atypical fibroxanthoma.Dermatol Surg, 1997; 23:105-110.21. Helwig EB, May D. Atypical fibroxanthoma of the skin withmetastasis. Cancer, 1986; 57:368-376.22. Kemp JD, Stenn KS, Arons M, Fischer J. Metastasizingatypical fibroxanthoma. Coexistence with chroniclymphocytic leukemia. Arch Dermatol, 1978; 114:1533.23. Giuffrida TJ, Kligora CJ, Goldstein GD. Localisedcutaneous metastasis from an atypical fibroxanthoma.Dermatol Surg, 2004; 30:1561.Correspondence and request for offprints to:Mrs Maria Lazaridou, DDS,MDAristotle University of ThessalonikiIoannou Xatzoudi 9, Neapoli56727, ThessalonikiGreece

BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141STOMATOLOGICAL SOCIETYUnusual Penetrating Metallic Foreign Bodies InjuredMaxillofacial and Orbital Region with Minimal DamageSUMMARYPenetrating injuries during work accidents represent a rare butcomplex variety of craniofacial trauma. Generally, the penetrating materialis stiff enough to cross through different anatomic structures and can causean impressive problem for the patient. On the arrival at the emergencydepartment, clinical situation of the patient must be evaluated to decide thetype of examination. Functional and cosmetic problems must be taken underconsideration and an immediate decision must be taken by the specialists fora rapid surgical treatment. The surgical approach depends on the position ofa foreign body.2 penetrating head injuries during work accident are presented, thepre- and intra-operative approach described and the particularities of thesecases are pointed out.Keywords: Penetrating Trauma; Metallic Foreign BodyA. Ntomouchtsis 1 , D. Maggoudi 2 , H. Panidou 3 ,A. Kondylidou 4 , K. Antoniades 11 Papanikolaou HospitalDepartment of Oral and Maxillofacial Surgery2 Theagenion HospitalDepartment of Oral and Maxillofacial Surgery3 Papanikolaou HospitalDepartment of Ophthalmology4 Aristotle UniversityDepartment of Dentoalveolar SurgeryOral Implantology and RadiologyThessaloniki, GreeceCASE REPORT (CR)Balk J Stom, 2011; 15:52-56IntroductionAccording to Agrillo et al 1 , a good cosmetic andfunctional outcome of penetrating injuries depend on 4main factors: (1) the extent of the traumatic injury; (2)clinical condition and age of the patient; (3) diagnosticaccuracy; and (4) the amount of time that has passedbetween trauma and operation. First aid for traumapatients requires their transportation to an emergencydepartment by qualified personnel. After this, amultidisciplinary approach is recommended, taking intoaccount all the anatomic structures involved and planningthe most suitable surgical strategy 1 .In order to assess the exact extent of themaxillofacial injuries, it is necessary to perform someexaminations, such as standard skull radiographs in 4projections, 2-dimensional computed tomography (CT)scans in axial and coronal projections, or 3-dimensionalCT scans of the maxillofacial area 2 . Preoperativeknowledge of the shape of the foreign body andits relationship to the surrounding structures usingappropriate imaging modalities is imperative 3 .Report of CasesCase AA 52-year-old farmer sustained an injury of hisleft eye during outdoor activity. After the injury, he wasexamined in the nearby hospital of his town and thenreferred to Papanikolaou Hospital of Thessaloniki nearly48 hours after being injured, under broad-spectrumantibiotic coverage and anti-tetanus prophylaxis.At the time of examination, he had hyposphagma,slight oedema around the left orbit, blepharoptosis anda dermal injury of the left upper eyelid. On furtherexamination by ophthalmologists, the left eye had peribulbaroedema, hyphema, intravitreous haemorrhage andreduction of visual acuity to counting fingers at 1 m. TheIOP was 15 mmHg. A slit lamps examination disclosediridoschesis at 6 o’clock. ENT examination revealed noabnormality of the nasal cavity. There was no systemicinvolvement.X-rays at the time of the injury and the requestedposttraumatic computer tomography revealed a metalbody with intra- and extra-conal extension, in immediatecontact to the left frontal, ethmoidal and nasal bones. The

Balk J Stom, Vol 15, 2011 Penetrating Injuries of the Maxillofacial and Orbital Regions 53distal part of the foreign body ended in the left superiorconcha. The optic nerve appeared normal. There wereno signs of any injures of the globe or any fractures orintracranial involvement (Figs.1-3).It was decided to explore the wound under generalanaesthesia. Through the entry wound the metallic bodywas found to be embedded in the medial wall of the orbit.On manipulation, the body showed slight movement andappeared to be fixed to deeper structures. In order to avoidfurther injuries of the orbital contents, with mild manoeuvresand under direct visual contact, the entry wound wasextending and the foreign body removed (Fig. 4).The patient recovered uneventfully. 3 months laterthe ptosis improved. New ophthalmologic examinationrevealed visual acuity of 3/10 and IOP of 9 mmHg.Fundus examination showed small hemorrhage near theoptic disc.Figure 3.Figure 1.Figure 4.Figure 2.Case BA 57-old man was brought to the emergencydepartment after a work accident. He was slightlyconfused, but able to answer to some questions. He hada metal foreign body of irregular shape embedded in hisleft mid-face, in the area of the left sinus. He presentedsoft tissue injuries of the lips and the chin, dermal lossat the tip of the nose, 3 broken teeth in the front of themandible and burning injuries on the neck, the cheekand the forehead (Figs. 5 and 6). After the evaluationby specialists of other disciplines and since there wereno signs of any injury of vital anatomic structures,

54 A. Ntomouchtsis et al. Balk J Stom, Vol 15, 2011radiographs (Figs. 7-9) and no computer tomography,were taken to estimate the exact position of the metalbody, because time was more critical in view of thepatient distress.The patient was transferred directly to surgery inthe operating room for careful removal under generalanaesthesia, with all facilities available in the event of anycomplication. A metal body of irregular shape and size 8cm x 5 cm was removed from the left side of the patient’sface (Fig. 10), along with a high number of small piecesof plastic which were also embedded in the trauma areaand seemed to have caused the burning injuries of theface. There was no intra operative haemorrhage or othercomplications.The front wall of the left sinus, along with thezygomaticomaxillary buttress was completely destroyedand there was no possibility of reconstruction. An antrorhinostomawas performed at the meatus inferior. Aprimary plastic closure of the face injuries was achieved.Antibiotic cover with cephalosporine secondgeneration, intra- and post-operatively, for 14 days wasrecommended. Our patient recovered uneventfully andhad no recurrent maxillary sinusitis or nasal obstruction.Figure 7.Figure 5.Figure 8.Figure 6. Figure 9.

Balk J Stom, Vol 15, 2011 Penetrating Injuries of the Maxillofacial and Orbital Regions 55DiscussionFigure 10.Foreign bodies can cause injuries of the orbitand extensive damage to the surrounding structures 4 .They may give rise to severe orbital complications andusually inorganic foreign bodies cause visual loss ororbital complications from direct trauma 5-8 . A retainedmetallic orbital foreign body may cause a variety ofsigns, symptoms, and clinical findings, based on its size,location and composition 9,10 . There have been describedcases with pyogenic infection, periostitis and fistulaformation. There may also be a risk of gas gangreneformation, development of tetanus, chronic sinusitis,when a sinus is involved, meningeal infection or cerebralabscess formation if cranial cavity is involved 11 . Evensight-threatening complications have been described 12 .Complications can appear long time after the injury 13 . Inthe case A, the 24-month follow-up period was uneventful.CT scan is the standard diagnostic test, becauseit demonstrates most foreign bodies and it is safe in thepresence of metallic bodies 14,15 . Recent reports haveshown helical CT scans to be as accurate as conventionalCT scans, while reducing the radiation exposure for thepatient 16,17 .The surgical approach used, depend on the positionof the foreign body. Most commonly, this is through theentry wound. Posteriorly located foreign bodies have anincreased risk of motility disturbances or optic neuropathyafter surgical removal 18 , whereas anteriorly placed foreignbodies are more easily removed 19-22 .In the case B, the examination was performed withsimple radiographs, because of the metallic nature of theforeign body and the possible artefacts in other imagingprocedures 23 , the urgency of the situation and becauseit was thought that any other method, like CT, wouldnot add anything important for the planed surgicalintervention.The proposed algorithms for the approach ofpenetrating injuries of the face 24,25 , after the exclusion ofany life threatening situation for the patient and with nocomplication from the orbital area, had no importancein the case A, because of the unique shape and size ofthe embedded foreign body. In the second case, theforeign body lost kinetic energy during the impact withthe maxillary region, saving, in this way, the orbitalstructures and the brain. Since there was no possibilityof osteosynthesis in the maxilla because of the extensivedestruction of the bone structures of the area, we decideda double approach from intraoral and through the facetrauma that left behind the metal body. A Caldwell- Lucoperation was unnecessary. The metallic object wascarefully removed because of the danger of a majorhaemorrhage and to avoid secondary iatrogenic injuryduring removal.Injury to the paranasal sinuses should beappropriately treated to decrease the risk of recurrentsinusitis and mucocele formation. Wound tracts shouldbe thoroughly irrigated and devitalized tissue debrided.Intraoral wounds should be closed early when possible.Prophylactic antibiotic coverage and tetanus toxoidbooster should be given. Long term follow-up isrecommended. Sometimes further imaging studies arenecessary to evaluate delayed traumatic injuries to cranialnerves and paranasal sinuses 26 .Although seldom fatal, the treatment of penetratingcraniofacial injuries requires a methodical approachbecause of the possible immediate complications that mayfollow the removal of the foreign body. The therapeuticrecord should be based on a multidisciplinary approach toobtain the best aesthetic and functional results. It must beemphasised that the prognosis of every injury by a foreignbody is strongly influenced by the nature and the locationof the injury and the extent of initial damage.References1. Agrillo A, Sassano P, Mustazza MC, Filiaci F. Complex-Type Penetrating Injuries of Craniomaxillofacial Region. JCraniofac Surg, 2006; 17(3):442-446.2. Gasparini G,Brunelli A, Rivaroli A, Lattanzi A, De PonteFS. Maxillofacial Traumas. J Craniofac Surg, 2002;13(5):645-649.3. Boahene KO, Thompson DM, Schulte DL, Brissett AE.Craniofacial Metal Bolt Injury: An Unusual Mechanism. JTrauma, 2004; 56:716-719.4. Peyman GA, Sanders DR, Goldberg MF. Principles andPractice of Ophthalmology. Vol III. 1st Ed. WB Saunders,1981; p 2466.

56 A. Ntomouchtsis et al. Balk J Stom, Vol 15, 20115. Macrae JA. Diagnosis and management of a wooden orbitalforeign body: case report. Br J Ophthalmol, 1979; 63:848-851.6. Charteris DG. Posterior penetrating injury of the orbit withretained foreign body. Br J Ophthalmol, 1988; 72:432-433.7. Wang WJ, Li CX, Sebag J, Ni C. Orbital fistula. Causes andtreatment of 20 cases. Arch Ophthalmol, 1983; 101:1721-1723.8. Lustrin ES, Brown JH, Novelline R, Weber AL. Radiologicassessment of trauma and foreign bodies of the eye andorbit. Neuroimaging Clin North Am, 1996; 6:219-237.9. Cooper W, Haik BG, Brazzo BG. Management of orbitalforeign bodies. In: Nesi FA, Levine MR, Lisman RD (eds).Smith’s Ophthalmic Plastic and Reconstructive Surgery. St.Louis: Mosby; 1998; pp 260-269.10. Spoor TC. Penetrating orbital injuries. In: Spoor TC, NestFA (eds). Management of Ocular, Orbital, and AdnexalTrauma. New York: Raven; 1988; pp 271-292.11. Vander JF, Nelson CC. Penetrating orbital injury withcavernous sinus involvement. Ophthalmic Surg, 1988;19:328-330.12. Duke-Elder S, MacFaul PA. Intraocular Foreign bodies. In:Duke-Elder S (ed). System of Ophthalmology. Vol XIV, PartI. London: Henry Kimpton, 1972; p 481.13. Dimitrakopoulos I, Lazaridis N, Karakasis D. Unusualretained foreign body in the orbit. J Oral Maxillofac Surg,1991; 49:420-421.14. Fulcher TP, McNab AA, Sullivan TJ. Clinical features andmanagement of intraorbital foreign bodies. Ophthalmology,2002; 109:494-500.15. Thomaidis V, Mangoudi D, Lazaridis N. An unusual case ofa low velocity bullet lodged in the parotid gland. Greek JOral Max Fac Surg, 1999; 14:1-5.16. Lakits A, Prokesch R, Scholda C, Bankier A. Orbital helicalcomputed tomography in the diagnosis and management ofeye trauma. Ophthalmology, 1999; 106:2330-2335.17. Lakits A, Prokesch R, Scholda C, et al. Helical andconventional CT in the imaging of metallic foreign bodies inthe orbit. Acta Ophthalmol Scand, 2000; 78:79-83.18. In-Young Chung, Seong-Wook Seo, Yong-Seop Han, EurieKim, Jim-Myung Jung. Penetrating Retrobulbar OrbitalForeign Body: A Transcranial Approach. Yonsei MedicalJournal, 2007; 48(2):328-330.19. Finkelstein M, Legmann A, Rubin PAD. Projectilemetallic foreign bodies in the orbit. A retrospective studyof epidemiologic factors, management, and outcomes.Ophthalmology, 1997; 104:96-103.20. Michon J, Liu D. Intraorbital foreign bodies. SeminOphthalmol, 1994; 9:193-199.21. Holt GR, Holt JE. Management of orbital trauma andforeign bodies. Otolaryngol Clin North Am, 1988; 21:35-52.22. Gönül E, Akbörü M, Izci Y, Timurkaynak E. Orbital foreignbodies after penetrating gunshot wounds: retrospectiveanalysis of 22 cases and clinical review. Minim InvasNeurosurg, 1999; 42:207-211.23. Fuller DG, Hutton WL. Prediction of postoperative vision ineyes with severe trauma. Retina, 1990; 10(Suppl 1):S20-34.24. Gussack GS, Jurkovich GJ. Penetrating facial trauma: amanagement plan. South Med J, 1988; 81:297-302.25. Dolin J, Scalea T, Mannor L, Sclafani S, Trooskin S. Themanagement of gunshot wounds to the face. J Trauma,1992; 33:508-515.26. Boahene KO, Thompson DM, Schulte DL, Brissett AE.Craniofacial Metal Bolt Injury: An Unusual Mechanism. JTrauma, 2004; 56:716-719.Correspondence and request for offprints to:A. NtomouchtsisPapanikolaou HospitalDepartment of Oral and Maxillofacial SurgeryThessaloniki, Grece

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Int J OralMaxillofac Surg, 1995; 24:417-426.2. Sternbach RA. Pain patients - traits and treatment. New York,London, Toronto, Sydney, San Francisko: Academic Press, 1974;pp 20-30.3. Koulourides T, Feagin F, Pigman W. Experimental changes inenamel mineral density. In: Harris RS (ed). Art and Science ofDental Caries Research. New York: Academic Press, 1968, pp355-378.