CASE (number) PRESENTATION HEADING

Table of contents:Vital treatmentCase 1 – Pulpitis: acute inflammation p. 3Case 2 – Pulpitis: accidental root perforation p. 13Case 3 – Pulpitis: inflammatory external resorption p. 24Case 4 – Pulpitis: accidental instrument separation p. 35Case 5 – Osteomyelitis: a differential diagnosticproblem p. 43Case 6 – Dental pain emergency treatment p. 51Necrotic treatmentCase 7 – Necrotic pulp: curved canals p. 57Case 8 – Dens invaginatus: pediatric endodontics p. 64Case 9 – Traumatic injury: molarization p. 73Case 10 – Endodontal-Periodontal lesion p. 82Case 11 – Apical periodontitis with a sinus-tract p. 97Case 12 – Apical periodontitis with obliterated canals p. 108RetreatmentCase 13 – Acute apical periodontitis: flare-up p. 115Case 14 – Retreatment and Apicoectomi p. 123Case 15 – Extra-radicular infection p. 134Case 16 – Surgical retreatment p. 1461

Case 17 – Apicoectomi: complicated location p. 155Case 18 – Cracked tooth p. 163Case 19 – Vertical root fracture p. 169Pain ManagementCase 20 – Neuropathic pain p. 1772

Case 1 - Pulpitis: acute inflammationPatient:White Norwegian female, 63 years old.The patient was referred from her private practitionerto the post graduate clinic for endodontic treatment oftooth 37, on Dec 12, 2006Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:At the referral dentist the patient complained aboutpain from tooth 37. She could not eat on the left side.Drinking cold drinks was also painful. The symptomshad started approximately 2 weeks earlier and hadlately increased. She knew that a part of the filling intooth 37 was missing. Caries was excavated, and thedental pulp was exposed. The patient was referred forendodontic treatment.3

Clinical findings:Tooth:37Extra oral:Intra oral:Dental:Periodontal:Other:normal skinnormal soft tissuePositive electric sensibility test and positive ice-test.The tooth was tender to percussion and was painfulupon biting. Occlusal IRMNo signs of pathologyThe other teeth in the upper and lower rightquadrants showed no signs relevant to the chiefcomplaint.Fig.2 PreoperativeRadiographic findings:Tooth :37Periodontal:The periodontal ligament space could be followedalong the roots and was slightly widened apically.Dental:The tooth was restored with a radiopaque fillingmaterial verified clinically as an OD amalgam. IRM inthe access preparation.4

Diagnosis:Tooth : 37Symptomatic pulpitisTreatment plan:Tooth : 37Pulpectomy and root-fillingTreatment:Date:12.12.2006Access cavity was prepared. Rubber dam was appliedand the field disinfected with chlorhexidine-ethanol.Vital tissue and bleeding from the pulp chamber wasevident. Only one canal was located. Preparation withRace rotary instruments and manually with NiTi files,to dimension:# 60, 21mm, ref point: occlusal surfaceFig 3. One canal in the middle of the root5

Fig.4 working lengthIrrigation with 1% NaOCl and 15% EDTA. The canalwas dried and root filled with gutta-percha and AHplussealer by System B, warm gutta-perchatechnique. IRM as a top filling.Fig.6 Masterpoint6

Fig.7 System B obturation systemFig.8 After cutting the master pointFig.9 endodontic treatment completedEvaluation:Radiographically the root-filling appeared dense andgood, with a 1,5 mm distance from the apex. Nocomplications during the treatment.Prognosis:FavorableFollow-up examination:The patient was asymptomatic. The clinicalexamination revealed normal findings, and the toothwas restored with a PFM (porcelain fused to metal)crown restoration. The radiographic examinationdemonstrated favorable healing.7

Fig.10 6 months follow-up8

Discussion:With vital pulpectomy, the clinical aim is removal of the entire vital pulptissue short of the anatomical apex followed by a bacteria tight, biocompatibleand stable root filling. With this treatment, inflamed tissue is removed to anapical level where wound surface can be kept to a minimum, the residual pulptissue is well vascularized, and the conditions for healing are optimal, providedthe entire treatment can be carried out under aseptic conditions (4).Given the fact that even following a carious exposure the infectiousprocess does not reach far into the pulpal space (9), a one- step treatmentseems reasonable since the procedure is basically surgical and does not demandas strong an emphasis on canal disinfection as the case with infected pulpnecrosis. The one-step treatment certainly presents several advantages (12). Thetotal time for treatment is reduced and it saves the patient both travel time andexpenses. From a treatment point of view, a one- appointment treatment alsooffers the advantage that curvatures, irregularities and other aberrations in thecanal anatomy as well as working length determinations are current to theoperator, thus facilitating the filling procedure that is likely to be easier than at alater appointment.It is generally accepted that a story of spontaneous or long lasting provoked painindicates irreversible and extended inflammatory changes of the pulp tissue anda more radical treatment has to be performed. In etiological terms, it is likelythat the pulpal infection has reached a level where its elimination is not possiblewithout removal of all of the pulp tissue (4).Severe pain to hot and sometimes cold liquids which lingers minutes andhours after the stimulus is removed, may be indicative of a severe inflammationassociated with deeper slow-reacting and high threshold unmyelinated C-neurofibers (11). The deep, dull, throbbing pain is caused by an increased pulpalpressure and firing of the C- fibers. In dentinal pain, the sharp, rapid pain is areaction of the A-delta fibers, which extend 150 µm into the dentin. In severepulpalgias, both A-delta and C-fibers become stimulated, when a stimulus isapplied to the tooth this results in a sharp pain which lingers as a deep dull painlong after the stimulus is removed (11).A factor of importance for the successful outcome of pulpectomy seems tobe the distance from the anatomical apex to the termination of the root-filling.The placement of the wound surface in vital teeth is guided by concerns otherthan those for treating infected root canals. The optimal wound level in teethwith vital pulp appears to be 1-2 mm from the radiographic apex (10). Thus,studies have shown that a distance from radiographically apex to root-fillingexceeding 3mm reduces the success rate compared to a termination of the filling0-3 mm from the radiographically apex (3,5). As there is no concern about hardor soft tissue infection when a vital pulp is present, the main objective will be tooptimize the technique of atraumatic and aseptic pulp surgery. The aim isplacement of the wound at the so called apical constriction (8). Overfilling should9

e avoided for the primary reason of not inducing more than necessary tissuetoxic, allergenic or foreign body reaction, which in turn may compromise apicalwound healing, induce an apical lesion and thereby endanger the possibility ofproperly assessing of the treatment (9).In controlled clinical and radiographical studies (5), success afterpulpectomy can be obtained in about 83-100% of the cases with favorableaseptic conditions, due to the fact that the vital pulp and the dentin are notinitially infected (10).Time is required to observe the treatment outcome. While in the absenceof infection, resolution to the surgical trauma should not take more than a coupleof weeks, the development of a lesion due to infection may require months oreven years to become diagnosable. The chemical irritation and foreign bodyreaction initiated by the root filling material may also cause periapical bonelesions that may take time to resolve (2). Consequently, the treatment outcomeobserved after a short time period may differ from that observed at a later timeperiods. Ørstavik (13) recorded that the peak incidence of emerging apicalperiodontitis was a year.Failures in these teeth may be caused by pulpal infection, although radiographicevidence of apical periodontitis is initially absent. The canals may also becontaminated during treatment, with bacteria from a bordering carious lesion orwith saliva (6), through coronal leakage (1,8) and through exposed dentinaltubules communicating with periodontal defects (7).In our case we had complete aseptic control, and the distance from theapex was correct. Therefore the prognosis is favorable.10

Reference list:1. Friedman S. Treatment outcome and prognosis of endodontic therapy. InØrstavik D, Pitt Ford TR, ed. Essential Endodontology: Prevention andTreatment of Apical Periodontitis 19982. Gesi A, Bergenholtz G. Pulpectomy-studies on outcome. Endod Topics 2003; 5:57- 703. Grahnen H, Hansson L. The prognosis of pulp and root canal therapy. A clinicaland radiographic follow-up examination. Odont Revy 1961; 12: 146- 1654. Hørsted-Bindeslev P, Løvschall H. Treatment outcome of vital pulp treatment.Endod Topics 2002; 2: 24- 345. Kerekes K, Tronstad L. Long-term results of endodontic treatment performedwith a standard technique. J Endod 1979; 5: 83- 906. Lin LM, Pascon EA, Skribner J, Gaengler P,Langeland K. Clinical, radiographic,and histological study of endodontic treatment failures. Oral Surg Oral Med OralPathol 1991; 11: 603- 6117. Lin LM, Skribner JE, Gaengler P. Factors associated with endodontic treatmentfailures. J Endod 1992;12: 625- 6278. Saunders WP, Saunders EM. Coronal leakage as a cause of failure in root canaltherapy: a review. Endod Dent Traumatol 1994; 10: 105- 1089. Shovelton DS. Studies of dentine and pulp in deep caries. Int Dent J 1970; 20:283- 29610. Spängberg L. Endodontic treatment of teeth without apical periodontitis. InØrstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention andTreatment of Apical Periodontitis 199811. Trope M, Sigurdsson A. Clinical manifestations and diagnosis. In Ørstavik D,Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of ApicalPeriodontitis 199812. Trope M, Bergenholtz G. Microbiological basis for endodontic treatment: can amaximal outcome be achieved in one visit? Endod Topics 2002; 1: 40- 5313. Ørstavik D. Time-course and risk analysis of the development and healing ofchronic apical periodontitis in man. Int Endod J 1996; 29: 150-15511

CASE 2Pulpitis: accidental root perforationPatient:White Norwegian female, 17 years old. Referred to thepost graduate clinic for evaluation and treatment oftooth 46, because of complications during endodontictreatment.Medical history:Non-contributoryFig.1 preoperative photoDental history and chief complaint:Tooth 46; deep composite filling distally due to cariesled to irreversible pulpitis. Her private practitionerstarted the endodontic treatment. There was anaccidental perforation to the periodontal ligament, andshe was referred to the Department of Endodontics.Clinical findings:Tooth: 46Extra oral:Intra oral:Normal skinNormal soft tissues13

Dental:Periodontal:Other:An O temporary filling with IRM.PPD within normal limits.No symptoms of pain.Fig.2 Radiographs: sent from the referral dentist:14.11.05 16.01.06Radiographic findings:Tooth: 46Periodontal:Dental:Diagnosis:The PDL was slightly widened apically around theroots.A radiopaque material was demonstrated inside thecanals verified clinically as Ca(OH)2.. The coronal parthad an OD composite.Tooth: 46 Necrotic pulpTreatment plan:Tooth: 46 sealing the perforations with MTARoot canal disinfection and filling14

Problem list:Perforation to the periodontal ligament.Treatment:Date: 13.03.06Medical and dental history. Treatment plan. Accesspreparation. Rubber dam was applied and the fielddisinfected with chlorhexidine-ethanol. Twoperforations were located in the mesially root, apicalthird.An attempt was made to find the original canals.Because of bleeding it didn’t seem realistic to finishThe rooot filling with gutta-percha.Three canals instrumented manually with NiTi files todimension:MB: # 45, 18 mm Ref. MBCML: # 45, 18 mm Ref. MLCD: # 60, 19, 5 mm Ref. MBCIrrigation with 1% NaOCl and 15% EDTA. The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.3 working length15

Fig.4 the canal shapeNext appointment; 05.05.06:The patient was asymptomaticRubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. The distal canal was filled by cold lateralcondensation technique with gutta-percha and AHplussealer.The mesially canals were sealed with MTA and a moistcotton pellet with sterile saline on top. IRM.Fig.5 Root filling with gutta-percha and MTA16

Evaluation:The root-filling appeared good.The patient was informed that the treatment outcomewas uncertain, that she might need an Apicoectomi inthe future.Follow-up examination: 20.10.2006The patient lives 20 miles out of Oslo, so her regulardentist took a control x-ray and sent it to me.No subjective symptoms.The x-ray shows no sign of pathology.Prognosis:FavorableFig.6 endodontic treatment completed17

Discussion:Root perforations may occur as a complication during endodontic treatment ordowel (post) preparation. Frequencies of such complications have been reportedto occur in up to 3% (5,11). Ingle et al (10) reported that failures inapproximately 10% of all failed cases root perforations resulted in endodontic.Over a period of 11 years, 55 root perforations were recorded at theDepartment of Cariology and Endodontics, School of Dentistry, University ofBergen (14).Forty-four of these perforations were diagnosed during endodonticor prosthodontic treatment, seven during routine endodontic recall and four priorto endodontic retreatment. Perforations occurred in all tooth groups, but weremore common in the maxilla than in the mandible (40 versus 15). In the maxillaarch the canine was the most frequently perforated tooth, followed by the lateralincisor. In the mandibular arch, the first molar was the most frequentlyperforated tooth followed by the second premolar. Of perforations occurringduring endodontic treatment, nine were located in the midroot level and 11 inthe apical third of the roots.Further analysis of specific procedures related to perforationsdemonstrated that attempts to negotiate calcified canals accounted for 11 out of26 perforations (42%). Nine out of 26 (35%) occurred during root canalinstrumentation, and the remaining six (23%) resulted from attempts to locatecalcified canal orifices. The perforations were treated with calcium hydroxide tocontrol bleeding that was often encountered at the level of perforations, and thedressing was maintained for at least 2 weeks prior to sealing the perforations.Twenty-eight perforations were repaired by orthograde fillings with gutta-perchaand Kloroperka N-Ø sealer, eight received a combined orthograde and surgicalrepair (gutta-percha / Kloroperka N-Ø sealer and amalgam), and in three casesonly a surgical approach was used (amalgam).Twelve perforations showed a size and location hopeless for repair, they weretherefore extracted. Four cases received no treatment but were recalled. Theoverall success rate in the primary treatment group was 56% while 36% becamefailures. A combined orthograde and surgical repair provided the most favorableoutcome with 92% successful cases.Further examination of the data suggest that there may be slightly greatertendency for treatment success when perforations are in the apical part of rootsrather than more coronally. Of the seven cervical level perforations, four failedand three were successful. Multiple factors may contribute to the relatively poorprognosis for perforations in the cervical portions of roots. Beavers et al (4)reported necrosis of the periodontal ligament coronal to the perforated areasubsequent to placement of calcium hydroxide. Bergenholtz et al (7) describedan unfavorable response to filling materials extruded through perforation defects.Hence, in the cervical region where perforations may be very close to epithelialattachment, any tissue destruction that stems from the treatment may cause lossof the epithelial attachment leading to formation of a permanent periodontaldefect. Two teeth with furcation level perforations were successfully treated.18

periodontal apparatus (16). They studied 16 clinical cases of root perforationsthat were all treated with MTA, three of the cases were furcal perforations, fivewere strip perforations, five were lateral perforations and three were apicalperforations. Seven of these patients presented with radiolucent lesions at thetime of repair. The follow- up radiographs ranged from 12-45 months. Theresults showed that all 16 cases demonstrated normal tissue architectureadjacent to the repair site at the recall visit. Teeth with existing lesions showedresolution of the lesion.Although MTA is one of the most researched materials in dentistry and showingremarkable results, the majority of the published data are based on in vitro andanimal studies. Research must be continued to evaluate more clinical outcomesin human subjects.20

Reference list:1. Alhadainy HA, Himel VT. Evaluation of the sealing ability of amalgam,Cavit,andglasionomer cement, in the repair of furcation perforations. Oral Surg OralMed Oral Pathol Oral Rad Endod 1993; 75: 362-3662. Arens DE, Torabinejad M. Repair of furcal perforations with mineral trioxideaggregate. Oral Surg Oral Med Oral Pathol Oral Rad Endod 1996; 82: 84-883. Balla R, Lo Monaco CJ, Skribner J, Lin LM. Histological study of furcationperforations treated with tricalcium phosphate, hydroxylapatite, amalgam andLife. J Endod 1991; 17: 234-2384. Beavers RA, Bergenholtz G, Cox CF. Periodontal wound healing followingintentional root perforations in permanent teeth of Macca mulatta. Int Endod J1986; 19: 36-445. Benenati FW, Roane JB, Biggs JT, Simon JH. Recall evaluation of iatrogenicRoot perforations repaired with amalgam and gutta-percha. J Endod 1986; 12:161-1666. Bergenholtz G, Lekhom U, Milthon R, Engstöm B. Influence of apical overinstrumentation and overfilling on retreated root canals. J Endod 1979; 5:310-3147. Bergenholtz G, Lekholm U, Milthon R, Heden G, Ödesjö B, Engström B.Retreatment of endodontic fillings. Scand J Dent Res 1979; 87: 217-2248. El Deeb ME, ElDeeb M, Tabibi A, Jensen JR. An evaluation of the use ofamalgam, Cavit, and calcium hydroxide in the repair of furcation perforation. JEndod 1982; 8: 459-4669. Hartwell GR, England MC. Healing of furcation perforations in primary teethafter repair with decalcified freeze-dried bone: a longitudinal study. J Endod1993; 19:357-36110. Ingle JI. A standardized endodontic technique utilizing newly designedinstruments and filling materials. Oral Surg Oral Med Oral Pathol 1961; 14:83-9111. Kerekes K, Tronstad L. Long-term results of endodontic treatment performedwith a standarized technique. J Endod 1979; 5: 83-9012. Koh ET, Torabinjead M, Pitt Ford TR, Brady K, Mc Donald F. Mineral trioxide21

aggregate stimulates biological response in human osteoblasts. J BiomedMaterRes 1997; 37: 432-43913. Koh ET, Mc Donald F, Pitt Ford TR, Torabinejad M. Cellular response tomineral trioxide aggregate. J Endod 1998; 24: 543-54714. Kvinnsland I, Oswald RJ, Halse A, Grønningsæter AG. A clinical androentgenological study of 55 cases of root perforations. Int Endod J 1989; 2275-8415. Lee SJ, Monsef M, Torabinejad M. Sealing ability of a mineral trioxideaggregate for repair of lateral root perforations. J Endod 1993; 19: 541-54416. Main C, Mirzayan N, Shabahang S, Torabinejad M. Repair of root perforationsusing mineral trioxide aggregate: A Long-term study. J Endod 2004; 2: 80-8317. Martin LR, Gilbert B, Dickerson AW. Management of endodontic perforations.Oral Surg Oral Med Oral Pathol 1982; 54: 668-67718. Nakata TT, Bae KS, Baumgartner JC. Perforation repair comparing mineraltrioxide aggregate and amalgam using an anaerobic bacterial leakage model.J Endod 1998; 24: 184-18619. Nicholls E. Treatment of traumatic perforations of the pulp cavity. Oral SurgOral Med Oral Pathol 1962; 15: 603-61220. Pitt Ford TR, Torabinejad M, Mc Kendry DJ, Hong CU, Kariyawasam SP. Useof mineral trioxide aggregate for repair of furcal perforations. Oral Surg OralMed Oral Pathol Oral Rad Endod 1995; 79: 756-76321. Resillez-Urioste F, Sanandajt K, Davidson RM. Use of resin-ionomer in thetreatment of mechanical root perforations: report of a case. Quintessence Int1998; 29: 115-11822. Rud J, Rud V, Munksgaard EC. Retrograde sealing of accidental rootperforations with dentin-bonded composite resin. J Endod 1998; 24: 671-67723. Schwarts RS, Mauger M, Clement DJ, Walker WA. Mineral trioxide aggregate:a new material for endodontics. J Am Dent Assoc 1999; 130: 967-97524. Seltzer S, Sinai I, August D. Periodontal effects of root perforations beforeand during endodontic procedures. J Dent Res 1970; 49: 332-33922

25. Torabinejad M, Hong CU, Mc Donald F, Pitt Ford TR. Physical and chemicalproperties of a new root-end filling material. J Endod 1995; 21: 349-35326. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Anti bacterial effect ofsome root filling materials. J Endod 1995; 21: 403-40627. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Cytotoxity of four rootend filling materials. J Endod 1995; 21: 489-49228. Torabinejad M, Hong CU, Lee SJ, Monsef M, Pitt Ford TR. Investigation ofmineral trioxide aggregate for root-end filling in dogs. J Endod 1995; 21:603-60829. Torabinejad M, Pitt Ford, Abedi HR, Kariyawasam SP, Tang HM. Tissuereaction to implanted root.end filling materials in the tibia and mandible inguinea pigs. J Endod 1998; 24: 468-47130. Weine FS. Endodontic Therapy, 3rd edn, p. 330. C.V Mosby Co., St Louis198223

CASE 3 - Pulpitis: Inflammatory external resorptionPatient:White Norwegian female, 77 years old. Referred to thepostgraduate clinic at the Department of Endodontics,from a general practitioner for treatment of tooth 33,on November 08, 2006Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:The patient had no symptoms from the tooth. Thegeneral practitioner wanted us to perform thenecessary treatment. He had detected a radiolucentarea in the mid part of the root at a regular check-up.The patient could not recall any history of trauma inthe area.24

Clinical findings:Tooth: 33Fig.2 tooth 33, buccal viewExtra oral:Intra oral:Dental:Periodontal:Other:Normal skinNormal findingsThe tooth was restored with a composite buccally atthe enamel-cementum border and one smallcomposite distally. The tooth was tender to neitherpercussion nor palpation.Chronic marginal periodontitis, with massive boneloss, especially in the lower front. Tooth 33 did notshow signs of increased PPD, and the patient tells thather periodontal problems have been stable for the lasttwo decades.The other teeth in the upper and lower quadrantsshowed no signs relevant to the chief complaint.Tooth 33 had a positive response to the electricsensibility test, and also to the ice-test.25

Radiographic findings:Tooth: 33Fig.3 preoperative x-rayPeriodontal:Dental:Normal PDL was followed along the root, normalapical conditions.A radiolucent resorption defect at the mid part of theroot surface, probed to be at the buccal surface.Diagnosis:Tooth: 33:Problem List:Treatment plan:Tooth: 33:Inflammatory external resorptionUnknown size of the defect.Root canal obliterated at the coronal part of theresorption defect. Look for a second canal.Root canal disinfection and fillingFilling the resorption defect with MTA, a surgicalintervention.Treatment:Date: 13.12 .2006Medical and dental history. Treatment plan.26

Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. One canalwas located and instrumented manually with NiTi filesto dimension:# 50, 23, 5 mm ref: ICEvan though the pulp responded to sensibility test,there was just a slight appearance of blood in thecanal. The resorption defect could be probed and theneed for an intracanal disinfection agent as ca (OH) 2was, at our opinion, necessary to control thedisinfection.Irrigation with 1% NaOCl and 15% EDTA. The canalwere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.4 working lengthNext appointment; 16.01.2007Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canal was irrigated with 1% NaOCl and 15%EDTA. The canal was dried with sterile paper pointsand filled by cold lateral condensation technique withgutta-percha and AH-plus sealer. IRM.Next appointment; 24.01.2007The patient met for surgery. Three carpules withXylocain and adrenaline were injected to establish27

anesthesia. The patient rinsed 1 minute withchlorhexidine mouthwash. Intrasulcular buccal incisionfrom distally on tooth 31 to the buccal surface ontooth 35 with surgical blade number 15. The flap waselevated and the cervical lesion was evident.We used a curette and a round bur to remove thegranulation tissue. The internal part of the resorptioncavity was filled with MTA. The flap was repositionedand sutured with 5, 4-0 silk sutures. Postoperativeinformation was given. Ice pack was kept over thesurgical site for 15 minutes. Analgesics wereprescribed: Pinex forte and Pinex. Chlorhexidinemouthwash was recommended.Fig.5 during surgery28

Fig.6 resorption defect with MTAFig.7 post surgeryNext Appointment: 31.01.2007After-surgery examination. The patient had beenasymptomatic. Favorable healing was demonstrated.The sutures were removed. Rubber dam was appliedand the field disinfected with chlorhexidine andethanol. IRM was placed over the gutta-percha downto the MTA. A composite filling was placed on top.29

Fig.8 One week post op.guttaperchaMTAFig.9 microscopic view30

composittIRMMTAFig.10 endodontic treatment competedEvaluation:Prognosis:No complications during treatment, the root-fillingappeared narrow, but dense and good.Favorable31

Discussion:External resorption can result from bacteria in the pulp cavity, surface of the rootor the gingival sulcus. Inflammatory resorption becomes progressive when, ontop of a denuded area of the root surface, there is an additional long-lastingstimulation, such as mechanical irritation of the tissue, increased pressure in thetissue, infection of the root canal, and finally, in combination with certaindiseases (4,5,8), such as hypoparathyroidsm, hypothyroidism, Paget´s diseaseand other endocrine disturbances. Herpes Zoster has also been reportedimplicated with resorptions (7). Local causative factors could be dental trauma,tumours (ameloblastoms, giant cell tumour and fibro-osseous lesions) and cysts,excessive mechanical or occlusal forces, impacted teeth, secondary bone graftingof alveolar clefts or intra coronal bleaching of pulpless teeth with 30-35%hydrogenperoxide (2). Apart from the above causative factors, resorption of noapparent cause is often reported in the literature (1,10). The term idiopathicresorption, which is used where no definite cause can be detected, reflects thelimited understanding on the causative factors of this pathological process.Denuded mineralized tissue is colonized by multinucleated cells whichinitiate the resorption process; however without further stimulation of theresorption cells, the process will end spontaneously.The protective mechanism against resorption is based on the premise that thecementum and predentin covering of dentin are essential elements in theresistance of the dental root to resorptions.Since the most external aspect of cementum is covered by a layer ofcementoblasts over a zone of non-mineralized cementoid, a surface that providesatisfactory conditions for osteoclast binding is not present (9). Another functionof the cemental layer is related to its ability to inhibit the movement of toxins ifpresent in the root canal space into the surrounding periodontal tissues (6). Theconsequence of an infected root canal space is, therefore, most likely to beapical periodontitis, as the toxins can communicate with the periodontal tissuesthrough the apical foramina or large accessory canals. However, if the cementallayer is lost or damaged, the inflammatory stimulators can pass from an infectedpulp space through the dentinal tubules into the surrounding periodontalligament, which, in turn, sets up an inflammatory response. Since the cementumis lost, this inflammatory response will result in both bone resorption and rootresorption.Thus, in order for root resorption to occur, two things must happen (9):1. The loss or alteration of the protective layer (pre-cementum or predentin)2. Inflammation must occur to the unprotected root surface.Inflammation in reaction to a traumatic injury varies according to the stimulus itis exposed to after the injury, and has the potential to cause extensive damageto the protective layer. The root resorption will continue until either no root32

structure remains or the stimulus is removed by the intervention of the dentist(9).The root resorption is diagnosed primarily by the radiolucent appearance of theroot and adjacent bone on X-rays. Diagnosis can be a major challenge asresorptive defects, facial or lingual/palatal, are most often missed duringexaminations, although newer radiographic techniques, such as ComputedTomography, display significant promise in improving the ability to identify thesedefects (3). The diagnosis is also occasionally assisted by the presence of clinicalsymptoms which are similar to apical periodontitis (9).External root resorption occurs, as the name implies, on the outer surface of theroot. Luxation injuries are the most likely injury where root resorption mayresult, and the long-term outcome is dependant on whether the healing responseis favorable or unfavorable.33

Reference list:1. Darbar UR, Jenkins CBG. Multiple external root resorption: case report. Austr Dent J1993; 38: 433-4352. Fuzz Z, Lin S, Tesis I. Root resorption- diagnosis, classification and treatment choicesbased on stimulation factors. Endod Dent Traumatol 2003; 19: 175-1853. Nance RS, Tyndall D, Levin LG, Trope M. Diagnosis of external root resorptions usingTACT (tuned-aperture computed tomography) Endod Dent Traumatol 2000; 16: 24-284. Pankhurst CI, Eley BM, Moniz C. Multiple idiopathic external root resorption. Oral SurgOral Med Oral Pathol 1988; 13: 516-5185. Samia F, Björn S. Root resorptions in a patient with hemifacial atrophies. J Endod1994;20: 299-3026. Selvig KA, Zander HA. Chemical analysis and microradiograhy of cementum andDentin from periodontally diseased human teeth. J Periodontol 1962; 33: 303-3107. Solomon CS, Coffiner MO, Chalfin HE. Herpes Zoster revisited: Implications in rootresorptions. J Endod 1986; 12: 210-2138. Tronstad L. Root resorptions- etiology, terminology and clinical manifestations. DentTraumatol 1986; 2: 263-2669. Trope M. Root resorptions due to dental trauma. End Topics 2002; 1: 79-10010. Webber RT. Traumatic injuries and the expanded role of calcium hydroxide. In:Gerstein, H, editor. Techniques in Clinical endodontics, 1 st edn. London, UK: W.B.Saunders Company, 1983. p. 181-21134

CASE 4 – Pulpitis: accidental instrument separation and rootperforationPatient:White, Norwegian male, 35 years old. The patient wasreferred from the undergraduate clinic to thepostgraduate clinic for retreatment of previously rootfilledtooth 46 and removal of a separated instrument,on November28, 2006.Fig.1 preoperational photoMedical history:Non-contributoryDental history and chief complaint:Three years ago, tooth 46 wasroot filled due to deep caries. When treated, an instrument separated in the mbcanal. It was decided to leave the instrument in the canal. However, the lingualcusp broke off, and the tooth needed a crown. It was therefore decided toretreat the root canals and try to remove the instrument. The undergraduatestudent had started the endodontic retreatment of tooth 46 and fractured aspiral filler size # 20, during negotiating and preparing of the ml canal. In the mbcanal the student also managed to accidentally perforate into the periodontalmembrane. The patient was asymptomatic.Clinical findings:Tooth:46Extra oral:normal skin35

Conventional retreatmentRoot canal disinfecton and fillingTreatment:Date:28.11.2006Medical and dental history. Treatment plan. IRM wasremoved. Rubber dam was applied and the fielddisinfected with chlorhexidine-ethanol. Three canalorifices were located, gutta-percha remnants weredemonstrated in two canals, - mb,ml and palatinalcanal was filled by the undergraduate student.. Thecoronal part of the separated spiral bur was visiblethrough the operating microscope. Removal of theinstrument required an access preparation withoverview. Ultrasound was used for preparation of thecanal orifice in the ml canal. A step was preparedaround the coronal part of the needel. Ultrasonic tipssuitable for removal of separated endodonticinstruments were further used in conjunction with15% EDTA irrigation until the instrument wasmovable. Finally, a cut ultrasonic tip was used tovibrate on top of the separated instrument until itcould be removed completely from the canal. The restof the gutta-percha was removed with Race rotaryinstruments. The instrument in the mb canal was notpossible to see in the microscope. It was notmovable, and we decided to leave it were it was. Theml canal was prepareted to dimension:Mb # 45, 20mm, ref point ML cuspIrrigation with 1% NaOCl, 15% EDTA. Two canalswere dried with sterile paper points and packed withCa(OH) 2. IRM as a temporary filling.37

Fig.3 instrument and spiral fillerin the mesial root.Fig.4 working lengthFig.5 ml canal orificeFig.6 removed spiral filler13.03.2007 The patient was asymptomatic. Rubber dam wasapplied and disinfected with chlorhexidine-ethanol.IRM and Ca(OH) 2were removed. Irrigation with 1%NaOCl and 15% EDTA. The mb root canal was filledwith MTA, the perforation being covered. The mlcanal was dried and filled by cold lateral condensationtechnique with gutta-percha and AH-plus sealer. IRMwas placed in the canal orifices and as a temporarytop filling. The patient was referred back to theundergraduate student for producing a PFM (porcelainfused to metal) crown as soon as possible.38

Fig.7 masterpointFig.8 endodontic treatmentcompletedEvaluation:Prognosis:The tooth is weekend by the perforation. No signs ofinfection. The tooth needed a crown, and the patientwas informed that the tooth has an uncertain future.QuestionableFollow-up examination: 6 weeks post-up: I called the patient and he saidthat the tooth was restored with a PFM crown. Nosymptoms of pain.39

Discussion:Management of a case with a broken instrument may involve an orthograde or asurgical approach. The three orthograde approaches are:1) attempt to remove the instrument2) attempt to bypass the instrument3) prepare and obdurate to the fractured segmentWhen these instruments can be removed, successful treatment or retreatmentgenerally occurs. If an instrument can be removed or bypassed and the canalcan be properly cleaned and filled, nonsurgical endodontics is the mostconservative approach. If the entire segment of the broken instrument is apicalto the curvature and safe access with visualization is not possible, then nonsurgical removal usually cannot be accomplished (3).The success of nonsurgical fractured instrument removal from root canalsdepends on several factors. Among them are the length and site of the fragment,the diameter and curvature of the root canal, and the friction and impaction ofthe instrument fragment into the canal wall (2). Rotary nickel-titaniuminstruments tend to be more difficult to remove than hand instruments. This isbecause they generally fracture in smaller fragments, further apically, at oraround the curve of narrow canals than hand instruments. Because of theirrotational motion, they tend to be wound in and impacted in the canal walls,occluding the canal lumen.Instruments located in the straight portion of the canal can usually be removed(3). When a fractured instrument lies partially around the canal curvature, butthe coronal aspect can still be visualized and accessed, the removal may bepossible, as in this case.No standardized procedure for successful instrument removal exists.Many techniques and devices have been tried – predominantly with fracturedhand instruments (2). These techniques have been time-consuming, have hadlimited success, and have imparted considerable risk to narrow and curvedcanals.Recently, special ultrasonic tips have been developed for use in differentpiezoelectric ultrasonic devices to assist in removal of fractured instruments. Thedifferent manufactures have stated that these tips are uniquely designed tooperate at a specific amplitude and at a frequency to maximize the safe removalof fractured instruments from root canals (5). Ward et al (5) studied 24 caseswhere they tried to remove fractured instruments from small, curved root canals.They used a technique with modified Gates-Glidden burs to perform a platformand then continuing with the use of special designed ultrasonic tips. All caseswhere the fractured instrument was situated before or at the curve weresuccessfully removed. In cases where the fractured instrument was situatedbeyond the curve, the technique was generally unsuccessful. They also stressed40

the importance of using a dental operating microscope to get optimalvisualization (5).Souter et al (4) evaluated in vitro and in vivo complications associated withfractured file removal. They used the same technique as Ward et al (5) toremove fractured instruments from different levels in the root canals (coronal,middle and apical third). They used the mesiolingual canals of 45 extractedhuman mandibular canals. The success rate, frequency of root perforations, androot strength were recorded for each group. Removal was successful in all caseswhere the file fragment was located in the coronal or middle third. Only 11 of 15files located in the apical third were successfully removed. Stripping perforationsoccurred in three cases, all where fragment was located beyond the curve.Fracture resistance declined significantly with more apically located filefragments. A review of 60 clinical cases showed similar rates of successful fileremoval and rate of perforations (4). Their conclusion was therefore that removalof fractured file fragment from the apical third should not routinely be attemptedbecause of the high frequency of complications (4).This has also been the conclusion of other studies (1), who suggested thatobjects in the apical third should be left in situ, with the canal coronal to theinstrument cleaned, shaped, and filled as normal. Apical surgery or extractionswere the recommended treatment options if further treatment was required.The position of the fractured instrument has also an influence on prognosis. Ifthe broken instrument prevents access to the root apex, it could influence theoperator’s ability to prepare, disinfect, and obdurate the entire root canal system.The prognosis is best when there is fracture of a large instrument in the latterpart of cleaning and shaping close to the working length. The prognosis is poorerfor those canals that have not been cleaned at all and in which a smallinstrument is broken far from the apex (1). In vital pulp cases, as well as thosecases where instrument fracture occurs after thorough instrumentation andirrigation, the chances for failure are less than if instrument fracture occurs in aninfected case before significant instrumentation and irrigation have beenperformed (1). Instrument fracture before completion of instrumentation in aninfected tooth results in a high chance of failure (1).41

Reference list:1. Fors UGH, Berg JO. Endodontic treatment of root canals obstructed by foreignobjects. Int Endod J 1986; 19: 2-102. Hülsmann M. Methods for removing metal obstructions from the root canal.Endod Dent Traumatol 1993; 9: 223-2373. Ruddle CJ. Non surgical retreatment. In: Cohen S, Burns RC, eds. Pathways ofthe pulp. 8 th ed. St. Louis: CV Mosby, 2002: 875-9294. Souter NJ, Messer H. Complications associated with fractured file removalusing an ultrasonic technique. J Endod 2005; 6: 450-4525. Ward JR, Parashos P, Messer H. Evaluation of an ultrasonic technique toremove fractured rotary nickel-titanium endodontic instruments from rootcanals: Clinical Cases. J Endod 2003; 11: 764-76742

CASE 5 – Osteomyelitis: a differential diagnostic problemPatient:White Norwegian male, 42 years old. Referred fromthe Department of Oral Surgery for necessarytreatment of the mandibular front teeth.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:Our patient had a long history of pain and treatment;- 1995: tooth 31: Acute apical periodontitis, the tooth was root filled- 1998: Accident, to the lower yaw, pain and discomfort without anydiagnostic solution, visiting several dentists- 2001: Tooth 31:sinus tract; Apicoectomi- 2002: Tooth 31:sinus tract persists- 2003: Tooth 31:extracted- 2004: Sinus tract in the area of 31; referred to Endodontist, but the teeth inthe area were positive to vitality testing.The Endodontist referred to Department of Oral surgery, faculty ofOslo.Tentative diagnosis was set to be Osteomyelitis. Treatment was explorativesurgery. Medication: Dalacin 150 mg x 4 for 1 month prior to surgery.43

Clinical findings:41 42 32palpation - - -percussion - - -mobility - - -period.ex. - - -el pulp test - - +c.d. snow - - +Fig.2 preoperative lingual view.Radiographic findings:Periodontal:Bone loss in the lower front.44

Dental:31 in a bridge, root was extracted. Radiolucent areaafter surgery.Fig.3 preoperative x-rayDiagnosis:Treatment plan:Tooth: 41: Necrotic pulp42: Necrotic pulpTooth : 41: Root canal disinfection and fillingTooth : 42: Root canal disinfection and fillingTreatment:Date: 16.02.2004 41: Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. One canalwas located and instrumented manually with NiTi filesto dimension:# 45, 20 mm ref: ICIrrigation with 1% NaOCl and 15% EDTA.The canalwas dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.42: Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. One canal45

was located and instrumented manually with NiTi filesto dimension:# 45, 22 mm ref: ICIrrigation with 1% NaOCl and 15% EDTA.The canalwas dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Next appointment; 21.03.2004Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.Both teeth were irrigated with 1% NaOCl and 15%EDTA. The canals were dried with sterile paper pointsand filled by cold lateral condensation technique withgutta-percha and AH-plus sealer. IRM.Tooth 41:Fig.4 working lengthFig.5 masterpoint46

Tooth 42:Fig 6.working length Fig.7 masterpoint Fig 8. endodontictreatmentcompletedEvaluation:Prognosis:No complications during treatment, the root-fillingsappeared satisfactory.FavorableFollow-up examination: 2 years post treatment:No subjective symptoms. The radiographicexamination demonstrated healing.47

Fig.9 13.02.2007, 2- year- follow-up48

Discussion:Periapical radiolucensis may have causes other than an infected pulp necrosisand are therefore important to identify before a treatment decision is taken.Examples include:• Anatomical structures• Developmental and physiological phenomena• Periapical scar tissue• Traumatic injury• Tumour• Periapical lesion of periodontal origin• Osteomyelitis• Radicular cystOn rare occasions endodontic infections may spread and involve large areas ofsurrounding bone and cause Osteomyelitis. This condition is accompanied bypain and elevated body temperature. The radiographic image may show a linearpattern of radiolucent bone, leaving islands of normal bone, witch later maybecome devitalized and transform to sequestrate(1).Apparently, the infection is spreading through the bone itself and is nolonger dependent on the infected tooth as a reservoir of the causativeorganisms. The radiographic appearance may also be sclerotizing and osteolyticoccurring in the same patient. A variant known as Garre´s Osteomyelitis ischaracterized by expansion of the cortical plate and mild clinical symptoms (2).In this case a microbiological sample was taken during surgery, but it showed nogrowth. This may be due to the antibiotic treatment before surgery.In the dental history of this case, a sinus tract is reported to be persistent. Stillthere is, to my knowledge, no fistelograms taken. This may have been of greathelp in solving this patients dental problems.49

Reference list:1. Happonen R.P., Bergenholtz G., Apical periodontitis. In Bergenholtz G.,Hørstad-Bindslev P.,Reit C.. Textbook of Endodontology,2003.2. Ørstavik D. Radiology of apical periodontitis. In Ørstavik D, Pitt Ford TR,ed.Essential Endodontology: Prevention and Treatment of Apical Periodontitis 199850

CASE 6 – Dental pain emergencyPatient:White Norwegian male, 37 years old. The patientcalled for an emergency appointment at our privatepractice. It was august 2, 2005, and his private dentist(PD) was on holiday and his office was closed. He wasin a lot of pain and he sounded desperate. He wasgiven an immediate appointment.Fig.1 preoperative photoMedical history: The patient’s physical condition was good. He was notusing any regular medication, but he had taken pain medication for several days.He did not have any known allergies.Dental history and chief complaint:The pain had started two weeks earlier. He had seenhis PD, who started a root canal treatment on tooth 17. When the anesthesiaeffect disappeared a couple of hours post treatment, the pain came back withthe same intensity as before the treatment. The PD prescribed antibiotics, andtold the patient to wait for a couple of days before calling back. However, thepain was so intolerable that he called another dentist. He continued the rootcanal treatment on tooth 17. When the pain persisted with the same intensity hefelt desperate and afraid. The next morning he came to our office.51

Clinical findings:The patient was rating his pain intensity to be 9 atthe Numerical Rating Scale, 10 being the worst possible pain. He had not sleptthe whole night, and the days before he had only slept for short periods of time,waken up from pain.Extra oral:Intra oral:Periodontal:normal skinnormal soft tissuePPD within normal limitsDental:Tooth 17 16 15Swelling _ _ _Tender topercussionSensibilitytesting_ + _+ (+) XNecrotic pulp _ (+) X52

Fig.2 preoperative x-rayRadiographic findings:Tooth 17 16 15Radiolucentarea_ _ +Started endo + - -Caries _ _ _Root filled _ _ +Diagnosis:16: Irreversible pulpitis with acute apical periodontitis15: chronic apical periodontitisTreatment plan: 16:- Complete removal of the pulp- Root canal disinfection- Occlusal reduction!7 and 15 needed treatment, but not at the emergency appointment.53

Treatment: 16Date:02.08.2005Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Fourcanals were located and instrumented with Raceinstrumentation system and manually with NiTi filesto dimension:Mb # 45, 21 mm ref: mb cuspMB2 # 40 ,21 mm ref: mb cuspMl # 45, 20 mm ref: ml cuspD # 60, 22 mm ref: mb cusp.Irrigation with 1% NaOCl and 15% EDTA.The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.3 working lengthEvaluation:Prognosis:No complications during treatment.FavorableFollow-up examination: The same afternoon the patient called the office andsaid that the pain was completely gone.54

Discussion:Vital pulpectomy gained general acceptance as the method of choice comparedto the previously most often preferred mortal pulpectomy, following severalstudies published in the period from about 1940-70. The basic principle for thistreatment was to leave out the instrumentation procedure and retain thedevitalized pulp tissue in the canal. The tissue was usually amputated at theentrance of the root canal, and subsequently sealed with a strong antisepticcement (paraformaldehyde, tricresol), the idea being to keep the fixed tissuepermanently disinfected (1,2,3).While still practised in some Asian and European countries (4,5), neither mortalpulpotomy nor mortal pulpectomy are no longer considered appropriate. Thepotential risk for leakage of the devitalizing agent to the gingival sulcus along theprovisional filling was especially discouraging. The current approach to invasivepulpal therapy by removing the vital pulp by mechanical means became a morewidespread procedure when improved agents for local anaesthesia wereintroduced in the 1920 (4).If the pulp remnant left in the root canal is more than 2 mm long, the risk ofpulp necrosis is high due to amputation injury. It is crucial for the treatmentoutcome of vital pulp therapy that the remaining pulp will stay alive after surgery(6). If the remaining pulp is short, the chances for revascularization are higherthan if the pulp stump is long, as the ratio between remaining pulp length andsize of apical constriction is small. It has been demonstrated however, that if thepulp is removed completely when strict asepsis is maintained, healing will occureven if the root canal filling is placed 2-4 mm short of the working length (6).In cases with necrotic pulp, however, great efforts must be spent on the mostapical part of the root canal, because disinfection of this area is crucial. The mostapical part of the infected pulp space has often branching of the main canals,and extensive apposition of cementum, that makes disinfection and mechanicaldebridement less effective and difficult. Furthermore, conventional antimicrobialagents are often diluted or inhibited by tissue fluids (6). As the major concern innecrotic cases is related to elimination of all infected soft and hard tissues fromthe apical part of the root canal, the placement of the wound surface must befurther apically than what is required in treatment of vital cases.The need for close apical preparation of teeth with necrotic pulp has beenconfirmed in several clinical studies of treatment outcome (6).In this case the use of sensibility testing could help in diagnosing the acing toothat an earlier point, and the endodontic treatment of 17 could have been avoided.55

Reference list:1. Baume JL, Holz J, Risk LB. Radicular pulpotomy for category III pulps. Part II.Instrumentation and technique. J Prost Dent 1971; 26: 649- 6572. Baume JL, Holz J, Risk LB. Radicular pulpotomy for category III pulps. Part III.Histological evaluation. J Prost Dent 1971; 26: 649- 6573. Engstrøm B, Spängberg L. Wound healing after partial pulpectomy. Ahistological study performed on contra lateral tooth pairs. Odont Tidskr 1967;75: 5- 184. Eriksen HM, Kirkevang L-L, Petersson K. Endodontic epidemiology and treatmentoutcome: general considerations. Endod Topics 2002; 2: 1-95. Gesi A, Bergenholtz G. Pulpectomy-studies on outcome. Endod Topics 2003; 5: 57- 706. Spängberg L. Endodontic treatment of teeth without apical periodontitis. InØrstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatmentof Apical Periodontitis 199856

CASE – 7 Necrotic pulp: curved canalsPatient:Asian male, 48 years old. The patient was referred tothe endodontic post-graduate clinic from the undergraduateclinic.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:The patient had been to treat tooth 37 for a carieslesion, and the cavity went in to the pulp chamber.The student reported that the caries was excavated,and eugenol and IRM was placed as a temporaryfilling. The patient was without symptoms.Clinical findings:Tooth: 37Extra oral:Intra oral:Dental:Periodontal:normal skinnormal soft tissuecaries buccally, IRM as a large temporary filling. Nosymptoms of pain.no signs of pathology57

Fig.2 preoperative photo, caries buccallyRadiographic findings:Tooth: 37Periodontal:Dental:materialThe periodontal ligament space could be followedalong the roots.The tooth was restored with a radiopaque fillingVerified clinically as an MO amalgam. The mesial roothas a curved shape.Diagnosis:Treatment plan:Tooth: 37: Necrotic pulpTooth: 37: Disinfection and root filling.Treatment:Date: 30.08.2005Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Threecanals were located and instrumented with the use ofendo-lift to size 20 and Race instruments todimension:Mb # 50, 21 mm ref: mb cuspMl # 50, 21 mm ref: ml cusp58

D # 60, 20mm ref: mb cusp.Irrigation with 1% NaOCl and 15% EDTA. The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.3 Working lengthFig.4 Endo-liftNext appointment; 12.10.2005Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. Three canals were dried with sterile paperpoints and filled by cold lateral condensationtechnique with gutta-percha and AH-plus sealer. IRM.59

Fig.5 MasterpointFig.6 Endodontic treatment completedEvaluation:Prognosis:No complications during treatment, the root-fillingappeared dense and good.FavorableFollow-up examination: 01.09.2006No subjective symptoms.The tooth is restored with a composite filling.No sign of pathology.Fig.7 1 year follow-up60

Discussion:The aims of root canal treatment are to disinfect the root canal systemthoroughly, completely obdurate the space created, so as to entomb anymicrobes that have escaped elimination and to prevent reinfection (9). A chemomechanical preparation technique is advocated to disinfect root canals (2),because it allows a greater number of root canals to be rendered bacteria free.The use of irrigation solutions have been shown to improve bacterial elimination,but could not predictably remove all bacteria. Mechanical debridement combinedwith antibacterial irrigation (0,5% sodium hypochlorite) can render 40-60 % ofthe treated teeth bacteria negative (1,7). Other studies by Ørstavik et al (12) andCard et al (3) suggested that the size of apical instrumentation may be importantfor the effective removal of canal bacteria. These studies found that with largerinstrumentation fewer bacteria remained in the canal and the healing was morerapid.An interappointment antimicrobial dressing is generally advocated toprevent recovery and multiplication of microorganisms remaining even aftercareful instrumentation and debridement of the root canal space (2). Studieshave shown that the application of a calcium hydroxide dressing brings thepercentage of bacteria - negative teeth to 90-100 percent (2,6).The root canal represents a special environment in which selectivepressures results in the establishment of a restricted group of the oral flora.Bacterial interrelationships and the nutritional supply are key factors indetermining the outcome of the infection. Endodontic treatment, apart fromdirectly eliminating bacteria, can completely disrupt the delicate ecology anddeprive persisting bacteria of their nutritional source (8).A correlation seems to exist between the size of the periapical lesion and thenumber of the bacterial species and cells present in the root canal. Teeth withlarge lesions usually harbor more bacterial species and have a higher density ofbacteria in their root canals than teeth with small lesions. Periapical status at thestart of treatment has been demonstrated to have fundamental impact on thefinal result (4,11,13).The success rate of initial therapy of apical periodontitis has been reported torange from 46% to 93% (5).It is well known that bacterial status at the time of the root-filling is of outmostimportance (10). Sjögren et al (7) demonstrated in their study, that teeth withpersistent infection at the time of obturation had a success rate of 68%, whereasteeth that sampled negative to bacterial growth had a success rate of 94%.How high the risk is for the treatment to fail will depend on asepsis, the chemomechanicalpreparation, the quality of the root-filling and the coronal restoration.In our case the tooth was initially a vital pulp therapy. However, by the time hemet for endodontic treatment there was no vitality left, and there was still61

unexcavated caries buccally. Therefore we decided to treat the tooth with anantibacterial interappointment dressing.62

Reference list:1. Byström A, Sundqvist G. Bacteriologic evaluation of the effect of 0, 5 percent sodiumhypochlorite in endodontic therapy. Oral Surg Oral Med Oral Pathol 1983; 55: 307-122. Byström A, Claesson R, Sundqvist G .The antibacterial effect of camphorated paramonochlorophenol,camphorated phenol and calcium hydroxide in treatment andinfected root canals. Endod Dent Traumatol 1985;1: 170-53. Card SJ, Sigurdsson A, Ørstavik D, Trope M. The effectiveness of Increased ApicalEnlargement in Reducing Intracanal Bacteria. J Endod 2002; 11: 779- 834. Engstrøm B, Hård af Segerstad L, Ramstrøm G, Frostell G. Correlation of positiveCultures with the prognosis for root canal treatemnt. Odontol Rev 1964; 15: 257- 705. Friedman S. Treatment outcome and prognosis of endodontic therapy. In Ørstavik D,Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of ApicalPeriodontitis 19986. Sjögren U, Figdor D, Spängberg L, Sundqvist G. The antimicrobial effect of calciumhydroxide as a short-term intracanal dressing. Int Endod J 1991; 24: 119-257. Sjögren U, Figdor D, Persson S, Sundqvist G. Influence of infection at the time of theroot- filling on the outcome of endodontic treatment of teeth with apical periodontitis.Int Endod J 1997; 30: 297-3068. Sundqvist G. Ecology of the Root Canal Flora. J Endod 1992; 9: 427-309. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. In Ørstavik D, PittFord TR,ed. Essential Endodontology: Prevention and Treatment of ApicalPeriodontitis199810. Waltimo T, Trope M, Haapasalo M, Ørstavik D. Clinical efficacy of treatmentProcedures in endodontic infection control and one year follow-up of periapicalhealing. J Endod 2005; 12: 863- 6611. Weiger R, Rosendahl R, Löst C. Influence of calcium hydroxide intracanal dressingson the prognosis of teeth with endodontically induced periapical lesions. Int Endod J2000; 33: 219-2612. Ørstavik D, Kerekes K, Molven O. Effects of extensive reaming and calciumhydroxide dressing on bacterial infection during treatment of apical periodontitis: apilot study. Int Endod J 1991; 24: 1-713. Ørstavik D, Qvist V, stoltze K. A multivariate analysis of the outcome of endodontictreatment. Eur J Oral Scien 2004; 112: 224-3063

CASE 8 – Dens invaginatus: pediatric endodonticsPatient:A nine year old white Norwegian female was referredto the Postgraduate Endodontic Clinic, Faculty ofDentistry, University of Oslo, by her general dentalpractitioner (GDP) May 2006 for treatment of theupper right lateral incisor (tooth 12).Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:10.05.2006Pain and swelling region 12. She was givenfenoxymethyl-penicillin; Apocillin 330 mg X 4, for 7days.64

Clinical findings:Tooth 12Fig.2 preoperative photoTooth 12 11 21 22IntraoralswellingNo No No NoPerc. test + - - -Palp. test + - - -Sens. test - + + +GPD - - - -65

Radiographic findings:Tooth 12 11 21 22RootDevelopopen (open) (open) openRadiolucencyDensinvag.+ - - -+ x x +Caries - - - -Fig.3 preoperative x-rayDiagnosis:Tooth : 12: Chronic apical periodontitisDens Invaginatus type 1 (Oehlers)Tooth: 22: Dens invaginatus type 1I called her dentist and discussed theneed for a composite in the foramensocum. He said that he would do so assoon as possible.66

Problem list:Root development in progressTreatment plan:Treatment:date 24.05.2006Tooth : 12: Root canal disinfection and filling withMTA.Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. The canalwas located and gently instrumented manually withNiTi files to dimension:# 60, 16 mm, ref: inc surface mlIrrigation with 1% NaOCl and 15 % EDTA.The canals were dried with sterile paper points anddressed with calcium hydroxide.IRM was placed as a top filling.Fig.4 Working lengthNext appointment; 26.09.2006Tooth 12 was asymptomatic and no intra-oral swellingwas palpated. Rubber dam was applied anddisinfected with chlorhexidine-ethanol. Ca(OH)2 wasremoved. Irrigation with 15% EDTA and 1% NaOCl.67

The canals were dried with sterile paper points andfilled with MTA. Wet cotton pellet. IRM as a top filling.Fig.5 endodontic treatment completedEvaluation:No symptoms, no signs of infection.The root is week, the MTA filling is questionable.Orthodontic treatment require extraction of severalteeth in the upper yaw. 12 is a currant choice.Prognosis:uncertainFollow-up examination: No subjective symptoms.68

Fig.6 05.12.2006Arrow shows a crack in the enamel. This confirms the uncertain prognosis.Anyway, it is of great interest to keep the tooth until the orthodontist is ready forextraction and replacement of several teeth. This may take several years.Fig.6 showing MTA and IRMMTAMTAIRM05.12.200669

Dens invaginatusType 1.Fig.7 4 types of dens invaginatus (Copy from Visual Endodontics).70

Discussion:Dens invaginatus is a dental malformation, often leading to endodonticcomplications.The etiology is unclear, but it is commonly believed that an invagination is theresult of a deep folding of the foramen coecum during tooth development (1).The prevalence of dens invaginatus varies considerably depending on the type ofclassification. Ruprecht et al found dens invaginatus in 1,7% of all examinedpatients(2).Location: The anomaly arises most commonly in the maxillary lateral incisor andless frequently in the central incisors. It also occurs in posterior teeth, extendingfrom the occlusal pit. Bilateral occurrence is a frequent finding; Grahnen et alreported 43%(1).The most common classification was introduced by Oehlers in 1957. (Figure 1)(3). Shultze and Brand introduced a more detailed classification also includinginvaginations starting at the incisal edge and dysmorphic root forms (figure 2)(4).The choice of treatment ranges from observation, fissure sealing, root canaltreatment to extraction. Root canal treatment can imply endodontic treatment ofthe invagination alone, or the main canal, or both (5). Pulp necrosis is oftenfound before root end closure(5).Endodontic treatment in conjunction with endodontic surgery is also commonwhen the anatomy hampers the ability to thoroughly clean and shape thecanal(s).(5). The treatment outcome is linked to the difficulty of cleaning andshaping and the present of a palato-radicular groove (PRG). The probability ofperiodontal breakdown is greater when a PRG is present. Mesial or distal PRGsare more often associated with pocket probing depth > 3mm (6).71

Reference list:1.Grahnen H, Lindahl B, Omnell K. Dens invaginatus. I. A clinicalroentgenological and genetical study of permanent upper lateral incisors.2.Ruprecht A, Batniji S, Sastry KAHR, El-Neweihi E. The incidence of dentalinvagination. Journal of Pedodontics 1986:10, 265-72.3.Oehlers F. Dens invaginatus. Variations of the invagination process andassociated anterior crown forms. Oral Surgery, Oral Medicine and OralPathology. 1957a;10:1204-18.4.Schulze C, Brand E. Uber Dens Invaginatus (dens in dente). ZahnarztligeWelt/reform 1972;81:569-73.5.Hulsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosisand treatment considerations. Int Endod J. 1997;30:79-90.6.Hou G-L, Tsai C-C: Relationship between palato-radicular grooves and localizedperiodontitis. J.Clin.Periodontol. 1993;20:678-82.72

CASE 9 – Traumatic injury: molarizationPatient:White Norwegian male, 12 years old. Referred to theDepartment of Endodontics for treatment of previouslytraumatized tooth 44.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:The boy fell from his bicycle and hurt some of histeeth. Tooth 44 had a concussion injury. He went tohis regular dentist for control. After 6 months thetooth tested negative to electrical vitality test, and atiny radiolucency was visible at the apex. He wasreferred to the Department of Endodontology forevaluation and treatment because of abnormalanatomy.Clinical findings:Tooth:44Extra oral:normal skin73

Intra oral:Dental:Periodontal:normal soft tissueIntact tooth with no restorations. Negative responseto electric sensibility test and to Endo-ice test.Normal findingsFig.2 tooth 44 preoperativeRadiographic findings:Tooth :44Periodontal:Dental:A tiny radiolucency was visible at the apex.The canal is separating into two or three smallercanals at the middle of the root.Fig.3 preoperative x-ray74

Diagnosis:Tooth :44: Chronic apical periodontitispreviously traumatized toothTreatment plan:Tooth :44: Root canal disinfection and fillingProblem list: anatomy, molarization tooth 44Treatment:Date:07.02.2007Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Threecanals were located and instrumented manually withNiTi files to dimension:Mb # 40, 22 mm ref: mb cuspMl # 40, 22 mm ref: ml cuspD # 40, 20mm ref: mb cuspFig.4 working lengthIrrigation with 1% NaOCl and 15% EDTA.The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.75

Next appointment; 07.03.2007Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. Three canals were dried with sterile paperpoints and filled by cold lateral condensationtechnique with gutta-percha and AH-plus sealer. IRMFig.5 MasterpointFig.6 Endodontic treatment completedEvaluation:Prognosis:No complications during treatment, the root-fillingappeared dense and good.Favorable76

Discussion:The classification of dental injuries is currently based on the World HealthOrganization’s Application of International Classification of Diseases to Dentistryand Stomatology (9), and modified by Andreasen (6). This classification can beapplied to both primary and permanent dentitions:Management of traumatic injuries include, after examination anddiagnosis, urgent care if indicated and definitive treatment. The latter requiresplanning both for the immediate and the long-term care (13). In cases ofluxation and avulsion injuries, the immediate concern is to stabilize the tooth inits normal position to allow re-attachment and re-organization of the periodontalligament support. Pulpal responses to traumatic injuries are affected by thedegree of injury to the neurovascular supply, which for the most part enterthrough the apical foramen. Three possible outcomes exist: Pulpal healing, pulpalnecrosis, or pulpal obliteration (1,2,5,11,12). The most desirable outcome afterdental trauma is pulpal healing. If the disruption of the neurovascular supply tothe pulp is less than total, for example in subluxation injuries, the pulp functionmay continue with reduced circulations until complete reconstitution is77

accomplished, usually within a few weeks. In cases of extensive or totalseverance of the apical blood supply, pulpal healing is rare if the apical diameteris < 0,5mm, such as is found in fully formed teeth.Pulpal necrosis following severance of the blood supply may proceed throughcoagulation necrosis (sterile necrosis) to gangrenous necrosis (infection ofinfarcted tissue). Of interest, with respect to pulpal necrosis in traumatized teethis the risk of infection-related (inflammatory) root resorption (4). This riskemphasizes the need for careful monitoring of pulpal responses after traumaticinjuries. The third type of pulpal response to trauma is obliteration of the rootcanal. This is frequently observed in luxation-type injuries associated withdisplacement (3,11). Rarely do such teeth require root canal treatment (3,11).Treatment recommendations for luxation injuries with minor involvementsuch as concussion and subluxation, is mostly symptomatic. Soft diet andpossibly occlusal adjustment to minimize discomfort on biting contact (7,13). Themore sever types of injuries, extrusive and lateral luxation; need both immediatecare (repositioning and stabilization for 2-4 weeks) and long-term considerations.In luxated teeth with pulp necrosis, root canal therapy is indicated. If neglected,infection-related root resorption is a distinct and dangerous possibility (4,13,14).Root resorption has been identified as repair-related (surface), infection-related(inflammatory), and ankylosis-related (replacement) resorption (4,14). Repairrelatedresorption is a transient process involving small areas on the root surfacefollowing luxation and avulsion injuries and can also be observed associated withroot fracture injuries (4). Typically, diagnosis can be made within 4 weeks afterinjury. Inflammatory resorption is a very aggressive type of injury-relatedresorption associated with root canal infection following trauma to a tooth (4).Luxation and avulsion injuries resulting in reduction or severance of pulpal bloodsupply, followed by bacterial invasion of the pulp, is the setting for initiation ofexternal (and sometimes internal) root resorption. These are both types ofinjuries that can cause damage to the cemental protection of the root surfaces,allowing dentinal tubules to become pathways for bacterial toxins within thecanal to trigger osteoclastic activity externally. Failure to remove bacteria fromthe root canal can result in this type of inflammatory resorption proceeding at arapid pace, resulting in total root resorption within a very short period of time(4,8,14).A relatively slower, but not necessarily more benign, resorptive process isankylosisrelated resorption. This type of resorption is associated with extensivetrauma to the PDL resulting in loss of vitality of the cells and extensive damageto the cementum. Lacking protective covering, the root cementum is exposed toosteoclasts that mistake cementum for bone and proceed to replace thecementum and dentine with new bone, resulting in a fusing of the bone and thetooth (8). An ankylosed tooth can be diagnosed clinically within 1 month by itspercussion sound (high, metallic) and radiographically within 2 months(disappearance of PDL space and invasion of bone into the root). Currently,78

there is no predictable method for arresting ankylosisrelated resorption after itsinitiation (10).Management of dental injuries includes follow-up control to complete orconfirm the diagnosis, assess response to treatment, determine need foradditional treatment or treatment change, and evaluate the treatment outcomeor complications. The following recommended schedule can be applied to themanagement of dental trauma patients (13):1 week. After 7-10 days, the splint placed on a replanted, avulsed tooth shouldbe removed and endodontic treatment, if indicated, should be initiated. 3-4weeks. The splint applied to luxated teeth can usually be removed after 3-4weeks. Radiographic examination should be performed to examine for thepossible beginning of root resorption or periradicular lesions. 6 weeks. At thistime, clinical and radiographic examinations may reveal evidence of pulp necrosisand infection-related (inflammatory) root resorption. 3-6 months. Examination atthis time may be necessary to establish definitive diagnosis of pulpal periodontalhealing complications. 1 year and up to 5 years. One year is a minimal controlperiod for traumatic dental injuries; some may require additional observationperiods to assess the final outcome.79

Reference list:1. Andreasen FM, Wistergaard Pedersen B. Prognosis of luxated permanent teeth- thedevelopment of pulp necrosis. Endod Dent Traumatol 1985; 1: 207-2202. Andreasen FM, Yu Z, Thomsen BL. Relationship between pulp dimensions anddevelopment of pulp necrosis after luxation injuries in the permanent dentition.Endod Dent Traumatol 1986; 2: 90-983. Andreasen FM, Yu Z, Thomsen ML, Andersen PK. Occurrence of pulp canalobliteration after luxation injuries in the permanent dentition. Endod Dent Traumatol1887; 3: 103- 1154. Andreasen FM, Andreasen JO. Root resorption following traumatic dental injuries.Proc Finn Dent Soc 1992; 88: 95-1145. Andreasen JO. Response of oral tissue to trauma. In: Andreasen JO, Andreasen FMeds. Textbook and Colour Atlas of Traumatic Injuries to the Teeth, 3rd edn.Copenhagen: Munksgaard, 1993: 77-1126. Andreasen JO, Andreasen FM. Classification, etiology and epidemiology of traumaticdental injury. In: Andreasen JO, Andreasen FM eds. Textbook and Colour Atlas ofTraumatic Injuries to the Teeth, 3rd edn. Copenhagen: Munksgaard, 1993: 151-1777. Andreasen FM, Andreasen JO. Luxation injuries. In: Andreasen JO, Andreasen FMeds. Textbook and Colour Atlas of Traumatic Injuries to the Teeth, 3rd edn.Copenhagen:Munksgaard, 1993: 315-3828. Andreasen JO, Borum M, Jacobsen HL, Andreasen FM. Replantation of 400 avulsedpermanent incisors. IV. Factors related to periodontal ligament healing. Endod DentTraumatol 1995; 11: 76-899. Application of the International Classification of Diseases to Dentistry andStomatology IDC-DA, 3rd edn. Geneva: WHO, 199510. Bakland LK, Andreasen JO. Dental Traumatology: essential diagnosis and treatmentplanning. Endod Topics 2004; 7: 14-3411. Jacobsen I, Kerekes K. Long-term prognosis of traumatized permanent anteriorTeeth showing calcifying processes in the pulp cavity. Scand J Dent Res 1977; 85:588-59812. Robertson A, Andreasen FM, Bergenholtz G, Andreasen JO, Norén JG. Incidence ofPulp necrosis subsequent to canal obliteration from trauma to permanent teeth. JEndod 1996; 22: 557-56080

13. The International Association of Dental Traumatology. Guidelines for the evaluationand management of traumatic dental injuries. Dental Traumatol 2001; 17: 1-4, 49-25, 97-102, 145-14814. Trope M. Root resorptions due to dental trauma. Endod Topics 2002; 1: 79-10081

CASE 10 – Endodontal – periodontal lesionPatient:White Norwegian male, 78 years old. Referred to theDepartment of Endodontics from a post graduatestudent in periodontics for evaluation and treatment.Medical history:Non-contributoryDental history and chief complaint:Because of acute pain the patient called his dentistfor an emergency appointment. He felt pain from the mandibular front teeth, andthey were mobile. He was feverish. His dentist examined him, and called theDepartment of Periodontics for an appointment. When they examined him, theytested sensibility on the mobile teeth, and found them to be necrotic, and therewas also the presence of a sinus tract. Therefore he was sent to us at theEndodontic department. Fortunate, this all happened at the same day,08.02.2007.Fig.1 preoperative photo82

Clinical findings:Tooth 42 41 31 32 33Vitality - - - - -Perk./Palp.Plaque/calculus+ + + + ++ + + + +Pockets - - + + -Mobile - - + + -Fig.2 preoperative photo83

Radiographic findings:Tooth 42 41 31 32 33Peri-apicalradiolucentRestorative- - + + -- - - - -Bone loss + + + + +Obliteration + + + + +Sinus tracttraced- - - + +Fig.3 radiographs that followed the referral84

Tentative Diagnosis:Tooth 32: acute exacerbation with a sinus tractTooth 31: chronic apical periodontitisTreatment plan:Information was given about the uncertainty of thistreatment. The patient was, however, interested intrying to keep his teeth.Tooth 31: Root canal disinfection and fillingTooth 32: Root canal disinfection and fillingApocillin, 660 mg,tabl.no.30Bacteriological sample.Possible diagnosis to be kept in mind; vertical root fracture and osteomyelitisTreatment:Date:08.02.2007Medical and dental history. Treatment plan.Bacteriological sample.Treatment of 32:Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. The canalwas located and instrumented manually with NiTi filesto dimension:# 50, 22mm ref: IC.Fig.4 working length 32Irrigation with 1% NaOCl and 15% EDTA.The canalwas dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.85

Test results from the microbiological sample: Treponema socranscii,Porphyromonas gingivalis, AA, Fusobacterium Nucleatum, Micromonas micros,Tannerella forsythia, Prevotella melaninogenica.Next appointment; 08.03.2007Fig.4 photo taken before treatmentThe sinus tract is still present. No pain. No mobility.Fig.5 gutta-percha in sinus tract.The gutta-percha in the sinus tract may not be able tofollow the tract all the way. In this case it stops in thepocket same place as one month earlier. I’m notconvinced that this is correct.Treatment of 32: Change of calsium hydroxide.Treatment of 31:Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. The canal86

was located and instrumented manually with NiTi filesto dimension:# 50, 23,5mm ref: IC.Fig.6 working length 31Irrigation with 1% NaOCl and 15% EDTA.The canalwas dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.7 post treatment photoWhen the rubber-dam was removed, liquid was poringout of the sinus tract and the pocket.Next appointment: 27.03.200787

Fig.8 preoperative photo 27.03.2007The patient was asymptomatic.Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. The canals were dried with sterile paper pointsand filled by cold lateral condensation technique withgutta-percha and AH-plus sealer. IRM.Fig.9 during treatmentFig.10 masterpoint X-ray88

Fig.11 endodontic treatment completedWhen the rubber dam was removed; exacerbationfrom the buccal pocket .Fig.10 post endodontic treatment89

Fig.11 gutta-percha in the buccal pocket.We decided to do an explorative surgery, 2 weeks later.Date:27.03.2007Fig.12 pre surgeryThe patient didn’t have any symptoms, and there was no exacerbation from thepocket. The pocket was narrow.90

Fig.13 Gutta-percha in pocket buccally.Fig.13 x-ray 12.04.2007We decided not to do the surgery and to make a new appointment in 3 months,and the patient got my telephone number in case of any change in the situation.91

Evaluation:Prognosis:No complications during treatment, the root-fillingappeared dense and good.Favorable for the endodontic treatment. Treatmentoutcome will depend upon the periodontal condition.92

Discussion:Despite numerous differences between chronic inflammatory disease ofperiodontal and endodontic origins, there are notable similarities, primarily that(1):1) both conditions share a common microbiota that often is associatedwith Gram-negative anaerobic bacteria, and2) elevated cytokine levels may be released systemically from acute andchronic manifestations of both disease processes (e.g., increased concentrationsof inflammatory mediators have been detected both in the gingival crevicularfluid of subjects with periodontal disease and in the periapical tissues ofendodontically involved teeth).The pulp and the periodontium are intimately related. As the tooth develops andthe root is formed, three main avenues for communication are created: dentinaltubules, lateral and accessory canals, and the apical foramen.Exposed dentinal tubules in areas of denuded cementum may serve ascommunication pathways between the pulp and the periodontal ligament.Exposure of dentinal tubules may occur due to development defects, disease orperiodontal procedures (12).Lateral and accessory canals may be present anywhere along the root (3,5,8,12).It is estimated that 30-40% of all teeth have lateral or accessory canals and themajority of them are found in the apical third of the root (6). De Deus (5) foundthat 17% of teeth had lateral canals in the apical third of the root, about 9% inthe middle third, and less than 2% in the coronal third. However, it seems thatthe prevalence of periodontal disease associated with lateral canals is relativelylow. Kirkham (8) studied 1000 human teeth with extensive periodontal diseaseand found that only 2% had lateral canals located in a periodontal pocket.The apical foramen is the principal and most direct route of communicationbetween the pulp and periodontium. Bacterial and inflammatory byproducts mayexit readily through the apical foramen to cause periapical pathosis. The apex isalso a portal of entry of inflammatory byproducts from deep periodontal pocketsto the pulp. Pulp inflammation and pulp necrosis extends into the periapicaltissues causing a local inflammatory response accompanied with bone and rootresorptions. In certain cases pulpal disease will stimulate epithelial growth thatwill affect the integrity of the periradicular tissues (9,14).It seems that the pulp is usually not directly affected by periodontal disease untilrecession has opened an accessory canal to the oral environment. At this stage,pathogens penetrating from the oral cavity through the accessory canal into thepulp may cause a chronic inflammatory reaction and pulp necrosis (12).93

However, as long as the accessory canals are protected by sound cementum,necrosis usually does not occur.Rubf et al (13) studied the profiles of periodontal pathogens in pulpal andperiodontal diseases associated with the same tooth. They used specific PCRmethods and detected the same pathogens in teeth with chronic apicalperiodontitis and chronic (adult) periodontitis. The isolated species wereActinobacillus actinomycetemcomitans,Tannerella forsythensis, Eiknellacorrodens, Fusobacterium nucleatum, Porphyromonas gingivals, Prevoellaintermedia and Treponema denticola. Spirochetes are associated with bothendodontic and periodontal diseases. The spirochete species most frequentlyfound in root canals are T.denicola (11) and T. maltophilum (7). T denicolapossesses an array of virulence factors associated wit periodontal disease andmay also participate in the pathogenesis of periradicular disease (11).The prognosis and treatment of each endodontic-periodontal disease type varies.Primary endodontic disease should only be treated by endodontic therapy andhas good prognosis. Primary periodontal disease should only be treated byperiodontal therapy. In this case, prognosis depends on severity of theperiodontal disease and patient’s response.Primary endodontic disease with secondary periodontal involvement should firstbe treated with endodontic therapy. Treatment results should be evaluated in 2-3 months and only then should periodontal treatment be considered. Thissequence of treatment allows sufficient time for initial tissue healing and betterassessment of the periodontal condition (4,10). It also reduces the potential riskof introducing bacteria and their byproducts during the initial healing phase. Inthese cases it is important to realize that periodontal healing could be adverselyaffected by aggressive removal of the periodontal ligament and underlyingcement during interim endodontic therapy (2). Prognosis of primary endodonticdisease with secondary periodontal involvement depends primarily on theseverity of periodontal involvement, periodontal treatment and patient’sresponse.Primary periodontal disease with secondary endodontic involvement and truecombined endodontic-periodontal diseases require both endodontic andperiodontal therapies, and the prognosis of these lesions depends primarily uponthe severity of the periodontal disease and the response to periodontal treatment(12).94

Reference list:1. Caplan DJ. Epidemiologic issues in studies of association between apicalperiodontitis and systemic health. Endod Topics 2004; 8: 15-352. Blomlöf L, Lindskog S, Hammarström L. Influence of pulpal treatments on celland tissue reactions in the marginal periodontium. J Periodontol 1988; 59:577-5833. Burch JG, Hulen S. A study of the prescence of accessory foramina and thetopography of molar furcations. Oral Surg Oral Med Oral Pathol 1974; 38:451-4554. Chapple I, Lumley P.The periodontal-endodontic interface. Dent Update 1999;26: 331-3345. De Deus QD. Frequency, location and direction of the lateral, secondary andaccessory canals. J Endod 1975; 1: 361-3666. Harington GW, Steiner DR. Periodontal-endodontic considerations. In: WaltonRE, Torabinejad M, editors, Principles andpractice of endodontics, 3 rd edn.Philadelphia: W.B. Saunders Co., 2002: 446-4847. Jung I-Y, Choi B-K, Kum K-Y, Yoo Y-J, Yoon T-C, Lee S-J, Lee C-Y.Identification of oral spirochetes at the species level and their association ofother bacteria in endodontic infections. Oral Surg Oral Med Oral Pathol OralRadiol Endod 2001; 92: 329-3348. Kirkham DB. The location and incidence of accessory pulpal canals inperiodontal pockets. J Am Dent Assoc 1975; 91: 353-3569. Nair PNR, Pajarola G, Schroeder HE. Types and incidence of human periapicallesion obtained with extracted teeth. Oral Surg Oral Med Oral Pathol 1996; 81:93-10110. Paul BF, Hutter JW. The endodontic-periodontal continuum revisited: Newinsights into etiology, diagnosis and treatment. J Am Dent Assoc 1997; 128:1541-154811. Rocas IN, Siqueira JF Jr, Santos KRN, Coelho AMA. “Red complex”(Bacteroides forsythus, Porphyromonas gingivalis, and Treponema denticola)in endodontic infections: A molecular approach. Oral Surg Oral Med OralPathol Oral Radiol Endod 2001; 91: 468-47112. Rotstein I, Simon JHS. Diagnosis, prognosis and decision-making in thetreatment of combined periodontal-endodontic lesions. Periodontol 2000;2004; 34: 165-20395

13. Rupf S, Kannengiesser S, Merte K, Pfister W, Sigusch B, Eschrich K.Comparison of profiles of key periodontal pathogens in the periodontium andendodonthium. Endod Dent Traumatol 2000; 16: 269-27514. Simon JHS. Incidence of periapical cysts in relation to the root canal. J Endod1980; 6: 845-84896

CASE 11- Apical periodontitis with a sinus tractPatient:Black African male, 22 years old. He was referred tothe Endodontic Department from his privatepractician.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:History of pain started during springtime 2005. He feltpain and extra-oral swelling in lower right jaw, andwent to see a doctor. He was referred to Ullevåluniversity hospital.First appointment; 04.10.05. Dr. Oddvar Moendescribes an “granulation polyp”. Odontogen origin isconsidered unlikely. An OPG was taken and didn’tindicate any relevant dental pathology. Thegranulation polyp is removed and sent to histologicaland bacteriologic examination. The patient is givenApocillin, 660 mg for one week, and he is givensickness leave for seven days.97

Second appointment; 18.10.05. Dr. Anne MarieRamsve. Test result. Pericoronitt 48. Apocillin 660 mgtabl no 40 and Flagyl 400 mg tabl 20.Treatment plan; ex 48 and excision of polyp.Third appointment; 01.11.05. Dr. Niels FredrikHågensli.Sinus tract from 46, vitality testing gives no respondfrom 46.Treatment plan; Treatment of necrotic pulp, tooth 46.Clinical findings:48 47 46 45El.pt + - + +Ice + - + +PPD - - - -Perc.t. - (+) (+) -Extra oral:Intra oral:Dental:Periodontal:normal skinsinus tract with an opening at the buccal mucosabetween 47 and 46.No visible caries.No mobility. PPD (periodontal probing depth) withinnormal limits.98

Fig. 2 gutta-perch point in sinus tractRadiographic findings:Tooth 47:Fig.3 x-ray gutta-percha point in sinus tractPeriodontal:Dental:Radiograph with a gutta-percha point in the sinustract confirmed the presence of a communicationbetween the oral mucosa and tooth 47.Radiopaque material was demonstrated in the coronalpart of tooth 47, verified clinically as an O compositefilling.Other: 48 caries M. No findings in relation to tooth 46 or 45that would influence the diagnosis or the treatment.Diagnosis:Tooth 47: Apical periodontitis with a sinus tract99

Treatment plan:Tooth 47: Root canal disinfection and fillingTreatment:07.06.06 Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Threecanals were located and instrumented manually withNiTi files to dimension:Mb # 45, 21 mm ref: mb cuspMl # 45, 20 mm ref: ml cuspD # 60, 22mm ref: mb cusp.Fig.4 Working lengthFig.5 MasterpointIrrigation with 1% NaOCl and 15% EDTA. The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Next appointment; 2 months.29.08.2006 Rubberdam was applied and the fielddisinfected with chlorhexidine and ethanol. CA (OH)2was removed. The canals were irrigated with 1%NaOCl and 15% EDTA. Three canals were dried withsterile paper points and filled by cold lateralcondensation technique with gutta-percha and AHplussealer. IRM.100

Fig 6.Endodontic treatment completed Fig.7 Post treatment, closure of sinus tractEvaluation:Prognosis:No complications during treatment, the root-fillingappeared dense and good.FavorableFollow-up examination: 20.11.06No subjective symptoms. The radiographicexamination didn’tdemonstrate apical periodontitisFig.8 6-months follow-up examination:101

Fig.9 complete healing of sinus tract102

Discussion:When apical inflammatory exudates drain to a body surface, a sinus tract hasdeveloped. The reason that a sinus tract develops is not fully understood. It maybe the mechanism with which the body controls the infection, or it may indicatea specific infection of some volume/ number/ virulence of the bacteria (16). Itmay develop as a result of an abscess or be without preceding symptoms, andthe diagnosis may be made without the patient even being aware of itsexistence. When longstanding, the tract can become epithelialzed (1).With adequate disinfection of the root canal and resolution of theperiapical inflammation, the sinus tract will heal without further treatment andthe epithelium, if present, will in most cases disintegrate (16). Commonly, thesinus tract will drain on the mucosa adjacent to the offending tooth. However itis possible that the opening can be relatively far from the involved tooth, or drainto the periodontal ligament mimicking a periodontal pocket. For these reasons, itis important to perform a thorough diagnostic examination and not rely tooheavily on the presence and location of the sinus tract opening. It is important totrace the sinus tract with an opaque object, for instance a gutta-percha point, todetermine the radiographic origin of the lesion. Disinfection of the root canalsystems should result in reversal of the chronic apical periodontitis and the sinustract will disappear quickly.In the great majority of teeth requiring root canal treatment, the goal iseither prevention or treatment of apical periodontitis. The final success is usuallydependant on successful infection control. Cleaning and shaping is the mostimportant step towards sterility of the canal. The goal of instrumentation andirrigation is to remove all necrotic and vital organic tissue as well as some hardtissue from the root canal system, and give the canal system a shape that allowsdebridement and predictable placement of locally used medicaments and apermanent root-filling of high technical quality.Irrigation of the root canal is an essential component in the process of root canalpreparation. There are five main benefits of using irrigants during the cleaning ofthe canal:1. Wetting of the canal walls and removal of debris by flushing2. Destruction of microorganisms3. Dissolution of organic matter4. Removal of smear layer and softening of the dentin5. Cleaning in areas that are inaccessible to mechanical cleansing methodsSodium hypochlorite was introduced to endodontics by Coolidge in 1919 (4), andhas remained a popular root canal irrigants because of its potent bactericidalactivity and ability to dissolve necrotic organic material. The antibacterial effecthas been clinically evaluated in a series of studies (2,3). NaOCl is used in103

concentrations varying from 0, 5% to 5, and 25%. Laboratory experiments usingthree Gram-negative anaerobic rods typically isolated from primary apicalperiodontitis, Porphyromonas gingivalis, P. endodontalis and Prevotellaintermedia demonstrated high susceptibility to NaOCl, and all three species werekilled within 15 s with all concentrations tested (0,5%- 5%) (17). Other in vitostudies has demonstrated a better antibacterial effect with high concentrations ofNaOCl (6,17). In vivo studies have failed to demonstrate the same. This isprobably due to the differences in conditions between in vitro and in vivo studies.In laboratory studies there are high volume of the medicament available forkilling, direct access to all microbes, and absence of other materials thatpotentially protect bacteria in vivo (8). Byström & Sundqvist (2,3) demonstratedthat 0,5% NaOCl, with or without the use of EDTA, improved the antibacterialefficiency of preparation compared with the use of saline irrigation. The sameauthors, could not demonstrate any significant difference in antibacterial effect invivo between 0,5% and 5% NaOCl. Peciuliene (12) studied the effect ofinstrumentation and NaOCl irrigation in previously root-filled teeth. Bacteria wereisolated in 33 of the 40 teeth examined before instrumentation.E.faecalis was found in 21 teeth, C. albicans in six teeth and Gram-negativeenteric rods and other microbes in 20 teeth. While no rods or yeast were foundin the second sample after the preparation and irrigation, E. faecalis stillpersisted in six teeth, which indicated that E. faecalis is much more resistiant tokilling by NaOCl than C.albicans and Gram-negative rods.NaOCl has been criticized for its unpleasant taste, relative toxicity, and its lackof ability to remove smear layer (15). Caustic effect on the maxillary sinus oradjacent structures has been demonstrated when NaOCl was accidentiallyexpressed into the periapical area (9,18). In addition to the strong bleachingeffect that can damage patients clothing. Pashley et al (11) compared thebiological effects of different concentrations of NaOCl solutions anddemonstrated greater cytotoxicity and caustic effects on healthy tissue with5,25% NaOCl than with 0,5% and 1% solutions. Therefore it might berecommended to use 0,5% - 1% NaOCl for canal irrigation. There has been anongoing search for alternative solutions that could replace NaOCl, because of theside-effects.Chlorhexidine, CHX has a wide antimicrobial spectrum and is effective againstboth Gram - positive and Gram-negative bacteria as well as yeast. It is able topermeate the cell wall or outer membrane and attacks the bacterial cytoplasmicor inner membrane, or the yeast plasma membrane. Its activity is pH dependentand is greatly reduced in the presence of organic matter (14).CHX gluconate has been shown to be superior to NaOCl in killing of E.faecalisand Staphylococcus aureus (2,6). A potential weakness of CHX in the root canalmay be its susceptibility to the presence of organic matter (14). In an in vitrostudy, Haapasalo et al (7) demonstrated that the effect of CHX is reduced,although not prevented, by the presence of dentine.104

Portenier et al (13) demonstrated total loss of activity of CHX by bovine serumalbumin. This might indicate the possibility that inflammatory exudates, rich inproteins such as albumin, entering the root canal through the apical foramen,may weaken the antibacterial effect of CHX.CHX lacks the tissue - dissolving ability, which is one of the obvious benefits ofNaOCl. While the in vito studies have demonstrated the antibacterial effect ofCHX against E. faecalis to be superior to that of NaOCl, there are no in vivostudies yet available that confirms this.Removal of the smear layer is an important step to facilitate disinfection of theroot canal. EDTA has little if any antibacterial activity. It is an effective chelatingagent (5) and removes the smear layer by chelating the inorganic component ofdentine.EDTA contributes to the elimination of bacteria in the root canal by facilitatingcleaning and removal of infected tissue. It has also been demonstrated thatremoval of the smear layer by EDTA improves the antibacterial effect of locallyused disinfecting agents in deeper layers of dentine (17). Studies have shownthat more debris was removed by irrigation with EDTA followed by NaOCl thanwith EDTA alone (10).Dental fluorosis is a type of hypocalcification of enamel characterized by whiteareas that may become discolored to brown. It is caused by consumption ofexcessive fluorides in the water supply (usually 2-8 ppm) during toothdevelopment. Technically this is chronic endemic dental fluorosis. Fluorosis is ageneral term for chronic fluoride poisoning.105

Reference list:1. Baumgartner JC, Pickett AB, Muller JT. Microscopic examination of oral sinustracts and their associated periapical lesions. J Endod 1984; 10: 146-1522. Byström A, Sundqvist G. Bacteriologic evaluation of the effect of 0,5 per centsodium hypochlorite in endodontic therapy. Oral Surg Oral Med Oral Pathol1983; 55: 307- 3123. Byström A, Sundqvist G. The antibacterial effect of sodium hypochlorite andEDTA in 60 cases of endodontic therapy. Int Endod J 1985; 18: 35- 404. Coolidge E. The diagnosis and treatment of conditions resulting from diseaseddental pulps. J Nation Dent Ass 1919; 6: 337- 3495. Czonstkowsky M, Wilson EG, Holstein FA. The smear layer in endodontics.Dent Clin North Am 1990; 34: 13- 256. Gomes PB, Ferraz CC, Vianna ME, Berber VB, Teixeira FB, Souza- Filho FJ. Invitro antibacterial activity of several concentrations of sodium hypochlorite andchlorhexidine gluconate in the elimination of Enterococcus faecalis. Int EndodJ 2001; 34: 424- 4287. Haapasalo HK, Siren EK, Waltimo TM, Ørstavik D, Haapasalo MP. Inactivationof local root canal medicaments by dentine: an in vitro study. Int Endod J2000; 33: 126- 1318. Haapasalo M, Endal U, Zandi H, Coil JM. Eradication of endodontic infection byinstrumentation and irrigation solutions. Endod Topics 2005; 10: 77- 1029. Hülsman M, Hahn W. Complications during root canal irrigation-literatureReview and case reports. Int Endod J 2000; 33: 186- 19310. Niu W, Yoshioka T, Kobayasi C, Suda H. A scanning electron microscopicstudy of dentinal erosion by final irrigation with EDTA and NaOCl solutions.Int Endod J 2002; 35: 934- 93911. Pashley EL, Birdsong NL, Bowman K, Pashley DH. Cytotoxic effects of NaOClon vital tissue. J Endod 1985; 11: 525- 52812. Peciuliene V, Reynaud A, Balciuniene I, Haapasalo M. Isolation of yeast andenteric bacteria in root-filled teeth with chronic apical periodontitis. Int Endod106

J 2001; 34: 429- 43413. Portenier I, Haapasalo H, Rye A, Waltimo T, Ørsavik D, Haapasalo M.Inactivation of root canal medicaments by dentine; hydroxylapatite andbovine serum albumin. Int Endod J 2001; 34: 184- 18814. Rusell AD. Antibacterial activity of chlorhexidine. J Hosp Infect 1993; 25:229-23815. Spängberg L, Engström B , Langeland K. Biologic effects of dentalmaterials.3. Toxicity and antimicrobial effect of endodontic antiseptics invitro. Oral Surg Oral Med Oral Pathol 1973; 36: 856- 87116. Trope M, Sigurdson A. Clinical manifestations and diagnosis. In Ørstavik D,Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment ofApical Periodontitis 199817. Ørstavik D, Haapasalo M. Disinfection by endodontic irrigants and dressings ofexperimentally infected dentinal tubules. Endod Dent Traumatol 1990; 6: 142- 149107

CASE 12 – Apical periodontitis with a sinus tract andobliterated canalsPatient:White Norwegian female, 60 years old, working as asecretary at the Faculty of Odontology. She detected asinus tract in the area of 26, and got an appointmentfor endodontic examination and treatment at theEndodontic Department.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:Tooth 26 was tender to chewing, and had been so fora couple of weeks. The gold crown was made about30 years ago.108

Clinical findings Tooth: 26Extra oral:Intra oral:normal skinSinus tract with an opening at the buccal mucosabetween tooth 25 and 26.Dental:Tooth 26 had an gold crown.The tooth was tender to palpation apically and had anegative response to the electric sensibility-test.Tooth 25 and 27 showed no signs relevant to the chiefcomplaint.Periodontal:No mobility. PPD (periodontal probing depth) withinnormal limits.Fig. 2 gutta-percha point in sinus tractRadiographic findings:Tooth :26Periodontal:Apical lesion around the mesio-buccal root of tooth26. Radiograph with a gutta-percha point in the sinustract confirmed the presence of a communicationbetween the oral mucosa and the lesion.109

Dental:Other:Radiopaque material was demonstrated in the coronalpart of tooth 26, verified clinically as the gold crownNo findings in relation to tooth 15 or 17 that wouldinfluence the diagnosis or the treatment.Fig.3 preoperative x-rayDiagnosis:Tooth : 26Apical periodontitis with a sinus tractTreatment plan:Tooth :26Problem list:Root canal disinfection and fillingObliterated canalsTreatment:Date:12.12.2006Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Threecanals were located and instrumented manually withNiTi files to dimension:Mb # 45, 21 mm ref: mb cuspDB # 45, 20 mm ref: ml cuspD # 60, 22 mm ref: mb cusp110

Irrigation with 1% NaOCl and 15% EDTA.The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Fig.4 working lengthNext appointment; 25.01.2007The sinus tract was no longer visible.The MB2 canal was located but not instrumentedduring the first appointment. An attempt was made tofind the canal, using round bur and ultra-sound. Thecanal was obliterated and we had to give up.Next appointment; 28.02.2007Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. Three canals were dried with sterile paperpoints and filled by cold lateral condensationtechnique with gutta-percha and AH-plus sealer. IRM.111

Fig.5 masterpointFig.6 endodontic treatment completedEvaluation:Prognosis:Since the mb root has a radiolucent area, it wasimportant to find both mb canals. The canal orificewas found, but because of obliteration it was notpossible to follow the canal all the way to the apex,without removing too much tooth structure. However,the sinus tract disappeared during treatment. Nocomplications during treatment, the root-fillingappeared dense and good.Favorable112

Discussion:This case was a variant of 26 with three roots with four canals. The two canals inthe mb root may share the same apex. The importance of careful scrutiny of thegroove on the floor of the chamber between the MB and palatal canals is obviousin the detection of the mesiolingual canal.Kulid et al (5) studied 51 maxillary first molars and 32 maxillary second molars,and concluded that the normal anatomy of the maxillary molars was two canalsin the mesiobuccal root.Hess (3) evaluated 513 extracted maxillary first and second molars, and foundthat 54% had 4 canals. Pineda et al (6) reported finding 4 canals in 51,5% offirst and second maxillary molars.Ibarrola et al (4) looked at the different factors affecting the negotiability ofsecond mesiobuccal canals in maxillary molars. The evaluation was done bystudying 87 extracted maxillary molars that had undergone previous endodontictreatment in the endodontic technique laboratory. Several factors that couldinterfere with the total or partial negotiation of MB2 canal were identified andincluded accumulation of debris and sealer that blocked access to these canals,dentinal debris produced with the path-finding instrument, the presence ofanatomical variations, diffuse calcifications, and pulp stones.Location of root canals has been evaluated in vivo and in vitro in researcharticles by using dental loupes, fiberoptic head lamps, scanning electronmicroscopic observation (4). The DOM (dental operating microscope) has beenshown to provide enhanced illumination and magnification for dental procedureson both hard and soft tissues (7). A study done by Baldassari-Cruz et al (1)looked at whether or not the use of DOM would increase detection of ML canalorifice in the MB root of extracted maxillary first and second molars, when notfound in unaided vision in an in vitro mannequin setting. Thirty-nine extractedmaxillary molars were used in the study. The result was that the ML canalorifices were detected in 20 of the teeth with a sharp explorer and a mirror. Inthe remaining teeth, 12 ML canal orifices were located by using the DOM. Theresults of their study indicated that the DOM increases the opportunity for thedentist to detect canal orifices.In this case DOM was used to detect and negotiate the MP canal.113

Reference list:1. Baldassari-Cruz LA, Lilly JP, Rivera EM. The influence of dental operatingmicroscope in locating the mesiolingual canal orifice. Oral Surg Oral Med OralPathol Oral Radiol Endod 2002; 93: 190-1942. Carr GB. Microscopes in endodontics. J Calif Dent Assoc 1992; 20: 55-583. Hess W, Zurcher E. The Anatomy of root canals of the teeth of permanentdentition. London: John Bane, Sons and Danielsson, 1925; pp. 32-34, 75, 774. Ibarrola JL, Knowles KI, Ludlow MO, McKinley Jr IB. Factors affecting thenegotiability of second mesiobuccal canals in maxillary molars. J Endod 1997;4: 236-2385. Kulid JC, Peters DD. Incidence and configuration of canal systems in themesiobuccal root of maxillary first and second molars. J Endod 1990; 13: 106-1126. Pineda F, Kuttler Y. Mesiobuccal and buccolingual roentgenographicinvestigation of 7275 root canals. Oral Surg Oral Med Oral Pathol 1972; 33:101-1107. Stropko JJ. Canal morphology of maxillary molars: clinical observations ofcanal configurations. J Endod 1999; 25: 446-450114

CASE 13 – Acute apical periodontitis with a flare-upPatient:White Norwegian female, 38 years old. The patient wasreferred from her private practitioner to the post graduate clinic for endodontictreatment of tooth 15, on March 20, 2006Fig 1: Preoperative photoMedical history:Non-contributoryDental history and chief complaint:Tooth 15 was restored with a PFM crown in 2003.After cementing the crown the tooth became symptomatic and root filled.Recently she had felt a numness in the area, and her regular dentist took aperiapical x-ray, witch showed a radiolucent area around the root apex. The rootfilling was too short, and the patient was referred to our clinic.115

Fig 2. tooth 15; a crown with a composite occlusally. Porcelain islost around the composite.Clinical findings:Tooth: 15Extra oral:Intra oral:Dental:normal skinnormal soft tissueTooth 15 was restored with a porcelain crown. It wasTender upon biting, tender to palpation apically andtender to percussion.No other findings on other teeth in the area.Periodontal:PPD within normal limitsRadiographic findings:Tooth: 15Periodontal:Dental:Other:Radiolucent area apically short root filled tooth, twoobliterated canals in the apical part.Tooth restored with a PFM crown.No findings116

Fig 3. PreoperativeDiagnosis:Treatment plan:Problem list:Tooth: 15 acute apical periodontitisTooth: 15 RetreatmentRoot canal disinfection and fillingCanal obliterationTreatment:Date: 20.03.2006Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Twocanals were located and instrumented manually withNiTi files and Race instrumentation system todimension:B # 50, 21 mm ref: B cuspP # 50, 20 mm ref: P cuspIrrigation with 1% NaOCl and 15% EDTA.The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.117

Fig 4. Working length 1 st and 2 nd step.Date:24.03.2006Flare up. The patient made contact in the weekend,because of severe pain. A firm palpable lesion haddeveloped over the root apex. Her symptoms startedon day three. She felt a pressure building up apicallyof tooth 15. She decided to contact a generalpractitioner and got an appointment with him.The private dentist performed an incision. A lot ofexudate and fluid emptied itself. The patient wasimmediately relieved. She was prescribed with acombination of antibiotics: Metronidazol andPhenoxymethyl-penicillin, and recommended to rinsewith Chlorhexidine mouthwash.Next appointment; 03.04.2006The patient was almost asymptomatic when arrivingat the clinic. A small fluctuant swelling could bepalpated, and the wound after the incision was visible.Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. Two canals were dried with sterile paper pointsand refilled with Ca(OH)2 and IRM.Next appointment; 08.06.2006The patient was asymptomatic. Rubber dam wasapplied and the field disinfected with chlorhexidineand ethanol. Ca(OH)2 was removed. The canals were118

irrigated with 1% NaOCl and 15% EDTA. Two canalswere dried with sterile paper points and filled by coldlateral condensation technique with gutta-percha andAH- plus sealer. IRM at the top.Fig 5: Masterpointcompeted.Evaluation:Fig 6: Endodontic treatmentThe root-filling appeared dense and good.Prognosis:FavorableFollow-up examination: No subjective symptoms.The radiograph showed good healing.Fig 7 1 year follow-up.119

Discussion:During the process of root canal instrumentation small amounts of debris,including pulp remnants, dentin filings, microorganisms and medicaments, maybe pushed out through the apical foramen into the periapical tissues. The hostreaction to this event is an inflammatory response to deal with the entry of theseforeign materials into the area. One of the consequences of the inflammatoryreaction is clinical symptoms which can range from no postoperative pain tomoderate or even severe pain, which may last several days (9).The periapical diagnosis of acute apical periodontitis, have been shown in moststudies to also result in a significantly higher flare-up rate. In addition, theradiographic presence of a periapical lesion, particularly larger lesions, alsoserves as a risk factor for development of flare-ups (9).Most studies regarding this issue have examined the types of treatment as areason for exacerbation (1,8), and in general have found little correlationbetween exacerbations and the nature of treatment.In most cases the amount of debris and number of bacteria are low so that thehost defense is able to rapidly eliminate the foreign material. In some cases,however sufficient numbers of virulent bacteria may be introduced into theperiapical tissues that have the capacity to interfere with the host defense andinduce an exacerbation.An exacerbation is by definition a periapical abscess which occurs in a toothundergoing endodontic treatment. Inoculation of microorganisms into theperiapical tissues typically occurs during instrumentation of the canal causing aperiapical abscess soon after treatment, within the first 24 hours. The symptomsare marked pain, often increasing in intensity, as well as clinical signs of mucosalredness or swelling and a general feeling of malaise. The swelling may be welllocalized in the form of a discrete lump adjacent to the tooth or may be broadand diffuse, spreading into the lip, cheek or face as facial cellulites (7).Studies which have examined the type of bacteria associated with periapicalabscess formation have revealed that the infections are polymicrobial, dominatedby anaerobes and that significant associations exist between particular bacteriaand signs and symptoms. Infection of the root canal with combinations ofbacteria containing the black pigmented anaerobes Pevotella intermedia,Porphyromonas endodontalis or Porphyromonas gingivalis increases the risk thata purulent apical inflammation will develop (6). The concomitant occurrence ofpeptostreptococci, especially peptostreptococcus micros with P. intermedia orP.endodontalis seems to increase the risk of post treatment abscess formation(6). Other studies (3) have demonstrated that Fusobacterium nucleatum isanother Gram-negative bacteria that may be a causative and/or contributingagent in endodontic flare-ups.The bacteria appear to be associated with the most severe forms ofinterappointment flare-ups, including pain. Structural components of its cell wall(i.e lipopolysaccharides) have been found to act as endotoxins that provokeinflammatory reactions. Synergistic associations with other pathogenic bacteria,120

such as Prevotella intermedia, Porphyromonas gingivalis and Peptostreptococcusmicros, may also add its pathogenic potential (3).The management of an acute exacerbation usually involves three measures:1. Re-cleaning the root canal2. Drainage3. Antibiotics and pain reliefRe-cleaning of the root canal in this case, was performed after the the incisionand drainage. We re-instrumented the canal, the patient was asymptomatic andwe used 2% chlorhexidine gluconate and NaOCl as antibacterial irrigants. NaOClis well known for its strong antibacterial activity ( 2,5). CHX has alsodemonstrated a wide antibacterial spectrum and is effective against both Grampositiveand Gram-negative bacteria as well as yeast (4). We decided to fill thecanal permanently with MTA after re-cleaning it, instead of remedicating withCa(OH) 2.The patient was also given antibiotics. The selection of an appropriate antibioticin the management of an exacerbation is based on the types of microorganismspresent and their known sensitivity. Since these infections are usuallypolymicrobial, they may contain some species which have the capacity forantibiotic resistance. However, it is not necessary for all microorganisms to besensitive to the antibiotics for an infection to resolve, since killing of some florachanges the nature and effectiveness of the collective consortium allowing animproved response by the host defence (7). The antibiotic of first choice is stillpenicillin, since it has the best balance of appropriate antimicrobial spectrum andrelatively low clinical toxicity. Depending on the clinical circumstances andseverity of infection, the penicillin can be supplemented with metronidazole,which is especially effective against Gram- negative anaerobes.121

Reference list:1. Balban FS, Skidmore AE, Griffin JA. Acute exacerbations following initialtreatment of necrotic pulps. J Endod 1984; 10: 78- 812. Byström A, Sundqvist G. The antibacterial action of sodiumhypochlorite andEDTA in 60 cases of endodontic therapy. Int Endod J 1985; 18: 35-403. Chavez de Paz LE. Fusobacerium nucleatum in endodontic flare- ups. OralSurg Oral Med Oral Pathol Oral Radiol Endod 2002; 93: 179-834. Shaker LA, Dancer BN, Russell AD, Furr JR. Emergence and development ofchlorhexidine resistance during sporulation of Bacillus subtilis 168.5. Siqueira JF jr, Rocas IN, Santos SR, Lima KC, Magalhaes FA, Uzeda M. Efficacyof instrumentation techniques and irrigatioen regimens in reducing thebacterial population within root canals. J Endod 2002; 28: 181-1846. Sundqvist GK, Eckerbom MI, Larsson ÅP, Sjögren U. Capacity of anaerobicbacteria from necrotic pulp to induce purulente infections. Infection andimmunity 1979; 25: 685- 6937. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. InØrstavik D, Pitt Ford TR, ed. Essential Endodontology: Prevention andTreatment of Apical Periodontitis 19988. Torabinejad M, Kettering JD, McGraw JC, Cummings RR, Dwyer TG, Tobias TS.Factors associated with interappointment emergencies of teeth with necroticpulps. J Endod 1988; 14: 261-669. Walton RE. Interappontment flare-ups: incidenve, related factors, preventionand management. Endod Topics 2002, 3, 67-76122

CASE 14 – Retreatment and ApicoectomiPatient:A 35 year old white Norwegian female was referred tothe Postgraduate Endodontic Clinic, Faculty ofDentistry, University of Oslo, from the UndergraduateClinic.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:16.08. 2001: Acute pulpitis tooth 36 due to deepcaries.At the next dental check-up in 2004 she visited in ourfaculty.Radiographic examination showed chronic apicalperiodontitis on tooth 36, distal root.No history of pain or discomfort.123

Clinical findings:Tooth: 36Extra oral:normal skinTooth 35 36 37IntraoralswellingTender topercussion_ _ __ _ _Tender topalpation_ _ _GPD _ _ _Other:No clinical findings or symptoms from the other teethin the upper and lower right quadrants relevant to thechief complaint.Radiographic findings:Tooth: 36Periodontal:Periapical lesions around distal roots.Dental:Other:The tooth was restored coronally with a radiopaquematerial verified clinically as a composite filling.The intraoral radiographic examinations demonstratedan acceptable distance from the periapical lesions tocanalis mandibularis.124

Fig.2 Preoperative x-rayDiagnosis:Treatment plan:Problem list:Tooth: 36: chronic apical periodontitisTooth: 36: Conventional retreatmentNegotiating of another distal canal?Root canal disinfection and filling.Why did it fail the first time?- distal root, short filling- anatomyTreatment:Date: 10.11.2004Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. Threecanals were located and instrumented manually withNiTi files to dimension:125

Fig.3 Working length x-raysMB: # 40/23mm, ref: mbcDL: # 45/22mm, ref: dlcBL: #40/21mm, ref: BCDB: #45/20mm ref: dbcIrrigation with 1% NaOCl and 15% EDTA. The canalswere dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Next appointment; 13.03.2005Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canals were irrigated with 1% NaOCl and 15%EDTA. Three canals were dried with sterile paperpoints and filled by cold lateral condensationtechnique with gutta-percha and AH-plus sealer. IRM.126

Fig.4 Masterpoint x-rayEvaluation:Prognosis:No complications during treatment, the root-fillingappeared dense and good.FavorableFollow-up examination:21.03.2006: No subjective symptoms from tooth 36.The tooth was restored with a PFM (porcelain fused tometal) crown.No signs of healing. There was still an apicalradiolucency around distal root.Diagnosis: tooth 36: chronic apical periodontitisTreatment: Apicoectomi tooth 36, distal root127

Problem list:The anatomical relations between the root apices inthe molar region in the left lower jaw and the canalismandibularis was important to define before we couldperform the Apicoectomi.The patient was referred to the Department ofRadiology for panoramic radiographic examination. Inthat way we could have an overview of the importantanatomical structures in the area.Fig.5 OPGThe patient met for surgery, 4 carpules with Xylocain-adrenaline were injected toestablish anesthesia. The patient rinsed for 1 minutewith Chlorhexidine mouthwash. Intrasulcular buccalincision from the distal surface of tooth 37 to themesial surface of tooth 33, with vertical releasingincision from tooth 33 towards the inferior aspect ofthe buccal mucosa. Surgical blade number 15 wasused. The flap was elevated. The apical lesion did notperforate the cortical bone. The intraoral radiographswere calibrated with a periodontal probe andmeasured the site of the lesion. Osteotomy wasperformed with a round bur no 16 with copiousirrigation with sterile saline, until the lesion waslocated and the mesial and distal roots were visible.Granulation tissue was removed by curettage.128

Resection of 3 mm of distal root with a long fissurebur on a high speed hand piece. It was difficult to seethe foramen, and we decided to leave the root withouta retrograde filling. Haemostasis in the bone cavitywas achieved with strypnongaze. The flap wasrepositioned and sutured with 7, 5-0 silk sutures.Postoperative information was given. Ice bag was keptat the patients’ right cheek, over the surgical site for15 minutes. Medications were prescribed: Pinex forteand Pinex. Chlorhexidine mouthwash wasrecommended.Fig.6 during surgeryFig 7. x-ray during surgeryFig.8 post surgery129

One week later:Prognosis:The patient was asymptomatic. No negative clinicalfindings. No numbness in the area where surgery wasperformed.FavorableFig.9 photo 6 months post-opFollow-up examination: 15.11.2006The patient was asymptomatic.No negative clinical findings.The radiographic examination demonstrated goodhealing.Fig.10 x-ray 6 months post-op130

Discussion;Endodontic re-treatment is generally considered to have a lower prognosis thanprimary endodontic cases, with the poorest outcome in retreated teeth/rootswith apical periodontitis.Studies that document retreatment in teeth with apical periodontitisdemonstrate that 56-84% of these lesions heal completely, on the other hand,studies of teeth without apical periodontitis, demonstrate a success rate of 89-100% (1).In addition to the preoperative status (2) the success rate of nonsurgicalretreatment in teeth with periapical pathosis also depends on the technicalstandard of the root-filling, with the lowest success rate when the root-fillingextended beyond the root apex (3).The major factors associated with endodontic failure are the persistence ofmicrobial infection in the root canal system and/ or the periradicular area (4,5).Bacteria located in areas such as isthmuses, ramifications, deltas, irregularitiesand dentinal tubules may sometimes be unaffected by endodontic disinfectionprocedures.In Sundqvist et al (6) and previous studies (7,8) the microbial flora detected inroot-filled canals could be characterized as monoinfections of predominantlyGram-positive microorganisms, with approximately equal proportions offacultative and obligate anaerobes.This composition differs markedly from that seen in infections of the untreatedcanal, which typically have a polymicrobial flora with approximately equalproportions of Gram-negative and Gram-positive bacteria and are dominated byobligate anaerobes (9,6)While selective pressures exist in the untreated canal that favor theestablishment of a very restricted group of the oral flora ( 9,10), specialconditions must also apply to the microorganisms that can persist in the rootfilledcanal.Enterococci are often reported to be low in numbers in untreated infected rootcanals with necrotic pulps (9). However, when the ecological prerequisites arealtered, enterococci may thrive and multiply.Gomes et al (11) reported multiplication of E.faecalis in some canals followingstandard biomechanical treatment procedures.Rocas et al (12) studied the association of Enterococcus faecalis with differentforms of periradicular disease. Statistical analysis showed that E. faecalis wassignificantly more associated with asymptomatic cases than with symptomaticones. E. faecalis was detected in 20 of 30 cases of persistent endodonticinfections associated with root-filled teeth.The average odds of detecting E. faecalis in cases of persistent infectionsassociated with treatment failure was 9.1.However, the major involvement of E. faecalis with asymptomatic periradiculardisease supports the assumption that enterococci are in general not highly131

virulent microorganisms, and their emergence as pathogens can be much morerelated to resistance to several antimicrobial agents than to high virulence.132

Reference list1. Friedman S. Treatment outcome and prognosis of endodontic therapy. InØrstavik D, Pitt Ford T, editors. Essential Endotology. Oxford: BlackwellScience Ltd; 19982. Bergenholtz G, Lekholm U, Milthon R, Engström B. Influence of apicalover instrumentation and overfilling on re-treated root canals. J Endod1979B; 5:310-3143. Sjögren U, Hagglund B, Sundqvist G, Wing K. Factors affecting the long-termresults of endodontic treatment. J Endod 1990; 16: 498-5044. Lin LM, Skibner JE, Gaengler P. Factors associated with endodontic treatmentfailures. J Endod 1992; 18: 625-6275. Nair PNR, Sjögren U, Krey G, Kahnberg KE, Sundqvist G. Intraradicularbacteria and fungi in root filled, asymptomatic human teeth with therapyresistantperiapical lesions: a long termlight and electron microscopic followupstudy. J Endod 1990; 16: 580-5886. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth withendodontic treatment and the outcome of consercative treatment. Oral Surgoral Med Oral Pathol 1998; 85: 86-937. Molander A, Reit C, Dahlén G. Kvist T. Microbiological examination of rootfilledteeth with apical periodontitis. Int Endod J1994; 27: 1048. Möller ÅJR. Microbiological examination of root canals and periapical tissues ofhuman teeth. Odont Tidskrift 1966-74:(supplement): 1-3809. Sundqvist G. Associations between microbial species in dental root canalinfections. Oral Microbiol Immunol 1992; 7: 257-26211. Gomes BPFA, Drucker DB, Lilley JD. Variations in the susceptilities ofcomponents of the endodontic microflora to biomechanical procedures. IntEndod J 1996; 29: 235-24112. Rocas IN, Siqueira JF, Santos KRN. Association of Enterococcus faecalis withDifferent forms of periradicular diseases. J Endod 2004; 5: 315-320133

CASE 15 - Ekstra-radiculær infectionPatient:White Norwegian female, 62 years old. The patientwas referred to the postgraduate clinic for evaluationand treatment of tooth 45.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:The patient was referred to private practice. Tooth 45was previously root filled, and because of chronicmarginal periodontitis it as not much bone around thetooth. Her private practitioner asked for evaluationand treatment of tooth 45. He wrote that he thoughtthe tooth was lost, but the patient insisted to try andkeep it as long as possible.Clinical findings:Tooth:45134

Extra oral:Intra oral:Dental:Periodontal:normal skinnormal soft tissuePFM (porcelain fused to metal) crown. The tooth wasslight tender to percussion. The crown had a good fit,and no signs of coronal leakage.A sinus tract was detected in a narrow pocketmesially.Radiographic findings:Tooth:45Periodontal:Dental:Other:Chronic marginal periodontitis, bone loss around thetooth, mostly mesially. Radiolucent area ofapproximately 10. mm in diameters.Root-filled tooth. Restored with a PFM crown.46: chronic apical periodontitis.Diagnosis:Problem List:Fig.2 preoperativeTooth: 45: Chronic apical periodontitis.The patient was informed that the treatment outcomehad an uncertain prognosis. She said that she waswilling to try and rescue the tooth. She already had135

extracted several teeth in her younger days, and shedidn’t want to give up without trying.Treatment plan:Tooth: 45: RetreatmentTreatment:Date: 17.08.2006Medical and dental history. Treatment plan.Access preparation. Rubber dam was applied and thefield disinfected with chlorhexidine-ethanol. One canalwas located and instrumented manually with NiTi filesto dimension:Mb # 60, 17 mm ref: mb cuspFig.3 persistent sinus tractExudate in the canal.Irrigation with 1% NaOCl and 15% EDTA.The canalwas dried with sterile paper points and packed withCa(OH)2 and IRM as a top filling.Next appointment; 14.09.2006Rubber dam was applied and the field disinfected withchlorhexidine and ethanol. Ca(OH)2 was removed.The canal was irrigated with 1% NaOCl and 15%EDTA. Still there was puss in the canal. The canal wasdried with sterile paper points and filled by cold lateral136

condensation technique with gutta-percha and AHplussealer. IRM.We decided to do an Apicoectomi as a last try to keepthe tooth. To minimize the expenses, I referred her tomyself at the Department of Endodontics.Fig.4 after retreatmentDiagnosis:Problem list:Tooth: 45: Ekstraradicular infection.The anatomical relations between the root apice andforamen mentale was important to define before wecould perform the Apicoectomi. When operating closeof a nerve foramen, there is a chance of parestesie inthe area. The patient was informed.The patient was referred to the Department ofRadiology for panoramic radiographic examination. Inthat way we could have an overview of the importantanatomical structures in the area.137

Fig.5 OPGDate: 12.12.2006The patient met for surgery, 3 carpules with Xylocainadrenalinewere injected to establish anesthesia. Thepatient rinsed for 1 minute with Chlorhexidinemouthwash. Intrasulcular buccal incision from thedistal surface of tooth 46 to the buccal surface oftooth 43, with vertical releasing incision from tooth 43towards the inferior aspect of the buccal mucosa.Surgical blade number 15 was used. The flap waselevated. The apical lesion did not perforate thecortical bone. The intraoral radiographs werecalibrated with a periodontal probe and measured thesite of the lesion. Osteotomy was performed with around bur no 16 with copious irrigation with sterilesaline, until the lesion was located and the root wasvisible. Granulation tissue was removed by curettage.Because of the resorption-defect we decided not tocut the root, just to clean the root-surface. The apicalforamen was demonstrated. Retrograde preparationwas performed with piezoelectric Satelec ultrasounddevice, using ultrasonic tip CT under constant coolingwith sterile saline, but there were very little space fora retrograde filling. The gutta-percha was removeduntil the inferior border of the post. The retropreparationwas dried with sterile paper points.Haemostasis in the bone cavity was achieved with138

strypnongaze. A retrograde filling with MTA wasmade. The flap was repositioned and sutured with 7,5-0 silk sutures. Postoperative information was given.Ice bag was kept at the patients’ upper lip, over thesurgical site for 15 minutes. Medications wereprescribed: Pinex forte and Pinex. Chlorhexidinemouthwash was recommended.Fig.6 during surgeryFig.7 during surgery139

Granulation tissue removed fromthe periapical cavity.Fig.8 post surgeryOne week postoperative:After surgery examination and suture removal. Thetooth was mobile grade 2. This had not been the casepreviously. A slight numbness’ in the area where weperformed the surgery, corresponding to the regioninnervated with nervus alveolaris inferior was evident.The healing was otherwise satisfactory, and thepatient had not experienced much pain.Evaluation:The retrograde filling of MTA is about 4 mm andappeared dense and good.After sequela with numbness’ in the area innervatedwith nervus alveolaris inferior are to be expected aftera surgical treatment like this. Preoperative informationis of outmost importance to avoid unnecessary anxietyand frustrations.The retro-filling appeared dense and of good quality.140

Prognosis:QuestionableFollow-up examination:3 months post-operativeThe patient was asymptomatic. No negative clinicalfindings. No numbness in the area where surgery wasperformed. No mobility.The radiographic examination demonstrated goodhealing.27.03.2007 27.03.2007Fig.9 3 months postopEvaluation:Uncertain prognosis because of short root and littlebone. The patient was satisfied with the result. Sheneeded time to prepare herself for a possibleextraction of the tooth.141

Discussion:The major factors associated with endodontic failure are the persistence ofmicrobial infection in the root canal system and/ or the periradicular area (3, 8).The clinician is often mislead by the notion that procedural errors, such asbroken instruments, perforations, overfilling, underfilling, ledges and so on arethe direct cause of endodontic failure. In most cases, procedural errors do notjeopardize the outcome of endodontic treatment unless a concomitant infectionis present. A procedural accident often impedes or makes it impossible toaccomplish appropriate intracanal procedures, and then there is a potential forfailure. There are however some cases in which the treatment has followed thehighest technical standards and yet failure occurs. Scientific evidence (9,10,13)indicates that some factors may be associated with the unsatisfactory outcomeof well-treated cases.They include: - microbial factors- Ekstraradicular and/ or intraradicular infections- intrinsic non microbial factors- extrinsic non microbial factorsBacteria located in areas such as isthmuses, ramifications, deltas, irregularitiesand dentinal tubules may sometimes be unaffected by endodontic disinfectionprocedures. In Sundqvist et al (14) and previous studies (5,7) the microbial floradetected in root-filled canals could be characterized as monoinfections ofpredominantly Gram-positive microorganisms, with approximately equalproportions of facultative and obligate anaerobes. This composition differsmarkedly from that seen in infections of the untreated canal, which typicallyhave a polymicrobial flora with approximately equal proportions of Gramnegativeand Gram-positive bacteria and are dominated by obligate anaerobes(13,14) While selective pressures exist in the untreated canal that favor theestablishment of a very restricted group of the oral flora ( 13,15), specialconditions must also apply to the microorganisms that can persist in the rootfilledcanal. Molander et al (6) examined the microbiological status of 100 rootfilledteeth with radiographically verified apical periodontitis- the pathology (P)group and of 20 teeth without signs of periapical pathosis- the technical group(T). In the P group 117 strains of bacteria were recovered in 68 teeth. In most ofthe cases examined, one or two strains were found. Facultative anaerobicspecies predominated among these isolates (69% of identified strains). Growthwas classified as sparse or very sparse in 53%, and as heavy or very heavy in42%. Enterococci were the most frequently isolated genera, showing heavy orvery heavy growth in 25 out of 32 cases (78%).Rocas et al (11) showed that E. faecalis was significantly associated withtreatment failures. Whereas this species was detected in 18% of the cases ofprimary endodontic infections, its prevalence in root-filled teeth was muchhigher: 67% of the cases. This finding suggests that this species can be inhibitedby other members of a mixed bacterial consortium commonly present in primaryinfections, and that the bleak environmental conditions within filled root canals142

may not prevent its survival. For a given microorganism to survive in a filled rootcanal, it must resist intracanal procedures of disinfections and endure periods ofstarvation. Studies have revealed that E. faecalis has the ability to penetrate andinvade dentinal tubules and adhere to collagen in the presence of human serum(4), sometimes to a deep extent. This property can enable this species to escapefrom the action of endodontic instruments and irrigants used during chemomechanical preparation. E. faecalis is also resistant to calcium hydroxide (1).E. faecalis can colonize root canals in single infections and such a relativeindependence of living without deriving nutrients from other bacteria is arguablyessential for its establishment in filled root canals (14). Finally, environmentalcues can also regulate gene expression in E faecalis, which can allow themicroorganisms to adapt to varying environmental conditions (2). This includesthe ability to survive in environments with scarce nutrients and to flourish whenthe nutrients is re- established.143

Reference list:1. Evans M, Davies JK, Sundqvist G, Figdor D. Mechanisms involved in theresistance of Enterococcus faecalis to calcium hydroxide. Int Endod J 2002;35: 221-2282. Jett BD, Huycke MM, Gilmore MS. Virulence of enterococci. Clin Microbiol Rev1994; 7: 462-4783. Lin LM, Skibner JE, Gaengler P. Factors associated with endodontic treatmentfailures. J Endod 1992; 18: 625-6274. Love MR. Enterococcus faecalis- a mechanism for its role in endodontic failure.Int Endod J 2001; 34: 399-4055. Molander A, Reit C, Dahlén G. Kvist T. Microbiological examination of rootfilledteeth with apical periodontitis. Int Endod J 1994; 27: 1046. Molander A, Reit C, Dahlén G. Kvist T. Microbial status of root-filled teeth withapical periodontitis. Int Endod J 1998; 31: 1-77. Möller ÅJR. Microbiological examination of root canals and periapical tissues ofhuman teeth. Odont Tidskrift 1966-74:(supplement): 1-3808. Nair PNR, Sjögren U, Krey G, Kahnberg KE, Sundqvist G. Intraradicularbacteriaand fungi in root filled, asymptomatic human teeth with therapy-resistantperiapical lesions: a long termlight and electron microscopic follow-up study. JEndod 1990; 16: 580-5889. Nair PNR, Sjögren U, Schumacher E, Sundqvist G. Radicular cyst affecting aroot- filled human tooth: a long-term post-treatment follow-up. Int Endod J1993; 26:225-23310. Nair PNR, Sjögren U, Figdor D, Sundqvist G. Persistent periapicalradiolucencies of root-filled human teeth, failed endodontic treatment, andperiapical scars. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87:617-62711. Rocas IN, Siqueira JF, Santos KRN. Association of Enterococcus faecalis withdifferent forms of periradicular diseases. J Endod 2004; 5: 315-32012. Sjögren U. Success and failure in endodontics. Odontol Dissertations. Umeå,Sweden: Umeå University; 199613. Sundqvist G. Associations between microbial species in dental root canalinfections. Oral Microbiol Immunol 1992; 7: 257-262144

14. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth withendodontic treatment and the outcome of consercative treatment. Oral Surgoral Med Oral Pathol 1998; 85: 86-9315. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. InØrstavik D, Pitt Ford T, editors. Essential endotology. Oxford: BlackwellScience Ltd; 1998145

CASE 16 – Surgical retreatmentPatient:White Norwegian male, 70 years old. The patient wasreferred to the postgraduate clinic for evaluation andretreatment of an apical infection on tooth 22 fromthe undergraduate clinic.Fig.1: preoperative photoMedical history:Non-contributoryDental history and chief complaint:The patient complained about tenderness in the areaof 22. Tooth 22 was root filled and a PFM crown with a post was cemented ontop. This was about 30 years ago, and the patient was very interested in keepingthe crown because he likes the look of it. The economical issue is also of greatinterest, and he wants to keep the costs as low as possible.Clinical findings:Tooth:22Extra oral:normal skin146

Intra oral:Dental:Periodontal:Other:normal soft tissuePFM (porcelain fused to metal) crown. The tooth wasslight tender to percussion. The crown had a good fit,and no signs of coronal leakage.normal findingsno clinical findings or symptoms from the other teethin the upper and lower right quadrants relevant to thechief complaint.Fig.2 Mirror image of the palatal view of 22.Radiographic findings:Tooth:22Periodontal:Dental:Periapical lesion around the root apex.The tooth was restored coronally with a radiopaquematerial verified clinically as the PFM crownrestoration. The crown appeared to have a good fit.A radiopaque material was demonstrated, extending1/3 in the root, corresponded to the post. A smallpiece of a root-filling is visible.147

Fig.3 preoperativeDiagnosis:Treatment plan:Tooth:22 : Acute apical periodontitisTooth:22 : Surgical retreatmentTreatment:Date:05.04.2005Date:03.05.2005Medical and dental history. Treatment plan.The patient met for surgery, 3 carpules with Xylocainadrenalinewere injected to establish anaesthesia. Thepatient rinsed for 1 minute with Chlorhexidinemouthwash. Intrasulcular buccal incision from thedistal surface of tooth 23 to the mesial surface oftooth 23 , with vertical releasing incision from tooth23 towards the inferior aspect of the buccal mucosa.Surgical blade number 15 was used. The flap waselevated. The apical lesion did not perforate thecortical bone. The intraoral radiographs werecalibrated with a periodontal probe and measured thesite of the lesion. Osteotomy was performed with around bur no 16 with copious irrigation with sterilesaline, until the lesion was located and the root wasvisible. Granulation tissue was removed by curettage.Resection of 3 mm of the root with a long fissure buron a high speed hand piece. The apical foramina wasdemonstrated. Retrograde preparation was performedwith piezoelectric Satelec ultrasound device, using148

ultrasonic tip CT under constant cooling with sterilesaline. The gutta-percha was removed until theinferior border of the post. The retro-preparation wasdried with sterile paper points. Haemostasis in thebone cavity was achieved with strypnongaze.Retrograde filling with MTA was placed. The flap wasrepositioned and sutured with 7, 5-0 silk sutures.Postoperative information was given. Ice bag was keptat the patients’ lip, over the surgical site for 15minutes. Medications were prescribed: Pinex forte,Pinex and Apocillin 660 mg. Chlorhexidine mouthwashwas recommended.Fig.4 during surgeryFig.5 during surgery, granuloma149

Fig.6 MTA in the canalFig.7 After surgery150

Fig.8 post-op x-ray10.05.2005 After surgery examination and suture removal. He had a hematomeat his right cheek. Otherwise the healing was satisfactory, and the patienthad not experienced much pain.Fig.9 one week post-opEvaluation:The retro filling appeared dense and good. Nocomplications during treatment.151

Prognosis:FavorableFollow-up examination: No subjective symptoms. The radiograph shows goodhealing.Fig.102 years follow-up.Fig.11 radiograph taken two year post-op.152

Discussion:Success rates ranging from 25-90% for surgical endodontic procedures have beenreported in the literature (1). Such disparity could be explained by the nature of thestudy, the different sample sizes, the period of recall, and the criteria used forevaluating clinical and radiographic parameters of healing. Furthermore, a number ofother factors can affect the prognosis in periradicular surgery, including patientdemographics and systemic conditions, tooth involved, amount and location of boneloss, quality of previous root canal treatment or retreatment, coronal restoration,occlusal microleakage, surgical materials and technique and surgeon skills (1,2).Zulo et al (3) did a prospective study to evaluate the outcome of surgicalendodontics. They used a well defined case selection and an evidence-based,contemporary surgical technique. Data were collected from all patients requiringsurgical treatment in a private practice setting limited to endodontics, during theperiod from January 1992 to December 1993. A total number of 114 patients wereselected and included in the study. The cases met the following criteria:1. One tooth was treated for each patient2. The tooth to be treated surgically had a dental history of failed root canaltreatment, and had at least one nonsurgical retreatment to enhancedebridement.3. The tooth to be treated surgically demonstrated a persistent periradicularlesion of strictly endodontic origin with or without clinical signs and symptomsof inflammation.4. The tooth to be treated exhibited an adequate final restoration with noclinical evidence of coronal leakage.Of the 114 cases treated, five patients could not be seen again. One tooth wasextracted for prosthetic reasons and four patients never responded to the recallrequest, representing a 4,3% drop-out rate. Of the remaining 109 cases, seven wereexcluded from this study for presenting with vertical root fractures. Ultimately, a totalnumber of 102 surgical cases were included in this study, of which 93 were classifiedas a success (91,2%) and nine as failures (8,8%) after the observation period of 1-4years.Zulo et al (3) concluded that with a strict endodontic surgical protocol and the use ofcontemporary techniques and materials (IRM was used in this study as a retrogradefilling material) will result in a predictably successful outcome in a wide range ofteeth.153

Reference list:1. Gutmann JL, Harrison JW. Surgical Endontics: Boston MA, USA: Blackwell ScientificPublications 19912. Rud J, Andreasen JO, Möller Jensen JE. A follow-up study of 1000 cases treated byendodontic surgery. Int Endod J 1972a; 1: 215-2183. Zulo ML, Ferreira MOF, Gutmann JL. Prognosis in periradicular surgery: a clinicalprospective study: Int Endod J 2000; 33: 91-98154

CASE 17 – Apicoectomi : complicated locationPatient:White Norwegian female, 61 years old. The patient wasreferred to the postgraduate clinic for evaluation andtreatment of a persistent apical infection after primaryendodontic treatment and retreatment at an Endodontist.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:Tooth 46 had been retreated because of a persistent sinustract after endodontic treatment. When the patient cameback to the Endodontist after three weeks of ca(OH)2dressing in the root canal, the sinus tract was still there.The dentist called our faculty and made an appointmentfor examination, and she said that she thought we wouldneed to do an Apicoectomi.Clinical findings:Tooth: 46Extra oral:Intra oral:Dental:normal skinsinus tract buccallyPFM (porcelain fused to metal) crown. The tooth wasslight tender to percussion. The crown had a good fit, andno signs of coronal leakage.155

Periodontal:Other:Normal findingsNo clinical findings or symptoms from the other teeth inthe upper and lower right quadrants relevant to the chiefcomplaint.Fig.2 gutta-percha in the sinus tractRadiographic findings:Tooth: 46Periodontal:Dental:Other:Periapical lesions around mesially and distal roots.The tooth was restored coronally with a radiopaquematerial verified clinically as the PFM crown restoration.The crown appeared to have a good fit.The intraoral radiographic examinations demonstrated anacceptable distance from the periapical lesions to canalismandibularis.Fig.3 preoperative x-ray156

Diagnosis:Tooth: 46:Apical periodontitis with a sinus tract.Extra radicular infectionTreatment plan:Tooth: 46:Apicoectomi.Problem list:The anatomical relations between the root apices in themolar region in the right lower jaw and the canalismandibularis was important to define before we couldperform the Apicoectomi.The patient was referred to the Department of Radiologyfor panoramic radiographic examination. In that way wecould have an overview of the important anatomicalstructures in the area.Fig.4 OPGTreatment:21.11.06 Medical and dental history. Treatment plan. The patientwas referred to the Department of Radiology for apanoramic examination and she got an appointment forApicoectomi.23.11.06 Panoramic examination at the Department of Radiology.157

28.11.06 the patient met for surgery, 5 carpules with Xylocainadrenalinewere injected to establish anesthesia. Thepatient rinsed for 1 minute with Chlorhexidine mouthwash.Intrasulcular buccal incision from the distal surface oftooth 47 to the mesially surface of tooth 43, with verticalreleasing incision from tooth 43 towards the inferioraspect of the buccal mucosa. Surgical blade number 15was used. The flap was elevated. The apical lesion did notperforate the cortical bone. The intraoral radiographs werecalibrated with a periodontal probe and measured the siteof the lesion. Osteotomy was performed with a round burno 16 with copious irrigation with sterile saline, until thelesion was located and the mesial and distal roots werevisible. Granulation tissue was removed by curettage.Resection of 3 mm of both roots with a long fissure bur ona high speed hand piece. Three apical foramina weredemonstrated. Retrograde preparation in both roots wasperformed with piezoelectric Satelec ultrasound device,using ultrasonic tip CT under constant cooling with sterilesaline. The retro-preparations were dried with sterilepaper points. Haemostasis in the bone cavity wasachieved with strypnongaze. Two retrograde fillings withMTA were placed. The flap was repositioned and suturedwith 7, 5-0 silk sutures. Postoperative information wasgiven. Ice bag was kept at the patients’ right cheek, overthe surgical site for 15 minutes. Medications wereprescribed: Pinex forte, Pinex and Apocillin 660 mg.Chlorhexidine mouthwash was recommended.Fig.5 during surgery158

Fig.6 During surgeryFig.7 post surgeryFig.8 x-ray post op05.12.06 after surgery examination and suture removal. Someedema was still present on the patient’s right side. A slightnumbness’ in the area where we performed the surgery,corresponding to the region innervated with nervusalveolaris inferior was evident. The healing was otherwisesatisfactory, and the patient had not experienced anypain. She was well informed, and she got a newappointment in 1 week.12.12.06 Satisfactory healing. The patient felt less num.Evaluation:This turned out to be a technically complicated anddemanding surgical treatment. The visibility during thecompletion of the retro-preparations and the retro-fillingswere poor. After sequela with numbness’ in the areainnervated with nervus alveolaris inferior are to beexpected after a surgical treatment like this. Preoperativeinformation is of outmost importance to avoid unnecessaryanxiety and frustrations.159

The retro-fillings appeared tiny.Prognosis:FavorableFollow-up examination:27.03.07 the patient was asymptomatic. No negative clinicalfindings. No numbness in the area where surgery wasperformed.The radiographic examination demonstrated good healing.Fig.9 3 months post op160

Discussion:Evaluating site is one of the most important steps in case selection for periradicularsurgery. Anatomic studies can provide some guidance, but individual variation isgreat, and there is no substitute for a complete clinical examination. A small oralopening, active facial muscles, shallow vestibule, and thick buccal alveolar bone allcan significantly increase the difficulty of the procedure, even in cases that appearstraightforward on radiographic examination.The primary anatomic structure of concern for periradicular surgery in the posteriormandible is the neurovascular bundle that courses through the mandibular canal andexits through the mental foramen.In our case healing of the lesion could first be observed after surgical retreatment.The importance of conservative retreatment of the canals before surgery has beenillustrated in Grung et al (1) showed a retreatment success rate 24% higher in casesof failed endodontic treatment, in which antibacterial measures and refilling of thecanal preceded apical surgery, than in cases in which apical surgery was the onlyprocedure performed. These results, in conjunction with Sjögren et al (2) suggestthat it is possible to attain very high success rates when both the intraradicular andthe extraradicular causes of endodontic treatment are well managed. A high successrate is dependent on the fact that defective root-fillings should, when possible beconventionally retreated and the supplemented, if no signs of periapical healing, withapical surgery (2).161

Reference list:1. Grung B, Molven O, Halse A. Periapical surgery in a Norwegian county hospital: follow-upfindings of 477 teeth. J Endod 1990; 16: 411-4172. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth with endodontictreatment and the outcome of consercative treatment. Oral Surg oral Med Oral Pathol1998; 85: 86-93162

CASE 18 – Cracked toothPatient:White Norwegian female, 30 years old. Referred to thepostgraduate clinic of Endodontics from theundergraduate clinic for treatment of tooth 16, August,2004.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:Tooth 16 was root-filled by an undergraduate student in2002, with a good result. The preoperative diagnosis waspulpitis due to caries profunda. The post operativeradiograph revealed a dense root-filling and the prognosiswas set to be good.When she was at a delayed follow-up examination of thetooth, on August 2004, a fistula was detected and thepatient was referred to the Department of Endodontics.She complained about tenderness on chewing.163

Fig.2 gutta-percha in sinus tract Fig.3 tooth 16Clinical findings:Tooth:16Extra oral:Normal skinIntra oral: A fistula was present buccally of tooth 16.Dental:Periodontal:Other:The tooth was restored with an occlusal composite witchwas of a poor condition. The tooth was tender topercussion.Mecially there was a narrow gingival pocket with aperiodontal probing depth of 7 mm.The other teeth in the upper and lower right quadrantsshowed no signs relevant to the chief complaintRadiographic findings:Tooth:16Periodontal:Dental:The PDL was widened mesially.A radiopaque material was demonstrated inside thecoronal part of the tooth verified clinically as thecomposite filling. A radiopaque material was observed inthe root canal corresponding to the root-filling material.The quality of the root-filling appeared dense and of goodquality.164

Fig.4 Preoperative X-rayFig.5 Gutta-percha point in sinus tractDiagnosis:Prognosis:Treatment plan:Tooth: 16: Cracked toothUncertainTooth: 16: Locate and verify the crack by the use ofoperating microscope.CrackUntreated mb2 canal• Composite restoration was partly removed for access cavity.• Fracture line mesially towards the distal.Treatment:Extraction165

Evaluation:If the tooth had been restored with porcelain fused tometal crown, the tooth would have had a good chance ofsurvival. The patient was given a poor advice when thedecision to make a composite restoration was made."Cracked tooth"166

Discussion:In this case we see a cracket tooth that will, eventually, lead to a vertical rootfracture. A vertical root fracture is a longitudinally oriented fracture of the root,extending from the root canal to the periodontium. It may be initiated in the crownor at the root apex, or, in some cases, along the root between these two points (5).The vertical root fracture may involve the full length of a root, a section of the rootwhich may be either the coronal or apical portion, it may extend into the crown ofthe tooth as well as involving the root, and it may involve both sides of the root(usual finding), but may in some instances involve only one side (5). It is generallyaccepted that vertical root fractures can be caused by various factors including pinand post placement, impact injuries, root canal filling procedures, and seating ofintracoronal restorations.Gehr et al (2) demonstrated in a survey of 100 cases of fractured teeth affecting 98patients during a 2-year period, that the presence of a root canal filling was thesingle most important clinical feature, in 71 of 100 cases. Endodontically treatedteeth are usually week as a result of loss of tooth material due to caries and accesscavities. In addition, the chance of fractures increases due to loss of moisture in thedentin of pulpless teeth (7). Bender et al (1) claimed that the extensive use of rotaryinstruments during preparation of the canal space, for example, cutting the dentin instraight lines particularly at the curvatures, weakened the root structures. Other havealso reported that extensive instrumentation of the root canal space may contributeto weakening of the root canal walls (3, 4), in addition to excessive pressure duringcompaction of gutta-percha (2).Chelating agents have also been suggested to cause embrittlement throughdecalcification of the dentin, and thereby increasing the fracture risk (6).Clinical symptoms seem to develop after fracture occurs, which involves theperiodontium and permits bacterial invasion and subsequent periodontal pocketformation. Once a root fracture involves the periodontium, clinical and radiographicappearance shows that pathologic destruction of the periodontal tissues progressesrapidly and leads to severe bone and attachment loss. Destruction of the periodontaltissues is widespread, extending the full length of the fracture. A periapicalradiograph with a gutta-percha cone inserted in the sinus tract is an importantdiagnostic tool (7).167

Reference list:1.Bender IB, Freedland JB. Adult root fracture. J Am Dent Assoc 1993; 107 413-92.Gehr ME, Dunlap RM, Anderson MH, Kuhl LV. Clinical survey of fractured teeth.AmDent Assoc 1987; 114: 174-73. Langer B, Stein SD, Wagenberg B. An evaluation of root resections. J Periodontol1981;52: 719-224. Meister F, Lommel TJ, Gerstein H. Diagnosis and posiible causes of vertical rootfracture. Oral Surg Oral Med Oral Pathol 1980; 49: 243-535. Pitts DL, Natkin E. Diagnosis and treatment of vertical root fractures. J Endod1983; 8: 338-466. Seidberg BH, Schilder H. An evaluation of EDTA in endodontics. Oral Surg OralMed Oral Pathol 1974; 37: 609-207. Tamse A. Iatrogenic vertical root fractures on endodontically treated teeth.Endod Dent Traumatol 1988; 4: 190-6168

CASE 19 – Vertical root fracturePatient:White Norwegian female, 57 years old. Referred to thepostgraduate clinic, Department of Endodontics, from herprivate practitioner for evaluation and treatment of tooth46.Fig.1 preoperative photoMedical history:Non-contributoryDental history and chief complaint:Tooth 46 had a history of root canal treatment,retreatment and apical surgery. The Apicoectomi wasdone two years ago, by an oral surgeon. The prognosiswas set to be good. The patient had however felt that ithad been something wrong with the tooth from the daythe endodontic treatment was completed. She had paincoming and going for several months. When she was at aregular follow-up examination of the tooth, on August 26,2006, she said that the pain had increased lately. The painwas spontaneous, especially during physical activity.169

Fig.2 Tooth 46Clinical findings:Tooth: 46Extra oral:Intra oral:Dental:normal skinnormal soft tissuePFM (porcelain fused to metal) crown. The tooth wastender to percussion and palpation. The crown seemed tohave a good fit, and no signs of coronal leakage.Periodontal:Other:no mobility or increased PPD (periodontal probing depth).The other teeth in the upper and lower right quadrantsshowed no signs relevant to the chief complaint.Radiographic findings:Tooth: 46Periodontal:Periapical lesions around mesial root, apical part. Becauseof previous Apicoectomi it could correspond to scar tissue.Dental:The tooth was restored coronally with a radiopaquematerial verified clinically as the PFM crown restoration.The crown appeared to have a good fit.A radiopaque material was demonstrated, extending 1/2 inthe distal root corresponding to a post.Other:The intraoral radiographic examinations demonstrated anacceptable distance from the periapical lesions to canalismandibularis.170

Fig 3 Preoperative x-rayTentative diagnosis:Tooth: 46: chronic apical periodontitis.Treatment plan:Problem list:Tooth: 46: ApicoectomiThe anatomical relations between the root apices in themolar region in the right lower jaw and the canalismandibularis was important to define before we couldperform the Apicoectomi.The patient was referred to the Department of Radiologyfor panoramic radiographic examination. In that way wecould have an overview of the important anatomicalstructures in the area.Fig.4 OPG171

Treatment:Date: 16.01.2007Date: 16.01.2007Date: 17.01.2007Medical and dental history. Treatment plan. The patientwas referred to the Department of Radiology for apanoramic examination and he got an appointment forApicoectomi.Panoramic examination at the Department of Radiology.the patient met for surgery, 5 carpules with Xylocainadrenalinewere injected to establish anesthesia. Thepatient rinsed for 1 minute with Chlorhexidine mouthwash.Intrasulcular buccal incision from the distal surface oftooth 47 to the mesial surface of tooth 43, with verticalreleasing incision from tooth 43 towards the inferioraspect of the buccal mucosa. Surgical blade number 15was used. The flap was elevated.The mesial root had a vertical root-fracture. The crownhad not at al a good fit! It was obvious that the tooth hada poor prognosis and that the treatment plan had to berewritten.Fig.5 during surgeryDiagnosis:Treatment:Vertical root fractureExtraction.The tooth was easy to remove; the mesial root was partedfrom the crown.172

Fig.6 after extractionFollow-up examination:Favorable healing of the extraction wound. Normal clinicalfindings. The radiographs demonstrated normal findings.The patient was asymptomatic, and had not experiencedmuch pain in the area after the extraction.173

Discussion:A vertical root fracture is a longitudinally oriented fracture of the root, extendingfrom the root canal to the periodontium. It may be initiated in the crown or at theroot apex, or, in some cases, along the root between these two points (1). Thevertical root fracture may involve the full length of a root, a section of the root whichmay be either the coronal or apical portion, it may extend into the crown of the toothas well as involving the root, and it may involve both sides of the root (usualfinding), but may in some instances involve only one side (1). It is generallyaccepted that vertical root fractures can be caused by various factors including pinand post placement, impact injuries, root canal filling procedures, and seating ofintracoronal restorations.Different instrumentation techniques have been evaluated regarding increasedfracture risk. Morfis (2) examined 460 teeth using different preparation techniques,the step-back technique in conjunction with lateral condensation of gutta-percha(group A) and the single cone technique (group B). He also evaluated the teethregarding to the type and the length of post, and the type of retention of the postused in all 460 teeth. After statistical evaluation of the result, he found that 3, 69%of the teeth had a vertical root fracture. Comparing the two groups, he found thatlateral condensation technique, in a canal prepared with “step-back” is morevulnerable for vertical root fractures. Long posts with length more than half of thelength of the root prepared with “step-back” technique were more responsible forvertical root fractures.To avoid or minimize the potential for vertical root fractures, minimalenlargement and flare preparation of the root canal space have been suggested (7),in addition to the use of nickel-titanium spreaders in curved canals during lateralcondensation (3).The misdiagnosis of vertical root fracture, as an endodontic failure, usuallyleads to root canal retreatment. This can occur when a sinus tract emerges from thealveolar mucosa, a periapical radiolucency is present at the radiograph, or if the rootcanal filling is not performed according to the standard criteria as shown in theradiograph. Thoroughly clinical and radiographic examination, including dentalhistory is mandatory.Pitts et al (1) have described the radiographic signs in teeth with vertical rootfractures. These included actual separation of root segments, radiolucent fracturelines, radiopaque signs, “halo ”-like radiolucency, periodontal-like lesions, resorptionalong fracture line, and loosened retro-filling or retro-filling material in a fracture line.Angular periodontal defect extending apically from the crestal bone, of variablewidth, and generally terminating at the level of the fracture line end was reported in29% of the cases of iatrogenic vertical root fracture examined by Tamse (4). Thepatient’s symptoms and clinical signs show a variety of clinical problems, includingpain of various kind, swelling, mobility, pockets and sinus tracts. The pockets causedby vertical root fracture are located adjacent to the site of the fracture, in contrast tothe normal sulcus depth usually seen around the other areas of the tooth (4). Pocketformation has been demonstrated to be a major finding in cases with vertical rootfractures. Sensitivity to palpation and percussion are also signs well known toaccompany root fractures. The diagnosis can occasionally be made at the time of thedental procedure. For example, a sharp cracking sound may be heard at the time of174

condensation the gutta-percha into the root canal. This sound was reported byMeister et al (5) in 6 out of 32 teeth with vertical root fractures. Positive evidence forvertical root fracture may be obtained by reproducing the pain by selective biting ona hard object or the use of dyes in a meticulously clean pulp chamber (4). For mostendodontically treated teeth clinically significant features develops after endodontictherapy is completed, the reason is that the therapy may have induced internalstress in the root or created micro fractures that initially were not exposed tobacterial contamination. Subsequent fractures or propagation of fractures then couldreach the sulcus, allowing bacterial invasion and rapid loss of bone and periodontalattachment (6).Regardless of the location and extent of a vertical root fracture, destruction ofperiodontal ligament and bone eventually occur in a linear fashion adjacent to thefracture. The aim of the treatment is elimination of the fracture. Depending on thesize and location of the fracture, treatment will range from partial root resection toextraction. In the great majority of cases of vertical root fracture, the gingival sulcuswill be involved and an irreversible periodontal pocket will usually be evident. Theindicated treatment is removal of the root. This means extraction for single-rootedteeth; however for multi-rooted teeth root amputation or hemi-section may befeasible (1).175

Reference list:1.Gehr ME, Dunlap RM, Anderson MH, Kuhl LV. Clinical survey of fractured teeth.AmDent Assoc 1987; 114: 174-72. Meister F, Lommel TJ, Gerstein H. Diagnosis and posiible causes of vertical rootfracture. Oral Surg Oral Med Oral Pathol 1980; 49: 243-533. Morfis AS. Vertical root fractures. Oral Surg Oral Med Oral Pathol 1990; 69: 631-54. Pitts DL, Natkin E. Diagnosis and treatment of vertical root fractures. J Endod1983; 8: 338-465. Schmidt KJ, Walker TL, Johnson JD, Nicoll BK. Comparison of Nickel-Titanium andStainless-Steel spreader penetration and accessory cone fit in curved canals.J Endod 2000; 1: 42-46. Tamse A. Iatrogenic vertical root fractures on endodontically treated teeth.Endod Dent Traumatol 1988; 4: 190-67. Trabert KC, Caputo AA, Abou- Rass M. Tooth fracture- a comparison ofendodontic and restorative treatments. J Endod 1978; 4: 341-5176

CASE 20 – Neuropathic painPatient:White Norwegian female, 55 years old. Referred from thepatient’s general practitioner to the Department ofEndodontics, for consultation and evaluation of treatmentand pain management. The patient had been in a caraccident in 2004.Fig.1 preoperative photoMedical history:The patient has several medical problems. She complainedabout problems with- allergies- eyes- intestinal- head and neckand she uses OTC drugs and alternative treatments likehomeopathy to release the troubles. Her regular medicaldoctor has not been able to help her solving theseproblems.Dental history and chief complaint:The referring dentist sais that she has plenty of fillings,but she used to have very little problems with them. She does not have a history ofpain and discomfort until recently. This started after the car accident. Tooth 36 waspainful and a root canal treatment was done. When the pain continued, anapicoectomy was performed without any relief of pain. Several antibiotic treatmenthas not solved the problem.177

The patient tells about a constant pain of varying degreesof intensity, localized to the mandibular left side. Occationally, the pain is spreadingtowards the maxillary left side molars and premolars, and to the temporal area. Shecan feel the pain when touching her skin at a certain point, and a light touch of thetooth 36 is causing pain.She further informs that she sleeps at night, and themornings are less painful - it develops during the day. Most days she carachterizesthe pain as low to moderate in intensity, but sometimes it is severe, but it is nevercompletely gone.Clinical examination:36 was tender to percussionAll teeth in both yaws were examined, and tested for the following:- Sensitivity testing- Percussion- Periodontal probing test- Palpation of muscels in face and neck- Crack-finder- three poins articulationThe result of the tests were: No findings.Radiographic examination:Fig.2 OPG178

Fig.3 Radiographic view of the dentitionResult of the radiographic examination: no findingsDiagnosis:Treatment:Neuropathic pain, it may be post traumatic to the caraccident.This patient was informed of the connection betweentraumatic injuries, periphery nerve damage andlongstanding persistent symptoms. A referral was sent toher general practitioner. The patient got a newappointment in 3 months time.Evaluation:Pain management is one of the most demanding andchallenging therapies there is. The important thing is to have an extensiveconsultation and to get all the facts including the patients’ whole dental record,before one could possibly make a statement. Often one most refer the patient toadditional specialists in other dental disciplines for examinations. Close cooperationwith the patient’s general practitioner, doctor and physiotherapist is mandatory.Prognosis:Uncertain. The patient needed to be careful followed-upfor a long time. Periphery nerve damage could heal or the symptoms could decreaseafter a prolonged healing period. It could also be consistent and without change anddiminishing of symptoms.Follow-up examination:Patient did not show for control. I called her, and she toldme that she had gone to another dentist for treatment. She wanted a secondopinion.179

I advised her not to receive any treatment without a pathological diagnosis wasmade. Any further interference in the area of 36, including extraction could make herpain more intense.We recommended her general practitioner to cooperate with the patients’ medicaldoctor to get a referral to a neurologist for examination, and suggestion of differenttreatment regimes with medications.180

Discussion:Odontogenic pain transmission is mediated primarily by peripheral sensory neuronsof the trigeminal nerve (9). The peripheral terminals of these nerves innervate thedental pulp and other oral tissues, whereas the central terminals releaseneurotransmitters, such as substance P, which are involved in the initiation of pain.These trigeminal sensory afferent neurons, along with sympathetic branches of thesuperior cervical ganglion and blood vessels, enter through the apical foramen of thetooth. Together, these nerves and blood vessels form the neurovascular bundle (9).There are myelinated and unmyelinated nerve fibers within the nerve bundles. Themyelinated fibers, called the A-fibers innervate the dentin. The unmyelinated fibers,known as C-fibers, innervate the body of the pulp and its blood vessels. The A-deltaand C-fibers of the dental pulp function as nociceptive mechanoreceptors that warnof tissue damage, whereas others are polymodal, with a wide, dynamic range (5).Inflammatory mediators such as histamine, bradykinin, prostaglandins, serotonin,substance P, CGRP, and leukotrienes, can cause pain directly by activating orsensitizing pulpal nociceptors. When the pulp becomes inflamed, the polymodalnociceptive fibers initiate and enhance this process by neurogenic inflammation.Substance P and calcitonin gene-related peptide (CGRP) can each contribute to theinflammatory process (2). Sensitization of neurons can also occur within the CNS (5).Secondary-order neurons can be changed or sensitized when they receive a constantbarrage of nociceptive input. Generally the changes are reversible; however, chronicsensitization may result in permanent changes to neuroprocessing. Permanentalterations may lead to chronic neuropathic pains. As central sensitization occurs,even normal input can be perceived as pain. Input carried by A-delta fibers, which donot mediate pain in most cases, can divert to nociceptive transmission. When thisoccurs, stimuli (e.g., a light touch to the tissues surrounding a sympathetic tooth)may be perceived as pain (8). Nociceptor fibers are stimulated by a variety ofphysical and chemical stimuli. During an infection or in the face of trauma, thetissues release noxious chemicals, including both peptides and lipids from which thenociceptor fibers are stimulated. Pain is perceived and recognized in the cortexbecause of incoming nociceptive (i.e., noxious stimulus) input (5). After activation,the C and A-delta fibers from the orofacial region transmit nociceptive signalsprimarily via trigeminal nerves to the trigeminal nucleus caudalis (N.caudalis) locatedin the medulla. N.caudalis plays an important role in processing nociceptive signals,and the output to higher brain regions can be increased (e.g hyperalgesia),decreased (e.g., analgesia), or misinterpreted (e.g., referred pain) as compared withincoming activity from the relevant C an A-delta fibers (9). These sensory fiberstransmit information by releasing excitatory neuropeptides, such as substance P andCGRP (9). In addition to activation and sensitization, the peripheral afferent fiberresponds to mediators (e.g., nerve growth factor (NGF) by increasing proteinsynthesis of substance P and CGRP and by undergoing sprouting of terminal fibers inthe inflamed tissue (3,4,9,10). Sprouting increases the density of innervations ininflamed tissue and may contribute to increased pain sensitivity in chronic pulpal orperiradicular inflammation. Toothache of neuropathic origin is either episodic orcontinuous. The episodic neuropathic toothache is characterized by a spontaneous,severe, sudden, sharp, lancinating, electrical shock pain that is felt in the tooth orradiates to a tooth. Furthermore, the pain episode lasts only seconds at a time,although paroxysms may occur in rapid succession (8). It is consistent with181

trigeminal neuralgia, which occurs between the fifth and eight decade of life andcauses distress for the patient (7). The pain involves one or more of the trigeminalnerve division and primarily involves either the maxillary or the mandibular division.The most prominent feature of episodic neuropathic toothache is the existence oftrigger points. These areas are often located in the skin of the lips, cheeks or gingiva.When touched, they provoke a painful response. Nevertheless, the possibility thatthese symptoms are being triggered by pulpal pathosis (instead of trigeminalneuralgia) must be ruled out (5). The cause of trigeminal neuralgia is unknown;empiric evidence suggests that the symptoms evolve as a consequence of vascularcompression of the Gasserion ganglion (where the cell bodies of the trigeminal nerveare located). The precise neurophysiologic mechanism has not been uncovered, andother theories for this particular disorder include viral infection of either neurons orthe Schwann cell sheath (5) Treatment modalities are varied and include medicalintervention with specific drugs that alleviate the neuralgic pain and various surgicalinterventions. For the dentist the most salient advice is to establish a diagnosis andavoid any invasive dental procedures. Invariably patients with trigeminal neuralgiahave undergone numerous endodontic procedures and extractions, but they continueto experience pain because pulpal and periodontal infectious processes have no rolein this syndrome. Therefore despite the patients insistence that the symptoms aretooth related, the diagnosis should be established and the patient should be referredto a neurologist for the definite therapy (1,6,11,12,14). Tegretol (carbamazepine),the standard medical therapy for trigeminal neuralgia, is quite effective.Unfortunately this particular drug is a bone marrow suppressant and will eventuallyproduce agranolocytosis. The side effect is dose dependant, and therefore will manypatients be maintained on tegretol without untoward side-effects. Continuousneuropathic toothache produces a persistent, ongoing unremitting pain. These painsmay be exacerbated by local provocation, such as percussion of the tooth. Neuriticpain (i.e., neuritis), deafferentation pains, or sympathetically maintained pains areconditions that can produce continuous toothaches. Neuritic pains that arise in themaxillary and mandibular divisions of the trigeminal nerve can cause dental pains.Neuritic pains result from a spread of inflammation from surrounding structures toneural structures. The pain is often continuous aching, and burning in nature.Occasionally neuropathic pain may arise after dental treatment, such as pulpextirpation, apicectomy or extraction. These conditions may appear as a phantomtoothache, described by the term atypical odontalgia, and is referred to as toothachewith no obvious organic cause (13). It is characterized by prolonged periods ofthrobbing or burning pain in the teeth or alveolar process that occurs in the absenceof any identifiable odontogenic cause. Usually the pain has been present for severalmonths or longer and repeated attempts at dental therapy have failed to resolve thepain. Although the pathophysiology of atypical odontalgia is not fully understood, itappears that the clinical characteristics best place it in the category ofdeafferentation pains. Sympathetic activity may also contribute to the maintenanceof the pain (5). Causalgia pain can involve the jaws, head and neck (8). Whenpresent, it may be confused with odontogenic pain. Causalgic pain is often associatedwith trauma, jaw fracture, or laceration and it may evolve after surgery. It has beenhypothesized that in Causalgia, nociceptor fibers become retracted in associationwith autonomic fibers (8). The skin overlying the painful area often becomeserymatous during pain episodes and the patients have a tendency to rub and scratch182

the involved area. The pain is characteristically paryxmal and burning, and it may beboth superficial and deep. When the predominant complaint is a deep component, itmay be confused with toothache. To arrive at a definitive diagnosis of Causalgia,historical trauma events and clinical features must be identified. Postherpethicneuralgia manifests similar features and should be considered in the differentialdiagnosis. Whether atypical facial pain are poorly localized or are centred in teeth,treatment should be approached cautiously. Many dentists have undertaken invasiveprocedures at the insistence of the patient, who firmly believes there is anodontogenic source. When the symptoms are mild, the pain should be managed withanalgesics and reassurance (8). Many patients with atypical facial pain respondfavourably to tricyclic antidepressants, particularly amitriptyline. This medicationaffects neurotransmitter substances and appears to have an analgesic property inaddition to its antidepressant effects (8).183

Reference list:1. Barker FG II et al. The long-term outcome of microvascular decompression for trigeminalneuropathy. N Eng J Med 1996; 334: 10772. Buck S et al. Pulpal exposure alters neuropeptide levels in inflamed dental pulp andtrigeminal ganglia: evaluation of axonal transport. J Endod 1999; 16: 7183. Buck S, Reese K, Hargreaves KM. Pulpal exposure alters neuropeptide levels in inflameddental pulp: evaluation of axonal transport. J Endod 1999; 25: 7184. Byers M et al. Effects of injury and inflammation on pulpal and periapical nerves. J Endod1990; 16: 785. Cohen AS, Brown DC. Orofacial pain emergencies: endodontic diagnosis andmanagement. In: Cohen, ST, Burns R, editors. Pathways of the pulp, 8th edn. St.Louis: CVMosby Co; 2002: p.31-766. Dalassio DJ. Management of the cranial neuralgias and atypical facial pain. A review. ClinJ Pain 1989; 5: 557. Drinnan AL. Differential diagnosis of orofacial pain. Dent Clin North Am 1987; 31: 6278. Eversole LR, Chase PF. Nonodontogenic orofacial pain and endodontics: pain disordersinvolving the jaws that simulate odontalgia. In: Cohen, ST, Burns R, editors. Pathways ofthe pulp, 8th edn. St.Louis: CV Mosby Co; 2002: p. 77-919. Hargreaves KM, Hutter JW. Endodontic Pharmacology. In: Cohen, ST, Burns R, editors.Pathways of the pulp, 8th edn. St.Louis: CV Mosby Co; 2002: p. 665-68210. Kimberly C, Byers M. Inflammation of rat molar pulp and periodontium causes increasedcalcitonin gene related peptide and axonal sprouting. Anat Rec 1988; 222: 28911. Main JH, Jordan RC, Barewal R. Facial neuralgias: a clinical review of 134 cases. J CanDent Assoc 1992; 58: 75212. Mc Laughlin MR et al. Microvascular decompression of cranial nerves: lessons learnedafter 4400 operations. J Neurosurg 1999; 90: 113. Rees RS, Harris M. Atypical odontalgia. Br J Oral Maxillofac Surg 1979; 16: 21214. Taarhj P. Decompression of the posterior trigeminal root in trigeminal neuralgia: a 30-year follow-up review. J Neurosurg 1982; 57: 14184

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