scientific thought and clinical practice - edit. dejan markovic

Scientific Thought and Clinical Practice

10 years of BaSS

Editor- in –Chief:Dejan Marković, B.D.S, M.D.S, PhD Assistant ProfesorClinic for Pediatric and Preventive DentistryFavulty of Dentistry, Unevirsity of Belgrade

Technical Editors:Ana Pucar, B.D.S, M.D.STamara Peric, B.D.S

Reviewers:

Dragan Beloica,Faculty of Dentistry, Belgrade, Serbia and MontenegroNicola Atanasov,Faculty of Stomatology, Sofia, BulgariaStephen Flint,Dublin Dental Hospital, IrelandHakki Tanyeri,Faculty of Dentistry, Istanbul, TurkeyHalid Sulejmanagić,Faculty of Dental Medicine, Sarajevo, Bosnia and HerzegovinaAbel Garcia Garcia,Complejo Hospitalario Universitario de Santiago, Santiago de Compostela,SpainPredrag Charles Lekic,Faculty of Dentistry, Manitoba, CanadaJelena Milašin ,

Sedin Kobašlija,Faculty of Dental Medicine, Sarajevo, Bosnia and HerzegovinaSlavoljub Živković,Faculty of Dentistry, Belgrade, Serbia and Montenegro

Faculty of Dentistry, Belgrade, Serbia and Montenegro

Contents

Editorial 5

Kimio Abe Jiang Teng Kazunar Ishibashi ToshihiroNishiura Anka Letic-Gavrilović

Secretion of Salivary Cystatin S by the Submandibular Glands of Rats Following Various Dental Treatment, Chronic Treatment With Isoproterenol and in Resistance Against Plaque Formation

6

D. Cenić-MiloševićP. Turčinović

Meditators Involved in Transmission and Modulation of Chronic Pain

24

Elena Kršljak Zoran Stajčić

Autotomy Phenomenon: Experimental Model of Neuralgic Pain

36

Carel L. Davidson Glass-Ionomer Cements, the Interesting Alternative For Resin-Based Composites

45

John W. Nicholson Glass-Ionomer Cements in Dentistry: the Current Position

58

Zoran R. Vulicević Ivana Davitkov, Dejan Marković, Aleksandar Todorović

Adhesive Dentistry :Future From the Past 69

Momir CarevićMarko Vulović,

National Program for Prevention of Oral Diseases Effect on Caries Distribution in Population of Serbia 1996 - 2001

89

N.Markova E.Ilieva

Epidemiology and Predictors of Early Childhood Caries / ECC /

97

Lutz Stösser Marcus Dell, Roswitha Heinrich-Weltzien

Bacterial and Enzymatic Tests in Caries Risk Assessment

106

Marko VulovićMomir Carević,

Public Health Issues Concerning Oral Health Care in Former Socialist Countries

119

M. Carčev H. Petanovski S. Carčeva

Replanation of Traumatically Extrated Teeth 126

Nurcan Buduneli Füsun Ünlü

Dental Management Ofeosinophilic Granuloma of Bone

136

Luigi Checchi Giulio Alessandri Bonetti Michele Bendandi Ana Pucar Marco Montevecchi

Orthodontic Extraction: the Extraction of the Third Molars in Close Proximity to the Mandibular Canal by an Orthodontic-Surgical Approach

142

Z. StajčićLj. Stojčev-Stajčić

Aesthetic Consideration in Oral and Maxillofacial Surgery

151

Ljubomir Todorović Chronic Orofacial Pain :Diagnostic and Therapeutic Challenge

159

Luigi Checchi Marco Montevecchi Monica Mele Giovanni Zucchelli

Treatment of Gingival Recession With Bilaminar Tehniquesthe Coronally Positioned Flap With Connective Tissue Graft

175

U.K.Gursoy I. Marakoglu

Densitometric Analysis in Periodontology 189

Vojislav Leković Zoran Aleksić,

Recent Advances in Regenerative Periodontal Therapy- a Combination of Autogenous Bone Grafting and Enamel Matrix Proteins

198

M. Ömer Görduysus Ümit Acer

Deceptiveness and Limitations of Roentgenograms in Endodontics; A Comparative Study With Radiovisiography and computerized Tomography

211

Darinka Stanišić-Sinobad Slobodan Dodić,

Possibilities of Occlusal Therapy in Management of Craniomandibular Disorders

222

Marija Stevanović Evaluation After Er:Yag Laser Application in Enamel, Dentin and Pulp

243

Dear colleagues,

the visionar idea of uniting Balkan dentists around scientific and professional progress will be completed by their 10th anniversary congress, this year. After ten years, we can conclude that the initial aim of founders, and also of those who have joined later, to improve dental profession in Balkan countries through vivid exchange of scientific and professional advances, is now fulfilled. More than ten thousands papers presented and many more participants on Balkan congresses during the last decade have shown strength and significance of scientific efforts Balkan dentists, their friends and co-workers from all over the world have made, and have underlined undoubted contribution to improvements in contemporary dentistry.

Lectures upon invitation of distinguished world scientists, as well as of outstanding lecturers from Balkan scientific institutions, have broaden horizons and contributed to professional progressing of their entire audience. The ambition of the 10th BaSS congress organizers was to refresh memories on previous gatherings and knowledges achieved, by publishing chosen lectures upon invitation.

Content of this monograph is only a part of more than a hundred presentations. Authors have kindly replied the invitation and updated their papers with the latest scientific findings. We hope that other invited lecturers who were not able to participate in this volume will contribute to the scientific development and dental profession in Balkan region and broader, by publishing their papers in our subsequent issue, until the following Congress.

Editor Prof.dr Dejan Marković


10 years of BaSS

Prof.dr Dejane Marković

SECRETION OF SALIVARY CYSTATIN S BY THE SUBMANDIBULAR GLANDS OF RATS FOLLOWING VARIOUS DENTAL TREATMENT, CHRONIC TREATMENT WITH ISOPROTERENOL AND IN RESISTANCE AGAINST PLAQUE FORMATION

Kimio Abe 1 Jiang Teng Kazunar Ishibashi Toshihiro Nishiura Anka Letic-Gavrilović

1Section of Biochemistry, Department of Functional Bioscience, Fukuoka Dental College, Japan


10 years of BaSS

This work was supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education in Japan

2

2 International Clinic for Neo-Organs, Roma, Italy

Summary Salivary cystatin S was first discovered on the polyacrylamide gel as the large mobile (LM) protein with a relatively high electrophoretic mobility secreted by the submandibular glands of rats treated with chronic isoproterenol injections. After the LM protein was cloned and sequenced the cDNA, it was identified as a salivary cystatin S belonging to family 2 of the cystatin superfamily. Secretion of salivary cystatin S by the salivary glands was strongly associated with various dental treatment such as repeated amputation of the lower incisor teeth and orthodontic appliances such as an incisal bite plane and for the lateral expansion. In addition, induction and/or secretion of salivary cystatin S and the expression of its mRNA were dramatically observed in the submandibular glands of the plaque-resistant rats. Following various dental treatment the secretory functions of the salivary glands were significantly varied and salivary cystatin S was characteristically induced in the submandibular glands and secreted into the oral cavity. Therefore, salivary cystatin S could probably play important roles to protect oral hard and soft tissues from various invaders. Key words : Salivary cystatin S, Plaque-resistant rat, Chronical isoproterenol injection, Orthodontic appliances, Incisor amputation Introduction It is well-known that the secretory functions may drastically be changed and salivary cystatin S is characteristically synthesized in the salivary glands of rats following chronic treatment with isoproterenol (IPR), repeated amputation of the lower incisor teeth, orthodontic treatment and intake of food including cysteine protease1-9 . In addition, plaque-resistant rats form virtually no plaque and do not develop gingivitis under the same dietary conditions but dramatically induce salivary cystatin S in saliva, the salivary glands and gingiva10, whereas plaque-susceptible rats with naturally occurring gingivitis, heavy plaque formation and marked periodontal pockets after being fed with commercially available powder chow 11,12, and have been registered as an animal model for gingivitis13, do not induce any salivary cystatin S in the salivary glands. Moreover, several investigators14-16 stated that the level of salivary cystatin S in whole saliva of periodontal patients was significantly less than that in whole saliva of healthy subjects. The present study was thus designed to review changes of the secretory functions throughout a series of our works, especially for induction, synthesis and/or secretion of salivary cystatin S by the salivary glands subjected to various


dental treatment, chronic treatment with IPR and in resistance against plaque formation. Materials and Methods 1. Saliva collection Young(1 to 8 weeks of age) and adult (12-52 weeks but mainly 12 weeks of ages ) male and female Sprague-Dawley (SD) rats were used in each experimental group. The plaque-resistant and plaque-susceptible rats originally generated from a Wistar-Kyoto strain were also distributed into each group. A l2-h light-dark cycle was maintained in the room by an automatic timing device with lights turned off at l8 h and the animals had ad libitum access to rat chow (Oriental Kobokogyo Co., Tokyo) and water. Ethical clearance for these studies was approved by the Asahi and Fukuoka Dental Colleges’ Animal Ethics Committee. The rats were fasted from l700 h to 0900 h prior to the collection of saliva, then anesthetized with sodium pentobarbital (Nembutal, 50 mg/kg body wt., i.p.), secured in the supine position with tape and tracheotomized to facilitate respiration during the saliva collection. Both submandibular ducts using thin and intramedic polyethylene tubes (PE 10, Beckton Dickinson) were intraorally cannulated by the method17. The submandibular glands did not secrete any saliva spontaneously in the absence of stimulation. With the exception of an initial drop, which was discarded, submandibular saliva was collected into microcentrifuge tubes kept in ice, and the volumes were estimated by weight, assuming the specific gravity of saliva to be l.0. IPR (30 mg/kg), physalaemin (0.02 mg/kg), bethanechol (1 mg/kg), methoxamine (6 mg/kg) and/or phenylephrine (6 mg/kg), and oxymetazoline (5 mg/kg) and/or clonidine (10 mg/kg) dissolved in isotonic saline were employed i.p. or i.v. as secretagogues suitable for five different types of receptors18. After the saliva collection, the salivary glands were weighed to estimate salivary flow rate and to extract several compositions including nucleic acids. 2. Various dental treatment An incisal bite plane constructed from cold-cured methyl methacrylate resin was used to both upper incisor teeth with the rats. A thin metal plate was inserted into the bite plane4,19 as seen in Fig. 1. An orthodontic appliance for upper incisor separation was also constructed from 0.016-inch wire with an open helical loop and fixed with a cold-cured methyl methacrylate to both the left and right maxillary central incisors of rats under anesthesia6. Thereafter, the

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orthodontic appliances were observed and modified if necessary every two days for 4 weeks.

Fig. 1 Lateral X-ray of a rat with an incisal bite plane in position. The white line between the teeth is the thin metal plate.

3. Repeated amputation of the lower incisors The lower incisors of rats in the experimental group were amputated under ether induced anesthesia at 3- or 4-day intervals for about 28 days. At 3, 7, 14 and 28 days after the repeated amputation the animals were used to collect submandibular and parotid saliva, extracts of three major salivary glands and the nucleic acids3.

4. Chronic treatment with IPR For chronic treatment with IPR-HCl, the drug (4 mg/kg or mainly 30 mg/kg) was administered i.p. once or twice a day for 4 or 6 days consecutively in the experimental group, while the control rats were just given sterile saline2,8.

5. Saliva, extracts and sera analyses Saliva samples were analyzed for total protein by the method20 with casein as a standard and then were kept frozen at -20 C until lyophilization could be carried out. After reconstitution of the lyophilized saliva, l5 % native polyacrylamide gel electrophoresis was carried out21. The polyacrylamide gels were stained with Wool Fast Blue BL22. The salivary cystatin S concentrations in submandibular saliva, sera, and the extracts of the submandibular glands and


gingiva were measured with ELISA23, 24. The band of salivary cystatin S was also determined by the Western blotting method25, using a polyclonal antibody against purified salivary cystatin S. The submandibular glands and gingiva kept at –80 were homogenized and then the homogenates were centrifuged at 105,000 x g for 1 h at 4 C to obtain their extracts. Sera were collected from the coagulated blood by centrifugation at 10,000 x g for 20 min at 4 C.

6. Antibody production to salivary cystatin S and its purification In brief, salivary cystatin S was purified by only two steps of native polyacrylamide gel electrophoresis and Immobiline-Canal isoelectric focusing and then a polyclonal antibody against this purified sample was evoked with an equal amount of Freund's complete adjuvant8, This polyclonal antibody is specific to the rat salivary cystatin S-3 but can react its S-l and S-2 with high homology separated from submandibular saliva of rats chronically treated with IPR8. The salivary cystatin S in submandibular saliva of plaque-resistant rats and Wistar rats subjected to chronic treatment with IPR for 4 days was also purified and antibodies against it were evoked by the method8,24 using two male white rabbits (2.5 kg). The IgG fraction was prepared by Affi-gel protein A column chromatography. Double immunodiffusion analysis was also performed on 1.2 % agarose gel.

7. Estimation of the nucleic acids and RNA-p Some salivary glands of the different groups of rats were studied histologically, and others were analyzed for DNA, RNA and RNA-p contents at 3, 7, 14, 21 and 28 days after enlargement induced by a certain types of dental treatment by the methods.

8. Northern blotting method The expression of salivary cystatin S mRNA was determined by the Northern hybridization method27 with a slight modification. RNA isolated by the acid-guanidium-phenol-chloroform method was used for Northern blot hybridization. Total RNA (15 μ g/lane) was subjected to electrophoresis through 1 % agarose gel containing 6.6 % formaldehyde, blotted onto positively charged nylon membranes (Amersham, UK) and cross-linked for 3 min with UV light. Digoxigenin-labelled DNA probes of salivary cystatin S were carried out by reverse transcription of mRNA with AMV reverse transcriptase XL and PCR amplification of cDNA by the instructions of the manufacturer (TaKaRa RNA PCR Kit, TaKaRa, Tokyo). The primers for amplification of salivary cystatin S cDNA with Tag DNA polymerase were commercially constructed10. With these primers, a 492-bp fragment of salivary cystatin S cDNA was amplified. The salivary cystatin S was probed with this amplified fragment and

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digoxigenin-labelled 11-dUTP. The hybridization probes were detected with anti-digoxigenin-alkaline phosphatase antibody.

9. Standard RT-PCR and competitive RT-PCR of mRNA for salivary cystatinS The RT-PCR and competitive RT-PCR were carried out to estimate the expression of mRNA for salivary cystatin S with the constructed primers of salivary cystatin S and a competitor28.

10. Statistical analysis All data were analyzed by the unpaired t-test and factorial analysis of variance. When factorial analysis of variance gave a significant F value, Duncan's New Multiple-Range Test was carried out on the adjusted means.

Results1. Enlargement with hypertrophy and hyperplasia of the salivary glands following a certain types of dental tratment and chronic IPR administration The submandibular and sublingual, but not parotid, glands were significantly enlarged at 7 to 28 days after repeated amputation of the lower incisors and a certain types of dental treatment with orthodontic appliances. The weights of submandibular and sublingual glands were about less twice their normal glands. In contrast to dental treatment, the submandibular and parotid, but not sublingual, glands after chronic injection with IPR were significantly enlarged by 36 h and reached to the maximum levels by 7 to 10 days after treatment. The weight of the parotid glands was approximately 4 to 5 times the weight of the control glands, whereas the submandibular glands were about

Changes of the DNA, RNA and RNA-p contents of the submandibular glands of rats subjected to repeated amputation of the lower incisor teeth for 21 days.●—● DNA/gland, ●…●: DNA/mg gland,

: RNA/gland, ; RNA/mg gland

—○ : RNA-p/gland, ○…○; RNA-p/mg gland, ▲—▲: RNA/DNA

Fig. 2


twice their normal glands. Together with the results of the histological studies, the DNA and RNA contents had significantly increased in the salivary glands of rats which suggested that both hypertrophy and hyperplasia had occured in these three major salivary glands after dental treatment and chronic treatment with IPR29 ( Fig. 2). Enlargement was completely abolished with atropine for only the sublingual glands but with phenoxybenzamine for both the submandibular and sublingual glands (Fig. 3).

Fig. 3 The effects of orthodontic treatment with different types of autonomic antagonists and morphine on body weight and the weights of the submandibular and sublingualglands for 1 week. Atro; atropine, 6-OHD; 6-hydroxydopamine, Phenox; phenoxybenzamine, Mor; morphine, C; 1 week after application, E; 1 week after application with different types of antagonists. *; p < 0.05, **; p < 0.02; ***; p < 0.01 by unpaired t-test. Values in the parenthesis denote No. of rats.

However, no enlargement was seen in any salivary gland of plaque-susceptible and plaque–resistant rats at any weeks of age. 2. Induction and/or secretion of salivary cystatin S by the submandibular glands of rats after various dental treatment, chronic treatment with IPR and in resistance of plaque formation Induction of salivary cystatin S by the submandibular glands of rats following dental treatment, chronic treatment with IPR and in the

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plaque-resistance were clearly observed (Fig. 4).

Fig.4 Electrophoretograms on 10 % native polyacrylamide gels including large mobile (LM ) proteins. The columns from left to right denote isoproterenol (the β-type protein), methoxamine (theα-type protein) stimuli in normal rats, and isoproterenol and methoxamine stimuli in rats subjected to chronic treatment of isoproterenol.

In rats subjected to repeated amputation of the lower incisor teeth and a certain types of orthodontic treatment, salivary cystatin S in the submandibular glands were induced at later stage than in rats subjected to chronic treatment with IPR and secreted into saliva by 28 days after dental treatment judged immunologically, electrophoretically and immunohistologically29. By the chemical sympathectomy with 6-hydroxydopamine, the induction and/or secretion of salivary cystatin S was dramatically enhanced by 7 days after a certain types of dental treatment30. In contrast, salivary cystatin S in the submandibular glands of rats subjected to chronic treatment with IPR was dramatically induced by a single IPR injection by 24 h and the amount increased dramatically to 400,000-fold by 7 days although in control rats salivary cystatin S was detectable from only two sources, submandibular saliva elicited by IPR and submandibular gland extracts, but could not be detectable in any other samples. The salivary cystatin S levels in submandibular saliva dramatically increased by 8 days and reached 30 % of the total salivary protein after chronic treatment with IPR 24. Salivary cystatin S was also present in the parotid and sublingual glands, and esophagus, small intestine, stomach, kidney and gingiva as well as sera of rats, probably translocated from submandibular saliva into, subjected to chronic treatment with IPR24,31. In contrast, the concentrations of salivary cystatin S in submandibular saliva, extracts of the submandibular glands and gingiva of plaque-resistant groups were significantly higher but after both groups had been subjected to chronic treatment with IPR they were not significantly different from those in plaque-susceptible groups. The concentration of salivary cystatin S in submandibular saliva of plaque-resistant, but not plaque-susceptible, groups increased significantly with increasing age (Table 1).


Table1.Comparison of salivary cystatin S concentrations in submandibular saliva between male RES and SUS rats in response to isoprotenol during development (means ± S.E.)

At 12 weeks of age, the concentration of salivary cystatin S in submandibular saliva of the plaque-resistant groups was over 3,500 times than in saliva of plaque-susceptible rats10 . The concentration of salivary cystatin S in the extract of the submandibular glands of male and female plaque-resistant groups was dramatically higher by 4,500-6,300 times than that of male and female plaque-susceptible groups. The salivary cystatin S in the extract of gingiva in the male plaque-resistant group was detectable by the ELISA method, but was not in the male plaque-susceptible group10. By the Western blotting method10, positive bands were detected only in submandibular saliva obtained from male and female plaque-resistant groups, but not from plaque-susceptible groups. 3. Agonist-dependent changes of secretory functions of the submandibular glands enlarged following various dental treatment, chronic treatment with IPR and in resistance of plaque formation

By the enlarged submandibular glands of rats subjected to repeated amputation of the lower incisor teeth and a certain types of orthodontic treatment, the secretory function did not greatly change except that the protein secretion were significantly reduced due to malnutrition devoid of the normal occlusion, following the excessive reduction of body weight. In contrast, the enlarged glands characteristically induced salivary cystatin S and secreted it into saliva after various dental treatment. This enlargement of the submandibular glands of rats was dramatically followed with hypertrophy and hyperplasia of the acinar cells, but not the granular convoluted tubule (GCT) cells. Therefore, the components such as proteases, epidermal growth factor and nerve growth factor, and —adrenoceptors, which were responsible for the -type proteinsecretion in response toα-adrenoceptor agonists, present in the GCT cells, were

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dramatically reduced following these dental treatment as well as chronic treatment with IPR. Therefore, a number of GCT cells were relatively reduced following such treatment, but their secretory functions were still conserved persistently for theα-type protein secretion following a certain types of dental treatment except that following repeated amputation of the lower incisors at 28 days after treatment, the α -type protein secretion was almost completely disappeared in the submandibular glands (Fig. 5).

Fig. 5. The IEF electrophoretograms of three types (α-, β- andγ) of protein in rat submandibular

saliva on gradient pH 3.5-9.0 gels. M denotes standard substances for pH.

In both groups of plaque-resistant and susceptible rats at all ages the proteins secreted by the submandibular glands in response to IPR, physalaemin and bethanechol were of the β-type as seen in the normal SD rats in contrast that the proteins were of the α -type in response to phenylephrine and oxymetazoline in both groups. These observation meant that the GCT cells were almost completely intact and could secrete their components different from those mentioned above. However, a little modifications were seen in response to


oxymetazoline in plaque-resistant rats which usually secreted the γ -type proteins in the normal submandibular glands of SD rats The agonist-dependent changes of secretory functions of the submandibular glands of plaque-resistant and plaque-susceptible rats were observed. For submandibular saliva elicited by IPR, physalaemin and bethanechol, the flow rates were significantly less in the plaque-resistant rats. In contrast, the concentration of protein in submandibular saliva in response to IPR, physalaemin and phenylephrine in plaque-resistant groups was significantly higher. Wet weights (mg/BW) of the submandibular glands, the volumes of saliva secreted and flow rates of plaque-resistant groups after chronic treatment with IPR were significantly less than those of plaque-susceptible groups10. In contrast, the concentration of protein in the plaque-resistant groups was significantly higher than that of plaque-susceptible groups subjected to chronic treatment of IPR. 4. The gene expression of salivary cystatin S The expression of mRNA of salivary cystatin S was also determined by the Northern blotting method (Fig. 6), RT-PCR and competitive RT-PCR. The gene expression of salivary cystatin S was observed in the submandibular glands of rats after 7 days subjected to a certain types of orthodontic treatment (Fig. 7) and in resistance against plaque formation, and the submandibular glands of Wistar rats subjected to chronic treatment with IPR for 4 days, but not in plaque-susceptible groups, or in Wistar and SD rats without chronic treatment with IPR and any orthodontic appliance (Fig. 6).

Fig. 6 Northern blotting of salivary cystatin S in the submandibular glands of the plaque-resistant, plaque-susceptible and Wistar rats with and without isoproterenol-treatment for 4 days. The gene expression of salivary cystatin S is seen in the plaque-resistant and isoproterenol-treated rats, but not in the plaque-susceptible and normal Wistar rats. 1 indicates plaque-susceptible (SUS), 2 plaque-resistant (RES), 3 normal Wistar and 4 isoproterenol-treated submandibular glands of Wistar rats.

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Fig. 7. The gene expression of salivary cystatin S in the submandibular glands of rats subjected to orthodontic treatment for the lateral expansion was observed after 7 days (7 D) by RT-PCR. Pair fed denotes control rats with paired food and Set the experimental groups. G3PDH denotes glyceraldehyde 3-phosphate dehydrogenase.

The gene expression of salivary cystatin S in the submandibular glands of SD rats during development was predominant at 7 weeks of age which coincided developmentally with the regression of terminal tubule cells and the differentiation of the GCT cells, respectively28.

Discussion In saliva secreted by the enlarged submandibular glands of rats subjected to repeated amputation of the lower incisor teeth, the concentrations of inorganic (K, Na, Ca and inorganic P) and organic substances (urea and sialic acid), and amylase activity did not greatly change during the experimental period for about 1 month with some exceptions, although the enlarged submandibular glands were significantly reduced their secretory functions for the protein secretion from 14 to 28 days after treatment29 as likely seen in the submandibular glands after orthodontic treatment with an incisal bite plane4,. Incidentially, the parotid gland, atrophied following these dental treatment, did not change their secretory functions during 1 month29. However, in the subligual glands at only 3 days, but not 7 days with an exception, subjected to orthodontic treatment, salivary flow rate, the concentrations of sialic acid and Ca, and the amounts of protein secreted


in saliva were significantly reduced19. From these results it was suggested that such variations of the salivary components were caused by the daily malnutrition following inadequate intake of foods due to irregular occulusion. The mechanism for enlargement of the sublingual and submandibular glands of rats subjected to various dental treatment was relatively different from that of rats subjected to chronic treatment with IPR by which caused enlargement of the parotid and submandibular glands of rats. The contents of DNA, RNA and RNA-p in the submandibular and sublingual glands, but not parotid glands, of rats subjected to various dental treatment were significantly higher at 7 and 14 days after treatment than those of control rats. Atropine completely inhibited enlargement of sublingual glands in contrast to that phenoxybenzamine (adrenergicα-blocker) also inhibited enlargement of both submandibular and sublingual glands30. Furthermore, in both submandibular and sublingual glands subjected to a certain types of orthodontic appliances, the contents of substance P significantly increased at both 3 and 7 days, but not at 14 and 28 days after treatment6. Therefore, both parasympathetic and sympathetic nerves as well as sensory nerves could probably associate with such events in three major salivary glands after various dental treatment. In contrast, the contents of both DNA and RNA in the submandibular and parotid glands subjected to chronic treatment with IPR were significantly higher than those of control rats at the relatively early stages. No enlargement was occurred in the sublingual glands of rats subjected to chronic treatment with IPR. The acinar cells were greatly enlarged with hypertrophy and hyperplasia in the submandibular and parotid glands of rats. Only enlarged submandibular gland subjected to a certain types of dental treatment and chronic treatment with IPR could drastically induce and secrete salivary cystatin S. It has not yet been elucidated the reasons why salivary cystatin S was drastically induced and secreted into the oral cavity by the submandibular glands of rats subjected to such treatment31. Further studies are necessary to elucidate genuine roles of salivary cystatin S secreted into the oral cavity, although some investigators elucidate that salivary cystatin S probably plays a role to protect the oral membrane and cavity from protease attacks derived from several bacteria32. It would be very useful to identify salivary biomarkers which distinguish patients with dental caries, gingivitis or periodontitis from healthy persons. No clear compositional differences have been discovered except some reports on salivary cystatin C or S in human whole and parotid saliva14-16, although many biomarkers, namely antibacterial factors, metabolic products, bacterial enzymes, cytokines and enzymes of host cells have been elucidated in saliva and gingival crevicular fluids obtained from patients with dental caries or periodontitis33. The levels of salivary cystatin S in submandibular saliva, extracts of the submandibular glands and gingiva in plaque-resistant rats increased

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substantially with increasing age and were significantly higher than those in plaque-susceptible rats10 in consistent with a report16. In brief, in saliva secreted by the submandibular glands of SD rats three types of protein were discovered and designated by us as theα-, β- andγ- types10, 18, 20-22, 34-40 (Fig. 5) . In saliva in response toβ2- adrenoceptor, cholinergic, peptidergic and β1-adrenoceptor, at relatively low doses, agonists, theβ- type protein , probably derived from the acinar cells, were dominatedly secreted. In contrast, in saliva in response to β1-adrenoceptor agonists such as tyrosine metabolites (catecholamines), at relatively high doses, the α -type protein, probably derived from the GCT cells, was characteristically secreted. The third type, which we have designated as the γ- type protein, could probably be present in human saliva and were secreted in response to 2-imidazoline derivatives such as clonidine, oxymetazoline, naphazoline and tetrahydrozoline, but not α-aminoclonidine which could secrete theα-type protein. The origins of the γ - type protein have not been yet clear. Therefore, further studies are necessary to elucidate the secretion route for the theγ- type protein by the submandibular glands of rats. Theγ- type protein contains significantly higher albumin and sIgA than the α - and β -types of proteins34,41. By the submandibular glands of rats subjected to various dental treatment and chronic treatment with IPR, the α -type protein was relatively, but not completely, disappeared due to hypertrophy and hyperplasia of the acinar cells and devoid in part of the GCT cells of the salivary glands. In both plaque-resistant and plaque-susceptible rats the proteins in submandibular saliva were of the β-type in all samples in response to IPR, physalaemin and bethanechol and in rats subjected to chronic treatment with IPR, as seen in normal SD rats18. These results suggest that the acinar cells of the submandibular glands could still work normally in both types of rats. In contrast to the β-type of protein, the α-type of protein was secreted in both groups of rats in response to oxymetazoline, which used to secrete the γ-type protein by SD rats18,34. Significantly higher levels of catecholamines in the salivary glands of plaque-resistant and plaque-susceptible groups than those of normal SD rats may be accountable for this discrepancy42. The plaque-susceptible groups responded to chronic treatment with IPR more strongly than plaque-resistant groups. It has already been suggested that a small amount of neurotransmitter release from very few impulses in postganglionic sympathetic secretomotor nerves is sufficient to activate acinar cells, whereas the GCT cells require a much higher local concentration of neurotransmitter and this greater release of neurotransmitter can only be achieved by high frequency impulse formation42. From data on the catecholamine content in the submandibular and adrenal glands, it may be suggested that plaque-resistant rats, as seen in a strain of the rat with hypertension, may have a much augmented adrenal-sympathetic system43,44.


The isoelectric point (pI 4.5), molecular weight (14,500), electrophoretic profile on pH 3.5-5 or 3.5-9.0 isoelectric focusing gels and sequence of the 26 N-terminal amino acids of the salivary cystatin S purified from submandibular saliva of plaque-resistant groups were identical to those of the rat salivary cystatin S-3 purified from submandibular saliva of a different strain , SD rats subjected to chronic treatment with IPR8,10. The gene expression of salivary cystatin S in the submandibular glands of rats subjected to repeated amputation of the lower incisor teeth and an application of an incisal bite plane has never been checked so far but similar results, as seen in the rats with an orthodontic appliance for the lateral expansion, could probably be obtained. The expression of the mRNA of salivary cystatin S in the submandibular glands was clearly observed in both male and female plaque-resistant, but not in plaque-susceptible or Wistar rats unless these were subjected to chronic treatment with IPR for 4 days. However, it has been elucidated in detail by quantitative competitive RT-PCR that the salivary cystatin S gene was already expressed at 7 days of age and that its concentration increased gradually. Then it reached a maximum at 28 days of age and decreased to constant levels after 26 weeks of age28. These expression patterns of salivary cystatin S gene were coincided with the regression of terminal tubule cells and the differentiation of the GCT cells. Incidentially, in the gene expression of the five adrenoceptor subtypes, unexpected results were obtained in the α1a-adrenoceptor subtype, which was most abundant and over 70 % within total five adrenoceptor subtypes (α1a,α1b, α 2A, β 1 and β 2) in the submandibular glands of both plaque-resistant and plaque-susceptible rats. The gene epression of β1-adrenoceptor subtypes, which probably play a role to synthesize salivary cystatin S in the acinar cells of the salivary glands, was unexpectedly low in both groups45. Therefore, further studies are necessary to elucidate the role of the gene expressed salivary cystatin S in the salivary glands. It can be concluded that salivary cystatin S induced following various dental treatment and chronic tratment with IPR could probably be a good biomarker to elucidate the roles of the salivary cystatin S in the oral cavity and also to discriminate two groups of plaque-resistant and plaque-susceptible rats. However, further studies in detail are necessary to elucidate the preventive actions of salivary cystatin S in the oral cavity.

This paper was presented at the II Congress of BaSS - Belgrade

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Timmerman MF, Snoek CM, Van der Velden U, Nieuw Amerongen AV. Protein composition of whole and parotid saliva in healthy and periodontitis subjects. J Periodont Res, 1996; 31: 57-65. 17. Yoshida Y, Sprecher RL, Schneyer CA, Schneyer LH. Role of β-receptors in sympathetic regulation of electrolytes in rat submaxillary saliva. Proc Soc Exp Biol Med, 1967; 126: 912-916 18. Abe K. Autonomic effects on protein secretion by rat submandibular salivary glands. Comp Biochem Physiol, 1987; 88C: 241-248. 19. Hioki S, Niwa K, Kishimoto T, Kawazoe T, Yokota Y, Abe K, Dawes C. The effects of an incisal bite plane on rat sublingual glands. J Dent Res, 1983; 62: 715-720. 20. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem, 1951; l93: 265-275. 21. Abe K, Dawes C. The effects of oxymetazoline on secretion of protein and some electrolytes by rat submandibular and parotid glands. Comp Biochem Physiol, 1985; 80C:347-353. 22. Abe K, Dawes C. The effects of electrical and pharmacological stimulation on the types of proteins secreted by rat parotid and submandibular glands. Arch Oral Biol, 1978; 23: 367-372. 23. Ishikawa E, Imagawa M, Hashida S, Yoshitake S, Hamaguchi Y, Ueno T. Enzyme-labeling of antibodies and their fragments for enzyme immunoassay and immunohistochemical staining. J Immunoassay, 1983; 4: 209-327. 24. Nishiura T, Ishibashi K, Abe K. Salivary cystatin levels in serum, submandibular saliva and various tissues of normal and isoproterenol-treated rats. Jpn J Oral Biol, 1994; 36: 20-26. 25. Towbin H, Staehelin T, Gordon J. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets. Procedure and some applications. Proc Natl Acad Sci USA, 1979; 76: 4350-4354. 26. Schmidt G, Thannhauser SJ. Method for the determination of deoxyribonucleic acid and phosphorus-proteins in animal tissues. J Biol Chem, 1945; 161: 83-89. 27. Barka T, Van der Noen H. Expression of the genes for cysteine proteinase inhibitors cystatin C and cystatin S in rat submandibular salivary gland. Arch Oral Biol, 1994; 39: 307-314. 28. Nishiura T, Abe K. Postnatal changes of gene expression for tissue inhibitors of metalloproteinase-1 and –2 and cystatin S and C, in rat submandibular gland demonstrated by quantitative reverse transcription-polymerase chain reaction. Arch Oral Biol, 1999; 44: 15-26. 29. Murata A. The effects of the periodic amputations of the lower incisor teeth on the major salivary glands of rats. J Gifu Dent Soc, 1981; 9: 40-66 (in Japanese). 30. Kamogashira K. The effects of the application of an orthodontic apparatus for a maxillary lateral expansion on both submandibular and sublingual glands of rats. J Kyushu Dent Soc 1987; 41: 233-256 (in Japanese).

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31. Nishiura T, Ishibashi K, Abe K. Translocation of orally administered rat salivary cystatin into serum and kidney. Arch Oral Biol, 1995; 40: 285-291. 32. Naito Y, Sasaki M, Umemoto T, Namikawa I, Sakae K, Ishihara Y, Isomura S, Suzuki I. Bacterial effects of rat cystatin S on an oral bacterium Porphyromonas gingivalis. Comp Biochem Physiol, 1995; 110 C: 71-75. 33. Embery G, Waddington R. Gingival crevicular fluid. Biomarkers of periodontal tissue activity. Adv Dent Res, 1994; 8: 329-336. 34. Shibaike S, Abe K, Okina A, Nishiura T. The effects of clonidine and three 2-imidazoline derivatives on the secretion of protein and some electrolytes by rat submandibular and parotid glands. Comp Biochem Physiol, 1992; 101C: 547-556. 35. Abe K, Yoneda K, Fujita R, Yokota Y, Dawes C. The effects of epinephrine, norepinephrine and phenylephrine on the types of proteins secreted by rat salivary glands. J Dent Res, 1980; 59: 1627-1634. 36. Okina A, Hidaka S, Tashiro M, Abe K. The effects of tyramine on salivary flow rate and protein secretion by rat submandibular glands. J Dent Res, 1993; 72: 897-906. 37. Okina A, Abe K, Inuzuka H, Yano T, Okina T, Nakashima T, Nishiura T. The effects of m-octopamine on salivary flow rates and protein secretion by rat submandibular glands. Comp Biochem Physiol, 1992; 103C: 469-476. 38 Okina A, Abe K, Tashiro M, Ishibashi K. The effects of p-octopamine on salivary flow rates and protein secretion by rat submandibular glands. J Dent Res, 1993; 72: 993-1000. 39. Abe K, Itoh T, Tashiro M, Okina A, Nakamura H, Nose T, Inoue H, Yu S-F. The effects of 5-hydroxydopamine on salivary flow rates and protein secretion by the submandibular and parotid glands of rats. Exp Physiol, 1996; 81: 645-653. 40. Tashiro M, Letic-Gavrilovic A, Nakamura H, Ohkuma K, Egashira Y, Omori H, Nagata H, Harada M, Abe K. The effects of 6-hydroxydopamine and potential antagonists on flow rates and protein secretion by rat submandibular glands. Serb J Stomatol, 1997; 44: 131-137. 41. Kiyama J. Characteristics of secretory immunoglobulin A secretion from rat salivary glands. Jpn J Oral Biol, 2000; 42: 302-314 (in Japanese). 42. Anderson LC, Garrett JR, Zhang X, Proctor GB, Shori DK. Differential secretion of proteins by rat submandibular acini and granular ducts on graded autonomic nerve stimulations. J Physiol (Lond), 1995; 485: 503-511. 43. Yano T. Salivary cystatin S secretion by the submandibular glands of plaque-susceptible rats. J Fukuoka Dent Coll, 1998; 25: 247-267 (in Japanese).. 44. Matsuo K, Sekine I, Nishimori I, Kunisada K, Izumi R, Niwa M, Ozaki M. Effects of chronic administration of arotinolol (ARL, S-596) on stroke-prone spontaneously hypertensive rats (SHRSP). 3. Studies on catecholamine contents in heart and adrenal gland. Pharmacometrics, 1984; 28: 467-471 (in Japanese). 45. Nan X L. Comparison of aquaporin and adrenoceptor subtypes mRNA expression in submandibular glands between plaque-resistant and –susceptible rats. J Fukuoka Dent Coll, 2003; 30: 1-13.



10 years of BaSS

MEDITATORS INVOLVED IN TRANSMISSION AND MODULATION OF CHRONIC PAIN

¹Faculty of Stomatology Pančevo ²Pharm-Olam, Group Ltd (Serbia & Montenegro)

D. Cenić-Milošević¹ P. Turčinović²

Summary This article presents a review of the neurotransmitters and neuromodulators in chronic pain states. Chronic pain, which is associated with prolonged tissue damage or injuries to the peripheral or central nervous system, results from a number of complex changes in nociceptive pathways. The tissue damage evoke interactions between neural and non-neural tissues which are important in producing hyperalgesia by changing membrane excitability and cell phenotype with expression of new molecules, including neurotransmitters, enzymes and chemical receptors. But the transmission of nociceptive information is modulated at the level of spinal cord and at the midbrain level according to the release of various mediators and complexity connections between different area of CNS. In chronic pain states, an increased neural excitability can be reduced with receptor selective drugs that block central chemical mediators or that control ectopic activity. Key words: Pain, chronic; Pain transmitters; Pain modulators Introduction “The astronauts will probably land on Mars in another decade. Unmanned spacecraft the eight billion miles to the farthest borders of our solar system, taking more than eight years to reach that most remote of planets, Pluto. But when man himself ventures out into the most distant reaches of limitless space, he can be certain of only one thing – even there he will still have to face his ancient implacable enemy, pain. For pain is as old as life itself and as new as your last heartbeat, and life and pain are inseparable, joined together for all eternity. Prehistoric man endured the hurt of arthritis and toothaches, of broken bones and infected ones, of childbirth and disease; and so will man of the twenty-first century”(1). The Nobel laureate Albert Schweitzer, physician who practiced in the African jungle for two decades, wrote «We must all die. But that Ican save him from dazs of torture, that is what I feel as my great and ever new privilege. Pain is a more terrible lord of mankind that even death itself»(2). Pain is a personal and complex sensory experience that is dificult to describe to another person. In fact, pain is an unpleasant sensory and emotional


experience associated with actual or potential tissue damage or described in terms of such damage (3). Certainly, one of the great paradoxes in pain is that it can be both, a symptom and a disease. As a symptom, acute, transient pain is associated with tissue damage and is a necessary safety signal for survival, protecting us from many of the dangers in our personal world. The chronic, intractable pain is asociated with tissue damage, inflammation or neuropathologies, and is a destructive disease turning the sufferer inward until his whole life begins to revolve around his pain (3). Moreover, in chronic pain states there is a superimposition of many other processes onto the basic events of nociception, which alters the relationship between stimulus and the response and affects the ability to modulate the resultant pain state (4). Chronic pain is a complex synthesis of biologic, psychologic, behavioral and neurohormonal – chemical factors (5). There are essentially three sensory centers in modulation of pain (5): the 1st center contains the peripheral receptors with fibers mediating impulses through the dorsal roots to the dorsal horn of the cord; the 2nd center is at the midbrain level and involves the thalamus, reticular system and hypothalamus; the 3rd center contains the cerebral cortex, where the pain is localized and qualified. In chronic pain, a rudimentary understanding of the complexity of events that occur in nociceptive pathways is beginning to emerge. Some of these events occur in precise time windows during the development and consolidation of the pain state, and can range from changes in the excitability of fine afferent nerves to drastic alterations in their cellular phenotype with the expression of new molecules, including neurotransmitters, enzymes and chemical receptors (5,6). Chronic central alterations in neurochemistry of pain produce hypersensitivity which enhances and prolongs relatively low levels of afferent input and allows normally innocuous stimuli to become painful. After a peripheral nerve injury, structal changes include loss of spinal interneurones, inappropriate rearrangements of afferent nerve processes in the spinal cord (7) and proliferation of sympathetic fibres into sensory ganglia which are not normally innervated to any significant degree (8,9). Modulation of receptor’s field After a peripheral injury a complex cascade of events is initiated. The initial insult results in the activation of the arachidonic acid cascade, which leads to the formation of prostaglandins and leukotrienes. These products are released from tissue and act to sensitize primary afferent terminals (10). Prostaglandins such as PGE2 and PGI2 can act directly on the peripheral terminals of nociceptors (11).

D. Cenić-Milošević

The original injury also results in the enzymatic conversion of kininogen into bradykinin (12-14). Prostaglandins (15,16) and leukotriens (17) act in concert with bradykinin to produce on enhanced activation of the primary afferent terminal. Bradykinin’s effects in the periphery are not nonspecific but are mediated by B2 bradykinin receptors, which are located on the terminals of primary afferent neurons (18,19). However, B1 receptors are expressed during prolonged inflammation and make a significant contribution to the hyperalgesia (20,21). Other inflammatory products including cytokines, such as interleukin1,6 and 8 (IL) and tumor necrosis factor alfa (TNF-alfa), also induce hyperalgesia by facilitating induction of B1 receptors, stimulating prostanoid production, and activating of sympathetic neurons. 5-Hydroxytryptamine (5-HT) is released from platelets and mast cells and produces mild and transient pain by direct activation of sensory neurones via 5-HT3 receptors. 5-HTalso induces a direct sensitization of nociceptors via 5-HT1 and 5-HT2 receptors (22,23). Apossible basis for sensitization by 5-HT, as well as by bradykinin and prostanoids, is a reduction of the slow inhibitory afterpotential that follows the action potential in some sensory neurones. The inhibition is due to cAMPgeneration and a reduction of the inhibitory K current. The overall effects is to increase the likelihood that the neurone will respond to a relatively weak stimulus with a train of action potentials rather than with a single spike. Histamine is released from mast cells and evokes the sensations of itch at low concentrations and pain at higher concentrations (24). Probably, these effects are produced by activation of histamine H1 receptors which increase membrane Ca-permeability and the release of tachykinins and calcitonin gene-related peptide (CGRP), resulting in further complex interactions including vascular changes and mast cell degranulation. These inflammatory mediators stimulate vascular endothelial cells to release the vasodilator nitric oxide (NO). NO is important for intercellular communication in peripheral tissue and in the CNS, including nociceptive pathways. This is usually achieved via the activation of guanylate cyclase and the production of cGMP (25). NO does not directly alter sensory neurone excitability, but acts indirectly in the antinociceptive effects of acetylcholine and morphine and promotes tachyphylaxis to bradykinin (26). However, peripheral NO mechanisms may be involved in neuropathic pain since nitric oxide synthase (NOS) is induced in sensory ganglia following peripheral axonal section. Furthemore, both pain and ectopic discharges that occur in peripheral fibres are reduced by NOS inhibition (27). How NOS inhibition alters nerve excitability is unclear, but changes in peripheral blood flow may contribute to this effect.


Interaction between neural and non-neural tissue The activation of afferent nerves induces an axon reflex and the release of sensory neuropeptides (substance P, neurokinin A, and CGRP). These peptides also change the excitability of sensory nerves nearby postganglionic sympathetic fibres. They also activate immune cells, alter local blood flow and induce the release of other active substances by plasma extravasation. A number of other peptides, such as a nerve growth factor (NGF), which are normally secreated by target tissues to regulate growth and maintain cellular phenotype of sensory and sympathetic neurones, can be increased by inflammation and nerve damage (28,29). Chemical pain transduction involves interaction with membrane receptors that are coupled to ion channels and the 2nd messenger system, resulting in changes of membrane excitability and cell phenotype. In this environment many chemical stimuli are available to initiate cascade of signals. In fact, there is enormous potential for signal amplification and modulation, as well as an opportunity for sinergism between neural and non-neural tissues (30). Such interactions are important in producing hyperalgesia. Changes in afferent nerves Activation of the primary afferent nerve terminals begins the transmission of nociceptive information. It is the release of nociceptive neurotransmitters from these primary afferent fibres that activates the second-order dorsal horn neurons. Supstance P, neurokinin A (NKA), CGRP, somatostatin and cholecystokinin are all present in small diameter unmyelinated primary afferents that terminate in the dorsal horn (31). In addition to neuropeptides, excitatory amino acids, such as glutamate and aspartate, which act on N-methyl-D-aspartate (NMDA) receptors, also play a distinct role in nociceptive transmission (31-35). Glutamate is co-localized with supstance P in the dorsal root ganglion cells and in the central terminals of primary afferent fibres (36). A role for supstance P may be to promote the release of excitatory amino acids from the spinal cord, leading to enhanced synaptic transmission. Glutamate mediated transmission is of fundamental importance in the hyperexcitability that is induced in the spinal cord and other central pathways in chronic pain (37). Spinal NMDA receptors are critical for producing “wind up” in the spinal cord. This is characterized by an increase in the excitability and discharge frequency of neurones in the dorsal horn (38). NMDA and peptide receptor mechanisms may also account for the spinal hyperexcitability following


peripheral nerve injury, during which normally innocuous mechanical stimuli, such as light touch, may evoke a feeling of intense pain (5). However, in neuropathic pain, further contribution to central hyperexcitability may occur through loss of inhibitory interneurones by excessive glutamate release (39). Modulation and transmission in CNS Numerous receptor systems have been localized at the dorsal horn of the spinal cord such as opioid, adrenergic, serotonin, GABA, cholinergic, adenosine, neuropeptide Y, calcitonin, somatostatin, neurotensin. Many of these receptor systems may function as specific modulators of nociceptive transmission (40-42). Although numerous neuropeptides, such as enkephalin, neurotensin and somatostatin are found within the hypothalamus (41,43-46), the functional significance of these neurotransmitters in pain processing is not known. Because the hypothalamus is highly integrated with limbic structures, the modulation of pain massage by emotional states (especialy in chronic pain) or prior experiences probably occurs at this level. The hypothalamus may be the activation site of migraine and cluster headaches (47). The posterior thalamus, which contains cells that regulate autonomic function, is closely related to the anterior hypothalamus, which contains the suprachiasmic nuclei. These nuclei control the principal circadian functions in mammals (46). This may explain the rhythmicity of many pains, including the time related cluster headaches and other pains (46,47). The hypothalamic pacemeker is mediated by the serotoninergic system (47). As in the hypothalamus, numerous neuropeptides and neurotransmitters have been localized within the periaqueductal gray substance (PAG) including enkephalin, dynorphin, neurotensin and supstance P (48-52). This region of the midbrain is well characterized site of descending inhibition (53-58). The PAG was the first brain site implicated in morphine produced analgesia (59). Activation of the PAG will inhibit nociceptive reflexes and second-order neurons. Although the locus coeruleus (LC)(60) is considered to be primarily a noradrenergic nucleus, some 5-HT is also present in the locus coeruleus along with numerous peptides (61-63). The locus coeruleus sends noradrenergic projections to the other brain regions (64) and activation of the LC will inhibit the firing of dorsal horn neurons and, also, nociceptive reflexes (65,66). The LC contains high density of opioid receptors (67,68) and morphine increases the activity of LC neurones. The nucleus raphe magnus is a 5-HT containing nucleus (61) that also contains a variety of other neurotransmitters (45,50). The largest input into the nucleus raphe magnus arises from the PAG and nucleus raphe magnus sends reciprocal serotoninergic and nonserotoninergic input into the PAG.


The role of the nucleus raphe magnus in descending inhibition has been characterized at the level of spinal transmission and spinal reflexes (54,55,57,69-73). It is certain that major role in modulation, in fact suppression of pain transmission, has the density of opioid receptor distribution. A high density of all three receptor types (mi, kapa, delta) are present in the dorsal horn of the spinal cord, thalamus, PAG and rostral ventral medulla sites. The same receptors are present on both spinal cord pain transmission neurons and upon the primary afferents that relay the pain message to them (74). The tooth pulp evoked potentials (TPEP’s), obtained as a response on electrical stimulation of tooth, represent a nociceptive pathway from receptor to the cortex (Fig.1).

Fig 1. Tooth pulp evoked potentials as an «objective index» of pain sensation: N1 – the first negative wave showing the first synaptic junction (substantia gelatinosa of nucl.caudalis pontis); P1 – the first positive wave showing nociceptive pathway through lemniscus medialis; N2/P2 – the second negative and the second positive waves showing nociceptive pathway at the thalamo-cortical level.

A – control registration B – registration 30 minutes after the administration of 50 mg tramadol per os C – registration one hour after the administration of 5 mg diazepam per os D – registration one hour after the administration of 7.5 mg flormidal per os E – registration one hour after the administration of 100 mg phenobarbitone per os.


In this case, a receptor – nociceptor is tooth pulp which is innervated solely by A-delta and C fibres, and although contradictory reports are available, it is generally accepted that the great majority of these fibres are of the nociceptive type. As TPEP’s demonstrate only the pain response (nociceptive response), their use in clinical practice is permited as an “objective” index of pain sensation (74) and in the diagnosis of orofacial pain syndroma (74,75). However, according to the registered TPEP’s, it is possible to determine the level on which the pain transmission is changed, and to find out, in experimental environment, the effects of receptor selective drugs (74,76). The native opioid peptides – endogenous opioids, exogenous opioids and central acting analgesics (Fig.1 – B) produce analgesia via three receptor types that are closely linked with AMP system and changes in Ca and K flux (77). It is well known that gamma amino butyric acid (GABA) is the most important inhibitory neurotransmitter at all levels of the neuraxis, including the spinal cord, hypothalamus, hippocampus, substantia nigra, cerebellar cortex and cerebral cortex.

That is the reason why benzodiazepines (diazepam and flormidal) (Fig.1 – C and D) and phenobarbiton (Fig.1 – E) change the pain response. In fact, benzodiazepines potentiate GABA-ergic neurotransmission by increasing the efficiency of GABA-ergic synaptic inhibition via membrane hyperpolarization, which leads to a decrease in the firing rate of neurons (76), while barbiturates also facilitate the actions of GABA by increasing the duration of the GABA-gated channel openings (78,79).

Furthemore, chronic pain behavior has added complexities, since human reactions can be modified by the environmental or sociological setting, and because of all of these facts, the treatment can begin with the acknowledgement that chronic pain is mechanistically diverse and is the outcome of multisystem dysfunction.


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44. Jacobowitz DM, O Donohue TL. Immunohistochemical identification and mapping in neurons of rat brain. Proc Natl Acad Sci, (USA), 1978; 75:6300-6304.

45. Jannes L, Stumpf WE, Kalivas PW. Topographical distribution in rat brain by immunohistochemistry. J Comp Neurol, 1982; 210:211-224.

46. Yamano M, Inagaki S, Kito S, et al. Enkephalinergic projection from the ventromedial hypothalamic nucleus to the midbrain central gray matter in the rat. Brain Res, 1986; 398:337-346.

47. Raskin NH. Serotonin receptors and headache. New Engl J Med, 1991; 325:353-354.

48. Elde R, Hokfelt T, Johansson O et al. Immunohistochemical studies using antibodies to leucine-enkephalin. Neuroscience, 1976; 1.349-351.

49. Kalivas PW, Jennes L, Nemeroff CB, et al. Topographical distribution of brain sites involved in hypotheria and antinociception. J Comp Neurol, 1982; 210:225-238.

50. Khachaturian H, Watson SJ, Lewis ME, et al. Dynorphin immunocytochemistry in the rat CNS. Peptides, 1982; 3:941-954.

51. Moss MS, Glazer EJ, Basbaum AL. The peptidergic organization of the cat periaqueductal gray. J Neurosci, 1983; 3:603-616.

52. Reicling DB, Kwiat GC, Busbaum AL. Anatomy, physiology and pharmacology of the periaqueductal gray contribution to antinociceptive controls. Prog Brain Res, 1988; 77:31-46.

53. Fields HL, Basbaum AI. Brainstem control of spinal pain transmission neurons. Annu Rev Physiol, 1978; 40:217-248.

54. Gebhart GF. Modulatory effects of descending system on spinal dorsal horn neurons. In: Yaksh TL (ed). Spinal afferent processing. New York: Plenum Press, 1986, pp 236-247.

55. Hammond DL. Control systems for nociceptive afferent processing. In: Yaksh TL (ed). Spinal afferent processing. New York: Plenum Press, 1986, pp 311-325.

56. Mayer DJ. Endogenous analgesia system. In: Liebeskind JC, Albe-Fessard DG (ed). Advances in pain research and therapy. New York: Raven Press, 1979, pp 428-436.

57. Mayer DJ, Price DD. Central nervous system of analgesia. Pain, 1976; 2:379-404. 58. Wang JL. Antinociceptive effect of intrathecally administered serotonin.

Anesthesiology, 1977; 47:269-271. 59. Tsou K, Jang CS. Studies on the site of analgesia action of morphine by

intracerebral microinjections. Scientia Sinica, 1964; 13:1099-1109.


60. Amaral DG, Sinnamon HM. The locus coeruleus: neurobiology of a central noradrenergic nucleus. Prog Neurobiol, 1977; 9:147-196.

61. Dalhstrom A, Fuxe K. Evidence for the existence of monoamine-containing neurons in the CNS. Acta Physiol Scand, 1964; 62:1-55.

62. Fuxe K. Evidence for the existence of monoamine neurons in CNS. Acta Physiol Scand, 1965; 64:37-84.

63. Sutin EL, Jacobowitz DM. Immunocytochemical localization of peptides and other neurochemicals in the rat laterodorsal tegmental nucleus and adjacent area. J Comp Neurol, 1988; 270:243-270.

64. Chu NS, Bloom FE. The catecholamine-containing neurons in the cat dorso – lateral pontine tegmentum. Brain Res, 1974; 66:1-21.

65. Jones SL, Gebhart GF. Characterization of coeruleospinal inhibition of the nociceptive tail-flick reflex in the rat. Brain Res, 1986; 364.315-330.

66. Jones SL, Gebhart GF. Inhibition of spinal nociceptive transmission from the midbrain, pons and medulla in the rat. Brain Res, 1988; 460:281-296.

67. Atweh SF, Kuhar MJ. Autoradiographic localization of opiate receptors in rat brain. Brain Res., 1977; 9:1-12.

68. Pert CB, Kuhar MJ, Snyder SH. Autoradiographic localization of the opiate receptor in rat brain. Life Sci, 1975; 16:1849-1854.

69. Llewelyn MB, Azami J, Roberts MHT. Brainstem mechanisms of antinociception. Neuropharmacology, 1986; 25.727-735.

70. Yaksh TL, Rudy TA. Narcotic analgesics. Pain, 1978; 4:299-359. 71. Besson JM, Oliveras JL, Chaouch A, et al. Role of the raphe nuclei in

stimulation-produced analgesia. Adv Exp Med Biol, 1981; 133:153-176. 72. Du HJ, Kitahata LM, Thalhammer JG, et al. Inhibition of nociceptive neuronal

responses in cat’s spinal dorsal horn by electrical stimulation and morpine microinjection in nucleus raphe magnus. Pain, 1984; 19:249-257.

73. Willis WD. Control of nociceptive transmission in the spinal cord. In: Ottoson D (ed). Progress in sensory physiology. New York: Springer, 1982, pp 175-192.

74. Lekic D, Cenic D. Pain and tooth pulp evoked potentials. Clinical Electro-encephalography, 1992; 1:37-46.

75. Todorovic Lj, Cenic D. The use of tooth pulp evoked potentials in the diagnosis of atypical facial pain and evaluation of results of treatment. Stom Glas S, 1992; 5:215-219. (in Serb)

76. Cenic D, Turcinovic P. Correlation between sedative-hypnotic effects of the benyodiazepines and the barbiturates. Book of Abstract of the 2nd Congress of the Balkan Stomatological Society, Belgrade, 1997; P177.

77. Fillingim B. R, Ness J. T, Glover L. T, Campbell M. C, Hastie A. B, Price D. D. and Staud R. Morphine responses and experimental pain: Sex differences in side effects and cardiovascular responses but not analgesia. Pain, 2005; 6:116-124.

78. Trevor AJ, Way WL. Sedatives – Hypnotics. In: Katzung BG (ed). Basic and clinical Pharmacology. Norwalk, Connecticut: Apppleton and Lange, 1995, pp 333-350.

79. Cronin N. J, Bradbury J. E. and Lidierth M. Laminar distribution of GABAA - and glycine – receptor mediated tonic inhibition in the dorsal horn of the rat lumbar spinal cord: effects of picrotoxin and strychnine on expression of Fos-like immunoreactivity. Pain, 2004; 112:156-163.



10 years of BaSS

AUTOTOMY PHENOMENON: EXPERIMENTAL MODEL OF NEURALGIC PAIN

Elena Kršljak, Zoran Stajčić

Department of Physiology, Faculty of StomatologyDr Subotica 8, Belgrade, Serbia&Montenegro

Summary

Autotomy is phenomenon of deafferentation of the rat limb by transection of the sciatic and saphenous nerves, inducing an automutilation of the limb as a response to painful stimuli generated from the amputation neuroma. It was first described by Wall et al in 1979. Autotomy has been proposed as an experimental model for neuralgic pain.It was shown that implantation of a polyethylene tube around the proximal end of the sciatic nerve increases autotomy behaviour. Autotomy is easily quantified by using the degree of autotomy score. It has been shown that some drugs can prevent or decrease the degree of autotomy, such as: tricyclic antidepressant, anesthetics, glycerol, morphine, streptomycin, ampicillin. Key words: Autotomy phenomenon, Sciatic nerve, Neuralgia Introduction

Wall et al ( 1979)25 have produced automutilation behaviour in rats after transection of the sciatic and saphenous nerves. As a result of this, animals start to attack their limbs. It is postulated that this behaviour is the result of the painfull impulses sent to the CNS from the amputation neuroma formed at the end of the transected sciatic nerve. Animals usually start biting their nails, then phalanges, ending with mutilation of the entire foot. This occurrence is named autotomy phenomenon by Wall et al (1979)25. The same behaviour has been observed following dorsal risotomy and named automutilation2,9. Blumenkopf6 has speculated that autotomy phenomenon can be considered as a patophysiological model of chronic pain and has introduced the term deafferentation. Wagner24 has used the term neuropathic behavior for the same phenomenon. However the majority of investigators has accepted the term autotomy4,6,21,25. History

The autotomy phenomenon was introduced in the scientific literature by Wall et al (1979)25. In this report rats and mice were taken as experimental animals and divided into 4 groups. In the first group both the sciatic and saphenus nerves were cut. In the second and the third group either sciatic or saphenus nerves were cut. In the forth group nerves were sectioned and polyethylene (PE) tube


was placed around the proximal nerve stump. It was shown that the autotomy behaviour was most frequently recorded in the PE tube group. Rats have been most commonly used experimental animals8,1214,16,21, followed by mice25. Some investigators have sectioned both, the sciatic and the saphenus nerves as one stage procedure4,8,9,11,16, whereas the others sectioned solely the sciatic nerve25. After transecting the sciatic nerve, the proximal end of the nerve21,25 is gently pulled into the PE tube which distal end is sealed by sterile bone wax21,25 ( Fig 1). The role of the PE tube is to prevent anastomosis of the nerve stump with adjecent nerve fibers. The PE tube can be used as a miniature cistern for different solutions to be investigated for their analgesic properties since they bathe the nerve stump for prolonged period of time. Barbera et al4 has injected such substances into the proximity of the nerve without implanting the PE tube. We have shown that frequency of the autotomy is much higher in animals where the PE tube is implanted11. The peripheral nerve transection is followed by period of latency, for about 2 weeks, when animals start biting the denervated limb25. Albe-Fessard et al2, Caudaletti7 instead of peripheral nerve section performed dorsal rhyzotomy of the suitable nerves in the cervical and thoracic part of the spinal cord.

Fig.1 The proximal end of the sciatic nerve is placed into the polyethylene tube Possible causes of autotomy There are two components of painful impulses that may cause the autotomy phenomenon. One is central10, related to brain activities and the other is peripheral associated with neuroma formation or abnormal activities of dorsal horn cells following rhyzotomy.

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There are opinions that the autotomy and “phantom pain” are the same phenomenon since it has been shown that substances reducing the phantom pain such as serotonin and triptofan also cause the suppression of the autotomy1. Others state that there is significant difference between these two phenomena because autotomy has a latency period, whereas phantom pain starts immediately after amputation2 lasting till the complete healing of the amputed part. The explanation for phantom pain is that this sensations of the amputated limbs, are represented in the thalamus, sensory and motor cortex( homunculuses). It is obvious that these 2 phenomena do not have the same mechanism of development.

Some authors explain the autotomy behaviour as a dermatome rule1. The others describe autotomy as excitability changes of the spinal cord and brain cells7,8. Futhermore, it has been shown that autotomy can be produced after dorsal rhysotomy7,8. Seltzer et al18 were able to produce autotomy by electric stimulation on the A-alpha and C sciatic nerve fibres. Interestingly, autotomy behaviour started immediately after such stimulation.

The prevail opinion in the literature is that autotomy phenomenon is caused by painful impulses originating from neuroma at the proximal end of the cut nerve1,4,8,16,18,21,25 ( Fig 2). Histopathological examination of the animals that developed autotomy revealed neuroma formation4,18,21,25. Barbera et al4 also proved neuroma formation after reentry and were able to produce painful impulses by small pressure on neuroma. Wagner et al24 noticed that Wallerian –like degeneration at the proximal end of the sciatic nerve influences the reduction the painful transmission and prevents the onset of autotomy phenomenon which was proved in our studies11,22. ( Fig.3) Based on current findings it can be strongly suggested that artificially created neuroma closed in PE tube is directly responsible for the autotomy behavior in experimental animals since the latency period of two weeks corresponds to the time required for neuroma to be formed.

Fig.2 Autotomy phenomenon is based on the neuroma transmitting painful impulses to

the CNS


Fig.3 Wallerian like degeneration on the proximal end of the transecting nerve

Autotomy scores Wall et al25 introduced a method for measuring the severity of autotomy by using numerical values which was based on the degree of damage of the foot. Minimal autotomy score was 0 and maximal 13. A0 describes the absence of autotomy. Scores from one to five (A1-A5) denote bitten nails (Fig.4). Scores

from five to ten (A5-A10) correspond to damaged phalanges (Fig.5). The maximal autotomy score (A13) is given to the destroyed entire foot (Fig.6). There has been unanimous use of autotomy score by investigators. If the autotomy behavior is produced after the dorsal root section of the forelimb, the denervated limbis divided into 10 zones. The ablation by biting one of the portions of the arm is counted 1. The ventral side is subdivided in the same way. The total of the forearm ablation is counted as 16, the

Fig.4 Four nails bitten

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ablation of one digit as 1 and half of a digit as 5. The complete mutilation of the forelimb is scored 2423 ( Fig.6)

Fig.5 An animal limb without two phalanges

Fig.6 The whole foot bitten off

Effects of drugs on autotomy phenomenon Published studies have been focused on substances and drugs blocking pain receptors or excitatory neurotransmitter receptors. The tested drug have been applied either systematically or topically at the free end of the transected nerve. Intraneural injection of RCA I, reduces the release of Substance P, which causes the decrease of painful impulses and autotomy behavior in rats. The opioid application and cryotherapy have been known to reduce the autotomy scores and suppress it, which Puke et al22 ascribed to the opiatory inhibitory effect on the substance P release in the gelatinous substance. Seltzer et al18 has shown that amitryptiline, tricyclic antidepressant is an effective analgesic against neuropathic chronic pains in humans. These drugs when applied in experimental animals reduce the autotomy behavior by inhibition of prostaglandin E2 and blocking H1 receptors. Puke et al17 pointed out the role of descendent inhibitory pain control in the autotomy control showing that clonidine dexmedetomidine alpha2 adrenoceptor agonists effectively suppress autotomy when administered on 14th and 21st day of the nerve sections. Local anesthetics and blockers of the nerve transmission in the C-fibers and also cause the suppression of the autotomy phenomenon. 10,18.Glycerol was shown by Rappaport et al16 to reduce autotomy and prevent ectopic activity in A-alpha and C-fibers by two possible modes. It could firstly, preferentially eliminate demyelinated large fibers through an osmotic action and secondly, reduce their excitability. Gonzales et al8 were able to show that 20-day application of phenobarbital could reduce the degree of autotomy. The same authors performed the anesthetic blokade of the cut nerve with local anesthetic placed between the nerve ends (1% solution of mepivacaine), which


resulted in a significant suppression of the autotomy scores. Kauppula et9 al injected anesthetic, lidocaine and bipuvacaine, before the nerve section, at the place of the future lesion, which influenced the reduction of the autotomy scores and postponed occurrence of this phenomenon. Seltzer et al18 reduced the autotomy scores by application of local anesthetic blocks.The autotomy behaviour in rats was reduced with a perineural infusion of lidocaine6. An Intrathecal lidocaine injection, before the nerve section, also resulted in the postponed occurrence of autotomy. Cryotherapy applied to block peripheral nerve functions and concurrently to prevent the autotomy phenomenon was used by Wagner et al(24).

The suppression of the autotomy phenomenon was caused with the aid of morphine dissolved in water in the rats with the sciatic nerve transection resulted in the reduction of the autotomy behavior(14) .

Saudeau et al(23) noticed, after unilateral section of the dorsal roots C5 to T1, that subcutaneous application of chloramphenicol and amoxycillin signigicantly reduced autotomy .Stajčić(28) showed that topically applied streptomycin after the sciatic nerve section in rats significantly reduced the autotomy phenomenon. Kršljak(11,13) has also shown that streptomycin and ampicillin injected into the PE tube significantly reduced the autotomy phenomenon ( Tab 1). The mechanism of the protective effect of ampicillin against autotomy is largely unknown.It could be suggested that ampicillin as well as streptomycin, produces some degenerative changes of the nerve stump, which have been confirmed by Stajčić et al ( 2002)22.

Tab.1

MANN-WHITNEY z -TEST- *** p < 0.001 Statistical significance compared streptomycin in relation to saline ** p < 0.01 Statistical significance compared ampicillin in relation to saline

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Sporel et20 al speculate that all drugs that reduced autotomy behavior can be considered anti-neuralgic drugs in humans. However, we think that the autotomy phenomen is a reliable experimental model for neuralgic pain, which can be used for testing new analgesic substances. References

1. Abbot FV and Young SN. The effect of tryptophan supplementation on autotomy Iduced by nerve lesions in rats. Pharmacol.-Biochem.-Behav, 1991; 40:301-304.

2. Albe- Fessard D, Giamberardino MA and Rampin 1990, Comparison of different animal models of chronic pain. Pain, 1990; 3:11-27

3. Alkadhi KA and McIsaac RJ. Ganglion-blocking effects of streptomycin. Arch.Int.Pharmacodyn.Ther..1978;232:58-67.

4. Barbera J, Garcia G, Lopez A and Jose L. The role of the neuroma in autotomy following sciatic nerve section in rats. Pain.198833,373-378

5. Best JA ,Marashi AH and Pollan LD. Neuromuscular Blockade After Clindamycin Administration: a case report. J Oral Maxillofac.Surg1999; 57:600-603.

6. Blumenkopf, B. and Lipman J.J. : Studies in autotomy: its pathophysiology and usefulness as a model of chronic pain. Pain 1992 : 49(1): 153- 156.

7. Caudeletti, S. and Ferri, S. : Intracerebroventricular salmon calcitonin reduces autotomy behavior in rats after dorsal rhizotomy. Pain 1992 : 48 (2): 275- 278.

8. Gonzalez-Darder, J.M., Ortega- Alvaro, A., Ruz-Franzi, I., Segura-Pastor, D. : Antinociceptive effects of phenobarbitol in “ tail-Flick” test and deafferentation pain. Anesth._ Analg. 1992: 75 : 81-86

9. Kauppila T and Pertovara A,1991, Effects of different sensory and behaviorall manipulations on autotomy caused by a sciatic lesion in rats. Exp.Neurol. 1991;111:128-130

10. Kauppila, T. : Nerve resuturation decreases autotomy in the rat. Exp. Neurol.1994 :125 (1) : 106-110.

11. Kršljak E. Stajčić Z. Evidence that ampicillin and streptomicin can supress autotomic behaviour in rats. Acta Veterinaria,2004:54:145-152.

12. Kršljak E., Stajčić Z. Autotomy phenomenon: experimental model of neurelgic pain. Balkan Journal of Stomatology, rewiev article , 1999; vol 3

13. Kršljak E.: Efekti ampicilina i hloramfenikola na fenomen autotomije. Stomatološki glasnik, 1998:45:215-218.

14. Luo, L., Wiesenfed,-Hallin, Z. : Effects of intrathecal local anesthetics on spinal excitability and the development of autotomy. Pain 1994 : 4: 6-10

15. Pittinger C, Eryasa Y,Adamson R. 1970, Antibiotics-induced paralysis.Anaesth Analg 1991; 49:487.


16. Rappaport ZH, Seltzer Z and Zagzad D, The effects of glycerol on autotomy. An experimental model of neuralgia pain. Pain1986; 26 :85-91.

17. Puke, M.J. et Wiesenfeld, H. Z. : The different effects of morphine and the alpha 2- adrenoceptor agonists clonidine and dexmedetomidine on the prevention and treatment of experimental neuropathic pain. Anesth.- Analg. 1993 : 77 : 104-109.

18. Seltzer Z, Beilin BZ, Ginzburg R Paran Y,Shimko T.1991, The role of injury discharge in the induction of neuropathic pain behavior in rats. Pain, 46, 327-336.

19. Sokoll MD and Gergis SD. Antibiotics and neuromuscular function. Anaesthesiology, 1981;55: 159-167.

20. Sporel-Ozakat RE,Edwards PM,Hepgul KT, Savas A and Gispen WH., A simple method for reducing autotomy in rats after peripheral nerve lesions. J. Neurosci.-Methods, 1991;36:263-265.

21. Stajcic Z. : The effects of streptomycin on autotomy . Pain , 1992 ; 48 : 257-259. 22. Stajcic Z., Saulacic N. and Dozic S., Effects of streptomycin on the rat infraorbital

nerve. J.Craniomaxillofac. Surg. 2002;30(5):304-7 23. Suaudeau C, Beaurepaire R, Rampin O, Albe - Fessard D. Antibitics and

morfinomimetic injections prevent automutilation behavior in rats after dorsal rhyzotomy. Pain, 1989;5:177-181.

24. Wagner R, Deleo JA, Heckman HM and Myers Peripheral nerve pathology following sciatic cryoneurolyses: relationship to neuropathic behaviors in the rat. Exp. Neorol, 1995;133:254-264.

25. Wall P D, Devor M, Inbal R, Scadding JW, Schonfeld D, Seltzer Z and Tomkiewicz, MM..1979, Experimental anaesthesia dolorosa. Pain, 1979, 7,103- 113.

26. Yamamoto T and Mizuguchi T. Time- dependent effects of oral morphine on autotomy following brachial nerve section in the rat. Neurosci-Lett, 1992;141:166-168.

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10 years of BaSS

GLASS-IONOMER CEMENTS, THE INTERESTING ALTERNATIVE FOR RESIN-BASED COMPOSITES

Emeritus Professor in Dental Materials Science at the University of Amsterdam, The Netherlands. Visiting Professor University of Siena, Italy.

Carel L. Davidson, PhD.

45

Introduction There is a continuous urge for novelties in dentistry originating from changing professional perceptions, changing demands from the patient and progress in industrial possibilities. The altering professional perceptions come along with raising consciousness that cariestreatment is not merely technique, but requires a bio-medical approach, that less-invasive techniques are possible, that bio-compatibility requires increased interest, that there are challenging new possibilities and that there exist new markets (Davidson, 2003). The patient has changed as they demand more esthetics, established bio-compatibility and lower costs. Today’s dentistry can be characterized by a move away from metal towards non-metal restorations. Motivation is mainly based on concern for esthetics and biocompatibility. In direct restorative dentistry this means a shift from amalgam to composites. For direct restorations, three essentially different materials are at our disposal: amalgam, resin-based composites and glass-ionomer cements. Amalgam Of all direct dental restorations in the Netherlands, in 1993, 30% were performed in tooth colored alternatives for amalgam; in 1997 this number was 50% and in 2002 this number was 70%! Restoring in tooth colored materials is nowadays the first option in the teaching programs at the dental schools in the Netherlands. The multi-phase silver amalgam excellently served dentistry for almost 200 years! Reasons for wanting alternative direct restorative materials were the limited flexural and edge strength and corrosion. The latter was main cause of undesired release of metal ions in the human body and poor aesthetics. Whether the use of amalgam in dentistry should be limited or avoided for biological reasons is still open for discussion. In the Netherlands, the official standpoint is that there is no scientific evidence that amalgam is a serious hazard for the patient, whilst the dental team can be at risk of mercury poisoning, if no adequate hygienic measures are taken (Dutch Health Council, 1998). The corrosion also leads to increased porosity, which on its turn contributes to higher brittleness. Because of its intrinsic brittleness, the restoration should be as bulky as possible, and by absence of adhesion, cavity preparation is based on macro-mechanical retention. Both measures imply that placement of amalgam is usually associated with excessive sacrifice of sound tooth structure (“extension for prevention”). Today, the opinion holds that, if prevention has failed, the dentist should only minimally sacrifice sound tooth structure when restoring the tooth. Within this concept, adhesion is essential. There are at the present two classes of materials

C. L. Davidson

which allow direct restorations with adhesive techniques. These are resin-based composites and glass-ionomer cements. Resin-based composites It goes beyond the scope of this paper to cover structure and properties of resin-based composites, but some essentials have to be addressed. In mechanical sense, the heavily filled resin-based composites with smaller filler particles can compete more or less with dental amalgam in mechanical perspective (Manhart et al., 2004). (see table 1).

Table 1. Some mechanical properties of a lathe-cut amalgam compared with tooth

structure resin-based composites (McCabe JF, 1996 and other sources)

With the latest generations of adhesives and restorative materials, the life time of a composite restoration almost equals that of an amalgam (Manhart et al., 2004). Greatest features of resin-based composites are their aesthetics and presumed ease of application. Indeed, the placement procedure seems easy and straight forward: minimal cavity preparation without special attention for macro-mechanical retention, recommended bonding procedure and placement is mandatory, where set-on-command is apparently guaranteed by sophisticated light-curing. Successful bonding to dentin is only possible if a certain substrate condition is guaranteed. Proper bonding requires deep knowledge and great skill; more than before, the quality of the restoration is determined by the dentist factor. The latest bonding generations became more operator friendly, but their clinical durability is reduced (De Munck et al. 2003). On top of this premature in situ degradation of bonding and composite limit the lifetime of these kinds of restorations (Söderholm, 2003). Therefore, it has to be emphasized that use of rubber-dam is obligatory. Notwithstanding this high-technology approach of resin- based composite application, it has to be understood that it takes approximately 2-4 times more time to make a composite than an amalgam restoration. Therefore, resin-based composite restorations cost much more chair time and for that reason are relatively expensive.

enamel dentin amalgam microfill hybrid hardness (KHN) 360 60 100 30 90 compressive strength (MPa) 250 280 360 260 300 tensile strength (MPa) 35 260 60 40 50 elastic modulus (GPa) 50 12 30 6 14


As a matter of fact, it takes a good dentist to make a good composite and a bad one to make a bad amalgam. If a plenty skilled dentists are available, resin-based composites may contribute to very satisfying dentistry, but problems arise if there exists a shortage. Table 2 shows the dentist density in a series of European countries. Country active dentists inhabitants inhabitants/dentist Austria 3 789 8 100 000 2138 Belgium 7 600 10 020 000 1342 Denmark 5 039 5 300000 1052 Finland 4 968 5 100 000 1027 France 40 229 58 700 000 1459 Germany 61 900 82 000 000 1325 Greece 11 728 10 500 000 895 Iceland 322 275 000 854 Ireland 1 531 3 600 000 2351 Italy 48 100 57 000 000 1185 Luxemburg 269 418 000 1554 Netherlands 7 162 15 700 000 2192 Norway 4 153 4 400 000 1059 Portugal 4 200 10 000 000 2381 Serbia and Montenegro 4 381 7 479 437 1707 Spain 15 723 39 500 000 2512 Sweden 8 650 8 850 000 1023 Switzerland 4 650 7 000 000 1505 Turkey 20 000 65 000 000 3250 UK 25 170 58 000 000 2304 Total 2 279 564 457 123 000 2005

Table 2. Dentist density in various West-European countries (EU Manual of Dental Practice 2000)

The variety in number of dentists per 1000 inhabitants is striking and might have repercussion on either the number of patients receiving dental care or on the quality of the dentistry in that particular area. This problem might be solved if the dental treatment was not becoming more and more demanding. The conclusion so far might be that consciously placing, the technique sensitive resin-based composite restorations offer highly aesthetic alternatives for amalgam. They can be used with minimal invasive treatment. Bonding to enamel is reliable, but that particularly the quality of the dentin bonding is questionable and that the bonding procedure is demanding and thus costly for wide-scale dentistry. Restorative systems which demands highly skilled dentists for the creation of reliable and durable restorations are less desirable in

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the perspective of reducing the continuing increase of costs of health services. There is a general demand for delegation of simple treatments to health team members with a lower degree of education. In dentistry the delegation of the restoration of small cavities to dental hygienists or dental nurses is widely explored. For such an approach more simple restorative systems are required. A possible solution in this area might be found in application of the direct bonding glass ionomer cements as a less demanding alternative to resin-based composites Glass ionomer cements The early conventional glass-ionomer materials were technique-sensitive, slow setting, opaque when set and sensitive to both desiccation and hydration during setting. This led to premature surface deterioration. Most of these problems have (more or less) been solved in newer generations of glass-ionomer cement. Setting has been accelerated and hydration problems have been reduced. However, unlike composites, their use in stressed situations is still questionable. The most common indication of the newer, heavily filled, reduced particle size glass-ionomer cements is in non-stress bearing build-ups, root caries, tunnel restorations and long term provisional restorations in primary and adult dentitions. The cement is formed as a result of poly-acidic attack of the outer shell of fluoride containing soluble aluminum-glasses. Dissimilar to resin- based composites that have no chemical reactivity after setting, glass ionomer cements remain reactive for a prolonged time. Also quite the opposite to resin-based composites, bond formation of glass ionomer cements to mineralized tissue is no problem. Although the bond strength reaches only 25% of that can be obtained with resin-based bonding systems, the bond is reliable and far more degeneration resistant than the resin systems, where the hybrid layer can break up with time (Pashley et al., 2004; Yoshida et al., 2004, ). Glass-ionomer cements do not require extra provisions for consistent retention or adhesion, as they adhere directly to, even humid, dental hard tissues (Mount, 1994; McLean, 1996) (See also Fig. 1). As filling material, glass-ionomer cement mimics tooth color not as good as composites do and show faster surface loss by wear, but since it is less technique demanding it may serve in many ways more


Fig. 1.GIC bond strength [MPa] to clean and contaminated substrates. successfully than resin-based composites. Dependant on tradition, in some countries (e.g. Australia, UK) full glass-ionomer Class III restorations are generally accepted, while the material is merely used as only dentine replacement in sandwich restorations. For the time being resin-based composites possesses superior surface characteristics. The resin-modification of glass-ionomer cements, introduced to obtain command set glass- ionomer cements, did not contribute to higher wear resistance (De Gee et.al, 1996). Resin modified glass-ionomer cements are materials in which a hydrophilic polymerizing resin is added to the glass-ionomer matrix. The admixed resin improves initial aesthetics and tensile strength and fracture toughness. Also desiccation and hydration problems are reduced. Resin-modified glass-ionomer cements set partly through an acid-base reaction and a polymerization of the resin component of the matrix. The resin component can be light-cured. Another portion of the setting process involves the typical acid-base process between the filler and the poly-acid matrix. The latter reaction does not progress as complete as is the case with traditional glass-ionomers. The hydrophilic character of the resin component also contributes to osmotic swelling. Another step in merging the characteristics of resin-based composites with those of traditional glass-ionomer cements was the introduction of the poly-acrylic acid modified composite resins, also called compomers. Compomers were intended as to optimally combine the properties of glass-ionomers and resin-based composites. If regarded as a more or less temporary restorative, compomers can replace resin-based composite in anterior proximal restorations and have become in many countries the material of first choice in pediatric

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dentistry. In almost all other applications, traditional composites and glass-ionomer cements are preferred because of greater strength and wear resistance and better dimensional stability. As a matter of fact, a disadvantage of compomers is that ease of handling was obtained at the cost the established specific properties of hybrid resin-based composites and a proper glass-ionomer reaction. Within the framework of mixing resins with inorganic materials, it has to be realized that conventional glass-ionomer is a pure inorganic material and thus is predisposed to acid erosion. Fig. 2 shows how decreasing pH affects wear significantly.

Fig. 2. pH-dependent erosive wear of conventional and light-curing glass-ionomers.

This acid susceptibility is less present for the resin-modified glass-ionomers. Note that wear as such for the resin-modified types is considerably faster than for conventional ones. Fig 3 shows how conventional glass-ionomers seriously can erode when used interdentally in risk patients. Also excessive consumption of soft drinks might put conventional glass-ionomer restorations at risk (See Table 3).

water 7.0 mineral water 4.1 coffee 3.8 orange juice 3.2 beer 4.3 seven-up 3.2 yoghurt 3.8 apple juice 2.8 wine 3.4 coca cola 2.7

Table 3. pH values of some soft drinks

For direct restorative dentistry, the slow setting of conventional glass-ionomer cements is felt as an inconvenience. Apart from the nuisance of waiting for finishing the restoration, a drawback of the slow setting is that the water


Sealants Thanks to their applicability under humid conditions and direct bonding to tooth enamel (Aboush and Jenkins, 1986), the inorganic glass-ionomer cements are also practicable alternatives for resin fissure sealings. Notwithstanding the affirmed low wear resistance of glass-ionomers, which causes the sealant to erode already after some months, its preventive effect was reported still effective after 5 years (Mejare and Mjör, 1990; Smales and Gao, 1997). Arends et al., (1989), Campos Serra and Cury (1992) and Glasspoole (2001) explained this result by effective fluoride released from the glass-ionomer, which forms in relatively short time a reservoir in the adjacent enamel in a fluoridated hydroxyl apatite structure. Even the temporary presence of this material would already be responsible for the prolonged prevention efficacy. SEM images, obtained by replica techniques from the fissures showed clinically imperceptible, retained material (see Fig. 5).

Fig. 5. Clinical and SEM aspect of a two-year old glass-ionomer fissure sealing in a 47. The transformation is visible at the borderline of the fissure.

The presence of this material may be responsible for the prolonged prevention efficacy (Arends et al, 1989; Campos Serra and Cury, 1992). Literature is not conclusive on the reason why this retained material is more resistant to erosion (Davidson, 1998; Okada et al, 2001). Shimokobe (1993) suggested that under oral conditions, glass-ionomer sealants might gradually change into a new,

C. L. Davidson

more durable structure with high retention. He expected that with help of the mineralizing potential of saliva, glass-ionomers might transform into an enamel-like structure called “pseudo enamel”. In addition to the satisfaction with glass-ionomer as an effective way of preventing fissure caries, Van Duinen et al (2004) observed clinically visible changes in the glass-ionomer as shown in Fig. 5 and 6. These changes referred to translucency, smoothness and hardness. In analogy to the (re-) mineralizing power on tooth structures (Segura et al, 1997), the potential of saliva as a reinforcing agent for restorative materials was suggested.

Fig. 6. Various SEM magnification aspects of the altered glass-ionomer sealing of Fig. 5.

The ideal pit and fissure sealant should be a full proof obstruction for the damaging effects of dental plaque at sites of the tooth that hardly can be cleaned with domestic measures. A tight-adhering, erosion-resistant, impermeable layer covering the tooth fulfills that goal. If the retention and its erosion resistance are guaranteed for a substantial number of years, there is nothing against the use of the, basically inactive, resin-based materials for this purpose. However, application of resins requires extensive tooth surface conditioning, whilst the hydrophobic material is essentially unwelcome in the humid oral environment. In contrast to this, the hydrophilic glass-ionomer requires only minor substrate conditioning and shows a tight adhesion to enamel but unfortunately will erode easily. The findings of Mejare and Mjor (1990) that teeth sealed with resins more frequently develop caries than teeth sealed with glass-ionomer, in spite of the fact that the bulk glass-ionomer sealant had visually vanished within a few


months, were explained. by SEM-imaging, which revealed still retained “glass-ionomer” in the depth of the fissure at sites, where clinically no remnants of the cement were detectable. These remnants may be the same as the “intermediate” layer as postulated by Wilson et al. (1983), being the product of an exchange reaction between the poly-acid and the hydroxyl-apatite. That deeply hidden, difficultly accessible inorganic layer should possess a high acid- resistance as it constantly will be covered by dental plaque. It is reasonable to attribute this quality for a great deal to fluoride from the glass-ionomer. Van Duinen et al. (2004) demonstrated that glass-ionomer adjacent to tooth structure and in contact with the oral fluids, frequently altered into a material with unexpected cutting resistance and displaying raised Calcium- and Phosphate content. It was remarkable that such an altered layer was only detectable after a couple of years’ performance, whilst its thickness increased with time. This indicates that, with time, the exchange process continues and consequently the glass-ionomer restoration gains in quality, starting from the outer surface and the junction with tooth structure. It appears that, glass-ionomer performs clinically better than from laboratory research may be expected (Okada et al, 2001; Ferrari and García-Godoy, 2002). As saliva and its minerals play a crucial role in mineralization processes (Boksman et al, 1987), it can be understood that only under in vivo circumstances the glass-ionomer surface changed into the new structure. Okada et al (2001) showed that glass-ionomer stored in saliva has an improved surface hardness compared to samples stored into water. Also in deeper areas exchange processes has been reported. Geiger and Weiner (1993) demonstrated between dentin and glass-ionomer an intermediate exchange layer containing fluoridated carbonate-apatite. Yet literature is not conclusive on the clinical efficacy of glass-ionomer cements fluoride as measure to prevent demineralization or promote remineralization of adjacent tooth structure (Mjör, 1996; Wilson et al., 1997; Seppä, 1992). It has to be stressed that in these review articles on clinical trials on secondary caries prevention by glass-ionomer vs. amalgam or composite restorations, the reason why glass-ionomer was used was not given. It might very well be so that glass-ionomer was merely selected in caries prone patients. It appears that, glass-ionomer performs clinically better than from laboratory research may be expected (Okada et al., 2001; Ferrari and García-Godoy, 2002). As saliva and its minerals play a crucial role in mineralization processes (Boksman et al., 1987), it can be understood that only under in vivo circumstances the glass-ionomer surface changed into the new structure. Okada et al. (2001) showed that glass-ionomer stored in saliva has an improved surface hardness compared to samples stored into water. Also in deeper areas exchange processes has been reported. Geiger and Weiner (1993) demonstrated between dentin and glass-ionomer an intermediate exchange layer containing fluoridated carbonate-apatite. The fluoride content in glass-ionomers is much higher than in the tooth. With ion exchange over time, fluoride ions might diffuse from the cement to the tooth. In the process, some of the hydroxy-

C. L. Davidson

apatite in the tooth would be permanently transformed into fluoro-hydroxy-apatite (Forss and Seppä, 1990). The lower is the pH, the greater gets the fluoride release, a feature that justifies glass ionomer cements to be called intelligent materials (Davidson, 1998).

Conclusions

In contrast to resin bonding, the adhesion of glass-ionomer to tooth structure is not technique sensitive and its quality increases with time. Therefore glass-ionomer might turn out to the more reliable restorative material in minimal invasive dentistry based on adhesive techniques. Glass-ionomer is not only bioactive, but has even features of an intelligent material.1. For socio-economical reasons, direct restorative techniques are preferred over indirectones. 2.Interest in amalgam is fading. 3. Resin based composites are unforgiving, and still are far from perfect. 4. Shortcomings of composites invariably have to be tackled by sophistication of placement techniques. 5. Glass-ionomers and their application technique is still open for improvements.6. Glass-ionomers are forgiving, bio-active and intelligent materials. 7. Glass-ionomers holds a great potential to become the first choice direct restorative material.

This paper was presented at the VII Congress of BaSS Kusadasi, Turkey


References

1. Aboush YEA, Jenkins CBG. An evaluation of the bonding of glass ionomer restoratives to dentine and enamel. Br Dent J 1986; 161: 179-183.

2. Arends J, Christoffersen J, Ruben J, Jongebloed WL. Remineralization of bovine dentin in vitro. The influence of F content in solution on mineral distribution. Caries Res 1989; 23: 309 - 314.

3. Boksman L, Gratton DR, McCutcheon E, Plotzke OB (1987). Clinical evaluation of glass-ionomer cement used as a fissure sealant. Quintessence Int 1987; 18: 707 - 709.

4. Campos Serra M, Cury JA. The in vitro effect of glass-ionomer cement restorations on enamel subjected to a demineralization and remineralization model. Quintessence Int 1992; 23: 143 - 147.

5. Davidson CL. Glass-ionomer cement, an intelligent material. Bull Group Int Rech Sci Stom Odontol 1998; 40: 38-41.

6. Davidson, CL. Restorative materials. In: Dental Caries, the disease and its clinical management. ed: O. Fejerskov and E. Kidd. Blackwell/Munksgaard Publ. Co. Oxford U.K. ISBN 1-4051-0718-9. pp. 276-282.

7. De Gee AJ, van Duinen RNB, Werner A, Davidson CL. Early and long term wear of conventional and resin-modified glass ionomers. J Dent Res 75 (8): 1613-1619, 1996

8. De Munck J, Van Meerbeek B, Yoshida Y, Inoue S, Vargas M, Lambrechts P, Vanherle G. Four-year water degradation of total etch adhesives bonded to dentin. J Dent Res 2003; 82: 136-140.

9. Ferrari M, García-Godoy F. Sealing ability of new generation adhesive-restorative materials placed on vital teeth. Am J Dent 2002; 15: 117-128.

10. Forss H, Seppä L, Prevention of enamel demineralization adjacent to glass ionomer filling materials. Scand J Dent Res 1990; 173-175.

11. Geiger SB, Weiner S. Fluoridated carbonatoapatite in the intermediate layer between glass-ionomer and dentin. Dent Mater 1993; 9: 33-36.

12. Glasspoole EA, Erickson RL, Davidson CL. Demineralization of enamel in relation to the fluoride release of materials. Am J Dent 2001; 14(1): 8-12.

13. Health Council of the Netherlands: Committee on Dental Restorative Materials. Dental Restorative Materials. Rijswijk: Health Council of the Netherlands, 1998; publication no. 1998/09.

14. Kleverlaan CJ, van Duinen RNB, Feilzer AJ. Mechanical properties of glass ionomer cements affected by curing methods. Dent Mater 20(1): 45-50, 2004

15. Marek MI. Alterations of Dental Amalgam. In: Eliades G. et al (eds), Dental Materials In Vivo. Publ: Quintessence Chicago, 2003: 61-77.

16. McCabe JF. Applied Dental Materials. 7th Edition Publ: Blackwell Munksgaard, 1996.

17. McLean JW. Dentinal bonding agents versus glass-ionomer cements. Quintessence Int 1996; 27: 659-667

18. Mejare I, Mjør IA. Glass-ionomer and resin-based fissure sealants: a clinical study. Scan J Dent Res 1990; 98: 345-50

19. Mjør IA. Glass ionomer cement restorations and secondary caries: A preliminary report. Quitessence Int 1996; 27: 171-174.

20. Mount GJ. Glass-ionomer cements: Past, present and future. Oper Dent 1994; 19: 82-90

C. L. Davidson

21. Smales RJ, Gao W, Ho FT. In vitro evaluation of sealing pits and fissures with newer glass-ionomers developed for the ART technique. J Clin Ped Dent 1997; 21(4): 321-323.

22. Okada K, Tosaki S, Hirota K, Hume WR. Surface hardness change of restorative filling materials stored in saliva. Dent. Mat 2001; 17: 34-39.

23. Pashley DH, Tay FR, Hashimoto M, Breschi L, Carvalho RM, Ito S. Degradation of dentin collagen by host-derived enzymes during aging. J Dent Res 4004; 83: 216-221.

24. Schuurs AHB, Davidson CL. Amalgaam. De feiten. Nijmegen, STI, 1998 STI, L. Hofmman. Pb.1191, 6501 BD Nijmegen. ISBN 90-6759-019-3.

25. Preston AJ, Agalamanyi EA, Higham SM, Mair LH. The recharge of esthetic dental restorative materials with fluoride in vitro-two years' results. Dent Mater 2003; 19(1): 32-7.

26. Segura A, Donly KJ, Stratmann RG. Enamel remineralization on teeth adjacent to Class II glass-ionomer restorations. Am J Dent 1997; 10: 247-250.

27. Seppä L, Salmenskivi S, Forss H. Enamel and plaque fluoride following glass ionomer application in vivo. Caries Res 1992; 9: 175-193.

28. Shimokobe H. Properties as a pit and fissure sealant. In: Glass-ionomer dental cement, the materials and their use. S. Katsuyama, T. Ishikawa and B Fujii (eds), Ishiyaku EuroAmerica Inc. Publishers, St.Louis, Tokyo, 1993.

29. Söderholm, K-J. Degradation mechanisms of dental resin composites. In: Eliades G. et al (eds), Dental Materials In Vivo. Ed. Chicago: Quintessence 2003: 99-124

30. Ten Cate JM, van Duinen RNB. Hypermineralization of dentinal lesions adjacent to glass-ionomer cement restorations. J Dent Res 1995; 74: 1266 – 1271.

31. Van Duinen RNB, Davidson CL, de Gee AJ, Feilzer AJ, In situ transformation of Glass-ionomer into an Enamel-like Material. Am J Dent 2004; 17; 223-227.

32. Van Duinen RNB, Kleverlaan CJ, de Gee AJ, Werner A, Feilzer AJ. 2003Early and long term wear of ‘fast-set’ conventional glass ionomer cements. Submitted to J Dent Res.

33. Wilson AD, Possner HJ, Powis DR. Mechanisms of adhesion of polyelectrolite cements to hydroxyapatite. J Dent Res 1983; 62: 590-592.



10 years of BaSS

GLASS-IONOMER CEMENTS IN DENTISTRY: THE CURRENT POSITION

School of Science,University of GreenwichChatham Maritime,Kent ,United Kingdom.

John W. Nicholson

Summary: Glass-ionomer cements have become important dental restorative and luting materials, finding particular application in paediatric dentistry. They form chemical bonds to enamel and dentine, which prove highly durable over time. They are biocompatible, and release fluoride ions which can be taken up by adjacent tooth structure. Modern glass-ionomers are much easier to use than the earlier versions, and high-viscosity materials have been developed for use with the Atraumatic Restorative Treatment (ART) technique. Resin-modified glass-ionomers have improved toughness compared with conventional glass-ionomers, and have established niche applications, also in paediatric dentistry. As well as in resin-modifed glass-ionomers, the fundamental chemistry of glass-ionomers has been employed in composte resin systems, both compomers and giomers. Both are essentially composite resins, and their properties and clinical indications are those of composites. In both cases, it is doubtful if the glass-ionomer chemistry adds anything significant to their performance. Introduction: Glass-ionomers have been used in various areas of restorative dentistry for approaching 30 years. Invented and originally described by Wilson and Kent [1], they consist of a basic glass powder and a water-soluble acidic polymer, such as poly(acrylic acid). The glass powder is a calcium (or strontium) aluminofluorosilicate [2]. Setting occurs by neutralization, and involves initial formation of calcium or strontium polyacrylate and later formation of aluminium polyacrylate. There is also evidence for a later, slow reaction involving the ion-depleted inorganic species from the acid-attacked glass [3]. Glass-ionomers are classified into three categories, namely conventional, metal-reinforced and resin modified [4-6]. All involve the acid-base setting chemistry of the original glass-ionomer, but in the case of resin-modified glass-ionomers this is augmented by a polymerization reaction of an additional monomer, typically 2-hydoxyethyl methacrylate, HEMA. Metal-reinforced glass-ionomers set only by the acid-base process, and are strengthened by the inclusion of finely divided metal powers, typically the silver-tin alloy of dental amalgams [7]. Recently fast-setting, high-viscosity conventional glass-ionomers have been developed [8]. These were developed during the early 1990s for use with the atraumatic restorative treatment (ART) technique in developing countries. These are considered later in this article, and the clinical success of the ART approach has relied on the improved properties of these newer glass-ionomer materials.


Properties of Glass-ionomers:

Adhesion Glass-ionomers form a natural adhesive bond to tooth structure (enamel or dentine) [9]. This seals the cavity, preventing leakage at the margins, protecting the pulp and eliminating secondary caries [11] The adhesive bond arises due to an ion-exchange process at the interface [4,10], and in strontium-based glass-ionomers, this has been shown to result in strontium migrating from the cement to well inside the tooth surface, and calcium migrating from the tooth to well inside the cement [12]. The result is a very durable bond to the tooth [10]. When determined relatively soon after placement, reported shear bond strengths of glass-ionomers are of the order of 3-7 MPa [6, 13]. However, because the material fails cohesively, this is actually a measure of the tensile strength. As the cement matures, the tensile strength increases, and failure rates in clinical service are very low [14]. Despite the good adhesion, conventional glass-ionomers show some microleakage at the margins of restorations. One in vitro study showed that conventional glass-ionomers were less reliable in sealing enamel margins than composite resin [15], and that there was significant dye penetration at the gingival margins.

Appearance Conventional glass-ionomers are tooth coloured, and have a degree of translucency, which gives them reasoable aesthetics. However, they are less aesthetic than composite resins, mainly because they remain relatively opaque compared with the tooth itself [11].

Fluoride release The glasses from which these cements are made contain fluoride, and some of this is transferred to the matrix during setting. From there it can be released, essentially without altering the physical properties of the cement [16]. Release has been shown to occur by two mechanisms, an early "wash-out" process, and a longer-term diffusion process [17]. The long-term nature of the release can continue over a long period of time, with one in vitro study showing release over a period of five years [18]. Fluoride release has been suggested to make glass-ionomers cariostatic when used clinically [19]. This is supported by in vitro studies using an artificial caries gel, when teeth restored with glass-ionomer and stored in this gel showed less decalcification than unrestored teeth stored similarly [20, 21]. However, clinical studies are more equivocal. For example, studies of the reasons given by dentists for replacement of restorations have shown that glass-

W. Nicholson

ionomers are as likely to be associated with secondary caries as composite resins [22, 23], which suggests that they may not be proving as cariostatic in clinical use as has been anticipated. As well as releasing fluoride, glass-ionomers are capable of taking up fluoride under appropriate conditions, eg from dentifrices, mouthwashes and topical fluoride solutions [24, 25]. This makes glass-ionomers permanent suppliers of fluoride, a feature that is advantageous for patients with high susceptibility to dental caries. Mechanical properties Glass-ionomers have good comporessive strengths, with modern restorative materials having values in excess of 200 MPa [26]. However, toughness is poor, and this leads to them being brittle and having low resistance to wear and abrasion [11]. This limits their use, and they cannot be used, for example, in repairing incisal edges of teeth, where composite resins again have the advantage. The longest recorded survival times for conventional glass-ionomers are consequently in areas of low stress, such as Class III and Class V restorations [16]. Clinical aplications of conventional glass ionomers: Glass-ionomers have found considerable use in paediatric dentistry for many years. The occurrence of caries in children is widespread, though declining, and restoration of carious teeth remains an important clinical procedure. Restoration of the primary dentition is less demanding than for the permanent dentition, because the restoration will be in use for much less time, and also experience lower biting forces than in adults [27, 28]. Glass-ionomers are well suited to these uses, and they have the additional advantages of fluoride release and adhesion [29]. The possibility of relatively quick placement is also advantageous when treating young children [28]. In adults, glass-ionomers are widely used to repair Class V cavities, a technique which exploits the inherent adhesion of these materials. Clinical results for this procedure are good, though in vitro studies suggest that resin-modified glass-ionomers, with their enhanced fracture toughness, and improved bond strength, are likely to give superior results [30]. Early glass-ionomer luting cements were particularly success. They were strong enough to cement stainless steel crowns, space maintainers and individual orthodontic brackets. Fluoride release was considered an added advantage in these applications [31]. They continue to be supplied for this purpose, and recent studies have suggested that capsulated versions of these materials, which benefit from controlled high-energy mixing by machine, give superior luting properties, at least in vitro [32].


Metal-containing glass-ionomers were developed in the 1980s in an attempt to create stronger and more durable cements. One approach was to add silver-tin alloy, and another was to preform a glass-silver metal hybrid material called a cermet. The latter was less successful, and resulting cements did not show any improvement in mechanical properties [7]. The main advantage of these materials was that the presence of silver made them radiopaque, but the fact that the fracture resistance and fracture toughness were no higher than for conventional glass-ionomers meant that these materials still could not be used in stress-bearing regions of the teeth [33]. However, there were some reports on the use of the cermet-containing cement as an amalgam substitute in children [34, 35]. However, this use declined with the introduction of resin-modified glass ionomers in the early 1990s [33]. One important application for conventional glass-ionomers is in the ART technique. This is based on two main principles, namely the removal of caries with hand instruments only and the restoration of the cavity with an adhesive materials, ie a conventional high-viscosity glass-ionomer [36]. The technique is available to all population groups, and employs minimal cavity preparation that conserves sound tooth material and reduces the trauma of repair. Clinical results with ART have been found to be good. For example, in one report, which involved a long-term oral health programme in schools in Zimbabwe, survival rates for one-surface ART restorations averaged 85.3% [37]. The most common cause of failure was unacceptable marginal defects (8.1%), with 6.1% falling out and 2.5% experiencing excessive wear. The mean treatment time for one-surface ART restorations without chairside assistance was 22.1 min. ART is therefore considered appropraite for population groups not receiving preventive and restorative care [37]. Resin Modified Glass-ionomers: Resin modified glass-ionomers are a subset of the main glass-ionomer class. They consist of the same components as conventional glass-ionomers, ie water, basic glass powder and polyacrylic acid, but with the addition of 2-hydroxyethyl methacrylate (HEMA) as the resin component [38]. They also usually contain photosensitive initiators designed to bring about free radical polymerization on irradiation with blue light from a conventional dental curing lamp. Certain brands also have HEMA side-chains grafted onto the polyacrylic acid backbone [39]. The overall effect of this highly varied chemistry is that resin modified glass-ionomers are complex materials [40]. There is some tendency for them to undergo phase separation. In their unset state, this is driven by the thermodynamic effects of the relatively non-polar HEMA in the aqueous solution of polyacrylic, and on setting, is exacerbated by the insolubility of

W. Nicholson

polyHEMA in water. Thus, the set material may consist of domains of differing composition. Regardless of this, their clinical performance is good, and they are now widely used and popular materials [41]. The presence of polyHEMA gives resin modified glass-ionomers some hydrogel character. This means that they will take up water [42-46], with the extent of uptake being determined by inter alia the chemical potential of water in the surrounding medium [45]. Experimental studies have shown that water uptake is greater from pure water, where the chemical potential is greatest, than from 0.9% NaCl solution [45]. A postive effect that resin modified glass-ionomers share with conventional glass-ionomers is the ability to release fluoride [47]. This has been shown to be greater in acid solution than in neutral [48]. Other ions have also been shown to be released by these materials by these materials, again with greater release under acidic conditions [48]. Resin-modified glass-ionomers have significantly higher flexural and tensile strengths than conventional glass-ionomers [11]. This means that they are more resistant to fracture. However, this has not resulted in improvements to their wear-resistance, and as a result they tend to be used in non-load bearing applications. Like conventional glass-ionomers, resin-modified glass-ionomers have found particular use in children's dentistry. Uses include restoration of the primary dentition [49, 50], luting and bonding of orthodontic bands. For restorative work, light-curable versions of these cments are used, with cure being brought about about with a dental curing lamp for up to 40 seconds per layer. For luting, resin-modified glass-ionomers that initiate polymerization simply by mixing two-component initiator systems can be employed, and these do not require the application of light On the other hand, some materials of this type exploit the translucency of the tooth, and these do employ light to bring about cure [51]. Compomers: Polyacid modified composite resins, informally known as “compomers” are complex materials that make some use of glass-ionomer chemistry [52]. They mainly consist of the same components as conventional dental composite resins, materilas that have been successfully used in clinical dentistry for many years [53]. However, they also contain minor amounts of an acid-functional monomer, and some reactive glass of the type used in glass-ionomer cements [54]. They therefore cure by polymerization but also have a later acid-base neutralization reaction due to the gradual uptake of water in situ. This gives them the desirable feature of fluoride ion release [55] and, in addition, some have been claimed to be able to adhere to tooth structure directly [56].


Since their introduction in the early 1990s, there have been a number of reports on the properties of compomers under different storage. An in vitro comparative study on the mechanical and physical properties of four compomers stored for 24 hour showed that these materials have acceptable properties for clinical use [57]. Water up-take is essential to promote the later acid-base reaction [58] but there is evidence that it has deleterious effects on the strength of these materials [59] and on their surface texture [60]. Mechanical properties such as compressive, diametral and biaxial flexural strengths of commercial compomers have been determined in different storage media at different times [61]. Environmental conditions were found to affect the strength of the materials with time with the most striking finding being that specimens stored in dry conditions underwent slight increases in strength, whereas all specimens stored in wet conditions became significantly weaker. Hence the water uptake, though essential to promote the secondary acid-base reaction, actually weakens the compomer. This would be expected to occur in the moist conditions of the mouth, and in this way the performance of these materials may be compromised. Giomers A giomer is a new type of restorative material that is based on composite resin, but filled with ground pre-reacted glass-ionomer cement particles. Giomers behave essentially as composite resins, and are light-curable. They need to be bonded using the typical resin bonding systems, which involve surface treatment and the application of bespoke bonding agents. However, they have the important property of fluoride release, which gives them some similarity to glass-ionomers. Unlike glass-ionomers, they do not have the initial burst of release, and their diffusion-based fluoride release is at a lower level than conventional glass-ionomers [62]. Because of their fundamental composite resin nature, giomers are easier to polish than glass-ionomers [63]. To date there have been few reports of the clinical performance of giomers. However, one three-year clinical study has appeared comparing the performance of a giomer and a composite resin in Class V cavities. Eight performance characteristics were measured, after which it was concluded that there were no significant differences between the two materials [64]. Not surprisingly, given their composition, giomers show very similar behaviour to composite resins. It is doubtful whether the inclusion of pre-prepared glass-ionomers makes any significant difference to these materials, and they are not fundamentally new materials, but a very slightly modified version of well-established materials. The modest fluoride release is unlikely to prove important.

W. Nicholson

Conclusions:

This review has shown tha glass-ionomer cements are important materials for use by dental clinicians, with particular benefits when used in paediatric dentistry. They bond to enamel and dentine, are biocompatible, and release fluoride. Among the modern glass-ionomer cements now being used clinically are the high-viscosity materials have been developed for use in the Atraumatic Restorative Treatment (ART) technique. Resin-modified glassionomers have better toughness compared with conventional glass-ionomers, and have established specific clinical applications, including in paediatric dentistry. The fundamental chemistry of glass-ionomers has also been employed in composite resin-based systems known respectively as compomers and giomers. Both have properties that are dominated by their essential composite resin nature and their clinical uses reflect this. However, both exhibit the property of fluoride release, and this may confer advantages under certain clinical conditions.

This paper was presented at the IX Congress of BaSS, Ohrid, FYROM

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ionomer composite resin systems, J. Esthet. Dent., 1994;6:227-244. 14. Tyas MJ. Cariostatic effect of glass ionomer cement: a five-year clinical study.

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restorations: a laboratory study. I., The influence of glass ionomer cement, Aust Dent. J., 1992;37:23-30.

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17. Verbeeck RMH, De Maeyer EAP, Marks LAM, De Moor RGJ, De Witte AMCJ, Trimpeneers LM. Fluoride release process of (resin-modified) glass-ionomer cements versus (polyacid-modified) composite resins, Biomaterials 1998;19:509-519.

18. Forsten L. Short- and long-term fluoride release from glass ionomers and other fluoride-containing filling materials in vitro, Scand. J. Dent. Res., 1990;98:179-185.

19. Mount GJ Glass ionomer cements: past, present and future, Oper. Dent., 1994;19:82-90.

20. Swift EJ Jr. An update on glass ionomer cements, Quintessence Int 1988;19:125-30.

21. Souto M, Donly KJ. Caries inhibition of glass ionomers, Am J Dent 1994;7:122-4. 22. Mjor IA. Glass-ionomer cement restorations and secondary caries: A

preliminary report. Quintessence Int 1996;27:171-174. 23. Wilson NHF, Burke FJT, Mjor IA. Reasons for placement and replacement of

restorations of direct restorative materials by a selected group of practitioners in the United Kingdom. Quintessence Int 1997;28:245-248.

24. Marinelle CB, Donly KJ, Wefel JS, Jakobsen JR, Denehy GE. An in vitro comparison of 3 fluoride regimens on enamel remineralization, Caries Res 1997;31:418-422.

25. Donly KJ, Nelson JJ. Fluoride release of restorative materials exposed to a fluoridated dentifrice, ASDC J Dent Child, 1997;64:249-250.

26. Williams JA, Billington RW. Changes in compressive strength of glass ionomer restorative materials with respect to time periods of 24 h to 4 months, J Oral Rehabil 1991;18:163-8.

27. Kilpatrick NM, Murray JJ, McCabe JF. The use of a reinforced glass-ionomer cement for the restoration of primary molars: a clinical trial, Br Dent J 1995;179:175-179.

28. Hickel R, Voss A. A comparison of glass cermet cement and amalgam restorations in primary molars, ASDC J Dent Child 1990;50:184-188.

29. McLean JW, Wilson AD. The clinical development of glass ionomer cement. II. Some clinical applications, Aust Dent J 1977;22:120-127.

30. Sonia G, Van Meerbeck B, Lambrechts P, Vanherle G. Marginal adaptation and retention of glass ionomer, resin modified glass ionomer and a polyacid

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modified resin composite in cervical Class V lesions. Dent Mater 1998;14:294-306.

31. Donly KJ, Istre S, Istre T. In vitro enamel reminerlaization at orthodontic band margins cemented with glass ionomer cement. Amer J Orthodont Dentofac Orthopod, 1995;107:461-464

32. Mitchell CA, Orr JF, Russell MD. Capsulated versus hand-mixed glass-ionomer luting cements for post retention, J Dent 1998;26:47-51.

33. Croll TP and Nicholson JW. Glass ionomer cements in children’s dentistry - a review of the literature. Pediatric Dent, 2002; 24: 423-425.

34. Croll TP, Phillips RW. Glass ionomer-silver cermet restorations in primary teeth Quintessence Int 1986;17:607-615.

35. Croll TP, Phillips RW. Six years’ experience with glass ionomer-silver cermet cement. Quintessence Int 1991;22:783-793.

36. Frencken JE, van’t Hof MA, van Amerongen WE, Holmgren CJ. Effectiveness of single-surface ART restorations in the permanent dentition: A meta analysis, J. Dent. Res., 2004;83:120-123.

37. Frencken JE, Makoni F, Sithole WD, Hackenitz E. Three-year survival of one-surface ART restorations and glass-ionomer sealants in a school oral health programme in Zimbabwe, Caries Res., 1998;32:119-126.

38. Wilson AD. Resin modified glass ionomer cements. Int J Prosthodont, 1990; 3: 425-429.

39. Mitra SB, Adhesion to dentin and physical properties of a light-cured glass ionomer liner/base. J Dent Res 1991; 70: 72-74.

40. Nicholson JW and Anstice HM, The physical chemistry of light-curable glass-ionomers, J Mater Sci Mater Med, 1994; 5: 119-122.

41. Chinelatti MA, Ramos RP, Chimello DT, Palma-Dibb RG. Clinical performance of a resin-modified glass-ionomer and two polyacid-modified resin composites in cervical lesions restorations: 1-year follow-up. J Oral Rehabil, 2004; 31:251-257.

42. Nicholson JW, Anstice HM and McLean JW, A preliminary report on the effect of storage in water on the properties of commercial light cured glass-ionone cements. Br Dent J 1992; 173: 98-101.

43. Kanchanavasita W, Pearson GJ and Anstice HM. Water sorption characteristics of resin-modified glass-ionomer cements. Biomaterials 1997;18:343-9.

44. Sidhu SK, Watson TF. Resin-modified glass ionomer materials, Am J Dent 1995;8:59-67.

45. Nicholson JW, The physics of water sorption by resin-modified glass-ionomer cement. J Mater Sci Mater Med 1997;8:691-695.

46. Yap AUJ, Lee CM, Water sorption and solubility of resin modified polyalkenoate cements. J Oral Rehabil, 1997;24:310-314.

47. Mitra SB, In vitro fluoride release from a light-cured glass-ionomer liner/base. J Dent Res 1991;70:75-78,

48. Forss H, Release of fluoride and other elements from light cured glass ionomers in neutral and acidic conditions. J Dent Res 1993;72:1257-1262.

49. Croll TP, Killian CM. Visible light-hardened glass ionomer-resin restorations for primary teeth: New developments, Quintessence Int 1992;23:679-682.

50. Croll TP, Killian CM. Glass ionomer-resin restoration of primary molars with adjacent Class II carious lesions, Quintessence Int 1993;24:723-727.


51. Croll TP, Helpin ML. Space maintainer cementation using light-hardened glass-ionomer/resin restorative cement. ASDC J Dent Child 1994;61:246-248.

52. McLean JW, Nicholson JW, Wilson AD. Proposed nomenclature for glass-ionomer dental cements and related materials, Quintessence Int 1994;25:587-589.

53. Anusavice KJ. Phillips’ Science of Dental Materials, WB Saunders, Philadelphia, 1994.

54. Meyer JM, Cattani-Lorente MA, Dupuis V. Compomers: between glass-ionomer cements and composites, Biomaterials 1998;19:529-539.

55. Shaw AJ, Carrick T, McCabe JF. Fluoride release from glass-ionomer and compomer restorative materials: 6-month data, J Dent 1998;26:355-359.

56. Dentsply, Dyract AP - The Compomer with Advanced Performance, in Technical Manual. 1997, Dentsply. p 11.

57. Latorre-Garcia M, Barcelo FH, Vera-Graziano R. Mechanical and physical properties of four compomers: in vitro comparative study, J Dent Res 2002. IADR San Diego (Abstr. 3291).

58. Eliades G, Kakaboura A, Palaghias G. Acid-base reaction and fluoride release profiles in visible light-cured polyacid-modified composite restoratives (compomers), Dent Mater 1998;14:57-63.

59. Nicholson JW, and Alsarheed M. Changes on storage of polyacid-modified composite resins, J Oral Rehabil, 1998;25:616-620.

60. Abur Bakr N, Han L, Okamoto A, Iwaku M. Color stability of compomer after immersion in various media. J Esthet Dent. 2000;12:258-63.

61. Adusei G, Deb S, Nicholson JW. Comparative studies of physical properties of commercial polyacid-modified composite resins (compomers), Dental Forum (Poland), (in press).

62. Yap AUJ, Tham SY, Zhu LY, Lee HY. Short-term fluoride release from various aesthetic restorative materials, Oper Dent, 2002;27:259-265.

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10 years of BaSS

ADHESIVE DENTISTRY :FUTURE FROM THE PAST

Faculty of Dentistry, University of BelgradeSerbia and Montenegro

Zoran R. Vulicević, Ivana Davitkov, Dejan Marković, Aleksandar Todorović

Summary

Today the goal of adhesive dentistry is to acomplish the development of a truly adhesive bond between a restorative material and the natural tooth structures. Contemporary dentin bonding agents and composite systems are offering possibility to adhere, seal, provide durable bond, long lasting surface in very harsh environment. Adhesive approach to the reconstructive dentistry is enhancing conservation of tooth structure during preparation. The aim of this paper is to present the development of dentin bonding agents and their present status, interface between tooth and composite resin with all relevant clinician procedures regarding this matter. The new classification of dentin bonding agents will be presented as recommendation to the practitioners. Results of some studies will be used in discussion to clear the influence of composite resin on dental tissue, bond strength and nature with some compatible materials such are metal and ceramics. Key words: dentin bonding agents, dental materials, adhesion, enamel and dentin tissue Introduction

Rapid changes occurring in the field of restorative dentistry during the last few decades have transformed the practice of dentistry. Not only do we see restorative changes occurring because of technologic advances in materials and devices but also because of patients’ demand for aesthetic, safe and durable dental care. The main breakthrough in aesthetic dentistry was opening the era of acid etching of enamel and latter dentin bonding procedures. Dentists must keep up with this rapid pace of change to stay in tune with latest developments. Therefore, it seams reasonable to gather some of scientific data and clinical experience in a state of the art aesthetic dentistry at the start of this century. This paper will present development of dentin bonding agents from the early beginnings with methacrylate-bonding to now days tissue sealing and resin infiltration. The efforts to distinguish the nature of the bond between composite systems, enamel and dentin tissue (mechanical vs. chemical bonding) will be presented. One could say that development of dentin bonding agents should lead to new generations of chemicals that provide intimate contact between cavity walls and restorations without microleakage.

The nature of a bond between two different materials might be mechanical, chemical, or a combination of these two. Typical example of mechanical bond is penetration of composite resin into etched enamel. After

Z. R. Vulićević et al

setting of the resin micromechanical interlocking is achieved. This is a base for good seal, adaptation and it prevents gap formation and microleakage around composite filling.

The benefits of the reliable and durable adhesion between tooth structures and composite resin are twofold: conservation of sound tooth tissues and elimination of bacteria penetration around cavity walls. The development of dentin bonding agents in the beginning was based on efforts to achieve chemical bonds, where one part of adhesive molecule bonds with Ca++ ions and another part copolymerizes with succesively applied composite resin. For this purpose a methacrylate was used1. The other possibility at that time was to establish covalent bond to dentin proteins, preferably collagen.

Fig.1: SEM micrograph of etched enamel with 37% orthophosphoric acid after 30 seconds.

Fig.2: SEM micrograph of DBA- dentin interface with Dentsply bonding agent.

Samples were demineralized and deproteinized.

Resin enamel bonding is the most reliable and most predictable of all

bonding procedures. The basis of this type of bond is etching enamel with phosphoric acid. This started with research of Buonacore in 1955 when he described the use of 85% phosphoric acid on enamel surface2. This acid was firstly applied on enamel surface for one minute. Even with such a strong concentration, the effect on the pulp was no more severe than that of distilled water according to research of Gwinett3,4. That opened the safe approach for this handy and elegant method in future conservative dentistry. Now days the use of 35 to 37% phosphoric acid is advocated for 15 to 30 second on enamel tissue5. During this time micro gaps can be find within the depth of 25 to 50 microns into subsurface enamel. Acid etching causes enamel prisms and interprismatic enamel to dissolve differently so that a microretentive pattern is formed6,7(Figure 1.). This gives a reliable basis for composite resin bonding. When the low viscosity bonding agents are placed on etched enamel surface, the resin enters the enamel gaps and forms resin tags deep into the structure of enamel. The use of the composite materials with acid etch technique can provide a durable and intimate marginal relationship with enamel. Bearing in mind the composition and structure of dentin tissue, one could easily recognize that obtaining adhesion to dentin in such a simple manner is not


almost completely denuded of hydroxyapatite, so possibility for additional chemical interaction is excluded. The adhesion mechanism to enamel and dentin is therefore based on diffusion and very similar to etch and rinse systems. Hybrid layers formed by these adhesives are 2-3μm wide, with morphological characteristics that closely resemble ones observed in etch and rinse systems46. Glass-Ionomer Based Adhesives

Glass-ionomer based adhesives (Fuji Bond LC – GC, Reactmer – Shofu) are usually used through two clinical application steps. In step one, polyalkenoic acid conditioner is applied, rinsed off and gently dried without dehydrating the surface, resulting in 0.5-1μm demineralization. Step two is the application of the bonding agent. Adhesion mechanism is twofold, and similar to mild self-etch adhesives: micro-mechanical, through hybridization, and chemical, through ionic bonding of carboxyl groups of the polyalkenoic acid with hydroxyapatite47. Laboratory Bond Strength Testing

One of possible ways to investigate and compare adhesive systems is laboratory bond strength testing. In the beginning, shear and tensile bond strength tests had been used. Along with the development of adhesive systems,

some drawbacks of these tests were recognized, like lack of standardization48. Another disadvantage of conventional tests is non-uniform stress distribution which, in contemporary adhesive systems, tends to produce mostly cohesive fractures of dentin, therefore precluding measurement of interfacial bond strength. In 1994, Sano et al. introduced microtensile bond strength test, using so-called hourglass designed specimens49. Although this method is more time consuming, the highest stress during testing is built-up right at the interface and fractures are mostly adhesive. It also makes

Fig.13: A sample prepared for microtensile bond strenght test. The upper half of the beam is made of composite resin and the lower half is dentin. Cross sectional area is 0,9mm2.


possible. Dentin tissue is surrounding pulp chamber and root canals. In coronal part it is covered with enamel and in root area with cementum. Dentin is composed of about 50% vol mineral, 30 % vol organic matter and 20 % vol fluid. By weight, 20% is organic material, primarily collagen and collagen-type compounds, and the inorganic percentage is about 70% presented as apatite or amorphous calcium phosphate. Structure of the dentin tissue can be described as a complex hydrated composite of four elements: oriented tubules surrounded by a highly mineralized peritubular zone, embedded in an intertubular matrix consisting largely of type I collagen with embedded apatite crystals, and dentinal fluid8. The dentinal tubules are not smooth tubes, but have irregular walls with many lateral branches and micro channels thet communicate with surrounding tubules. They are filled with odontoblastic processes close to the pulp chamber and they permit the fluid movement which is related to pain and sensitivity9. The normal mineral content of dentin can be found in two areas between tubules: in the intertubular dentin and concentrated in peritubular dentin. The apatite crystals are much smaller than in enamel tissue and therefore much more difficult to study. Crystallite orientation has some relationship with tubule direction. Dentin liquor is an extracellular tissue liquid with high protein content formed in the pulp. Due to the pulpal tissue pressure of 20 to 30 mm Hg, the dentin fluid flows outward. After tooth preparation with rotating instruments a specific structure is formed on the surface of dentin. It is a 1 to 5μm thick smear layer, that consists of hydroxyapatite crystals and denaturized collagen, and it can not be removed with cotton or water. This biological liner reduces sensitivity and lowers the rate of flow of the dentin liquor. However, smear layer in this form is not a reliable bonding surface10. Adhesive systems have most commonly been classified into generations, mostly according to the time of the release into dental market. The first dentin bonding generation was actually unfilled resin, based on a Bowen resin bis GMA which just improved wetting of enamel. Bond strength values with etched enamel were satisfactory - 15 to 20 Mpa, but bond to dentin was negligible. Second generation of DBA was based on organic phosphate esters and methacrylate which were bonded to calcium ions of hydroxyapatite in dentin (Figure 2.). Bond strength values with dentin ranged from 2 to 5 MPa. Unfortunately, the bond did not last as it was quickly broken due to hydrolysis of its ester bonds. The era of priming and conditioning the exposed dentin tissue started with the third generation of dentin bonding agents11. For the very first time bond strength values reached 7 to 15 MPa. The idea was to increase the wetability of dentin, and today it is a state of the art. There have been two major groups of dentin bonding agents: one where the smear layer was removed with chelating agents such is EDTA, or the other group with priming agents which modified the structure of the smear layer. A representative of the first group was Gluma bonding system where for the first time the resin tags were reported (Figure 3.), as a basis for micromechanical


retention. With second group (Superlux Prep, Prisma Universal bond 2) crystal like formations were reported as an interface between dentin tissue and composite resin12,13(Figure 4.).

Fig.3: SEM micrograph of Gluma bonding

resin tags that penetrated dentin after EDTA pretreatment. Samples were demineralized and deproteinized.

Fig.4: SEM micrograph of modified smear

layer with Prisma Universal Bond 2. Samples were demineralized and

deproteinized.

Classification of Contemporary Adhesive Systems

In the past few years, the so called “generation” classification has been criticized, as being mainly chronologically based, thus lacking scientific background and fairly describing adhesion mechanisms.

Contemporary adhesive systems are now classified in a different manner. The new classification evolved from the description of fundamental principle of adhesion. Basic adhesion mechanism is an exchange process comprising of removing inorganic tooth structure and replacing it with resin monomers14. Upon polymerization, resin monomers become micro-mechanically interlocked into created porosities, due to diffusion mechanisms, and it is believed that relationship achieved this way contributes the most to the final quality and longevity of the tooth-restoration interface (Figure 5.). Possibility for chemical interaction of resin monomers with tooth tissue was considered to be of secondary or no importance at all, depending on the adhesive system itself. Recently, the idea of possible advantages of chemical interaction between functional monomers and tooth tissue has drawn new attention, mostly in terms of potential benefits against hydrolytic degradation to which adhesive systems are exposed over a long period of clinical service15,16.

Depending on adhesion strategy and the intensity of exchange process, modern adhesive systems can be categorized into three major groups14: etch and rinse (formerly referred to as “total-etch systems”), self-etch and glass-ionomer based adhesives. Between each group, adhesives can be further classified according to the number of clinical steps required for application.


Fig.5: SEM micrograph of a two-step etch and rinse adhesive system PQ Clear (Ultradent) interface with dentin. Samples were demineralized (6N HCl, 30 seconds) and deproteinized (2.5% NaOCl, 10 minutes)* to enable the examination. A: adhesive layer. H: hybrid layer. R: resin tag. D: dentin.

Fig.6: SEM micrograph of enamel ground

with 600 grit Silicon carbide paper and etched with 37,5% orthophosphoric acid

(Gel Etchant – Kerr) for 15 seconds. A well defined etching pattern is visible.

Etch and Rinse Adhesives

Etch and rinse adhesive systems are used either through two or three clinical application steps. First step always involves application of the conditioner or acid etchant (30-40% phosphoric acid) on both enamel and dentin. In three-step etch and rinse systems (also categorized into 4th generation), first step is followed by application of the primer, or adhesion promoter, and in the third step bonding agent or adhesive resin. Two-step etch and rinse systems were next to be introduced (also known as 5th generation dentin bonding agents), offering primer and adhesive combined into one bottle. Bonding to phosphoric acid-etched enamel remains the most predictable and effective procedure in adhesive dentistry (Figure 6.).

Mechanism of adhesion to dentin is similar for three- and two-step etch and rinse systems. The first, etch and rinse phase, completely removes smear layer, opens dentinal tubules and demineralizes dentin surface to a depth of 3-5μm17. By this step, collagen fibrils become almost completely exposed, denuded of hidroxyapatite and form a micro-retentive network. Monomers that are successively applied should completely infiltrate the spaces between collagen fibers in order to achieve micro-mechanical interlocking, described and referred to as a hybrid layer18-22. Besides the process of hybridization, resin penetrates into opened dentin tubules and forms resin tags (Figure 7.). However, the length of resin tags itself does not influence bond strength and is considered to be of secondary importance. The adhesion mechanism in etch and rinse systems is purely based on micro-mechanical interlocking, since no chemical interaction is possible between collagen fibers depleted from hydroxyapatite and functional groups of monomers23.


Fig.7: SEM micrograph of a two-step etch and rinse adhesive system PQ Clear (Ultradent) interface with dentin. Samples were demineralized and deproteinized. An extensive resin penetration into dentin tubules is visible, along with forming of numerous lateral tags. A: adhesive layer. H: hybrid layer. R: resin tag. L: lateral tag. D: dentin.

Features of three-step etch and rinse systems

In three-step etch and rinse systems, primer and adhesive resin are applied in separate clinical steps. On dentin, priming step should assure transforming hydrophilic into hydrophobic state. Primer wets exposed collagen fibers, carries monomers into porosities between fibers and at the same time displaces residual moisture from the surface through evaporation of the solvent included in its formulation. Following priming step, adhesive resin is applied, aiming to fill remaining porosities between fibers, form resin tags that seal dentinal tubules and stabilize hybrid layer. Adhesive resin should also provide methacrylate double bonds for co-polymerization with the restorative resin. Unlike dentin, enamel tissue does not require a separate priming step, since being hydrophobic in nature. On the other hand, application of primer onto acid-etched dentin doesn’t negatively influence adhesion with enamel. When a wet bonding approach is followed (described later), and cavity is left moist after rinsing of the acid, it is important to apply primer on enamel to ensure that residual surface moisture is displaced through evaporation of the primer solvent. Features of two-step etch and rinse systems

Two-step etch and rinse systems were introduced in attempt to reduce the number of application steps and simplify the bonding procedure. Since priming and bonding step were joined, these systems needed to be formulated as more hydrophilic, compared to conventional three-step etch and rinse systems. The solvent to monomer ratio in these systems is also higher, which can result in applying the adhesive in a layer too thin. Bearing in mind that the layer too thin won’t polymerize, due to oxygen inhibition, some manufacturers recommend applying adhesive resin in multiple layers. This way, actual clinical


application time is not reduced, and in general, these systems have been described as being more technique sensitive than three-step systems24. Wet and dry bonding approach

The main reason for widely discussed technique sensitivity of etch and rinse systems is the questionable degree of surface wetness needed after rinsing the acid. While enamel should preferably be dry to allow penetration of adhesive monomers, proper treating of dentin is more complex. As mentioned before, etching and rinsing step leaves dentin surface demineralized to a depth of 3-5μm. More importantly, collagen fibers are exposed and left without inorganic support of hydroxyapatite. In order to achieve penetration of resin monomers into such a structure and assure interlocking, collapse of collagen fibers needs to be prevented. It has been described that overdrying of dentin surface induces collapse of collagen fibers which form a coagulate, thereby impeding proper resin penetration25. Depending on the kind of solvent of the primer (or primer/adhesive in two-step systems), two different clinical approaches have been described. One method is referred to as wet bonding, and it was introduced in the early ‘90s by Kanca26 and Gwinett27. This technique should be used with acetone based adhesive systems. The cavity is left visibly wet after rinsing the phosphoric acid, and wet bonding concept relies on the ability of acetone to displace residual water, at the same time carrying resin monomers into porosities of the collagen web. Acetone solvent is then gently dried to evaporate, while monomers stay left behind. The critical step in this approach is the precise amount of surface wetness. If a cavity is left too wet, solvent will not be able to displace all the water, and consequently, polymerization will be affected. The other, so-called “dry bonding” approach is less technique sensitive. This approach is advised to be used with water/ethanol based adhesives. In general, cavity should be slightly dried, since these primers can re-hydrate and re-expand the collapsed collagen fibers.

Regardless of the bonding technique used, the possibility for discrepancy between depth of dentin demineralization and monomer infiltration28-30 was recognized as a main drawback of etch and rinse adhesives. It was shown that leakage can exists within the porosities of the hybrid layer even in the absence of gap. This specific form of leakage is referred to as nanoleakage, and in its initial description it was explained by incomplete infiltration of resins into acid etched dentin31. Self-Etch Adhesives

The self-etching adhesive concept is generally based on the use of non-rinsing acidic monomers that simultaneously condition (etch) and prime enamel and dentin. This concept was first introduced in the early ‘90s with


Scotchbond 2 (3M), but this adhesive was applied on dentin alone, requiring a selective acid etching of enamel. Contemporary self-etching adhesives are applied on both enamel and dentin. According to the number of clinical application steps, further classification can be made to two-step and one-step systems.

In two-step systems (also referred to as 6th generation), application of a self-etching primer is followed by adhesive resin (AdheSE – Ivoclar Vivadent, Contax - DMG Hamburg, Clearfil SE – Kuraray, OptiBond Solo plus self-etch system – Kerr, Unifil Bond – GC).

One-step systems combine conditioning, priming and bonding into a single clinical step (following “generations” approach, classified into 7th generation). These systems can be further divided into two sub-groups. One group represents one-step two-components adhesive systems in which two components are mixed shortly before applying (Adper Prompt L-Pop – 3M ESPE, Prompt L-Pop 2 – 3M ESPE, Futurabond NR – Voco). The other group represents so called “all in one adhesives”, the newest achievement in adhesion to tooth structure. These are one-step one-component self-etching adhesives, that require no mixing (i-Bond – Kulzer, G-Bond – GC).

Self-etching systems are often referred to as utilizing the most promising adhesive approach. Since rinsing phase is excluded, so is the need for establishing the debatable optimal level of moisture on cavity surfaces, which significantly reduces technique sensitivity. These systems are user-friendly due to reduced number of application steps and reduced application time. Another important characteristic of self-etching systems is simultaneous demineralization and infiltration of resin monomers. This feature was believed to ensure that no discrepancies are possible between two processes, unlike etch and rinse systems.

However, recently published studies demonstrated the phenomenon of nanoleakage in some self-etching systems32 and concluded that the general concept that self-etch adhesives etch and infiltrate to the same extension in dentine doesn’t apply to all adhesives in this category. It was also pointed that the original description of nanoleakage should be redefined, since tracer identified spaces within the adhesive and hybrid layer are believed to form as a result of incomplete water removal from the adhesive itself, rather than incomplete resin infiltration33,34. Water is a common part of all self-etching systems. It ionizes acidic monomers, therefore enabling demineralization of tooth tissues. Lately, a lot of research has been focused on simplified, more hydrophilic one-step systems. Studies reported that these adhesives do not seal dentin very well, since being permeable to dentinal fluid, resulting in formation of water droplets along the adhesive-composite interface35.

Concern is often raised regarding the quality of adhesion of self-etching systems with enamel since the pH value of self-etching primers is a few times higher compared to phosphoric acid (Figure 8. and 9.). Numerous studies


showed that bond strength of self-etch systems to enamel was either in the range of etch and rinse systems, or lower36-39.

In addition to classification according to number of clinical steps, self-etching systems can be divided depending on etching aggressiveness, into mild, moderate and strong40,23. This particular classification may be meaningful as it is based on morphologic findings at the tooth-adhesive interface.

Fig.8: SEM micrograph of enamel ground with 600 grit Silicon carbide paper and etched with 37,5% orthophosphoric acid (Gel Etchant – Kerr) for 15 seconds.

Fig.9: SEM micrograph of enamel ground with 600 grit Silicon carbide paper and conditioned and primed with a self-etching primer (AdheSE – Ivoclar Vivadent).

Mild Self-Etch Adhesives

Mild self-etch adhesives have a pH of around 2, and demineralize dentin to a depth of 1μm, in a way that collagen fibers are not completely deprived of hydroxyapatite. Smear layer is dissolved and becomes an integral part of a hybrid layer which is less than 1μm thick (Figure 10.). Although hybrid layer is noticeably thinner compared with etch and rinse systems, it has been shown that this feature doesn’t negatively affect bond strength of self-etch systems41,42. An important characteristic of mild self-etch

Fig.10: SEM micrograph of a mild one-step one-component adhesive G-BOND (GC Corp.) interface with dentin. Samples were demineralized and deproteinized. Hybrid layer is not visible. Resin tags formation is minimal, with non-uniform tags and no lateral tags. C: composite resin. R: resin tag. D: dentin.


systems is possibility for additional chemical interaction between functional groups of monomers and calcium of hydroxyapatite that is surrounding collagen fibers. Using X-ray Photoelectron Spectroscopy (XPS)43 it is possible to investigate both the existence of a chemical interaction and its intensity, through quantification of the degree of ionic bond formation between acidic groups of functional monomers with calcium of hydroxyapatite. In a recently published study it was shown that investigated functional monomers (4-MET, phenyl-P and 10 MDP) of different mild self-etching systems do interact chemically with hydroxyapatite within a clinically reasonable time44. It has also been shown that the chemical bonding potential of the acid/acidic monomer will be higher if the calcium salt that it forms is less soluble45. Moderate self-etch adhesives

Moderate self-etch adhesives have a pH of around 1.5, which is why micro-mechanical interlocking at dentin and enamel induced by systems from this group is more intense compared to mild self-etch adhesives (Figure 11. and 12). Also, residual hydroxyapatite is present at the hybrid layer base, and might serve as a receptor for additional chemical reaction.

Figures 11 and 12: SEM micrographs of moderate two-step two-component adhesives AdheSE - Ivoclar Vivadent (figure 7) and Contax – DMG Hamburg (figure 8) interface with

dentin. Samples were demineralized and deproteinized. Resin tag formation with corresponding lateral tags is visible. Hybrid layer is not clearly visible. A: adhesive. R: resin

tag. L: lateral tag. D: dentin.

Strong self-etch systems

Strong self-etch systems have a pH of 1 or less, and degree of demineralization induced on enamel and dentin is the highest among self-etching systems. Dentin is demineralized in a way that hydroxyapatite is


possible to measure bond strength on any area of the tooth, on sclerotic or on caries affected dentin, and even calculate means and variances for single tooth. In the last decade this method has been widely excepted and at the same time criticized and modified. Shono et al50 introduced the so-called non trimming version of microtensile test, which uses sticks (beams) made half of dentin/enamel and half of composite resin, with a cross-sectional area of bellow 1mm2(Figure 13.). In a recently published study51 these two methods were compared and hourglass specimens were found to show more defects near the bonding interface, probably because trimming is usually done free-hand. In attempt to standardize the microtensile test as much as possible, some researchers use MicroSpecimen Former, which enables producing specimens in the form of sticks that are trimmed at the interface to a cylindrical shape52. Although there is a correlation between laboratory and clinical effectiveness23, long term, controlled clinical trials remain the most relevant way to completely eveluate new material or treatment method. Biocompatibility Testing

Most of the testing regarding biocompatibility of dental materials point out on their possible citototoxicity. Today, during the standard procedure of pre-clinical investigation, application of different tests recommended by ISO 10993 is supposed to present possible citotoxicity of tested materials, all with intention to introduce standards in this kind of testing53. During the citotoxicity testing of some hybrid materials samples (ISO10993-5:

Test for citotoxicity), Marković (2001) noticed while working on human diploid line WI 38 change in acidity of MEM-Eagle medium and reduction of cell culture ranging from moderate to full cell destruction (Figure 14.). Change in acidity undoubtedly disturb stability and cause variability of cell culture. Further investigation on degree of diffusion of potentially toxic substances through dentin would be of great importance54-56. Tests of tissue response on implanted materials (ISO10993-6) in the same investigation showed moderate response on surrounding tissues. Mild aseptic inflammatory reaction was registered in tissue surrounding implanted sample, together with appearance of cystic formation. In the

Fig.14; Appearance of cell cultures 48h following setting of test samples (Luxat). Reduction in number and loss of fibroblast cell morphology. Remaining cells are of filamentous appearance with no signs of mitotic activity.


center of allergic reaction around particles of tested material, eosinophilic cells in various stages of differentiation may be noticed (Figure 15.). Pre-clinical testing of dental materials where a direct contact of material with cell culture or living tissues of experimental animals is accomplished show that it provokes significant reaction that has to be declared as an undesirable one57-59. However, investigations carried

out by the authors Bergenholz (1989)60, Brannstrom (1982)61, and Cox (1987)62 point to significance of bacteria presence bellow the filling and their influence on pulp tissue. Therefore, the aim of adhesive dentistry is to provide proper marginal adaptation of cavity filling in order to prevent possible changes on pulp tissue.

Investigation of the authors Kanca (1992)63, Pashley (1993)4 White64 and Cox (1994)65 conducted on Rhesus monkeys and the influence of total etch technique on their pulp tissue, where the teeth were extracted and analyzed after 3, 25 and 80 days, showed that with routine dentine etching, irritability factor was not confirmed.

The influence of composite materials and components that might be obtained from them, have to be observed in the light of buffer capacity of remaining dentine, smear layer, dentin permability and length and extending direction of dental tubules, since a simple interpretation of results of biocompatibility tests may led to a wrong conclusion on influence of many dental materials66. Synergism Of Adhesive Systems With Other MaterialS

Bonding to metal surfaces has always proven to be difficult. The metal structure cen be precious or nonprecious alloy, depending on the thickness and the amount that will be exposed. For adequate bonding it is necessary to obtaine the clean surface and adhesion promoting primer. In laborathory conditions, adhesion can be improved by the use of silica coatings. These coatings are connected with heating which is not possible in oral surrounding. Up to now the simplest way intraoraly to clean the surface seems to be sand blasting. Metal surface must be send blasted with clean at least 110 microne grain size Aluminum oxide and 2 bar of air pressure. Various compounds have been used as priming agents (Figure 16.). One recently developed and introduced interface lining is Kevloc System. It uses the principle of direct

Fig.15: Particles of tested materials (a) inside the muscle tissues in strong eosinofilic (e) aseptic reaction.


acrylizing of metal surface. Kevloc primer and layer is fused to the metal surface. With this procedure surface penetration and water resistant coating is achieved. Kevloc replaces complicated handling with easy and simple application, acheving a strong bond between metal and resin67(Figure 17.).

Fig.16:Pretreatment of metal surfaces prior lutting with composite resin

Fig.17: Reinforced interface with Kevlock System provides reliable basis for long lasting prosthodontic constructions made from composite resin, such is ArtGlass, on metal alloy.

To bond composite resin with organic base to a porcelain surface with inorganic base there is a need for modification of the porcelain surface to enhance the compatibility of resin and to achieve high bond strength. Silane primer is the best coupling agent to achieve reliable bond strength. To explain proper porcelain bonding there is a need to clear the chemistry of both silane compound and the porcelain surface itself. Porcelain contains silica in adition with other alkaline oxides. As the water is absorbed on the surface of porcelain this layer could become strongly alkaline. Therefore there is a need to place hydrofluoric acid based porcelain etchant, which will wash away alkaline layer. After this etching procedure a single component silane in alcohol or acetone solution is used. An organosilane compound is hydrolyzed in the presence of water and this silanol is reactive and it reacts with the porcelain surface. With a layer of unfilled resin durable and long lasting adhesion can be obtained with composite resin68. Conclusion

At the end one could ask: What will be the future in adhesive dentistry? Where is the bonding agent that will be capable of preventing both displacement of the restoration and the formation of gaps? The future of dentin bonding agents is to become simple for use, one-step, multi purpose, biocompatible, containing fillers with –OH ions with high pH values, more elastic, with real Fluoride adsorption and release, strong and reliable.


Composite resins are to be based on epoxy resins and resins which will not shrink but expand slightly during setting, mechanically improved, stable, with glass particles and strips or fibers. Also, curing time is to be shorter and setting improved. The benefits for clinicians will be in simple bulk placement, elimination of postoperative sensitivity and secondary caries, with extensive durability and longevity achieved. If our predictions are wrong, than Edmund Burke, an 18th century statesman was right when he said: “You can never plan the future by the past”. This paper is presented at the II Congress of BaSS – Belgrade References

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21. Vulicevic Z.R. Investigation of relationship and bond strength between composite resin and dentin Ph.D, Belgrade, 1994

22. Vulicevic Z.R, Beloica D, Vulovic M. SEM investigation of the dentin/adhesive interface IADR meeting Singapore, June 1995. Journal of dental research 1995; Vol 74; Abstracts of papers

23. Van Meerbeek B, De Munck J, Yoshida Y, Inoue S, Vargas M, Vijay P, Van Landuyt K, Lambrechts P,Vanherle G. Buonocore Memorial Lecture – Adhesion to Enamel and Dentin: Current Status and Future Challenges. Operative Dentistry, 2003, 28-3, 215-235

24. Unterbrink GL, Liebenberg WH. Flowable resin composites as “filled adhesives”: Literature review and clinical recommendations. Quintessence International 1999; 30 (4) 249-257

25. Pashley DH, Carvalho RM. Dentine permeability and dentine adhesion. J Dent. 1997 Sep;25(5):355-72.

26. Kanca J 3rd. Effect of resin primer solvents and surface wetness on resin composite bond strength to dentin. Am J Dent. 1992 Aug;5(4):213-5.

27. Gwinett AJ. Moist versus dry dentin: Its effect on shear bond strength. American Journal of Dentistry 1992; 5(3) 127-129

28. Wang Y, Spencer P. Hybridization efficiency of the adhesive/dentin interface with wet bonding. J Dent Res 2003;82:141—5.

29. Van Meerbeek B, Inokoshi S, Braem M, Lambrechts P, Vanherle G. Morphological aspects of the resin-dentin interdiffusion zone with different dentin adhesive systems. J Dent Res 1992;71:1530—40.

30. Sano H, Shono T, Takatsu T, Hosoda H. Microporous dentin zone beneath resin-impregnated layer. Oper Dent 1994;19:59—64.

31. Sano H, Takatsu T, Ciucchi B, Horner JA, Matthews WG, Pashley DH. Nanoleakage: leakage within the hybrid layer. Oper Dent 1995;20:18—25.


32. Carvalho RM, Chersoni S, Frankenberger R, Pashley DH, Prati C, Tay FR. A challenge to the conventional wisdom that simultaneous etching and resin infiltration always occurs in self-etch adhesives. Biomaterials. 2005 Mar;26(9):1035-42.

33. Tay FR, Pashley DH, Yoshiyama M. Two modes of nanoleakage expression in single-step adhesives. J Dent Res 2002; 81(7):472—6.

34. Tay FR, Pashley DH. Water treeing - a potential mechanism for degradation of dentin adhesives. Am J Dent 2003;16:6-12.

35. Chersoni S, Suppa P, Grandini S, Goracci C, Monticelli F, Yiu C, Huang C, Prati C, Breschi L, Ferrari M, Pashley DH, Tay FR. In vivo and in vitro permeability of one-step self-etch adhesives. J Dent Res. 2004 Jun;83(6):459-64.

36. Perdigao J, Lopes L, Lambrechts P, Leitao J, Van Meerbeek B, Vanherle G. Effects of a self-etching primer on enamel shear bond strengths and SEM morphology. Am J Dent. 1997 Jun;10(3):141-6.

37. Hayakawa T, Kikutake K, Nemoto K. Influence of self-etching primer treatment on the adhesion of resin composite to polished dentin and enamel. Dent Mater. 1998 Mar;14(2):99-105.

38. Kanemura N, Sano H, Tagami J. Tensile bond strength to and SEM evaluation of ground and intact enamel surfaces. J Dent. 1999 Sep;27(7):523-30

39. Inoue S, Vargas MA, Abe Y, Yoshida Y, Lambrechts P, Vanherle G, Sano H, Van Meerbeek B. Microtensile bond strength of eleven contemporary adhesives to enamel. Am J Dent. 2003 Oct;16(5):329-34.

40. Tay FR, Pashley DH. Aggresiveness of contemporary self-etching systems. I: Depth of penetration beyond dentin smear layers. Dental Materials 17 (2001) 296-308

41. Inoue S, Van Meerbeek B, Vargas M, Yoshida Y, Lambrechts P, Vanherle G. (2000) Adhesion mechanism of self-etching adhesives in: Tagami J, Toledano M & Prati C (eds) Advanced Adhesive Dentistry Proceedings book of the Granada 3rd International Kuraray Symposium December 3-4 1999, Cirimido: Grafiche Erredue p 131-148.

42. De Munck J, Van Meerbeek B, Satoshi I, Vargas M, Yoshida Y, Armstrong S, Lambrechts P, Vanherle G. Microtensile bond strengths of one- and two-step self-etch adhesives to bur-cut enamel and dentin. Am J Dent. 2003 Dec;16(6):414-20.

43. Yoshida Y, Van Meerbeek B, Nakayama Y, Snauwaert J, Hellemans L, Lambrechts P, Vanherle G, Wakasa K. Evidence of chemical bonding at biomaterial-hard tissue interfaces. J Dent Res. 2000 Feb;79(2):709-14.

44. Yoshida Y, Nagakane K, Fukuda R, Nakayama Y, Okazaki M, Shintani H, Inoue S, Tagawa Y, Suzuki K, De Munck J, Van Meerbeek B. Comparative study on adhesive performance of functional monomers. J Dent Res. 2004 Jun;83(6):454-8.

45. Yoshida Y, Van Meerbeek B, Nakayama Y, Yoshioka M, Snauwaert J, Abe Y, et al. (2001). Adhesion to and decalcification of hydroxyapatite by carboxilic acids.J Dent Res 80;1565-1569.

46. Inoue S, Van Meerbeek B, Vargas M, Yoshida Y, Lambrechts P, Vanherle G. (2000) Adhesion mechanism of self-etching adhesives in: Tagami J, Toledano M & Prati C (eds) Advanced Adhesive Dentistry Proceedings book of the Granada 3rd International Kuraray Symposium December 3-4 1999, Cirimido: Grafiche Erredue p 131-148.


47. Fukuda R, Yoshida Y, Nakayama Y, Okazaki M, Inoue S, Sano H, Suzuki K, Shintani H, Van Meerbeek B. Bonding efficacy of polyalkenoic acids to hydroxyapatite, enamel and dentin. Biomaterials. 2003 May;24(11):1861-7.

48. Pashley DH, Sano H, Ciucchi B, Yoshiyama M, Carvalho RM. Adhesion testing of dentin bonding agents: A review. Dent Mater 11:117-125, March, 1995

49. Sano H, et al. Relationship between surface area for adhesion and tensile bond strength – evaluation of a micro-tensile bond test. Dent Mater 1994;10(4):236-40

50. Shono Y, Ogawa T, Terashita M, Carvalho RM, Pashley EL, Pashley DH. Regional Measurement of Resin-Dentin Bonding as an Array. J Dent Res 78(2): 699-705, February, 1999

51. Goracci C, Sadek FT, Monticelli F, Cardoso PEC, Ferrari M. Influence of substrate, shape, and thickness on microtensile specimens' structural integrity and their measured bond strengths. Dental Materials (2004) 20, 643-654

52. De Munck J, Van Meerbeek B, Satoshi I, Vargas M, Yoshida Y, Armstrong S, Lambrechts P, Vanherle G. Microtensile bond strengths of one- and two-step self-etch adhesives to bur-cut enamel and dentin. Am J Dent. 2003 Dec;16(6):414-20.

53. Marković D.: Biocompatibility of Glass-Ionomer Cements, Zadužbina Andrejević, Beograd, 2001.

54. Marković D.: Testing of biocompatibility of glass-ionomer cements – citotoxicity test. Stom Glas S, Vol. 49, 2002:75-80

55. Markovic D., V. Zivojinovic, V. Kokovic and V. Jokanovic. Hydroxyapatite as the root canal system filling material: a citotoxicity testing, Materials Science Forum, 453-454, (2004), 555-561.

56. Polić Đ., Marković D., Keserović B., Popović O., Vulićević Z.: Preparation of cell cultures for SEM analysis. 2nd Congress of the Balkan Stomatological Society, April 1997 Belgrade.

57. A. Paljm; D. Marković: Experimental animals in testing on response of oral mucosa on permanent filling materials. Arhive of Oncology 1998;6(sppl.2):83

58. Vulićević Z., Marković D.: In Vitro and In Vivo Investigation of Hydroxyapatit Root Sealer Biocompatibility., ESE Geteborg, jun 1997.

59. D. Marković; A. Paljm: Testing of Biological Tolerance of GIC and Compomers – An Animal Test. 35 Annual Meeting of the CED of IADR, Nica, Francuska 1998.

60. Bergenholz,G. 1989 Bacterial leakage around dental restorations-impact on pulp. In: Quality Evaluation of Dental Restorations (ed.K.J.Anausavice),p.243 Quint.Pub.Comp.Chicago

61. Brannstrom,M. Glantz PO, Nordenwall,K.: Cavity cleaners and etchants. In Smith,D.C. Williams,D.: Biocompatibility of dental materials.CRC,Boca Raton 1982 (p.102)

62. Cox CF,Keall CL, Keall HJ, et al. Biocompatibility of surface-sealed dental materials against exposed pulps. J Prosthet Dent 1987;57:1-8

63. Kanca, J.:Improving bond strength through acid etcing of dentin and bonding to wet dentin surfaces.J Am Dent Assoc 123:35, 1992

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65. Cox,CF,Suzuki,S.:Re-evaluating pulp protection: Calcium hydroxide liners vs. cohesive hybridization.Jam Dent Assoc 125,July 1994


66. Živković S., S. Bojović, D. Pavlica and D. Marković: Testing of microleacage of five restorative materials. Stom. Glas. S. vol 46, 1999: 27 – 31

67. Todorovic A, Vulicevic Z.R. Enamel metal interface reinforcement by the use of Kevloc® FDI Annual World Dental Congress, Vienna October 1-5. 2002.

68. Vulicevic Z.R, Beloica D, Vulovic M. Tensile bond strength of resin bonding and polycarboxylate cements IADR meeting, San Francisco, March 13-17. 1996.



10 years of BaSS

NATIONAL PROGRAM FOR PREVENTION OF ORAL DISEASES EFFECT ON CARIES DISTRIBUTION IN POPULATION OF SERBIA1996 – 2001

Clinic for Pediatric and Preventive Dentistry Faculty of Dentistry, University of Belgrade

Marko Vulović, DDS, MSc, PhD, ProfessorMomir Carević, DDS, MSc, PhD, Associate Professor

Summary

The highest level of caries prevalence in 12 years old in Serbia was recorded in 1980's (DMFT 6,8) while in some regions was above DMFT 10,0 (Western Serbia). Such high DMFT gave the initiative idea for creating a National program for prevention of oral diseases in population of Serbia. Evaluation of program results indicates that the National Program for Prevention of Oral Diseases in Serbia yielded excellent results in improving oral health especially in decreasing of DMFT in twelve year olds (from 6.0 in 1986 to 3.5 in 1995) until the introduction of UN sanctions in Yugoslavia. Since its official commencement in 1996, due to well-known difficult economic and political situation in our country, the program suffered from lack of finical support, but in spite of all hardships, the program maintained the achieved level of oral health and even made slight improvement during its mandate period (1996 to 2001): Slight decrease of children with baby bottle caries (7% - 6.5% respectively) was recorded; increasement of caries free children in age of three (55.5% - 60.9%), six (35.5% - 38.7%) and twelve (19.4% - 21.2%); and slight decrease of DMFT in twelve years old (from 3.4 to 3.2 respectively) was recorded as well. According to the obtained data it is evident that the National Program for Prevention of Oral Diseases in Population of Serbia in spite of the all difficulties in past decade stood up against all challenges, maintaining the achieved level of oral health until introduction of UN sanctions and contributed even slight improvement of oral health in population of Serbia.

Key Words: caries, program, prevention

Epidemiological studies of oral pathology in inhabitants of Serbia in 1980’s indicated an exceptionally high frequency of oral diseases occurrence, especially dental caries and periodontal diseases, in spite of rapidly improved level of curative dentistry 8,10.

Studies conducted in Serbia after World War II has shown that caries prevalence in 12 year old was considerable low 5,6. Extensive and rapid urbanization and industrialization caused changes of living habits, which influenced rapid increase of oral diseases, primarily caries occurrence 7,8,9.

The highest level of caries prevalence in 12 years old in Serbia was recorded in 1980's (DMFT 6,8) while in some regions was above DMFT 10,0 (Western Serbia)10. At the some time dentistry in Serbia had its rapid development as well in manpower and equipment, but strictly oriented toward therapeutic dentistry. This argument and such high DMFT gave the initiative

M. Carević et al

idea for creating a National program for prevention of oral diseases in population of Serbia.

In the late eighties (1987-1988) the Program was completed and experimentally implemented in few regions in Serbia. At first in a few Public Health Care Centers in the Capital town - Belgrade, and by the end of 1990 it was implemented in the most of regional Public Health Care Centers across of Serbia.

Although from the beginning the Program yielded significant results, it was modified in early nineties in accordance with the gained experience. In 1994 the Serbian government recognized it as a National Program for Prevention of Oral Diseases in Population of Serbia and its official commencement was in 1996, with five years of implementing period.

The Program was based on the contemporary concept of prevention of oral diseases, similar to those existing in the Scandinavian countries, our own experience and the demands proposed by WHO for achieving the global goals "Health for all by the year 2000" 4.

The Program resembles joint activities of dentistry, pediatrics, gynecology, visiting-nurses and other members of health care services. Other community based services and intersectorial co-operation of education, mass media, food producers, water plants, etc., were recommended as well in targeting risk populations groups such as pregnant women, infants, small children, preschool and school children, handicaps and adult population over 65 years old 11.

Preventive models and activities recommended by this program were those for which there is clear evidence of their efficacy and effectiveness in implementation on community basis such as:

- Fluoride prevention: fluoridation of public water supplies (Water fluoridation low 1971, 1976, 1994), fluoride tablets, fluoride rinses, fluoridated toothpaste.

- Diet counseling: reduction of frequency of food and drinks intake and sugar consumption control.

- Oral hygiene: supervised (school, kindergarten) and unsupervised (home) brushing and flossing.

- Fissure sealing: permanent molars (ages 6-7 and 10-12).

The basic activity given by the Program was dental health education with purpose to promote oral health and to raise individual responsibility for health in general, as well oral health11,12,13. With that purpose many publications were published and distributed (booklets, posters, slides, videos, etc.).


Evaluation of the Program effect on oral health status of targeted population groups was based on collected data from the annual reports from the Public Dental Health Services, guided by uniform criteria according to the main goals of the Program.

Fig. 1. DMFT of 12-year-olds in Serbia - 1986-1995(trendline)

6,15

3,6 3,5

y = -0,92x + 6,85R2 = 0,918

0

1

2

3

4

5

6

7

8

1986. 1990. 1994. 1995.

TFM

D

Looking at the present data it is evident that oral health status in general is better then ten years ago. Evaluation of program results indicates that the National Program for Prevention of Oral Diseases in Serbia yielded excellent results in improving oral health especially in decreasing of DMFT in twelve year olds (from 6.0 in 1986 to 3.5 in 1995) until the introduction of UN sanctions in Yugoslavia. (Fig.1)

M. Carević et al

Fig. 2. Baby bottle caries in Serbia - 1996-2001

7,0 6,8 6,4 6,5

y = -0,19x + 7,15R2 = 0,7934

0

2

4

6

8

1996. 1998. 2000. 2001.

%

Since its official commencement in 1996, due to well-known difficult economic and political situation in our country, the program suffered from lack of finical support, but in spite of all hardships, the program maintained the achieved level of oral health and even made slight improvement during its mandate period (1996 to 2001); Slight decrease of children with baby bottle caries (7% - 6.5% respectively) was recorded (Fig.2)


Fig. 3. Caries free children in age of 3, 6, 12

0

10

20

30

40

50

60

70

1996. 1998. 2000. 2001.

%

age 3 age 6 age 12

Increasement of caries free children in age of three (55.5% - 60.9%), six (35.5% - 38.7%) and twelve (19.4% - 21.2%) (Fig.3); and slight decrease of DMFT in twelve years old (from 3.4 to 3.2 respectively) was recorded as well (Fig.4).

Fig. 4. DMFT of 12-year-olds in Serbia - 1996-2001(trendline)

3,4 3,5 3,2 3,2

y = -0,09x + 3,55R2 = 0,6

0

1

2

3

4

5

6

1996. 1998. 2000. 2001.

TFM

D

M. Carević et al

According to the present data it is evident that the designed National Program for Prevention of Oral Diseases in Population of Serbia has shown its efficiency in depressing caries prevalence for relatively short time after its implementation.

The promising concept of the oral health preventive program was disturbed by the poor economic ability of the country, especially affected by UN sanctions in 1992, culminating with NATO bombardment of Yugoslavia in 1999.

Great number of refugees (over 700.000) had additional impact on oral health in Serbia. A number of targeted pilot studies among refugees show that their DMFT was higher than their schoolmates who were born and breaded at the examined locations. The data about their oral health was not separated from the annual reports (they have equal rights in getting Health Care as regular inhabitants of Serbia), and were included in general data of oral health status of inhabitants of Serbia.

All of the above mentioned hardships had a bad effect on the health care system, but the worse on dental health care, and as well on the Program of Prevention of Oral Diseases. Government was forced to give the priorities to the urgent medical care, while some segments of medical health care, especially dental health care, as a "non vital part", was left a side for better days to come. Even thaw that Government gave the priority to the Program as well, there was no money left for its implementation because of the drastic reduction in financing dental health care.

It can be concluded that National Program for Prevention of Oral Diseases in Population of Serbia in spite of the all difficulties in past decade stood up against all challenges, maintaining the achieved level of oral health until introduction of UN sanctions and contributed even slight improvement of oral health in youngest population of Serbia.

This paper was presented at the II Congress of BaSS - Belgrade


References

1. Beloica D. i sar.: Dečja stomatologija. Beograd, Elit-Medica, 2003.

2. Carević M., Vulović M.: Dijagnostika rizika za pojavu karijesa. SGS., 1992; 39:47-49.

3. Carević M., Vulović M.: Early Childhood Caries Prevalence in Serbia.

4. 9th Congress of the Balkan Stomatological Society, Book of Abstracts ,Ohrid, FYROM, 2004.

5. FDI.: Goals for oral Health in the Year 2000. FDI Newsletter, 1982.

6. Graovac Ž.: Karijes mlečnih zuba. SGS, 1954;1:12-18.

7. Graovac Ž. i sar.: Rasprostranjenost zubnog kvara u SR Srbiji. SGS, 1966; Br. 3.

8. Graovac Ž.: Osnovi dečje stomatologije. Beograd, Naučna knjiga, 1969.

9. Popović V.: Bolesti usta i zuba u stanovništva Beograda. Stomatološki fakultet, Beograd, 1987.

10. Stošić P. i sar.: Karakteristike narodne patologije iz oblasti stomatologije u SR Srbiji. IV Kongresa stom. Jugoslavije, Sarajevo, Zbornik radova ,1968.

11. Stošić P. i sar. Dečja i preventivna stomatologija. Beograd, Dečje novine, 1984.

12. Vulović M. i sar.: Program preventivne stomatološke zdravstvene zaštite stanovnika Republike Srbije. Beograd, Zavod za udžbenike i nastavna sredstva, 1996.

13. Vulović M.: Dental Health Care Program in Serbia. Dundee, Book of Abstracts: I Congress of European Assotiation for Public Dental Health, 1996.

14. Vulović M., Carević M.: Strategies for Prevention of Oral Diseases. Buchurest, Romania, Book of Abstracts: 6th Congress of the Balkan Stomatological Society, 2001.

15. Vulović M. i sar.: Preventivna stomatologija. Beograd, Elit-Medica, 2002.

16. Vulović M., Carević M.: Caries Prevelence of 12-year Old in Serbia. Ohrid, FYROM, Book of Abstracts: 9th Congress of the Balkan Stomatological Society, 2004.

17. WHO: A Strategy for Health Promotion Program at the Regional Office for Europe. Copenhagen, Regional Office for Europe, 1990.

18. WHO: Oral Health for the 21th Century. Geneva, Oral Health Unit, 1993.

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10 years of BaSS

EPIDEMIOLOGY AND PREDICTORS OF EARLY CHILDHOOD CARIES / ECC /

N.Markova, E.Ilieva

Early childhood caries (ECC) is of epidemic proportions in some

European and US minority populations and in many developing countries all over the world. There are relatively few studies of caries prevalence in preschool children and the data that are available often are grouped into broad age categories. The international trend in industrialized countries shows declining dmft scores since 1967, although the absolute level of dmft is high in some countries. For example, in 1992 Japanese 4-year-olds had a mean dmft score of 5.7, while Finnish 4-olds had a mean dmft score of 0.6 (8). Furthermore, the rate of decline may be leveling off (3). Mayanagi et al. (8) also report a relatively high prevalence of caries in the primary dentition (percentage of children affected) among 5-year-olds in both developed and developing countries, ranging from 92% in China to 75% in Scotland and 42% in England and Wales. Milnes (9) comprehensive review of the epidemiology of maxillary anterior caries examines numerous studies from Europe (primarily England), Africa, Asia, Middle East, and North America. The highest prevalence of maxillary anterior caries is found in Africa and Southeast Asia/48%/, although this caries pattern remains widespread in developed countries of Western Europe/12%/. The English studies are of particular interest because relatively large, community-based samples are used along with a common definition of maxillary anterior caries/4-18%/. Caries scores in US children range from approximately 1 to 12 but the many different caries measures (dmft, dmfs, dfs, dft) make comparison difficult (2,7,12,13). In contrast to these high caries levels, a US national survey of children aged 2 to 4 years reports a mean dmfs of 1.2, with 17% having caries (6). Reports limited to the prevalence of maxillary anterior caries in the United States also illustrate a wide range affecting from less than 5% to more than 70% in some Native American populations (2). Data are sparse or inaccurate because: preschool-age children are hot readily accessible for examination; examined samples may be non-representative; infant feeding practices vary in different cultural and ethnic groups, making extrapolation of finding inappropriate; infants and toddlers often are difficult to examine thoroughly; and criteria for ECC have varied among existing studies with respect to location of dental decay and number of teeth affected, e.g., any labiolingual lesion in a maxillary incisors or a dmft score of 5 or greater (13) Although prevalence of ECC have varied in individual surveys from about 1% to as high as nearly 70%, the national prevalence of the condition in Bulgaria concerning 3 year-olds has been estimated to be no greater than 60.84% (14). An investigation, an object of our comment was held in 2004 at 372 three years old children. The observation’s objects are: individuals, teeth and tooth surfaces

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with caries and free of caries. The comparison with epidemiological studies with children of the same are held in 1996 and 2001 have been made. Fig. 1.

52.8

23.13 21.24

0

20

40

60%

1996 2001 2004

Caries prevalence per person (Ep) at 3 years old children

The comparison of the results of Ep shows statistically significant

differences of 2001 and 2004 compared with 1996. The reduction of Ep for the last 3 years is obvious, but without significant difference. Nevertheless we can speak about decreasing of Ep during last years, that is compatible with the data of scientific literature. (Fig.1). Fig. 2.

10.01

3.09 4.38

0

5

10

15%

1996 2001 2004

Caries prevalence per teeth (Et) at 3 yers old children

The Et index shows another way of development. Comparison of the results in 2001 and 2004 to these in 1996 decrease of Et with statistically


significant differences. The result from the last 3 years shows controversial tendency - statistically significant increase of the Et. Compared with the reduced group of children with caries, the increase of the percent of the affected teeth means that the number of affected teeth in the mouth of one sick child is increasing. (Fig.2) Fig. 3.

1.99

0.62 0.92

0

0.5

1

1.5

2dmft

1996 �. 2001 �. 2004 �.

dmft at 3 years old children

This conclusion has been confirmed at same rate from the from the in investigation of dmft. There is increase of the average level in 2004 compared with 2001. The difference is not yet statistically significant (u=1,87), but the results are compatible to data for Et-index. (Fig. 3) Fig. 4

11.39

24.05

10.1317.72

36.71

0

10

20

30

40%

1 2 3 4 5 andmore

number of carious teeth

Distribution of children according to number of carious teeth

N.Markova et al

Fig. 5a, 5b.

Distribution in the group with 5 and more carious teeth

55.20%

44.80%

5-9 lesions 10 and more

Distribution in the group with 10 and more carious teeth

46.10%

38.50%7.70%

7.70%

10111216

To be understanding the meaning of caries prevalence in the group of

sick children is necessary to follow-up the percentage of children with different number of carious teeth. The results show that children with 5 and more lesions are statistically more than all the other groups excluding the group with 2 carious teeth. (Fig. 4) In the group with 5 and more lesions there also are differences. Their analysis show that nearly equal are the group of children with 5-9 carious teeth and that of children with 10 or more carious teeth. In the last subgroup statistically more are the children with 10 and 11 lesions. A clear tendency of prevalence of children with more carious teeth is seen. (Fig. 5a, 5b)


Fig. 6.

51,9

11,4

36,7

0

20

40

60%

molars ant maxteeth

molars+ant max

teeth

Caries atack of different teeth group

With teeth are most often attack at 3 years old children? The biggest is

the percentage of children with involved molars – more than half of sick children. On the second place is the group of children with the worse clinical symptoms – involved molars and anterior maxillary teeth. The least percentage is for the group with involved only anterior maxillary teeth. (Fig. 6) Fig. 7.

Caries involvement of different tooth surfaces

15,61% 33,66%

18,70%18,70%

13,33%

occ

mes

mes

dis

ora

The results for the most often involved tooth surfaces are similar to the teeth. Oclusal surfaces are statistically significant more affected than all the others – mesial, bucal, distal, oral. Next are mesial and bucal surfaces with significant differences to distal ones. There is no such difference compared to oral surfaces. These data show that in spite of the proven specifications of the

N.Markova et al

caries of the 3 year old children, in early age prevails fissure caries, determined by the retentive surfaces and incomplete mineralisation. Fig. 8.

0,56

0,89

0,07 0,03

0

0,2

0,4

0,6

0,8

1d,f

non-treated treated

Comparison of treated and non-treated caries in 2001 and 2004 year

20012004

For further view of the already described tendency the development of

Dental Caries Treatment Index in 2001 and 2004 has been followed up. The comparison of average rates of active caries in both years shows statistically significant increase in 2004 year. Decrease, but not statistically significant, is seen at the treated caries. The number of filled teeth at 3 years old children is extremely small compared with the need of treatment. Predictors of ECC Swedish investigators in a prospective, longitudinal study showed than predictors of caries development before 2.5 years of age were MS concentration, immigrant background and the consumption of candy (4). Predictors for developing caries during the next year were the same as those before age 2.5 years, plus mother’s education and consumption of sugar-containing beverages. The probability of caries development was 87% when all the variables associated with caries were present at 1 year of age (5). A study of 677 children aged 1-6 years who attended one of 20 day-care centers in Finland showed that MS were increased by consumption of sucrose snacks and reduced by regular use of fluoride tablets (10). Cessation of toothbrushing at the centers did not affect MS levels. Those with positive tests for MS had significantly greater dmf scores than did those with negative tests. Findings of another Finnish study showed that visible plaque on the labial surfaces of maxillary incisors of children who averaged 19 months of age at baseline was the best predictor of caries risk during the following 1.5 years (1). Visible plaque had a positive prognostic (predictive) value of 63% and a negative prognostic value of 97% during the interval. More children with


visible dental plaque at 1 an 2 years of age has developed caries by the age of 3 than those without visible plaque at those ages. Those who were caries free at age 3 had received more help with toothbrushing and had used more frequently fluoride toothpaste than those who developed caries by age 3. Wendt also shows that oral hygiene and dietary habits established by 1 year of age are maintained throughout early childhood. He also reported that immigrant status was correlated with the development of caries by age 3. Slavkin (11) has indicated than genetics may confer susceptibility or resistance factors with respect to tooth decay, which might affect the development of ECC. A study of oral health behavioral, cognitive and socioeconomic factors associated with increments of dental caries in children aged 3-5 years showed than higher MS and initial dmfs scores and parental reports of more frequents toothbrushing of their children’s teeth were associated with greater increments of dental caries (4,13).

Although research should continue on determining the prevalence of ECC in various racial, ethnic and socioeconomic groupings, we are reaching the point where high risk of the disease in communities can be predicted on the basis of socioeconomic factors, immigrant status and ethnic/racial background. Research, thus, should focus on developing profiles or indexes to predict the prevalence of ECC in communities based on these factors. Research also is needed to develop an index to identify individual children at high risk of ECC. Some factors for consideration for this index are: low socioeconomic status, low birthweight, siblings with the condition, low exposure to fluoride, high consumption of refined carbohydrates and poor oral hygiene practices. Key words : Early childhood caries, predictors, risk factors, prevention.

N.Markova et al

References :

1. Alaluusua S, Malmivirta R. Early plaque accumulation – a sign for caries risk in young children. Community Dent Oral Epidemiol. 1994;22:273-6.

2. Barnes GP, Parker WA, Lyon TC, Drum MA, Coleman GC. Ethnicity, location, age and fluoridation factors in baby bottle tooth decay and caries prevalence of Head start children. Public Health Rep.1992;107:167-172.

3. Downer MC. Time trends in dental decay in young children. Health Trends 1989;21:7-9

4. Grindefjord M, Dahllof G, Nilsson B, Modeer T. Stepwise predictor of dental caries in children up to 3.5 years of age. Caries Res 1996;30:256-66.

5. Grindefjord M, Dahllof G, Nilsson B, Modeer T. Prediction of dental caries development in 1-year-old children. Caries Res 1995;29:343-8.

6. Kaste LM, Selwitz RH, Oldakowski RJ, Brunelle JA, Winn DM, Brown Lj. Coronal caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-1991. J Dent Res 1996;75(Spec Iss):631-41.

7. Louie R.,Brunell JA, Maggiore ED, Beck RW. Caries prevalence in Head Start children, 1986-87. J Public Health Dent 1990;50:299-305.

8. Mayanagi H, Saita MH, Kamiyama K. Cross-sectional comparisons of caries time trends in nursery school children in Sendai, Japan. Community Dent Oral Epiodemiol 1995;23:344-9.

9. Milnes AF. Description and epidemiology of nursing caries.J.Publ. Health Dent.1996;56:38-50.

10. Raito M, Mottonen M, Uhari M. Toothbrushing and the occurrence of salivary mutans streptococci children at day care centers. Caries Res 1995;29:280-4.

11. Slavkin H.Streptococcus mutans, ECC and new opportunities.J.AM.Dent.Assoc.,1999;130:1787-1792.

12. Tang JM, Althman DS, Robertson DC, O`Sullivan DM, Douglass JM, Tinanoff N. Dental caries prevalence and treatment levels in Arizona preshchool children. Public Health Rep 1997;112:65-75

13. Tinanoff N,O’Sullivan DM.Early childhood caries: overvew and recent findings.Pediatric.Dent.1997;19:12-60.

14. Todorova M.,D.Stranski,Tz.Iolov.Caries prevalence of children 2-18 yaers-olds in Bulgaria.Stom.Sofia,1979;1-16.



10 years of BaSS

BACTERIAL AND ENZYMATIC TESTS IN CARIES RISK ASSESSMENT

Friedrich-Schiller-Universität JenaPoliklinik für Präventive Zahnheilkunde, Erfurt, Germany

Lutz Stösser, Marcus Dell, Roswitha Heinrich-Weltzien

1

1

Supported by 3M ESPE, Germany.

Summary

A reliable identification of the caries risk group characterized by a caries experience above average could contribute considerably to the improvement of oral health. Preferred methods and parameters of reviewed risk assessment studies, such as sensitivity and specificity were mentioned in the context of a particular caries risk assessment study with schoolchildren, used as an example. Many clinical and laboratory parameters showed a significant correlation to the caries incidence observed during 4 years. Multiple regression analysis classified correctly at most 75 % of the subjects. Using dichotomization rules for different sizes of the risk group microbial and sociodemographic variables were added to the regression model. Salivary samples could be used in predictive studies for determination of the total load of the oral cavity with cariogenic microorganisms. The lactic acid indicator, ClinproTM Cario Diagnosis, might represent a further tool to improve caries risk prediction. Key words: Caries risk prediction, caries experience,S. mutans, lactic acid.

Now with the caries decline continuing to the point that half of children aged 5 to 16 years in many "western" countries are free of dental caries in their permanent dentition, the value of persuading factors related to high caries risk is greater than ever before. Despite the caries decline, a substantial number of children remained susceptible to a high caries experience. A reliable identification of this caries risk group characterised by a caries experience above average could contribute considerably to the improvement of public oral health of children or adolescents. Providing preventive procedures to those at greatest risk to dental caries requires accurate methods of identifying these children (Beck 1998, Ericsen and Dimitrov 2003, Stamm et al. 1991).

Epidemiological research has convincingly demonstrated that health and disease are determined by the dynamic interaction of many factors which may support, co-act or inhibit each other. Traditional scientific approach tries to explain and understand the interaction by isolating and studying separately factors involved in the disease process. Bivariate association has dominated dental research for a long time (Bibby and Shern 1978, Klock and Krasse 1979). Now with the development of hard- and software simple past methods were replaced by multiple regression models so that the independent and joint effects of risk factors could be considered in more detail. The interactions of these factors are visually summarised within the Keyes venn diagram (fig. 1) showing the relation of major etiological conditions of dental caries which could be start point for investigation (Bratthall 2000, Helfenstein et al. 1997, Palenstein Heldermann et al. 2001, Stamm et al. 1991).


Fig. 1: Etiologic precondition of caries and

possible indicators or predictors of caries risk

Nowadays dental caries is considered as an infectious disease caused by a group of specific bacteria which metabolise carbohydrates at the tooth surface and produce considerable amounts of organic acids as waste products. These acids are represented mainly by lactic acid which is one of the most acidic metabolic compounds and which is responsible for the pronounced pH-drop of dental plaque following sugar intake (fig. 2). Without sugar challenge plaque produces so called weak organic acids (e.g. acetate, propionate, butyrate) but surplus of sugar leads to an intensive, so-called homo-enzymatic production of lactic acid which is the strongest among the acids analysed in dental plaque (Edgar and Geddes 1986). Furthermore the acid diffuses into the dental hard tissue and dissolves minerals. Carbonate containing apatite is dissolved first; in addition calcium ions leave the crystal lattice because phosphate residues become less negatively charged and therefore they are unable to hold all calcium ions. This bacterial effect is a chronically progressive, non-self limiting process. After 12-24 hours of undisturbed microbial development dental plaque becomes a very active producer of acid if carbohydrate is available and causes intensive demineralisation (Featherstone 2000). Microorganisms involved in this process are mainly streptococci, lactobacilli and actinomycetes. They have different capacities to produce acid from carbohydrates and their acid tolerance

L.Stösser et al

Fig. 2: Stephan curve, pattern of organic acid produced by

dental plaque and semiquantitative Clinpro Cario L-Pop score for lactic acid could be very different as well. The last, so-called aciduric property labels microorganisms in more or less cariogenic representatives. Mutans Streptococci are one of the most important bacteria within this concept of acid production and tolerance (Stösser 1988). Therefore their contribution was often a target of caries risk assessment studies (Thibodeau and O´Sullivan1996, Kneist et al. 1999). The present paper reviews parameters associated with caries and their highly complex interrelation. A better understanding of the relation of these factors to caries including microbial tests should aid the development of more effective risk assessment methods than being available currently to distinguish caries-prone and caries-resistant individuals. In particular the contribution of microbial tests in risk assessment should be analysed and compared with a recently developed intraoral lactic acid determination (Schmid et al. 2002). Caries risk assessment study of Erfurt – General conditions

The purpose of an own investigation (Stösser et al. 2000) used as a representative example for this review was to identify the best predictors for caries increment in permanent dentition of an 8- and 12-year-old cohort of schoolchildren (n=151 or 204, respectively) at baseline from a set of clinical, microbial, salivary, behavioural and socio-economic variables and to develop a model for the prediction of caries increment. Additionally, the analysis should determine the relation between the definition of risk (dichotomization) and the


accuracy of the prediction. The sample consisted of 355 children examined three times, with two year intervals between the examinations (fig. 3).

Fig.3: Course of the Caries Risk Study of Erfurt with parameters recorded in 1993-97

L.Stösser et al

WHO criteria (1987) were used for classification of tooth surface status. Addi-tionally white spots and stained fissures, approximal plaque index (API), papillary bleeding index (PBI), unstimulated and stimulated flow rates, pH, buffer capacity as well as hydroxylapatite saturation (HAP) of saliva and S. mutans (Sm) and lactobacilli counts (Lb) were estimated. Before the first examination, a question-naire was completed with questions about socio-economic characteristics, oral hygiene habits and history of fluoride exposure (fig. 3). Details were published in the past (Stösser 1998). The probability of a subject falling into the high caries risk group was fitted with logistic regression (Fischer et al. 1999). Three dichotomization criteria called “any”, “epidemiological” or “extreme” for the caries variable DMFS increment were used according to Beck et al. (1992). Subjects at “any” risk were defined as those having positive mean DMFS scores. For the second criteria, subjects at “epidemiological” risk were defined as those who collected the upper approximate 70 % of the mean DMFS total. According to the last criteria, subjects at “extreme” risk were defined as those 10 % of all subjects with the highest mean DMFS values.

Results of risk assessment

The clinical findings at the end of the study do not reflect a priori the different caries challenges in the subpopulation examined but the average characterized the situation in general (fig. 4).

Fig.4: Final clincal results of a caries risk assessment study of Erfurt

The explanatory value of these clinical and laboratory parameters for caries incidence of 2.2 or 3.8 DMFS for the respective cohorts was estimated by calculating the correlation by Spearman or with the Wilcoxon test (Hartung 1986). The highest values of correlation were noted for past caries experience and its components (DS + FS) followed by initial caries lesions, IS (fig. 5).

Fig.5: Correlation of parameters recorded and caries observed as well as logistic

regression of caries risk prediction (by Stösser et al. 2000)


The risk prediction was made by fitting baseline data into a multiple logistic

regression analysis. These values were cross-classified according to their predicted caries risk and the observed actual caries increment (Kingman 1990, Fischer et al. 1999, Fischer 2004).

Furthermore, a stepwise technique was used to understand the discriminating power of clinical and laboratory parameters in different combinations within the model. The single variable of initial caries (IS) always identified correctly 71 % of children having developed new caries lesions during the study period. The model achieved its highest sensitivity, specificity and accuracy by introduction of past caries experience together with initial lesions and showed the best achievable prediction with an accuracy of 75.7 %. Having taken into consideration more clinical or laboratory variables, such as the amount of plaque, S. mutans and lactobacilli scores or buffering and hydroxylapatite saturation of saliva, the prediction and validity of calculations did not improve (fig. 5).

Fig.6: Caries risk prediction for different dichotomized groups by DMFS cut-off points

Dichotomization of caries risk

The target of any risk assessment study determines the cut-off point agreed, because a low level leads to a large risk group, as already known (Kingman 1990, Stamm et al. 1991). By multiple regression analysis a risk group of 60 % of the children was calculated with the dichotomization rule “any” (fig. 6); the sensitivity, specificity and accuracy of this model amounted to 74 %. Only past caries experience and initial caries lesions represented the predictors necessary for this classification. The model for the “epidemiological” risk group (37%) required

L.Stösser et al

additionally a microbial mutans score and approximal plaque index. The “extreme” risk group comprised 28 % of the subjects and was discriminated by further parameters, such as pH of unstimulated saliva and education of the head of the family (fig. 6). Microbial tests

Salivary samples have particular predictive value for determination of the general microbial load of the oral cavity. In the above mentioned trial the random variation of the number of mutans streptococci was not as large as expected and the majority of schoolchildren involved did not heavily change their oral microbial score. Only 7-13 % of the subjects showed a deterioration of 2 or more scores being relevant for supposed high caries risk (Stösser et al. 2000). At the same time it becomes apparent that the highest S. mutans value coincided with ageing of the schoolchildren reflecting the increased number of teeth surfaces.

Fig.7: Stability of S. mutans scores (Dentocult, Orion) and their effect on caries incidence

If the subjects were ranked according to their S. mutans contamination, they demonstrated different caries incidences reflecting the microbial exposure (fig. 7). Children with high S. mutans scores developed significantly more caries lesions while low S. mutans scores caused a lower tooth decay; the consequence of the above mentioned deterioration of S. mutans scores was a moderately elevated caries challenge in the group concerned. The special cariogenicity of S. mutans was also confirmed by these facts (Grindefjord et al. 1993; Raito et al. 1996; Thibodeau and O´Sallivan, 1996) although S. mutans and lactobacilli scores did not improve considerably the sensitivity or specificity of prediction. At the end of the study 33 subjects among the high S. mutans carriers did not show any caries increment during the four year period of interest.


This observation supported the conclusion of conditional predictive power of S. mutans scores. This was in accordance to Hausen (1997) who claimed that microbial tests are inferior to clinical parameters and such assays could be recommended to be carried out only in subpopulations without any decayed tooth (Kingman 1990). Lactic acid formation as predictor of caries risk

The majority of experimental tests for caries risk prediction determine the protective function of saliva or the bacterial exposition by S. mutans and/or lactobacilli outside the oral cavity by laboratory methods. A new approach was developed (Schmid et al. 2002) by which lactic acid formation, being the driving force of cariogenic demineralisation, was taken into consideration under in situ conditions of dental plaque because acid production of this biofilm might differ in its properties from planktonic bacterial suspensions in the laboratory. Two tests were inaugurated to determine lactic acid concentration in the oral cavity with an impression material for site specific evaluation (Clinpro Cario Diagnosis, 3M ESPE) or with a swab indicator for general consideration (Clinpro Cario L-Pop, 3M ESPE). The biochemical mechanism of determination shown in figure 8 leads to a blue discoloration of the swab; its intensity is in correlation to the amount of acid produced. The impression shows blue "hot spots" of active lactic acid production by cariogenic dental plaque because the alginat contains sucrose for lactic acid production and the colour indicator (fig. 8).

Fig.8:Clinpro Cario Diagnosis lactic acid determination as site specific test by impression or for general consideration by Clinpro Cario L-Pop swab

L.Stösser et al

The correct reflection of the intraoral lactic acid load after ingestion of a

10 % sucrose solution could be confirmed by Clinpro Cario L-Pop (CCP) and by the method of an indwelling pH electrode as well (Stößer at al. 1990). The highest lactic acid concentration was recorded after 15 minutes by the Stephan curve with pH 4.4-4.5 and corresponded to the highest CCP score of 7.2 (fig. 2). Furthermore clinical use of the CCP showed a slightly more intensive acid load of the oral cavity within a caries risk group of adolescents characterised by a high DMFS value of 13.3 (fig. 9).

Fig.9: Clinical data and biochemical results of lactic acid determination with a caries risk

sample of adolescents In comparison to a non-caries risk group with a low DMFS of 2.8 and less initial lesions (IS 7.4) the CCP score was lower, too. Microbial caries risk tests (CRT, Vivadent) for S. mutans or lactobacilli reflected the same difference between these groups but both showed a high variation. Site specific caries risk investigation within the same group of adolescents was made by a modified Navy plaque index (Rustogi et al.1992, Borutta et al. 1997); areas of lactic acid production within the Clinpro Cario Diagnosis (CCD) impressions were recorded followed by plaque revelation with Miraton (Hagen GmbH) and the same plaque scoring (fig. 10).


Fig.10:Impression with Clinpro Cario-Diagnosis and revelation of plaque

The comparison of the impression data based on lactic acid production or revelation of plaque by Miraton showed a high concordance of both methods but some plaque areas could be stained by one method only (fig. 11). The lactic acid positive areas could probably represent locations of special cariogenic risk and should be taken into consideration of further longitudinal research.

Fig.11:Number of plaque areas stained by plaque revelator or Clinpro Cario Diagnosis

L.Stösser et al

The number of variables associated with dental caries is so extensive and their interaction is so complex that further research is needed to develop appropriate multivariate methods. Salivary samples can be used in predictive studies for determination of the total load of cariogenic microorganisms. The random variation of the number of bacteria is however large. Therefore the lactic acid formation could probably be an additional tool for further improvement in caries risk prediction.

This paper was presented at the V Congress of BaSS Thessaloniki, Greece

References

1. Beck JD, Weintraub JA, Disney JA, Graves RC, Stamm JW, Kaste LM, Bohannan HM. University of North Carolina caries risk assessment study. Comparison of high risk predicition, any risk prediction, and any risk etiological models. Community Dent Oral Epidemiol 1992;20:313-21.

2. Beck JD. Risk revisited. Community Dent Oral Epidemiol 1998;26:200-225. 3. Bibby BG, Shern RJ (eds). Proceedings: Methods of caries prediction.

Washington DC, London: Information Retrieval Inc, 1978. 4. Borutta A. Plaque removal efficacy of a newly developed powered toothbrush

in the primary dentition of pre-school children. J Clin Dent 1997;8:151-155. 5. Bratthall D: Introducing the Significant Caries Index together with a proposal

for a new global oral health goal for 12-year-olds. Int Dent J 2000;50:378-384. 6. Edgar WM, Geddes DAH. Plaque acidity models for cariogenicity testing –

Some theoretical and practical observations. J Dent Res 1986;65:1498-1502. 7. Ericsen HM, Dimitrov V. Ecology of oral health. A complexity perspective. Eur

J Oral Sci 2003; 111: 285-290. 8. Featherstone JDB. The science and practice of caries prevention. 2000;131:887-

899. 9. Fischer T, Kneist S, Heinrich-Weltzien R, Stößer L. Analysis of longitudinal

caries data of children using a generalised linear repeated measurement model. Caries Res 1999;33:316-317.

10. Fischer T. Ein verallgemeinertes lineares Modell bei Vorliegen von Messwiederholungen zur Kariesrisikobestimmung bei 7-17jährigen Schülern. Med. Diss. (Charite) Berlin 2004.

11. Grindefjord M, Dahllöf G, Ekström G, Höjer B, Modeér T. Caries prevalence in 2.5 year old children. Caries Res 1993;27:505-510.

12. Hartung J. Statistik: Lehr- und Handbuch der angewandten Statistik (5.Aufl.) München, Oldenburg 1986.

13. Hausen H. Caries prediction - the state of the art. Community Dent Oral Epidemiol 1997;25:87-96.


14. Helfenstein U, Steiner M, Menghini G. The use of generalised additive models

(GAM) in dentistry. Community Dent Health 1997;14:221-226. 15. Kneist S, Heinrich-Weltzien R, Stösser L. Saliva tests and dental health.

Intependent Dent 1998;3;102-108. 16. Kneist S, Heinrich-Weltzien R, Fischer T, Klein C, Rupf S, Eschrich K.

Handelsübliche Speicheltests zum Mutans-Nachweis – Übersicht und Effizienzbewertung. Quintessenz 1999;50:33-43.

17. Kingman A. Statistical issues in risk models for caries. In Bader JD (ed). Risk Assessment in Dentistry. Chapel Hill, University of North Carolina Dental Ecology, 1990;193-200.

18. Klock B, Krasse B. A comparison between different methods for prediction of caries activity. Scand J Dent Res 1979;87:129-139.

19. Palenstein Helderman WH, van’t Hof MA, van Loveren C. Prognosis of caries increment with past caries experience variables. Caries Res 2001;35:186-192.

20. Raito M, Pienihäkkinen K, Scheinin A. Assessment of single indicators in relation to caries increment in adolescents. Acta Odontol Scand 1996;54:113-117.

21. Rustogi KN, Curtis JP, Volpe AR, Kemp JH, McCool JJ and Korn LH. Refinement of the Modified Navy Plaque Index to increase plaque scoring efficiency in gumline and interproximal tooth areas. J Clin Dent 1992;3:C9-12.

22. Schmid B, Fischeder D, Arndt S, Haeberlein I. Site-specific detection of lactic acid production on tooth surfaces. Caries Res 2002; 36:174.

23. Stamm JW, Stewart PW, Bohannan HM, Disney JA, Graves RC, Abernathy JR. Risk assessment for oral diseases. Adv Dent Res 1991;5:4-17.

24. Stösser L. Die kariogene Bedeutung der acidogenen und acidurischen Eigenschaften des Streptococcus mutans. Stomatol. DDR 1988;38:679–683.

25. Stösser L, Tietze W, Künzel W, Limberger K. Intra-orale pH-Messung zur Bestimmung des azidogenen Potentials von Nahrungsmitteln. Oralprophylaxe 1990;12:145 – 153.

26. Stösser L (ed). Kariesdynamik und Kariesrisiko. Berlin: Quintessence, 1998. 27. Stösser L, Kneist S, Heinrich-Weltzien R, Fischer T, Tietze W. Current research

on caries risk assessment. In: Stookey GK (ed): Early Detection of Dental Caries II: Proceedings of the 4th Annual Indiana Conference Indianapolis, India. Indianapolis, IN: Indiana University School of Dentistry, 2000, 31-56.

28. Thibodeau EA, O´Sullivan DM. Salivary mutans streptococci and dental caries pattern in pre-school children. Community Dent Oral Epidemiol 1996;24:164-168.

29. WHO. Oral Health Surveys: Basic Methods. 3rd Ed World Health Organisation, Genf 1987.

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10 years of BaSS

PUBLIC HEALTH ISSUES CONCERNING ORAL HEALTH CAREIN FORMER SOCIALIST COUNTRIES

Clinic for Pediatric and Preventive Dentistry School of Dentistry, University of Belgrade

Marko Vulović, DDS, MSc, PhD, Professor Momir Carević, DDS, MSc, PhD, Associate Professor

Introduction Reduction of dental caries in developed countries of Northern and Central Europe in the last 20 years has not occurred because of the undoubted advances in the dental treatment but because of the widespread introduction of comprehensive oral diseases preventive programs and promotion of oral health, especially use of fluorides. Oral health in developing countries of Eastern Europe in generally did not follow the pattern of oral health improvement as in developed countries of Northern and Central Europe. Prevalence rate of dental caries remained high in most of Eastern Europe. For example DMFT in twelve years old in this countries is still between DMFT 3-5. The main reason for higher occurrence of oral diseases in this countries are not due to the lower level of dental treatment, but due to the missing or improper implementation of Programs of oral health care. Public Dental Health has to be based and supported by National Programs of Oral Health Care which are existing in most of the Northern European countries, concerning rationale use of scientifically approved most effective and inexpensive measures in prevention of oral diseases, proper education and distribution of manpower employed in Public Dental Health Services.

Key words: caries, prevalence, prevention

Public health is defined as “the science and art of preventing disease,

prolonging life and promoting health trough the organized society” 1. In other words the aim of public health (PH) is to improve health in population, so dental public health can be defined as “the science and art of preventing oral diseases, promoting oral health and improving the quality of life through the organized efforts of society”4.

There have been three phases of activities in PH as organized care since the middle of the 19th century, and we stand now at the fourth phase 2.

The first phase (1840-1890) was period of rapid urbanization and industrialization with desperate living condition for the poor. Public health was based on sanitary reform. This was a period when medical and epidemiological researches were detecting causal relationships involving malnutrition, unhygienic condition and infectious diseases.

The second phase (1880-1930) was characterized by the advances in bacteriology and immunization bringing personal prevention on a population basis. This was a period of growth in the maternal and child welfare (school meals and milk were introduced to compensate malnutrition among the poor).

M. Vulović et al

The third phase (1930-1975) was therapeutic phase. Medical services were focused to hospitals, increasing complexities of medical treatments and less emphasis on public health in terms of prevention and health promotion.

The fourth phase, so called "the new public hearth" is characterized by the growing awareness of the limitation of therapy to tackle chronic lifestyle diseases. Over the last 20 years focus of public health has been changing5. The 1977 World Health Assembly resolution added impetus with the aim that by the year 2000 all citizens of the world would attain a level of the health permitting them to live socially and economic productive lives. Several health policy documents followed giving specific health goals 6,13,14. The next step was the national setting of targets by many governments, for example, within Europe, as "Health for all by the year 2000 " policies and strategies 16.

However, one of the notable trends, common across the world, has been increasing difference between the rich and poor in economic and social conditions both within and between countries. Many studies have shown that this phenomenon underlies the growing disparity in health between these group "in society” 8,10. This has become accentuated because the occurrence of the most prevalent diseases, cancer, hearth disease and dental caries, are determined by our lifestyle.

Concerning oral health, the two principal diseases are dental caries and periodontal disease with common etiologic factors such as sugars in the diet and bacterial dental plaque. Oral cancer afflict a minority, but the prevalence is increasing in some countries. The two major risk factors are smoking and alcohol consumption.

Living standard and lifestyle, which has crucial influence on diet, oral hygiene, smoking and etc., are of great importance for the occurrence of oral diseases. This finding is in common with other chronic condition affecting general health, for example coronary heart disease.

Dental caries is probably the most common of all chronic diseases of modern society. There is now sufficient epidemiological evidence to show that in high developed countries we find either a maintenance of high caries prevalence or a considerable low where water fluoridation and other preventive methods have been widely used 15. Nevertheless, dental caries still accounts as a major cause of tooth loss in age group up to 40 years of age, while periodontal diseases seem to have even greater importance in this respect.

There are great variations in the prevalence of dental caries within the European Region, being at low to very low levels in Northern Europe, and moderate to high levels in Central and Eastern Europe 11.

The reduction in dental caries in developed countries of Northern and Central Europe in the last 20 years has not occurred because of the undoubted advances in the dental treatment but because of the widespread introduction of comprehensive oral diseases preventive programs and promotion of oral health, especially use of fluorides 7,10,15.


Oral health in developing countries of Eastern Europe in generally did not followed the pattern of oral health improvement in developed countries. Prevalence rate of dental caries remained high in most of Eastern Europe. For example DMFT in twelve year old in this countries is still between DMFT What is the main reason?! Where is the problem?

Former socialist countries of Eastern Europe had very centralized and government controlled health care system, with all expenses covered by government. In other words free of charge. This concept seems to be very promising, especially in reaching oral health and as well general health global goals (“Health for all up to year 2000”) 6. This countries has accepted from the very beginning the concept of Primary Health Care (PHC) proposed by WHO, based on equitable distribution, community involvement, prevention and health promotion, appropriate technology and multisectorial approach (Declaration of Alma Ata – WHO/UNICEF, 1978).

It seems that problem was not in the main concept of organization. The problem seems to be somewhere else;

First: The promising government concept of health care was disturbed by the poor economic ability of the society which could not support financially the given tasks of health care and health promotion.

Second: Rapid increase of living standard and changes of lifestyle caused drastic increase of oral diseases with demand of very expensive curative treatment, which public (government supported) insurance could not support as well.

Third: At the same time insurance users didn't share the responsibility for their own health, because there were no sanction if they faille to follow preventive measures proposed by the health authorities and in same time very expensive treatment was as well free of charge. This was the main reasons of irrational distribution between health and disease. It seems that both, doctors and patients, are more willing to treat disease instead of preventing it.

Fourth: On the other hand, the promoting factor of this irrationality was evaluation and financing of health service. The health service activities were evaluated and paid by the treatment done (for example according to number of filled teeth, extracted teeth, number of crowns, prosthetic appliances etc.) in other words finances were directed for disease treatment rather than prevention. System was cot up in his own trap: PROMOTING PREVENTION - FINANCING DISEASE.

Fifth: Another problem seems to be in distribution of manpower. Distribution of personnel within oral health care system reflects the irrationality of the system as well. For example, a high proportion of dental hygienists or preventive therapists may demonstrate a preventive philosophy or policy at the system level. In contrary to the Western European Countries where exist

9,1 1 3-5

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specially trained medical staff with different level of education in preventive dentistry (dental hygienists, community dentistry workers, specialist of community dentistry etc.) in Eastern European countries we stand today that high professionally trained dentist with curriculum based on curative dentistry (disease treatment) are employed in preventive dentistry (to prevent oral diseases). They are trained to work in preventive dentistry (during postgraduate studies - specialization) but on the other hand still curative oriented.

Recent social changes in most Eastern European (former socialist) Countries demanded changes of health care systems as well. Open demands were focused on rationalization of health care system (improvement of Public Health Care, Primary Dental Health Care equally distributed on public and private services, etc.), insurance improvement, financing of health care and etc. In other words PDHC is to be responsible for planing and caring out Program of Oral Health by unique policy, to provide treatment of oral diseases in risk groups (pregnant women, children, old people) and basic dental treatment for all ( emergency etc). In this terms PDHC is to remain in government control.

Current transformation of health care systems in most Former Socialist Countries (undergoing transition), from very centralized and government controlled dental health services based on very expensive curative care which governments could not support any longer, and common belief that oral diseases are not threatening life, has excluded stomatology completely from primary health care system and left it within very expensive private practice oriented dentistry.

As we have experienced so far in Serbia, dental private practitioners have very little interest in dealing with prevention of oral diseases. Their interest is mainly focused on treatment which is bringing more profit.

Having all this in mind, and to avoid total absence of primary dental health care from the National health care system, dental profession in Serbia has recommended to the Ministry of Health - that it is of great importance that dentistry become a part of the unique primary health care system based on:

1. National Program for Prevention of Oral Diseases in Population of Serbia

- oral health promotion - preventive dental health care of whole population - early diagnosing and treatment of oral diseases of preschool and

school children - orthodontic treatment of children up to 18 years old with participation - prosthetic treatment of children up to 18 years old with participation 2. Urgent dental treatment for whole population - first aid - acute oral diseases - oral trauma and etc.


3. Basic dental health care - fillings - tooth extraction - conservative treatment of prior. diseases - prosthetics with participation Population groups: 1. with special needs (handicaps) 2. at high medical risk - hemophilia - cardiovascular diseases - diabetes - cancer and etc. 3. older than 65 years 4. social aid beneficiaries 4. Surgical treatment of neoplasm (benign and malign) in oro-facial region Finances for proposed dental care (PDHC) should be provided by

government through the National Health Insurance as a part of finances directed for primary health care (PHC), which will be available under same conditions for both, government and private dental services.

Conclusion

The main reason for higher occurrence of oral diseases in Eastern European countries is not due to the lower level of dental treatment, but due to the missing or improper implementation of Programs of oral health care. Public Dental Health has to be based and supported by National Programs of Oral Health Care which are existing in most of the Northern European countries concerning rationale use of scientifically approved most effective and inexpensive measures in prevention of oral diseases, proper education and distribution of manpower employed in Public Dental Health Services. With such recommended approach lower socio-economic groups who are dominant in former socialist countries undergoing transitions, which suffer the worst health problems, and with most difficulty in accessing health care, will get opportunity to fulfill their demands for oral health improvement.

This paper was presented at the IV Congress of BaSS – Istanbul, Turkey

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References

1.Acheson D.: Public Health in England: Report of the Committee of Inquiry in the Future Development of the Public Health Function. HMSO, London, 1988

2.Ashton J.: Institutes of public health and medical schools: grasping defeat from the jaws of victory? Journal of Epidemiology and Community Health, 1993, 47:165-168.

3.Carevic M., Vulovic M.: Effect of National Program for Prevention of Oral Diseases in Serbia (1996-2000). Kushedassi, Turkey, Abstracts Book 7th Congress of Balkan Stomatological Society, 2002.

4.Downer M.C., Gelbier S. and Gibbons D.E.: Introduction to Dental Public Health.London, FDI World Press, 1994.

5.Dean K.: Editorial: Creating a new knowledge base for the new public health. Journal of Epidemiology and Community Health 48, 1994, 217-219

6.FDI: Goals for Oral Health in the Year 2000. FDI Newsletter, March 1982. 7.Murray J.J.: Prevention of Oral Disease. Oxford, New York, Tokyo, Oxford University

Press. 1996. 8.Petersen P.E.: Social Inequalities in Dental Health-Towards a Theoretical Explanation.

Community Dental and Oral Epidemiology, 1990, 18: 153-158 9.Petersen P.E.: Changing Oral Health Profiles of Children in Central and Eastern Europe -

Challenges for the 21st Century. IC Digest, 2003, 2: 12-13 10.Pine C.M.: Community Oral Health. Wright. Oxford, Boston, Johannesburg, Melbourne,

New Delhi, Singapore, 1997. 11.Reich E.: Trends in Caries and Periodontal Health Epidemiology in Europe. International 12.Dental Journal, 2001, 51: 392-398 Vulović M. i sar.: Program preventivne stomatološke

zdravstvene zaštite stanovnika Republike Srbije. Beograd, Zavod za udžbenike i nastavna sredstva, 1996.

13.WHO: Global Strategy for Health for All by the Year 2000. World Health Organization. Global, 1981.

14.WHO: Targets for Health for All: Targets in Support of the European Regional Strategy for Health for All. World Health Organization, Copenhagen, 1985

15.WHO Regional Office for Europe. Experience on Water Fluoridation in Europe. Copenhagen, 1987.

16.WHO: Public Health in European Community. Health Promotion Program 1996-2000.European Commission, 1997.



10 years of BaSS

REPLANTATION OF TRAUMATICALLY EXTRACTED TEETH

Faculty of Dentistry Skopje, Skopje, FYR Macedonia Department for Paediatric and Preventive Dentistry Department for Orthodontics

M. CarčevH. PetanovskiS. Carčeva

1

2

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Summary

The authors present contemporary views regarding the treatment of traumatically extracted teeth. Apart from emphasizing the significance of taking a detailed history and performing thorough clinical examination, a special attention is focused on several aspects of the implantation procedure. Finally, factors determining the success of the procedure, as well as the outcome of the treatment are discussed in detail.

Key Words: Tooth Replantation, technique; Immobilisation

Introduction:

Traumatic extraction or avulsion is a kind of injury when due to a physical trauma the tooth is completely extruded out of the alveolar socket. (Fig. 1) The traumatic extraction is often accompanied by lacerations and bleeding of soft tissues of the face and mouth, and because of the impressiveness of the injuries, the most common reaction is fright and upset.

Fig 1. A patient, 12 years of age. Avulsion of the tooth 11


The absence of rational behaviour in these moments is often reason for negligence of the extruded tooth, leaving it in a position of the injury, or if it is found, it is often transported to the dental office in dry handkerchief. If the traumatic injury takes place in late hours or during the weekend, the extruded tooth remains folded in dry handkerchief for few hours or even few days. According to Andreasen3 and Cornell5 the mode of transportation of the tooth to the dental office and how quick it will be put back into the alveolar socket are decisive for the success of the replantation.

Epidemiology:

According to the data enclosed by Andreasen3, the frequency of teeth avulsion compared of all of the types of teeth injuries subject of different epidemiological studies, accounts for 0.5 to 16% in the permanent dentition, and 7-13% in the deciduous dentition. The data reported by Beloica4 from the Clinic of Paediatric and Preventive Dentistry in Belgrade, testify for more frequent cases of avulsion in deciduous comparing to the permanent dentition. Grossman7 concluded that avulsion is most frequent at the age between 10 and 14, while according to Andreasen1 the maxillary incisors are almost 10 times more exposed to these injuries compared to the mandibular incisors.

At the Clinic of Paediatric and Preventive Dentistry in Skopje 30 replantations of traumatically extracted teeth have been performed in the last ten years. Although traumatic extraction is not a frequent injury, the knowledge of the replantation technique and problems related to it is indispensable because every dentist during his/her clinical practice may come to a situation of dealing with this kind of injury. The higher prevalence of traumatic extractions in the child age imposes the need for knowing the biological traits of young permanent teeth.

Treatment of Patients with Traumatic Extraction

Taking history The most important data upon which the further course of the therapy

depends in the case of traumatic extracted teeth regard to the extra oral time, i.e. the time that passes from the moment of tooth extrusion until the moment of coming to the dental office. If that time is shorter than 2 hours, it is necessary

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that the most important data are collected and that the replantation is started immediately, while the other data should be put aside and taken after the replantation is finished. Detailed anamnesis could be taken beforehand only if the extra oral time is longer than 2 hours.

If the patient, together with the extruded tooth could not immediately reach the dental office, he/she should be advised to rinse the tooth with cold water and if possible, to put it back into the alveolar socket. If, because of any other reason this is not possible, the advice is to hold the tooth under the tongue and to immediately come to the dental office. Another convenient way of transportation of the tooth to the dental office is to store it in physiological solution. An appropriate alternative for physiological solution is a solution made of 1 coffee spoon of salt and 2 dl of water. The third alternative is transportation of the tooth in cotton pad or clean handkerchief damped in water.

Clinical examination

The clinical examination should be as short as possible. The traumatized area around the extruded tooth should be cleaned with sterilized cotton pad damped in physiological solution in order to enable more precise detection of the degree of the injury. If the examination shows that it is a matter of tooth extrusion without injury of the surrounding tissues, especially if the tooth resides out of the alveolar socket not more than 30 min, the replantation should start immediately. Radiographic examination should be undertaken only in cases when there is a justified doubt of alveolar bone fracture or if the patient had not found the tooth and we want to exclude or confirm its possible complete intrusion into the alveolar socket. If the extra oral time is longer than 2 hours, then the injured area should be thoroughly examined and radiogram should be obtained. Replantation procedure

Before replantation, the tooth should be thoroughly cleaned with tampon damped in physiological solution. Any chemical or mechanical procedures are contraindicated, as well as putting the tooth in antibiotic (penicillin) or resection of the apical part of the root. Preparation of the tooth for replantation

The condition of the tooth apex and the extra oral time are 2 key factors that determinate the time and the type of possible endodontic treatment.

With teeth having non-completed the root growth, if the extra oral time is not longer than 2 hours, the endodontic treatment should not be carried out because according to the experience of many authors, as well as ours, revascularization and revitalization of the pulp is highly possible. Absence of


clinical difficulties and continuing the growing process are signs of preserved pulp vitality of the replanted tooth. Electrical vitality examination during the first few months does not give reliable data, because the function of the nerve fibres starts to re-establish after 35 days. If after 30 days of the replantation, we can notice signs of root resorption accompanied by clinical difficulties (pain, red colouring of the mucus membrane in the apical region, percussion sensibility) we should immediately start with extirpation of the pulp and filling the root canal with calcium-hydroxide.

If the extra oral time is longer than 2 hours, first we carry out an endodontic treatment and after that, the tooth replantation. However, there are opposing opinions. Andreasen2, for example, states that in these cases the tooth replantation should be carried out first, while the endodontic treatment should be carried out 2-3 weeks after the replantation because it is experimentally proven that application of calcium-hydroxide prior to the replantation may have stimulating effect on the cementoblasts causing ankylosis, which puts limit to the healing process of the periodontal ligament by forming collagen fibres.

With teeth having completed root growth, depending on the extra oral time, there are 2 factors determining the course of the replantation treatment. When the extra oral time is shorter than 2 hours, replantation should start immediately in order to prevent further damage and necrosis of the remaining parts of the root periodontal ligament, because the endodontic treatment will prolong the extra oral time. 2-3 weeks after the replantation, endodontic treatment is carried out by filling the root canal with calcium-hydroxide. Endodontic treatment prior to replantation is regularly carried out in teeth which extra oral time is longer than 2 hours. The chances of revitalization of the teeth with completed root growth are only theoretical.

In order to decrease the risk of root resorption, which is the most common complication after the replantation, Cornell5 recommends that the tooth should be stored in 1-2% sodium-fluoride solution, 4-5 minutes prior to replantation. If the extra oral time is shorter than 2 hours, application of fluorides should be avoided because they can have cytotoxic effect on the root vital tissue. Preparation of the alveolar socket

The preparation of the alveolar socket starts with rinsing the blood coagulum with physiological solution or with cotton pad winded up on a stick. The alveolus should not be cooled because that procedure could accelerate root resorption after the replantation. If alveolar fracture is present, the replantation of the tooth should be performed with local anaesthetics.

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Technique of replantation After the preparation of the alveolar socket, the tooth crown is put

back into the alveolus holding it between the thumb and the fingerpost with loose pressure and rotating movements until the tooth is positioned in its place. At the end, the alveolus is repositioned in order to correct its expansion.

Immobilisation of the replanted tooth There are many ways of fixation of the replanted teeth, but common

opinion is that the stainless steel wire and composite splints are most convenient nowadays, due to its easy shaping and ensuring solid fixation of the replanted tooth8 (Fig. 2).

Fig. 2. Immobilization performed with stainless steel wire and composite splint

The immobilization wire should be 0.8-1 mm thick. First we fix the most distal tooth, and the last - the replanted tooth. The splint is postured labial in the maxilla and lingual in the mandible to ensure that it does not disturb the occlusion.

Prevention of tetanus and application of antibiotics Prevention of tetanus is carried out with active and passive

immunization. Better quality is obtained by active immunization, but if the patient is not protected in this way, the passive immunization is carried out immediately after the replantation with application of antitoxin (anti-tetanus


immunoglobulin). After the replantation, there is no need of antibiotic therapy because

the replantation procedure itself is not indication for ordering antibiotics. Duration of immobilization

The opinions about the duration of the replanted tooth immobilization vary widely. The recommendations for the duration of the immobilization vary from 2 to 6 weeks, or longer. However, the opinion that the immobilization should last not more than 2 weeks is commonly accepted as the prolonged rigid immobilization may cause more harm than good because it increases the risk of ankylosis and root resorption9. Splints removal

Firstly, the wire arch is cut in the inter-dental areas using diamante borer, the composite above the wire is removed, and after that the wire and the remains of the composite material are removed from the healthy adjacent teeth using excavator or instrument for tartar removal. The composite is removed from the replanted tooth exclusively with diamante borer and turbo machine in order to avoid additional traumatism of the tooth. After the teeth are free of composite, they are covered with a fluoride preparation.

Since the replanted tooth is not firmly fixed, the patient is advised to save the teeth in the frontal region for the following 2 years and to maintain rigorous oral hygiene.

Replantation of traumatically extracted deciduous teeth

Although some authors have been carrying out replantation of traumatically extracted deciduous teeth, according to our own experience and that of other authors, replantation of the deciduous teeth is not advisable and should not be carried out because it is regularly accompanied by early complications, such as pulp necrosis or root resorption9, while the inflammatory process may later occur and damage the offspring of the permanent tooth. Factors that determinate the success of the replantation

The success of the extruded teeth replantation depends on many factors the most important of which being: the extra oral time, the treatment of the extruded tooth and the way of its transportation to the dental office, the

M. Carčev et al

degree of preservation of the periodontal tissue on the root surface, the condition of the alveolar bone and the application of fluorides during the replantation.

1. The extra oral time after the tooth extrusion is considered the most important factor for the success of the replantation. According to Andreasen3, 79-96% of the replanted teeth show signs of root resorption, but if the extra oral time is shorter than 30 minutes the resorption can be found in only 10% of the cases.

2. The way of preservation and the medium in which the extruded tooth is stored is considered not less important comparing to the extra oral time. Andreasen3 states that even the prolonged storing of the tooth in physiological solution or in saliva will not have grater influence on the damage of the periodontal ligament, than when the extra oral time is short, but the tooth is stored in dry place. The mechanical cleaning of the root, as well as its cleaning with soap, 3% hydrogen or alcohol will have more harmful effect on the periodontal ligament causing death of the cementoblasts and coagulation of the collagen fibres.

3. Preservation of the periodontal ligament has important role for the success of the replantation. Every procedure that involves scrubbing and removing of the periodontal ligament remnants from the root before the replantation is highly contraindicated3. The cells of the periodontal ligament is presumed that can survive about 2 hours, while the healing process of the periodontal tissue left on the root of the replanted tooth is 2-3 weeks.

4. Alveolar fracture has unfavourable impact on the root of the replanted tooth and accelerates its resorption. Curettage of the alveolus is reason for accelerated root resorption, so this procedure is also contraindicated.

5. The opinion frequently found in literature that the root apex should be removed before the replantation has proven to be wrong, because that procedure accelerates the resorption. The easier reposition of the tooth in the alveolar socket is mentioned as a motive for carrying out this procedure, considering the fact that the residue of blood coagulum may prevent it. The coagulum may be removed with injection of physiological solution or with tampon, thus avoiding the scratching of the alveolar socket. Other reason for apex resection is the tendency for more expressed exposure of the pulp in the apical part and its faster revitalization. However, this procedure has shown to be unjustified because only accelerated resorption is experimentally registered, but not faster revitalization. These reasons justify the assumption that apicectomy before the replantation is contraindicated.

6. It is experimentally proven that storing the tooth 4-5 minutes in solution of 1-2% sodium fluoride significantly reduces root resorption5. The mechanism of beneficial influence of the fluoride is not completely cleared up, but it is presumed that the fluoride is built in the cement, thus making it more


resistant on the root surface. According to Cornell5, local application of fluorides to the root prior to its replantation is crucial, but it should be applied only on teeth with extra oral time longer than 2 hours.

Follow-up and prognosis of the replanted teeth

Every replanted tooth should be followed, clinically and radiographically, disregarding the condition of its apex and the extra oral time. In teeth for which we expect revitalization, electrical and thermal stimulation are not always credible signs of preserved vitality. Continue of the root growth, as well as the narrowing of the pulp chamber although indirect, are more certain signs of preserved vitality of the pulp.

The prognosis of the replanted teeth is not favourable. The previous clinical experience testifies of frequent complications. The most common complication is the root resorption (Fig. 3). However, with teeth having unfinished root growth and extra oral time shorter than 30 minutes, root resorption is found in only 10% of the cases. This fact itself goes in favour of the conclusion that the replantation should mean competition with the time, because the time passed from the tooth extrusion until its putting back into the alveolus can not been compensated even by the best performed replantation. Regardless of frequent pathological changes of the tooth pulp and root, the replantation should be considered as justified if the tooth is preserved for only few years. This procedure exerts the huge psychological significance, insures esthetical function, preserving of space and undisturbed jaw growth.

Fig. 3. Radiogram of the tooth 11, taken 4 years after the replantation - A complete root resorption is evident

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References

1. Cornell RW. Management of the avulsed tooth. Clinical Transplantation in dental specialties. Saint Louis: The CV Mosby Co, 1980. 2. Beloica D. Teeth injuries. Beograd: Djecje novine, 1990. (in Serb) 3. Andreasen JO. Etiology and pathogenesis of traumatic dental injuries in the clinical study of 1298 cases. Scand J Dent Res, 1971; 78:329. 4. Andreasen JO. Traumatic injuries of teeth. Copenhagen, Philadelphia: Munksgaard and WB Sauders Co, 1981. 5. Grossman LI, Ship I. Survival rate of replanted teeth. Oral Surg, 1970; 29:899-904. 6. Camp JH. Replantation teeth following trauma. Sent Louis: The CV Mosby Co, 1980. 7. Andreasen JO. A time-related study of root resorption activity after replantation of mature permanent incisors in monkeys. Swed Dental J, 1980; 4:101-105. 8. Skrinjaric I. Traumas of teeth in children, Zagreb: Globus, 1988. (in Croat) 9. Gregg TA, Boyd DH. Treatment of avulsed permanent teeth in children. UK National Guidelines in Paediatric Dentistry. Int J Paediatr Dent, 1998; 8(1):75-81.


DENTAL MANAGEMENT OFEOSINOPHILIC GRANULOMA OF BONE:A literature review

Department of Periodontology, Faculty of Dentistry, Ege University, İzmir, Turkey

Nurcan Buduneli DDS, PhDFüsun Ünlü DDS, PhD, Professor

Scientific Thought and Clinical Practice 10 years of BaSS

Summary: Langerhans’ cell histiocytosis, comprises 3 different clinical entities;

Hand-Schüller-Christian disease, Letterer-Siwe disease and eosinophilic granuloma (EG) of bone. They are all characterized by abnormal proliferation of histiocytes and eosinophilic leukocytes destroying local tissue secondary to cellular infiltration. EG of bone is the most common, but fortunately the mildest form, which usually affects adolescents and young adults. The skull, mandible, ribs, and long bones are the most frequently affected parts in the skeletal system. Oral cavity lesions are frequently the initial signs and symptoms leading to diagnosis. The involvement of periodontal tissues in EG is well recognized and may sometimes mimic severe localized periodontitis lesions with pronounced gingival recession and alveolar bone destruction resulting in tooth loss. In suspected cases, the differential diagnosis should include early-onset periodontitis, odontogenic cysts and tumors, multiple myeloma, osteomyelitis, and malignant lymphoma. For an accurate diagnosis the histopathological examination of the lesions is mandatory. The accepted treatment of EG of bone includes surgical curettage of the lesion, localized low dose radiotherapy and rarely chemotherapy. Treatment modalities can be planned depending on the extent, location, and accessibility of the involvement. Since diseases like EG of bone are mostly prone to the preliminary diagnosis of dental practitioners, it is highly important to be well aware of the related diagnostics and management aspects. Key words: eosinophilic granuloma, periodontal manifestations, etiology, management Introduction:

Langerhans’ cell histiocytosis, formerly known as histiocytosis X syndrome is composed of three different clinical entities; Hand-Schüller-Christian disease, Letterer-Siwe disease and eosinophilic granuloma (EG) of bone.17 While the exact etiology of this rare syndrome remains largely obscure, the diagnosis and treatment may pose a problem to the clinician. Until the present time, immunological abnormality in terms of a hypersensitivity reaction towards an unknown antigen, a bacteriological infection and an inflammatory process have been proposed for the etiology of Langerhans’ cell histiocytosis.7,14 These 3 diseases are all characterized by abnormal proliferation of histiocytes and eosinophilic leukocytes destroying local tissue secondary to cellular infiltration.2,8,17 Hand-Schüller-Christian disease (chronic disseminated form) typically involves a triad of symptoms; diabetes insipidus, exophthalmus, and multiple lytic bone lesions. Letterer-Siwe disease (acute disseminated form) usually affects children under the age of three and has a


rather fatal course. There is widespread involvement of multiple organs, particularly lymph nodes, liver and spleen and the patient usually dies within a relatively short period of time, after the diagnosis. EG of bone is the most common but fortunately the mildest form, which usually affects adolescents and young adults. Having similar clinical and histopathological features, a risk of transformation among these there diseases is not unlikely.

The purpose of this article is to review the clinical presentation of EG of bone and to highlight the management aspects. Clinical features:

EG of bone is more common in males than females. The skull, mandible, ribs, and long bones are the most frequently affected parts in the skeletal system. However, lytic lesions can be found in any other bone with the exception of hands and feet. Oral cavity lesions are frequently the initial sings and symptoms leading to the diagnosis. The involvement of periodontal tissues in EG is well recognized and may sometimes mimic severe localized periodontitis lesions with pronounced gingival recession and alveolar bone destruction resulting in tooth loss. A sore mouth, foeter exore, pus, pain, swelling, loosening of teeth and retarded healing after extraction are among the main oral findings in EG. The lesions are more common in the mandible than the maxilla and are often detected in the radiographs as unifocal or multifocal round or oval radiolucencies with well-defined margins (scooped-out shape).22

Floating-teeth sign is another characteristic radiographic appearance. Sclerosis in the alveolar bone lesions, periosteal new bone formation, and slight root resorption are less frequent radiographic findings in EG of bone.6 In suspected cases, the differential diagnosis should include early-onset periodontitis, odontogenic cysts and tumors, multiple myeloma osteomyelitis, and malignant lymphoma. For an accurate diagnosis the histopathological examination of the lesions is mandatory. The abundance of histiocytic cells having common features with Langerhans’ cells which are scattered among large numbers of eosinophils is a characteristic histologic finding.2,18 The immunohistochemical staining of the proliferating cells show pronounced positivity with S100 antigen, which is considered to be the most reliable marker for Langerhans’ cell histiocytosis. CD1a surface antigen is another diagnostic marker that can be used in immunohistochemical techniques. Moreover, electron microscopy may be helpful where available, to show the characteristic Birbeck granules in histiocytes.

A confirmatory biopsy analysis of EG should be followed by examination of the skeletal system and the whole body for additional lesions. General medical and radiographic examination can be achieved by skeletal scintigraphy, tomograms of the abdomen and pelvis as well as a chemical profile and a complete blood count.13 Management of a patient with EG of bone requires a

N. Buduneli et al

multidisciplinary approach between specialists and careful follow-up examinations.

Dental management:

After detection of the whole body for any other possible lesion and consulting with a physician, the dental surgeon may plan the treatment of the case. The accepted treatment of EG of bone includes surgical curettage of the lesion, localized low dose radiotherapy and rarely chemotherapy.1,3,10,17 Both corticostreoids and cytotoxic drugs have been used for the treatment of histiocytosis X.5,15 Treatment modalities can be planned depending on the extent, location, and accessibility of the involvement.12 In the accessible areas, aggressive surgical curettage is usually an appropriate way of treatment of unifocal eosinophilic granuloma, where there is no additional organ pathology.

Not all teeth involved by the disease require removal, except those with pronounced mobility and lytic bone destruction around the apices of the roots. Surgical curettage should be as thorough as possible and in some cases can be followed by filling with cancellous bone chips in order to prevent fractures or excessive bone defects. Solitary lesions usually respond well to conservative surgical excision or low dose radiotherapy and may heal spontaneously leaving only scar tissue.19 Low dose (300-1000 rads) radiation therapy is useful in surgically inaccessible areas, in lesions of the weight-bearing bones, and in areas, where surgery will cause dysfunction or disfigurement.4 Jaw lesions are frequently treated by enucleation to avoid long-term growth complications produced by radiotherapy.10 Radiotherapy administration of 100 to 200 rads daily for two or more weeks may be recommended.21 The possible side effects of irradiation on the growth centers, and the developing dentition should also be considered.

Disruption of normal growth should not be the outcome of therapy. For localized unifocal lesions, another treatment option is intralesional injection of corticostreoids (vinblastine sulphate).9 In more aggressive or multifocal cases steroids can be prescribed systemically. However, it can be stated that chemotherapy should be reserved for disseminated forms of the Langerhans’ cell histiocytosis syndrome; namely Letterer-Siwe disease and Hand-Schüller-Christian disease.

In treatment of EG chemotherapy is rarely used in surgically inaccessible areas, or in case of recurrence following surgery or radiotherapy.20 The prognosis for a true unifocal EG of bone appears to be good, with surgery alone or with combined therapy consisting surgery and irrradiation.1,11 It is pleasant that the recurrence rate is low regardless of the treatment method. Even more than that the unifocal bone lesions may heal spontaneously leaving only a scar tissue, but this is rare and unpredictable. Therefore, cases should be put on a regular clinical follow-up regimen to avoid the risk of recurrence and


expansion. Good regeneration of bone without any evidence of recurrence has been reported even in multifocal EG cases.16 Case report

A male patient aged 24 was referred to the Department of Periodontology with a preliminary diagnosis of juvenile periodontitis in April 1994. The true nature of the sequential jaw lesions was found to be EG of bone after confirmatory biopsy analysis with S100 antigen. The whole body and skeletal system as well as the blood values were detected for ant other signs and symptoms of possible lesions and all were found to be normal. The severely affected molar teeth had to be extracted and systemic corticosteroids (vinblastine sulphate) had to be prescribed due to the sequential and recurrent progression of lesions.

After four years of clinical follow-up no new lesion was detected, the patient did not have related complaints any more and the extraction sites healed completely, yet with a significant alveolar bone resorption. The patient had received the appropriate prosthetic treatment and is still on regular follow-up regimen. As a conclusion, since diseases like EG of bone are mostly prone to the preliminary diagnosis of dental practitioners, it is highly important to be well aware of the related diagnostic and management aspects. References

1. Artzi Z, Gorsky M, Raviv M. Periodontal manifestations of adult onset of histiocytosis. J Periodontol, 1989; 60:57-66

2. Ben-Ezra JM, Koo CH. Langerhans’ cell histiocytosis and malignancies of the M-PIRE system. Hematopathology, 1993; 99:464-471

3. Beyer D, Herzog M, Zanella FE, Bohndorf K, Walter E, Hüls A. Röntgen diagnostik von Zahn-und Kieferkrankungen. Springer Verlag, 1987, pp 291-296

4. Bhaskar PB, White CS, Baughman R. et al. Eosinophilic granuloma of the mandibular condyle. Oral Surg Oral Med Oral Pathol, 1993; 76:557-560

5. Bilgiç H, Köylü R, Seber O, Ekiz K, Demiriz M, Taştan B. Histiocytosis X: a clinicopathological study. J Health Sci, 1994; 5-6:69-79

6. Dagenais M, Pharoah MJ, Sikorski PA. The radiographic characteristics of histiocytosis X. Oral Surg Oral Med Oral Pathol, 1992; 74:230-236

7. Hratman KS. Histiocytosis Z: A review of 114 cases with oral involvement. Oral Surg Oral Med Oral Pathol, 1980; 49:38-54

8. Ide F, Iwase T, Saito I et al. Immunohistochemical and ultrastructural analysis of the proliferating cells in histiocytosis X. Cancer, 1984; 53:917-921

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6

9. Jones LR, Toth BB, Cangr A. Treatment for solitary eosinophilic granuloma of the mandible by streoid injection: report of a case. J Oral Maxillofac Surg, 1989; 47:306-309

10. Kaban LB. Pediatric Oral and Maxillofacial Surgery. W.B. Saunders Company 1990, pp 384-386

11. McDonald RE, Avery DR. Dentistry for the child and adolescents. 5th Edition. The C.V. Mosby Company 1988, pp 185-187

12. Moghadam KH, Saedi S, Gier RE. Adult-onset multifocal histiocytosis X presenting as a periodontal problem. J Oral Maxillofac Surg, 1991; 49:417-419

13. Nicopoulou-Karayianni K, Mombelli A, Lang NP. Diagnostic problems of periodontitis-like lesions caused by eosinophilic granuloma. J Clin Periodontol, 1989; 16:505-509

14. Osband ME, Lipton JM, Lavin P. Histiocytosis X. New England J Med, 1981; 304:146-153

15. Piatelli A & Paolantonio M. Eosinophilic granuloma of the mandible involving the periodontal tissues. A case report. J Periodontol, 1995; 66:731-736

16. Punnia Moorthy A. Eosinophilic granuloma manifesting as a periodontal problem. Br Dent J, 1985; 161:66-67

17. Regezi JA, Sciubba JJ. Oral Pathology: clinical-pathological correlations. Philadelphia: W.B. Saunders 1993; pp 413-416

18. Ruco LP, Stopacciaro A, Vitolo D et al. Expression of adhesion molecules in Langerhans’ cell histiocytosis. Histopathology, 1991; 23:29-37

19. Saunders JGC, Eveson JW, Addy M et al. Langerhans’ cell histiocytosis presenting as bilateral eosinophilic granulomata in the molar region of the mandible. A case report. J Clin Periodontol, 1998; 25:340-342

20. Ünlü F, Gürses N, Seçkin T, Ünal T. Multifocal eosinophilic granuloma with sequential periodontitis-like lesions. J Clin Periodontol, 1997; 24:384-387

21. Whitcher BL, Webb J. Treatment of recurrent epsinophilic granuloma of the mandible following radiation therapy. J Oral Maxillofac Surg, 1986; 44:565-570

22. Yu Q, Wang P-Z, Shi H-M et al. Radiographic findings in Langerhans’ cell disease affecting the mandible. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 1995; 79:251-254



10 years of BaSS

ORTHODONTIC EXTRACTION: THE EXTRACTION OF THE THIRD MOLARS IN CLOSE PROXIMITY TO THE MANDIBULAR CANAL BY AN ORTHODONTIC-SURGICAL APPROACH

¹*Department of Periodontology, School of Dentistry, University of Bologna, Via S.Vitale 59 Bologna, Italy.²*Department of Periodontology and Oral Medicine, Shool of Dentistry, University of Belgrade, Dr Subotica 4, Belgrade, Serbia and Montenegro

Luigi Checchi¹Giulio Alessandri Bonetti¹Michele Bendandi¹Ana Pucar²Marco Montevecchi¹

Summary The purpose of this study was to describe an orthodontic-surgical approach to performing riskless extractions of those third molars with contiguity between the roots and the mandibular canal. The approach consists of different phases. First the surgical risks have to be assessed. A first topographic diagnosis is made using a panoramic radiograph and then, if there is a suspected contact between root and mandibular canal, a CT scan is done. When the proximity is confirmed, “the orthodontic extraction procedure” will start with the creation of an orthodontic anchorage. This phase is followed by a surgical exposure of the third molar crown in order to bond a bracket to the occlusal surface. A stainless steel sectional wire is anchored from the first molar to the third molar to produce the extrusive forces. After a positive clinical assessment of the extrusion level, a new radiological check is requested to evaluate the tooth movement. When the tooth is out of the mandibular canal, the surgeon can perform a safe and easy third molar extraction. With this therapeutic approach the extraction of an impacted lower third molar will be:

� easier and quicker, � with less post-operative discomfort, � without risk of paresthesia or mandibular fracture, � with periodontal advantages.

In conclusion the orthodontic-surgical approach to the high-risk extraction of impacted lower third molar has proved to be a quite simple technique for the dentist and minimally traumatizing for the patient. Key Words: third molar, tooth impaction, orthodontic extrusion, extraction.


Introduction:

The extraction of lower third molar is one of the most frequent procedures in oral surgery and it can bring about various complications; among these, the neurological ones (paresthesia), are the most feared since they are likely to lead to legal disputes between dentist and patient. Once it has been decided that the wisdom tooth has to be extracted, it is necessary to assess the risk of nerve damage consequent to the surgical procedure either by a direct trauma of the lower alveolar nerve, more rarely of the lingual nerve, or by an indirect trauma due to nerve compression following an edema or a post-extraction hematoma (5,8,15,17). The onset of such complications is affected by many factors as the patient’s age (2); the medical history; the level of tooth impaction (8); tooth inclination (3,8); root morphology (8); the skill of the operator (1,8), but must importantly the contiguity between the roots and the mandibular canal influences the incidence of neurological complications (3,8,15). For this reason, it is important to carry out appropriate radiographic exams to make a precise topographic diagnosis of the third molar before the surgery, thus being able to assess the surgical risks and decide the most convenient approach. If those radiographs show a suspected proximity between tooth and mandibular canal, a dental CT scan must be performed to fix precisely the topographic relationships among these anatomic structures so as to be able to assess the extractive risk before the operation.

Fig.1: A first topographic diagnosis is made using a panoramic radiograph. If there is a contact between root and mandibular canal a CT scan is done

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If the proximity between root and canal is confirmed, the “orthodontic extraction” will start by the creation of the orthodontic anchorage.A stainless steel lingual arch, welded to bands, is cemented on the first molars and a stainless steel sectional wire is tied into orthodontic brackets from the second molar to the first bicuspid, buccally on the extrusion side. Then an open flap is done to expose the crown of the impacted tooth and to apply an orthodontic bracket on it.There are two different clinical cases of impaction of wisdom teeth that affect the duration of the extrusion therapy:- vertically or distally inclined; the extrusive force produces a movement of extrusion, without rotation, along the path of physiologic eruption of the tooth and in 3 to 6 months produces a setting apart from the mandibular canal. - horizontally or mesially inclined; it often requires longer therapy (6-12 months) because it is difficult to have a mere axial extrusion movement without rotation. In order to make the tooth movement easier, avoiding impaction of the third molar on the distal surface of the second molar, it is useful to reduce the occlusal surface of the crown during tooth

Fig.2:The orthodontic ancorage

Fig.3:Surgical exposure of the third molar crown


exposure. However, it is important to make a clinical distinction by means of the CT scan not only on the sagittal level but also on a transversal level. The extrusive force must be direct in such a way so as to set apart the roots from the mandibular canal not only vertically but also frontally. The orthodontic extrusion of the third molar is done by a cantilever. A rectangular stainless steel sectional wire (placed into the auxiliary tube on the first molar and tied to the bracket on the wisdom tooth) is the active part of the system. Once it has been bended and activated it allows to generate the extrusion movement of the third molar.

Fig.4: The orthodontic extrusion. A cantilever is placed into the auxiliary tube on the first molar and tied to the bracket on the third molar

Fig5 : Clinical evaluation of the extrusion

The sectional wire has to be reactivated after 4-6 weeks. On the basis of a positive clinical judgement, a new panoramic radiograph it is done to evaluate the tooth movement and to decide the moment to perform the extraction. When the surgeon has checked the absence of true relationship between root and canal by a new panoramic radiograph, the extraction is performed without risk of neurological complications.

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Initial Final Fig.6. Radiographic evaluation of the extrusion

Fig.7. Clinical Case

Initial

End of the extrusion

Control after 2 years


Initial Final

Fig.8 Discussion The use of the so called “Orthodontic extraction” eliminates the risk of direct and indirect trauma to the alveolar nerve by the increased distance between the roots and the mandibular canal, the reduction of the time instrumentation during extraction and the more favourable position for the surgery. For these reasons the extraction is quicker, easier and safer (4,7,12). Bone apposition is another advantage of this technique as a consequence of the extrusive movement. In fact there is a reduction of the possibility of mandibular fracture due to the increase in mandibular resistance (6,11); and a better periodontal status on the distal surface of the second molar after the third molar extraction (7). It is known from the literature that the surgical extraction of an impacted third molar often results in an infrabony periodontal defect on the distal surface of the adjacent second molar (9,10). The “Orthodontic extraction” technique solves this problem because there is a conservative management of the alveolar bone, due to the simplicity of the surgery, and to the (coronally) alveolar bone extrusion distally to second molar. The “orthodontic extraction” technique, however, is not without drawbacks. The procedure requires two minor surgical procedures: the exposure of the third molar crown and the extraction of the tooth.

. .

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The procedure is generally more time-consuming if compared with the mere extraction. Anyway this technique has been progressively developed during the years and it has been improved with regards to predictability of the clinical results and above all reduction of therapy length. This method cannot be used on a routine basis; it should only be used after an accurate selection of clinical cases of tooth impaction. Conclusions The cooperation among various specialists, in both the diagnostic and operative phases, is of paramount importance in order to establish the best possible treatment plan for the patient. The cooperation between the orthodontist and the oral surgeon has led to the “Orthodontic extraction”. The orthodontic-surgical approach to the high-risk extraction of impacted lower third molar has proved to be a technique without risk of paresthesia or mandibular fracture and with periodontal advantages (4,12). It is favourably accepted by the patient because it is considered a biologically, conservative and safe therapeutic choice and a technique that allows extraction of lower third molars otherwise impossible for the high risk of complications. The procedure is generally more time-consuming if compared with the mere extraction. Anyway this technique has been progressively developed during the years and it has been improved with regards to predictability of the clinical results and above all reduction of therapy length. This method cannot be used on a routine basis; it should only be used after an accurate selection of clinical cases of tooth impaction.


References 1) Brann CR, Brickley MR, Shepard JP. Factors influencing nerve damage during lower third molar surgery. Br Dent J 1999;186:514. 2) Bruce RA, Frederickson GC, Small GS. Age of patients and morbidity associated with mandibular third molar surgery. J Am Dent Ass 1980;101:240. 3) Bui CH, Seldin EB, Dodson TB. Types, frequencies, and risk factors for complications after third molar extraction. J Oral Maxillofac Surg 2003;61:1379. 4) Checchi L, Alessandri Bonetti G, Pelliccioni GA. Removing high-risk impacted mandibular third molars: a surgical-orthodontic approach. J Am Dent Ass 1996;127:1214. 5) Chiapasco M, De Cicco L, Marrone G. Side effects and complications associated with third molar surgery. Oral Surg Oral Med Oral Pathol 1993;76: 412. 6) Halmos DR, Ellis E, Dodson TB. Mandibular third molars and angle fractures. J Oral Maxillofac Surg 2004;62:1076. 7) Hirsch A, Shteiman S, Boyan BD, Schwartz Z. Use of orthodontic treatment as an aid to third molar extraction: a method for prevention of mandibular nerve injury and improved periodontal status. J Periodontol 2003;74(6):887. 8) Kipp DP, Goldstein BH, Weiss WW Jr: Dysesthesia after mandibular third molar surgery: a retrospective study and analysis of 1,377 surgical procedure. J Am Dent Ass 1980;100:185. 9) Kugelberg CF, Ahlstrom U, Ericson S, Hugoson A. Periodontal healing after impacted lower third molar surgery: a retrospective study. Int J Oral Surg 1985;14:29. 10) Kugelberg CF, Ahlstrom U, Ericson S, Hugoson A, Thilander H. The influence of anatomical, pathophysiological and other factors on periodontal healing after impacted lower third molar surgery: a multiple regression analysis. J Clin Periodontol 1991;18: 37. 11) Libersa P, Roze D, Cachart T, Libersa JC. Immediate and late mandbular fractures after third molar removal. J Oral Maxillofac Surg 2002;60:163. 12) Marchetti C, Alessandri Bonetti G, Pieri F, Checchi L. Orthodontic extraction: Conservative treatment of impacted mandibular third molar associated with a dentigerous cyst. A case report. Quintessence Int 2004;35;371. 13) Monaco G, Montevecchi M, Alessandri Bonetti G, Gatto MRA, Checchi L. Reliability of panoramic radiography in evaluating the topographic relationship between the mandibular canal and impacted third molars. J Am Dent Ass 2004;135:312. 14) Phillips C, White RP Jr, Shugars DA, Zhou X. Risk factors associated with prolonged recovery and delayed clinical healing after third molar surgery. J Oral Maxillofac Surg 2003;61:1436-48. 15) Rud J. Third molar surgery: relationship of root to mandibular canal and injuries to inferior dental nerve. Dansk resumè. Tandlaegebladet 1983;87:619. 16) White RP. Recovery after third-molar surgery. Am J Orthod Dentofacial Orthop 2004;126:289. 17) Wofford DT, Miller RI. Prospective study of dysesthesia following odontectomy of impacted mandibular third molars. J Oral Maxillofac Surg 1987;45:15.

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10 years of BaSS

AESTHETIC CONSIDERATION IN ORAL AND MAXILLOFACIAL SURGERY

1Dental/Medical Clinic "Beograd-Centar", Narodnog fronta 35, 11000 Belgrade, Serbia2Clinic of Oral Surgery, Faculty of Stomatology, Dr. Subotića 4, Belgrade, Serbia

Z. Stajčić Lj. Stojčev-Stajčić 2

1

Summary The purpose of this article is to deal with aesthetic consideration of an oral and maxillofacial surgeon when performing routine surgical procedures in the mouth and the face. The most frequently involved components in oral and maxillofacial surgery that may interfere with facial appearance are teeth, gums, lips, facial skin and underneath skeleton. Majority of respective surgical procedures has to fulfill strict aesthetic requirements which urges a surgeon to consider cosmesis when planning surgery. Characteristic cases are described do demonstrate authors phylosophy and skill in attempts to preserve esthetics while performing relatively complex procedures. Key words: aesthetic surgery, surgery oral maxillofacial

The face is the field where an oral and maxillofacial surgeon exercises his skill and knowledge in order to provide a cure to a diseased or disfigured patient. The face is, unfortunately, the most exposed part of the body and any alteration may produce serious psychological disturbances in an unhappy patient. The primary goal of oral and maxillofacial surgery is to remove lesion, eradicate disease and restore function with simultaneous endeavors not to leave patients with unpleasant defects or ugly scars. Since pleasant facial appearance mostly depends on facial harmony and happy smile this article is intended to deal with components of the face and the mouth that are most frequently involved in routine oral and maxillofacial surgical work with respect not to interfere with facial appearance. Teeth Replantation

Loss of anterior teeth due to trauma may contribute to extremely unpleasant appearance (Fig. 1a) therefore every attempt should be made for their replacement1. Replantation in children is routinely performed irrespective of the time of injury. Whenever possible, periodontium should be preserved and the tooth replanted withouth pulpectomy. Immobilization should be kept in place 10 - 14 days (Fig. 1b) and patient advised to exert light and frequent pressure on the replanted and splinted tooth with the tip of the tonque. By doing so, ankylosis is less likely to occur. Endodontic treatment is postponed for a month and following the removal of the pulp, the root canal is temporary filled by calcium hydroxide for a period of 6 - 12 months and then replaced with permanent root canal filling with gutta-percha (Fig. 1c).

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Fig. 1. A 9-year-old boy with avulsed upper left central and lateral incisors. a) Empty sockets with fracture of the alveolar bone in the region of 22; b) The teeth replanted and splinted with wire and composite; c) Condition after completion of treatment. In the event ankylosis of replanted tooth does occur, resorbtion of the root by osteoclasts takes some time by which the alveolar bone, instead of being resorbed, grows to a certain extent which can by favourable for future insertion of implants. Implantation

In cases of missing upper central incisor with diastema (Fig. 2a), insertion of an implant (Fig. 2b) is the only acceptable solution that can serve as a foundation for the construction of aesthetically acceptable ceramic crown (Fig. 2c). In cases of total teeth loss, six implants (Fig. 3a) can support a bridge of 12 crowns with a good function and pleasing aesthetic results (Fig. 3b).2

Fig. 2. Missing upper left central incisor in patient with diastema that is replaced by an implant and metal ceramic crown. a) Condition following removal of the tooth; b) Implant following Osseo integration; c) a crown constructed on the implant.


Fig. 3. Edentulous upper jaw that was restored with six implants and metal ceramic bridge. a) Condition after osseo integration. Cover screws removed, implants ready for an impression; b) Metal ceramic bridge constructed. Gums

A gummy smile is the expression for patients that while smiling show not only teeth but a great part of gums. In the event of vertical maxillary excess these are treated by LeFort I maxillary osteotomy with impaction. In cases with short crowns a gingivoplasty is performed providing a sufficient width of attached gingiva is present. Gingival recession that most frequently affects upper canines (Fig. 4a) and lower incisors is successfully treated using a two-layer sliding mucoperiosteal flap (Figs. 4b-d)3.

Fig. 4. Treatment of buccal gingival recession. a) Preoperative condition on the upper right canine with a flap outlined with ink; b) A two-layer mucoperiosteal flap raised with inner portion sutured into the defect; c) The outer portion placed over the inner and sutured; d) Condition 6 months postoperatively.

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Lips Benign and malignant lesions that involve lips require appropriate

surgical excision and immediate reconstruction. When small lesions are present the most important measure is to restore the vermilion-skin border. Malignant tumours of the lips necessitate both functional and aesthetic reconstruction. For defects that do not exceed two thirds of the lower lip, Karapandzic repair gives most satisfactory results (Fig. 6)4. Reconstruction of the entire lower lip is, as far as the aesthetics is concerned, most successfully performed using Webster modification of Fries flaps4 (Fig. 7). Reconstruction of skin defects following the excision of malignant tumours in the vicinity of the lip vermilion (Fig. 5a) requires meticulous planning otherwise the distortion of the vermilion is most likely. In such cases a triangular skin island sliding flap has proved to be reliable technique that gives satisfactory results (Fig. 5 bc).

Fig. 5. Recurrent basal cell carcinoma of the upper lip skin in the vicinity of the vermilion. a) Preoperative condition with triangular flap outlined with ink; b) skin island flap placed into the defect and sutured; c) Postoperative result with inconspicuous scar and no distortion of the vermilion.

The Face

Making incisions in the face is inevitable maneuver in routine oral and maxillofacial surgical practice. Every attempt should be made to place an incision in such a way that it leaves inconspicuous scar postoperatively. In trauma cases such as midface fractures a coronal approach offers wide surgical access and the scar that is placed in the hair. Lower blepharoplasty incision is used for approach to the orbital floor fractures5. A typical parotidectomy incision is replaced by face-lift incision that gives a sufficient surgical access for


safe removal of the gland with tumour and leaves almost invisible scar that is well hidden in the tragus, behind the earlobe and in the hair (Fig. 8). The most striking disfigurement of the face is the result of dentofacial deformities. This problem is dealt by orthognathic surgery which is the filed of maxillofacial surgery where astonishing improvement of facial appearance can be achieved without a single scar in the face6. In cases where both jaws are deformed or a single jaw exhibits pronounced deformity, so called bimaxillary orthognathic surgery is indicated to correct these and accomplish skeletal and dental harmony7,8,9 (Fig. 9). It has to be pointed out that this type of surgery is almost impossible without pre and postoperative orthodontic treatment that is aimed to correct dentoalveolar anomalies and achieve good and stable occlussion10,11. The most difficult cases within dentofacial deformities such as Hemifacial Microsomia (Fig. 10) and Hanhart's syndrome are treated with pericranial and osteopericranial flaps in addition to bimaxillary surgery12,13.

Fig. 6. A male patient with malignant tumour of the lower lip reconstructed with Karapandzic arterial flaps. a) Preoperative condition; b) Condition following the repair.

Fig. 7. A male patient with squamous cell carcinoma of the entire lower lip reconstructed with Webster repair. a) Preoperative condition with flaps outlined with ink; b) Postoperative result.

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Fig. 8. A female patient with benign parotid tumour. a) Preoperative finding; b) Face-lift incision applied, skin raised giving good surgical access to the gland; c) The facial nerve exposed following the removal of the tumour; d) Postoperative condition with well hidden scars.

Fig. 9. A patient with pronounced mandibular prognathism treated with bymaxillary surgery. a) Preoperative condition; b) Postoperative result.

Fig. 10. A male patient with Hemifacial Microsomia. a) Preoperative condition; b) Postoperative result achieved with bimaxillary orthognathic surgery and osteopericranial flap.



References

1. Stajčić Z. Dentoalveolar reconstructive surgery. Bilten oralnih hirurga Srbije, 1999 ; 10 – 13.

2. Stajcic Z. Metal endosseous implants - current concepts. Stom Glas S, 1993 ; 40 (Suppl. 1) : 72 - 73.

3. Stajčić Z, Čakić S, Stojčev Lj. Two-layer sliding mucoperiosteal flap for the treatmment of buccal gingival recession. Balk J Stom, 2000 ; 4 : 117 - 119.

4. McGregor IA, McGregor FM. Cancer of the face and mouth.Edinburgh London Melbourne New York, Churchill Livingstone, 1986, pp. 135 - 176.

5. Rončević R. Stajčić Z. Surgical treatment of posttraumatic enophthalmos: a study of 73 cases. Ann Plast Surg, 1994 ; 32 : 288-294.

6. Stajčić Z. Simultaneous movement of the maxilla and the mandible in the correction of severe mandibular prognathism. Stom Glas S, 1990 ; 37 : 41 - 48.

7. Stajčić Z, Rončević R. Facial nerve paralysis following combined maxillary and mandibular osteotomy. 1990 ; 18 : 192 - 194.

8. Juniper, R.P. Stajčić Z. Pterygoid plate separation using an ascillating saw in Le Fort I osteotomy. J Cranio Max-Fac Surg, 1991 ; 19 : 153 - 154.

9. Stajčić Z. Altering the angulation of a curved osteotome - does it have effects on the type of pterygomaxillary disjunction in Le Fort i osteotomy? Int J Oral Maxillofac Surg, 1991 ; 20 : 301 - 303.

10.Stajčić Z. Team approach in the treatment of dentofacial anomalies. Stom Glas S, 1993 ; 40 (Suppl. 1) : 56 - 57.

11.Vidović B., Stajčić Z. Orthodontic-surgical treatment of mandibular retrognathism associated with long face. Galenika-Dental, 2003 ; 2 : 7 - 9.

12.Rončević R, Stajčić Z. Correction of facial deformities with pericranial and osteopericranial flaps. Br J Plast Surg, 1994 ; 47 : 230-235.

13.Rončević R, Stajčić Z, Nikolić Z. Hanhart’s syndrome with facial asymmetry. A case report. Br J Plast Surg, 1995 ; 48 : 511-514.

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10 years of BaSS

CHRONIC OROFACIAL PAIN :DIAGNOSTIC AND THERAPEUTIC CHALLENGE

Clinic of Oral Surgery and Orofacial Pain Centre, Faculty of Stomatology,Beograd, Serbia and Montenegro

Ljubomir Todorović

Summary

Chronic orofacial pain is reviewed, especially from the aspect of common diagnostic and therapeutic dilemmas. Chronic orofacial pain is a more frequent phenomenon than usually regarded, as time rich with emotional tension greatly favours the specific release of endogenous conflicts, which may also be manifested by chronic orofacial pain, especially psychogenic orofacial pain.

In this article, characteristic modalities of neurogenic, somatic and psychogenic pain in the orofacial region are described, pointing to the main diagnostic criteria and therapeutic possibilities. The rationale for setting up and organizing pain clinics is stressed, as treatment by several specialists at the same place is more convenient, both to the patient and the practitioner, and gives a better chance for success than referral to other specialists, especially to psychiatric clinics. Key words: Pain, facial, chronic; Pain, neurogenic; Pain, somatic; Pain psychogenic Introduction

Orofacial pain is the most frequent reason patients seek dental attention. However, the precise diagnosis of orofacial pain is not always simple. In that respect, the greatest diagnostic (and therapeutic) problem presents chronic pain, especially when there is no obvious organic cause (for example, malignant disease).

Pain is an unpleasant emotional experience resulting from either physical or psychological trauma1. Painful experience includes not only a perception of sensations evoked by noxious stimuli, but also the reaction or response to such stimuli2. Unless the patient is supposed to be a conscious malingerer or layer, the painful experience is always unpleasant and always real1. The psychological component of this experience has always been accepted3 and psychological factors, such as previous experience, prejudice, emotional status etc, may significantly influence and intensify it or cause the persistence of pain even when the original tissue damage has disappeared4.

Pain of more than 6 months’ duration is considered to be chronic5. In contrast to acute pain, which serves a biologic purpose as either a protective mechanism or a warning signal, chronic pain does not serve any biologic purpose and appears to be permanent and intensified by psychological factors4. In fact, chronic pain may be considered as a product of complex interaction of biologic, i.e. organic and psychological factors, and of an acquired “illness

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behaviour” as well as some behavioural factors (bruxism habit, chronic muscle contraction) which significantly contribute to arising pain5.

Chronic orofacial pain may have many different clinical presentations. However, all these conditions (except cancer pain, which may have chronic presentation but does not have diagnostic or therapeutic dilemmas) can be grouped into three main pain categories4: neurogenic pain (caused by structural abnormalities within the neural components), somatic pain (caused by abnormalities in normal structures, but sometimes having referred pain characteristics) and psychogenic pain (caused primarily by disturbances in the psychogenic sphere, but also showing sometimes changes within the neural component). Neurogenic Pain

Neurogenic pain is estimated to be caused by a functional abnormality within the nervous system4. However, the exact etiopathogenetic mechanism of the most prominent representative of this chronic orofacial category - a paroxysmal (idiopathic) trigeminal neuralgia is still not precisely determined. Paroxysmal Trigeminal Neuralgia

Paroxysmal trigeminal neuralgia (PTN) is a precisely defined clinical entity, with a clinical picture that distinguishes it from other, more or less similar orofacial pain syndromes. Although known for centuries, PTN still produces controversies, beginning with terminological (idiopathic or primary trigeminal neuralgia, tic douloureux, etc) closing with therapeutic (a plethora of treatment modalities, no one guaranteeing permanent pain relief). Clinical presentation. PTN is characterized by lancinating pain, the most intensive pain ever experienced by humans6. Pain is most frequently described as a sudden, sharp, severe stabbing or lancinating, lasting relatively briefly (from a few seconds to a minute). It is of paroxysmal nature, repeating throughout the day (rarely at night). Pain is characteristically provoked by stimulation of one, more or less constant sensory region of the skin of the face or oral mucosa, so-called trigger-zone, which is one of the patognomonic symptoms. Trigger-mechanism is usually provoked by light touch, talking, chewing or swallowing. After provoking a trigger-mechanism, pain is elicited within a single division of the trigeminal nerve (most often maxillary or mandibular). Immediately after the attack, there is a short “refractory period” when it is impossible to provoke pain. The patient is usually pain-free between attacks, but sometimes a dull, constant pain may persist between attacks of sharp pain.


Periods of spontaneous remission of pain attacks are characteristic for the PTN. They can be brief (few months) or more protracted (till a year) - an especially confusing feature because coincidental treatment may be given the (undeserved) credit for bringing on what is in fact a spontaneous subsidence of pain7. However, the spontaneous remissions gradually get shorter, especially in untreated cases1. Spontaneous recovery has not been reported. Diagnostic criteria. As pain, a most prominent symptom of the PTN, demonstrates individual experience which is difficult to present objectively, the diagnosis of PTN is not always simple. It is primarily based on the detailed description of pain characteristics, as well as on the elimination of other possible causes of pain.

Classic criteria for making the diagnosis of PTN are8,9: (1) the intensive, brief pain of paroxysmal character, with complete remissions occurring between attacks; (2) the existence of a trigger-zone provokable by even a light sensory stimulation; (3) unilateral pain confined to the distribution of the affected nerve-division; (4) normal neurological findings at examination, without objective sensory or motor disturbances.

There are no laboratory tests or radiographic findings pointing to the PTN. Nevertheless, each patient with presumable diagnosis of PTN should be submitted to detailed clinical and radiographic examination, including the routine laboratory tests, in order to exclude other syndromes and diseases with similar clinical presentation. In diagnosing PTN, a positive response to local anaesthetic injection or the undertaken medication reinforces the clinical impression and confirms the diagnosis10. Specific changes of somatosensory evoked potentials in PTN patients are also observed11, but it is not clear whether these results may be used with certainty in differential diagnosing of the PTN12.

The PTN may be confused with three main types of syndromes9: (1) paroxysmal (idiopathic) neuralgia involving other nerves; (2) symptomatic neuralgia; and (3) facial pain other than paroxysmal neuralgia.

Idiopathic neuralgia may affect, although only occasionally, other nerves than trigeminal - the glossopharyngeal and the superior laryngeal nerves. Many pain characteristics are similar to the PTN, but pain appears in tonsils and the root of the tongue, referring to the ear and the throat. It is usually provoked by swallowing or speaking13. The diagnosis of glossopharyngeal neuralgia may be established by simple local anaesthetic spraying of the throat: a relief of pain indicate the glossopharyngeal neuralgia9.

Symptomatic (secondary) trigeminal neuralgias are caused by both peripheral and central lesions of the trigeminal nerve. Intracranial causes of secondary neuralgias may be the posterior and the middle cranial fossa lesions, and extracranial causes comprise compression or entrapment of peripheral trigeminal branches14. In the very beginning of the disease, symptoms may imitate PTN, but gradually pain becomes more constant, usually accompanied

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by signs of affection of other nerves (neurological, sensory or motor dis-turbances). Detailed oral, otorhinolaryngological, neurological and radiographic examinations, as a rule, reveal the cause of pain (in contrast to the PTN).

Chronic orofacial pain other than idiopathic neuralgia may sometimes mimic true PTN pain. This is especially the case with vascular and psychogenic pains. However, pain in these conditions is more constant, localized on the wider region and, especially with psychogenic pain, not confined precisely to the certain nerve division. Nevertheless, sometimes a great clinical experience is needed to differentiate these syndromes from PTN solely on the basis of clinical characteristics of pain. Treatment. Due to unknown aetiology and pathogenesis of the PTN, there is no uniform mode of treatment. Several drugs and procedures were proposed in due course, but only some of them maintained judgement of time.

Generally speaking, treatment of PTN can be medical or surgical. Numerous surgical procedures, which can be didactically grouped into intracranial and extracranial ones, are reserved for patients who do not respond to medication10, or cannot use it for other reasons (for example, allergy).

Medical treatment in many treatment protocols takes the first line15

owing to the discovery of Blom16 that the antiepileptic drug carbamazepine (TegretolR, MazepineR), can provide pain relief in PTN patients. Although there is other anticonvulsant medication useful in the treatment of PTN, car-bamazepine is still the sovereign remedy for that purpose, effective in 60-90% of the treated patients8,16-19. Moreover, this drug is so specific in abolishing PTN pain that can be used even for diagnostic purpose20. The therapeutic dose of the drug gradually rises from 200-400 mg daily to the maximal 1200 mg daily dose owing to the attained effect. Unfortunately, in 25-50% of the patients, after several years of successful treatment, carbamazepine becomes ineffective21.

An analysis of results of the carbamazepine treatment of PTN, performed at the Clinic of Oral Surgery, Faculty of Stomatology in Belgrade22, however, showed slightly poorer effect of this medication than is usually presented (Tab. 1). The positive effect of the treatment, in this series, was noticed in only 11 of 19 patients (58%), with pain relief of 12 months maximum. At the same time, side-effects were noticed in 7 patients, although not of a serious character (dizziness, drowsiness and sluggishness).

Peripheral nerve blocks (blockades) are, usually, the next step in the PTN treatment. This term comprises the injection of some neurolytic substances in the vicinity of the affected peripheral nerve for the purpose of relieving pain. The injection technique is the same as for the anaesthetic blocks performed routinely for achieving local anaesthesia, only with the substances other than local anaesthetics.


Table 1. Clinical Data of Patients with PTN and Results of Carbamazepine Treatment

Patient TheAffected Nerve*

Duration of PTN

Initial Dose**

Painless Period

Side- effects

1. V3 3 months 0.6 3months yes 2. V3 4 weeks 0.6 4months # 3. V2/3 5 years 0.6 5days 4. V3 1 month 0.6 12 months 5. V2 2 years 0.6 0 # 6. V3 7 years 0.6 0 yes 7. V2 l month 0.6 0 yes 8. V2 8 years 1.2 6 weeks 9. V3 l month 0.6 0 yes 10. V3 4 years 0.6 1 month yes 11. V3 4 years 1.2 1 month 12. V3 3 months 0.6 0 yes 13. V3 2 years 0.6 0 # 14. V2 2 years 0.6 6 months/still 15. V2/3 3 years 1.2 0 16. V2/3 3 months 1.2 0 yes 17. V3 1 month 0.6 3 months yes/# 18. V3 2 years 0.6 9 months/still 19. V3 1 week 0.6 3 months/still

* - V2 – Maxillary Nerve; V3 – Mandibular Nerve ** - g/daily # - refuses therapy The use of solely local anaesthetics for the same purpose (peripheral

nerve block) is least effective, producing pain relief in PTN only sporadically and in the beginning of the condition8,15. Controlled, double blind study of the effect of peripheral nerve blocks with local anaesthetic (lidocaine) and the solution of streptomycin in lidocaine in the treatment of PTN, performed in two separate institutions (Yugoslavia and UK)23, however, showed that local anaesthetic may be efficient in some patients, with a pain relief period of more than 30 months (Tab. 2). Nevertheless, local anaesthetics are used primarily for diagnosing PTN, as test-blocks performed at the first visit. If the pain relief is achieved even after the relapse of local anaesthesia, our policy is not to undertake any other procedure till the recurrence of pain. So, in these cases, peripheral nerve blocks with local anaesthetics may be regarded as a therapeutic procedure.

Ethyl-alcohol (95%) is most frequently used for peripheral nerve blocks. Alcohol causes neurolysis when contacting peripheral nerve8, producing anaesthesia of the region innervated by the treated nerve division, which is an unpleasant consequence of the alcohol blockade.

Lj. Todorović

Table 2. Treatment Results of Peripheral Streptomycin/Lidocaine versus Lidocaine Alone Injections in the Treatment of PTN

* - L - Lidocaine Alone; S/L - Solution of Streptomycin in Lidocaine ** - V2 – Maxillary Nerve; V3 – Mandibular Nerve

In addition, pain recurs after 6 to 24 months8, and subsequent blocks

are more difficult to perform and less effective due to the fibrous tissue formed after previous injection8. This is the reason some authors do not recommend peripheral alcohol blocks as a treatment modality for PTN patients10.

It seems that anhydrous organic alcohol glycerol is a better alternative to ethyl-alcohol for peripheral nerve blocks in PTN. Due to its hygroscopic properties, it diffuses through perineurium, absorbing water and subsequently damaging nerve axons24. It is shown that glycerol has a satisfactory effect on pain relief in PTN when applied peripherally in the vicinity of the affected nerve25. A preliminary study, conducted at the Clinic of Oral Surgery in Belgrade22, showed pain relief from 6 to 24 months in 70% of patients with PTN treated with peripheral glycerol nerve blocks (Tab. 2). It is suggested that glycerol should be injected 20-30 minutes after local anaesthetic, as not to be unnecessarily diluted22.

An attempt to use the solution of streptomycin in lidocaine for peripheral nerve block in PTN patients deserves attention, preliminary results of the procedure being firstly reported in 198626. The procedure comprised 5 peripheral nerve blocks, the time between each injection varying from 3-7 days

Patient Blockade* Treated Nerve**

Painless Period

Recurrence

1. L V3 0 2. S/L V2 5 months yes 3. L V3 17 months no 4. S/L V2 3 weeks yes 5. L V2 26 months no 6. L V2 0 7. S/L V2 2 weeks yes 8. S/L V3 30months no 9. L V3 0 10. S/L V3 3 months yes Ii. S/L V2 6 months yes 12. S/L V3 0 13. S/L V3 14 months no 14. L V2 0 15. L V2 8 months yes 16. S/L V3 6 months no 17. L V2 0


according to the intensity and frequency of pain attacks. Even this preliminary study showed very encouraging results, the double blind, controlled one demonstrated a slightly less favourable, but still beneficial effect23.

Open surgery on peripheral nerves, so-called peripheral neurectomy, has long been advocated for the treatment of PTN8. By surgical avulsion of a certain segment of the affected peripheral nerve, a relatively long period of pain relief is achieved. The major disadvantage of peripheral neurectomy is that total anaesthesia of the corresponding region results, while pain relief is only temporary. Repeating the procedure is much more difficult because of the presence of fibrous scar tissue, and should be performed at the other site. These are the reasons peripheral neurectomy is not widely used10.

Cryosurgical techniques, based on the freezing effect of liquid nitrogen probes at the surgically exposed nerve, have been used for the treatment of PTN for approximately two decades27,28. Cryoanalgesia can be achieved even without surgical exposure of the affected nerves. The advantages of cryotherapy are relatively fast recovery of sensation (approximately after 3 months), relatively long remissions, the possibility of performing on an out-patient basis and the absence of major complications.

Intracranial percutaneous or open surgery is usually left for resistant cases of PTN, when other procedures fail. It comprises blockade of the gasserian ganglion, percutaneous retrogasserian coagulation or major surgery on the sensory root of the trigeminal nerve. The injection of glycerol into the trigeminal cistern30 has increasingly gained followers10. Pain relief is comparatively long (even more than 6 years) and recurrence is quite low (l2-31%)30-32. Percutaneous retrogasserian radio frequent rhizotomy selectively destroys preganglionic trigeminal nerve fibres, through small electrode, by thermo-coagulation of trigeminal rootlets33, giving favourable effect but comparatively frequent recurrence. Major intracranial surgery is out of the scope of oral and maxillofacial surgery.

In conclusion, it should be stressed that an ideal procedure in the PTN treatment does not exist. The treatment plan is, therefore, individual, adapted to every single patient, as well as to the possibilities and experience of the therapist. Even if there are some differences in treatment protocols between institutions treating PTN patients, general trend is directed to less invasive procedures, primarily medical therapy, and open surgery being left for resistant cases and in late stages of the condition. At the Orofacial Pain Centre at the Faculty of Stomatology in Belgrade, priority is given to less invasive procedures in the treatment of PTN, such as medical treatment and peripheral nerve blockades with glycerol or the solution of streptomycin in lidocaine. The results of these types of treatment are quite satisfactory23,25,26, which justifies the recommendation of using such procedures as a first step in the treatment of PTN patients.

Lj. Todorović

Somatic Pain

Somatic pain may be divided into superficial and deep somatic pain4. Superficial somatic pain has a bright quality of stimulating nature and is involved in acute pain; deep somatic pain, on the other hand, has a dull, deep, depressing quality, and is often involved in chronic orofacial pain.

Musculoskeletal pain falls into the category of deep somatic pain; in the orofacial region, this pain category refers to temporomandibular joint and masticatory muscle problems, usually coexisting and overlapping with signs and symptoms. This is the reason why the term facial arthromyalgia, proposed by Harris34, seems to be the most appropriate for the chronic pain syndrome otherwise variably called the temporomandibular joint dysfunction syndrome, myofascial pain dysfunction syndrome or, at the beginning, Costen’s syndrome. However, in quite a number of patients, temporomandibular joint dysfunction can be distinguished from myofascial pain dysfunction. In the rest of unclear cases it is crucial to recognize and identify the basic and primary cause of discomfort as the treatment may significantly vary, from solely to combined medical, dental and surgical. Temporomandibular Joint Pain

Temporomandibular joint pain arises due to the “internal derangement”, defined as an abnormal relationship of the articular disc (meniscus) to the mandibular condyle, glenoid fossa and articular eminence35. The first sign of the internal derangement is a painless joint sound (click), which occurs on movement of the joint, indicating a subluxation of the posterior band of the meniscus. The click remains painless as long as the main insertions of the meniscus into the mandibular condyle poles are not threatened36. A painful click arises when the main insertions begin to fail and the whole meniscus begins to luxate. This is possible only if there is a stretching or tearing of the insertions of the meniscus into the condylar poles, and this is accompanied by pain and tenderness to palpation over the lateral pole - a usual clinical finding36.

Arthralgia is characterized by continuous, localized joint pain that increases with jaw function. The maximum jaw opening motion is sometimes limited or deviated to the affected side. The joint is usually tender on palpation. The condition is termed also as capsulitis and synovitis37. Localized arthralgia/arthritis can be caused by external trauma to the joint or by repetitive malfunction of the jaw (fingernail biting, bruxism, and clenching teeth)36,38. Due to subluxation, meniscus no longer separates the condyle from its fossa to the same degree as in its correct anatomical position and a malocclusion may result36. On the other hand, occlusion may affect the joint indirectly, by altering muscle activity, and directly. However, many studies suggest there is no demonstrable relationship between the occlusion and


temporomandibular joint pain39. Finally, as the direct relationship between emotional factors, inducing the increased muscle activity, and temporomandibular joint dysfunction has been demonstrated40, a hypothesis is developed, connecting emotional status, muscle activity and joint dysfunction, although correlations between these factors have not been clearly established39.

Due to different possible etiological factors, it is am parent that, consequently, the treatment also can be directed to various presumable sources. There are several treatment modalities, from simple reassurance and occlusal correction (necessary to allow bilateral mastication), to joint surgery comprising arthrocentesis, meniscoplasty or menisectomy41,42. The usual policy is a conservative approach - to try with the least invasive procedures (occlusal correction, making bite-guard appliances, physiotherapy, psychotropic medication), leaving surgery for those cases where conservative treatments have failed42. Muscular (Myofascial) Pain

Masticatory muscle myalgia can occur as a result of direct muscle tissue trauma, forceful jaw-closing habits (bruxism) or prolonged protective muscle activity secondary to regional pain43. Typical characteristics of myofascial pain are dull, aching, continuous pain increasing with function, with local palpable tender bands in the muscle and trigger points within these bands44. Trigger points are tender to palpation and exogenous factors such as tension, trauma or weather changes, which may increase pain from mild to ago-nizing4. In early stages, the pain may be more localized, but with chronicity, the trigger point can refer pain to more distant sites45.

The mechanism for these chronic muscle pain phenomena is not clear, but speculations include theories involving localized hypoxia, central sensitization and neurogenically induced pain-peptide secretion at the tender sites”3.

Specific myofascial trigger point therapies include stretch and (cold) spray, post-isometric relaxation, injection of trigger points, massage applied to the taut bands and trigger points and physiotherapy (ultrasound, electrical stimulation)”. However, the success of the treatment depends on the precise differential diagnosis to the temporomandibular joint pain and psychogenic pain syndromes. Psychogenic Pain

Chronic orofacial pain of psychogenic nature is a much more frequent phenomenon than is usually regarded47. The time rich with emotional tension greatly favours the specific release of endogenous conflicts, which may be manifested by chronic orofacial pain as well. According to some reports48, 2-5%

Lj. Todorović

of patients with chronic orofacial pain have no demonstrable organic disease, or have an exaggerated response to minimal pathology.

Psychogenic pain, like any psychosomatic disturbance, can arise in three ways34, each manifesting differing degrees of severity and chronicity: (1) as a manifestation of stress in an otherwise fit and stable person; (2) as a symptom of psychiatric illness; or (3) as a feature of an unchanging hypochondriacally personality trait. It is important to recognize that this pain is real, arisen initially in dilated blood vessels34. It is supposed that there is a disturbance of the central descending pain inhibitory system that normally filters chronic peripheral discomfort in these patients49. Psychogenic pain is characteristically constant and nagging, of aching and burning nature, located deep into tissues and difficult to describe50. It is not well localized and crosses over normal neurological boundaries. The typical patient is, according to Miller51, a middle aged female, edentulous, haggard and importunate. As there is no oral or dental abnormality which can be associated to the apparent symptoms, the term “atypical facial pain” is frequently used, although it is not officially recommended52. However, the term “atypical” seems to be more convenient than the term “psychogenic” in routine communication, especially with a patient, because it does not suggest that the pain is imagined - a fact which could cause the patient to become upset.

Psychogenic orofacial pain can be manifested differently, the most interesting (and characteristic) presentation being atypical odontalgia49,53,54. This condition is characterized by continuous or throbbing pain localized in a single tooth (or several teeth in the region), otherwise indistinguishable from that of an acute pulpitis or periodontitis. Affected teeth are extremely sensitive to pressure or thermal stimuli. Some cases appear to have been precipitated by a dental procedure, such as the fitting of a bridge or an extraction3. The main feature of the condition is the lack of any detectable sign of dental pathology, although the detailed anamnesis can reveal previous attempts to “treat” the condition by unnecessary dental procedures (pulpectomies, root fillings, apicoectomies, extractions, etc.)”’.Although symptoms may vary, a carefully taken history usually reveals some emotional problems or recurrent migrainous attacks. This is the reason the condition is assumed to be a state of hyperalgesia of pulpal/periodontal pain receptors, suggesting a vascular disturbance.

To arrive at an accurate diagnosis of psychogenic pain, the first and most important step is to take a complete history and to obtain relevant information, such as: chief complaint(s), location of pain and its characteristics (quality, intensity, temporal behaviour, provoking, aggravating or relieving factors), chronology of complaints and personal and past medical history4. Objective signs of any kind of oral pathology usually lack. However, investigations of tooth pulp evoked potentials (TPEP) have revealed some indicative, although discrete, changes in patients with psychogenic pain55. These changes are seen in a shorter latency of the first negative wave on the side with pain compared to the opposite side or to control patients. Also, the


second negative wave has a prolonged latency on the side with pain, with a plateau instead of an amplitude peak (Fig. 1). Changes of TPEP in psychogenic pain patients indicate the existence of slower impulse transmission and the reduction of cognitive inhibitory pain control at both synaptic junctions (at pons and thalamus).

Fig. 1. Typical TPEP in: (a) Healthy individual: N1 - the first negative wave showing the first synaptic junction; P1 -the first positive wave showing impulse transmission in lemniscus medialis; N2/P2 - the second negative and the second positive waves showing impulse transmission at the thalamo-cortical level; (b) A patient with atypical facial pain: on the side with pain the changed N2 wave, with plateau phenomenon

Treatment of psychogenic orofacial pain is not simple, especially if one persistently tries to find out an organic cause of present pain. The patient usually undergoes unnecessary dental or surgical treatment without any improvement (it even gets worse), and pain moves from one tooth or place to another. The patient should be subjected to essential dental care only, with additional explanation that the actual pain is a migraine-like pain in the teeth and surrounding tissues due to dilated blood vessels or hyperactive muscles, provoked by emotional pressure and stress. Finally, it was shown that tricyclic antidepressants improve symptoms in patients with psychogenic pain, as well as with facial arthromyalgia56. It seems that they are successful even in the absence of depression. The explanation of antidepressants’ efficacy probably lies in the fact that they increase the serotonin, noradrenaline and dopamine concentrations in synapses, preventing their re-uptake57. Tricyclic antidepressants are effective in the vast majority of psychogenic pain patients49;however, the improvement can not be demonstrated immediately, but a few months after the beginning of the therapy.

Lj. Todorović

Possible Conclusions

Many patients experiencing or anticipating chronic orofacial pain seek oral and dental treatment. In addition, an orofacial region is one of the most complex of all regional areas in terms of identification of pain48, having an extremely complex cranial and cervical innervation and an intricate vascular supply. There are many other pain modalities and types apart from those mentioned in this review (for example, different vascular pains, post-traumatic and secondary neuralgias, etc.). It is obvious that precise diagnosing of all types of chronic orofacial pain requires a lot of experience and undertaking of the most promising procedures only after careful evaluation of all available data.

Whenever a patient presents for evaluation chronic orofacial pain, it is essential: (1) to take a detailed and complete history; (2) to perform a detailed clinical examination of the orofacial region; (3) not to have prejudice that the patient necessarily has an organic condition provoking pain; (4) to have thorough insight into all possible causes of orofacial pain, i.e. organic, functional and psychogenic; and (5) to have no hesitation in referring a patient for further evaluation if there is no obvious cause of pain found instead of performing unnecessary (usually irreversible) dental procedures.

Having in mind the fact that chronic orofacial pain presents a diagnostic and therapeutic challenge to health practitioners, it should be dealt with by clinicians of different specialities, and it seems that the multidisciplinary concept in treating orofacial pain patients is the best approach. The basic rationale of setting up and organizing specialized pain clinics is the necessity of treating pain patients by several specialists at the same time and place. Only joint management of chronic orofacial pain patients provides an overall insight into pain cause itself and the necessary diagnostic and treatment procedures.


References 1. Harris M. Facial Pain. In: Rowe AHR, Alexander AG, Johns RB (eds): A Companion to Dental Studies, vol. 3 - Clinical Dentistry. Oxford-London-Edinburgh-Boston-Palo Alto-Melbourne: Blackwell Scientific Publications, 1986, pp 44-53. 2. Dubner R. Neurophysiology of Pain. Dent Clin North Am, 1978; 23:11-30. 3. Harris M. Psychogenic aspects of facial pain. Br Dent J, 1974; 136:199-202. 4. Pertes RA, Heir GM. Chronic Orofacial Pain. A Practical Approach to Differential Diagnosis. Dent Clin North Am, 1991; 35:123-140. 5. Harness DM, Rome HP. Psychological and Behavioral Aspects of Chronic Facial Pain. Otolaryngol Clin North Am, 1989; 2:1073-1094. 6. Merskey H. Pain terms. A list of definitions and notes on usage. Pain, 1979; 6:249-252. 7. Sweet WH. Trigeminal Neuralgia. In: Foley KM, Payne RM (eds): Current Therapy of Pain. Toronto-Philadelphia: BC Decker Inc, 1989, pp 116-125. 8. Bayer DB, Stenger TG. Trigeminal Neuralgia. An overview. Oral Surg, 1979; 48:393-399. 9. Walker AE. The Differential Diagnosis of Trigeminal Neuralgia. In: Hassler R, Walker AE (eds): Trigeminal Neuralgia: Pathogenesis and Pathophysiology. Stuttgart: Georg Thieme Verlag, 1970, pp 30-34. 10. Donlon WC, Jacobson AL, Truta MP. Neuralgias. Otolaryngol Clin North Am, 1989; 22(6):1145-1l58. 11. Leandri M, Parodi CI, Favale E. Early trigeminal evoked potentials in tumours of the base of the skull and trigeminal neuralgia. Electroenceph Clin Neurophysiol, 1988; 71:114-124. 12. Ceni� D, Todorovi� Lj. The Differential Diagnosis of Pain Syndromes in Orofacial Region Using Tooth Pulp Evoked Potentials. Stom Glas S, 1993: 40(Supp. 1):s124 (in Serb) 13. Orton CI. Glossopharyngeal Neuralgia: Its Diagnosis and Treatment. Br J Oral Surg, 1972; 9:228-232. 14. Harris M. Orofacial Neuropathology. In: Moore JR (ed): Surgery of the Mouth and Jaws. Oxford-London-Edinburgh-Boston-Palo Alto-Melbourne: Blackwell Scientific Publications, 1985, pp 806-809. 15. Heyck H. Headache and Facial Pain: Differential Diagnosis, Pathogenesis, Treatment. Stuttgart-New York: Georg Thieme Verlag, 1981, pp 138-181. 16. Blom S. Trigeminal neuralgia: its treatment with a new anticonvulsant drug (G-32883). Lancet, 1962; 1:839-840. 17. Lipton S. Relief of pain in clinical practice. Oxford-London-Edinburgh-Melbourne: Blackwell Scientific Publications, 1979, pp 66-90. 18. Braunhofer J, Jesch W. Klinische Erfahrungen mit einem neuen Dibenzoazepinderivat (G 32883) in der Behandlung der Trigeminusneuralgie. Med Welt, 1964/1; 4:200-203. 19. Carnaille H, De Coster J, Tyberghein J, Dereymaeker A. Etude statistique de pres de 700 cas de facialgies traitees par le Tegretol. Acta Neurol Belg, 1966; 66:175-196. 20. Sweet WH. The treatment of trigeminal neuralgia (tic douloureux). N Engl J Med, 1986; 315:174-177. 21. Dalessio DJ. Medical treatment of trigeminal neuralgia. Clin Neurosurg, 1977; 24:579-583. 22. Staj�i� Z, Todorovi� Lj. Idiopathic Trigeminal Neuralgia: The Most Severe Pain in the Face. Stom Glas S, 1984; 41:71-80 (in Serb) 23. Stajcic Z, Juniper RP, Todorovic L. Peripheral Streptomycin/Lidocaine Injections versus Lidocaine Alone in the Treatment of Idiopathic Trigeminal Neuralgia: A double blind controlled trial. J Cranio-Max-Fac Surg, 1990; 18:243-246.

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24. Rengachary SS, Watanabe IS, Singer P, Bopp WJ. Effect of glycerol on peripheral nerve: an experimental study. Neurosurgery, 1983; 13:681-688. 25. Stajcic Z. Peripheral glycerol injections in the treatment of idiopathic trigeminal neuralgia: A preliminary study. Int J Oral Maxillofac Surg, 1989; 18:255-257. 26. Sokolovic M, Todorovic L, Stajcic Z, Petrovic V. Peripheral streptomycin/lidocaine injections in the treatment of idiopathic trigeminal neuralgia. J Max-Fac Surg, 1986; 14:8-9. 27. Barnard DJW, Lloyd JW, Glynn CJ. Cryosurgery in the management of intractable facial pain. Br J Oral Surg, 1978; 16:135-142. 28. Zakrzewska JM, Nally FF, Flint SR. Cryotherapy in the management of paroxysmal trigeminal neuralgia: Four year follow-up of 39 patients. J Max-Fac Surg, 1986; 14:5-7. 29. Juniper RP. Trigeminal neuralgia - treatment of the third division by radiologically controlled cryoblockade of the inferior dental nerve at the mandibular lingula. A study of 31 cases. Br J Oral Maxillofac Surg, 1991; 29:154-158. 30. Hakanson S. Trigeminal neuralgia treated by the injection of glycerol into the trigeminal cistern. Neurosurgery, 1981; 9:638-646. 31. Waltz TA, Dalessio DJ, Ott KH, Copeland B, Abbott G. Trigeminal cistern glycerol injections for facial pain. Headache, 1985; 25:354-357. 32. Dieckmann G, Veras G, Sogabe K. Retrogasserian glycerol injection or percutaneous stimulation in the treatment of typical and atypical trigeminal pain. Neurological Research, 1987; 9:48-49. 33. Sweet WH, Wepsic JG. Controlled thermocoagulation of trigeminal ganglion and rootlets for differential destruction of pain fibers. Part 1. Trigeminal neuralgia. J Neurosurg, 1974; 40:143-156. 34. Harris M. Medical Versus Surgical Management of Temporomandibular Joint Pain and Dysfunction. Br J Oral Maxillofac Surg, 1987; 25:113-120. 35. Dolwick MF. Diagnosis and Etiology. In: Helms CA, Katzberg RW, Dolwick MF (eds): Internal Derangements of the Temporomandibular Joint. San Francisco: University of California Press, 1983, p 31. 36. Juniper RP. The Pathogenesis and Investigation of TMJ Dysfunction. Br J Oral Maxillofac Surg, 1987; 25:105-112. 37. Solberg WK. Temporomandibular disorders: management of problems associated with inflammation, chronic hypomobility and deformity. Br Dent J, 1986; 160:421-428. 38. Okeson JP. Fundamentals of Occlusion and Temporomandibular Disorders. St Louis: The CV Mosby Company, 1985. 39. Rothwell PS. The Temporomandibular Joint Pain/Dysfunction Syndrome. In: Moore JR (ed): Surgery of the Mouth and Jaws. Oxford-London-Edinburgh-Boston-Palo Alto-Melbourne: Blackwell Scientific Publications, 1985, pp 588-599. 40. Fine EW. Psychological factors associated with non-organic temporomandibular joint pain dysfunction syndrome. Br Dent J, 1971; 131:402-407. 41. Dimitroulis G, Dolwick MF, Martinez A. Temporomandibular Joint Arthrocentesis and Lavage for the Treatment of Closed Lock: A Follow-up Study. Br J Oral Maxiilofac Surg, 1995; 33:23-27. 42. Leopard PJ. Surgery of the Non-Ankylosed Teniporornandibular Joint. Br J Oral Maxillofac Surg, 1987; 25:138-148. 43. Clark GT, Takeuchi H. Temporomandibular Dysfunction, Chronic Orofacial Pain and Oral Motor Disorders in the 21st Century. CDA Journal, 1995; 23(4):4l-50. 44. Solberg WK. Temporomandibular disorders: Physical tests in diagnosis. Br Dent J, 1986; 160:273-277.


45. Travel JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore: Williams and Wilkins, 1983. 46. Simons DG. Myofascial Pain Syndromes. In: Foley KM, Payne RM (eds): Current Therapy of Pain. Toronto-Philadelphia: BC Decker Inc, 1989, pp 251-266. 47. Todorovi� Lj, Ceni� D, Poti� J. Chronic Orofacial Pain of Psychogenic Nature - An Increasing Reality. Stom Glas S, 1995; 42:135-141. (in Serb) 48. Gerschman J, Burrows G, Reade P. Chronic Orofacial Pain. Advances in Pain Research and Therapy, 1979; 3:317-323. 49. Harris M. Psychogenic facial pain. Int J Oral Surg, 1981; 10(Suppl. 1):183-186. 50. Drinnan AJ. Differential Diagnosis of Orofacial Pain. Dent Clin North Am, 1987; 31(4):627-643. 51. Miller H. Pain in the face. Br Med J, 1986; 2:577-580. 52. Merskey H (ed). Classification of chronic pain, descriptions of chronic pain syndromes and definitions of pain terms. IASP Subcommittee on Taxonomy. Pain, 1986; 3(Suppl.):3-9. 53. Rees RT, Harris M. Atypical odontalgia. Br J Oral Surg. 1978-79; 16:212-218. 54. Reik L. Atypical odontalgia: A localized form of atypical facial pain. Headache, 1984; 24:222-224. 55. Todorovi� Lj, Ceni� D. The Use of Tooth Pulp Evoked Potentials in the Diagnosis of Atypical Facial Pain and Evaluation of Results of Treatment. Stom Glas S, 1992; 39:215-219. (in Serb) 56. Feinmann C, Harris M. Psychogenic facial pain. Part 2: Management and prognosis. Br Dent J, 1984; 156:205-208. 57. Feinmann C. Pain Relief by Antidepressants: Possible Modes of Action. Pain, 1985; 23:1-8.


10 years of BaSS

TREATMENT OF GINGIVAL RECESSION WITH BILAMINAR TECHNIQUESTHE CORONALLY POSITIONED FLAP WITH CONNECTIVE TISSUE GRAFT

Department of Periodontology, School of Dentistry, University of Bologna, Via S.Vitale 59 Bologna, Italy.

Luigi ChecchiMarco MontevecchiMonica MeleGiovanni Zucchelli

Summary Periodotal mucogingival techniques continually evolve and many are the surgical approaches currently described for the treatment of the gingival recession. Aim of the present paper is to outline the indication for the coronally positioned flap with connective tissue graft and describe the surgical technique. Key words: coronally positioned flap, connective tissue graft, gingival recession, root coverage Introduction: The gingival margin is clinically recognized by a festooned line which follows, in state of health, the pattern of the cemento-enamel junction (CEJ) at a distance of 1-2 mm. In state of health it exists a great individual variability in the more or less festooned pattern of the gingival margin that is genetically determined as the teeth shape. Two typologies of teeth are known: the square one and the cylindrical one. To square teeth (mesio-distal dimension like the apico-coronal one) it corresponds a flat pattern of the gingival margin, since flat it is the CEJ. To cylindrical teeth (mesio-distal dimension smaller than the apico-coronal one) it corresponds a festooned pattern of the margin, proportional to the festooned pattern of the CEJ. A very frequent parodontal pathology is the gingival recession. In a study by Kassab and Choen it has been pointed out that 88% of patients being older than 65 have at least one recession and that its extension and number increase with the age. It consists on a shift in an apical direction of the gingival margin and on the exposition of a more or less wide part of the root surface. This disharmony may be apparent in the patient’s smile or even at a functional level (phonics, chewing). Often the root exposure due to gingival recession may cause dentine hypersensitivity and consequently patient discomfort and/or inadequate oral hygiene. The irregular outline of the gingival margin, even in the absence of tooth hypersensitivity, may render plaque control more difficult for the patient, even more when gingival recession is triangular sharped with acute angles (the so-called “Stillman cleft”).

L.Checchi et al

Etiology The loss of the soft tissues is well represented either in populations having an high standard of oral hygiene2-3-4-5-6-7 or in those having values of low plaque indexes8-9-10. In particular when the plaque indexes are low the recession is often present on the buccal area associated with abrasion of the enamel and the exposed root surface3-4-5-10. Several studies done on populations with a different level of oral hygiene at first suggested the division of the recessions into two main groups, one related to mechanical elements and another one associated with the periodontal disease7-11-12. Today the causes determining the gingival recession are divided into:

� Traumatic � Bacterial � Mixed � Viral

The traumatic recessions are the more frequent and can be dued to many causes: brushing, thread trauma, orthodontic trauma, prosthetic trauma, occlusal trauma. The causes associated with the brushing are various: very hard and not rounded bristles, incorrect use, unsuitable movement for the periodontal morfo-type of the patient, favourish the abrasion of the dental surface and the ulceration of the gingival one. Some authors think that an incorrect brushing is the most frequently cause associated with the gingival recession outbreak. The traumatic injuries progress from the outer to the inner part in centripetal direction, involving at first the oral epithelium, than the connective and finally the junction epithelium. The pathogenic mechanism is represented by an ulceration (reversible phase) that deepen until it reaches its entire thickness (irreversible phase). This kind of recession is often associated with tooth abrasions on buccal areas2-13-14. The bacterial recessions are noticed when there is not a loss of inter-proximal attachment. On the contrary the recession is not a “pure” injuries, but a clinical mark of the periodontal disease. The bacterial plaque determines a heavy damage and the clinical marks are those of the tissue inflammation. The plaque enters in the furrow and triggers an inflammatory reaction, which involves at first the junction epithelium, then the connective and finally the oral epithelium. The ulceration is centrifugal from the inner to the outer part. The reduction of the space before occupied by the connective, determines a reduction of the vascularization, with a consequent ischemic involution of the epithelium. It causes a gingival collapse and so the


beginning of the gingival recession. It has to be noted how the pathogenic mechanism of the bacterial recessions is opposite to that of the traumatic recessions. Mixed recession (with a combined et etiology). It is frequent the clinical remark of a recession determined at first by a brushing trauma and then colonized by the bacterial plaque. In a pure injury caused by brushing the gingival margin in tonic, instead when it also shows an inflammatory suffering of the gingival margin, then it means that the bacterial plaque contributed to increase such an injury. The gingival recession induced by virus is an injury difficult to diagnose because it is often confused with the abrasive one caused by brushing. They are caused by herpetic viruses, they are rare and are characterized by having a semilunar disposition, they are shown as ulcerations of the epithelium with the connective exposition. The differential diagnosis is made easier by the painful symptomatology of the injury, the vesicular appearance, multiple and also cutaneous localizations. Classification of the recession The classification of the recessions have the goal to include the defect in a category, that gives a specific indication in the formulation of the prognosis, on the possibility of a root coverage in the phase of the surgical therapy. The classification by Sullivan and Atkins in 196815 is tied up by therapeutic methods of the period in which it has been conceived (free gingival grafts): Narrow and not too deep recessions: they do not usually need the therapeutic intervention. If the surgical procedure of root coverage is used, the wide vascularization of apical mesial and distal origin allows to expect a favourable prognosis. Narrow and deep recessions: the revascularization of any grafts coming from mesial or distal. Wide not too deep recessions: the vascularization coming mainly from apical allows to maintain grafts of a width not larger than 2 mm. Wide and deep recessions: the loss of the tissue has gone beyond the mucogingival line. It can be surgically recovered a height not larger than 1-2 mm. Nowadays it is used as reference Miller’s classification of 198516, based on the root coverage prognosis. The possibility to bring back the gingival margin to the CEJ depends, according to such a classification, on the integrity of the periodontal interdental support; if there is not the loss of junction ad of mesial and distal support; if there is not the loss of junction and of mesial and distal support, the recession may be completely recovered: the prognosis is optimal and there is an aesthetic recovery.

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ClassI marginal tissue recession which does not extend to the mucogingival junction. There is no periodontal loss (bone or soft tissue) in the interdental area, and 100% root coverage can be anticipated, Class II marginal tissue recession which extends to or beyond the mucogingival junction. There is no periodontal loss (bone or soft tissue) in the interdental area, and 100% root coverage can be anticipated, Class III marginal tissue recession which extends to or beyond the mucogingival junction. Bone or soft tissue loss in the interdental area is present or there is malpositioning of the teeth which prevents the attempting of 100% root coverage. Partial root coverage can be anticipated. Class IV marginal tissue recession which extends to or beyond the mucogingival junction. The bone or soft tissue loss in the interdental area and/or malpositioning of the teeth is so severe that root coverage cannot be anticipated. All four Sullivan and Atkins’ classes fall into Class I and Class II; Class III and Class IV recessions deal with interdental loss or extrusion that prevents attempting 100% root coverage. Treatment of the recession with bilaminar techniques In the last years a great number of surgical techniques have been proposed for the treatment of gingival recessions:

� Free gingival grafts � Pedicle flaps (with a coronal or lateral shift) � Regenerative techniques (guided tissue regeneration) � Bilaminar techniques

In this share it has been given a particular attention to the bilaminar techniques, connective graft associated to the coronal shifted flap, for the treatment of the single or multiple recessions with the aim of valuing the advantages obtained by this therapeutic approach towards the tissue recovery. In 1985 Langer and Raetzke17-19 introduced the subepithelial connective grafts, later defined also with the term of bilaminar techniques, since the receiving site is covered by two layers of tissue: the first one, that takes a direct touch with the root surface, is represented by the same connective graft, the second one is given by the previously risen flap and then repositioned. The bilaminar techniques are identified with the studies of Langer and Langer 198517, Nelson 198718 and Raetzke 198519. Most of the success of a root coverage technique depends on a right preliminary analysis of the case and on the surgical technique choice.


The coronal positioned flap20 (CPF) is a technique that gives excellent aesthetics results; it can permit not to take the connective tissue from another oral place, is relatively easy to do and permits to treat many recessions at the same time. On the contrary, the taking from the palate, even though executed with not too many invasive techniques, it is equally source of pain and trouble for the patient. Moreover, being limited the quantity of tissue to be taken (generally from the palate), it has to be considered that it is hardly desirable the coverage of more than three teeth in the same surgical seat. The reason why it is chosen a bilaminar technique instead of the pedicle ones depends on the clinic case taken in exam. In fact in literature discordant data have been quoted about the percentage of root coverage, which can be obtained with the simple CPF. The selection of the recession to treat with this kind of surgery seems to be the determining element to obtain a high expectation of its executive success. The bilaminar technique is proposed as alternative to the simple CPF when:

Surgical technique

The subject presented 3 recessions on adjacent teeth (11-12-13-14) in aesthetic area of the mouth (Fig1).

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1. an increase of the thickness and the width of keratinized tissue is needed2. the root surface presents a lack of the hard tissues in terms of abrasion or root caries3. for the root coverage of single or multiple recessions which present a residual keratinized tissue smaller than 3 mm (Allen e Miller 1989)21

All the recession defects fall into class I according to the definitions given by Miller16. The defect of hard tissue on the root of the canine required a bilaminar technique, consisting of a connective tissue graft covered by a CPF (Fig 2). The connective tissue graft (harvested from the palate) is placed inside the root concavity in order to compensate the abrasion space and to prevent soft tissue flap collapse inside it. Following local anesthesia (2% carbocaine with 1:100,000 epinephrine - Astra), a horizontal incision was made with a scalpel in order to design an “envelope” type of flap22. The incision was extended to include one tooth on each side of the teeth to be treated, in order to facilitate the planned coronal repositioning of the flap tissue over the exposed root surfaces (Fig 3). The horizontal incision of the flap was made up with oblique submarginal

incisions in the interdental areas and continued with intrasulcular incisions at the recession defects. Each surgical papilla was dislocated with respect to the anatomic papilla by the oblique submarginal interdental incisions: in particular the surgical papillae mesial to the flap mid-line were dislocated more apically and distally while the papillae distal to the mid-line were shifted in a more apical and mesial position.

Fig. 3

Fig. 2


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The envelope flap was raised with a split-full-split approach in the corono-apical direction22: the oblique interdental incisions were carried out keeping the blade paral-lel to the long axis of the teeth in order to dissect split-thickness the surgical papillae. Gingival tissue apical to the root exposures was raised full-thickness in order to provide with more thickness that portion of the flap critical for root coverage. The most apical portion of the flap was elevated split-thickness to facilitate its coronal displace-ment. The root surfaces were mechanically treated with the use of curettes. It must be considered that only that portion of the root exposure with loss of clinical attachment (gingival recession + probable gingival sulcus/pocket) was instrumented. Exposed root surfaces in areas of anatomic bone dehiscence were not instrumented to avoid damaging any connective tissue fibers still inserted in the root cementum. The remaining tissue of the anatomic interdental papillae was de-epithelialized to create connective tissue beds to which the surgical papillae were sutured. A sharp dissection into the vestibular lining mucosa was then carried out to eliminate muscle tension. It must be considered that the “adequate” coronal displacement of the flap results from the elimination of lip and muscle tensions in the apical portion of the flap. During coronal advancement each surgical papilla rotated towards the ends of the flap and finally resided at the center of the interproximal area. Flap mobilization was considered “adequate” when the marginal portion of the flap was able to passively reach a level coronal to the cemento-enamel junction at each single tooth in the surgical site. The flap, in fact, should be stable in its final position even without the sutures. The connective tissue graft was harvested from palate. The site was de-epithelialized by means of a rounded diamond bur. The mesio-distal length of the graft was 6 mm greater than the width of the recession measured at the level of the CEJ. The apico-coronal dimension of the graft was equal to the depth of the bone dehiscence (measured from the CEJ to the buccal bone crest) minus the pre-operative height of keratinized tissue apical to the recession defect. The thickness of the graft was less than 1mm. The connective tissue graft was positioned apical to the CEJ, at a distance equal to the height of keratinized tissue originally present apical to the recession defect, and it was anchored at the base of the interdental anatomic papillae with two interrupted sutures (Vicryl 5/0 C3, Ethicon) (Fig 4). The graft, acting as a bio-filler inside the concave abrasion area, gives stability to the covering flap, which is coronally advanced in excess (about 1mm) with respect to the clinical CEJ23 (Fig 4, 5). Sling sutures (Vicryl 5/0 C3, Ethicon) were performed to accomplish a precise adaptation of the buccal flap on the exposed root surfaces and to stabilize every single surgical papilla over the interdental connective tissue bed (Fig 6).

Fig.4

Fig.5

Fig.6


It was prescribed to the patient nimesulide (Aulin, Roche), 100 mg tablets every 8 hours for 2 days. The patient was instructed not to brush the teeth in the treated area but to mouthrinse with chlorhexidine solution (0.12%) twice daily for 1 min.Fourteen days after the surgical treatment, the sutures were removed. Plaque control in the surgically treated area was maintained by chlorhexidine rinsings for additional 2 weeks. After this period the patient was again instructed in mechanical tooth cleaning of the treated tooth region using a soft toothbrush and a roll-technique. The patient was recalled for prophylaxis 1, 3 and 5 weeks after suture removal and, subsequently, once every 3 months until the final examination (12 months) Fig (7, 8).

Discussion

The choice of the surgical technique for the treatment of the gingival recessions has to be always made paying attention in valuing the clinical situation and the needs of the patient. For this reason, it has to be guided by the duty of minimizing the number of the surgical phases, to reduce the pain and the post surgical troubles of the patient, considering the final aesthetic result. The effectiveness of a surgical technique in the treatment of the gingival recessions is measured in the capacity to obtain root coverage. This last can be expressed as a percentage of both root coverage and cases with a complete root coverage, which does not depend on the kind of surgery but on the periodontal state of health and on the anatomical characteristics of the site to treat. Only in

Fig. 7, 8.

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presence of an integrity of the interproximal periodontal support it is possible to bring back the gingival margin at the level of the cemento-enamel junction. In literature a great number of surgical techniques directed to the root coverage are reported, the choice towards bilaminar techniques is giuded by the presence of a clinical situation in which the simple pedicle flap would not allow to obtain the desired clinical result. The characteristic of the bilaminar methods, proposed for the first time during the second half of the eighties17-19, consists on the facts that the connective grafts are interposed between the receiving site and a pedicle flap. In this way the connective tissue receives in the first phase of recovery a double blood supply: either from the periostal underlying bed or from the overlying pedicle flap. Another advantage of the bilaminar technique is given by the collecting technique. The taken connective graft presents a smaller thickness compared with the required one from an epithelio-connective technique and this allows having a recovery of the donor site, generally the palate, without any risks of necrosis of the underlying tissues. When permitted by the thickness of the palate, it is possible to use “trap door” technique described by Harris20, where the palatine wound recovers primarily with a great reduction of the risk of secondary haemorrhage and a lower post surgical trouble. When the thickness of the donor site seems not to guarantee a right amount for the collecting of a graft, it is necessary to choose other techniques that introduce the de-epithelialization of the graft. The de-epithelialization can be executed extra-orally after the collecting of the graft or before the collecting in the intra-oral site, and in this last case with several advantages. With a diamond bur all the epithelium is eliminated, the underlying tissue has to be bleeding to indicate the right elimination of the epithelium. With the aid of tweezers and scalpel the dissection in the involved area is started, taking care to maintain a uniform thickness. The donor site is finally sutured and left recovering for second intention. Considering the use of the connective graft and CPF together the advantage consist on the possibility to treat recessions of the soft tissues associated with root caries or abrasions. The graft allows the filling of the depression placed on the root surface so, acting as “biological filler” makes easy the following coronal shift of the coverage flap and the restoration of the right emergency profile. The CPF can be steadied through an horizontal periosteal suture in apical area. This procedure not only permits a better stability of the flap, limiting the muscular tractions, but it also presses the tissues with a consequent reduction of the coagula. This reduction produces undoubted advantages on the process of recovery and then, of result. Unfortunately such stratagem is not always well accepted by patients in the operation following days, since it provokes pain and sense of traction. The authors, then, try to limit the use paying an extreme attention to the flap passivation, in the use of a pressing on the operated area with a wet and hot


gauze and specific post surgical suggestions. It is suggested then, to limit the use of this suture in situations with a particularly low fornix. The presence of gingival recessions on the anterior areas of the dental arches, can represent an aesthetic problem for the patient who, many times, complain the exaggerated length of some of his teeth, which becomes evident when smiling. Moreover what troubles the patient is the loss of the harmony of colours and thickness. In these cases, when is not possible to adopt surgical techniques with pedicle flaps, the bilaminar techniques represent a good compromise. The coverage flap masks the white “keloid” appearance of the graft, guaranteeing a camouflage of it. This has been also the reason why, during the years, it has been done several changes to the original techniques that provided the use of a partially de-epithelialized connective graft. The epithelial portion of the graft was left displayed in the oral environment and was not covered by the flap with the aim to restore the gingival margin. The colour difference between the epithelial portion of the graft and the flap placed as coverage of the connective portion of the same, brings to an anaesthetic result. Today it is tried to reduce the dimensions of the connective graft and to guarantee, using the anatomical papilla correctly de-epithelialized, the entire coverage of the graft and the coronal support for the flap. As conclusion, the CPF associated with the connective graft is proposed as a valid therapy for the coverage of the gingival recessions, as the primary option in all those cases where the quality and the amount of the marginal tissues of the pedicle flap do not guarantee an optimal recovery and when it is necessary to fill the deficit of root tissue, consequent to the presence of both root abrasion and caries.

This paper was presented at the IX Congress of BaSS - Ohrid

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References

1. Kassab MM, Cohen RE. The etiology and prevalence of gingival recession. J Am Dent Assoc 2003 Feb; 134(2): 220-225.

2. Checchi L, Daprile G, Gatto MR, Pelliccioni GA. Gingival recession and toothbrushing in an Italian School of Dentistry: a pilot study. J Clin Periodontol. 1999 May; 26(5):276-80

3. Loe et al. The natural history of periodontal disease in man: prevalence, severity, extent of gingival recession in conjunction with root surface citric acid conditioning. J of Periodontol 1992; 63: 489-95.

4. Murtoramaa et al. Periodontal status in university students. J Clin Periodontol 1987; 14: 462-65.

5. Sangnes G. Traumatization of teeth and gingival related to habitual tooth cleaning procedures. J Clin Periodontol 1976; 94-103.

6. Sangnes G, Gjermo P. Prevalence of oral soft and hard tissue lesion related to mechanical tooth cleaning procedures. Community Dentistry and Oral Epidemiology 1976; 4: 77-83.

7. Serino et al. The prevalence and distribution of gingival recession in subject with high standard of oral hygiene. J Clin Periodontol 1994; 21: 57-73.

8. Baelum V et al. Oral hygiene, gingivitis and periodontal breakdown in adult Tanzanias. J Periodontol Res 1986; 21: 221-232.

9. Baelum V et al. Periodontal disease in adult Kenyasns. J Clin Periodontol 1998; 15: 445-452.

10. Yoneyama et al. Probing depth, attachment loss and gingival recession. Findings from a clinical examination in Ushiku, Japan. J Clin Periodontol 1998; 15: 581-91.

11. Baker D & Seymour G (1976). The possible pathogenesis of gingival recession. A histological study of induced recession in the rat. J Clinic Periodontol; 3:208-19.

12. Löe H, Anerud A et al. (1992). The natural history of periodontal disease in man. The rate of periodontal destruction before 40 years of age. J of Periodontol; 49: 607-20.

13. Guidard EA, Caffesse RG. Treatment of localized gingival recession III. Comparison of results obtained with lateral sliding and coronally repositioned flaps. J Periodontol 1978; 457-461.

14. Urbani G, Lombardo G, Cavalleri et al. Le recessioni gengivali. Supplemento a il Dentista Moderno 1993: 1-53.

15. Sullivan HC, Atkins JH. Free autogenous gingival graft I Principles of successful grafting. Periodontics 1968; 6: 121-129.

16. Miller P. D. (1985). A classification of marginal tissue recession. The Int J Periodont Rest Dent 4(2): 9-13.

17. Langer and Langer. Subepithelial connective tissue graft technique for root coverage. J Periodontol 1985; 56 715-20.

18. Nelson SW. The subpedicle connective tissue graft. A bilaminar reconstructive procedure for coverage of denuded root surfaces. J Periodontol 1987; 58: 95-102

19. Ratzke PB. Covering localized areas of root exposure employing the “envelope techinique”. J Periodontol 1985; 56: 397-402.


20. Harris RJ, Harris AW. The coronally positioned pedicle graft with inlaid margins: a predictable method to obtain root coverage of shallow defects. Int J Period Res Dent 1994; 14: 229-41.

21. Allen EP, Miller PD. Coronal positioning of existing gingival: shirt term results in the treatment of shallow marginal tissue recessions. J Periodontol 1989: 60: 316-19.

22. Zucchelli G, De Sanctis M. Treatment of multiple recession type defects in patients with aesthetic demands. J Clin of Periodontol 2000; 71:1506-1514

23. Zucchelli G, Amore C, Sforza NM et al. Bilaminar techniques for the treatment of recession-type defects. A comparative study. J Clin of Periodontol 2003; 30: 862-870.

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10 years of BaSS

DENSITOMETRIC ANALYSIS INPERIODONTOLOGY

University of Cumhuriyet Faculty of Dentistry Department of PeriodontologySivas Turkey

U.K.Gursoy (DDS, PhD)I. Marakoglu (DDS, PhD)

Summary:

Beginning from the exploration of x-ray, densitometric analysis is in common use of medical diagnosis. Today densitometric analysis begins to take place in dental clinics especially in periodontology with precise bone density change detection. Although microdensitometry and photodensitometric analysis were most common methods to assess bone density changes, recent developments in radiography and nuclear medicine let the clinicians use computer supported densitometric techniques also. Both in disease progression and healing process, early changes which could affect the treatment and maintenance procedures could easily be designated by the help of densitometric analysis. It seems that densitometric analysis, with its ability to detect minor changes in alveolar bone and easy usage, will take conventional radiographs place. Key Words: Densitometric Analysis; Alveolar Bone; Periodontology. Introduction

Periodontitis is a host mediated inflammatory disease induced by a group of bacteria, which results in a loss of connective tissue attachment and alveolar bone. As loss of attachment and alveolar bone are essential characteristics in periodontal disease, those changes must be detected in a clear and objective manner1. Nevertheless, main objective of the periodontal therapy is the reconstruction of gingiva, cementum, bone and periodontal ligament on a previously infected root surface. Over the last two decades 6 to 12 month surgical re-entries has been the gold standard of evaluation for most clinical regenerative studies. One of the greatest limitations with this form of analysis is recruiting the patients for re-entry. Although clinical soft tissue measurements, like pocket depth measurements or bleeding indexes have played an important role in the assessment of regenerative procedures, they do not provide any information regarding the hard tissue response to the therapy2. Conventional radiography, which is used both in evaluation of disease progression and healing period, is a non-invasive diagnostie tool that detects by measuring the alveolar bone height. Alveolar bone loss is conventionally calculated by measuring the distance between the alveolar crest and cemento-enamel junction on radiographs. However, the reduction seen on the conventional radiography is the bone loss occurred, not the continuing loss3. Healthy cortical bone covers the resorption changes on conventional radiograph readings on periodontal defect when active periodontal destruction happened in active disease period. Hence, conventional radiography is an

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insensitive technique for detecting small bony lesions or sites in which periodontitis had just started or progressed4. Today, with the help of new enhanced digital image analyse techniques, changes in alveolar bone can be detected not only in bone height but also in density. Assessing of alveolar bone density provides us to detect early bone loss and gain around the teeth when bone loss is still permanent3. Densitometric analysis is being performed in medicine for a long time, beginning from shortly after the discovery of X-ray. First attempt was to evaluate the mineral structure of teeth in 1930’s5. In the past, bone density measurement techniques were associated with large precision errors relative to estimated rates of change. Technical and biological factors generally affect the ability to interpret bone loss rates. Technology of bone densitometry has undergone rapid changes over last decade with dual-energy X-ray absorptiometry6. Nowadays, bone density can be reliably evaluated from radiographs, computerized tomography(CAT scans), peripheral bone densitometry by single photon apsorptiometry(SPA), dual-photon absorptiometry(DPA), and dual energy X-ray technology (DEXA) as well as peripheral dual energy X-ray pDEXA7. In dental research, microdensitometry was used for densitometric analysis in jaws8 and later phodensitometry9, subtraction radiography10 and computer assisted densitometric image analysis (CADIA)11 techniques was performed. Even if they were not so common in use, quantitative computed tomography12 and 125I-absorptiometry13 were performed to detect alveolar bone density changes also. Microdensitometric Analysis Beginning from the mid 60’s, microdensitometry offered a more quantitative and objective technique than the visual method evaluating radiographic bone height and mineralization. Several investigators used it in order to determine the size and quantity of trabeculae in bone14, amount of bone resorption in the area of bone implants15, and the effect of regenerative alterations of the alveolar bone after flap operation16. Israel14 has reported that size and quantity of trabeculae in bone can be determined by using microdensitometric analysis. Miller et al.15 reported Joyce-Loebel microdensitometery as a new system of measuring bone density in 1964 in order to measure bone density. This densitometer prints out a 2-dimensional analogue map of the density patterns seen in a photographic negative or other transperencies. This instrument has proved itself useful both in the quantitative and qualitative analysis of bone density as determined radiographically8. This technique takes an aluminium step-wedge as reference and determines the changes in bone mineralization by the help of this reference. Aluminium was chosen because its atomic number is close to calcium. In 1977 Turgut and Kansu16 combined a study about bone regeneration in post operative flap


procedure by assessing the interdental bone density changes; and they stated the bone resorption till 3rd month postoperatively by using microdensitometry. Also in that study they found lower density scores in the posterior region in comparison to the anterior region and expressed the importance of anatomic structures in densitometric analysis. As they couldn’t find any difference between the densitometric analyse results of men and women they noticed that sex does not affect the results of densitometry. In 1972 Matsue et al.17 stated that the microdensitometry is more quantitative and objective technique than the visual method of evaluating radiographic bone height and mineralization following transplantation. 1251-Absorptiometry Radiographic and nuclear medicine diagnostic techniques reached the sensitivity that can detect small bone changes. A non radiographic diagnostic method, 125I-absorptiometry, introduced by Henrikson13, is the most precise method to detect periodontal bone mass changes. It is based on the absorption by bone of a low-energy gama beam by bone, originating from a radioactive source of 125I. This method has been shown to measure bone mass with a high degree of exactness and precision. The use of this system in posterior sites limited by technical considerations, and the nature of the beam of 125I makes precise alignment even more critical than with other techniques18. Photodensitometric Analysis Photodensitometric analysis has been developed in order to facilitate the densitometric analysis in posterior regions, especially in furcations. Photodensitometry is a quantitative method that is based on correlating bone density changes with a density reference device in the radiograph3. It implies the use of photodensitometer and a computer assisted transformation of the optical density into millimetres of aluminium equivalents. A microdensitometer together with a microcomputer is used in density readings18. In 1990 after assessing the interdental bone density changes by photodensitometry, Dubrez et al.9 reported statistically significant bone gain in a postoperative 1-year period after scaling and root planning. Ersoy and Ataoğlu19 assessed the alveolar bone density by photodensitometry in patients they performed closed root surface curettage and they found 14.4% decrease in density in 2 months postoperatively, and later in 6 and 12 months they found an increase of 8.6% and 16.9%, respectively. In a similar study, Alptekin et al20 examined the effect of low dose doxycyclin on alveolar bone density in adult periodontitis patients by photodensitometric method and they could not found any significant effect. In that study they used transmission densitometry on assessing the scores. Colbert and Bachtell21 coined the term radiographic

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absorptiometry for similar analysis of radiographs with computer-controlled calculations of the radiographic image. Kuhl and Nummikoski3 measured the accuracy and precision of a radiographic absorptiometry method by using an occlusal density reference wedge in quantification of localised alveolar bone density changes and they found the accuracy of the intraoral radiographic absorptiometry method low when used for absolute quantification of bone density. However, they suggested that the precision of the method is good and the correlation is linear, indicating that the method can be used for serial assessment of bone density changes at individual changes. Subtraction Radiography Subtraction radiography, which has been used in medical diagnose for a long time, began to use in dental, especially in periodontal diagnosis18. Subtraction of 2 serially obtained radiographs is a technique that increases detectability21. Changes in density and/or volume of bone can be detected as lighter areas (bone gain) or dark areas (bone loss). Quantitative changes in comparison with baseline images can be detected using an algorithm for gray scale levels. This is accomplished by means of a computer. Radiographs taken with identical exposure geometry can be scanned using microphotometer that determines a grey-level value for each picture point. After superimposition of 2 subsequent radiographs, this technique can show differences in relative densities18. The success of the technique is contingent on the ability to cancel unchanged anatomical structures. Hence, it suffers from artefacts introduced by inexact replication of the projection geometry, uncontrolled variations in film exposure and processing, and tissue changes resulting from normal growth or development22,23. A photographic subtraction technique was first described by Ziedses des Planetes in 1934 and has been used mainly for angiographic examinations. The theory of photographic subtraction has been described in detail by Hardstedt and Welander. Hardstredt determined the conditions for optimal results and described the requirements that have to be met with regard to film density, contrast, exposure and processing24. In early attempts, Hausman et al.25 detected differences in crestal bone height of 0,87mm with reliability. Jeffcoat et al.24 have shown a strong relationship between probing attachment loss detected using sequential measurements made with an automated periodontal probe and bone loss detected by subtraction radiography. Because many physiologic as well as pathologic changes of dental interest occur with bone, digital subtraction radiography should be of value whenever it is of significant interest to study such changes longitudinally. It should be particularly valuable in research aimed at studying the effects of different treatment procedures or the progression of lesions left untreated24. Studies of observer performance in radiographic diagnosis of periapical lesions


have demonstrated significant variations among examiners regarding the size of such lesions, as well as of changes in size between examinations26-28. It has been found that examiners could completely fail to perceive lesions which were detected at earlier stages in a series of radiographs of periapical lesions with increasing size28. In diagnosis of periodontal disease there is a need for accurate detection of subtle changes in the crest of alveolar bone, for which the conventional radiographic technique is less well suited29. Under most ideal conditions, digital subtraction images permit the detection of 5% change in mineral mass per volume, whereas traditional visualisation of serial radiographs requires a change of at least 30%22,30. This method has a great diagnostic potential, even in clinical practice, because of the development of personal computers with capability for digitising and image processing 18. Computer Assisted Densitometric Image Analysis (CADIA) CADIA is one form of subtraction radiography that allows the investigator to quantify changes by comparing the radiographic density in a predetermined region of interest(ROI) between baseline and follow up radiographs2. In this system, a video camera, which interfaced with an image processor, and a computer that allow the storage and mathematical manipulation of the images, measures the light transmitted through a radiograph, and the signals from the camera are converted into grey-levels18. Bragger et al1 reported that CADIA is an objective method to quantitatively follow alveolar bone density changes over time and appears to be the most sensitive of previously described radiographic interpretation techniques. They compared the ability of CADIA to detect alveolar bone changes on radiographs with interpretation of digital subtraction images and conventional radiographic interpretation. In their evaluations of bone loss at osteoctomy/osteoplasty sites and they found 72.7% negative change by digital subtraction images, 50.9% negative change by conventional interpretation, and 81.8% density change by CADIA. In an other study, Bragger et al11 performed crown lengthening procedures for restorative purposes and assessed the density changes by CADIA: a statistically significant density loss was assessed 4-6 weeks post surgically at test sites treated by periodontal surgical procedures, compared to corresponding controls. Deas et al31 using replicate measurements of clinical attachment levels and CADIA, demonstrated that the prevalence of progressing lesions in periodontitis (38% of sites per patient) as detected by this radiographic method, might be much higher than previously thought. The CADIA system appears to offer an objective method to follow alveolar bone density changes quantitatively over time. The density change information stored in a digital form and its detection does not depend on human perception or a diagnostic decision making process. In contrast to the perhaps most precise method for assessment alveolar bone mass, the 125I-absorptiometry, this method is not restricted to the anterior region, and viewing and analysing of a

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larger area of diagnostic interest or several areas at the same time is possible. Patient exposure to X-rays is not increased since routinely taken dental radiographs may be analysed. However, there are some disadvantages of the system; it requires superimposable serial radiographs that can be obtained by applying custom-made bite-blocks and a Rinn system modificafion 1. Quantitative Computed Tomography (QCT)

Computed tomography rapidly gets used in medicine in order to assess the bone minerelization quantitatively. QCT can be performed in single-energy or dual-energy modes, which differ in accuracy, precision and radiation. Kiemetti et al12 determined the mineral density of the trabecular bone of the mandible by single-energy QCT and compared the results with the bone mineral densities of their lumbar area. The bone mineral density of the lumbar area and that of the femoral collum correlated well with each other, but the bone mineral density of the trabecular bone of the mandible did not correlate with either of the other two bone mineral density measurements. Kribbs et al32 found that in elderly subjects mandibular density did not correlate with any skeletal measurements except vertebral bone.

One of the most recent advances in the assessment of bone changes involves the use of nuclear medicine. Nuclear medicine techniques for the study of bone metabolism use a bone seeking radiopharmaceutical, such as diphosphonate subject, which labelled with a radionucleide, Tc 99m. This compound is injected intravenously, and after a waiting period to allow for bony uptake and clearance of the radiopharmaceutical, uptake by the bone is measured with a miniaturised semiconductor probe radiation detector 18.

As it provides the clinician with the basis for applying preventive or corrective measures, early detection of periodontal bone loss is important. Reduction of alveolar crestal bone density is one early sign of periodontal disease and precedes the loss of height of the alveolar bone crest. However, conventional comparisons of radiographs cannot detect small changes reliably due to great variations in the anatomical structure and radiographic image density and contrast33. Conventional radiographs do not let to have ideas about the continuing bone reposition or resorption18. There are several studies that mention the bone density changes before loss in bone crest height34. In conclusion, it should be noted that the densitometric analysis represents the future in dental imaging because of its ability to detect bone changes that is often undetected when using the conventional radiographs.


U.K.Gursoy et al

References

1. Bragger U, Pasquali L, Rylander H, Carnes D, Kornman KS. Computer assisted densitometric image analysis in periodontal radiography. A Methodological Study. J Clin Periodontol 1988; 15:27-372. Toback GA, Brunsvold MA, Nummikoski PV, Master LB, Mellonig JT, Cochran DL. The accuracy of radiographic methods in assessing the outcome of periodontal regenerative therapy. J Periodontol 1999;70: 1479-14893. Kuhl ED, Nummikoski PV. Radiographic absorptiometry method in measurement of localised alveolar bone density changes. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;89:375-814. Bragger U, Bürgin W, Fourmousis I, Schmid G, Schild U, Lang NP. Computer-assisted densitometric image analysis of digital subtraction images:In vivo error of the method and effect of thresholding. J Periodotol 1998;69:967-9745. Goodwin PN. Methodologies for the measurement of bone density and their precision and accuracy. Seminars in Nuclear Medicine 1987;Vol XVII, No 4: 293-3046. Pasariello R, Albanese CV, Kvasnova M. Bone densitometry in clinical practice. Eur Radiol 1997;7(Suppl. 2):2-107. Becker W, Hujoel PP, Becker BE, Willingham. Osteoporosis and implant failure: An exploratory case-control study. J Periodontol 2000;71 :625-6318. Matsue I, Collings CK, Zimmerman ER, Vail WC. Microdensitometric analysis of human autogenous alveolar bone implants. J Periodontol 1970;41:489-4959. Dubrez B, Graf JM, Vuagnat P, Cimasoni G. Increase of interproximal bone density after subgingival instrumentation quantitative radiographical study. J Periodontol 1990;6 1:725-73110. Janssen PTM, van Aken J. Problems around the in vitro and in vivo application of quantitative digital subtraction radiography. J Clin Periodontol 1989;16:323-33011. Bragger U, Pasqulai L, Kornman KS. Remodelling of interdental alveolar bone after periodontal flap procedures assessed by means of computer-assisted densitometric image analysis(CADIA). J Clin Periodontol 1988;15:558-56412. Kiemetti E, Vainio P, Lassila V, Alhavla E. Trabecular bone mineral density of mandible and aiveolar height in postmenopausal women. Scand J Dent Res 1993;101:166-7013. Henrikson CO. Iodine as a source for odontoİogical roentgenology. Acta Radiol 1976;13;37714. Israel H. Microdensitometric analysis for study of skeletal growth and aging in the living subject. Amer J of Physical Anthropology 1968;29: 28715. Miller CS, Parsons FG, Kofsky IK. Simplified two dimensional microdensitometry. Nature 1964;202: 1196.16. Turgut E, Kansu H. Flap operasyonunu takiben standardize edilen paralel teknikle alman seri radyograflarin mikrodensitometrik analizleriyle kemik rejenerasyonunun takibi. Hacettepe Un Dishekimliği Fakultesi Dergisi 1977; 1:48-56


17. Matsue I, Zimmerman ER, Collings LK, Best JT. Microdensitometric analysis of human autogenous bone implants II. Two dimensional density and pattern analysis of interproximal alveolar bone. J Periodontol 1971 ;42:435-43818. Carranza FA, Newman MG. Clinical Periodontology Philadelphia, W.B.Saunders Company, 1996 pp 380-38119. Ersoy M, Ataoglu T. Kapali kok yuzey kuretajinin alveolar kemik densitesi uzerine etkisi. Selcuk Un. Dishekimligi Fak. Dergisi 1996;6: 101-10520. Alptekin NO, Duran I, Gozlu M, Erdem EO, Ozkaya T. Eriskin periodontitis tedavisinde donusumlu uygulanan dusuk doz doksisiklinin alveoler kemik densitesine etkisi. Cumhuriyet Un. Dishekimligi Fak. Dergisi 1999;2:42-4721. Colbert C, Bachtell RS. Radiographic absorptiometry (Photodensitometry). In: Cohn SH, editor. Non-invasive measurements of bone mass and their clinical application. Boca Raton:CRC Press.1981 pp.52-8422. Ortman LF, Duniford R, McHenry K, Hausmaıın E. Subtraction radiography and computer assisted densitometric analysis of standardised radiographs. A comparison study with 125I absorptiometry. J Periodont Res 1985;20:644-65123. Webber RL, Ruttiman UE, Grondahl HG. X-ray image subtraction as a basis for assessment of periodontal changes . J Periodont Res 1982;17:509-51124. Gröndahl HG, Gröndahl K, Webber RL, Bethesda MD. A digital subtraction technique for dental radiography. J Oral Surg 1983;55:96- 102.25. Hausmann E, Allen K, Carpio L. Computerised methodology for detection of alveolar crestal bone loss from serial intraoral radiographs. J Periodontol 1992;63:65726. Duinkerke ASH, Poel ACM. Variations in the interpretation of periapical radiolucencies. Oral Surg. 1975;40:414-42227. Goldman M, Pearson AH, Darzenta N Endodontic success -Who’s reading the radiographs? Oral Surg 1972;33:432-43728. Duinkerke ASH, Poel ACM van de, Doesburg WH, Lemmens WAJG. Densito-metric analy sis of experimentally produced periapical radiolucencies. Oral Surg 1977;43:782-79729. Lang NP, Hill RW. Radiographs in periodontics J Clin Periodontol 1977;4:16-2830. Hausmann E. Radiographic and dental imaging in periodontal practice. J Periodontol 2000;71:497-50331. Daes D, Pasquali LA, Yuan CH, Komman KS. The relationship between the probing attachment loss and computed radiographic analysis in monitoring the progres-sion of periodontitis. J Periodontol 1991;62: 13532. Kribbs PJ, Chesnut CH, Ott SM, Kilcoyne RE Relationships between mandibular and skeletal bone in a population of normal women. J Prosthet Dent 1990;63:86-8933. Nummikoski PV, Steffensen B, Hamilton K, Dove SB. Clinical validation of a new subtraction radiography techmnique for periodontal bone loss detection. J Periodotol 2000;71,508-605


10 years of BaSS

RECENT ADVANCES IN REGENERATIVE PERIODONTAL THERAPY- A COMBINATION OF AUTOGENOUS BONE GRAFTING AND ENAMEL MATRIX PROTEINS

University of Belgrade, Faculty of Dentistry, Perio Dpt.

Vojislav Leković, DDS, PhDZoran Aleksić, DDS, MS

Summary Objective: Enamel matrix proteins (EMP) have been introduced as a new approach for regenerative periodontal treatment. The purpose of this study was to evaluate the clinical effectiveness of enamel matrix proteins (EMP) used in combination with autogenous bone graft (ABG) in treatment of periodontal infrabony defects. Materials and Methods: The study employed a split mouth design. Twenty paired intrabony defects were surgically treated and re-entered six months later. Experimental sites were treated with EMP and grafted with ABG. Control sites were treated with an OFD. The primary outcomes evaluated in the study were changes in probing depth, clinical attachment level and defect bone fill. Results: Preoperative pocket depths, attachment levels and intra-operative bone measurements were similar for control and experimental sites. Post surgical measurements taken at six months revealed a significantly greater reduction in pocket depth in the experimental group (3.96 ± 1.31 mm on buccal sites and 3.88 ± 1.23 mm on lingual sites) when compared to the control group (1.91 ± 0.81 mm on buccal sites and 1.97 ± 0.73 mm on lingual sites). The experimental sites also presented with significantly more attachment gain (3.18 ± 1.19 mm on buccal sites and 3.14 ± 1.16 mm on lingual sites) than the control sites (1.58 ± 0.89 mm on buccal sites and 1.52 ± 0.76 mm on lingual sites). Surgical reentry of the treated defects revealed a significantly greater amount of defect fill in favor of the experimental group (3.89 ± 1.15 mm on buccal sites and 3.82 ± 1.08 mm on lingual sites) as compared to the control group (1.41 ± 0.81 mm on buccal sites and 1.44 ± 0.92 mm on lingual sites). Conclusions: Based on the results of the present study, it was concluded that enamel matrix proteins in combination with autogenous bone graft enhance the results achieved with standard surgical procedure in promoting true periodontal regeneration. Key words:Periodontal regeneration, enamel matrix proteins, autogenous bone graft. Introduction A primary goal of regenerative periodontal therapy is to reproduce the tooth supporting tissue, lost as a result of the infectious disease process.1-3 `True periodontal regeneration` is the reformation of a functionally oriented periodontal ligament with collagen fibers inserting in both regrown alveolar bone and reformed acellular cementum over a previously diseased root surface.3 To achieve this outcome the first concept of periodontal regeneration was focused on the reconstruction of osseous lesions.This has proven to be an


effective therapy and many types of bone grafts have been utilized, but the ability for regeneration of cementum and periodontal ligament was very limited.7,8 Guided tissue rgeneration was a pioneering technique that set the second stage for the evolution of periodontal regeneration. The principle of GTR is to promote periodontal regeneration through the use of selected cell repopulation of the periodontal defect.21,23,24 This is accomplished, in part, by barrier membranes, which exclude the gingival epithelium and connective tissues.This allows repopulation of the defect with cells from the periodontal ligament and bone tissues and has been shown to increase the amount of periodontal regeneration.16,24 Nyman et al.1 , Lekovic et al.17 and Sculean et al.12 , suggest that more periodontal regeneration occurs when bone grafts are combined with barrier membranes. Although GTR successfully promotes passive periodontal regeneration, application of the method is often difficult while there is substantial variation of clinical predictability, degree of efficacy and it is not known if there is some critical size required for space.18,11,23,21 The Biology-based approaches set the ground for the current third evolutionary stage in periodontal regeneration by emphasizing the importance of extracellular matrices and suggesting the use of growth factors, viable cells for tissue engineering and gene therapy with the overall goal of enhancing the desired outcome of therapy.2,15,16,25 The periodontal regeneration is a complex but orderly process involving the reformation of three different tissues at probably different time points. This will require a series of sequential interactions among cells and between cells and the extracellular matrix. All of these tissues are not only a functional unit but also a developmental unit of dental origin.10,13,14 One way of promoting periodontal regeneration, therefore, is to try to mimic the biologic processes involved in nascent tooth development, especially the development of the root and the supporting tissues. This approach in periodontal regeneration is called Biomimetics.2,3 Enamel matrix proteins have been shown to be involved in the formation of new tooth attachment.5,7,20 Due to their role in the formation of periodontal tissues, EMP have been recently investigated as a therapeutic approach for periodontal regeneration.25,26,27 The biologic concept behind enamel matrix induced periodontal regeneration is based on the discovery that enamel matrix proteins not only are involved in enamel formation but also play a key role in the formation of the root and attachment apparatus. It has been shown that porcine derived EMP are able to enhance the proliferation and protein production by human periodontal ligament cells in vitro (Gestrelius et al., 1997). Porcine derived EMP have also been used in periodontal regenerative procedures in animal models (Zetterström et al., 1997; Hammarström et al., 1997) and humans (Heijl et al., 1997) and shown to be effective in improving clinical attachment levels and radiographic bone fill. Several reports on patients

V.Leković et al

have shown that periodontal regeneration can be achieved with EMPs at the histologic level (Heijl, 1997; Mellonig, 1999; Cochran et al.2003;). While the use of EMP is a novel concept in periodontal regeneration, osseous grafting is a technique well established among researchers and clinicians.9,10,14,17,18 Several bone graft materials have been evaluated in Periodontics with various degrees of success (for a comprehensive review, see Garrett, 1996). Clinical trials evaluating bone graft materials often used open flap debridment (OFD) as a control procedure.28,29,30 Results of these trials invariably showed that grafted sites perform better than controls. Therefore, even though a graft material that promotes periodontal regeneration on a complete and predictable basis is still not available, benefits from osseous grafting are no longer disputed. Autogenous bone, long considered the gold standard of grafting materials, is currently the only osteogenic graft available to clinical practitioners.2,3 Grafted autogenous bone heals into growing bone through the processes of osteogenesis, osteoinduction and osteoconduction. Autogenous bone can be harvested from the iliac crest or intraoral sites. Resorption following transplantation has been reported to be less with mandibular bone grafts than with iliac crest grafts. Bone grafts obtained intraorally generally result in less morbidity.4,6 However, intraoral donor sites provide a significantly smaller volume of bone than the iliac crest. The donor site usually depends on the volume and type of bone desired and necessary. Autogenous bone is highly osteogenic and best fulfills the dental grafting requirements of providing a scaffold for bone regeneration. Combining osseous grafting with the wound healing promoted by EMP has the potential to result in a synergistic effect of both materials. This assumption is based on the fact that two distinct wound-healing principles may be applied together in one clinical situation. While a autogenous bone graft has the ability to exert osteogenic effects besides maintaining defect space, EMP can work at the periodontal ligament level to promote the formation of new cementum and the development of a new functional attachment unit. The purpose of this study was to evaluate the effectiveness of EMP combined with autogenous bone graft in reducing probing depths, improving clinical attachment levels and promoting bone fill in periodontal intrabony defects as compared to results obtained by OFD alone. Materials and methods Twenty healthy patients (mean age 43 years ± 8 months, 11 smokers and 9 non-smokers) with matched pairs of interproximal defects were recruited for the study. Inclusion criteria consisted of patients having two similar interproximal defects with pocket depths greater that 5 mm following initial therapy. The two selected defects could not be present in the same interproximal area and had to


present in the same arch (either contralateral or same side).The exclusion criteria consisted of endodontically treated test and adjacent teeth, patients with systemic illnesses, immune-compromised patients, or patients taking any drug known to cause gingival enlargement. Patients allergic or sensitive to any medication to be used in the study were also excluded. Patients were informed as to the character and purpose of the study and were required to sign an informed consent. The University Institutional Review Board approved the study design and consent. Initial therapy consisted of oral hygiene instructions, which was repeated until patients achieved an O’Leary plaque score (O’Leary et al., 1972) of 25% or below. Scaling and root planing of the quadrant(s) involving experimental and control teeth was performed under local anesthesia. Occlusal adjustment was performed if trauma from occlusion was diagnosed. Six to eight weeks following phase I therapy, a re-evaluation was performed to confirm the need for periodontal surgery. The study used a split mouth design where two interproximal sites were randomly (toss of a coin) assigned to the EMP/ABG or OFD groups. EMP/ABG sites were treated with the combination of a commercially available enamel matrix protein preparation (Emdogain®,Straumann-ITI, Switzerland) and autogenous bone grafting. OFD sites acted as controls and received a flap surgery without any graft material or membrane. Occlusal stents were fabricated with cold-cured acrylic resin on a cast model obtained from an alginate impression. The occlusal stent was made to cover the occlusal surface of the tooth being treated and the occlusal surfaces of at least one tooth in the mesial and distal directions. Stents were also extended apically on the buccal and lingual surfaces as to cover the coronal third of the teeth involved. All steps described above were developed in order to obtain an occlusal stent that was both stable when in position and easy to be removed by the therapist. Prior to surgery, the Plaque Index (Silness & Löe, 1964) and the Gingival Sulcus Index (Mühleman & Son, 1971) were measured. With the acrylic stent in position, the periodontal probe was inserted into the crevicular space at the angle necessary to reach the deepest area of the interproximal pocket. Probe angulation varied between 10 and 20 degrees. A pencil mark was made where the probe made contact with the acrylic stent and a groove was made on the pencil-marked area with a cylindrical low-speed burr. Using the groove as guide, the periodontal probe was re-inserted into the pocket and pocket depth (using the gingival margin as reference), gingival recession (using the most apical of the stent as reference) and relative attachment level (using the most apical end of the stent as reference) were recorded. Measurements were performed with a Marquis periodontal probe and recorded to the nearest millimeter. The same measurements were repeated on buccal and lingual surfaces of each interproximal defect.

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The surgical procedure was performed by local infiltration of 2% lidocaine containing epinephrine at a concentration of 1:100,000. Buccal and lingual sulcular incisions were used and mucoperiosteal flaps were elevated. Care was exercised to preserve as much interproximal soft tissue as possible. Complete debridement of the defects as well as scaling and root planing were achieved with the use of an ultrasonic device and hand curettes. Measurements of the osseous defects were made utilizing the same grooves previously employed to record pocket depth and attachment levels. The distance between the most apical end of the stent and point at which the groove-adapted probe made contact with the bottom of the defect was the one recorded on buccal and lingual sites. Other grooves, one buccal and one lingual, were fabricated as described in the previous paragraph in order to measure the distance between the most apical end of the stent and the interproximal alveolar crest (Figure 1) Experimental sites were treated with EMP in accordance to the manufacturer’s instructions. Root surfaces adjacent to the defects were treated with a 24% EDTA gel (Straumann-ITI,Switzerland) for two minutes. Surgical areas were then rinsed abundantly with sterile saline solution and EMP where then applied on the root surfaces in the apico-coronal direction (Figure 2,3). Defects were then grafted with autogenous bone graft, which had been previously mixed with sterile saline solution. The autogenous bone graft was tightly packed in the defects to the level of the surrounding bony walls (Figure 4). OFD assigned sites were treated with identical surgical procedures, excluding the EDTA treatment of the root, application of EMP, or grafting with ABG. Flaps were sutured at the original levels using 4-0 silk. Periodontal dressing was placed over the area and antibiotics

Fig1. Experimental defect in situ

Fig.2. Root surface modification

with the Pref-Gel®


(amoxicillin 500 mg, three times a day for 14 days) and 0.12% chlorhexidine rinses (two times a day for 14 weeks) were prescribed. Oral analgesics (ibuprofen 800 mg, three times a day as needed) were also prescribed.Dressing and silk sutures were removed at one week postoperatively. Surgical wounds were gently cleansed with chlorhexidine on a cotton swab and a new dressing was placed for an additional week. Treated teeth were splinted to an adjacent tooth using cold-cured resin if post-surgical mobility was found to be of class 1 or more at the end of the first post-operative week. Mechanical oral hygiene consisting of brushing, flossing and/or use of interproximal brushes was initiated at the end of the second postoperative week. Patients were examined weekly up to one month after surgery and then at three and six months. Postoperative care included reinforcement of oral hygiene and mechanical plaque removal whenever necessary. Six months after the initial surgery, all clinical measurements were repeated and surgical re-entries performed (Figure 5). The surgical reentries

Fig. 3. Aplication of Emdogain®

Fig.4. Experimental defect filled with autogenous bone

Fig. 5. Re-entry after six months

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consisted of buccal and lingual full thickness flaps and removal of all soft tissue from the exposed treated defect. All measurements described for the first surgical procedures were repeated during reentries using the acrylic stent as described earlier. Measurements were averaged out (mean ± standard error) and statistical comparisons between control and experimental sites at baseline and six months postoperatively were made using paired student’s “t” tests. “P” values ≤0.005 were regarded as statistically significant. Results All twenty patients completed the study. Surgical sites, EMP/ABG or OFD treated, healed uneventfully. No cases of flap dehiscence or infection were detected. All wounds appeared completely covered with soft tissue by day 14. With regards to number of bony walls, treated defects were as follows: EMP/ABG sites: 13 two-wall and 7 three-wall. Control sites: 16 two-wall and 4 three-wall. Changes in probing depth are reported on Table 1.

Site OFD EMPs/ABG “p” Value Mean Difference

Buccal 1.91 ± 0.81 3.96 ± 1.31 <0.001 2.05 ± 0.74 Mean Reduction Lingual 1.97 ± 0.73 3.88 ± 1.23 <0.001 1.91 ± 0.69

TABLE 1: Probing Depth Measured from the Gingival Margin.

Probing Depth (n = 20 paired defects) While both EMP/ABG and OFD sites showed a significant pocket depth reduction at 6 months, reduction on buccal and lingual measurements of EMP/ABG treated sites were greater (differences from controls of 2.05 ± 0.74 mm and 1.91 ± 0.69 mm, respectively). EMP/ABG treated sites also presented with significantly greater gain in clinical attachment (Table 2).

Site OFD EMPs/BPBM “p” Value Mean Difference

Mean Gain Buccal 1.58 ± 0.89 3.18 ± 1.19 <0.001 1.60 ± 0.28

(Initial - 6 mo) Lingual 1.52 ± 0.76 3.14 ± 1.16 <0.001 1.62 ± 0.26

TABLE 2: Attachment Levels Measured from the Acrylic Stent.

Attachment Level (n = 20 paired defects)


Differences in clinical attachment gain between EMP/ABG and OFD sites were of 1.60 ± 0.28 mm on buccal aspects and 1.62 ± 0.26 mm on lingual aspects in favor of the EMP/ABG treated sites. Gingival recession values were not significantly different between both groups (Table 3).

Site OFD EMP/ABG “p” Value Mean Difference

Mean Change Buccal 1.19 ± 1.26 1.16 ± 1.22 >0.05 0.03 ± 0.02

(Initial - 6 mo) Lingual 1.21 ± 1.28 1.28 ± 1.24 >0.05 0.07 ± 0.02

TABLE 3: Gingival Recession Measured from the Acrylic Stent.

Gingival Recession (n = 20 paired defects) Table 4 reports changes in osseous measurements for EMP/ABG and OFD treated sites. EMP/ABG treated sites presented with significantly greater bone fill than control sites. Differences from controls were of 2.48 ± 0.25 mm for buccal measurements and 2.38 ± 0.31 mm for lingual measurements in favor of EMP/ABG treated sites.

Site OFD EMP/ABG “p” Value Mean Difference

Mean Fill Buccal 1.41 ± 0.81 3.89 ± 1.15 <0.001¶ 2.48 ± 0.25

(Initial - 6 mo) Lingual 1.44 ± 0.92 3.82 ± 1.08 <0.001¶ 2.38 ± 0.31

TABLE 4: Defect Fill Measured from the Acrylic Stent.

Defect Fill (n = 20 paired defects) Plaque measurements and sulcular bleeding index were not significantly different between EMP/ABG and OFD sites at baseline or at 6 months. A small reduction in plaque index and sulcular bleeding was observed for both groups at 6 months when compared to baseline values, but the differences between the two groups were not statistically significant (Tables 5 and 6).

OFD EMP/ABG “p” Value

Initial 0.73 ± 0.67 0.71 ± 0.69 >0.05

6 Months 0.49 ± 0.62 0.50 ± 0.71 >0.05

“p” Value >0.05 >0.05

TABLE 5: Changes in Plaque Index

Plaque Index

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OFD EMP/ABG “p” Value

Initial 1.41 ± 0.81 1.49 ± 0.89 >0.05

6 Months 1.08 ± 0.70 1.19 ± 0.71 >0.05

“p” Value >0.05 >0.05

TABLE 6: Changes in Sulcus Bleeding Index:

Sulcus Bleeding Index Discussion

The results of this study support the hypothesis that a combination of osseous grafting with ABG and EMP have the ability to significantly reduce pocket depth, improve attachment levels and promote bone fill in intrabony defects in humans. Data generated by this study showed that the overall results achieved with a combination of EMP and ABG were not only statistically but also clinically significant from the control treated areas. EMP/ABG treatment of intrabony lesions clearly resulted in the periodontal therapeutic goal of a shallow gingival crevice compatible with predictable and effective maintenance. OFD was chosen as the control modality of treatment in this study so that differences observed in experimental sites could be attributed to the materials being implanted and not to the surgical technique employed. Probing depth resolution is a main outcome of periodontal regenerative procedures in clinical practice. Even though a reduction in pocket depth does not imply successful regeneration, postoperative pocket depth will have a direct impact on maintenance of a treated area. As well, pocket depth often will dictate the need for further therapy in a previously treated area. The combined EMP/ABG therapy reduced pockets by 3.88 to 3.96 mm, which is considered maintainable by most clinicians. The control sites treated in this study, for the reason described above, were retreated for the elimination of the residual post-surgical pocket depth at reentry. The modality of therapy employed on control sites was either regenerative (EMP/ABG) or resective depending on the depth and clinical characteristics of the residual lesion. Clinical attachment gain observed in the EMP/ABG group was in the 3.14-3.18 mm range, roughly 1.60 mm better than the average 1.52-1.58 mm range noticed with OFD. It appears obvious that the EMP, or the ABG or both were responsible for this advantage. Given the study design, however, it is not possible to determine which of the treatments used - EMP or ABG – was


responsible for the attachment gain. With regards to attachment gain promoted by EMPs Heijl and co-workers (1997) reported a gain in the 2.1-2.3 mm range. Even though extrapolations from results of other trials should be done with caution, it could be speculated that the greater mean attachment gain achieved in this study (3.14-3.18 mm) as compared to the two reports listed above where a single (instead of a combined) therapy was used may be due to a synergistic effect of EMP and ABG.

Defect fill with bone is a desirable outcome of periodontal regeneration. The bone fill observed in sites treated with EMP and ABG was in the 3.82-3.89 mm range, values which are comparable to ones reported for autogenous bone grafts (Shallhorn et al., 1970; Hiatt & Shallhorn, 1973; Froum et al., 1976). Autogenous bone is considered by many to be the gold standard as a periodontal grafting material but is often difficult to obtain in sufficient quantity. The ability to obtain similar results with other bone graft materials where availability is not a limiting factor presents the clinicians with a distinct advantage when treating large and/or multiple defects.

A limitation of reentry periodontal regeneration studies such as this one is the inability to assess the histologic characteristics of the regenerated tissues including the nature of the attachment between the newly formed bone and the previously diseased root surface. Block sections are necessary to confirm the presence of new attachment. It has been shown that new attachment is a possibility with either EMP (Heijl, 1997; Mellonig, 1999) or ABG (Cochran et al., 2003), but the predictability of such an outcome remains unknown.

In summary, intrabony periodontal defects can be successfully treated with a combination of enamel matrix proteins and autogenous bone grafting.

This paper was presented at the V Congress of BaSS – Thessaloniki, Greece

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10. Sculean A, Donos N, Blaes , Lauermann M, Reich E, Brecx M. Treatment of infrabony defects with enamel matrix proteins and guided tissue regeneration. A prospective controlled clinical study. J Clin Periodontol 2001;28:397-403.

11. Sculean A, Donos N, Blaes, Lauermann M, Reich E, Brecx M. The effect of postsurgical antibiotics on the healing of infrabony defects following treatment with enamel matrix proteins. J Periodontol 2001;72:190-195.

12. Sculean A, Donos N,Miliauskaite A, Arweiler N, Brecx M. Treatment of infrabony defects with enamel matrix proteins or bioabsorbable membranes. A 4-year follow-up split mouth study. J Periodontol 2001;72:1965-1701.

13. Froum SJ,Weinberg MA, Rosenberg E, Tarnow D. A comparative study utilizing open flap debridment with and without enamel matrix derivate in the treatment of periodontal infrabony defects. A 12-month re-entry study. J Periodontol 2001;72:25-34.

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15. Camargo PM, Lekovic V, Weinlaender M, Vasilic N, Kenney EB, Madzarevic M. The effectiveness of enamel matrix proteins used in a combination with bovine porous bone mineral in the treatment of infrabony defects in humans. J Clin Periodontol 2001;28:1016-1022.

16. Lekovic V, Camargo PM, Weinlaender M, Vasilic N, Djordjevic M, Kenney EB. The use of bovine porous bone mineral in combination with enamel matrix proteins or with an autologous fibrinogen/fibronectin system in the treatment of intrabony periodontal defects in humans. J Periodontol 2001; 72: 1157-1163;

17. Lekovic V, Camargo PM, Weinlaender M, Kenney EB, Vasilic N. The use of bovine porous bone mineral, enamel matrix proteins, and a bioabsorbable membrane in intrabony periodontal defects in humans. J Periodontol. 2001; 72:583-589.

18. Lekovic V, Camargo PM, Weinlaender M, Nedic M, Aleksic Z, Kenney EB. A comparison between enamel matrix proteins used alone or in combination with bovine porous bone mineral in the treatment of intrabony periodontal defects in humans. J Periodontol 2000;71:1110-1116.


19. Cortellini P, Pini-Prato G, Tonetti MS. Periodontal regeneration of human infrabony defects II. Re-entry procedures and bone measures. J Periodontol 1993;64:261-268.

20. Okuda K, Momose M, Miyazaki A, Murata M, Yokoyama S, Yonezawa Y, Wolf L, Yoshie H. Enamel matrix derivate in the treatment of human infrabony osseous defects. J Periodontol 2000.71:1821-1828.

21. Yukna R, Melloning J.Histologic evaluation of periodontal healing in humans following regenerative therapy with enamel matrix derivate. A 10-case series. J Periodontol 2000;71:752758.

22. McClain P K, Shallhorn RG. Long-term assessment of combined osseous composite grafting, root conditioning, and guided tissue regeneration. Int J Periodont Rest Dent 1993; 13: 9-27.

23. Shallhorn RG, McClain PK. Combined osseous composite grafting, root conditioning, and guided tissue regeneration. Int J Periodont Rest Dent 1988; 8: 8-31.

24. Anderegg CR, Martin SJ, Gray JL, Mellonig JT, Gher ME. Clinical evaluation of the use of decalcified freeze-dried bone allograft with guided tissue regeneration in the treatment of molar furcation invasions. J Periodontol 1991;62: 264-268.

25. Hammarström L. Enamel matrix derivative (EMDOGAIN®) in the treatment of intrabony periodontal defects. J Clin Periodontol 1997; 24: 705-714.

26. Gestrelius S, Andersson C, Lidström D, Hammarström L, Somerman M. In vitro studies on periodontal ligament cells and enamel matrix derivatives. J Clin Periodontol 1997; 24: 685-692.

27. Zetterström O, Andersson C, Eriksson L, et al. Clinical safety of enamel matrix derivative (EMDOGAIN®) in the treatment of periodontal defects. J Clin Periodontol 1997; 24: 697-704.

28. Hammarström L, Heijl L, Gestrelius S. Periodontal regeneration in a buccal dehiscence model in monkeys after application of enamel matrix proteins. J Clin Periodontol 1997; 24: 669-677.

29. Heijl L, Heden G, Svärdström G, Östgren, A. Enamel matrix derivative (EMDOGAIN®) in the treatment of intrabony periodontal defects. J Clin Periodontol 1997; 24: 705-714.

30. Heijl L. Periodontal regeneration with enamel matrix derivative in one human experimental defect. A case report. J Clin Periodontol 1997; 24: 693-696.

31. O’Leary TJ, Drake RB, Naylor JE. The plaque control record. J Periodontol 1972; 43: 38-40.

32. Silness J, Löe H. Periodontal disease in pregnancy. II. Correlation between oral hygiene and periodontal condition. Acta Odontol Scand 1964; 22: 121-135.

33. Mühleman H, Son S. Gingival sulcus index: A leading symptom in initial gingivitis. Helv Odontol Acta 1971; 42: 195-209.

34. Waerhaug J. Healing of the dento-epithelial junction following subgingival plaque control. II. As observed on extracted teeth. J Clin Periodontol 1978; 49: 119-129.

V.Leković et al


10 years of BaSS

DECEPTIVENESS AND LIMITATIONS OF ROENTGENOGRAMS IN ENDODONTICS; A COMPARATIVE STUDY WITH RADIOVISIOGRAPHY ANDCOMPUTERIZED TOMOGRAPHY

¹Professor, Hacettepe University, Faculty of Dentistry, Department of Endodontics, Ankara-Turkey²Formerly Research and Teaching Assistant, Hacettepe University, Faculty of Dentistry, Department of Endodontics, Ankara-Turkey

¹M. Ömer Görduysus DDS, PhD, Professor²Ümit Acer DDS, PhD

Abstract

This research was designed to compare the limitations and deceptiveness of conventional radiographs with radiovisiography (RVG) and computerized tomography (CT) in determination of procedural errors during routine root canal therapy (RCT). In 50 single and multirooted extracted teeth were used randomly and, custom made procedural errors were created as their anatomical structures allowed to simulate potential errors during RCT. Then they were photographed and the X-rays of all teeth were taken at a standart angle with parallel technique, the second step was taking the X-rays and pictures from proximal aspects to prove the errors. Additionally, RVG and CT images were taken. The RVG images and the X-rays were evaluated comparatively by the same combined group of dentists, endodontists and students to find out the hidden procedural errors on. In RVG group to determine the procedural errors, the failure rate was 79% (The statistical result was significant, p=0,00001). In the X-ray group the failure rate was 71,8% (The statistical result was significant, p=0,0042). We could not obtain the expected outcome from CT. CT could only differ the unfilled canals from others; could not visualize the difference of densities of any filling materials or instruments existing in the canals. We concluded that during the root canal therapy, RVG was the better to finding out the procedural errors in comparison to routine x-rays, but both of them were not precise sufficiently. Keywords: Computerized tomography, procedural error, radiographic limitations, radiovisiography, unfilled canal. Introduct�on

Radiography may be the most accurate and least subjective diagnostic aid available to the endodontist. Further constraints arise from the assessment of equivocal three-dimensional diasease processes that vary over time from two-dimensional radiographic images (1). Although radiographs are inseparable parts of endodontic therapy; e.g. they have some disadvantages; magnification, distortion, superpositioning (overlapping of roots) and they also causes some troubles on diagnosis of bucco-lingual lesions, crack lines. Therefore, sometimes roentgen films lead us to misdiagnosis of cases or they are deceptive for evaluation, examination of root canal fillings and procedural errors. Although conventional periapical radiographs produce acceptable details in the mesio-distal direction, the observation of details in buccolingual dimension is inadequate (2). Other disadvantages of film-based techniques include the time required to process the film interrupting the dental treatment, and variability of image quality associated with chemical film processing. In addition, film processing

M. Ö. Görduysus et al

and storage require much space, and manipulation of film-based images is impossible after processing (3). Everyday, specialists, general practitioners and students perform many root canal treatments and these fillings are evaluated by instructors in dental schools or in private practices by the doctors. But sometimes very successfully looking root canal fillings on X-ray may be a really substandard one because of deceptiveness of radiographs. In recent years, new imaging techniques have been developed with the aim of improving the clarity of the image whilst reducing the radiation dose (4). The first radiovisiography (RVG) system was introduced to the international market in 1987. RVG offers following advantages, e.g. the images are produced nearly instantaneously which there is a reported reduction in the radiation dose to the patient, chemical processing is eliminated, images can be stored electronically or on thermal prints, digital images can be transmitted over telephone lines for consultations or referrals, and RVG images can be manipulated by computerized functions (5). These computerized functions include the manipulation of digital images allowing for variation in image presentation; e.g. contrast and brightness manipulation, digital filtering, zoom function, millimeter gridding, reverse imaging, color intensity mapping, gray-level enhancement, upside-down flip, pseudo-coloring, image recalling and printing. The gray-scale image type relies on image presentation through 256 shades of gray. Reverse imaging converts the digital image to a negative, and color intensity mapping substitutes different colors for gray-scale values (6). The operating principle of these machines is first to obtain a suitable TV image of a specimen, after which each line of the TV frame is then divided into a number of picture points. Each point is assigned a ‘gray-level’ value (usually from 0 to 64) depending upon the brightness or darkness of that region of the specimen. Areas with similar gray-level values may be detected by adjusting ‘thresholds’ to a range which excludes all parts of the image with brighter or darker gray-level values (7).

The most common advantage of radiovisiography system for the patients is the creation of cooperation between the patient and the dentist by examining whole of his treatment on the monitor. By this way the patient gets knowledge about his treatment and trusts the dentist more. In dentistry computerized tomography has been widely used in oral implantation to determine the structure of mandible. CT can image the transversal informations missing from X-rays. It also gives three-dimensional images, and can clearly image the relation-ship between the anatomically neighbouring structures and bone. Although CT has advantages over conventional tomography, it also has some disadvantages such as motion and metal artifacts, increased radiation exposure, limited availability, and higher cost (2).


CT produces its images by dividing the region of the body which is going to be determined into millimeters (8). Unlike the two-dimensional systems, the information derived from any object within the slice is unaffected by variations in the material on either side of the slice (9). CT can provide the necessary information prior to surgery which brings problems that occur during standart implant procedures such as malpositioned implants, damage to neurovascular structures, or intraoperative bleedings threatening the patient’s life (10). The purpose of this study was to determine the limitations and deceptiveness of conventional systems versus radiovisiography (RVG) and computerized tomography (CT) comparatively in certain cases with procedural errors like perforations, broken instruments, inadequate root canal fillings, stripping, superpositioned roots in vivo and in diagnosis statistically. Mater�als and methods Randomly selected 50 teeth were used for this study (14 anteriors, 12 premolars, 24 molars). These teeth were numbered from 1 to 50. The preoperative X-rays of each were taken at the beginning of the study. We have decided what kinds of custom made procedural errors we were going to create as their anatomical structures allow. The procedural errors were broken instruments, over and underfillings, perforations, zipping, stripping, fractures, false canal, inadequate

root canal fillings. These iatrogenic errors were created while filling the canals in some strategic points which are examining difficult with X-rays. The idea when creating these errors were to think clinical procedural errors and select the teeth to reflect such errors. Procedural errors were also selected on the basis that at the normal angle the error would not be seen, but when the mesial and distal aspects were taken, the error was going to be seen from one direction.

Fig 1: The photograph of the sample. The overfilled gutta-percha can be viewed at the perforated apical portion.


Following step, all these teeth were filled with AH26 and gutta-percha and during cleaning, shaping and filling, the hidden errors were created purposely. Then all the teeth were photographed in order to prove the error if the error was seen from outside of the root (Fig. 1). All specimens were mounted in custom-built Plexiglass devices with the attachment of the Rinn positioning ring (Rinn Corp. Elgin, IL) that provided a uniform orientation, constant source-to-object distance of 4.5cm, and object-to-film distance of 2.5cm. The film was held parallel to the long axis of the jaws, and both were perpendicular to the X-ray beam. Kodak Ultraspeed (Eastman Kodak Co., Rochester, NY), size 2 film, was used and exposed for 0.64 s at 70 kVp, 15 mA (Siemens Heliodent). Each specimen was positioned with a standart orientation that allowed the use of parelleling techniques throughout (Fig. 2). Later, these teeth were radiographed from different aspects such as 30

degrees mesial or distal to the teeth where we also tried to keep standardization procedures and tried to prove the iatrogenic errors on different aspects (Fig. 3). After conventional radiographs, the samples were imaged with dental digital radiographic (DDR) techniques and computerized tomography.

Fig 2: The periapical X-ray of the first sample. At that standart (normal) angle no procedural errors can be detected.

Fig3: The periapical X-ray of the first sample from 30 degrees of mesial aspect. There is a broken instrument in the canal which is hidden and not visible at the figure 2. Also an apical zipping and overfilling of gutta-percha can be seen clearly.


Same mounts were used to ensure consistency of angulation and source-to-object distance for the RVG images. Trophy (model 32000) use a radiation source (fixed at 70 kVp and 8 mA) that is integrated with the imaging system. The settings used were that of a lower molar (Trophy designation 48). These exposure parameters for Trophy were measured at 0.25 or 0.29 s (15 and 17 impulses) by using a Mini-X-digital kVp/exposure time monitor (Frank Barker Associates, Pequannock, NJ). Trophy images were taken from the same aspects where we could not see the procedural errors in conventional techniques (Fig. 4). Our aim was to determine the results of the two techniques in the same directions and to examine if RVG was adequate where X-ray images were limited. Trophy images were printed using a UP 850 video thermal printer (Sony). Then enhanced images of each were examined, and printed. The images were manipulated if the observation of details would get better without any other exposures and changing the direction, as the computer functions allowed. The enhancements were such as gray-scale, color intensity mapping, reverse image, contrast and brightness manipulation and zoom. Again the thermal prints were obtained.

Fig 4: RVG image of the first sample taken with the same paralel technique that the procedural arrors cannot be detected on X-ray.

The CT images were obtained at 120 kV and 150 mA by using a spiral CT scan (Siemens Volume Zoom) with a speed of 1mm per rotation and 1mm slice thickness. The images were reconstructed from the raw data to obtain oblique cuts, which were 1mm apart (Fig. 5). We have prepared a questionaire form that includes the X-ray and the RVG images from the same directions that we took first where examining the errors was so difficult, for the randomly selected examiners from the Department of


Endodontics in Hacettepe. They analyzed all the images in a darkroom and noted what they could see as a procedural error. Then they were scored according to the number of their right and wrong answers. After 20 days interexaminer agreement test was also applied to the evaluators. Hypothesis test of two proportions for independent samples was used for the statistical analysis in finding out the success rate of X-ray and RVG alone, and their success according to each other. We ourselves also examined the images of CT and compared with X-rays and RVG for the procedural errors.

Fig5: CT of the second sample with 1mm slice thickness. Second cana is not filled.

Results

According to the statistical results in X-rays, the success rate was 21% indicating highly significant differences (p=0,00001). In RVG, the success rate was 28,2%, with significant diffrences (p=0,0042). And when we compared the failings in determining the procedural errors of both X-rays and RVG to each other, the difference between the rates 79% and 71,8% was found significant statistically (p=0,0051). As a result, RVG was more successful on imaging the procedural errors from the same angle over conventional radiography. When the second image from a different angle was taken, we could examine the procedural errors standing behind the structures in front. The procedural errors in CT images could not be seen clearly, on the contrary we were expecting getting well on 1mm slices and three-dimensional images at the beginning of the study. Superpositions were never seen because of three-dimensional imaging. As there were no superpositions, we could be able to examine the exact number of unfilled canals or roots, but we could not be able


to differ any kinds of materials that have different density in a canal such as gutta-percha, broken instruments, any of the filling materials. D�scuss�on

To obtain maximum information it is necessary to expose at least two radiographs of the area under investigation, one taken at the normal, standart (direct) angle and the other with an altered angulation (11). In endodontics, altering the angulation can be useful to determine the number, location, shape, size and direction of curvature of roots and canals; identify superimposed roots and canals; establish the position of root curvatures; locate the position of root apices in relation to anatomical landmarks; distinguish between anatomical landmarks and radiolucent apical pathology; establish the position of iatrogenic errors (perforations, fractured instruments etc.); distinguish between internal and external root resorption; locate foreign bodies following trauma; establish the position of root fractures or resorptive processes (11). Roots that are superimposed on a standart radiograph can be visualized when a mesial or distal view is taken (11).

In general, because of excessive time loss and cost we happen to take just one radiograph at a standart angle. If the endodontist does not feel any need for further care in cases of canal variations or procedural errors that cannot be detected at a normal angle, then the patient is at risk for a less effective treatment (12). Even if the radiographs that endodontists evaluate look to be perfect, the iatrogenic errors may not be visible on the radiographs at the first angulation. Zakariasen et al. (1984) reported that when raiographs from three different angles were taken of each periapical area, intraobserver agreement rose from 70% to 87%. The data from this study indicate that unreliability of endodontic radiographic interpretation is a serious problem and that incorrect/failure diagnoses are occuring (13).

One of the problem noted with the RVG images was the inability to see a file in the canal when the image was enhanced to make the apex clearly visible. Too much enhancement resulted in a loss of fine detail, such as the tip of the file disappering from the image (14). Conversely, in our study we found that the RVG images were superior to the X-rays because of magnification and enhancement, and especially the procedural errors that were created in small areas were more clearly visualized by that magnification. According to the results of Melius et al. (15), the 0.1mm difference between the digital and conventional radiographs had no clinical significance. Because of this, a dental film read without magnification has about the same amount of observable information as a filmless dental radiograph (16).

The data in our study indicated that digital radiographs have so many advantages over X-rays. These are; less radiation dosage, real-time images, image enhancement during interpretation, image storage without loss of any


knowledge, no need for darkroom, better diagnosis (17). In our study RVG images could not directly visualize the errors different from the X-rays, but because of the enhancement of the images, and the density changes we could make, RVG images could prove the errors where we estimated. It is suggested that the other advantage of digital radiography is environmental protection, because the use of developer and fixing solutions will become history (17).

One of the problems we have met with RVG was the difficulty on placing the hard sensor especially to the palate, because of this, many times we could not be able to see the apices of roots and we had to increase the number of RVG images with extra radiation dosages. Prints of images of RVG can be achieved. The prints do not have quality of the monitor-displayed images and the advantage of operating with the image in the dynamic electronic form is lost (17). This point is in agreement with our study too; an ideal image on monitor cannot be the same as the print of the real image. In spite of all these advantages, filmless dental radiology has not really become popular in the world. Probably the single most important reason for this is cost (16). These systems cost three to five times that of a conventional radiographic system. As with all new technology, it is expected that the cost will drop as the system improves.

In contrast to conventional radiography and radiovisiography, all the anatomical structures and canal variations lying behind a root canal treatment can always be detected in computerized tomography. The most significant advantage of CT that makes it superior to other systems is the imaging ability of transversal details and buccolingual aspects that are missing in other techniques. Buccal and lingual root canals cannot be differentiated on the radiographs because they are superimposed (2). CT has disadvantages over other systems such as motion and metal artifacts, increased radiation exposure, limited availability, and higher cost (2). But the radiation dosage and exposure time used for CT scans are decreasing because of improvement in technology in recent years (2). Reconstructing is time-consuming (9). In addition, the equipment needs too large space and educated personnel for reconstruction is necessary.

If the endodontist in a clinic wants to take a series of radiographs from one patient at once, the radiation dosage is going to be reported as approximately 2 rad, and it is equal to the dosage in CT.

In this study, differing the density of any radioopaque material in a canal such as filling materials, broken instruments, was impossible. We think that the first reason was the existence of silver inside AH26, and the second reason was the pixel spacing of 1-2mm that was too thick for the structure of a canal. The little spread that the silver created in the canal resulted in ignorance of whole image. While passing to a radiolucent area from a dense radioopaque area (the canal with root canal treatment), some kinds of radiolucent artifacts were seen like shadow. These radiolucencies were just artifacts, but they could make the endodontist think that voids were present in the root canal treatment.


In a study of Youssefzadeh et al. (18), the metallic artifacts of the post overlied the buccal root and deteriorated the image quality, and the fracture line could not be detected. In our study, CT resolution was insufficent to render the exact shape of the canals, but we could demonstrate the width of the canals comparatively. In the radiographs we daily take in clinics, extra roots and canals are missing (12). It is suggested that computerized tomography might be used within the field of endodontics when a differential diagnosis or more information was needed for the clinical management of periapical bone lesions. In that regard it was important to know that dose reduction methods had been established so that the technique might be used with low radiation risk (19). Tidmarsh has pointed out (20) that psychological factors played a particularly important role in the process of visual interpretation. It seems that at times an observer sees only what he or she wants to see. It is also suggested that such factors as tiredness, whether the observer was upset, and closeness of involvement with the case might all influence the results. We also think that if the examiners had more experience about the evaluation of RVG images, then the results would have changed so much.

Conclusion

The present study indicates that most of the procedural errors during the endodontic therapy, we could not see on conventional radiographs and could not also be seen on RVG. Either routine radiography or RVG are generally deceptive to determine if any procedural error is exist. On the other hand, a very satisfying looking root canal filling may not be a real good one indeed unless we can not be seen from different aspect or could be evaluated by different techniques. However the advantageous difference of RVG comes from the advantage of magnification and manuplation of the images even if it is too little. We suggest that because of the advantages that RVG has brought, it should be routinely used in the field of endodontics. Additionally, whenever the two-dimensional system (conventional technique) is used, we suggest that the second angulation should be used (paralactic film technique). We suggest that CT should just be used at times of need such as implantology or apical surgery; it should be used as a last applied technique. Overall to evaluate the quality of the RCT performed, the hidden and unvisible (unexamined) procedural errors must be keept in mind and their potential dangers to failure of the case shouldn’t be figured out. Using the recent and contemporary technology in the field of endodontics and dental diagnostics is very critical factor to improve the success rate, patient satisfaction and clinical practice.

This paper was presented at the VIII Congress of BaSS – Tirana, Albania


References 1. Lavelle C.L.B., Wu C.J. (1995) Digital radiographic images will benefit endodontic services, Endod. Dent. Traumatol. 11:253-260. 2. Velvart P., Hecker H., Tillenger G. (2001) Detection of the apical lesion and the mandibular canal in conventional radiography and computed tomography, Oral Surg. Oral Med. Oral Pathol. Oral Radiol. 92:682-688. 3. Versteeg C.H., Sanderink G.C.H., Van der Stelt P.F. (1997) Efficacy of digital intraoral radiography in clinical dentistry, Journal of Dentistry 25:215-224. 4. Griffiths B.M., Brown J.E., Hyatt A.T., Linney A.D. (1992) Comparison of three imaging techniques for assessing endodontic working length, Int. Endod. J. 25:279-287. 5. Mistak E.J., Loushine R.J., Primack P.D., West L.A., Runyan D.A. (1998) Interpretation of periapical lesions comparing conventional, d,rect digital, and telephonically transmitted radiographic images, J. Endod. 24:262-266 6. Barbat J., Messer H.H. (1998) Detectability of artificial periapical lesions using direct digital and conventionl radiography, J. Endod. 24:837-842. 7. Pitts N.B. (1984) Detection and measurement of approximal radiolucencies by computer-aided image analysis, Oral Surg 58:358-366. 8. Tachibana H., Matsumoto K., Applicability of X-ray computerized tomography in endodontics (1990) Endod. Dent. Traumatol. 6:16-20. 9. Hounsfield G.N., Computerized tranverse axial scanning (tomography): Part 1. Description of system (1973) Br. J. Radiol. 46:1016-1022. 10. Dula K., Mini R., Van der Stelt P.F., Lambrecht J.T., Schneeberger P., Buser D. (1996) Hypothetical mortality risk associated with spiral computed tomography of the maxilla and mandible, Eur. J. Oral Sci. 104:503-510. 11. Fava L.R.G., Dummer P.M.H. (1997) Periapical radiograpyhic techniques during endodontic diagnosis and treatment, Int. Endod. J. 30:250-261. 12. Robinson S., Czerny C., Gahleitner A., Bernhart T., Kainberger F.M., Dental CT evaluation of mandibular first premolar root configurations and canal variations (2002) Oral Surg. Oral Med. Oral Pathol. Oral Radiol. Endod. 93:328-332. 13. Kenneth L., Zakariasen, Scott D.A., Jensen J.R., Endodontic recall radiographs: how reliable is our interpretation of endodontic success or failure and what factors affect our reliability? (1984) Oral Surg. Oral Med. Oral Pathol. 57:343-347. 14. Leddy B.J., Miles D.A., Newton C.W., Brown C.E., Interpretation of endodontic file lengths using RadioVisioGraphy (1994) J. Endod. 20:542-545. 15. Melius B., Jiang J., Zhu Q., Measurement of the distance between the minor foremen and the anatomic apex by digital and conventional radiography (2002) J. Endod. 28:125-126. 16. Vandre R.H., Webber R.L., Future trends in dental radiology (1995) Oral Surg. Oral Med. Oral Pathol. 80:471-478. 17. Wenzel A., Gröndahl H.G., Direct digital radiography in the dental office (1995) Int. Dent. J. 45:27-34. 18. Youssefzadeh S., Gahleitner A., Dorffner R., Bernhart T., Kainberger F.M., Dental vertical root fractures: value of CT in detection (1999) Radiology 210:545-549. 19. Cotti E., Vargiu P., Dettori C., Mallarini G., Computerized tomography in the management and follow-up of extensive periapical lesion (1999) Endod. Den. Traumatol. 15:186-189. 20. Tidmarsh B.G. (1987) Radiographic interpretation of endodontic lesions- a shadow of reality, Int Dent. J. 37:10-15.



10 years of BaSS

POSSIBILITIES OF OCCLUSAL THERAPY IN MANAGEMENT OF CRANIOMANDIBULAR DISORDERS

Faculty Of Stomatology, Clinic For Prosthodontic,University Of Belgrade

Darinka Stanišić–Sinobad, ProfessorSlobodan Dodić, Associate Professor

Introduction

Craniomandibular disorders ( CMD) are considered to be one of the signifficant problems of contemporary man resulting greatly from his stressfull environment and way of life. Affecting mainly the structures of the orofacial system ,this group of disturbances has become one of the challenges for the dental proffesion today.

Over the years functional disturbances of the masticatory system have been identified by a variety of terms: Costen syndrome1, temporomandibular joint dysfunction syndrome2, functional temporomandibular joint disturbances3, pain disfunction syndrome4, myofacial pain – dysfunction syndrome5 and so on. Currently in the literature the term “ craniomandibular disorders” is used interchangeably with the term “temporomandibular disorders”6,7,8. These terms , which gained popularity, have been defined as collective terms embracing a great number of clinical problems that involve various functional and structural disturbances of temporomandibular joints, orofacial muscles and associated structures. Over the last two decades the terms craniomandibular disorders( CMD) and temporomandibular disorders (TMD) have been used to express a comprehensive set of head and neck conditions , but the most common symptoms and signs mostly specific to the orofacial region include:

- dull aches or pains anterior to the ear , sometimes extending to the face , head and neck,

- tenderness of the muscles of mastication - joint noises ( clicking , crepitations) and - limitations and deviations of jaw movements8,9,10,11,12

Epidemiology

Since the beginning of the l990s a considerable number of cross-sectional and longitudinal epidemiologic studies from many different parts of the world have been published , but those from the Scandinavian countries dominate.13,14,15,16,17,18,19,20 The results of all these studies show that symptoms and especially signs of CMD are quite common in these populations. The longitudinal studies showed an increase of symptoms and signs with increasing age, from childhood to young adults and the middle-aged. Reported sex differences are actually small. The reported figures from patients studies vary from 3: 1 to 8:1 female to male, but epidemiological surveys show that signs and symptoms of CMD are present in both sexes in equal proportions. However, women usually seek medical advice more than men


and may be more willing to admit the appropriate treatment. This fact probably accounts for the disproportion between the sexes in the patient studies.10,21

The signs and symptoms of CMD presented in dfferent studies vary in character and frequency. The definitions are also different from study to study. The prevalence of symptoms has been recorded through various kinds of methods such as telephone calls, personal interviews, or questionnaires of different design. The results have been evaluated by various disfunction indexes ( Helkimo 1974, Schiffman and Fricton 1990 ). These different methods necessarily give a variety of contrasting results what makes it difficult to compare different sudies.22

Summarising the results of numerous epidemiological studies it can be concluded that 50- 75% of the population have signs of a disorder at some stage during their life, whereas an estimated 20%-25% of the population have symptoms of a craniomandibular disorder. However, only 3%-4% of these seek some kind of treatment.

It is interesting that studies which examine the prevalence of CMD in adolescents and young adults report that an average of 42%- 76% of these populations showed at least one clinical sign of CMD.23,24,25,26,27 In the study which included 500 persons between 18 and 25 years of age from various regions of Republic Serbia , the signs and symptoms of CMD were found in 72,3% of young persons from Vojvodina, , in 56,3% of persons from Belgrade and in 71,5% of persons from the region of central Serbia, that is , an average of 65,4% of young persons in Serbia had at least one clinical sign associated with CMD28 ( graph 1). The presence of signs and symptoms of CMD, as well as the presence of occlusal discrepancies in these population groups were evaluated using the Helkimos dysfunction and occlusal indexes 29.The prevalence of certain signs and symptoms in the group having the positive Helkimos disfunction index is summarised in table 1.

D.Stanišić–Sinobad et al

Graph 1.- Prevalence of CMD in Serbian adolescent population28

Di>072.3%

Di=027.7%

73

28

Di>056.3%

Di=043.7%

1190

Di>071.5%

Di=028.5%

138

55

Di>065.4%

Di=034.6%

327173

Vojvodina(n=101)

Belgrade(n=206)

Central Serbia without Belgrade (n=193)

Total n=500


Table 1

The prevalent signs and symptoms of CMD in individuals having the positive Helkimo’s dysfunction index ( Di>0)28

Classification

Many classification systems for CMD have been proposed over the years in an attempt to decrease confusion and controversy which still exists concerning the etiology, pathology and treatment modalities in this area. One of the simplest and most promissing of these at the moment is the classification proposed by the American Academy of orofacial pain that is integrated with an existing medical diagnostic classification used by the International Headache Society.9 This classification recognises the three main categories of CMD: The TM joint diaorders, masticatory muscle disorders and congenital and developmental disorders with many subcategories among each of them. Although all these categories can cause several or all of the symptoms, this classification offers a meaningful approach to diagnosys and management of patients suffering from CMD.

Nr.of individuals having the

positive Helkimos

dysfunction index

Signs No. of individuals

% Symptoms No. of individuals

%

327 ( 65,4%)

Limitation in jaw

movements deviations

(deflexions) on jaw opening

245 74,9 Pain on mandibular movements

17 5,2

Joint clicking on opening (closing )

126 38,5 Palpatory sensibility

of TMJ

19 5,8

Palpatory sensibility

of masticatory

muscles

34 10,4


Etiology

One of the main problems where CMD is concerned is the poor understanding of the etiology of this disturbances in each individual patient. A number of hypotheses about the primary causes of CMD have been suggested through the literature, but generally overall agreement exists only in that , the etiology of CMD is extremely complex, heterogenous and multifactorial. The great number of etiologic factors , well known to every clinician dealing with these problems can be summarised as followes:

- the predisposing factors which increase the risk of CMD, - the initiating factors which cause the onset of CMD , - the perpetuating factors which enhance the progression of CMD and

interfere with healing.9,30,31,32

The dividing line between these categories is not clear and each of them involves a number of various factors that very often mix and cover each other.However , the main ones which can be derived from very heterogenous etiology and must never be overlooked are:

- the biomechanical factors ( macro and micro trauma), - the psychological factors ( emotional stress, personality

characteristics), - the genetic factors ( congenital, developmental , postural disturbances

), - the occlusal factors ( malocclusions, occlusal interferences, lack of

posterior dental support).11,12,30,32 The role of occlusion in etiology of CMD

The influence of occlusal codition in onset of CMD has been strongly debated for many years and still is a source of controversy. Up to the eighties in the last century , the occlusal factors such as the presence of uncured malocclusions, discrepances between intercuspal and retruded contact position greater than two milimeters, retrusive and nonworking side interferences and loss of posterior teeth were considered to be the primary causes of CMD. Many famous names starting with Costen J.B. 1934. supported this hypothesis .1,2,3,4,5,31,



However, the contemporary scientific and clinical evidence did not confirm a direct correlation between the occlusal factors and CMD symptoms. In fact , many scientist deny any influence of occlusion in the onset of CMD. It appears that many individuals are able to adapt to occlusal discrepances and to function within tolerable limits without the emergence of signs and symp-toms of CMD.9,11,32 Between these oposite groups of opinions are those who believe that occlusion does not have a primary role in the etiology of CMD , but it has a secundary influence and can exacerbate symptoms after the onset of CMD caused by other sources such as trauma, congenital deformities, systemic deseases and what has been particularly emphasised in the last two decades , emotional stress and the personality factor.33,34,35,36 Pullinger et all 1993. concluded that no single occlusal factor could be connected directly to signs and symptoms of CMD in the investigated group. The similar occlusal condition persisted very often in healthy subjects.However, some occlusal features such as the skeletal anterior open bite, the slide between retruded contact position and intercuspal position greater than 2 mm , overjets of greater than 4mm and five or more missing posterior teeth , occurred mainly in subjects with CMD and were rare in healthy subjects.37 In a cross-sectional study including 500 young persons between 18 and 25 years of age from various regions of Serbia Dodic S. (2003.) found that among 229 persons without occlusal discrepances ( Helkimos occlusal index Oi =0) , 135 (58,95% ) showed the signs and symptoms of CMD ,that is ( Helkimos dysfunction index Di>0).However, in the group of 271 persons with evident occlusal discrepances (Oi >0), 192 (70,85%) of persons showed the signs and symptoms of CMD ( Di >0). The multiple logistic regres-sion analysis ( χ2- test , ODDS RATIO ) showed the risk of onset the CMD in the group having occlusal discrepances to be 1,2- 2,5 greater than in group without such discrepances ( table 2. ).28

Table 2. Distribution of subjects according to the values of the Helkimos dysfunction index (Di) and occlusal index (Oi) in the sample of 500 young adults from various regions of Serbia28

The relationship of occlusal factors and CMD is an extremely critical issue in dentistry. It is obvious that occlusal condition should be considered only as one of many factors that can contribute to the development of CMD. However, to appreciate the role of occlusion in CMD one must better understand the dynamic , functional relationship which exists between the individual occlusal condition , TM joints and neuromuscular system. This dynamic relationship is responsible for all mandibular movements and for continous protection of all orofacial tissues. Having this relationship in mind it can be concluded that an individual occlusal condition can influence the TM joints and masticatory muscles in at least two ways: - directly by distribution of forces elicited by masticatory muscles and - indirectly by monitoring muscle function via the bio feed-back mechanism. a) It is assumed that tht occlusal complex accepts the majority of compresive forces acting during various functions of the masticatory system. In the normal conditions with preserved natural dentition TM joints are exposed only to the shear forces of various intensity. The fact , that articular surfaces of the joint are lined with dense fibrous tissue ,with the fibrocartilage disc interposed between them is a big functional advantage of the TM joints. Owing to viscoelasticity of the fibrous articular layer and presence of viscoelastic disc the forces transmitted to the joints are spread uniformly , minimising damage.38,39 However, the optimal distribution of functional forces on the joint tissues can be expected only if a harmony exists between the individual occlusal condition and the musculoskeletaly ( orthopedicaly ) stable relationship of the articular components.12

Occlusal index (Oi)

Oi = 0 Oi > 0 Total Dysfunction index

(Di) No % No % No %

Di=0 94 41.05 79 29.15 173 34.6

Di>0 135 58.95 192 70.85 327 65.4

total 229 100 271 100 500 1002- test 2=7.76 ; p<0.01.


Unfortunately, such a harmony can rarely be found among adult individuals and even among children. It is much more common to find an unstable occlusal condition due to the loss of posterior teeth, periodontal deseases, migrations of teeth, exccesive abrasion of the teeth and various kinds of interferences during mandibular movements. In such conditions , when the teeth are brought into the maximum possible occlusal contact and loading occurs the condiles can loose their optimal orthopedic stability. Unusual movements of the condiles ( translatory shift between the condiles and their discs) can occur in an attempt to gain stability. Over a period of time, these movements become a source of continously repeated microtrauma which can lead to damage of joint tissues and a series of intracapsular disorders.34,35,40,41,42 Whether an intracapsular disorder will develop or not depends on individual adaptability of the joint tissues, degree of joint instability and amount of loading. According to current studies the discrepancies between the musculoskeletaly stable position of the condyles and maximum intercuspation greater than 2mm increase significantly the risk of intracapsular disorders.37 However, the main factor that influences the likelyhood of developing CMD is the amount of loading acting on teeth and TM joints during various functions of the orofacial system. For example, in bruxing individuals with unstable joint relationships , CMD is far more likely to be developed than in individuals with the same degree of joint instability, but without bruxing habits .12 In this way it can be explained why CMD do not develop in subjects with severe malocclusions and develop in others with minor occlusal discrepances. b) The neuromuscular harmony is essential for functional ability, comfort and longterm stability of the orofacial system. Every mandibular movement is generated and monitored owing to the reciprocical action of the peripheral and central nervous system and the sinergic answer of the masticatory muscles. Functional and structural disturbances in any one of the components of the OF system may be reflected by functional or structural disorders in one or more of its other componnts. In that regard , the occlusal contact patterns of the teeth ( e.g. malocclusions, occlusal interferences) can influence the activity of masticatory muscles and even induce masticatory muscle pain.43,44,45 Activities of the masticatory muscles can be divided into two categories: functional muscle activitieses which include chewing, speaking and swalloving and parafunctional activities which include clenching and grinding of the teeth , various oral habits and any increase in the level of muscle tonus that is not necessary for normal function. Functional activities of masticatory muscles enable the necessary functions of the OF system to be performed with minimum forces and with minimum


damage to any structure. These activities are directly influenced by the occlusal condition and bio feed- back mechanism . The parafunctional activities are very common among adult population and even among children.46,47,48 The etiology of diurnal parafunctional activities and nocturnal bruxism is not well known. It seems that nocturnal bruxism is generated at the CNS level and that emocional stress has an excitatoy effect on this activity .12,46,49,50 The influence of interfeering tooth contacts on parafunctional activities is still debating. Many references deny such an influence51, but the other point to the direct relationship between the occlusal interferences and bruxism.52 However, all of them agree that parafunctional activities have an damaging effect on the health of all orofacial structures and may be responsible for their breakdown. There are many reasons for that. The forces of tooth contact during parafunctional activities are much greater than forces during normal functional activities. Instead of being inhibited by tooth contacts , they can actually be provoked by certain tooth contacts. Tooth wear patterns suggest that most parafunctional activities occur in eccentric positions of the mandible what results in application of heavy forces to a few teeth in an unstable joint position. Instead of normal isotonic muscle contraction the parafunctional activities elicite the nonphysiologic isometric muscle contraction over a long period of time. The result of this type of muscle function is an increase in metabolic by-products within the muscle tissues with the consequenting symptoms of fatique, pain and spasm.12

General concepts in management of CMD

Successful management of patients with CMD and orofacial pain is very often a difficult and confusing task that exceeds the professional knowlidge of a dental clinician., especially when the problem is chronic and is accompanied by psychological factors.Although many treatment modalities have been recommanded , non of them are effective always for every type of disorder and for every patient. Effective treatment selection depends on thorough understanding of the disorder and its etiology and accurate diagnosis.

The management program for a CMD patient can be divided into three parts: emergency therapy, initial or short-term therapy and long-term management. The initial therapy that is directed toward informing and educating the patient with respect to his problem and offering him the emergency care is essential for succesful management of CMD. Initial therapy should be reversible and palliative.The posttraumatic pain, an active triger point or an acute disc displacement followed by restricted mandibular


oppening may require emergency treatment. It always includes patient education, some home-care instructions and certain medication to control pain and inflamation , but may involve also the intraoral apliance therapy, physical therapy, pharmacotherapy, and some kind of behavioral and psiycho-therapy. Patients who respond to initial or short term therapy with a significant reduction in pain and dysfunction should be reevaluated at the conclusion of initial therapy . At this point the clinician should make a decidion on which course of long-term management to pursue and determine the probability of effectiveness of each of the various treatment modalities . Anyhow, various modalities of irreversible occlusal therapy, psychotherapy, farmacotherapy and sometimes surgery should be considered at this point.3,7,11,12,33 The occlusal therapy

The influence of occlusal condition in development of CMD is still a debating question. However, there is a lot of evidence that muscle hiperactivity as a consequence of interfeering occlusal contacts , or parafunctional activity may present a potential danger to all orofacial structures and even leed to CMD symptoms. In that regard the occlusal therapy should be considered as one of the important modalities in management of CMD . Occlusal therapy is considered to be any treatment that is directed toward altering the individual mandibular position or occlusal contact pattern . There are generally two modalities of occlusal therapy:

- reversible occlusal therapy that uses various types of occlusal apliances and alters the patients occlusal condition temporarily and

- irreversible occlusal therapy that encompasses any treatment in dentistry which changes the patients occlusal condition or mandibular position permanently such are the : selective grinding, restorative procedures , orthodontic treatment or combination of these treatments.

Generally, the occlusal therapy is indicated always when the patients occlusal contact pattern results in an unphysiologic muscle function or unstable position of one or both joints. Indications for reversible occlusal therapy are very wide. Actually , the reversible apliance therapy is the initial treatment in majority of patients suffering from a masticatory musce or TM joint disorder.. However, when the irreversible occlusal therapy is concerned much caution must be involved in establishing the proper diagnosis and


treatment plan. Irreversible ( permanent ) occlusal therapy in patients with signs and symptoms of CMD is indicated only when the great probability egsists that the primary or signifficant contributing ethiologic factor creating CMD is the patients occlusal condition or unstable mandibular position.12

Selecting the therapeutic mandibular position for occlusal therapy

The first step in performing an appropriate occlusal treatment in patients with CMD is to select the optimal reference ( therapeutic ) position of the mandible which should be used in fabrication of temporary apliances and if needed in fabrication of permanent restorations. The choice of therapeutic mandibular position depends primarily on the basic goals of occlusal therapy. If the basic goal of occlusal therapy is to relieve pain and to enable the recovery of joint tissues in an acute disc displacement situation , the therapeutic position of the mandible should be that position nearst to intercuspal position which eliminates the symptoms.However, if there is evidence that patients occlusal condition created the unphysiologic muscle function or unstable condilar position , or the contributing factors such as bruxism elicited muscle hyperactivity and overloading of teeth and joints, the basic goal of occlusal therapy must be to achieve harmony between the occlusal contact pattern, joint stability and muscle function. In these situations the therapeutic position of the mandible should be that position which ensures the physiologic optimal relationship of joint components and orthopedic stability of the joints. According to the latest references this position implies that the condyles assume the most superior-anterior position in their fossae, resting against the respective articular eminences with the articular discs properly interposed when the upper and lower teeth achieve the maximum number of occlusal contacts and the loading occurs. This position of the mandible is also designated as the centric relation position because of its reproducibility and a possibility of a mandibular hinge movement.3,11,12

However, to accept the idea of establishing a maximum number of intercuspal contacts in the position of the mandible when the condyles assume their most superior-anterior position in the fossae ( which means centric relation ), one should have in mind that the concept of centric relation has changed in recent years. We should never more think about the centric relation as a” most retruded position of the mandible , or the “ligamentous position “ of the condyles in the fossae.3,12,52,53 In fact , the term “centric relation “ itself can cause confusion , because in occlusal therapy we are actually looking for an orthopedicaly stable position of the codyles that garanties the healing of joint tissues , relaxation of elevator muscles and efficient function with minimum forces.


Reversible occlusal therapy( appliance therapy)

Occlusal applinace therapy is a noninvasive and reversible biomechanical method of managing pain and disfunction of temporomandibular joints and associated musculature. The occlusal applinance ( splint ) is a removable interocclusal device made of hard acrylic resin which covers the upper ,or lower dental arch .

a. b. Fig. 1. a.- The stabilisation splint made for the upper dental arch, maximum nubber of contacts in centric relation b.- Canine guidance established with the splint. The most commonly used appliance therapy is the stabilisation appliance therapy. There is rich evidence in the current literature that proves the benefitial influence of stabilisation appliances in reducing the CMD symptoms in 70% - 90% of patients , particularly when used in conjunction with other treatment methods.54,55,56,57,58 The beneficial effect of stabilisation appliances in majority of patients suffering from CMD is still not entirely clear. According to occlusal theory these appliances change the patients occlusal condition and create an occlusal scheme that is more able to withstand any strong parafunctional forces placed on the masticatory system.They stabilise the condyles in their physiologicaly optimal position , decrease the joint loading, provide the maximum number of contacts between the mandibular supporting cusps and appliances flat plane , increase the vertical dimension of occlusion, provide an optimal canine guidance ( fig1.a,b).In this way they help the hyperactive masticatory muscles to rest and to regenerate their normal


function what eliminates pain, muscle spasm and tenderness in majority of patients.

According to muscular theory these appliances decrease significantly the myoelectrical activity of mandibular elevators during clenching and also their postural activity.59,60 Beneficial results of stabilisation appliance therapy are attributed also to minimal changes in vertical dimension of occlusion and finaly to placebo effects. It is difficult to assess what role an increase of vertical dimension plays in the benefit from occlusal splints, but it was demonstrated that dysfunction symptoms were reduced faster and more completely in the patients with the greatest increase in vertical dimension.61 These type of appliances are most beneficial in patients with symptoms related to a myogenous disorder, for egsample in patients with diurnal parafunctional activities or nocturnal bruxing events, in patients with local muscle soreness, chronic centrally mediated mialgia and posttraumatic retrodiscitis. In patients with symptoms related to an anterior disc displacement and clicking joints an anterior repositioning splintis mach more recommended. This is an interocclusal device that stabilises the mandible in an anterior ( protrusive ) position for a certain period of time(fig.2.)

Fig.2.a,b - The anterior repositioning splint

a

b.


The aim of this treatment is to stabilise the mandible temporarily in an positon that eliminates symptoms of an intracapsular disorder and enables the recovery of the retrodiscal tissues. The proper appliance selection depends upon an accurate diagnosis, patients occlusal condition, presence of parafunctional habits, patients occupation and esthetic requirements. Sometmes one type of appliance may not suffice. A comlex case with pathologic tissue changes , involving both joint and muscle components may need a combination of appliances. Irreversible occlusal therapy

The main objectives of the reversible occlusal therapy in patients with CMD are to relieve pain and to restore an acceptable level of orofacial functions. When the patient has reached a certain improvement and has attained acceptable function , the need for long-term management should be assessed. The patient who has been asymptomatic for a minimum of three months should be weaned from the splint. The objective of the weaning process is to eliminate the occlusal splint and to allow the patient to return to his former occlusion. At this delicate point several important questions must be answered before beginning of any other treatment: - should the appliance therapy be continued with a decreased amount of time of splint usage, or a repositioning splint should be converted to a stabilisation one ? - should the splint be completely eliminated and the patient returned to his own occlusion ? - is there any need for a more complex irreversible occlusal treatment? - which modality of irreversible occlusal treatment should be performed in that particular patient?

Answers to these questions can be obtained after a detailed evaluation of patients general health, , an evaluation of patients occlusal condition concerning its stability and after identification of all perpetuating and contributing factors that can egsacerbate the symptoms of CMD. Using a splint on a long-term basis can be effective , but also may cause remodelng of the TMJ surfaces and undesirable occlusal changes. If the primary etiologic factor creating the CMD was emotional stress, accidental trauma, or a systemic desease , and the patient is symptom free after 2-3 months of wearing a stabilisation splint , the splint can be eliminated after a period of time weaning. Permanent (irreversible ) occlusal therapy, that is directed towards altering permanently the patients egsisting contact pattern or mandibular position is indicated only when signifficant evidence


egsists that the primary etiologic factor creating the CMD was prevalent the patients occlusal condition.3,7,9,11,12,29,30

Long-term management must be directed primarily at eliminating or minimising those contributing factors that could cause returning of signs and symptoms of CMD.In spite of the fact that occlusal factors by themselves can not cause the onset of CMD , they are main contributing factors that may exacerbate and perpetuate symptoms of CMD emerged for other reasons ( bruxism, trauma, emotional stress ).11,12 The presence of parafunctional activities specifically nocturnal bruxism and clenching must be carefully egsamined. These habits can reverse any progress achieved by reversible occlusal therapy and must be considered in long-term management. Modification of patients bahavior, habits and lifestyle are sometimes of essential importance.

The main objective of every long –term occlusal treatment is to provide a physiologic occlusion that will stabilise the condyles in their orthopedically optimal position, that will distribute the occlusal forces over the dental arches and joints without overloading any structure and provide an acceptable , symptom free function. Generally, the following modalities of irreversible occlusal therapy can be performed in patients with CMD :

- selective grinding ( occlusal equilibration ), - restorative treatment using the occlusal fillings, fixed or removable

prosthetic appliances, - ortodontic treatment , or - combination of these treatments.

When irreversible changes of the egsisting occlusion are indicated , the

patients occlusal status should be carefully evaluated through the use of intraoral egsamination of the present teeth and their parodontal tissues , through analysis of diagnostic casts mounted in an acceptable articulator and analysis of selected dental and cephalometric radiographs. Both, the static and dynamic relationships of dental arches should be assessed and all occlusal interferences and deficiences identified because they can contribute to occlusal and joint instability and endanger the benefitial results of reversible occlusal treatment. According to current references all irreversible therapeutic procedures should be performed in accordance with the concept of mutually protected occlusion. This will establish :

- maximum number of occlusal contacts in the chosen , therapeutic mandibular position ( ICP, CR, or another therapeutic position),

- elimination of vertical and lateral components of RCP-ICP slide , - axial loading of all posterior teeth during mandibular closure,


- sufficient anterior or canine guidance to disoclude posterior teeth during excursive mandibular movements,

- an stable free-way space in the rest position of the mandible. Sequence of treatment procedures in occlusal therapy of patients with CMD

The proper treatment sequencing is an important part in managing the patients with CMD. The reversible , noninvasive forms of occlusal therapy should always be used before any other modality of treatment. The results of reversible occlusal therapy are most important in determining the need for more invasive , irreversible restorative procedures. If the initial , reversible treatment fails to eliminate symptoms , the diagnosis must be reegsamined for accuracy. Failure of the reversible apliance therapy suggests that patients occlusal condition did not create the CMD symptoms ,or the patient did not fulfill all therapeutic requirements.

If the irreversible occlusal therapy is indicated , the best way is to start with the least amount of dental alterations that will fulfill the treatment objectives. Treatment may range from simple equilibration of few occlusal interferences to full-mouth reconstruction, orthodontics , orthognathic surgery , or a combination of these modalities.

Occlusal equilibration or selective grinding is indicated in cases where minor changes on dental surfaces are needed to achieve the desired occlusal contact pattern. Since the selective grinding must always be accomplished among the enamel , the great occlusal discrepances can not be resolved in this way. Another factor that must be considered during equilibration procedure is the vertical dimension of occlusion. The initial apliance therapy increases VDO, while equilibration , if not done carefully , can reduce VDO. In some patients this can cause an exacerbation of symptoms. However, in others reduction of VDO can be beneficial part of overall occlusal therapy ( patients with the long-face syndrome and anterior open bite ) .11

If selective grinding is not sufficient in elimination of occlusal disrepances , restoration of the teeth may be indicated using various types of fillings, inlays ,onlays or fixed and removable prosthodontic restorations. In the cases with great inter and intra arch discrepances prosthodontic treatment alone will not be sufficient in achieving the stable occlusion and a satisfactory maxillomandibular relationship. In such cases an orthodontic treatment should be performed firstly , and after that an appropriate prosthodontic treatment.



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49. Lazic V. Analiaz mišične aktivnosti i stanja okluzije u pacijenata sa noćnim parafunkcijama. Doktorska disertacija , Univerzitet u Beogradu 2003.

50. Kirveskari P., Le B.Y., Salonen M., Forsell H., Grans L. …Effect of elimination of occlusal interferences on signs and symptoms of craniomandibular disorder in young adults. J.oral Rehabil 1989., 16(21-26)

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10 years of BaSS

EVALUATION AFTER ER:YAG LASER APPLICATION IN ENAMEL, DENTIN AND PULP

Faculty of Dentistry, Cyril and Metodi UniversitySkopje,Macedonia.

Marija Stevanovic

Summary

Ever since lasers for medical applications became available, attempts have been made to use them in dentistry. Once decay or other pathologies are discovered, the Er: YAG laser is a convenient instrument to perform safe, minimally invasive treatment. Using Hydrokinetic energy, the laser allows the operator to eliminate the thermal damage, vibration, and micro fractures of enamel associated with even the most sophisticated and advanced high-speed hand pieces available today. The objectives of this study are:

� To examine the morphological and compositional changes of human enamel and dentin after laser irradiation.

� To investigate the pulpal response to cavity preparations in healthy human teeth using the Er:YAG laser.

In order to answer these questions the following methods have been used:

� Ten intact extracted teeth were irradiated with Er:YAG laser set at 350 mJ energy per puls and 6 Hz frequency. The morphology and the cavities in enamel and dentin were investigated on scanning electron microscope.

� A total of 10 healthy firs premolars that were to be removed due to space problem were used and prepared with the laser. Cavities were superficial, media and deep. Following the laser irradiation the cavities were closed temporarily and teeth were extracted after 24 hours. Specimens were fixed, decalcified for light microscopy.

SEM observations showed that the cavities produced by the laser irradiation in enamel were crater-like round or slightly oval with clear margins and no signs of melting or carbonification. Some favourable morphological changes of the irradiated dentin were achieved by the Er:YAG laser: highly irregular surface and absence of smear layer which provides a suitable surface for physical bonding mechanisms of composite materials. Results also showed that Er:YAG laser under investigation is a pulp preserving hard tissue drilling method, if used with specific energy and frequency settings at wavelength of 2,94 μm. Key words: Er:YAG laser, dentin, enamel, pulp

M.Stevanovic

Laser is an optical electronic device that produces a light beam, which can be projected trough space with no dispersion or loss of potential. Ever since the use of first lasers in medicine, there have been attempts to use them in dentistry, too. Great expectations that laser can take the place of classical dental preparation caused damage on hard dental tissue and pulp. In conventional laser applications, tissue is ablated by evaporating and pyrolysis.

This procedure is unsuitable for removal of dental hard tissues due to high melting and evaporating temperatures. The development of a new solid-state laser, the Er:YAG laser, made accessible a new laser wavelength that has the special characteristic of coinciding with the maximum absorption peak of water. Unlike other lasers, this high degree of absorption combined with the pulsed operating mode of the Er:YAG laser permits excellent material ablation rates in conjunction with minimal thermal influence.

The depth of penetration of the Er:YAG laser beam in water is approximately 1μm. The absorption of hydroxylapatite also has a relative maximum at 2,94μm but this is negligible compared to the high degree of absorption in water. The radiation is absorbed in outermost surface layers of the tissue. Even the low portion of water contained in enamel is sufficient for good absorption. Since the impact point of the focused laser beam is limited to a small area minimising heating of the surrounding area.

The effective ablation of dental hard tissues using the Er:YAG laser has been applied in cavity preparation, and it proved to be effective in caries removal1,2. The efficiency of the Er:YAG laser to ablate hard dental tissues has been found to be comparable to preparation with conventional drills and burs. Compared to other laser systems, Er:YAG laser can ablate dental hard tissues more effectively, due to the high absorption in both water and hydroxyapatite and since it minimally increases temperature in the surrounding tissues, especially when constant cooling is achieved with water spray3. When hard dental tissues were irradiated by an Er:YAG laser accompanied with water spray, not only the temperature increase was minimal but also there was no severe carbonization, melting or cracking of the material.

Histological studies in animals showed that pulp response to Er:YAG laser is similar to the response to high-speed handpieces, and no pulpal inflammatory responses were observed when water-cooling was applied4, 5. The purpose of this study was to examine the morphological and compositional changes of human enamel and dentin after laser irradiation and to investigate the pulpal response to cavity preparations in healthy human teeth using the Er:YAG laser.


Material and method

Ten intact extracted teeth were irradiated with Er:YAG laser emitting at 2,95μm, set at 350 mJ energy per puls and 6 Hz frequency for enamel preparation and 250 mJ energy and 4 HZ frequency for dentin preparation under continuous water mist. The morphology and the cavities in enamel and dentin were investigated on scanning electron microscope and compared to the effect of the conventional method.

A total of 10 healthy firs premolars that were to be removed due to space problem were used and prepared with the laser. Cavities were superficial, media and profunda. Following the laser irradiation the cavities were closed temporarily and teeth were extracted after 24 hours. Specimens were fixed with 10% formalin solution, decalcified and sectioned for light microscopy.

Results

SEM analysis after laser irradiation on enamel showed crater-like formations (Fig.1.), round and oval with presence of flakes and scales along the wall. There was no evidence of carbonisation or melting of the enamel. Some samples showed few cracks in the surrounding area (Fig.4). The crater showed a conical shape and a well-defined margin (Fig. 2.). High magnification showed an ablation pattern of enamel rods that resembled a honeycomb (Fig.3). SEM observations after Er:YAG laser irradiation on dentin with water-cooling showed a scaly or irregular surface and absence of smear layer with exposed orifices of the dentinal tubules (Fig.5). The intertubular dentin suffered more ablation than the peritubular dentin causing the tubules to protrude (Fig. 6). Irradiation without water spray for cooling created molten lava-like sites, severe cracking of the dentin, and irregular structure with micro holes (Fig. 7) Light microscopy after preparation of superficial and media cavities with Er:YAG laser didn’t reveal any pathological changes in the pulp tissue which remained normal with all the components: central zone, cellular zone, acellular zone, odontoblasts (Fig. 8 and 9). In deep cavities, close to the pulp, prepared with the Er:YAG laser, light microscopy showed: vascular dilatation, hyperaemia, mild disruption of odontoblasts, hydrops degeneration with vacuoles in the odontoblast protoplasm (Fig. 10 and 11). Discussion

The effect of the Er:YAG laser on biologic tissue is due to a process best described as a thermo-mechanical effect on the tissue. The water contained in the tissue causes the ablation process due to absorption and permits highly

M.Stevanovic

efficient ablation in conjunction with minimal pulse energy requirements. Short duration of the laser pulse is also responsible for its low-strain effect since the exposure to the laser beam lasts just part of the second.

Thermo-mechanical ablation takes place because of the fact that water contained in the tissue is transferred from liquid to vapour state very fast by absorption of short laser pulses. The resulting rapid expansion of the water very briefly generates a pressure sufficiently high to remove tissue substance. Only a part of the tissue volume, i.e. the water portion needs to be evaporated. Therefore another characteristic of the ablation process is that removal only begins when a specific energy density is exceeded. This energy is approximately twice higher for enamel than for dentin. When operating subablatively, the tissue is merely heated up and dehydrated. SEM examination showed cavities with round or conical shape and no carbonisation and melting of the enamel were found. Similar morphological findings have been reported in other studies6.

Hibst and Keller reported that enamel and dentin are removed by water vaporisation and micro explosions. Enamel ablation results from repeated heating and explosive expansions of the water within the crystalline lattice enamel. The initial effect of the Er:YAG laser application to enamel is to vaporise the hydrous interprismatic matrix, resulting in loosened and disrupted enamel prisms. Continuing the laser exposure, more energy is deposited on the site and inorganic components of the enamel are melted and vaporised, resulting in cavitations. While escaping from the tissue the high pressure vapour ejects some of the loosened enamel prisms1,2.

Cracks in the cavity margin after laser irradiation were observed. The presence of cracks in some samples is due to mechanical stress caused by laser pulse sequence. Gusti claims that such cracks result from laser impact if they are arranged radially around the cavity like sunrays6. The floor of the crater showed honeycomb-like appearance, which indicates that the Er:YAG laser irradiated dental tissues is compatible with the requirements of adhesive dentistry.

In the present study when Er:YAG laser was applied in dentin with a water mist, neither carbonisation nor melting in the lased areas or in the surrounding tissues was found. There was no evidence of charring or cracking of the dentin. These findings correspond to the previous studies of Er:YAG laser irradiation, emphasizing that minimal thermal damage to the surrounding tissues can be expected when continuous water spray is used7. The lased dentin surface also showed microirregularites and absence of a smear layer. It can be assumed that micro irregularities originate from the micro explosions through rapid water evaporation, which is the chief mechanism of hard tissue ablation with this type of laser. On the contrary, Er:YAG laser irradiation without water-cooling showed severe carbonisation, molten lava-like surface and irregular


structures with micro holes. This is a result of the high temperatures achieved during laser irradiation without water-cooling.

The Er:Yag treated teeth in superficial and media cavities retained normal architecture of the pulp, vascularity and cellularity appeared to be unchanged. There was no inflammatory cell infiltrate evident. Changes in the pulp tissue were noticed only in deep cavities irradiated with the Er:YAG laser revealing vascular dilatation, hyperaemia, mild disruption of odontoblasts, hydrops degeneration with vacuoles in the odontoblast protoplasm. These kinds of changes are a result of a defensive activity in the pulp and are reversible.

Nair reported of similar results in his study when he investigated short term and long term pulpal effect after Er:YAG laser irradiotion. Long term effect reveled distinct apposition of tertiary dentine formation immediately under the laser defect8. Hyperaemia as a reaction, during laser treatment, is not dye to temperature rise in the pulp chamber because temperature rise was not observed in hard dental tissues also.

Glockner investigated the rise of pulp temperature during laser treatment and realised that not only that the temperature does not rise but there is a significant fall to 30�C. This effect is due to the non-contact pulsing mode of irradiation9.

Wigdor claims that pulpal histologic appearance of the Er:YAG laser treated teeth shows promise because there do not appear to be abnormal changes caused by the laser when compared to normal findings of the pulp tissue3. The results of the present study show that the Er:YAG laser can successfully be used for cavity preparations and caries removal. If used with constant water cooling, as recommended by the manufacturer, there is no thermal damage to hard tissues or the pulp.

Fig 1. Crater like formation after one

laser puls.

Fig.2. Well-defined margin with the surrounding tissue

M.Stevanovic

Fig.3. Honeycomb-like formations in

the crater Fig.4 Cracks in the enamel after laser

irradiation

Fig5. Dentin after laser irradiation

Fig.6. Dentin after laser irradiation

Fig7. Dentin after laser irradiation

without water cooling

Fig8. Pulp after laser irradiation in superfitial cavities


Fig9. Normal pulp after laser irradiation in media cavities

Fig. 10. Changes in the pulp after laser irradiation in deep cavities

Fig.11. Vacuoli in odontoblast cells .

This paper was presented at the X Congress of BaSS – Belgrade

M.Stevanovic

References 1. Hibst R., Keller U. Experimental Studies of the Application of the Er:YAG Laser

on Dental Hard Substances: I Measurement of the Ablation Rate. Lasers in SuRgery and Medicine 1989 9: 338-344.

2. Keller U., Hibst R. Experimental Studies of the Application of the Er:YAG Laser on Dental Hard Substances: II Light Microscopic and SEM Investigations. Lasers in Surgery and Medicine 1989 9: 345-351.

3. Widgor H., Abt E., Ashrafi S., Walsh J. The effect of lasers on dental hard tissues. JADA 1993 124: 65-70.

4. Keller U., Hibst R., Mohr W. Histologische Untersuchungen der Pulpareaktion nach ER:YAG Laserbestrahlung. Dtsch Zahnartztl Z 47, 222-224 (1992) 4.

5. Keller U., Raab W.H.-M., Hibst R., Die Pulpareaktion Wahrend der Bestrahlung von Zahnhartsubstanzen mit dem Er:YAG Laser. Dtsch Zahnarztl Z 46, 158-160(1991) 2.

6. Giusti JCM., Santos-Pinto L., Lizarelli RFZ., Bagnato SV. Ablation Rates and Morphological Patterns of Deciduous Tooth Enamel after Er:YAG Laser Irradiation: An In Vitro Study. J Oral Laser applications 2002: 2: 159-164.

7. Matsumoto K., Hossain M., Tsuzuki N., Yamada Matsumoto K., Hossain M., Tsuzuki N., Yamada Y. Morphological and Compositional Changes of Human Dentin after Er:YAG Laser Irradiation. J Oral Laser Applications 2003; 3: 15-20.

8. Nair PN., Baltensperger MM., Luder HU., Eyrich GK. Pulpal Response to Er:YAG laser drilling of dentine healthy human third molars. Lasers Surg Med. 2003;32(3):203-9.

9. Glockner K, Rumpler J, Ebeleseder K, Stadtler P. Intrapulpal Temperature during Preparation with the Er:YAG Laser compared to the Conventional Burr: An in Vitro Study. J. Clin. Laser Med.& Surg. 16 (3) 1998; 153-157.


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