Table of contents: Vital treatment
Case 1 – Pulpitis: acute inflammation p. 3
Case 2 – Pulpitis: accidental root perforation p. 13
Case 3 – Pulpitis: inflammatory external resorption p. 24
Case 4 – Pulpitis: accidental instrument separation p. 35
Case 5 – Osteomyelitis: a differential diagnostic
problem p. 43
Case 6 – Dental pain emergency treatment p. 51 Necrotic treatment
Case 7 – Necrotic pulp: curved canals p. 57
Case 8 – Dens invaginatus: pediatric endodontics p. 64
Case 9 – Traumatic injury: molarization p. 73
Case 10 – Endodontal-Periodontal lesion p. 82
Case 11 – Apical periodontitis with a sinus-tract p. 97
Case 12 – Apical periodontitis with obliterated canals p. 108 Retreatment
Case 13 – Acute apical periodontitis: flare-up p. 115
Case 14 – Retreatment and Apicoectomi p. 123
Case 15 – Extra-radicular infection p. 134
Case 16 – Surgical retreatment p. 146
1 Case 17 – Apicoectomi: complicated location p. 155
Case 18 – Cracked tooth p. 163
Case 19 – Vertical root fracture p. 169
Pain Management
Case 20 – Neuropathic pain p. 177
2
Case 1 - Pulpitis: acute inflammation
Patient: White Norwegian female, 63 years old. The patient was referred from her private practitioner to the post graduate clinic for endodontic treatment of tooth 37, on Dec 12, 2006
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: At the referral dentist the patient complained about pain from tooth 37. She could not eat on the left side. Drinking cold drinks was also painful. The symptoms had started approximately 2 weeks earlier and had lately increased. She knew that a part of the filling in tooth 37 was missing. Caries was excavated, and the dental pulp was exposed. The patient was referred for endodontic treatment.
3 Clinical findings: Tooth:37
Extra oral: normal skin
Intra oral: normal soft tissue
Dental: Positive electric sensibility test and positive ice-test. The tooth was tender to percussion and was painful upon biting. Occlusal IRM
Periodontal: No signs of pathology
Other: The other teeth in the upper and lower right quadrants showed no signs relevant to the chief complaint.
Fig.2 Preoperative
Radiographic findings: Tooth :37
Periodontal: The periodontal ligament space could be followed along the roots and was slightly widened apically.
Dental: The tooth was restored with a radiopaque filling material verified clinically as an OD amalgam. IRM in the access preparation.
4 Diagnosis: Tooth : 37 Symptomatic pulpitis
Treatment plan: Tooth : 37 Pulpectomy and root-filling
Treatment:
Date:12.12.2006 Access cavity was prepared. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Vital tissue and bleeding from the pulp chamber was evident. Only one canal was located. Preparation with Race rotary instruments and manually with NiTi files, to dimension:
# 60, 21mm, ref point: occlusal surface
Fig 3. One canal in the middle of the root
5
Fig.4 working length
Irrigation with 1% NaOCl and 15% EDTA. The canal was dried and root filled with gutta-percha and AH- plus sealer by System B, warm gutta-percha technique. IRM as a top filling.
Fig.6 Masterpoint
6
Fig.7 System B obturation system Fig.8 After cutting the master point
Fig.9 endodontic treatment completed
Evaluation: Radiographically the root-filling appeared dense and good, with a 1,5 mm distance from the apex. No complications during the treatment.
Prognosis: Favorable
Follow-up examination: The patient was asymptomatic. The clinical examination revealed normal findings, and the tooth was restored with a PFM (porcelain fused to metal) crown restoration. The radiographic examination demonstrated favorable healing.
7
Fig.10 6 months follow-up
8 Discussion: With vital pulpectomy, the clinical aim is removal of the entire vital pulp tissue short of the anatomical apex followed by a bacteria tight, biocompatible and stable root filling. With this treatment, inflamed tissue is removed to an apical level where wound surface can be kept to a minimum, the residual pulp tissue is well vascularized, and the conditions for healing are optimal, provided the entire treatment can be carried out under aseptic conditions (4). Given the fact that even following a carious exposure the infectious process does not reach far into the pulpal space (9), a one- step treatment seems reasonable since the procedure is basically surgical and does not demand as strong an emphasis on canal disinfection as the case with infected pulp necrosis. The one-step treatment certainly presents several advantages (12). The total time for treatment is reduced and it saves the patient both travel time and expenses. From a treatment point of view, a one- appointment treatment also offers the advantage that curvatures, irregularities and other aberrations in the canal anatomy as well as working length determinations are current to the operator, thus facilitating the filling procedure that is likely to be easier than at a later appointment.
It is generally accepted that a story of spontaneous or long lasting provoked pain indicates irreversible and extended inflammatory changes of the pulp tissue and a more radical treatment has to be performed. In etiological terms, it is likely that the pulpal infection has reached a level where its elimination is not possible without removal of all of the pulp tissue (4). Severe pain to hot and sometimes cold liquids which lingers minutes and hours after the stimulus is removed, may be indicative of a severe inflammation associated with deeper slow-reacting and high threshold unmyelinated C- neurofibers (11). The deep, dull, throbbing pain is caused by an increased pulpal pressure and firing of the C- fibers. In dentinal pain, the sharp, rapid pain is a reaction of the A-delta fibers, which extend 150 µm into the dentin. In severe pulpalgias, both A-delta and C-fibers become stimulated, when a stimulus is applied to the tooth this results in a sharp pain which lingers as a deep dull pain long after the stimulus is removed (11). A factor of importance for the successful outcome of pulpectomy seems to be 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 other than those for treating infected root canals. The optimal wound level in teeth with 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-filling exceeding 3mm reduces the success rate compared to a termination of the filling 0-3 mm from the radiographically apex (3,5). As there is no concern about hard or soft tissue infection when a vital pulp is present, the main objective will be to optimize the technique of atraumatic and aseptic pulp surgery. The aim is placement of the wound at the so called apical constriction (8). Overfilling should
9 be avoided for the primary reason of not inducing more than necessary tissue toxic, allergenic or foreign body reaction, which in turn may compromise apical wound healing, induce an apical lesion and thereby endanger the possibility of properly assessing of the treatment (9). In controlled clinical and radiographical studies (5), success after pulpectomy can be obtained in about 83-100% of the cases with favorable aseptic conditions, due to the fact that the vital pulp and the dentin are not initially infected (10). Time is required to observe the treatment outcome. While in the absence of infection, resolution to the surgical trauma should not take more than a couple of weeks, the development of a lesion due to infection may require months or even years to become diagnosable. The chemical irritation and foreign body reaction initiated by the root filling material may also cause periapical bone lesions that may take time to resolve (2). Consequently, the treatment outcome observed after a short time period may differ from that observed at a later time periods. Ørstavik (13) recorded that the peak incidence of emerging apical periodontitis was a year. Failures in these teeth may be caused by pulpal infection, although radiographic evidence of apical periodontitis is initially absent. The canals may also be contaminated during treatment, with bacteria from a bordering carious lesion or with saliva (6), through coronal leakage (1,8) and through exposed dentinal tubules communicating with periodontal defects (7).
In our case we had complete aseptic control, and the distance from the apex was correct. Therefore the prognosis is favorable.
10 Reference list: 1. Friedman S. Treatment outcome and prognosis of endodontic therapy. In Ørstavik D, Pitt Ford TR, ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
2. Gesi A, Bergenholtz G. Pulpectomy-studies on outcome. Endod Topics 2003; 5: 57- 70
3. Grahnen H, Hansson L. The prognosis of pulp and root canal therapy. A clinical and radiographic follow-up examination. Odont Revy 1961; 12: 146- 165
4. Hørsted-Bindeslev P, Løvschall H. Treatment outcome of vital pulp treatment. Endod Topics 2002; 2: 24- 34
5. Kerekes K, Tronstad L. Long-term results of endodontic treatment performed with a standard technique. J Endod 1979; 5: 83- 90
6. Lin LM, Pascon EA, Skribner J, Gaengler P,Langeland K. Clinical, radiographic, and histological study of endodontic treatment failures. Oral Surg Oral Med Oral Pathol 1991; 11: 603- 611
7. Lin LM, Skribner JE, Gaengler P. Factors associated with endodontic treatment failures. J Endod 1992;12: 625- 627
8. Saunders WP, Saunders EM. Coronal leakage as a cause of failure in root canal therapy: a review. Endod Dent Traumatol 1994; 10: 105- 108
9. Shovelton DS. Studies of dentine and pulp in deep caries. Int Dent J 1970; 20: 283- 296
10. Spängberg L. Endodontic treatment of teeth without apical periodontitis. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
11. Trope M, Sigurdsson A. Clinical manifestations and diagnosis. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
12. Trope M, Bergenholtz G. Microbiological basis for endodontic treatment: can a maximal outcome be achieved in one visit? Endod Topics 2002; 1: 40- 53
13. Ørstavik D. Time-course and risk analysis of the development and healing of chronic apical periodontitis in man. Int Endod J 1996; 29: 150-155
11
12 CASE 2 Pulpitis: accidental root perforation
Patient: White Norwegian female, 17 years old. Referred to the post graduate clinic for evaluation and treatment of tooth 46, because of complications during endodontic treatment.
Medical history: Non-contributory
Fig.1 preoperative photo
Dental history and chief complaint: Tooth 46; deep composite filling distally due to caries led to irreversible pulpitis. Her private practitioner started the endodontic treatment. There was an accidental perforation to the periodontal ligament, and she was referred to the Department of Endodontics.
Clinical findings: Tooth: 46
Extra oral: Normal skin
Intra oral: Normal soft tissues
13
Dental: An O temporary filling with IRM.
Periodontal: PPD within normal limits.
Other: No symptoms of pain.
Fig.2 Radiographs: sent from the referral dentist:
14.11.05 16.01.06
Radiographic findings: Tooth: 46
Periodontal: The PDL was slightly widened apically around the roots.
Dental: A radiopaque material was demonstrated inside the canals verified clinically as Ca(OH)2.. The coronal part had an OD composite.
Diagnosis: Tooth: 46 Necrotic pulp
Treatment plan: Tooth: 46 sealing the perforations with MTA
Root canal disinfection and filling
14 Problem list:
Perforation to the periodontal ligament.
Treatment: Date: 13.03.06 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Two perforations were located in the mesially root, apical third. An attempt was made to find the original canals. Because of bleeding it didn’t seem realistic to finish The rooot filling with gutta-percha.
Three canals instrumented manually with NiTi files to dimension:
MB: # 45, 18 mm Ref. MBC ML: # 45, 18 mm Ref. MLC D: # 60, 19, 5 mm Ref. MBC
Irrigation with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.3 working length
15
Fig.4 the canal shape
Next appointment; 05.05.06: The patient was asymptomatic
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. The distal canal was filled by cold lateral condensation technique with gutta-percha and AH- plus sealer.
The mesially canals were sealed with MTA and a moist cotton pellet with sterile saline on top. IRM.
Fig.5 Root filling with gutta-percha and MTA
16
Evaluation: The root-filling appeared good. The patient was informed that the treatment outcome was uncertain, that she might need an Apicoectomi in the future.
Follow-up examination: 20.10.2006 The patient lives 20 miles out of Oslo, so her regular dentist took a control x-ray and sent it to me. No subjective symptoms. The x-ray shows no sign of pathology.
Prognosis: Favorable
Fig.6 endodontic treatment completed
17 Discussion: Root perforations may occur as a complication during endodontic treatment or dowel (post) preparation. Frequencies of such complications have been reported to occur in up to 3% (5,11). Ingle et al (10) reported that failures in approximately 10% of all failed cases root perforations resulted in endodontic. Over a period of 11 years, 55 root perforations were recorded at the Department of Cariology and Endodontics, School of Dentistry, University of Bergen (14).Forty-four of these perforations were diagnosed during endodontic or prosthodontic treatment, seven during routine endodontic recall and four prior to endodontic retreatment. Perforations occurred in all tooth groups, but were more common in the maxilla than in the mandible (40 versus 15). In the maxilla arch the canine was the most frequently perforated tooth, followed by the lateral incisor. In the mandibular arch, the first molar was the most frequently perforated tooth followed by the second premolar. Of perforations occurring during endodontic treatment, nine were located in the midroot level and 11 in the apical third of the roots. Further analysis of specific procedures related to perforations demonstrated that attempts to negotiate calcified canals accounted for 11 out of 26 perforations (42%). Nine out of 26 (35%) occurred during root canal instrumentation, and the remaining six (23%) resulted from attempts to locate calcified canal orifices. The perforations were treated with calcium hydroxide to control bleeding that was often encountered at the level of perforations, and the dressing was maintained for at least 2 weeks prior to sealing the perforations. Twenty-eight perforations were repaired by orthograde fillings with gutta-percha and Kloroperka N-Ø sealer, eight received a combined orthograde and surgical repair (gutta-percha / Kloroperka N-Ø sealer and amalgam), and in three cases only a surgical approach was used (amalgam). Twelve perforations showed a size and location hopeless for repair, they were therefore extracted. Four cases received no treatment but were recalled. The overall success rate in the primary treatment group was 56% while 36% became failures. A combined orthograde and surgical repair provided the most favorable outcome with 92% successful cases. Further examination of the data suggest that there may be slightly greater tendency for treatment success when perforations are in the apical part of roots rather than more coronally. Of the seven cervical level perforations, four failed and three were successful. Multiple factors may contribute to the relatively poor prognosis for perforations in the cervical portions of roots. Beavers et al (4) reported necrosis of the periodontal ligament coronal to the perforated area subsequent to placement of calcium hydroxide. Bergenholtz et al (7) described an unfavorable response to filling materials extruded through perforation defects. Hence, in the cervical region where perforations may be very close to epithelial attachment, any tissue destruction that stems from the treatment may cause loss of the epithelial attachment leading to formation of a permanent periodontal defect. Two teeth with furcation level perforations were successfully treated.
18 However, in these two cases, the perforations were not exposed to saliva prior to treatment. These findings are in keeping with general guide-lines for treatment of perforations such as those presented by Weine (30) who recommended sealing perforations as soon as possible, to minimize bacterial contaminations and damage to the periodontal ligament (19,24). A variety of different materials including calcium hydroxide, dental amalgam, Cavit (ESPE), composite resin, glasionomer cement, freeze-dried bone and tricalciumphosfate (5,8,9,17,21,22,28) have been reported in the literature as repairing materials for perforations. Amalgam has been the most commonly used perforation repair material. However, studies have demonstrated that it has poor sealing ability, resulting in inflammation and inadequate regeneration of periradicular tissues (3). Alhadainy and Himel (1) compared the sealing ability of Cavit-G, glasionomer, and amalgam, and found that glasionomer provides a better seal because of its ability to adhere to dentin. In this study, Cavit also outperformed amalgam, possibly because of Cavit’s hydrophilic nature and ease of placement compared to amalgam.
In addition to providing a good seal, the material of choice for repair of root perforations must be biocompatible, non-toxic, insoluble in the presence of tissue fluids, and capable of promoting regeneration of the periradicular tissue. Mineral trioxide aggregate (MTA) is a relatively new material that has been successfully used to repair perforations (2,16,20,23). MTA consists of a fine powder primarily composed of tricalciumsilicate, tricalcium aluminate, tricalcium oxide and silicate oxide that, upon hydration, forms a collodial gel that solidifies in approximately 3 h (25). Therefore, when used as a root repair material, although the periradicular tissues provide some moisture from the external surface of the material, to assure proper setting, moisture must also be provided from the internal aspect of the root using a moist cotton pellet (16). The biocompatibility of MTA has been demonstrated in vitro (27) and by being implanted in the mandible and tibia of guinea pigs (29). In a dye leakage study, Lee et al (15) investigated the sealing ability of MTA in lateral perforations and reported that MTA allowed significantly less leakage than IRM or amalgam. Nakata et al (18) compared the sealing ability of MTA and amalgam in furcal perforations of extracted human teeth using an anaerobic bacterial leakage model. Their results showed that MTA allows significantly less leakage compared with amalgam. The reduction of bacterial leakage of MTA was though a result of its sealing ability rather than an antimicrobial property of the material (26) One of the major consequences after repair of root perforations has been the inflammatory reaction in the surrounding tissues. MTA has not only been shown to be biocompatible but has also demonstrated the ability to allow regeneration of dental hard tissues (12,13). Main et al (16) showed that MTA had the ability to promote regeneration of cementum, thus facilitating regeneration of the
19 periodontal apparatus (16). They studied 16 clinical cases of root perforations that were all treated with MTA, three of the cases were furcal perforations, five were strip perforations, five were lateral perforations and three were apical perforations. Seven of these patients presented with radiolucent lesions at the time of repair. The follow- up radiographs ranged from 12-45 months. The results showed that all 16 cases demonstrated normal tissue architecture adjacent to the repair site at the recall visit. Teeth with existing lesions showed resolution of the lesion. Although MTA is one of the most researched materials in dentistry and showing remarkable results, the majority of the published data are based on in vitro and animal studies. Research must be continued to evaluate more clinical outcomes in human subjects.
20 Reference list:
1. Alhadainy HA, Himel VT. Evaluation of the sealing ability of amalgam,Cavit,and glasionomer cement, in the repair of furcation perforations. Oral Surg Oral Med Oral Pathol Oral Rad Endod 1993; 75: 362-366
2. Arens DE, Torabinejad M. Repair of furcal perforations with mineral trioxide aggregate. Oral Surg Oral Med Oral Pathol Oral Rad Endod 1996; 82: 84-88
3. Balla R, Lo Monaco CJ, Skribner J, Lin LM. Histological study of furcation perforations treated with tricalcium phosphate, hydroxylapatite, amalgam and Life. J Endod 1991; 17: 234-238
4. Beavers RA, Bergenholtz G, Cox CF. Periodontal wound healing following intentional root perforations in permanent teeth of Macca mulatta. Int Endod J 1986; 19: 36-44
5. Benenati FW, Roane JB, Biggs JT, Simon JH. Recall evaluation of iatrogenic Root perforations repaired with amalgam and gutta-percha. J Endod 1986; 12: 161-166
6. Bergenholtz G, Lekhom U, Milthon R, Engstöm B. Influence of apical over instrumentation and overfilling on retreated root canals. J Endod 1979; 5: 310-314
7. Bergenholtz G, Lekholm U, Milthon R, Heden G, Ödesjö B, Engström B. Retreatment of endodontic fillings. Scand J Dent Res 1979; 87: 217-224
8. El Deeb ME, ElDeeb M, Tabibi A, Jensen JR. An evaluation of the use of amalgam, Cavit, and calcium hydroxide in the repair of furcation perforation. J Endod 1982; 8: 459-466
9. Hartwell GR, England MC. Healing of furcation perforations in primary teeth after repair with decalcified freeze-dried bone: a longitudinal study. J Endod 1993; 19:357-361
10. Ingle JI. A standardized endodontic technique utilizing newly designed instruments and filling materials. Oral Surg Oral Med Oral Pathol 1961; 14: 83-91
11. Kerekes K, Tronstad L. Long-term results of endodontic treatment performed with a standarized technique. J Endod 1979; 5: 83-90
12. Koh ET, Torabinjead M, Pitt Ford TR, Brady K, Mc Donald F. Mineral trioxide
21 aggregate stimulates biological response in human osteoblasts. J Biomed Mater Res 1997; 37: 432-439
13. Koh ET, Mc Donald F, Pitt Ford TR, Torabinejad M. Cellular response to mineral trioxide aggregate. J Endod 1998; 24: 543-547
14. Kvinnsland I, Oswald RJ, Halse A, Grønningsæter AG. A clinical and roentgenological study of 55 cases of root perforations. Int Endod J 1989; 22 75-84
15. Lee SJ, Monsef M, Torabinejad M. Sealing ability of a mineral trioxide aggregate for repair of lateral root perforations. J Endod 1993; 19: 541-544
16. Main C, Mirzayan N, Shabahang S, Torabinejad M. Repair of root perforations using mineral trioxide aggregate: A Long-term study. J Endod 2004; 2: 80-83
17. Martin LR, Gilbert B, Dickerson AW. Management of endodontic perforations. Oral Surg Oral Med Oral Pathol 1982; 54: 668-677
18. Nakata TT, Bae KS, Baumgartner JC. Perforation repair comparing mineral trioxide aggregate and amalgam using an anaerobic bacterial leakage model. J Endod 1998; 24: 184-186
19. Nicholls E. Treatment of traumatic perforations of the pulp cavity. Oral Surg Oral Med Oral Pathol 1962; 15: 603-612
20. Pitt Ford TR, Torabinejad M, Mc Kendry DJ, Hong CU, Kariyawasam SP. Use of mineral trioxide aggregate for repair of furcal perforations. Oral Surg Oral Med Oral Pathol Oral Rad Endod 1995; 79: 756-763
21. Resillez-Urioste F, Sanandajt K, Davidson RM. Use of resin-ionomer in the treatment of mechanical root perforations: report of a case. Quintessence Int 1998; 29: 115-118
22. Rud J, Rud V, Munksgaard EC. Retrograde sealing of accidental root perforations with dentin-bonded composite resin. J Endod 1998; 24: 671-677
23. Schwarts RS, Mauger M, Clement DJ, Walker WA. Mineral trioxide aggregate: a new material for endodontics. J Am Dent Assoc 1999; 130: 967-975
24. Seltzer S, Sinai I, August D. Periodontal effects of root perforations before and during endodontic procedures. J Dent Res 1970; 49: 332-339
22 25. Torabinejad M, Hong CU, Mc Donald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. J Endod 1995; 21: 349-353
26. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Anti bacterial effect of some root filling materials. J Endod 1995; 21: 403-406
27. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Cytotoxity of four root end filling materials. J Endod 1995; 21: 489-492
28. Torabinejad M, Hong CU, Lee SJ, Monsef M, Pitt Ford TR. Investigation of mineral trioxide aggregate for root-end filling in dogs. J Endod 1995; 21: 603-608
29. Torabinejad M, Pitt Ford, Abedi HR, Kariyawasam SP, Tang HM. Tissue reaction to implanted root.end filling materials in the tibia and mandible in guinea pigs. J Endod 1998; 24: 468-471
30. Weine FS. Endodontic Therapy, 3rd edn, p. 330. C.V Mosby Co., St Louis 1982
23 CASE 3 - Pulpitis: Inflammatory external resorption
Patient: White Norwegian female, 77 years old. Referred to the postgraduate clinic at the Department of Endodontics, from a general practitioner for treatment of tooth 33, on November 08, 2006
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: The patient had no symptoms from the tooth. The general practitioner wanted us to perform the necessary treatment. He had detected a radiolucent area in the mid part of the root at a regular check-up. The patient could not recall any history of trauma in the area.
24 Clinical findings: Tooth: 33
Fig.2 tooth 33, buccal view
Extra oral: Normal skin
Intra oral: Normal findings
Dental: The tooth was restored with a composite buccally at the enamel-cementum border and one small composite distally. The tooth was tender to neither percussion nor palpation.
Periodontal: Chronic marginal periodontitis, with massive bone loss, especially in the lower front. Tooth 33 did not show signs of increased PPD, and the patient tells that her periodontal problems have been stable for the last two decades.
Other: The other teeth in the upper and lower quadrants showed no signs relevant to the chief complaint. Tooth 33 had a positive response to the electric sensibility test, and also to the ice-test.
25 Radiographic findings: Tooth: 33
Fig.3 preoperative x-ray
Periodontal: Normal PDL was followed along the root, normal apical conditions.
Dental: A radiolucent resorption defect at the mid part of the root surface, probed to be at the buccal surface.
Diagnosis: Tooth: 33: Inflammatory external resorption
Problem List: Unknown size of the defect. Root canal obliterated at the coronal part of the resorption defect. Look for a second canal.
Treatment plan: Tooth: 33: Root canal disinfection and filling Filling the resorption defect with MTA, a surgical intervention.
Treatment: Date: 13.12 .2006 Medical and dental history. Treatment plan.
26 Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. One canal was located and instrumented manually with NiTi files to dimension:
# 50, 23, 5 mm ref: IC
Evan though the pulp responded to sensibility test, there was just a slight appearance of blood in the canal. The resorption defect could be probed and the need for an intracanal disinfection agent as ca (OH) 2 was, at our opinion, necessary to control the disinfection. Irrigation with 1% NaOCl and 15% EDTA. The canal were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.4 working length
Next appointment; 16.01.2007
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canal was irrigated with 1% NaOCl and 15% EDTA. The canal was dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
Next appointment; 24.01.2007
The patient met for surgery. Three carpules with Xylocain and adrenaline were injected to establish
27 anesthesia. The patient rinsed 1 minute with chlorhexidine mouthwash. Intrasulcular buccal incision from distally on tooth 31 to the buccal surface on tooth 35 with surgical blade number 15. The flap was elevated and the cervical lesion was evident. We used a curette and a round bur to remove the granulation tissue. The internal part of the resorption cavity was filled with MTA. The flap was repositioned and sutured with 5, 4-0 silk sutures. Postoperative information was given. Ice pack was kept over the surgical site for 15 minutes. Analgesics were prescribed: Pinex forte and Pinex. Chlorhexidine mouthwash was recommended.
Fig.5 during surgery
28
Fig.6 resorption defect with MTA
Fig.7 post surgery
Next Appointment: 31.01.2007
After-surgery examination. The patient had been asymptomatic. Favorable healing was demonstrated. The sutures were removed. Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. IRM was placed over the gutta-percha down to the MTA. A composite filling was placed on top.
29
Fig.8 One week post op.
guttapercha
MTA
Fig.9 microscopic view
30 compositt
IRM
MTA
Fig.10 endodontic treatment competed
Evaluation: No complications during treatment, the root-filling appeared narrow, but dense and good.
Prognosis: Favorable
31 Discussion:
External resorption can result from bacteria in the pulp cavity, surface of the root or the gingival sulcus. Inflammatory resorption becomes progressive when, on top of a denuded area of the root surface, there is an additional long-lasting stimulation, such as mechanical irritation of the tissue, increased pressure in the tissue, infection of the root canal, and finally, in combination with certain diseases (4,5,8), such as hypoparathyroidsm, hypothyroidism, Paget´s disease and other endocrine disturbances. Herpes Zoster has also been reported implicated 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 grafting of alveolar clefts or intra coronal bleaching of pulpless teeth with 30-35% hydrogenperoxide (2). Apart from the above causative factors, resorption of no apparent cause is often reported in the literature (1,10). The term idiopathic resorption, which is used where no definite cause can be detected, reflects the limited understanding on the causative factors of this pathological process. Denuded mineralized tissue is colonized by multinucleated cells which initiate the resorption process; however without further stimulation of the resorption cells, the process will end spontaneously. The protective mechanism against resorption is based on the premise that the cementum and predentin covering of dentin are essential elements in the resistance of the dental root to resorptions. Since the most external aspect of cementum is covered by a layer of cementoblasts over a zone of non-mineralized cementoid, a surface that provide satisfactory conditions for osteoclast binding is not present (9). Another function of the cemental layer is related to its ability to inhibit the movement of toxins if present in the root canal space into the surrounding periodontal tissues (6). The consequence of an infected root canal space is, therefore, most likely to be apical periodontitis, as the toxins can communicate with the periodontal tissues through the apical foramina or large accessory canals. However, if the cemental layer is lost or damaged, the inflammatory stimulators can pass from an infected pulp space through the dentinal tubules into the surrounding periodontal ligament, which, in turn, sets up an inflammatory response. Since the cementum is lost, this inflammatory response will result in both bone resorption and root resorption. 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 pre- dentin) 2. Inflammation must occur to the unprotected root surface.
Inflammation in reaction to a traumatic injury varies according to the stimulus it is exposed to after the injury, and has the potential to cause extensive damage to the protective layer. The root resorption will continue until either no root
32 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 the root and adjacent bone on X-rays. Diagnosis can be a major challenge as resorptive defects, facial or lingual/palatal, are most often missed during examinations, although newer radiographic techniques, such as Computed Tomography, display significant promise in improving the ability to identify these defects (3). The diagnosis is also occasionally assisted by the presence of clinical symptoms which are similar to apical periodontitis (9). External root resorption occurs, as the name implies, on the outer surface of the root. Luxation injuries are the most likely injury where root resorption may result, and the long-term outcome is dependant on whether the healing response is favorable or unfavorable.
33 Reference list: 1. Darbar UR, Jenkins CBG. Multiple external root resorption: case report. Austr Dent J 1993; 38: 433-435
2. Fuzz Z, Lin S, Tesis I. Root resorption- diagnosis, classification and treatment choices based on stimulation factors. Endod Dent Traumatol 2003; 19: 175-185
3. Nance RS, Tyndall D, Levin LG, Trope M. Diagnosis of external root resorptions using TACT (tuned-aperture computed tomography) Endod Dent Traumatol 2000; 16: 24-28
4. Pankhurst CI, Eley BM, Moniz C. Multiple idiopathic external root resorption. Oral Surg Oral Med Oral Pathol 1988; 13: 516-518
5. Samia F, Björn S. Root resorptions in a patient with hemifacial atrophies. J Endod 1994;20: 299-302
6. Selvig KA, Zander HA. Chemical analysis and microradiograhy of cementum and Dentin from periodontally diseased human teeth. J Periodontol 1962; 33: 303-310
7. Solomon CS, Coffiner MO, Chalfin HE. Herpes Zoster revisited: Implications in root resorptions. J Endod 1986; 12: 210-213
8. Tronstad L. Root resorptions- etiology, terminology and clinical manifestations. Dent Traumatol 1986; 2: 263-266
9. Trope M. Root resorptions due to dental trauma. End Topics 2002; 1: 79-100
10. Webber RT. Traumatic injuries and the expanded role of calcium hydroxide. In: st Gerstein, H, editor. Techniques in Clinical endodontics, 1 edn. London, UK: W.B. Saunders Company, 1983. p. 181-211
34 CASE 4 – Pulpitis: accidental instrument separation and root perforation
Patient: White, Norwegian male, 35 years old. The patient was referred from the undergraduate clinic to the postgraduate clinic for retreatment of previously root- filled tooth 46 and removal of a separated instrument, on November28, 2006.
Fig.1 preoperational photo
Medical history: Non-contributory
Dental history and chief complaint: Three years ago, tooth 46 was root filled due to deep caries. When treated, an instrument separated in the mb canal. It was decided to leave the instrument in the canal. However, the lingual cusp broke off, and the tooth needed a crown. It was therefore decided to retreat the root canals and try to remove the instrument. The undergraduate student had started the endodontic retreatment of tooth 46 and fractured a spiral filler size # 20, during negotiating and preparing of the ml canal. In the mb canal the student also managed to accidentally perforate into the periodontal membrane. The patient was asymptomatic.
Clinical findings: Tooth:46
Extra oral: normal skin
35 Intra oral: normal soft tissue
Dental: Lingual part of the tooth is replaced with an IRM.
Periodontal: PPD within normal limits
Radiographic findings: Tooth :46
Periodontal: The periodontal ligament space could be followed along the roots and was slightly widened apically.
Dental: Root filled tooth with an instrument at the apical part of the mesial root.
Fig.2 preoperative x-ray
Diagnosis: Tooth :46 Root-filled tooth , unsatisfactory root filling.
Problem list; MB canal: instrument separated in the apical part Perforation distally in the coronal part of the canal ML canal: spiral filler in the canal
Treatment plan: Tooth : 46 Removal of the separated instrument Removal of the spiral filler MTA on the perforation
36 Conventional retreatment Root canal disinfecton and filling
Treatment: Date:28.11.2006 Medical and dental history. Treatment plan. IRM was removed. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canal orifices were located, gutta-percha remnants were demonstrated in two canals, - mb,ml and palatinal canal was filled by the undergraduate student.. The coronal part of the separated spiral bur was visible through the operating microscope. Removal of the instrument required an access preparation with overview. Ultrasound was used for preparation of the canal orifice in the ml canal. A step was prepared around the coronal part of the needel. Ultrasonic tips suitable for removal of separated endodontic instruments were further used in conjunction with 15% EDTA irrigation until the instrument was movable. Finally, a cut ultrasonic tip was used to vibrate on top of the separated instrument until it could be removed completely from the canal. The rest of the gutta-percha was removed with Race rotary instruments. The instrument in the mb canal was not possible to see in the microscope. It was not movable, and we decided to leave it were it was. The ml canal was prepareted to dimension:
Mb # 45, 20mm, ref point ML cusp Irrigation with 1% NaOCl, 15% EDTA. Two canals were dried with sterile paper points and packed with Ca(OH) . IRM as a temporary filling. 2
37
Fig.3 instrument and spiral filler Fig.4 working length in the mesial root.
Fig.5 ml canal orifice Fig.6 removed spiral filler
13.03.2007 The patient was asymptomatic. Rubber dam was applied and disinfected with chlorhexidine-ethanol. IRM and Ca(OH) were removed. Irrigation with 1% 2 NaOCl and 15% EDTA. The mb root canal was filled with MTA, the perforation being covered. The ml canal was dried and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM was placed in the canal orifices and as a temporary top filling. The patient was referred back to the undergraduate student for producing a PFM (porcelain fused to metal) crown as soon as possible.
38
Fig.7 masterpoint Fig.8 endodontic treatment completed
Evaluation: The tooth is weekend by the perforation. No signs of infection. The tooth needed a crown, and the patient was informed that the tooth has an uncertain future.
Prognosis: Questionable
Follow-up examination: 6 weeks post-up: I called the patient and he said that the tooth was restored with a PFM crown. No symptoms of pain.
39
Discussion: Management of a case with a broken instrument may involve an orthograde or a surgical approach. The three orthograde approaches are: 1) attempt to remove the instrument 2) attempt to bypass the instrument 3) prepare and obdurate to the fractured segment
When these instruments can be removed, successful treatment or retreatment generally occurs. If an instrument can be removed or bypassed and the canal can be properly cleaned and filled, nonsurgical endodontics is the most conservative approach. If the entire segment of the broken instrument is apical to the curvature and safe access with visualization is not possible, then non surgical removal usually cannot be accomplished (3). The success of nonsurgical fractured instrument removal from root canals depends 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 of the instrument fragment into the canal wall (2). Rotary nickel-titanium instruments tend to be more difficult to remove than hand instruments. This is because they generally fracture in smaller fragments, further apically, at or around the curve of narrow canals than hand instruments. Because of their rotational 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, but the coronal aspect can still be visualized and accessed, the removal may be possible, as in this case. No standardized procedure for successful instrument removal exists. Many techniques and devices have been tried – predominantly with fractured hand instruments (2). These techniques have been time-consuming, have had limited success, and have imparted considerable risk to narrow and curved canals. Recently, special ultrasonic tips have been developed for use in different piezoelectric ultrasonic devices to assist in removal of fractured instruments. The different manufactures have stated that these tips are uniquely designed to operate at a specific amplitude and at a frequency to maximize the safe removal of fractured instruments from root canals (5). Ward et al (5) studied 24 cases where they tried to remove fractured instruments from small, curved root canals. They used a technique with modified Gates-Glidden burs to perform a platform and then continuing with the use of special designed ultrasonic tips. All cases where the fractured instrument was situated before or at the curve were successfully removed. In cases where the fractured instrument was situated beyond the curve, the technique was generally unsuccessful. They also stressed
40 the importance of using a dental operating microscope to get optimal visualization (5). Souter et al (4) evaluated in vitro and in vivo complications associated with fractured file removal. They used the same technique as Ward et al (5) to remove fractured instruments from different levels in the root canals (coronal, middle and apical third). They used the mesiolingual canals of 45 extracted human mandibular canals. The success rate, frequency of root perforations, and root strength were recorded for each group. Removal was successful in all cases where the file fragment was located in the coronal or middle third. Only 11 of 15 files located in the apical third were successfully removed. Stripping perforations occurred in three cases, all where fragment was located beyond the curve. Fracture resistance declined significantly with more apically located file fragments. A review of 60 clinical cases showed similar rates of successful file removal and rate of perforations (4). Their conclusion was therefore that removal of fractured file fragment from the apical third should not routinely be attempted because of the high frequency of complications (4). This has also been the conclusion of other studies (1), who suggested that objects in the apical third should be left in situ, with the canal coronal to the instrument cleaned, shaped, and filled as normal. Apical surgery or extractions were the recommended treatment options if further treatment was required. The position of the fractured instrument has also an influence on prognosis. If the broken instrument prevents access to the root apex, it could influence the operator’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 latter part of cleaning and shaping close to the working length. The prognosis is poorer for those canals that have not been cleaned at all and in which a small instrument is broken far from the apex (1). In vital pulp cases, as well as those cases where instrument fracture occurs after thorough instrumentation and irrigation, the chances for failure are less than if instrument fracture occurs in an infected case before significant instrumentation and irrigation have been performed (1). Instrument fracture before completion of instrumentation in an infected tooth results in a high chance of failure (1).
41 Reference list:
1. Fors UGH, Berg JO. Endodontic treatment of root canals obstructed by foreign objects. Int Endod J 1986; 19: 2-10
2. Hülsmann M. Methods for removing metal obstructions from the root canal. Endod Dent Traumatol 1993; 9: 223-237
3. Ruddle CJ. Non surgical retreatment. In: Cohen S, Burns RC, eds. Pathways of th the pulp. 8 ed. St. Louis: CV Mosby, 2002: 875-929
4. Souter NJ, Messer H. Complications associated with fractured file removal using an ultrasonic technique. J Endod 2005; 6: 450-452
5. Ward JR, Parashos P, Messer H. Evaluation of an ultrasonic technique to remove fractured rotary nickel-titanium endodontic instruments from root canals: Clinical Cases. J Endod 2003; 11: 764-767
42 CASE 5 – Osteomyelitis: a differential diagnostic problem
Patient: White Norwegian male, 42 years old. Referred from the Department of Oral Surgery for necessary treatment of the mandibular front teeth.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental 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 any diagnostic 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 in the area were positive to vitality testing. The Endodontist referred to Department of Oral surgery, faculty of Oslo.Tentative diagnosis was set to be Osteomyelitis. Treatment was explorative surgery. Medication: Dalacin 150 mg x 4 for 1 month prior to surgery.
43
Clinical findings:
41 42 32 palpation - - - 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 area after surgery.
Fig.3 preoperative x-ray
Diagnosis: Tooth: 41: Necrotic pulp 42: Necrotic pulp Treatment plan: Tooth : 41: Root canal disinfection and filling Tooth : 42: Root canal disinfection and filling
Treatment: Date: 16.02.2004 41: Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. One canal was located and instrumented manually with NiTi files to dimension:
# 45, 20 mm ref: IC
Irrigation with 1% NaOCl and 15% EDTA.The canal was dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
42: Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. One canal
45 was located and instrumented manually with NiTi files to dimension:
# 45, 22 mm ref: IC
Irrigation with 1% NaOCl and 15% EDTA.The canal was dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Next appointment; 21.03.2004
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. Both teeth were irrigated with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
Tooth 41:
Fig.4 working length Fig.5 masterpoint
46 Tooth 42:
Fig 6.working length Fig.7 masterpoint Fig 8. endodontic treatment completed
Evaluation: No complications during treatment, the root-fillings appeared satisfactory.
Prognosis: Favorable
Follow-up examination: 2 years post treatment: No subjective symptoms. The radiographic examination demonstrated healing.
47
Fig.9 13.02.2007, 2- year- follow-up
48 Discussion:
Periapical radiolucensis may have causes other than an infected pulp necrosis and 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 cyst
On rare occasions endodontic infections may spread and involve large areas of surrounding bone and cause Osteomyelitis. This condition is accompanied by pain and elevated body temperature. The radiographic image may show a linear pattern of radiolucent bone, leaving islands of normal bone, witch later may become devitalized and transform to sequestrate(1). Apparently, the infection is spreading through the bone itself and is no longer dependent on the infected tooth as a reservoir of the causative organisms. The radiographic appearance may also be sclerotizing and osteolytic occurring in the same patient. A variant known as Garre´s Osteomyelitis is characterized by expansion of the cortical plate and mild clinical symptoms (2).
In this case a microbiological sample was taken during surgery, but it showed no growth. 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. Still there is, to my knowledge, no fistelograms taken. This may have been of great help 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 1998
50 CASE 6 – Dental pain emergency
Patient: White Norwegian male, 37 years old. The patient called for an emergency appointment at our private practice. It was august 2, 2005, and his private dentist (PD) was on holiday and his office was closed. He was in a lot of pain and he sounded desperate. He was given an immediate appointment.
Fig.1 preoperative photo
Medical history: The patient’s physical condition was good. He was not using 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 seen his PD, who started a root canal treatment on tooth 17. When the anesthesia effect disappeared a couple of hours post treatment, the pain came back with the same intensity as before the treatment. The PD prescribed antibiotics, and told the patient to wait for a couple of days before calling back. However, the pain was so intolerable that he called another dentist. He continued the root canal treatment on tooth 17. When the pain persisted with the same intensity he felt desperate and afraid. The next morning he came to our office.
51
Clinical findings: The patient was rating his pain intensity to be 9 at the Numerical Rating Scale, 10 being the worst possible pain. He had not slept the whole night, and the days before he had only slept for short periods of time, waken up from pain.
Extra oral: normal skin
Intra oral: normal soft tissue
Periodontal: PPD within normal limits
Dental:
Tooth 17 16 15
Swelling _ _ _
Tender to _ + _ percussion
Sensibility + (+) X testing
Necrotic pulp _ (+) X
52
Fig.2 preoperative x-ray
Radiographic findings:
Tooth 17 16 15
Radiolucent _ _ + area
Started endo + - -
Caries _ _ _
Root filled _ _ +
Diagnosis: 16: Irreversible pulpitis with acute apical periodontitis 15: chronic apical periodontitis
Treatment 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: 16
Date:02.08.2005 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Four canals were located and instrumented with Race instrumentation system and manually with NiTi files to dimension:
Mb # 45, 21 mm ref: mb cusp MB2 # 40 ,21 mm ref: mb cusp Ml # 45, 20 mm ref: ml cusp D # 60, 22 mm ref: mb cusp.
Irrigation with 1% NaOCl and 15% EDTA.The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.3 working length
Evaluation: No complications during treatment.
Prognosis: Favorable
Follow-up examination: The same afternoon the patient called the office and said that the pain was completely gone.
54 Discussion:
Vital pulpectomy gained general acceptance as the method of choice compared to the previously most often preferred mortal pulpectomy, following several studies published in the period from about 1940-70. The basic principle for this treatment was to leave out the instrumentation procedure and retain the devitalized pulp tissue in the canal. The tissue was usually amputated at the entrance of the root canal, and subsequently sealed with a strong antiseptic cement (paraformaldehyde, tricresol), the idea being to keep the fixed tissue permanently disinfected (1,2,3). While still practised in some Asian and European countries (4,5), neither mortal pulpotomy nor mortal pulpectomy are no longer considered appropriate. The potential risk for leakage of the devitalizing agent to the gingival sulcus along the provisional filling was especially discouraging. The current approach to invasive pulpal therapy by removing the vital pulp by mechanical means became a more widespread procedure when improved agents for local anaesthesia were introduced in the 1920 (4).
If the pulp remnant left in the root canal is more than 2 mm long, the risk of pulp necrosis is high due to amputation injury. It is crucial for the treatment outcome 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 higher than if the pulp stump is long, as the ratio between remaining pulp length and size of apical constriction is small. It has been demonstrated however, that if the pulp is removed completely when strict asepsis is maintained, healing will occur even 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 most apical part of the root canal, because disinfection of this area is crucial. The most apical part of the infected pulp space has often branching of the main canals, and extensive apposition of cementum, that makes disinfection and mechanical debridement less effective and difficult. Furthermore, conventional antimicrobial agents are often diluted or inhibited by tissue fluids (6). As the major concern in necrotic cases is related to elimination of all infected soft and hard tissues from the apical part of the root canal, the placement of the wound surface must be further apically than what is required in treatment of vital cases. The need for close apical preparation of teeth with necrotic pulp has been confirmed in several clinical studies of treatment outcome (6).
In this case the use of sensibility testing could help in diagnosing the acing tooth at 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- 657
2. Baume JL, Holz J, Risk LB. Radicular pulpotomy for category III pulps. Part III. Histological evaluation. J Prost Dent 1971; 26: 649- 657
3. Engstrøm B, Spängberg L. Wound healing after partial pulpectomy. A histological study performed on contra lateral tooth pairs. Odont Tidskr 1967; 75: 5- 18
4. Eriksen HM, Kirkevang L-L, Petersson K. Endodontic epidemiology and treatment outcome: general considerations. Endod Topics 2002; 2: 1-9
5. Gesi A, Bergenholtz G. Pulpectomy-studies on outcome. Endod Topics 2003; 5 : 57- 70
6. Spängberg L. Endodontic treatment of teeth without apical periodontitis. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
56 CASE – 7 Necrotic pulp: curved canals
Patient: Asian male, 48 years old. The patient was referred to the endodontic post-graduate clinic from the under- graduate clinic.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: The patient had been to treat tooth 37 for a caries lesion, 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 temporary filling. The patient was without symptoms.
Clinical findings: Tooth: 37
Extra oral: normal skin
Intra oral: normal soft tissue
Dental: caries buccally, IRM as a large temporary filling. No symptoms of pain. Periodontal: no signs of pathology
57
Fig.2 preoperative photo, caries buccally
Radiographic findings: Tooth: 37
Periodontal: The periodontal ligament space could be followed along the roots.
Dental: The tooth was restored with a radiopaque filling material Verified clinically as an MO amalgam. The mesial root has a curved shape.
Diagnosis: Tooth: 37: Necrotic pulp
Treatment plan: Tooth: 37: Disinfection and root filling.
Treatment:
Date: 30.08.2005 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canals were located and instrumented with the use of endo-lift to size 20 and Race instruments to dimension:
Mb # 50, 21 mm ref: mb cusp Ml # 50, 21 mm ref: ml cusp
58 D # 60, 20mm ref: mb cusp.
Irrigation with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.3 Working length Fig.4 Endo-lift
Next appointment; 12.10.2005
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Three canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
59 Fig.5 Masterpoint Fig.6 Endodontic treatment completed
Evaluation: No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable
Follow-up examination: 01.09.2006 No subjective symptoms. The tooth is restored with a composite filling. No sign of pathology.
Fig.7 1 year follow-up
60 Discussion: The aims of root canal treatment are to disinfect the root canal system thoroughly, completely obdurate the space created, so as to entomb any microbes that have escaped elimination and to prevent reinfection (9). A chemo mechanical 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 combined with antibacterial irrigation (0,5% sodium hypochlorite) can render 40-60 % of the treated teeth bacteria negative (1,7). Other studies by Ørstavik et al (12) and Card et al (3) suggested that the size of apical instrumentation may be important for the effective removal of canal bacteria. These studies found that with larger instrumentation fewer bacteria remained in the canal and the healing was more rapid. An interappointment antimicrobial dressing is generally advocated to prevent recovery and multiplication of microorganisms remaining even after careful instrumentation and debridement of the root canal space (2). Studies have shown that the application of a calcium hydroxide dressing brings the percentage of bacteria - negative teeth to 90-100 percent (2,6). The root canal represents a special environment in which selective pressures results in the establishment of a restricted group of the oral flora. Bacterial interrelationships and the nutritional supply are key factors in determining the outcome of the infection. Endodontic treatment, apart from directly eliminating bacteria, can completely disrupt the delicate ecology and deprive persisting bacteria of their nutritional source (8).
A correlation seems to exist between the size of the periapical lesion and the number of the bacterial species and cells present in the root canal. Teeth with large lesions usually harbor more bacterial species and have a higher density of bacteria in their root canals than teeth with small lesions. Periapical status at the start of treatment has been demonstrated to have fundamental impact on the final result (4,11,13). The success rate of initial therapy of apical periodontitis has been reported to range from 46% to 93% (5).
It is well known that bacterial status at the time of the root-filling is of outmost importance (10). Sjögren et al (7) demonstrated in their study, that teeth with persistent infection at the time of obturation had a success rate of 68%, whereas teeth 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 chemo- mechanical preparation, 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 he met for endodontic treatment there was no vitality left, and there was still
61 unexcavated caries buccally. Therefore we decided to treat the tooth with an antibacterial interappointment dressing.
62 Reference list: 1. Byström A, Sundqvist G. Bacteriologic evaluation of the effect of 0, 5 percent sodium hypochlorite in endodontic therapy. Oral Surg Oral Med Oral Pathol 1983; 55: 307-12
2. Byström A, Claesson R, Sundqvist G .The antibacterial effect of camphorated para- monochlorophenol, camphorated phenol and calcium hydroxide in treatment and infected root canals. Endod Dent Traumatol 1985;1: 170-5
3. Card SJ, Sigurdsson A, Ørstavik D, Trope M. The effectiveness of Increased Apical Enlargement in Reducing Intracanal Bacteria. J Endod 2002; 11: 779- 83
4. Engstrøm B, Hård af Segerstad L, Ramstrøm G, Frostell G. Correlation of positive Cultures with the prognosis for root canal treatemnt. Odontol Rev 1964; 15: 257- 70
5. Friedman S. Treatment outcome and prognosis of endodontic therapy. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
6. Sjögren U, Figdor D, Spängberg L, Sundqvist G. The antimicrobial effect of calcium hydroxide as a short-term intracanal dressing. Int Endod J 1991; 24: 119-25
7. Sjögren U, Figdor D, Persson S, Sundqvist G. Influence of infection at the time of the root- filling on the outcome of endodontic treatment of teeth with apical periodontitis. Int Endod J 1997; 30: 297-306
8. Sundqvist G. Ecology of the Root Canal Flora. J Endod 1992; 9: 427-30
9. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis1998
10. Waltimo T, Trope M, Haapasalo M, Ørstavik D. Clinical efficacy of treatment Procedures in endodontic infection control and one year follow-up of periapical healing. J Endod 2005; 12: 863- 66
11. Weiger R, Rosendahl R, Löst C. Influence of calcium hydroxide intracanal dressings on the prognosis of teeth with endodontically induced periapical lesions. Int Endod J 2000; 33: 219-26
12. Ørstavik D, Kerekes K, Molven O. Effects of extensive reaming and calcium hydroxide dressing on bacterial infection during treatment of apical periodontitis: a pilot study. Int Endod J 1991; 24: 1-7
13. Ørstavik D, Qvist V, stoltze K. A multivariate analysis of the outcome of endodontic treatment. Eur J Oral Scien 2004; 112: 224-30
63 CASE 8 – Dens invaginatus: pediatric endodontics
Patient: A nine year old white Norwegian female was referred to the Postgraduate Endodontic Clinic, Faculty of Dentistry, University of Oslo, by her general dental practitioner (GDP) May 2006 for treatment of the upper right lateral incisor (tooth 12).
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: 10.05.2006
Pain and swelling region 12. She was given fenoxymethyl-penicillin; Apocillin 330 mg X 4, for 7 days.
64 Clinical findings:
Tooth 12
Fig.2 preoperative photo
Tooth 12 11 21 22
Intraoral No No No No swelling
Perc. test + - - -
Palp. test + - - -
Sens. test - + + +
GPD - - - -
65 Radiographic findings:
Tooth 12 11 21 22
Root open (open) (open) open Develop
Radio- + - - - lucency
Dens + x x + invag.
Caries - - - -
Fig.3 preoperative x-ray
Diagnosis: Tooth : 12: Chronic apical periodontitis Dens Invaginatus type 1 (Oehlers) Tooth: 22: Dens invaginatus type 1 I called her dentist and discussed the need for a composite in the foramen socum. He said that he would do so as soon as possible.
66
Problem list: Root development in progress
Treatment plan: Tooth : 12: Root canal disinfection and filling with MTA. Treatment: date 24.05.2006 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. The canal was located and gently instrumented manually with NiTi files to dimension:
# 60, 16 mm, ref: inc surface ml
Irrigation with 1% NaOCl and 15 % EDTA. The canals were dried with sterile paper points and dressed with calcium hydroxide. IRM was placed as a top filling.
Fig.4 Working length
Next appointment; 26.09.2006 Tooth 12 was asymptomatic and no intra-oral swelling was palpated. Rubber dam was applied and disinfected with chlorhexidine-ethanol. Ca(OH)2 was removed. Irrigation with 15% EDTA and 1% NaOCl.
67 The canals were dried with sterile paper points and filled with MTA. Wet cotton pellet. IRM as a top filling.
Fig.5 endodontic treatment completed
Evaluation: No symptoms, no signs of infection. The root is week, the MTA filling is questionable. Orthodontic treatment require extraction of several teeth in the upper yaw. 12 is a currant choice.
Prognosis: uncertain
Follow-up examination: No subjective symptoms.
68
Fig.6 05.12.2006
Arrow 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 for extraction and replacement of several teeth. This may take several years.
Fig.6 showing MTA and IRM
MTA
MTA
IRM
05.12.2006
69
Dens invaginatus Type 1.
Fig.7 4 types of dens invaginatus (Copy from Visual Endodontics).
70 Discussion: Dens invaginatus is a dental malformation, often leading to endodontic complications. The etiology is unclear, but it is commonly believed that an invagination is the result of a deep folding of the foramen coecum during tooth development (1). The prevalence of dens invaginatus varies considerably depending on the type of classification. Ruprecht et al found dens invaginatus in 1,7% of all examined patients(2). Location: The anomaly arises most commonly in the maxillary lateral incisor and less frequently in the central incisors. It also occurs in posterior teeth, extending from the occlusal pit. Bilateral occurrence is a frequent finding; Grahnen et al reported 43%(1). The most common classification was introduced by Oehlers in 1957. (Figure 1) (3). Shultze and Brand introduced a more detailed classification also including invaginations starting at the incisal edge and dysmorphic root forms (figure 2) (4). The choice of treatment ranges from observation, fissure sealing, root canal treatment to extraction. Root canal treatment can imply endodontic treatment of the invagination alone, or the main canal, or both (5). Pulp necrosis is often found before root end closure(5). Endodontic treatment in conjunction with endodontic surgery is also common when the anatomy hampers the ability to thoroughly clean and shape the canal(s).(5). The treatment outcome is linked to the difficulty of cleaning and shaping and the present of a palato-radicular groove (PRG). The probability of periodontal breakdown is greater when a PRG is present. Mesial or distal PRGs are more often associated with pocket probing depth > 3mm (6).
71 Reference list:
1.Grahnen H, Lindahl B, Omnell K. Dens invaginatus. I. A clinical roentgenological and genetical study of permanent upper lateral incisors.
2.Ruprecht A, Batniji S, Sastry KAHR, El-Neweihi E. The incidence of dental invagination. Journal of Pedodontics 1986:10, 265-72.
3.Oehlers F. Dens invaginatus. Variations of the invagination process and associated anterior crown forms. Oral Surgery, Oral Medicine and Oral Pathology. 1957a;10:1204-18.
4.Schulze C, Brand E. Uber Dens Invaginatus (dens in dente). Zahnarztlige Welt/reform 1972;81:569-73.
5.Hulsmann M. Dens invaginatus: aetiology, classification, prevalence, diagnosis and treatment considerations. Int Endod J. 1997;30:79-90.
6.Hou G-L, Tsai C-C: Relationship between palato-radicular grooves and localized periodontitis. J.Clin.Periodontol. 1993;20:678-82.
72 CASE 9 – Traumatic injury: molarization
Patient: White Norwegian male, 12 years old. Referred to the Department of Endodontics for treatment of previously traumatized tooth 44.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: The boy fell from his bicycle and hurt some of his teeth. Tooth 44 had a concussion injury. He went to his regular dentist for control. After 6 months the tooth tested negative to electrical vitality test, and a tiny radiolucency was visible at the apex. He was referred to the Department of Endodontology for evaluation and treatment because of abnormal anatomy.
Clinical findings: Tooth:44
Extra oral: normal skin
73 Intra oral: normal soft tissue
Dental: Intact tooth with no restorations. Negative response to electric sensibility test and to Endo-ice test. Periodontal: Normal findings
Fig.2 tooth 44 preoperative
Radiographic findings: Tooth :44
Periodontal: A tiny radiolucency was visible at the apex.
Dental: The canal is separating into two or three smaller canals at the middle of the root.
Fig.3 preoperative x-ray
74
Diagnosis: Tooth :44: Chronic apical periodontitis previously traumatized tooth
Treatment plan: Tooth :44: Root canal disinfection and filling Problem list: anatomy, molarization tooth 44
Treatment: Date:07.02.2007 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canals were located and instrumented manually with NiTi files to dimension:
Mb # 40, 22 mm ref: mb cusp Ml # 40, 22 mm ref: ml cusp D # 40, 20mm ref: mb cusp
Fig.4 working length
Irrigation with 1% NaOCl and 15% EDTA.The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
75
Next appointment; 07.03.2007
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Three canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM
Fig.5 Masterpoint Fig.6 Endodontic treatment completed
Evaluation: No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable
76
Discussion:
The classification of dental injuries is currently based on the World Health Organization’s Application of International Classification of Diseases to Dentistry and Stomatology (9), and modified by Andreasen (6). This classification can be applied to both primary and permanent dentitions:
Management of traumatic injuries include, after examination and diagnosis, urgent care if indicated and definitive treatment. The latter requires planning both for the immediate and the long-term care (13). In cases of luxation and avulsion injuries, the immediate concern is to stabilize the tooth in its normal position to allow re-attachment and re-organization of the periodontal ligament support. Pulpal responses to traumatic injuries are affected by the degree of injury to the neurovascular supply, which for the most part enter through the apical foramen. Three possible outcomes exist: Pulpal healing, pulpal necrosis, or pulpal obliteration (1,2,5,11,12). The most desirable outcome after dental trauma is pulpal healing. If the disruption of the neurovascular supply to the pulp is less than total, for example in subluxation injuries, the pulp function may continue with reduced circulations until complete reconstitution is
77 accomplished, usually within a few weeks. In cases of extensive or total severance of the apical blood supply, pulpal healing is rare if the apical diameter is < 0,5mm, such as is found in fully formed teeth. Pulpal necrosis following severance of the blood supply may proceed through coagulation necrosis (sterile necrosis) to gangrenous necrosis (infection of infarcted tissue). Of interest, with respect to pulpal necrosis in traumatized teeth is the risk of infection-related (inflammatory) root resorption (4). This risk emphasizes the need for careful monitoring of pulpal responses after traumatic injuries. The third type of pulpal response to trauma is obliteration of the root canal. This is frequently observed in luxation-type injuries associated with displacement (3,11). Rarely do such teeth require root canal treatment (3,11). Treatment recommendations for luxation injuries with minor involvement such as concussion and subluxation, is mostly symptomatic. Soft diet and possibly occlusal adjustment to minimize discomfort on biting contact (7,13). The more sever types of injuries, extrusive and lateral luxation; need both immediate care (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). Repair- related resorption is a transient process involving small areas on the root surface following luxation and avulsion injuries and can also be observed associated with root fracture injuries (4). Typically, diagnosis can be made within 4 weeks after injury. Inflammatory resorption is a very aggressive type of injury-related resorption associated with root canal infection following trauma to a tooth (4). Luxation and avulsion injuries resulting in reduction or severance of pulpal blood supply, followed by bacterial invasion of the pulp, is the setting for initiation of external (and sometimes internal) root resorption. These are both types of injuries that can cause damage to the cemental protection of the root surfaces, allowing dentinal tubules to become pathways for bacterial toxins within the canal to trigger osteoclastic activity externally. Failure to remove bacteria from the root canal can result in this type of inflammatory resorption proceeding at a rapid 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 is ankylosisrelated resorption. This type of resorption is associated with extensive trauma to the PDL resulting in loss of vitality of the cells and extensive damage to the cementum. Lacking protective covering, the root cementum is exposed to osteoclasts that mistake cementum for bone and proceed to replace the cementum and dentine with new bone, resulting in a fusing of the bone and the tooth (8). An ankylosed tooth can be diagnosed clinically within 1 month by its percussion 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 its initiation (10). Management of dental injuries includes follow-up control to complete or confirm the diagnosis, assess response to treatment, determine need for additional treatment or treatment change, and evaluate the treatment outcome or complications. The following recommended schedule can be applied to the management of dental trauma patients (13): 1 week. After 7-10 days, the splint placed on a replanted, avulsed tooth should be removed and endodontic treatment, if indicated, should be initiated. 3-4 weeks. The splint applied to luxated teeth can usually be removed after 3-4 weeks. Radiographic examination should be performed to examine for the possible beginning of root resorption or periradicular lesions. 6 weeks. At this time, clinical and radiographic examinations may reveal evidence of pulp necrosis and infection-related (inflammatory) root resorption. 3-6 months. Examination at this time may be necessary to establish definitive diagnosis of pulpal periodontal healing complications. 1 year and up to 5 years. One year is a minimal control period for traumatic dental injuries; some may require additional observation periods to assess the final outcome.
79 Reference list:
1. Andreasen FM, Wistergaard Pedersen B. Prognosis of luxated permanent teeth- the development of pulp necrosis. Endod Dent Traumatol 1985; 1: 207-220
2. Andreasen FM, Yu Z, Thomsen BL. Relationship between pulp dimensions and development of pulp necrosis after luxation injuries in the permanent dentition. Endod Dent Traumatol 1986; 2: 90-98
3. Andreasen FM, Yu Z, Thomsen ML, Andersen PK. Occurrence of pulp canal obliteration after luxation injuries in the permanent dentition. Endod Dent Traumatol 1887; 3: 103- 115
4. Andreasen FM, Andreasen JO. Root resorption following traumatic dental injuries. Proc Finn Dent Soc 1992; 88: 95-114
5. Andreasen JO. Response of oral tissue to trauma. In: Andreasen JO, Andreasen FM eds. Textbook and Colour Atlas of Traumatic Injuries to the Teeth, 3rd edn. Copenhagen: Munksgaard, 1993: 77-112
6. Andreasen JO, Andreasen FM. Classification, etiology and epidemiology of traumatic dental injury. In: Andreasen JO, Andreasen FM eds. Textbook and Colour Atlas of Traumatic Injuries to the Teeth, 3rd edn. Copenhagen: Munksgaard, 1993: 151-177
7. Andreasen FM, Andreasen JO. Luxation injuries. In: Andreasen JO, Andreasen FM eds. Textbook and Colour Atlas of Traumatic Injuries to the Teeth, 3rd edn. Copenhagen:Munksgaard, 1993: 315-382
8. Andreasen JO, Borum M, Jacobsen HL, Andreasen FM. Replantation of 400 avulsed permanent incisors. IV. Factors related to periodontal ligament healing. Endod Dent Traumatol 1995; 11: 76-89
9. Application of the International Classification of Diseases to Dentistry and Stomatology IDC-DA, 3rd edn. Geneva: WHO, 1995
10. Bakland LK, Andreasen JO. Dental Traumatology: essential diagnosis and treatment planning. Endod Topics 2004; 7: 14-34
11. Jacobsen I, Kerekes K. Long-term prognosis of traumatized permanent anterior Teeth showing calcifying processes in the pulp cavity. Scand J Dent Res 1977; 85: 588-598
12. Robertson A, Andreasen FM, Bergenholtz G, Andreasen JO, Norén JG. Incidence of Pulp necrosis subsequent to canal obliteration from trauma to permanent teeth. J Endod 1996; 22: 557-560
80 13. The International Association of Dental Traumatology. Guidelines for the evaluation and management of traumatic dental injuries. Dental Traumatol 2001; 17: 1-4, 49- 25, 97-102, 145-148
14. Trope M. Root resorptions due to dental trauma. Endod Topics 2002; 1: 79-100
81 CASE 10 – Endodontal – periodontal lesion
Patient: White Norwegian male, 78 years old. Referred to the Department of Endodontics from a post graduate student in periodontics for evaluation and treatment.
Medical history: Non-contributory
Dental history and chief complaint: Because of acute pain the patient called his dentist for an emergency appointment. He felt pain from the mandibular front teeth, and they were mobile. He was feverish. His dentist examined him, and called the Department of Periodontics for an appointment. When they examined him, they tested sensibility on the mobile teeth, and found them to be necrotic, and there was also the presence of a sinus tract. Therefore he was sent to us at the Endodontic department. Fortunate, this all happened at the same day, 08.02.2007.
Fig.1 preoperative photo
82 Clinical findings:
Tooth 42 41 31 32 33
Vitality - - - - -
Perk./ + + + + + Palp.
Plaque/ + + + + + calculus
Pockets - - + + -
Mobile - - + + -
Fig.2 preoperative photo
83 Radiographic findings:
Tooth 42 41 31 32 33
Peri-apical - - + + - radio- lucent Restor------ative
Bone loss + + + + +
Obliteration + + + + +
Sinus tract - - - + + traced
Fig.3 radiographs that followed the referral
84 Tentative Diagnosis: Tooth 32: acute exacerbation with a sinus tract Tooth 31: chronic apical periodontitis
Treatment plan: Information was given about the uncertainty of this treatment. The patient was, however, interested in trying to keep his teeth. Tooth 31: Root canal disinfection and filling Tooth 32: Root canal disinfection and filling Apocillin, 660 mg,tabl.no.30 Bacteriological sample.
Possible diagnosis to be kept in mind; vertical root fracture and osteomyelitis
Treatment: Date:08.02.2007 Medical and dental history. Treatment plan. Bacteriological sample. Treatment of 32: Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. The canal was located and instrumented manually with NiTi files to dimension: # 50, 22mm ref: IC.
Fig.4 working length 32
Irrigation with 1% NaOCl and 15% EDTA.The canal was dried with sterile paper points and packed with Ca(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; 08.03.2007
Fig.4 photo taken before treatment
The 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 to follow the tract all the way. In this case it stops in the pocket same place as one month earlier. I’m not convinced that this is correct. Treatment of 32: Change of calsium hydroxide.
Treatment of 31: Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. The canal
86 was located and instrumented manually with NiTi files to dimension:
# 50, 23,5mm ref: IC.
Fig.6 working length 31
Irrigation with 1% NaOCl and 15% EDTA.The canal was dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.7 post treatment photo
When the rubber-dam was removed, liquid was poring out of the sinus tract and the pocket. Next appointment: 27.03.2007
87
Fig.8 preoperative photo 27.03.2007
The patient was asymptomatic. Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
Fig.9 during treatment
Fig.10 masterpoint X-ray
88
Fig.11 endodontic treatment completed
When the rubber dam was removed; exacerbation from the buccal pocket .
Fig.10 post endodontic treatment
89
Fig.11 gutta-percha in the buccal pocket.
We decided to do an explorative surgery, 2 weeks later.
Date:27.03.2007
Fig.12 pre surgery
The patient didn’t have any symptoms, and there was no exacerbation from the pocket. The pocket was narrow.
90
Fig.13 Gutta-percha in pocket buccally.
Fig.13 x-ray 12.04.2007
We 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: No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable for the endodontic treatment. Treatment outcome will depend upon the periodontal condition.
92 Discussion:
Despite numerous differences between chronic inflammatory disease of periodontal and endodontic origins, there are notable similarities, primarily that (1): 1) both conditions share a common microbiota that often is associated with Gram-negative anaerobic bacteria, and 2) elevated cytokine levels may be released systemically from acute and chronic manifestations of both disease processes (e.g., increased concentrations of inflammatory mediators have been detected both in the gingival crevicular fluid of subjects with periodontal disease and in the periapical tissues of endodontically involved teeth).
The pulp and the periodontium are intimately related. As the tooth develops and the root is formed, three main avenues for communication are created: dentinal tubules, lateral and accessory canals, and the apical foramen.
Exposed dentinal tubules in areas of denuded cementum may serve as communication pathways between the pulp and the periodontal ligament. Exposure of dentinal tubules may occur due to development defects, disease or periodontal 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 the majority of them are found in the apical third of the root (6). De Deus (5) found that 17% of teeth had lateral canals in the apical third of the root, about 9% in the middle third, and less than 2% in the coronal third. However, it seems that the prevalence of periodontal disease associated with lateral canals is relatively low. Kirkham (8) studied 1000 human teeth with extensive periodontal disease and found that only 2% had lateral canals located in a periodontal pocket.
The apical foramen is the principal and most direct route of communication between the pulp and periodontium. Bacterial and inflammatory byproducts may exit readily through the apical foramen to cause periapical pathosis. The apex is also a portal of entry of inflammatory byproducts from deep periodontal pockets to the pulp. Pulp inflammation and pulp necrosis extends into the periapical tissues causing a local inflammatory response accompanied with bone and root resorptions. In certain cases pulpal disease will stimulate epithelial growth that will affect the integrity of the periradicular tissues (9,14).
It seems that the pulp is usually not directly affected by periodontal disease until recession has opened an accessory canal to the oral environment. At this stage, pathogens penetrating from the oral cavity through the accessory canal into the pulp 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 and periodontal diseases associated with the same tooth. They used specific PCR methods and detected the same pathogens in teeth with chronic apical periodontitis and chronic (adult) periodontitis. The isolated species were Actinobacillus actinomycetemcomitans,Tannerella forsythensis, Eiknella corrodens, Fusobacterium nucleatum, Porphyromonas gingivals, Prevoella intermedia and Treponema denticola. Spirochetes are associated with both endodontic and periodontal diseases. The spirochete species most frequently found in root canals are T.denicola (11) and T. maltophilum (7). T denicola possesses an array of virulence factors associated wit periodontal disease and may 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 and has good prognosis. Primary periodontal disease should only be treated by periodontal therapy. In this case, prognosis depends on severity of the periodontal disease and patient’s response. Primary endodontic disease with secondary periodontal involvement should first be treated with endodontic therapy. Treatment results should be evaluated in 2- 3 months and only then should periodontal treatment be considered. This sequence of treatment allows sufficient time for initial tissue healing and better assessment of the periodontal condition (4,10). It also reduces the potential risk of introducing bacteria and their byproducts during the initial healing phase. In these cases it is important to realize that periodontal healing could be adversely affected by aggressive removal of the periodontal ligament and underlying cement during interim endodontic therapy (2). Prognosis of primary endodontic disease with secondary periodontal involvement depends primarily on the severity of periodontal involvement, periodontal treatment and patient’s response. Primary periodontal disease with secondary endodontic involvement and true combined endodontic-periodontal diseases require both endodontic and periodontal therapies, and the prognosis of these lesions depends primarily upon the 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 apical periodontitis and systemic health. Endod Topics 2004; 8: 15-35
2. Blomlöf L, Lindskog S, Hammarström L. Influence of pulpal treatments on cell and tissue reactions in the marginal periodontium. J Periodontol 1988; 59: 577-583
3. Burch JG, Hulen S. A study of the prescence of accessory foramina and the topography of molar furcations. Oral Surg Oral Med Oral Pathol 1974; 38: 451-455
4. Chapple I, Lumley P.The periodontal-endodontic interface. Dent Update 1999; 26: 331-334
5. De Deus QD. Frequency, location and direction of the lateral, secondary and accessory canals. J Endod 1975; 1: 361-366
6. Harington GW, Steiner DR. Periodontal-endodontic considerations. In: Walton rd RE, Torabinejad M, editors, Principles andpractice of endodontics, 3 edn. Philadelphia: W.B. Saunders Co., 2002: 446-484
7. 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 of other bacteria in endodontic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001; 92: 329-334
8. Kirkham DB. The location and incidence of accessory pulpal canals in periodontal pockets. J Am Dent Assoc 1975; 91: 353-356
9. Nair PNR, Pajarola G, Schroeder HE. Types and incidence of human periapical lesion obtained with extracted teeth. Oral Surg Oral Med Oral Pathol 1996; 81: 93-101
10. Paul BF, Hutter JW. The endodontic-periodontal continuum revisited: New insights into etiology, diagnosis and treatment. J Am Dent Assoc 1997; 128: 1541-1548
11. 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 Oral Pathol Oral Radiol Endod 2001; 91: 468-471
12. Rotstein I, Simon JHS. Diagnosis, prognosis and decision-making in the treatment of combined periodontal-endodontic lesions. Periodontol 2000; 2004; 34: 165-203
95 13. Rupf S, Kannengiesser S, Merte K, Pfister W, Sigusch B, Eschrich K. Comparison of profiles of key periodontal pathogens in the periodontium and endodonthium. Endod Dent Traumatol 2000; 16: 269-275
14. Simon JHS. Incidence of periapical cysts in relation to the root canal. J Endod 1980; 6: 845-848
96 CASE 11- Apical periodontitis with a sinus tract
Patient: Black African male, 22 years old. He was referred to the Endodontic Department from his private practician.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint:
History of pain started during springtime 2005. He felt pain and extra-oral swelling in lower right jaw, and went to see a doctor. He was referred to Ullevål university hospital.
First appointment; 04.10.05. Dr. Oddvar Moen describes an “granulation polyp”. Odontogen origin is considered unlikely. An OPG was taken and didn’t indicate any relevant dental pathology. The granulation polyp is removed and sent to histological and bacteriologic examination. The patient is given Apocillin, 660 mg for one week, and he is given sickness leave for seven days.
97 Second appointment; 18.10.05. Dr. Anne Marie Ramsve. Test result. Pericoronitt 48. Apocillin 660 mg tabl no 40 and Flagyl 400 mg tabl 20. Treatment plan; ex 48 and excision of polyp.
Third appointment; 01.11.05. Dr. Niels Fredrik Hågensli. Sinus tract from 46, vitality testing gives no respond from 46. Treatment plan; Treatment of necrotic pulp, tooth 46.
Clinical findings:
48 47 46 45
El.pt + - + +
Ice + - + +
PPD - - - -
Perc.t. - (+) (+) -
Extra oral: normal skin
Intra oral: sinus tract with an opening at the buccal mucosa between 47 and 46.
Dental: No visible caries.
Periodontal: No mobility. PPD (periodontal probing depth) within normal limits.
98
Fig. 2 gutta-perch point in sinus tract
Fig.3 x-ray gutta-percha point in sinus tract
Radiographic findings: Tooth 47:
Periodontal: Radiograph with a gutta-percha point in the sinus tract confirmed the presence of a communication between the oral mucosa and tooth 47.
Dental: Radiopaque material was demonstrated in the coronal part of tooth 47, verified clinically as an O composite filling.
Other: 48 caries M. No findings in relation to tooth 46 or 45 that would influence the diagnosis or the treatment.
Diagnosis: Tooth 47: Apical periodontitis with a sinus tract
99 Treatment plan: Tooth 47: Root canal disinfection and filling
Treatment:
07.06.06 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canals were located and instrumented manually with NiTi files to dimension:
Mb # 45, 21 mm ref: mb cusp Ml # 45, 20 mm ref: ml cusp D # 60, 22mm ref: mb cusp.
Fig.4 Working length Fig.5 Masterpoint
Irrigation with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Next appointment; 2 months.
29.08.2006 Rubberdam was applied and the field disinfected with chlorhexidine and ethanol. CA (OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Three canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH- plus sealer. IRM.
100
Fig 6.Endodontic treatment completed Fig.7 Post treatment, closure of sinus tract
Evaluation: No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable
Follow-up examination: 20.11.06 No subjective symptoms. The radiographic examination didn’t demonstrate apical periodontitis
Fig.8 6-months follow-up examination:
101
Fig.9 complete healing of sinus tract
102
Discussion: When apical inflammatory exudates drain to a body surface, a sinus tract has developed. The reason that a sinus tract develops is not fully understood. It may be the mechanism with which the body controls the infection, or it may indicate a specific infection of some volume/ number/ virulence of the bacteria (16). It may develop as a result of an abscess or be without preceding symptoms, and the diagnosis may be made without the patient even being aware of its existence. When longstanding, the tract can become epithelialzed (1). With adequate disinfection of the root canal and resolution of the periapical inflammation, the sinus tract will heal without further treatment and the epithelium, if present, will in most cases disintegrate (16). Commonly, the sinus tract will drain on the mucosa adjacent to the offending tooth. However it is possible that the opening can be relatively far from the involved tooth, or drain to the periodontal ligament mimicking a periodontal pocket. For these reasons, it is important to perform a thorough diagnostic examination and not rely too heavily on the presence and location of the sinus tract opening. It is important to trace the sinus tract with an opaque object, for instance a gutta-percha point, to determine the radiographic origin of the lesion. Disinfection of the root canal systems should result in reversal of the chronic apical periodontitis and the sinus tract will disappear quickly. In the great majority of teeth requiring root canal treatment, the goal is either prevention or treatment of apical periodontitis. The final success is usually dependant on successful infection control. Cleaning and shaping is the most important step towards sterility of the canal. The goal of instrumentation and irrigation is to remove all necrotic and vital organic tissue as well as some hard tissue from the root canal system, and give the canal system a shape that allows debridement and predictable placement of locally used medicaments and a permanent root-filling of high technical quality.
Irrigation of the root canal is an essential component in the process of root canal preparation. There are five main benefits of using irrigants during the cleaning of the canal:
1. Wetting of the canal walls and removal of debris by flushing 2. Destruction of microorganisms 3. Dissolution of organic matter 4. Removal of smear layer and softening of the dentin 5. Cleaning in areas that are inaccessible to mechanical cleansing methods
Sodium hypochlorite was introduced to endodontics by Coolidge in 1919 (4), and has remained a popular root canal irrigants because of its potent bactericidal activity and ability to dissolve necrotic organic material. The antibacterial effect has been clinically evaluated in a series of studies (2,3). NaOCl is used in
103 concentrations varying from 0, 5% to 5, and 25%. Laboratory experiments using three Gram-negative anaerobic rods typically isolated from primary apical periodontitis, Porphyromonas gingivalis, P. endodontalis and Prevotella intermedia demonstrated high susceptibility to NaOCl, and all three species were killed within 15 s with all concentrations tested (0,5%- 5%) (17). Other in vito studies has demonstrated a better antibacterial effect with high concentrations of NaOCl (6,17). In vivo studies have failed to demonstrate the same. This is probably due to the differences in conditions between in vitro and in vivo studies. In laboratory studies there are high volume of the medicament available for killing, direct access to all microbes, and absence of other materials that potentially protect bacteria in vivo (8). Byström & Sundqvist (2,3) demonstrated that 0,5% NaOCl, with or without the use of EDTA, improved the antibacterial efficiency of preparation compared with the use of saline irrigation. The same authors, could not demonstrate any significant difference in antibacterial effect in vivo between 0,5% and 5% NaOCl. Peciuliene (12) studied the effect of instrumentation and NaOCl irrigation in previously root-filled teeth. Bacteria were isolated in 33 of the 40 teeth examined before instrumentation. E.faecalis was found in 21 teeth, C. albicans in six teeth and Gram-negative enteric rods and other microbes in 20 teeth. While no rods or yeast were found in the second sample after the preparation and irrigation, E. faecalis still persisted in six teeth, which indicated that E. faecalis is much more resistiant to killing by NaOCl than C.albicans and Gram-negative rods. NaOCl has been criticized for its unpleasant taste, relative toxicity, and its lack of ability to remove smear layer (15). Caustic effect on the maxillary sinus or adjacent structures has been demonstrated when NaOCl was accidentially expressed into the periapical area (9,18). In addition to the strong bleaching effect that can damage patients clothing. Pashley et al (11) compared the biological effects of different concentrations of NaOCl solutions and demonstrated greater cytotoxicity and caustic effects on healthy tissue with 5,25% NaOCl than with 0,5% and 1% solutions. Therefore it might be recommended to use 0,5% - 1% NaOCl for canal irrigation. There has been an ongoing search for alternative solutions that could replace NaOCl, because of the side-effects. Chlorhexidine, CHX has a wide antimicrobial spectrum and is effective against both Gram - positive and Gram-negative bacteria as well as yeast. It is able to permeate the cell wall or outer membrane and attacks the bacterial cytoplasmic or inner membrane, or the yeast plasma membrane. Its activity is pH dependent and is greatly reduced in the presence of organic matter (14). CHX gluconate has been shown to be superior to NaOCl in killing of E.faecalis and Staphylococcus aureus (2,6). A potential weakness of CHX in the root canal may be its susceptibility to the presence of organic matter (14). In an in vitro study, 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 serum albumin. This might indicate the possibility that inflammatory exudates, rich in proteins 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 of NaOCl. While the in vito studies have demonstrated the antibacterial effect of CHX against E. faecalis to be superior to that of NaOCl, there are no in vivo studies yet available that confirms this.
Removal of the smear layer is an important step to facilitate disinfection of the root canal. EDTA has little if any antibacterial activity. It is an effective chelating agent (5) and removes the smear layer by chelating the inorganic component of dentine.
EDTA contributes to the elimination of bacteria in the root canal by facilitating cleaning and removal of infected tissue. It has also been demonstrated that removal of the smear layer by EDTA improves the antibacterial effect of locally used disinfecting agents in deeper layers of dentine (17). Studies have shown that more debris was removed by irrigation with EDTA followed by NaOCl than with EDTA alone (10).
Dental fluorosis is a type of hypocalcification of enamel characterized by white areas that may become discolored to brown. It is caused by consumption of excessive fluorides in the water supply (usually 2-8 ppm) during tooth development. Technically this is chronic endemic dental fluorosis. Fluorosis is a general term for chronic fluoride poisoning.
105
Reference list:
1. Baumgartner JC, Pickett AB, Muller JT. Microscopic examination of oral sinus tracts and their associated periapical lesions. J Endod 1984; 10: 146-152
2. Byström A, Sundqvist G. Bacteriologic evaluation of the effect of 0,5 per cent sodium hypochlorite in endodontic therapy. Oral Surg Oral Med Oral Pathol 1983; 55: 307- 312
3. Byström A, Sundqvist G. The antibacterial effect of sodium hypochlorite and EDTA in 60 cases of endodontic therapy. Int Endod J 1985; 18: 35- 40
4. Coolidge E. The diagnosis and treatment of conditions resulting from diseased dental pulps. J Nation Dent Ass 1919; 6: 337- 349
5. Czonstkowsky M, Wilson EG, Holstein FA. The smear layer in endodontics. Dent Clin North Am 1990; 34: 13- 25
6. Gomes PB, Ferraz CC, Vianna ME, Berber VB, Teixeira FB, Souza- Filho FJ. In vitro antibacterial activity of several concentrations of sodium hypochlorite and chlorhexidine gluconate in the elimination of Enterococcus faecalis. Int Endod J 2001; 34: 424- 428
7. Haapasalo HK, Siren EK, Waltimo TM, Ørstavik D, Haapasalo MP. Inactivation of local root canal medicaments by dentine: an in vitro study. Int Endod J 2000; 33: 126- 131
8. Haapasalo M, Endal U, Zandi H, Coil JM. Eradication of endodontic infection by instrumentation and irrigation solutions. Endod Topics 2005; 10: 77- 102
9. Hülsman M, Hahn W. Complications during root canal irrigation-literature Review and case reports. Int Endod J 2000; 33: 186- 193
10. Niu W, Yoshioka T, Kobayasi C, Suda H. A scanning electron microscopic study of dentinal erosion by final irrigation with EDTA and NaOCl solutions. Int Endod J 2002; 35: 934- 939
11. Pashley EL, Birdsong NL, Bowman K, Pashley DH. Cytotoxic effects of NaOCl on vital tissue. J Endod 1985; 11: 525- 528
12. Peciuliene V, Reynaud A, Balciuniene I, Haapasalo M. Isolation of yeast and enteric bacteria in root-filled teeth with chronic apical periodontitis. Int Endod
106 J 2001; 34: 429- 434
13. Portenier I, Haapasalo H, Rye A, Waltimo T, Ørsavik D, Haapasalo M. Inactivation of root canal medicaments by dentine; hydroxylapatite and bovine serum albumin. Int Endod J 2001; 34: 184- 188
14. Rusell AD. Antibacterial activity of chlorhexidine. J Hosp Infect 1993; 25: 229-238
15. Spängberg L, Engström B , Langeland K. Biologic effects of dental materials.3. Toxicity and antimicrobial effect of endodontic antiseptics in vitro. Oral Surg Oral Med Oral Pathol 1973; 36: 856- 871
16. Trope M, Sigurdson A. Clinical manifestations and diagnosis. In Ørstavik D, Pitt Ford TR,ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
17. Ørstavik D, Haapasalo M. Disinfection by endodontic irrigants and dressings of experimentally infected dentinal tubules. Endod Dent Traumatol 1990; 6: 142- 149
107 CASE 12 – Apical periodontitis with a sinus tract and obliterated canals
Patient: White Norwegian female, 60 years old, working as a secretary at the Faculty of Odontology. She detected a sinus tract in the area of 26, and got an appointment for endodontic examination and treatment at the Endodontic Department.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: Tooth 26 was tender to chewing, and had been so for a couple of weeks. The gold crown was made about 30 years ago.
108 Clinical findings Tooth: 26
Extra oral: normal skin
Intra oral: Sinus tract with an opening at the buccal mucosa between tooth 25 and 26.
Dental: Tooth 26 had an gold crown. The tooth was tender to palpation apically and had a negative response to the electric sensibility-test. Tooth 25 and 27 showed no signs relevant to the chief complaint.
Periodontal: No mobility. PPD (periodontal probing depth) within normal limits.
Fig. 2 gutta-percha point in sinus tract
Radiographic findings: Tooth :26
Periodontal: Apical lesion around the mesio-buccal root of tooth 26. Radiograph with a gutta-percha point in the sinus tract confirmed the presence of a communication between the oral mucosa and the lesion.
109 Dental: Radiopaque material was demonstrated in the coronal part of tooth 26, verified clinically as the gold crown
Other: No findings in relation to tooth 15 or 17 that would influence the diagnosis or the treatment.
Fig.3 preoperative x-ray
Diagnosis: Tooth : 26 Apical periodontitis with a sinus tract
Treatment plan: Tooth :26 Root canal disinfection and filling
Problem list: Obliterated canals
Treatment: Date:12.12.2006 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canals were located and instrumented manually with NiTi files to dimension:
Mb # 45, 21 mm ref: mb cusp DB # 45, 20 mm ref: ml cusp D # 60, 22 mm ref: mb cusp
110 Irrigation with 1% NaOCl and 15% EDTA.The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Fig.4 working length
Next appointment; 25.01.2007
The sinus tract was no longer visible. The MB2 canal was located but not instrumented during the first appointment. An attempt was made to find the canal, using round bur and ultra-sound. The canal was obliterated and we had to give up.
Next appointment; 28.02.2007
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Three canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
111
Fig.5 masterpoint
Fig.6 endodontic treatment completed
Evaluation: Since the mb root has a radiolucent area, it was important to find both mb canals. The canal orifice was found, but because of obliteration it was not possible to follow the canal all the way to the apex, without removing too much tooth structure. However, the sinus tract disappeared during treatment. No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable
112 Discussion:
This case was a variant of 26 with three roots with four canals. The two canals in the mb root may share the same apex. The importance of careful scrutiny of the groove on the floor of the chamber between the MB and palatal canals is obvious in 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 canals in the mesiobuccal root.
Hess (3) evaluated 513 extracted maxillary first and second molars, and found that 54% had 4 canals. Pineda et al (6) reported finding 4 canals in 51,5% of first and second maxillary molars.
Ibarrola et al (4) looked at the different factors affecting the negotiability of second mesiobuccal canals in maxillary molars. The evaluation was done by studying 87 extracted maxillary molars that had undergone previous endodontic treatment in the endodontic technique laboratory. Several factors that could interfere with the total or partial negotiation of MB2 canal were identified and included accumulation of debris and sealer that blocked access to these canals, dentinal debris produced with the path-finding instrument, the presence of anatomical variations, diffuse calcifications, and pulp stones.
Location of root canals has been evaluated in vivo and in vitro in research articles by using dental loupes, fiberoptic head lamps, scanning electron microscopic observation (4). The DOM (dental operating microscope) has been shown to provide enhanced illumination and magnification for dental procedures on 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 canal orifice in the MB root of extracted maxillary first and second molars, when not found in unaided vision in an in vitro mannequin setting. Thirty-nine extracted maxillary molars were used in the study. The result was that the ML canal orifices were detected in 20 of the teeth with a sharp explorer and a mirror. In the remaining teeth, 12 ML canal orifices were located by using the DOM. The results of their study indicated that the DOM increases the opportunity for the dentist 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 operating microscope in locating the mesiolingual canal orifice. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002; 93: 190-194
2. Carr GB. Microscopes in endodontics. J Calif Dent Assoc 1992; 20: 55-58
3. Hess W, Zurcher E. The Anatomy of root canals of the teeth of permanent dentition. London: John Bane, Sons and Danielsson, 1925; pp. 32-34, 75, 77
4. Ibarrola JL, Knowles KI, Ludlow MO, McKinley Jr IB. Factors affecting the negotiability of second mesiobuccal canals in maxillary molars. J Endod 1997; 4: 236-238
5. Kulid JC, Peters DD. Incidence and configuration of canal systems in the mesiobuccal root of maxillary first and second molars. J Endod 1990; 13: 106- 112
6. Pineda F, Kuttler Y. Mesiobuccal and buccolingual roentgenographic investigation of 7275 root canals. Oral Surg Oral Med Oral Pathol 1972; 33: 101-110
7. Stropko JJ. Canal morphology of maxillary molars: clinical observations of canal configurations. J Endod 1999; 25: 446-450
114 CASE 13 – Acute apical periodontitis with a flare-up
Patient: White Norwegian female, 38 years old. The patient was referred from her private practitioner to the post graduate clinic for endodontic treatment of tooth 15, on March 20, 2006
Fig 1: Preoperative photo
Medical history: Non-contributory
Dental 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 a periapical x-ray, witch showed a radiolucent area around the root apex. The root filling was too short, and the patient was referred to our clinic.
115
Fig 2. tooth 15; a crown with a composite occlusally. Porcelain is lost around the composite.
Clinical findings: Tooth: 15
Extra oral: normal skin
Intra oral: normal soft tissue
Dental: Tooth 15 was restored with a porcelain crown. It was Tender upon biting, tender to palpation apically and tender to percussion. No other findings on other teeth in the area.
Periodontal: PPD within normal limits
Radiographic findings: Tooth: 15
Periodontal: Radiolucent area apically short root filled tooth, two obliterated canals in the apical part.
Dental: Tooth restored with a PFM crown.
Other: No findings
116
Fig 3. Preoperative
Diagnosis: Tooth: 15 acute apical periodontitis
Treatment plan: Tooth: 15 Retreatment Root canal disinfection and filling
Problem list: Canal obliteration
Treatment:
Date: 20.03.2006 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Two canals were located and instrumented manually with NiTi files and Race instrumentation system to dimension:
B # 50, 21 mm ref: B cusp P # 50, 20 mm ref: P cusp
Irrigation with 1% NaOCl and 15% EDTA.The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
117
Fig 4. Working length 1st and 2nd step.
Date:24.03.2006 Flare up. The patient made contact in the weekend, because of severe pain. A firm palpable lesion had developed over the root apex. Her symptoms started on day three. She felt a pressure building up apically of tooth 15. She decided to contact a general practitioner and got an appointment with him. The private dentist performed an incision. A lot of exudate and fluid emptied itself. The patient was immediately relieved. She was prescribed with a combination of antibiotics: Metronidazol and Phenoxymethyl-penicillin, and recommended to rinse with Chlorhexidine mouthwash.
Next appointment; 03.04.2006 The patient was almost asymptomatic when arriving at the clinic. A small fluctuant swelling could be palpated, and the wound after the incision was visible. Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Two canals were dried with sterile paper points and refilled with Ca(OH)2 and IRM.
Next appointment; 08.06.2006 The patient was asymptomatic. Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were
118 irrigated with 1% NaOCl and 15% EDTA. Two canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH- plus sealer. IRM at the top.
Fig 5: Masterpoint Fig 6: Endodontic treatment competed.
Evaluation: The root-filling appeared dense and good.
Prognosis: Favorable
Follow-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, may be pushed out through the apical foramen into the periapical tissues. The host reaction to this event is an inflammatory response to deal with the entry of these foreign materials into the area. One of the consequences of the inflammatory reaction is clinical symptoms which can range from no postoperative pain to moderate or even severe pain, which may last several days (9). The periapical diagnosis of acute apical periodontitis, have been shown in most studies to also result in a significantly higher flare-up rate. In addition, the radiographic presence of a periapical lesion, particularly larger lesions, also serves as a risk factor for development of flare-ups (9). Most studies regarding this issue have examined the types of treatment as a reason for exacerbation (1,8), and in general have found little correlation between exacerbations and the nature of treatment. In most cases the amount of debris and number of bacteria are low so that the host defense is able to rapidly eliminate the foreign material. In some cases, however sufficient numbers of virulent bacteria may be introduced into the periapical tissues that have the capacity to interfere with the host defense and induce an exacerbation. An exacerbation is by definition a periapical abscess which occurs in a tooth undergoing endodontic treatment. Inoculation of microorganisms into the periapical tissues typically occurs during instrumentation of the canal causing a periapical abscess soon after treatment, within the first 24 hours. The symptoms are marked pain, often increasing in intensity, as well as clinical signs of mucosal redness or swelling and a general feeling of malaise. The swelling may be well localized in the form of a discrete lump adjacent to the tooth or may be broad and diffuse, spreading into the lip, cheek or face as facial cellulites (7). Studies which have examined the type of bacteria associated with periapical abscess formation have revealed that the infections are polymicrobial, dominated by anaerobes and that significant associations exist between particular bacteria and signs and symptoms. Infection of the root canal with combinations of bacteria containing the black pigmented anaerobes Pevotella intermedia, Porphyromonas endodontalis or Porphyromonas gingivalis increases the risk that a purulent apical inflammation will develop (6). The concomitant occurrence of peptostreptococci, especially peptostreptococcus micros with P. intermedia or P.endodontalis seems to increase the risk of post treatment abscess formation (6). Other studies (3) have demonstrated that Fusobacterium nucleatum is another Gram-negative bacteria that may be a causative and/or contributing agent in endodontic flare-ups. The bacteria appear to be associated with the most severe forms of interappointment flare-ups, including pain. Structural components of its cell wall (i.e lipopolysaccharides) have been found to act as endotoxins that provoke inflammatory reactions. Synergistic associations with other pathogenic bacteria,
120 such as Prevotella intermedia, Porphyromonas gingivalis and Peptostreptococcus micros, may also add its pathogenic potential (3).
The management of an acute exacerbation usually involves three measures: 1. Re-cleaning the root canal 2. Drainage 3. Antibiotics and pain relief
Re-cleaning of the root canal in this case, was performed after the the incision and drainage. We re-instrumented the canal, the patient was asymptomatic and we used 2% chlorhexidine gluconate and NaOCl as antibacterial irrigants. NaOCl is well known for its strong antibacterial activity ( 2,5). CHX has also demonstrated a wide antibacterial spectrum and is effective against both Gram- positive and Gram-negative bacteria as well as yeast (4). We decided to fill the canal permanently with MTA after re-cleaning it, instead of remedicating with Ca(OH) . 2 The patient was also given antibiotics. The selection of an appropriate antibiotic in the management of an exacerbation is based on the types of microorganisms present and their known sensitivity. Since these infections are usually polymicrobial, they may contain some species which have the capacity for antibiotic resistance. However, it is not necessary for all microorganisms to be sensitive to the antibiotics for an infection to resolve, since killing of some flora changes the nature and effectiveness of the collective consortium allowing an improved response by the host defence (7). The antibiotic of first choice is still penicillin, since it has the best balance of appropriate antimicrobial spectrum and relatively low clinical toxicity. Depending on the clinical circumstances and severity 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 initial treatment of necrotic pulps. J Endod 1984; 10: 78- 81
2. Byström A, Sundqvist G. The antibacterial action of sodiumhypochlorite and EDTA in 60 cases of endodontic therapy. Int Endod J 1985; 18: 35-40
3. Chavez de Paz LE. Fusobacerium nucleatum in endodontic flare- ups. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2002; 93: 179-83
4. Shaker LA, Dancer BN, Russell AD, Furr JR. Emergence and development of chlorhexidine resistance during sporulation of Bacillus subtilis 168.
5. Siqueira JF jr, Rocas IN, Santos SR, Lima KC, Magalhaes FA, Uzeda M. Efficacy of instrumentation techniques and irrigatioen regimens in reducing the bacterial population within root canals. J Endod 2002; 28: 181-184
6. Sundqvist GK, Eckerbom MI, Larsson ÅP, Sjögren U. Capacity of anaerobic bacteria from necrotic pulp to induce purulente infections. Infection and immunity 1979; 25: 685- 693
7. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. In Ørstavik D, Pitt Ford TR, ed. Essential Endodontology: Prevention and Treatment of Apical Periodontitis 1998
8. Torabinejad M, Kettering JD, McGraw JC, Cummings RR, Dwyer TG, Tobias TS. Factors associated with interappointment emergencies of teeth with necrotic pulps. J Endod 1988; 14: 261-66
9. Walton RE. Interappontment flare-ups: incidenve, related factors, prevention and management. Endod Topics 2002, 3, 67-76
122 CASE 14 – Retreatment and Apicoectomi
Patient: A 35 year old white Norwegian female was referred to the Postgraduate Endodontic Clinic, Faculty of Dentistry, University of Oslo, from the Undergraduate Clinic.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: 16.08. 2001: Acute pulpitis tooth 36 due to deep caries. At the next dental check-up in 2004 she visited in our faculty. Radiographic examination showed chronic apical periodontitis on tooth 36, distal root. No history of pain or discomfort.
123 Clinical findings: Tooth: 36
Extra oral: normal skin
Tooth 35 36 37
Intraoral _ _ _ swelling
Tender to _ _ _ percussion
Tender to _ _ _ palpation
GPD _ _ _
Other: No clinical findings or symptoms from the other teeth in the upper and lower right quadrants relevant to the chief complaint.
Radiographic findings: Tooth: 36
Periodontal: Periapical lesions around distal roots.
Dental: The tooth was restored coronally with a radiopaque material verified clinically as a composite filling.
Other: The intraoral radiographic examinations demonstrated an acceptable distance from the periapical lesions to canalis mandibularis.
124 Fig.2 Preoperative x-ray
Diagnosis: Tooth: 36: chronic apical periodontitis
Treatment plan: Tooth: 36: Conventional retreatment Negotiating of another distal canal? Root canal disinfection and filling.
Problem list: Why did it fail the first time?
- distal root, short filling - anatomy
Treatment:
Date: 10.11.2004 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. Three canals were located and instrumented manually with NiTi files to dimension:
125 Fig.3 Working length x-rays
MB: # 40/23mm, ref: mbc BL: #40/21mm, ref: BC DL: # 45/22mm, ref: dlc DB: #45/20mm ref: dbc
Irrigation with 1% NaOCl and 15% EDTA. The canals were dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Next appointment; 13.03.2005
Rubber dam was applied and the field disinfected with chlorhexidine and ethanol. Ca(OH)2 was removed. The canals were irrigated with 1% NaOCl and 15% EDTA. Three canals were dried with sterile paper points and filled by cold lateral condensation technique with gutta-percha and AH-plus sealer. IRM.
126 Fig.4 Masterpoint x-ray
Evaluation: No complications during treatment, the root-filling appeared dense and good.
Prognosis: Favorable
Follow-up examination: 21.03.2006: No subjective symptoms from tooth 36. The tooth was restored with a PFM (porcelain fused to metal) crown. No signs of healing. There was still an apical radiolucency around distal root.
Diagnosis: tooth 36: chronic apical periodontitis
Treatment: Apicoectomi tooth 36, distal root
127
Problem list: The anatomical relations between the root apices in the molar region in the left lower jaw and the canalis mandibularis was important to define before we could perform the Apicoectomi. The patient was referred to the Department of Radiology for panoramic radiographic examination. In that way we could have an overview of the important anatomical structures in the area.
Fig.5 OPG
The patient met for surgery, 4 carpules with Xylocain-adrenaline were injected to establish anesthesia. The patient rinsed for 1 minute with Chlorhexidine mouthwash. Intrasulcular buccal incision from the distal surface of tooth 37 to the mesial surface of tooth 33, with vertical releasing incision from tooth 33 towards the inferior aspect of the buccal mucosa. Surgical blade number 15 was used. The flap was elevated. The apical lesion did not perforate the cortical bone. The intraoral radiographs were calibrated with a periodontal probe and measured the site of the lesion. Osteotomy was performed with a round bur no 16 with copious irrigation with sterile saline, until the lesion was located 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 fissure bur on a high speed hand piece. It was difficult to see the foramen, and we decided to leave the root without a retrograde filling. Haemostasis in the bone cavity was achieved with strypnongaze. The flap was repositioned and sutured with 7, 5-0 silk sutures. Postoperative information was given. Ice bag was kept at the patients’ right cheek, over the surgical site for 15 minutes. Medications were prescribed: Pinex forte and Pinex. Chlorhexidine mouthwash was recommended.
Fig.6 during surgery Fig 7. x-ray during surgery
Fig.8 post surgery
129 One week later: The patient was asymptomatic. No negative clinical findings. No numbness in the area where surgery was performed.
Prognosis: Favorable
Fig.9 photo 6 months post-op
Follow-up examination: 15.11.2006
The patient was asymptomatic. No negative clinical findings. The radiographic examination demonstrated good healing.
Fig.10 x-ray 6 months post-op
130 Discussion;
Endodontic re-treatment is generally considered to have a lower prognosis than primary endodontic cases, with the poorest outcome in retreated teeth/roots with apical periodontitis. Studies that document retreatment in teeth with apical periodontitis demonstrate 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 nonsurgical retreatment in teeth with periapical pathosis also depends on the technical standard of the root-filling, with the lowest success rate when the root-filling extended beyond the root apex (3). The major factors associated with endodontic failure are the persistence of microbial infection in the root canal system and/ or the periradicular area (4,5). Bacteria located in areas such as isthmuses, ramifications, deltas, irregularities and dentinal tubules may sometimes be unaffected by endodontic disinfection procedures. In Sundqvist et al (6) and previous studies (7,8) the microbial flora detected in root-filled canals could be characterized as monoinfections of predominantly Gram-positive microorganisms, with approximately equal proportions of facultative and obligate anaerobes. This composition differs markedly from that seen in infections of the untreated canal, which typically have a polymicrobial flora with approximately equal proportions of Gram-negative and Gram-positive bacteria and are dominated by obligate anaerobes (9,6) While selective pressures exist in the untreated canal that favor the establishment of a very restricted group of the oral flora ( 9,10), special conditions must also apply to the microorganisms that can persist in the root- filled canal. Enterococci are often reported to be low in numbers in untreated infected root canals with necrotic pulps (9). However, when the ecological prerequisites are altered, enterococci may thrive and multiply. Gomes et al (11) reported multiplication of E.faecalis in some canals following standard biomechanical treatment procedures. Rocas et al (12) studied the association of Enterococcus faecalis with different forms of periradicular disease. Statistical analysis showed that E. faecalis was significantly more associated with asymptomatic cases than with symptomatic ones. E. faecalis was detected in 20 of 30 cases of persistent endodontic infections associated with root-filled teeth. The average odds of detecting E. faecalis in cases of persistent infections associated with treatment failure was 9.1. However, the major involvement of E. faecalis with asymptomatic periradicular disease supports the assumption that enterococci are in general not highly
131 virulent microorganisms, and their emergence as pathogens can be much more related to resistance to several antimicrobial agents than to high virulence.
132 Reference list
1. Friedman S. Treatment outcome and prognosis of endodontic therapy. In Ørstavik D, Pitt Ford T, editors. Essential Endotology. Oxford: Blackwell Science Ltd; 1998
2. Bergenholtz G, Lekholm U, Milthon R, Engström B. Influence of apical over instrumentation and overfilling on re-treated root canals. J Endod 1979B; 5:310-314
3. Sjögren U, Hagglund B, Sundqvist G, Wing K. Factors affecting the long-term results of endodontic treatment. J Endod 1990; 16: 498-504
4. Lin LM, Skibner JE, Gaengler P. Factors associated with endodontic treatment failures. J Endod 1992; 18: 625-627
5. Nair PNR, Sjögren U, Krey G, Kahnberg KE, Sundqvist G. Intraradicular bacteria and fungi in root filled, asymptomatic human teeth with therapy- resistant periapical lesions: a long termlight and electron microscopic follow- up study. J Endod 1990; 16: 580-588
6. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth with endodontic treatment and the outcome of consercative treatment. Oral Surg oral Med Oral Pathol 1998; 85: 86-93
7. Molander A, Reit C, Dahlén G. Kvist T. Microbiological examination of root- filled teeth with apical periodontitis. Int Endod J1994; 27: 104
8. Möller ÅJR. Microbiological examination of root canals and periapical tissues of human teeth. Odont Tidskrift 1966-74:(supplement): 1-380
9. Sundqvist G. Associations between microbial species in dental root canal infections. Oral Microbiol Immunol 1992; 7: 257-262
11. Gomes BPFA, Drucker DB, Lilley JD. Variations in the susceptilities of components of the endodontic microflora to biomechanical procedures. Int Endod J 1996; 29: 235-241
12. Rocas IN, Siqueira JF, Santos KRN. Association of Enterococcus faecalis with Different forms of periradicular diseases. J Endod 2004; 5: 315-320
133 CASE 15 - Ekstra-radiculær infection
Patient: White Norwegian female, 62 years old. The patient was referred to the postgraduate clinic for evaluation and treatment of tooth 45.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: The patient was referred to private practice. Tooth 45 was previously root filled, and because of chronic marginal periodontitis it as not much bone around the tooth. Her private practitioner asked for evaluation and treatment of tooth 45. He wrote that he thought the tooth was lost, but the patient insisted to try and keep it as long as possible.
Clinical findings: Tooth:45
134
Extra oral: normal skin
Intra oral: normal soft tissue
Dental: PFM (porcelain fused to metal) crown. The tooth was slight tender to percussion. The crown had a good fit, and no signs of coronal leakage.
Periodontal: A sinus tract was detected in a narrow pocket mesially.
Radiographic findings: Tooth:45
Periodontal: Chronic marginal periodontitis, bone loss around the tooth, mostly mesially. Radiolucent area of approximately 10. mm in diameters.
Dental: Root-filled tooth. Restored with a PFM crown.
Other: 46: chronic apical periodontitis.
Fig.2 preoperative Diagnosis: Tooth: 45: Chronic apical periodontitis. Problem List: The patient was informed that the treatment outcome had an uncertain prognosis. She said that she was willing to try and rescue the tooth. She already had
135 extracted several teeth in her younger days, and she didn’t want to give up without trying.
Treatment plan: Tooth: 45: Retreatment
Treatment:
Date: 17.08.2006 Medical and dental history. Treatment plan. Access preparation. Rubber dam was applied and the field disinfected with chlorhexidine-ethanol. One canal was located and instrumented manually with NiTi files to dimension:
Mb # 60, 17 mm ref: mb cusp
Fig.3 persistent sinus tract
Exudate in the canal. Irrigation with 1% NaOCl and 15% EDTA.The canal was dried with sterile paper points and packed with Ca(OH)2 and IRM as a top filling.
Next appointment; 14.09.2006
Rubber dam was applied and the field disinfected with chlorhexidine 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 was dried with sterile paper points and filled by cold lateral
136 condensation technique with gutta-percha and AH- plus sealer. IRM. We decided to do an Apicoectomi as a last try to keep the tooth. To minimize the expenses, I referred her to myself at the Department of Endodontics.
Fig.4 after retreatment
Diagnosis: Tooth: 45: Ekstraradicular infection.
Problem list: The anatomical relations between the root apice and foramen mentale was important to define before we could perform the Apicoectomi. When operating close of a nerve foramen, there is a chance of parestesie in the area. The patient was informed. The patient was referred to the Department of Radiology for panoramic radiographic examination. In that way we could have an overview of the important anatomical structures in the area.
137
Fig.5 OPG
Date: 12.12.2006 The patient met for surgery, 3 carpules with Xylocain- adrenaline were injected to establish anesthesia. The patient rinsed for 1 minute with Chlorhexidine mouthwash. Intrasulcular buccal incision from the distal surface of tooth 46 to the buccal surface of tooth 43, with vertical releasing incision from tooth 43 towards the inferior aspect of the buccal mucosa. Surgical blade number 15 was used. The flap was elevated. The apical lesion did not perforate the cortical bone. The intraoral radiographs were calibrated with a periodontal probe and measured the site of the lesion. Osteotomy was performed with a round bur no 16 with copious irrigation with sterile saline, until the lesion was located and the root was visible. Granulation tissue was removed by curettage. Because of the resorption-defect we decided not to cut the root, just to clean the root-surface. The apical foramen was demonstrated. Retrograde preparation was performed with piezoelectric Satelec ultrasound device, using ultrasonic tip CT under constant cooling with sterile saline, but there were very little space for a retrograde filling. The gutta-percha was removed until the inferior border of the post. The retro- preparation was dried with sterile paper points. Haemostasis in the bone cavity was achieved with
138 strypnongaze. A retrograde filling with MTA was made. 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 the surgical site for 15 minutes. Medications were prescribed: Pinex forte and Pinex. Chlorhexidine mouthwash was recommended.
Fig.6 during surgery
Fig.7 during surgery
139 Granulation tissue removed from the periapical cavity.
Fig.8 post surgery
One week postoperative: After surgery examination and suture removal. The tooth was mobile grade 2. This had not been the case previously. A slight numbness’ in the area where we performed the surgery, corresponding to the region innervated with nervus alveolaris inferior was evident. The healing was otherwise satisfactory, and the patient had not experienced much pain.
Evaluation: The retrograde filling of MTA is about 4 mm and appeared dense and good. After sequela with numbness’ in the area innervated with nervus alveolaris inferior are to be expected after a surgical treatment like this. Preoperative information is of outmost importance to avoid unnecessary anxiety and frustrations. The retro-filling appeared dense and of good quality.
140
Prognosis: Questionable
Follow-up examination: 3 months post-operative The patient was asymptomatic. No negative clinical findings. No numbness in the area where surgery was performed. No mobility. The radiographic examination demonstrated good healing.
27.03.2007 27.03.2007
Fig.9 3 months postop
Evaluation: Uncertain prognosis because of short root and little bone. The patient was satisfied with the result. She needed time to prepare herself for a possible extraction of the tooth.
141 Discussion: The major factors associated with endodontic failure are the persistence of microbial 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 as broken instruments, perforations, overfilling, underfilling, ledges and so on are the direct cause of endodontic failure. In most cases, procedural errors do not jeopardize the outcome of endodontic treatment unless a concomitant infection is present. A procedural accident often impedes or makes it impossible to accomplish appropriate intracanal procedures, and then there is a potential for failure. There are however some cases in which the treatment has followed the highest technical standards and yet failure occurs. Scientific evidence (9,10,13) indicates that some factors may be associated with the unsatisfactory outcome of well-treated cases. They include: - microbial factors - Ekstraradicular and/ or intraradicular infections - intrinsic non microbial factors - extrinsic non microbial factors Bacteria located in areas such as isthmuses, ramifications, deltas, irregularities and dentinal tubules may sometimes be unaffected by endodontic disinfection procedures. In Sundqvist et al (14) and previous studies (5,7) the microbial flora detected in root-filled canals could be characterized as monoinfections of predominantly Gram-positive microorganisms, with approximately equal proportions of facultative and obligate anaerobes. This composition differs markedly from that seen in infections of the untreated canal, which typically have a polymicrobial flora with approximately equal proportions of Gram- negative and Gram-positive bacteria and are dominated by obligate anaerobes (13,14) While selective pressures exist in the untreated canal that favor the establishment of a very restricted group of the oral flora ( 13,15), special conditions must also apply to the microorganisms that can persist in the root- filled canal. Molander et al (6) examined the microbiological status of 100 root- filled teeth 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 of the cases examined, one or two strains were found. Facultative anaerobic species predominated among these isolates (69% of identified strains). Growth was classified as sparse or very sparse in 53%, and as heavy or very heavy in 42%. Enterococci were the most frequently isolated genera, showing heavy or very heavy growth in 25 out of 32 cases (78%). Rocas et al (11) showed that E. faecalis was significantly associated with treatment failures. Whereas this species was detected in 18% of the cases of primary endodontic infections, its prevalence in root-filled teeth was much higher: 67% of the cases. This finding suggests that this species can be inhibited by other members of a mixed bacterial consortium commonly present in primary infections, and that the bleak environmental conditions within filled root canals
142 may not prevent its survival. For a given microorganism to survive in a filled root canal, it must resist intracanal procedures of disinfections and endure periods of starvation. Studies have revealed that E. faecalis has the ability to penetrate and invade 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 escape from the action of endodontic instruments and irrigants used during chemo mechanical preparation. E. faecalis is also resistant to calcium hydroxide (1). E. faecalis can colonize root canals in single infections and such a relative independence of living without deriving nutrients from other bacteria is arguably essential for its establishment in filled root canals (14). Finally, environmental cues can also regulate gene expression in E faecalis, which can allow the microorganisms to adapt to varying environmental conditions (2). This includes the ability to survive in environments with scarce nutrients and to flourish when the nutrients is re- established.
143 Reference list: 1. Evans M, Davies JK, Sundqvist G, Figdor D. Mechanisms involved in the resistance of Enterococcus faecalis to calcium hydroxide. Int Endod J 2002; 35: 221-228
2. Jett BD, Huycke MM, Gilmore MS. Virulence of enterococci. Clin Microbiol Rev 1994; 7: 462-478
3. Lin LM, Skibner JE, Gaengler P. Factors associated with endodontic treatment failures. J Endod 1992; 18: 625-627
4. Love MR. Enterococcus faecalis- a mechanism for its role in endodontic failure. Int Endod J 2001; 34: 399-405
5. Molander A, Reit C, Dahlén G. Kvist T. Microbiological examination of rootfilled teeth with apical periodontitis. Int Endod J 1994; 27: 104
6. Molander A, Reit C, Dahlén G. Kvist T. Microbial status of root-filled teeth with apical periodontitis. Int Endod J 1998; 31: 1-7
7. Möller ÅJR. Microbiological examination of root canals and periapical tissues of human teeth. Odont Tidskrift 1966-74:(supplement): 1-380
8. Nair PNR, Sjögren U, Krey G, Kahnberg KE, Sundqvist G. Intraradicularbacteria and fungi in root filled, asymptomatic human teeth with therapy-resistant periapical lesions: a long termlight and electron microscopic follow-up study. J Endod 1990; 16: 580-588
9. Nair PNR, Sjögren U, Schumacher E, Sundqvist G. Radicular cyst affecting a root- filled human tooth: a long-term post-treatment follow-up. Int Endod J 1993; 26:225-233
10. Nair PNR, Sjögren U, Figdor D, Sundqvist G. Persistent periapical radiolucencies of root-filled human teeth, failed endodontic treatment, and periapical scars. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999; 87: 617-627
11. Rocas IN, Siqueira JF, Santos KRN. Association of Enterococcus faecalis with different forms of periradicular diseases. J Endod 2004; 5: 315-320
12. Sjögren U. Success and failure in endodontics. Odontol Dissertations. Umeå, Sweden: Umeå University; 1996
13. Sundqvist G. Associations between microbial species in dental root canal infections. Oral Microbiol Immunol 1992; 7: 257-262
144 14. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth with endodontic treatment and the outcome of consercative treatment. Oral Surg oral Med Oral Pathol 1998; 85: 86-93
15. Sundqvist G, Figdor D. Endodontic treatment of apical periodontitis. In Ørstavik D, Pitt Ford T, editors. Essential endotology. Oxford: Blackwell Science Ltd; 1998
145
CASE 16 – Surgical retreatment
Patient: White Norwegian male, 70 years old. The patient was referred to the postgraduate clinic for evaluation and retreatment of an apical infection on tooth 22 from the undergraduate clinic.
Fig.1: preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: The patient complained about tenderness in the area of 22. Tooth 22 was root filled and a PFM crown with a post was cemented on top. This was about 30 years ago, and the patient was very interested in keeping the crown because he likes the look of it. The economical issue is also of great interest, and he wants to keep the costs as low as possible.
Clinical findings: Tooth:22
Extra oral: normal skin
146 Intra oral: normal soft tissue Dental: PFM (porcelain fused to metal) crown. The tooth was slight tender to percussion. The crown had a good fit, and no signs of coronal leakage.
Periodontal: normal findings
Other: no clinical findings or symptoms from the other teeth in the upper and lower right quadrants relevant to the chief complaint.
Fig.2 Mirror image of the palatal view of 22.
Radiographic findings: Tooth:22
Periodontal: Periapical lesion around the root apex.
Dental: The tooth was restored coronally with a radiopaque material verified clinically as the PFM crown restoration. The crown appeared to have a good fit. A radiopaque material was demonstrated, extending 1/3 in the root, corresponded to the post. A small piece of a root-filling is visible.
147
Fig.3 preoperative
Diagnosis: Tooth:22 : Acute apical periodontitis
Treatment plan: Tooth:22 : Surgical retreatment
Treatment:
Date:05.04.2005 Medical and dental history. Treatment plan.
Date:03.05.2005 The patient met for surgery, 3 carpules with Xylocain- adrenaline were injected to establish anaesthesia. The patient rinsed for 1 minute with Chlorhexidine mouthwash. Intrasulcular buccal incision from the distal surface of tooth 23 to the mesial surface of tooth 23 , with vertical releasing incision from tooth 23 towards the inferior aspect of the buccal mucosa. Surgical blade number 15 was used. The flap was elevated. The apical lesion did not perforate the cortical bone. The intraoral radiographs were calibrated with a periodontal probe and measured the site of the lesion. Osteotomy was performed with a round bur no 16 with copious irrigation with sterile saline, until the lesion was located and the root was visible. Granulation tissue was removed by curettage. Resection of 3 mm of the root with a long fissure bur on a high speed hand piece. The apical foramina was demonstrated. Retrograde preparation was performed with piezoelectric Satelec ultrasound device, using
148 ultrasonic tip CT under constant cooling with sterile saline. The gutta-percha was removed until the inferior border of the post. The retro-preparation was dried with sterile paper points. Haemostasis in the bone cavity was achieved with strypnongaze. Retrograde filling with MTA was placed. The flap was repositioned and sutured with 7, 5-0 silk sutures. Postoperative information was given. Ice bag was kept at the patients’ lip, over the surgical site for 15 minutes. Medications were prescribed: Pinex forte, Pinex and Apocillin 660 mg. Chlorhexidine mouthwash was recommended.
Fig.4 during surgery Fig.5 during surgery, granuloma
149
Fig.6 MTA in the canal
Fig.7 After surgery
150
Fig.8 post-op x-ray
10.05.2005 After surgery examination and suture removal. He had a hematome at his right cheek. Otherwise the healing was satisfactory, and the patient had not experienced much pain.
Fig.9 one week post-op
Evaluation: The retro filling appeared dense and good. No complications during treatment.
151 Prognosis: Favorable
Follow-up examination: No subjective symptoms. The radiograph shows good healing.
Fig.10 2 years follow-up.
Fig.11 radiograph taken two year post-op.
152 Discussion: Success rates ranging from 25-90% for surgical endodontic procedures have been reported in the literature (1). Such disparity could be explained by the nature of the study, the different sample sizes, the period of recall, and the criteria used for evaluating clinical and radiographic parameters of healing. Furthermore, a number of other factors can affect the prognosis in periradicular surgery, including patient demographics and systemic conditions, tooth involved, amount and location of bone loss, 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 surgical endodontics. They used a well defined case selection and an evidence-based, contemporary surgical technique. Data were collected from all patients requiring surgical treatment in a private practice setting limited to endodontics, during the period from January 1992 to December 1993. A total number of 114 patients were selected and included in the study. The cases met the following criteria: 1. One tooth was treated for each patient 2. The tooth to be treated surgically had a dental history of failed root canal treatment, and had at least one nonsurgical retreatment to enhance debridement. 3. The tooth to be treated surgically demonstrated a persistent periradicular lesion of strictly endodontic origin with or without clinical signs and symptoms of inflammation. 4. The tooth to be treated exhibited an adequate final restoration with no clinical evidence of coronal leakage.
Of the 114 cases treated, five patients could not be seen again. One tooth was extracted for prosthetic reasons and four patients never responded to the recall request, representing a 4,3% drop-out rate. Of the remaining 109 cases, seven were excluded from this study for presenting with vertical root fractures. Ultimately, a total number of 102 surgical cases were included in this study, of which 93 were classified as a success (91,2%) and nine as failures (8,8%) after the observation period of 1-4 years. Zulo et al (3) concluded that with a strict endodontic surgical protocol and the use of contemporary techniques and materials (IRM was used in this study as a retrograde filling material) will result in a predictably successful outcome in a wide range of teeth.
153 Reference list: 1. Gutmann JL, Harrison JW. Surgical Endontics: Boston MA, USA: Blackwell Scientific Publications 1991
2. Rud J, Andreasen JO, Möller Jensen JE. A follow-up study of 1000 cases treated by endodontic surgery. Int Endod J 1972a; 1: 215-218
3. Zulo ML, Ferreira MOF, Gutmann JL. Prognosis in periradicular surgery: a clinical prospective study: Int Endod J 2000; 33: 91-98
154 CASE 17 – Apicoectomi : complicated location
Patient: White Norwegian female, 61 years old. The patient was referred to the postgraduate clinic for evaluation and treatment of a persistent apical infection after primary endodontic treatment and retreatment at an Endodontist.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: Tooth 46 had been retreated because of a persistent sinus tract after endodontic treatment. When the patient came back to the Endodontist after three weeks of ca(OH)2 dressing in the root canal, the sinus tract was still there. The dentist called our faculty and made an appointment for examination, and she said that she thought we would need to do an Apicoectomi.
Clinical findings: Tooth: 46
Extra oral: normal skin
Intra oral: sinus tract buccally
Dental: PFM (porcelain fused to metal) crown. The tooth was slight tender to percussion. The crown had a good fit, and no signs of coronal leakage.
155
Periodontal: Normal findings
Other: No clinical findings or symptoms from the other teeth in the upper and lower right quadrants relevant to the chief complaint.
Fig.2 gutta-percha in the sinus tract
Radiographic findings: Tooth: 46
Periodontal: Periapical lesions around mesially and distal roots.
Dental: The tooth was restored coronally with a radiopaque material verified clinically as the PFM crown restoration. The crown appeared to have a good fit.
Other: The intraoral radiographic examinations demonstrated an acceptable distance from the periapical lesions to canalis mandibularis.
Fig.3 preoperative x-ray
156
Diagnosis: Tooth: 46: Apical periodontitis with a sinus tract. Extra radicular infection
Treatment plan: Tooth: 46: Apicoectomi.
Problem list: The anatomical relations between the root apices in the molar region in the right lower jaw and the canalis mandibularis was important to define before we could perform the Apicoectomi. The patient was referred to the Department of Radiology for panoramic radiographic examination. In that way we could have an overview of the important anatomical structures in the area.
Fig.4 OPG
Treatment: 21.11.06 Medical and dental history. Treatment plan. The patient was referred to the Department of Radiology for a panoramic examination and she got an appointment for Apicoectomi.
23.11.06 Panoramic examination at the Department of Radiology.
157 28.11.06 the patient met for surgery, 5 carpules with Xylocain- adrenaline were injected to establish anesthesia. The patient rinsed for 1 minute with Chlorhexidine mouthwash. Intrasulcular buccal incision from the distal surface of tooth 47 to the mesially surface of tooth 43, with vertical releasing incision from tooth 43 towards the inferior aspect of the buccal mucosa. Surgical blade number 15 was used. The flap was elevated. The apical lesion did not perforate the cortical bone. The intraoral radiographs were calibrated with a periodontal probe and measured the site of the lesion. Osteotomy was performed with a round bur no 16 with copious irrigation with sterile saline, until the lesion was located and the mesial and distal roots were visible. Granulation tissue was removed by curettage. Resection of 3 mm of both roots with a long fissure bur on a high speed hand piece. Three apical foramina were demonstrated. Retrograde preparation in both roots was performed with piezoelectric Satelec ultrasound device, using ultrasonic tip CT under constant cooling with sterile saline. The retro-preparations were dried with sterile paper points. Haemostasis in the bone cavity was achieved with strypnongaze. Two retrograde fillings with MTA were placed. The flap was repositioned and sutured with 7, 5-0 silk sutures. Postoperative information was given. Ice bag was kept at the patients’ right cheek, over the surgical site for 15 minutes. Medications were prescribed: Pinex forte, Pinex and Apocillin 660 mg. Chlorhexidine mouthwash was recommended.
Fig.5 during surgery
158
Fig.6 During surgery Fig.7 post surgery
Fig.8 x-ray post op
05.12.06 after surgery examination and suture removal. Some edema was still present on the patient’s right side. A slight numbness’ in the area where we performed the surgery, corresponding to the region innervated with nervus alveolaris inferior was evident. The healing was otherwise satisfactory, and the patient had not experienced any pain. She was well informed, and she got a new appointment in 1 week.
12.12.06 Satisfactory healing. The patient felt less num.
Evaluation: This turned out to be a technically complicated and demanding surgical treatment. The visibility during the completion of the retro-preparations and the retro-fillings were poor. After sequela with numbness’ in the area innervated with nervus alveolaris inferior are to be expected after a surgical treatment like this. Preoperative information is of outmost importance to avoid unnecessary anxiety and frustrations.
159 The retro-fillings appeared tiny.
Prognosis: Favorable
Follow-up examination:
27.03.07 the patient was asymptomatic. No negative clinical findings. No numbness in the area where surgery was performed. The radiographic examination demonstrated good healing.
Fig.9 3 months post op
160 Discussion:
Evaluating site is one of the most important steps in case selection for periradicular surgery. Anatomic studies can provide some guidance, but individual variation is great, and there is no substitute for a complete clinical examination. A small oral opening, active facial muscles, shallow vestibule, and thick buccal alveolar bone all can significantly increase the difficulty of the procedure, even in cases that appear straightforward on radiographic examination.
The primary anatomic structure of concern for periradicular surgery in the posterior mandible is the neurovascular bundle that courses through the mandibular canal and exits 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 been illustrated in Grung et al (1) showed a retreatment success rate 24% higher in cases of failed endodontic treatment, in which antibacterial measures and refilling of the canal preceded apical surgery, than in cases in which apical surgery was the only procedure performed. These results, in conjunction with Sjögren et al (2) suggest that it is possible to attain very high success rates when both the intraradicular and the extraradicular causes of endodontic treatment are well managed. A high success rate is dependent on the fact that defective root-fillings should, when possible be conventionally retreated and the supplemented, if no signs of periapical healing, with apical surgery (2).
161 Reference list:
1. Grung B, Molven O, Halse A. Periapical surgery in a Norwegian county hospital: follow-up findings of 477 teeth. J Endod 1990; 16: 411-417
2. Sundqvist G, Figdor D, Sjögren U. Microbiology analysis of teeth with endodontic treatment and the outcome of consercative treatment. Oral Surg oral Med Oral Pathol 1998; 85: 86-93
162 CASE 18 – Cracked tooth
Patient: White Norwegian female, 30 years old. Referred to the postgraduate clinic of Endodontics from the undergraduate clinic for treatment of tooth 16, August, 2004.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint:
Tooth 16 was root-filled by an undergraduate student in 2002, with a good result. The preoperative diagnosis was pulpitis due to caries profunda. The post operative radiograph revealed a dense root-filling and the prognosis was set to be good. When she was at a delayed follow-up examination of the tooth, on August 2004, a fistula was detected and the patient was referred to the Department of Endodontics. She complained about tenderness on chewing.
163
Fig.2 gutta-percha in sinus tract Fig.3 tooth 16
Clinical findings: Tooth:16
Extra oral: Normal skin
Intra oral: A fistula was present buccally of tooth 16.
Dental: The tooth was restored with an occlusal composite witch was of a poor condition. The tooth was tender to percussion.
Periodontal: Mecially there was a narrow gingival pocket with a periodontal probing depth of 7 mm.
Other: The other teeth in the upper and lower right quadrants showed no signs relevant to the chief complaint
Radiographic findings: Tooth:16
Periodontal: The PDL was widened mesially.
Dental: A radiopaque material was demonstrated inside the coronal part of the tooth verified clinically as the composite filling. A radiopaque material was observed in the root canal corresponding to the root-filling material. The quality of the root-filling appeared dense and of good quality.
164
Fig.4 Preoperative X-ray Fig.5 Gutta-percha point in sinus tract
Diagnosis: Tooth: 16: Cracked tooth
Prognosis: Uncertain
Treatment plan: Tooth: 16: Locate and verify the crack by the use of operating microscope.
Crack
Untreated mb2 canal
• Composite restoration was partly removed for access cavity. • Fracture line mesially towards the distal.
Treatment: Extraction
165 Evaluation: If the tooth had been restored with porcelain fused to metal crown, the tooth would have had a good chance of survival. The patient was given a poor advice when the decision 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 root fracture. 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 crown or 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 root which may be either the coronal or apical portion, it may extend into the crown of the 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 generally accepted that vertical root fractures can be caused by various factors including pin and post placement, impact injuries, root canal filling procedures, and seating of intracoronal restorations.
Gehr et al (2) demonstrated in a survey of 100 cases of fractured teeth affecting 98 patients during a 2-year period, that the presence of a root canal filling was the single most important clinical feature, in 71 of 100 cases. Endodontically treated teeth are usually week as a result of loss of tooth material due to caries and access cavities. In addition, the chance of fractures increases due to loss of moisture in the dentin of pulpless teeth (7). Bender et al (1) claimed that the extensive use of rotary instruments during preparation of the canal space, for example, cutting the dentin in straight lines particularly at the curvatures, weakened the root structures. Other have also reported that extensive instrumentation of the root canal space may contribute to weakening of the root canal walls (3, 4), in addition to excessive pressure during compaction of gutta-percha (2).
Chelating agents have also been suggested to cause embrittlement through decalcification of the dentin, and thereby increasing the fracture risk (6).
Clinical symptoms seem to develop after fracture occurs, which involves the periodontium and permits bacterial invasion and subsequent periodontal pocket formation. Once a root fracture involves the periodontium, clinical and radiographic appearance shows that pathologic destruction of the periodontal tissues progresses rapidly and leads to severe bone and attachment loss. Destruction of the periodontal tissues is widespread, extending the full length of the fracture. A periapical radiograph with a gutta-percha cone inserted in the sinus tract is an important diagnostic tool (7).
167
Reference list: 1.Bender IB, Freedland JB. Adult root fracture. J Am Dent Assoc 1993; 107 413-9
2.Gehr ME, Dunlap RM, Anderson MH, Kuhl LV. Clinical survey of fractured teeth.Am Dent Assoc 1987; 114: 174-7
3. Langer B, Stein SD, Wagenberg B. An evaluation of root resections. J Periodontol 1981;52: 719-22
4. Meister F, Lommel TJ, Gerstein H. Diagnosis and posiible causes of vertical root fracture. Oral Surg Oral Med Oral Pathol 1980; 49: 243-53
5. Pitts DL, Natkin E. Diagnosis and treatment of vertical root fractures. J Endod 1983; 8: 338-46
6. Seidberg BH, Schilder H. An evaluation of EDTA in endodontics. Oral Surg Oral Med Oral Pathol 1974; 37: 609-20
7. Tamse A. Iatrogenic vertical root fractures on endodontically treated teeth. Endod Dent Traumatol 1988; 4: 190-6
168 CASE 19 – Vertical root fracture
Patient: White Norwegian female, 57 years old. Referred to the postgraduate clinic, Department of Endodontics, from her private practitioner for evaluation and treatment of tooth 46.
Fig.1 preoperative photo
Medical history: Non-contributory
Dental history and chief complaint: Tooth 46 had a history of root canal treatment, retreatment and apical surgery. The Apicoectomi was done two years ago, by an oral surgeon. The prognosis was set to be good. The patient had however felt that it had been something wrong with the tooth from the day the endodontic treatment was completed. She had pain coming and going for several months. When she was at a regular follow-up examination of the tooth, on August 26, 2006, she said that the pain had increased lately. The pain was spontaneous, especially during physical activity.
169
Fig.2 Tooth 46
Clinical findings:
Tooth: 46
Extra oral: normal skin
Intra oral: normal soft tissue
Dental: PFM (porcelain fused to metal) crown. The tooth was tender to percussion and palpation. The crown seemed to have a good fit, and no signs of coronal leakage.
Periodontal: no mobility or increased PPD (periodontal probing depth).
Other: The other teeth in the upper and lower right quadrants showed no signs relevant to the chief complaint.
Radiographic findings: Tooth: 46
Periodontal: Periapical lesions around mesial root, apical part. Because of previous Apicoectomi it could correspond to scar tissue.
Dental: The tooth was restored coronally with a radiopaque material verified clinically as the PFM crown restoration. The crown appeared to have a good fit. A radiopaque material was demonstrated, extending 1/2 in the distal root corresponding to a post.
Other: The intraoral radiographic examinations demonstrated an acceptable distance from the periapical lesions to canalis mandibularis.
170
Fig 3 Preoperative x-ray
Tentative diagnosis: Tooth: 46: chronic apical periodontitis.
Treatment plan: Tooth: 46: Apicoectomi
Problem list: The anatomical relations between the root apices in the molar region in the right lower jaw and the canalis mandibularis was important to define before we could perform the Apicoectomi. The patient was referred to the Department of Radiology for panoramic radiographic examination. In that way we could have an overview of the important anatomical structures in the area.
Fig.4 OPG
171 Treatment:
Date: 16.01.2007 Medical and dental history. Treatment plan. The patient was referred to the Department of Radiology for a panoramic examination and he got an appointment for Apicoectomi. Date: 16.01.2007 Panoramic examination at the Department of Radiology.
Date: 17.01.2007 the patient met for surgery, 5 carpules with Xylocain- adrenaline were injected to establish anesthesia. The patient rinsed for 1 minute with Chlorhexidine mouthwash. Intrasulcular buccal incision from the distal surface of tooth 47 to the mesial surface of tooth 43, with vertical releasing incision from tooth 43 towards the inferior aspect of the buccal mucosa. Surgical blade number 15 was used. The flap was elevated. The mesial root had a vertical root-fracture. The crown had not at al a good fit! It was obvious that the tooth had a poor prognosis and that the treatment plan had to be rewritten.
Fig.5 during surgery
Diagnosis: Vertical root fracture
Treatment: Extraction. The tooth was easy to remove; the mesial root was parted from the crown.
172
Fig.6 after extraction
Follow-up examination: Favorable healing of the extraction wound. Normal clinical findings. The radiographs demonstrated normal findings. The patient was asymptomatic, and had not experienced much pain in the area after the extraction.
173 Discussion: 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 crown or at the root apex, or, in some cases, along the root between these two points (1). The vertical root fracture may involve the full length of a root, a section of the root which may be either the coronal or apical portion, it may extend into the crown of the 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 (1). It is generally accepted that vertical root fractures can be caused by various factors including pin and post placement, impact injuries, root canal filling procedures, and seating of intracoronal restorations.
Different instrumentation techniques have been evaluated regarding increased fracture 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 teeth regarding to the type and the length of post, and the type of retention of the post used 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 that lateral condensation technique, in a canal prepared with “step-back” is more vulnerable for vertical root fractures. Long posts with length more than half of the length of the root prepared with “step-back” technique were more responsible for vertical root fractures. To avoid or minimize the potential for vertical root fractures, minimal enlargement 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 lateral condensation (3). The misdiagnosis of vertical root fracture, as an endodontic failure, usually leads to root canal retreatment. This can occur when a sinus tract emerges from the alveolar mucosa, a periapical radiolucency is present at the radiograph, or if the root canal filling is not performed according to the standard criteria as shown in the radiograph. Thoroughly clinical and radiographic examination, including dental history is mandatory. Pitts et al (1) have described the radiographic signs in teeth with vertical root fractures. These included actual separation of root segments, radiolucent fracture lines, radiopaque signs, “halo ”-like radiolucency, periodontal-like lesions, resorption along fracture line, and loosened retro-filling or retro-filling material in a fracture line. Angular periodontal defect extending apically from the crestal bone, of variable width, and generally terminating at the level of the fracture line end was reported in 29% of the cases of iatrogenic vertical root fracture examined by Tamse (4). The patient’s symptoms and clinical signs show a variety of clinical problems, including pain of various kind, swelling, mobility, pockets and sinus tracts. The pockets caused by vertical root fracture are located adjacent to the site of the fracture, in contrast to the normal sulcus depth usually seen around the other areas of the tooth (4). Pocket formation has been demonstrated to be a major finding in cases with vertical root fractures. Sensitivity to palpation and percussion are also signs well known to accompany root fractures. The diagnosis can occasionally be made at the time of the dental procedure. For example, a sharp cracking sound may be heard at the time of
174 condensation the gutta-percha into the root canal. This sound was reported by Meister et al (5) in 6 out of 32 teeth with vertical root fractures. Positive evidence for vertical root fracture may be obtained by reproducing the pain by selective biting on a hard object or the use of dyes in a meticulously clean pulp chamber (4). For most endodontically treated teeth clinically significant features develops after endodontic therapy is completed, the reason is that the therapy may have induced internal stress in the root or created micro fractures that initially were not exposed to bacterial contamination. Subsequent fractures or propagation of fractures then could reach the sulcus, allowing bacterial invasion and rapid loss of bone and periodontal attachment (6). Regardless of the location and extent of a vertical root fracture, destruction of periodontal ligament and bone eventually occur in a linear fashion adjacent to the fracture. The aim of the treatment is elimination of the fracture. Depending on the size and location of the fracture, treatment will range from partial root resection to extraction. In the great majority of cases of vertical root fracture, the gingival sulcus will be involved and an irreversible periodontal pocket will usually be evident. The indicated treatment is removal of the root. This means extraction for single-rooted teeth; however for multi-rooted teeth root amputation or hemi-section may be feasible (1).
175
Reference list:
1.Gehr ME, Dunlap RM, Anderson MH, Kuhl LV. Clinical survey of fractured teeth.Am Dent Assoc 1987; 114: 174-7
2. Meister F, Lommel TJ, Gerstein H. Diagnosis and posiible causes of vertical root fracture. Oral Surg Oral Med Oral Pathol 1980; 49: 243-53
3. Morfis AS. Vertical root fractures. Oral Surg Oral Med Oral Pathol 1990; 69: 631-5
4. Pitts DL, Natkin E. Diagnosis and treatment of vertical root fractures. J Endod 1983; 8: 338-46
5. Schmidt KJ, Walker TL, Johnson JD, Nicoll BK. Comparison of Nickel-Titanium and Stainless-Steel spreader penetration and accessory cone fit in curved canals. J Endod 2000; 1: 42-4
6. Tamse A. Iatrogenic vertical root fractures on endodontically treated teeth. Endod Dent Traumatol 1988; 4: 190-6
7. Trabert KC, Caputo AA, Abou- Rass M. Tooth fracture- a comparison of endodontic and restorative treatments. J Endod 1978; 4: 341-5
176 CASE 20 – Neuropathic pain
Patient: White Norwegian female, 55 years old. Referred from the patient’s general practitioner to the Department of Endodontics, for consultation and evaluation of treatment and pain management. The patient had been in a car accident in 2004.
Fig.1 preoperative photo
Medical history: The patient has several medical problems. She complained about problems with - allergies - eyes - intestinal - head and neck and she uses OTC drugs and alternative treatments like homeopathy to release the troubles. Her regular medical doctor has not been able to help her solving these problems.
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 of pain and discomfort until recently. This started after the car accident. Tooth 36 was painful and a root canal treatment was done. When the pain continued, an apicoectomy was performed without any relief of pain. Several antibiotic treatment has not solved the problem.
177 The patient tells about a constant pain of varying degrees of intensity, localized to the mandibular left side. Occationally, the pain is spreading towards the maxillary left side molars and premolars, and to the temporal area. She can feel the pain when touching her skin at a certain point, and a light touch of the tooth 36 is causing pain. She further informs that she sleeps at night, and the mornings are less painful - it develops during the day. Most days she carachterizes the pain as low to moderate in intensity, but sometimes it is severe, but it is never completely gone.
Clinical examination: 36 was tender to percussion
All 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 articulation
The result of the tests were: No findings.
Radiographic examination:
Fig.2 OPG
178
Fig.3 Radiographic view of the dentition
Result of the radiographic examination: no findings
Diagnosis: Neuropathic pain, it may be post traumatic to the car accident.
Treatment: This patient was informed of the connection between traumatic injuries, periphery nerve damage and longstanding persistent symptoms. A referral was sent to her general practitioner. The patient got a new appointment in 3 months time.
Evaluation: Pain management is one of the most demanding and challenging therapies there is. The important thing is to have an extensive consultation 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 to additional specialists in other dental disciplines for examinations. Close cooperation with the patient’s general practitioner, doctor and physiotherapist is mandatory.
Prognosis: Uncertain. The patient needed to be careful followed-up for a long time. Periphery nerve damage could heal or the symptoms could decrease after a prolonged healing period. It could also be consistent and without change and diminishing of symptoms.
Follow-up examination: Patient did not show for control. I called her, and she told me that she had gone to another dentist for treatment. She wanted a second opinion.
179 I advised her not to receive any treatment without a pathological diagnosis was made. Any further interference in the area of 36, including extraction could make her pain more intense.
We recommended her general practitioner to cooperate with the patients’ medical doctor to get a referral to a neurologist for examination, and suggestion of different treatment regimes with medications.
180 Discussion: Odontogenic pain transmission is mediated primarily by peripheral sensory neurons of the trigeminal nerve (9). The peripheral terminals of these nerves innervate the dental pulp and other oral tissues, whereas the central terminals release neurotransmitters, such as substance P, which are involved in the initiation of pain. These trigeminal sensory afferent neurons, along with sympathetic branches of the superior cervical ganglion and blood vessels, enter through the apical foramen of the tooth. Together, these nerves and blood vessels form the neurovascular bundle (9). There are myelinated and unmyelinated nerve fibers within the nerve bundles. The myelinated 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-delta and C-fibers of the dental pulp function as nociceptive mechanoreceptors that warn of 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 or sensitizing pulpal nociceptors. When the pulp becomes inflamed, the polymodal nociceptive fibers initiate and enhance this process by neurogenic inflammation. Substance P and calcitonin gene-related peptide (CGRP) can each contribute to the inflammatory process (2). Sensitization of neurons can also occur within the CNS (5). Secondary-order neurons can be changed or sensitized when they receive a constant barrage of nociceptive input. Generally the changes are reversible; however, chronic sensitization may result in permanent changes to neuroprocessing. Permanent alterations 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 do not mediate pain in most cases, can divert to nociceptive transmission. When this occurs, 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 of physical and chemical stimuli. During an infection or in the face of trauma, the tissues release noxious chemicals, including both peptides and lipids from which the nociceptor fibers are stimulated. Pain is perceived and recognized in the cortex because of incoming nociceptive (i.e., noxious stimulus) input (5). After activation, the C and A-delta fibers from the orofacial region transmit nociceptive signals primarily via trigeminal nerves to the trigeminal nucleus caudalis (N.caudalis) located in 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 with incoming activity from the relevant C an A-delta fibers (9). These sensory fibers transmit information by releasing excitatory neuropeptides, such as substance P and CGRP (9). In addition to activation and sensitization, the peripheral afferent fiber responds to mediators (e.g., nerve growth factor (NGF) by increasing protein synthesis of substance P and CGRP and by undergoing sprouting of terminal fibers in the inflamed tissue (3,4,9,10). Sprouting increases the density of innervations in inflamed tissue and may contribute to increased pain sensitivity in chronic pulpal or periradicular inflammation. Toothache of neuropathic origin is either episodic or continuous. The episodic neuropathic toothache is characterized by a spontaneous, severe, sudden, sharp, lancinating, electrical shock pain that is felt in the tooth or radiates to a tooth. Furthermore, the pain episode lasts only seconds at a time, although paroxysms may occur in rapid succession (8). It is consistent with
181 trigeminal neuralgia, which occurs between the fifth and eight decade of life and causes distress for the patient (7). The pain involves one or more of the trigeminal nerve division and primarily involves either the maxillary or the mandibular division. The most prominent feature of episodic neuropathic toothache is the existence of trigger 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 that these symptoms are being triggered by pulpal pathosis (instead of trigeminal neuralgia) must be ruled out (5). The cause of trigeminal neuralgia is unknown; empiric evidence suggests that the symptoms evolve as a consequence of vascular compression of the Gasserion ganglion (where the cell bodies of the trigeminal nerve are located). The precise neurophysiologic mechanism has not been uncovered, and other theories for this particular disorder include viral infection of either neurons or the Schwann cell sheath (5) Treatment modalities are varied and include medical intervention with specific drugs that alleviate the neuralgic pain and various surgical interventions. For the dentist the most salient advice is to establish a diagnosis and avoid any invasive dental procedures. Invariably patients with trigeminal neuralgia have undergone numerous endodontic procedures and extractions, but they continue to experience pain because pulpal and periodontal infectious processes have no role in this syndrome. Therefore despite the patients insistence that the symptoms are tooth related, the diagnosis should be established and the patient should be referred to 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 eventually produce agranolocytosis. The side effect is dose dependant, and therefore will many patients be maintained on tegretol without untoward side-effects. Continuous neuropathic toothache produces a persistent, ongoing unremitting pain. These pains may be exacerbated by local provocation, such as percussion of the tooth. Neuritic pain (i.e., neuritis), deafferentation pains, or sympathetically maintained pains are conditions that can produce continuous toothaches. Neuritic pains that arise in the maxillary and mandibular divisions of the trigeminal nerve can cause dental pains. Neuritic pains result from a spread of inflammation from surrounding structures to neural structures. The pain is often continuous aching, and burning in nature. Occasionally neuropathic pain may arise after dental treatment, such as pulp extirpation, apicectomy or extraction. These conditions may appear as a phantom toothache, described by the term atypical odontalgia, and is referred to as toothache with no obvious organic cause (13). It is characterized by prolonged periods of throbbing or burning pain in the teeth or alveolar process that occurs in the absence of any identifiable odontogenic cause. Usually the pain has been present for several months or longer and repeated attempts at dental therapy have failed to resolve the pain. Although the pathophysiology of atypical odontalgia is not fully understood, it appears that the clinical characteristics best place it in the category of deafferentation pains. Sympathetic activity may also contribute to the maintenance of the pain (5). Causalgia pain can involve the jaws, head and neck (8). When present, it may be confused with odontogenic pain. Causalgic pain is often associated with trauma, jaw fracture, or laceration and it may evolve after surgery. It has been hypothesized that in Causalgia, nociceptor fibers become retracted in association with autonomic fibers (8). The skin overlying the painful area often becomes erymatous during pain episodes and the patients have a tendency to rub and scratch
182 the involved area. The pain is characteristically paryxmal and burning, and it may be both superficial and deep. When the predominant complaint is a deep component, it may be confused with toothache. To arrive at a definitive diagnosis of Causalgia, historical trauma events and clinical features must be identified. Postherpethic neuralgia manifests similar features and should be considered in the differential diagnosis. Whether atypical facial pain are poorly localized or are centred in teeth, treatment should be approached cautiously. Many dentists have undertaken invasive procedures at the insistence of the patient, who firmly believes there is an odontogenic source. When the symptoms are mild, the pain should be managed with analgesics and reassurance (8). Many patients with atypical facial pain respond favourably to tricyclic antidepressants, particularly amitriptyline. This medication affects neurotransmitter substances and appears to have an analgesic property in addition to its antidepressant effects (8).
183 Reference list:
1. Barker FG II et al. The long-term outcome of microvascular decompression for trigeminal neuropathy. N Eng J Med 1996; 334: 1077
2. Buck S et al. Pulpal exposure alters neuropeptide levels in inflamed dental pulp and trigeminal ganglia: evaluation of axonal transport. J Endod 1999; 16: 718
3. Buck S, Reese K, Hargreaves KM. Pulpal exposure alters neuropeptide levels in inflamed dental pulp: evaluation of axonal transport. J Endod 1999; 25: 718
4. Byers M et al. Effects of injury and inflammation on pulpal and periapical nerves. J Endod 1990; 16: 78
5. Cohen AS, Brown DC. Orofacial pain emergencies: endodontic diagnosis and management. In: Cohen, ST, Burns R, editors. Pathways of the pulp, 8th edn. St.Louis: CV Mosby Co; 2002: p.31-76
6. Dalassio DJ. Management of the cranial neuralgias and atypical facial pain. A review. Clin J Pain 1989; 5: 55
7. Drinnan AL. Differential diagnosis of orofacial pain. Dent Clin North Am 1987; 31: 627
8. Eversole LR, Chase PF. Nonodontogenic orofacial pain and endodontics: pain disorders involving the jaws that simulate odontalgia. In: Cohen, ST, Burns R, editors. Pathways of the pulp, 8th edn. St.Louis: CV Mosby Co; 2002: p. 77-91
9. 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. 665-682
10. Kimberly C, Byers M. Inflammation of rat molar pulp and periodontium causes increased calcitonin gene related peptide and axonal sprouting. Anat Rec 1988; 222: 289
11. Main JH, Jordan RC, Barewal R. Facial neuralgias: a clinical review of 134 cases. J Can Dent Assoc 1992; 58: 752
12. Mc Laughlin MR et al. Microvascular decompression of cranial nerves: lessons learned after 4400 operations. J Neurosurg 1999; 90: 1
13. Rees RS, Harris M. Atypical odontalgia. Br J Oral Maxillofac Surg 1979; 16: 212
14. Taarhj P. Decompression of the posterior trigeminal root in trigeminal neuralgia: a 30- year follow-up review. J Neurosurg 1982; 57: 14
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