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Histological evaluation of contaminated furcal perforation in dogs’ teeth repaired by MTA with or without internal matrix
Histological evaluation of contaminated furcal perforation in dogs’ teeth repaired by MTA with or without internal matrix Abdullah Al-Daafas, BDS, MSc,a and Saad Al-Nazhan, BDS, MSD,b Riyadh, Saudi Arabia KING FAHAD SECURITY FORCE COLLEGE AND KING SAUD UNIVERSITY
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:e92-e99)
Perforation is a communication between the root canal system and the surrounding tissues through the floor of the pulp chamber or root canal wall of the tooth.1,2 It can occur as a result of a large carious lesion in or adjacent to the floor of the pulp chamber, internal or external root resorption, and during endodontic treatment or after space preparation. The long-term prognosis of a perforated tooth is dependent upon the location of the perforation, how long the perforation is exposed to oral contamination, and the ability to seal the perforation.1 Experimental studies of periodontal tissue reaction after perforations in monkeys’ and in dogs’ teeth, together with some clinical investigation of perforations in human teeth, suggest that perforation in the cervical third of the root or in the floor of the pulp chamber have the least favorable prognosis after treatment.3,4 These types of perforation usually increase the possibility of epithelial proliferation and periodontitis.1,5 Nonsurgical immediate repair using proper filling material may prevent the resulting communication between perforation site and gingival sulcus and thus favorable prognosis could be achieved.6 Amalgam has been the standard material for repairing furcal perforation for many years.7,8 Recently, mineral trioxide aggregate (MTA) material was found to be superior to most of the dental materials that have been tried to repair furcal perforation.9,10 Repair of the perforated defect is usually complicated by the fact that the size of the defect may allow extrusion of the material into the periodontal ligament space and surrounding structures. This may preclude success regardless of the material used. The concept of The study was supported by the Research Center of the Dental College, King Saud University, Riyadh, Saudi Arabia. a Endodontist, King Fahad Security Force College, Dental Clinics. b Associate Professor, King Saud University, College of Dentistry, Division of Endodontics. Received for publication Mar 29, 2006; returned for revision Sep 6, 2006; accepted for publication Sep 7, 2006. 1079-2104/$ - see front matter © 2007 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2006.09.007
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using internal biocompatible matrices such as calcium sulfate, hydroxyapatite, or HAPSET (Lifecore Biomedical, Chaska, MN, USA) was suggested in an attempt to control the extrusion of the filling materials as well as increase the sealing ability of the repaired materials.6,11-13 Calcium sulfate has also been used as a bone substitute for filling defects. According to Bahn,14 it acts as a space filler, and the most important advantage of its use is its natural rate of resorption, which compared closely with the rate of new bone growing into a defect. Therefore, its use as an internal matrix under repaired material of defected contaminated perforation might enhance the healing of the damaged tissue. Although one published study9 that deals with repairing contaminated furcation perforation using MTA alone has been investigated histologically, no such study has been performed for the use of internal matrices as a promoter of bone healing with MTA. Therefore, the purpose of this study was to investigate the histologic healing response of experimentally induced furcal perforations in dogs’ teeth contaminated with saliva and repaired with MTA with or without internal matrices (calcium sulfate). Results were compared to amalgam. MATERIALS AND METHODS Filling materials Two materials, the grey type of MTA (Pro Root MTA, Dentsply Tulsa Dental, Tulsa, OK, USA; #990903) and amalgam (Dispersalloy regular set two spill, Dentsply Caulk International, Inc, Milford, DE, USA; #656-2892) were used as filling materials to repair the perforation of this study. Calcium sulfate (CAPSET, Lifecore Biomedical, Inc, Chaska, MN, # 75030272) was selected as an internal matrix. Experimental animals A total of 72 teeth from 9 healthy adult beagle strain dogs, weighing 11 to 17 kg and approximately more than 1 year old were used. All used teeth were intact, free from caries or periodontal disease, and had complete root development. Both sides of the mandibular
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third and fourth premolars, and maxillary second and third premolars were used. The teeth were randomly divided into 4 experimental groups of 15 teeth each, and 2 control groups with 6 teeth each.
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Experimental procedure The experimental procedure was conducted in accordance with the protocol outlined by the Research Center of the Dental College, King Saud University animal ethics committee. The experimental procedure was carried out at the animal house of King Khalid University Hospital of King Saud University. Each dog was anesthetized with an intramuscular injection of Ketamine (8-10 mg/kg) and Atropine (0.02-0.04 mg/kg), followed by an intravenous injection of Xylazine (2.2 mg/kg), and intubated with a cuffed endotracheal tube before beginning the experimental procedure. A preoperative radiograph was taken for each tooth. The teeth were then isolated with rubber dam. The tooth surfaces and surrounding field were cleaned using a cotton pellet socked with 30% hydrogen peroxide for 1 minute, then tooth surfaces were disinfected with 5% iodine tincture for 1 minute. All medicaments used in this study were freshly prepared at the College of Pharmacy of King Saud University, Riyadh, Saudi Arabia. An access opening was made using a No. 4 sterile carbide round bur and water spray. The pulp tissue was removed and the root canals were instrumented to the apical delta using step-back technique, cleaned with 1% sodium hypochlorite, and filled with laterally condensed gutta-percha and AH26 sealer cement. The excess filling material was removed from the pulp chamber floor with a hot endodontic excavator. A 1.4-mm-diameter perforation was created in the center of the pulp chamber floor of the experimental and positive control teeth using a sterile No. 4 round bur at low speed. The perforation depth was limited to 2 mm into the alveolar bone. This was guided by use of a rubber stopper as a marker on the shank of the bur. Hemorrhage was controlled by rinsing the area with saline solution and use of cotton pellets. Radiographs were taken, and the access cavity of all the experimental teeth was left open to saliva contamination for 4 weeks for bacterial contamination and the formation of inflammatory lesions in the furcation area. The presence of a lesion was confirmed radiographically. The animals were then anesthetized and the perforations were curetted under aseptic technique by using a small spoon excavator to remove the debris and inflamed tissue, cleaned with 2.5% sodium hypochlorite, and dried with paper points. The experimental teeth were treated as follows:
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Group 1: Negative control. No perforation was created in the pulp chamber after finishing the root canal filling. The access cavity was left open without coronal filling. Group 2: Positive control. The furcal perforation and access cavity were left open without coronal filling. Group 3: MTA. MTA was mixed according to the manufacturer’s instructions then carried into the cavity by a small amalgam carrier and condensed with Schilder plugger No.11 using light pressure. The coronal access cavity was filled with MTA. Group 4: MTA with calcium sulfate as artificial floor. Medical-grade calcium sulfate powder was mixed with an accelerating diluent solution on a sterile glass pad using a sterile spatula. The material was placed in the defect cavity with a Messing gun and condensed gently with Schilder plugger No.11 until the entire defect was filled. After 5 minutes, the dentin wall of the perforated cavity was refreshed with a small spoon excavator then the cavity was rinsed with saline to remove debris of the calcium sulfate. The perforation site and the access cavity were filled with MTA as in group 3. Group 5: Amalgam. Amalgam was mixed and carried to the perforation site with small amalgam carrier and condensed with a small amalgam plugger. The coronal access cavity was filled with amalgam. Group 6: Amalgam with calcium sulfate. Calcium sulfate mixed and placed in the defected cavity as in group 4. The perforated site and the access cavity were filled with amalgam as in group 5.
Subsequent to the repair of all perforation sites, radiographs of all teeth in the study were exposed. Histological preparation The animals were killed by use of an overdose of sodium pentobarbital after 4 months. Each animal was perfused with 10% buffered formalin then each experimental tooth with the surrounding alveolar bone was cut in a block section using a hand saw and placed in 10% buffered formalin for 24 hours. The specimens were decalcified separately in 10% hydrochloric acid, 1% EDTA, and 1% sodium acetate, which were changed daily. The end point of decalcification was determined radiographically. Each block was trimmed 1 mm away from the edge of perforation in the buccolingual direction in dogs numbered 1 to 5, and in mesiodistal direction in dogs numbered 6 to 9. The amalgam filling in group numbers 4 and 5 was removed from each tooth. The specimens were washed in running water for 24 hours. Then a code number was given for each specimen. The specimens were processed by using an open processing system (Shandon, Duplex processor, Cheshire, UK), in which the specimens were
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Fig. 1. Photomicrograph of mesiodistal section of Group 2 (positive control). A, Epithelial proliferation with severe inflammatory response (Masson’s trichrome, ⫻40). B, Magnification of A showing osteoclast cells (Howships) within lacunae (black arrow) (⫻200). C, Magnification of same area of bone resorption. Note multinucleated osteoclasts (white arrows) (⫻400).
dehydrated in a series of ethyl alcohol 70%, 95%, and absolute alcohol in 18 hours. The specimens were embedded in paraffin wax (Winlab, Freezing point 51-53 C, Leicestershire, UK). Step-serial sections of each block were cut using a microtome (Leica, RM2145, Nussloch, Germany) at a setting of 5-m thickness through the area of the furcal perforation. Slides were stained with hematoxylin and eosin and Masson’s trichrome. They were then examined under light microscopy (Leitz, Laborlux S, Binocular microscope, Wetzlar, Germany) by 2 examiners. Photographs of selected areas were taken using a digital camera (Olympus, BX41TF, Tokyo, Japan). The histological sections were assessed for inflammation and type of healing at the furcation area adjacent to the repaired materials. They were scored according to criteria used by Salman et al.15 The severity of inflammation was classified as none where there was no infiltration of inflammatory cells present, mild where a few scattered inflammatory cells were present, moderate where inflammatory cells did not obscure the normal tissues, and severe when
massive infiltration of inflammatory cells replaced normal tissue. The presence or absence of root dentin or bone resorption, bone or cementum deposition, and epithelium at the furcation site was noted. Scores (most frequent) were obtained, tabulated, and statistically analyzed. The Kruskal-Wallis test was used to analyze data of inflammation, bone deposition, and bone resorption. RESULTS The coronal fillings of all the experimental teeth were intact at the end of the experimental period except for 1 tooth with MTA in group 3. This tooth had fractured in the buccolingual direction. One specimen from groups 1, 2, 4, and 6, and 2 specimens from group 3 were excluded from the study because of technical problems during the histological preparation. Histological examination of the negative control group revealed normal alveolar bone with evidence of osseous remodeling and no inflammatory change. Inflammatory infiltrate with severely chronic inflamma-
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tum deposition over the MTA (Fig. 2, Table I). The newly formed cementum was cellular and sometimes formed as an irregular layer. Deposition of cementum was noted in resorbed cavities along the side of the root and new bone had been formed adjacent to the collagen fiber capsule in 12 specimens. The use of calcium sulfate under the MTA caused mild to moderate chronic inflammatory infiltration in 10 specimens (Table I). No extruded material or ankylosis was observed. The fibrous layer that separates the zone of inflammation and interradicular bone was seen. Eleven specimens demonstrated the presence of stratified squamous epithelium in the furcation area. Eight specimens of 14 had cementum deposition over the MTA and in earlier resorbed cavities along the side of the root (Fig. 3). Evidence of osteoblast activity was seen in 11 specimens, in which 5 cases exhibited new bone formation.
Fig. 2. Photomicrograph of group 3 (MTA), buccolingual section. A, A layer of new irregular cementum bridge (arrows) over the excess material (MTA) (hematoxylin and eosin, ⫻40). B, Magnification of box marked in A shows narrow periodontal ligament space (arrows) between cementum and bone, and free from inflammatory cell (⫻100).
tory cells was observed under proliferating epithelium that extended into surrounding bone in the positive control group. Abscess formation and collagen fiber capsule surrounding the area of inflammation were observed in most of the specimens and root resorption was present. There was no deposition of cementum or bone and the osteoclast activity was remarkable in interradicular bony septum bordering the perforation site (Fig. 1). MTA repair When MTA was used alone, most of the specimens were free of inflammatory cells infiltrated with cemen-
Amalgam Using amalgam alone to close the perforated site caused mild to moderate chronic inflammatory reaction. The zone of inflammation was surrounded by striations of collagen fibers. Granulomatous lesions covered with stratified squamous epithelium were present in the bifurcation area of 7 specimens of 13 (Fig. 4). The epithelium did not seem to proliferate apically and in some cases it was seen as a lining immediately adjacent to the perforation site. Cementum deposition was not seen in any of the amalgam specimens. The evidence of osteoblast activity was seen in 9 specimens in which 6 specimens exhibited new bone formation. The extruded material was observed in most of the specimens. The use of calcium sulfate under amalgam caused a mild to moderate chronic inflammatory reaction in most of the specimens. The zone of inflammation was surrounded by a fibrous layer. Epithelial proliferation was present in the bifurcation area of 13 specimens of 14 (Fig. 5). No extruded material or ankylosis was observed. No specimen showed deposition of cementum over the amalgam. Bone formation was evident in 6 specimens, and in 3 specimens an evidence of osteoblast activity bordering the bony trabeculae was seen. Osteoclastic activity was seen in 7 specimens where it was marked in 1 specimen. Statistical analysis MTA alone had the lowest score of inflammation (Table II). This was followed by amalgam, MTA with calcium sulfate, and amalgam with calcium sulfate. A significant difference was found among the experimental groups (P⫽ .023). The migration of epithelium in the defect areas repaired by MTA with calcium sulfate and amalgam with calcium sulfate appeared more common when compared with MTA or amalgam alone.
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Table I. The histological findings of all the groups Group Group Group Group Group Group Group
1: 2: 3: 4: 5: 6:
Negative control Positive control MTA MTA with calcium sulfate Amalgam Amalgam with calcium sulfate
No.
Inflammation
Epithelium
Cementum
Bone apposition
Bone resorption
5 6 14 14 13 14
0 6 8 11 10 13
0 6 5 11 7 13
5 0 10 8 0 0
1 1 12 11 9 9
1 5 2 7 6 7
Fig. 3. Photomicrograph of group 4 (MTA with calcium sulfate). Mesiodistal section, shows apposition of cementum (black arrow) and deposition of cementum in resorbed cavity (white arrow). There are no inflammatory cells in the periodontal tissue (PDL) (hematoxylin and eosin, ⫻40).
However, this difference was not statistically significant (P⫽ .093). When the 4 experimental groups were compared to positive control, the MTA and amalgam group showed a statistically significant difference. No statistically significant difference was noted for cementum formation over MTA and MTA with calcium sulfate (P⫽ .430). MTA showed the highest score of bone deposition, followed by amalgam, amalgam with calcium sulfate, and MTA with calcium sulfate. It was a significant difference between the groups (P⫽ .045). Furthermore, MTA showed the lowest score of bone resorption. No significant difference was found between the groups (P⫽ .067). DISCUSSION The success rate when using only MTA, without calcium sulfate, was excellent. This result is in agreement with earlier reports.9 However, our findings for amalgam were better than earlier reports.9 In general our rate of repairs were better than reported by Seltzer et al.3 who found, in a histological study using mon-
Fig. 4. Photomicrograph of group 5 (amalgam), buccolingual section. A, Epithelium proliferation from palatal side (arrows), absence of cementum around repaired material, and moderate inflammation (hematoxylin and eosin, ⫻40). B, Magnification of A shows a layer of proliferated epithelium (arrows), and chronic inflammatory cells, mostly lymphocytes and plasma cells (⫻100).
keys’ teeth, that perforated areas had a poor chance for healing after 6 to 10 months of observation. We attribute the difference to time interval of exposing the defected area to saliva, methodology and materials used, and the animal model.
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Fig. 5. Photomicrograph of group 6 (amalgam with calcium sulfate) buccolingual section shows epithelial proliferation (arrows) and fibrous layer (Fl) that surrounded the zone of mild inflammation (Masson’s trichrome, ⫻40).
Dogs were selected for this study because their teeth have suitable furcation that provides good accessibility and visibility. Their teeth are large enough to facilitate the study of tissue reaction and allow ample room for perforation without hemisection of the tooth.16 However, the morphologic character of the dog’s tooth is different from that of a human tooth. The posterior teeth of the dog lack a root trunk and the furcation is often as close as 1 to 2 mm from the cementoenamel junction.15 As a result, epithelialization of a furcation perforation of dogs’ teeth is perhaps more likely than in the human, where the furcation lies more deeply within the alveolus. Thus, any technique shown to produce favorable results in dogs may understate the response in human. On the other hand, the proximity of the cementoenamel junction to the furcation may explain the high rate of epithelization seen in the experimental groups in the present study. This might be a limitation for using the dog model when studying perforation repair. The size of perforations in this investigation was standardized at 1.4 mm, which is similar to several previous studies.7-9,13,17,18 The bur was allowed to penetrate 2 mm into the alveolar bone to enhance the inflammatory response.13 The other factor that enhances the formation of the interradicular lesion was to leave the perforation site open for saliva contamination for 4 weeks.2,13 A good prognosis, however, can be achieved when the perforation is repaired immediately.9,19 Clinically, a time delay may increase the difficulty of repairing the defect because of the resorption of bone in the area of the defect.2,3,17 Sterilization of the perforation defect before applying the filling material was recommended by Kvinnsland et al.20 In this study the perforation site was curetted and
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washed with 2.5% sodium hypochlorite before repairing under aseptic conditions. Pitt Ford et al.9 attributed the good response in some specimens in which repair of delayed furcal perforations was effective with the use of 2.5% sodium hypochlorite. In this study all perforation defects of the experimental groups and the entire access cavities were filled with the same material to achieve good sealing. Many previous studies had used amalgam and MTA to seal the access cavity after repairing the perforated site with either the same or different material.7-9,21 Weldon et al.10 showed that filling the furcation perforation and the entire access cavity with same material produced less leakage and therefore prognosis might be improved. The histological sections in this investigation were prepared in 2 directions as suggested in several earlier studies.3,7,8,9,13,18,22 Half of the specimens were prepared in the buccolingual direction to better observe sinus tracts through the gingival sulcus, inflammation, and epithelium migration. The other half were prepared in the mesiodistal direction to better evaluate the depth of the gingival pocket, type of attachment, and extent of inflammation in relation to the root surface. Inflammation caused by infection was seen in the positive control group as a breakdown of the interradicular bone and the migration of epithelium.3,7,8 We found the lowest incidence of epithelium migration when using MTA. It is believed that this may be because of good biocompatibility and sealing ability of the material. Deposition of hard tissue over MTA with or without calcium sulfate was observed in the majority of specimens. In addition, new cementum was fused to the original cementum on the root surface. This supports earlier reports of repair when using MTA9,21,23-26 and this may due to a number of factors such as sealing ability, biocompatibility, and alkaline pH on setting. Koh et al.27 stated that it is possible that MTA offers a biologically active substrate for bone cell proliferation and stimulates interleukin production. The causes for cementum deposition over the filling material have been extensively discussed in the literature. Holland28 reported that calcium hydroxide in contact with pulp tissue or culture medium produces deposition of calcite crystals that originated from a reaction of the calcium from calcium hydroxide with carbon dioxide from the pulp tissue. Seux et al.29 also observed a rich extracellular network of fibronectin in close contact with these crystals, and concluded that their findings strongly support the role of calcite crystals and fibronectin as an initiating step in the formation of a hard tissue barrier. The same crystals that were observed with calcium hydroxide were reported with MTA by Holland et al.30 According to Torabinejad et
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Table II. Severity of inflammation for the groups. Group Group Group Group Group Group Group
1: 2: 3: 4: 5: 6:
Negative control Positive control MTA MTA with calcium sulfate Amalgam Amalgam with calcium sulfate
No.
None (%)
Mild (%)
Moderate (%)
Severe (%)
5 6 14 14 13 14
5 (100) 0 (0.0) 6 (42.8) 3 (21.4) 3 (23.0) 1 (7.1)
0 (0.0) 0 (0.0) 4 (28.5) 2 (14.2) 4 (30.7) 4 (28.5)
0 (0.0) 1 (16.6) 3 (21.4) 7 (50) 4 (30.4) 6 (42.8)
0 (0.0) 5 (83.3) 1 (7.1) 2 (14.2) 2 (15.3) 3 (21.4)
al.,31 MTA has 2 specific phases composed of calcium oxide and calcium phosphate after reaction with water. Thus, MTA has calcium oxide on its surface that could react with tissue fluids to form calcium hydroxide. For this reason it is believed that MTA actively promotes hard tissue formation rather than being inert or an irritant like most other materials. New cementum may be derived from either the remaining periodontal ligament or it is derived from the ingrowing connective tissue.26 Cementum deposition was not observed when using amalgam for repair. In the current investigation, ankylosis was seen in 2 specimens associated with MTA without calcium sulfate. This finding is consistent with those reported by Holland et al.24 In addition, Beavers et al.19 observed ankylosis after 7 days from repairing the furcal perforation with calcium hydroxide. Ankylosis is an infrequent complication in the healing of furcal perforation because of the low thermal trauma generated while perforating.2,9,15,22 Although slow speed was used for the perforations in this study, increased temperature may have been generated when inserting the bur into the alveolar bone. This may also have caused resorption and deposition of new bone and cementum. Deposition of bone was found more often than resorption especially with MTA without calcium sulfate. No extrusion of the filling material was noted in the groups that used calcium sulfate compared to those without calcium sulfate. Amalgam extruded into the interradicular area resulted in inflammation, which has been observed in earlier studies.9,13 We used an internal matrix under amalgam repairs as it was reported as advantageous.13 Similar findings were not observed in the present study. This may be attributed to the delayed treatment of the perforated site, which was used here. When the MTA was accidentally extruded into the interradicular area, deposition of hard tissue over the material with the presence of a healthy periodontium was observed. The extrusion of repair materials should be expected in cases of delayed repair of the perforation compared to immediate repair. During immediate repair of modest perforations the periodontal ligament and surrounding hard tissue will act as a barrier.
CONCLUSION Furcation perforation has poor prognosis if the perforation site is not immediately repaired. The healing after delayed repair of furcal perforation shows no statistical significant difference among the 4 test groups. However, placement of MTA alone shows better healing response compared to other groups. The use of calcium sulfate as internal matrix under MTA or amalgam did prevent extrusion of the repaired material into the contaminated perforated area but it caused unfavorable inflammatory reaction. Moreover, uses of calcium sulfate did not aid bone regeneration or prevent epithelium migration into the defected perforation area. Therefore, using calcium sulfate as an internal matrix for MTA is not recommended. REFERENCES 1. Sinai I. Endodontic perforations: their prognosis and treatment. J Am Dent Assoc 1977;95:90-5. 2. Jew R, Weine F, Keen J. A histologic evaluation of periodontal tissues adjacent to root perforations filled with Cavit. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1982;54:124-35. 3. Seltzer S, Sinai I, August D. Periodontal effects of root perforations before and during endodontic procedures. J Dent Res 1970;49:332-9. 4. Meister F, Lommel T, Gerstein H, Davies E. Endodontic perforations which resulted in alveolar bone loss. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1979;47:463-70. 5. Lantz B, Persson P. Periodontal tissue reactions after surgical treatment of root perforations in dog’s teeth: a histologic study. Odont Revy 1970;21:51-62. 6. Lemon R. Nonsurgical repair of perforation defects. Dent Clin North Am 1992;36:349-457. 7. El Deeb ME, El Deeb M, Tabibi A, Jensen J. An evaluation of the use of amalgam, Cavit and calcium hydroxide in the repair of furcation perforation. J Endod 1982;8:459-66. 8. Balla R, LoMonaco C, Skribner J, Lim L. Histological study of furcation perforation treated with tricalcium phosphate, hydroxyapatite, amalgam, and life. J Endod 1991;19:591-5. 9. Pitt Ford T, Torabinejad M, Hong C, Kariyawasam S. Use of mineral trioxide aggregate for repair of furcal perforations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:756-63. 10. Weldon J, Pashley D, Loushine R, Weller R, Kimbrough W. Sealing ability of mineral trioxide aggregate and Super-EBA when used as furcation repair materials, a longitudinal study. J Endod 2002;28:467-70. 11. Alhadainy H, Himel V. An in vitro evaluation of plaster of Paris
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barriers used under amalgam and glass ionomer to repair furcation perforations. J Endod 1994;20:449-52. Jantarat J, Dashper S, Messer H. Effect of matrix placement on furcation perforation repair. J Endod 1999;25:192-6. Rafter M, Baker M, Alves M, Daniel J, Remeikis N. Evaluation of healing with use of an internal matrix to repair furcation perforations. Int Endod J 2002;35:775-83. Bahn S. Plaster: a bone substitute. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1966;21:672-8. Salman M, Quinn F, Dermody J, Hussey D, Claffey N. Histological evaluation of repair using a bioresorbable membrane beneath a resin-modified glass ionomer after mechanical furcation perforation in dogs’ teeth. J Endod 1999;25:181-6. Alhadainy H. Animal model for the study of perforation of pulp chamber floor. Int Endod J 1996;29:195. Himel V, Brady J, Weir J. Evaluation of repair of mechanical perforations of the pulp chamber floor using biodegradable tricalcium phosphate or calcium hydroxide [abstr]. J Endod 1985;11:161-5. Aguirre R, Deeb M, El Deeb M. Evaluation of the repair of mechanical furcation perforations using amalgam, gutta-percha or indium foil. J Endod 1986;12:249-56. Beavers R, Bergenholtz G, Cox C. Periodontal wound healing following intentional root perforations in permanent teeth of Macaca mulatta. Int Endod J 1986;19:36-44. Kvinnsland I, Oswald R, Halse A, Gronnings A. A clinical and roentgenological study of 55 cases of root perforation. Int Endod J 1989;22:75-84. Yildirim T, Gençog˘lu N, Firat I, Perk C, Guzel O. Histologic study of furcation perforations treated with MTA or Super EBA in dogs’ teeth. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:120-4. Alhadainy H, Himel V, Lee B, Elbaghdady Y. Use of a hydroxyapatite-based material and calcium sulfate as artificial floors to repair furcal perforations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:723-9. Holland R, Souza V, Nery M, Filho J, Bernabe P, Dezan E.
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Reaction of dogs’ teeth to root canal filling with mineral trioxide aggregate or a glass ionomer sealer. J Endod 1999;25:728-30. Holland R, Filho J, Souza V, Nery M, Bernabe P, Junior E. Mineral trioxide aggregate repair of lateral root perforations. J Endod 2001;27:281-4. Apaydin E, Shahrokh S, Torabinejad M. Hard tissue healing after application of fresh or set MTA as root end filling material. J Endod 2004;30:21-4. Torabinejad M, Pitt Ford T, McKendry D, Abedi H, Miller D, Kariyawasam S. Histological assessment of mineral trioxide aggregate as a root end filling in monkeys. J Endod 1997;23:225-8. Koh E, McDonald F, Pitt Ford R, Torabinejad M. Cellular response to mineral trioxide aggregate. J Endod 1998;24:543-7. Holland R. Histochemical response of amputed pulps to calcium hydroxide. Rev Bras Pesq Med Biology 1971;4:83-95. Seux D, Couble M, Hartman D, Gauthier J, Magloire H. Odontoblast like cytodifferentiation of human dental pulp cells in vitro in the presence of a calcium hydroxide containing cement. Arch Oral Biol 1991;36:117-28. Holland R, Souza V, Nery M, Filho J, Bernabe P, Dezan E. Reaction of rat connective tissue to implanted dentin tubes filled with mineral trioxide aggregate or calcium hydroxide. J Endod 1999;25:161-6. Torabinejad M, Hong C, McDonald F, Pitt Ford T. Physical and chemical properties of a new root-end filling material. J Endod 1995;21:349-53.
Reprint requests: Saad Al-Nazhan, BDS, MSD Associate Professor King Saud University, College of Dentistry Division of Endodontics PO Box 60169 Riyadh 11545 Saudi Arabia [email protected]; [email protected]
(Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:e92-e99)
Perforation is a communication between the root canal system and the surrounding tissues through the floor of the pulp chamber or root canal wall of the tooth.1,2 It can occur as a result of a large carious lesion in or adjacent to the floor of the pulp chamber, internal or external root resorption, and during endodontic treatment or after space preparation. The long-term prognosis of a perforated tooth is dependent upon the location of the perforation, how long the perforation is exposed to oral contamination, and the ability to seal the perforation.1 Experimental studies of periodontal tissue reaction after perforations in monkeys’ and in dogs’ teeth, together with some clinical investigation of perforations in human teeth, suggest that perforation in the cervical third of the root or in the floor of the pulp chamber have the least favorable prognosis after treatment.3,4 These types of perforation usually increase the possibility of epithelial proliferation and periodontitis.1,5 Nonsurgical immediate repair using proper filling material may prevent the resulting communication between perforation site and gingival sulcus and thus favorable prognosis could be achieved.6 Amalgam has been the standard material for repairing furcal perforation for many years.7,8 Recently, mineral trioxide aggregate (MTA) material was found to be superior to most of the dental materials that have been tried to repair furcal perforation.9,10 Repair of the perforated defect is usually complicated by the fact that the size of the defect may allow extrusion of the material into the periodontal ligament space and surrounding structures. This may preclude success regardless of the material used. The concept of The study was supported by the Research Center of the Dental College, King Saud University, Riyadh, Saudi Arabia. a Endodontist, King Fahad Security Force College, Dental Clinics. b Associate Professor, King Saud University, College of Dentistry, Division of Endodontics. Received for publication Mar 29, 2006; returned for revision Sep 6, 2006; accepted for publication Sep 7, 2006. 1079-2104/$ - see front matter © 2007 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2006.09.007
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using internal biocompatible matrices such as calcium sulfate, hydroxyapatite, or HAPSET (Lifecore Biomedical, Chaska, MN, USA) was suggested in an attempt to control the extrusion of the filling materials as well as increase the sealing ability of the repaired materials.6,11-13 Calcium sulfate has also been used as a bone substitute for filling defects. According to Bahn,14 it acts as a space filler, and the most important advantage of its use is its natural rate of resorption, which compared closely with the rate of new bone growing into a defect. Therefore, its use as an internal matrix under repaired material of defected contaminated perforation might enhance the healing of the damaged tissue. Although one published study9 that deals with repairing contaminated furcation perforation using MTA alone has been investigated histologically, no such study has been performed for the use of internal matrices as a promoter of bone healing with MTA. Therefore, the purpose of this study was to investigate the histologic healing response of experimentally induced furcal perforations in dogs’ teeth contaminated with saliva and repaired with MTA with or without internal matrices (calcium sulfate). Results were compared to amalgam. MATERIALS AND METHODS Filling materials Two materials, the grey type of MTA (Pro Root MTA, Dentsply Tulsa Dental, Tulsa, OK, USA; #990903) and amalgam (Dispersalloy regular set two spill, Dentsply Caulk International, Inc, Milford, DE, USA; #656-2892) were used as filling materials to repair the perforation of this study. Calcium sulfate (CAPSET, Lifecore Biomedical, Inc, Chaska, MN, # 75030272) was selected as an internal matrix. Experimental animals A total of 72 teeth from 9 healthy adult beagle strain dogs, weighing 11 to 17 kg and approximately more than 1 year old were used. All used teeth were intact, free from caries or periodontal disease, and had complete root development. Both sides of the mandibular
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third and fourth premolars, and maxillary second and third premolars were used. The teeth were randomly divided into 4 experimental groups of 15 teeth each, and 2 control groups with 6 teeth each.
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Experimental procedure The experimental procedure was conducted in accordance with the protocol outlined by the Research Center of the Dental College, King Saud University animal ethics committee. The experimental procedure was carried out at the animal house of King Khalid University Hospital of King Saud University. Each dog was anesthetized with an intramuscular injection of Ketamine (8-10 mg/kg) and Atropine (0.02-0.04 mg/kg), followed by an intravenous injection of Xylazine (2.2 mg/kg), and intubated with a cuffed endotracheal tube before beginning the experimental procedure. A preoperative radiograph was taken for each tooth. The teeth were then isolated with rubber dam. The tooth surfaces and surrounding field were cleaned using a cotton pellet socked with 30% hydrogen peroxide for 1 minute, then tooth surfaces were disinfected with 5% iodine tincture for 1 minute. All medicaments used in this study were freshly prepared at the College of Pharmacy of King Saud University, Riyadh, Saudi Arabia. An access opening was made using a No. 4 sterile carbide round bur and water spray. The pulp tissue was removed and the root canals were instrumented to the apical delta using step-back technique, cleaned with 1% sodium hypochlorite, and filled with laterally condensed gutta-percha and AH26 sealer cement. The excess filling material was removed from the pulp chamber floor with a hot endodontic excavator. A 1.4-mm-diameter perforation was created in the center of the pulp chamber floor of the experimental and positive control teeth using a sterile No. 4 round bur at low speed. The perforation depth was limited to 2 mm into the alveolar bone. This was guided by use of a rubber stopper as a marker on the shank of the bur. Hemorrhage was controlled by rinsing the area with saline solution and use of cotton pellets. Radiographs were taken, and the access cavity of all the experimental teeth was left open to saliva contamination for 4 weeks for bacterial contamination and the formation of inflammatory lesions in the furcation area. The presence of a lesion was confirmed radiographically. The animals were then anesthetized and the perforations were curetted under aseptic technique by using a small spoon excavator to remove the debris and inflamed tissue, cleaned with 2.5% sodium hypochlorite, and dried with paper points. The experimental teeth were treated as follows:
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Group 1: Negative control. No perforation was created in the pulp chamber after finishing the root canal filling. The access cavity was left open without coronal filling. Group 2: Positive control. The furcal perforation and access cavity were left open without coronal filling. Group 3: MTA. MTA was mixed according to the manufacturer’s instructions then carried into the cavity by a small amalgam carrier and condensed with Schilder plugger No.11 using light pressure. The coronal access cavity was filled with MTA. Group 4: MTA with calcium sulfate as artificial floor. Medical-grade calcium sulfate powder was mixed with an accelerating diluent solution on a sterile glass pad using a sterile spatula. The material was placed in the defect cavity with a Messing gun and condensed gently with Schilder plugger No.11 until the entire defect was filled. After 5 minutes, the dentin wall of the perforated cavity was refreshed with a small spoon excavator then the cavity was rinsed with saline to remove debris of the calcium sulfate. The perforation site and the access cavity were filled with MTA as in group 3. Group 5: Amalgam. Amalgam was mixed and carried to the perforation site with small amalgam carrier and condensed with a small amalgam plugger. The coronal access cavity was filled with amalgam. Group 6: Amalgam with calcium sulfate. Calcium sulfate mixed and placed in the defected cavity as in group 4. The perforated site and the access cavity were filled with amalgam as in group 5.
Subsequent to the repair of all perforation sites, radiographs of all teeth in the study were exposed. Histological preparation The animals were killed by use of an overdose of sodium pentobarbital after 4 months. Each animal was perfused with 10% buffered formalin then each experimental tooth with the surrounding alveolar bone was cut in a block section using a hand saw and placed in 10% buffered formalin for 24 hours. The specimens were decalcified separately in 10% hydrochloric acid, 1% EDTA, and 1% sodium acetate, which were changed daily. The end point of decalcification was determined radiographically. Each block was trimmed 1 mm away from the edge of perforation in the buccolingual direction in dogs numbered 1 to 5, and in mesiodistal direction in dogs numbered 6 to 9. The amalgam filling in group numbers 4 and 5 was removed from each tooth. The specimens were washed in running water for 24 hours. Then a code number was given for each specimen. The specimens were processed by using an open processing system (Shandon, Duplex processor, Cheshire, UK), in which the specimens were
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Fig. 1. Photomicrograph of mesiodistal section of Group 2 (positive control). A, Epithelial proliferation with severe inflammatory response (Masson’s trichrome, ⫻40). B, Magnification of A showing osteoclast cells (Howships) within lacunae (black arrow) (⫻200). C, Magnification of same area of bone resorption. Note multinucleated osteoclasts (white arrows) (⫻400).
dehydrated in a series of ethyl alcohol 70%, 95%, and absolute alcohol in 18 hours. The specimens were embedded in paraffin wax (Winlab, Freezing point 51-53 C, Leicestershire, UK). Step-serial sections of each block were cut using a microtome (Leica, RM2145, Nussloch, Germany) at a setting of 5-m thickness through the area of the furcal perforation. Slides were stained with hematoxylin and eosin and Masson’s trichrome. They were then examined under light microscopy (Leitz, Laborlux S, Binocular microscope, Wetzlar, Germany) by 2 examiners. Photographs of selected areas were taken using a digital camera (Olympus, BX41TF, Tokyo, Japan). The histological sections were assessed for inflammation and type of healing at the furcation area adjacent to the repaired materials. They were scored according to criteria used by Salman et al.15 The severity of inflammation was classified as none where there was no infiltration of inflammatory cells present, mild where a few scattered inflammatory cells were present, moderate where inflammatory cells did not obscure the normal tissues, and severe when
massive infiltration of inflammatory cells replaced normal tissue. The presence or absence of root dentin or bone resorption, bone or cementum deposition, and epithelium at the furcation site was noted. Scores (most frequent) were obtained, tabulated, and statistically analyzed. The Kruskal-Wallis test was used to analyze data of inflammation, bone deposition, and bone resorption. RESULTS The coronal fillings of all the experimental teeth were intact at the end of the experimental period except for 1 tooth with MTA in group 3. This tooth had fractured in the buccolingual direction. One specimen from groups 1, 2, 4, and 6, and 2 specimens from group 3 were excluded from the study because of technical problems during the histological preparation. Histological examination of the negative control group revealed normal alveolar bone with evidence of osseous remodeling and no inflammatory change. Inflammatory infiltrate with severely chronic inflamma-
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tum deposition over the MTA (Fig. 2, Table I). The newly formed cementum was cellular and sometimes formed as an irregular layer. Deposition of cementum was noted in resorbed cavities along the side of the root and new bone had been formed adjacent to the collagen fiber capsule in 12 specimens. The use of calcium sulfate under the MTA caused mild to moderate chronic inflammatory infiltration in 10 specimens (Table I). No extruded material or ankylosis was observed. The fibrous layer that separates the zone of inflammation and interradicular bone was seen. Eleven specimens demonstrated the presence of stratified squamous epithelium in the furcation area. Eight specimens of 14 had cementum deposition over the MTA and in earlier resorbed cavities along the side of the root (Fig. 3). Evidence of osteoblast activity was seen in 11 specimens, in which 5 cases exhibited new bone formation.
Fig. 2. Photomicrograph of group 3 (MTA), buccolingual section. A, A layer of new irregular cementum bridge (arrows) over the excess material (MTA) (hematoxylin and eosin, ⫻40). B, Magnification of box marked in A shows narrow periodontal ligament space (arrows) between cementum and bone, and free from inflammatory cell (⫻100).
tory cells was observed under proliferating epithelium that extended into surrounding bone in the positive control group. Abscess formation and collagen fiber capsule surrounding the area of inflammation were observed in most of the specimens and root resorption was present. There was no deposition of cementum or bone and the osteoclast activity was remarkable in interradicular bony septum bordering the perforation site (Fig. 1). MTA repair When MTA was used alone, most of the specimens were free of inflammatory cells infiltrated with cemen-
Amalgam Using amalgam alone to close the perforated site caused mild to moderate chronic inflammatory reaction. The zone of inflammation was surrounded by striations of collagen fibers. Granulomatous lesions covered with stratified squamous epithelium were present in the bifurcation area of 7 specimens of 13 (Fig. 4). The epithelium did not seem to proliferate apically and in some cases it was seen as a lining immediately adjacent to the perforation site. Cementum deposition was not seen in any of the amalgam specimens. The evidence of osteoblast activity was seen in 9 specimens in which 6 specimens exhibited new bone formation. The extruded material was observed in most of the specimens. The use of calcium sulfate under amalgam caused a mild to moderate chronic inflammatory reaction in most of the specimens. The zone of inflammation was surrounded by a fibrous layer. Epithelial proliferation was present in the bifurcation area of 13 specimens of 14 (Fig. 5). No extruded material or ankylosis was observed. No specimen showed deposition of cementum over the amalgam. Bone formation was evident in 6 specimens, and in 3 specimens an evidence of osteoblast activity bordering the bony trabeculae was seen. Osteoclastic activity was seen in 7 specimens where it was marked in 1 specimen. Statistical analysis MTA alone had the lowest score of inflammation (Table II). This was followed by amalgam, MTA with calcium sulfate, and amalgam with calcium sulfate. A significant difference was found among the experimental groups (P⫽ .023). The migration of epithelium in the defect areas repaired by MTA with calcium sulfate and amalgam with calcium sulfate appeared more common when compared with MTA or amalgam alone.
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Table I. The histological findings of all the groups Group Group Group Group Group Group Group
1: 2: 3: 4: 5: 6:
Negative control Positive control MTA MTA with calcium sulfate Amalgam Amalgam with calcium sulfate
No.
Inflammation
Epithelium
Cementum
Bone apposition
Bone resorption
5 6 14 14 13 14
0 6 8 11 10 13
0 6 5 11 7 13
5 0 10 8 0 0
1 1 12 11 9 9
1 5 2 7 6 7
Fig. 3. Photomicrograph of group 4 (MTA with calcium sulfate). Mesiodistal section, shows apposition of cementum (black arrow) and deposition of cementum in resorbed cavity (white arrow). There are no inflammatory cells in the periodontal tissue (PDL) (hematoxylin and eosin, ⫻40).
However, this difference was not statistically significant (P⫽ .093). When the 4 experimental groups were compared to positive control, the MTA and amalgam group showed a statistically significant difference. No statistically significant difference was noted for cementum formation over MTA and MTA with calcium sulfate (P⫽ .430). MTA showed the highest score of bone deposition, followed by amalgam, amalgam with calcium sulfate, and MTA with calcium sulfate. It was a significant difference between the groups (P⫽ .045). Furthermore, MTA showed the lowest score of bone resorption. No significant difference was found between the groups (P⫽ .067). DISCUSSION The success rate when using only MTA, without calcium sulfate, was excellent. This result is in agreement with earlier reports.9 However, our findings for amalgam were better than earlier reports.9 In general our rate of repairs were better than reported by Seltzer et al.3 who found, in a histological study using mon-
Fig. 4. Photomicrograph of group 5 (amalgam), buccolingual section. A, Epithelium proliferation from palatal side (arrows), absence of cementum around repaired material, and moderate inflammation (hematoxylin and eosin, ⫻40). B, Magnification of A shows a layer of proliferated epithelium (arrows), and chronic inflammatory cells, mostly lymphocytes and plasma cells (⫻100).
keys’ teeth, that perforated areas had a poor chance for healing after 6 to 10 months of observation. We attribute the difference to time interval of exposing the defected area to saliva, methodology and materials used, and the animal model.
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Fig. 5. Photomicrograph of group 6 (amalgam with calcium sulfate) buccolingual section shows epithelial proliferation (arrows) and fibrous layer (Fl) that surrounded the zone of mild inflammation (Masson’s trichrome, ⫻40).
Dogs were selected for this study because their teeth have suitable furcation that provides good accessibility and visibility. Their teeth are large enough to facilitate the study of tissue reaction and allow ample room for perforation without hemisection of the tooth.16 However, the morphologic character of the dog’s tooth is different from that of a human tooth. The posterior teeth of the dog lack a root trunk and the furcation is often as close as 1 to 2 mm from the cementoenamel junction.15 As a result, epithelialization of a furcation perforation of dogs’ teeth is perhaps more likely than in the human, where the furcation lies more deeply within the alveolus. Thus, any technique shown to produce favorable results in dogs may understate the response in human. On the other hand, the proximity of the cementoenamel junction to the furcation may explain the high rate of epithelization seen in the experimental groups in the present study. This might be a limitation for using the dog model when studying perforation repair. The size of perforations in this investigation was standardized at 1.4 mm, which is similar to several previous studies.7-9,13,17,18 The bur was allowed to penetrate 2 mm into the alveolar bone to enhance the inflammatory response.13 The other factor that enhances the formation of the interradicular lesion was to leave the perforation site open for saliva contamination for 4 weeks.2,13 A good prognosis, however, can be achieved when the perforation is repaired immediately.9,19 Clinically, a time delay may increase the difficulty of repairing the defect because of the resorption of bone in the area of the defect.2,3,17 Sterilization of the perforation defect before applying the filling material was recommended by Kvinnsland et al.20 In this study the perforation site was curetted and
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washed with 2.5% sodium hypochlorite before repairing under aseptic conditions. Pitt Ford et al.9 attributed the good response in some specimens in which repair of delayed furcal perforations was effective with the use of 2.5% sodium hypochlorite. In this study all perforation defects of the experimental groups and the entire access cavities were filled with the same material to achieve good sealing. Many previous studies had used amalgam and MTA to seal the access cavity after repairing the perforated site with either the same or different material.7-9,21 Weldon et al.10 showed that filling the furcation perforation and the entire access cavity with same material produced less leakage and therefore prognosis might be improved. The histological sections in this investigation were prepared in 2 directions as suggested in several earlier studies.3,7,8,9,13,18,22 Half of the specimens were prepared in the buccolingual direction to better observe sinus tracts through the gingival sulcus, inflammation, and epithelium migration. The other half were prepared in the mesiodistal direction to better evaluate the depth of the gingival pocket, type of attachment, and extent of inflammation in relation to the root surface. Inflammation caused by infection was seen in the positive control group as a breakdown of the interradicular bone and the migration of epithelium.3,7,8 We found the lowest incidence of epithelium migration when using MTA. It is believed that this may be because of good biocompatibility and sealing ability of the material. Deposition of hard tissue over MTA with or without calcium sulfate was observed in the majority of specimens. In addition, new cementum was fused to the original cementum on the root surface. This supports earlier reports of repair when using MTA9,21,23-26 and this may due to a number of factors such as sealing ability, biocompatibility, and alkaline pH on setting. Koh et al.27 stated that it is possible that MTA offers a biologically active substrate for bone cell proliferation and stimulates interleukin production. The causes for cementum deposition over the filling material have been extensively discussed in the literature. Holland28 reported that calcium hydroxide in contact with pulp tissue or culture medium produces deposition of calcite crystals that originated from a reaction of the calcium from calcium hydroxide with carbon dioxide from the pulp tissue. Seux et al.29 also observed a rich extracellular network of fibronectin in close contact with these crystals, and concluded that their findings strongly support the role of calcite crystals and fibronectin as an initiating step in the formation of a hard tissue barrier. The same crystals that were observed with calcium hydroxide were reported with MTA by Holland et al.30 According to Torabinejad et
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Table II. Severity of inflammation for the groups. Group Group Group Group Group Group Group
1: 2: 3: 4: 5: 6:
Negative control Positive control MTA MTA with calcium sulfate Amalgam Amalgam with calcium sulfate
No.
None (%)
Mild (%)
Moderate (%)
Severe (%)
5 6 14 14 13 14
5 (100) 0 (0.0) 6 (42.8) 3 (21.4) 3 (23.0) 1 (7.1)
0 (0.0) 0 (0.0) 4 (28.5) 2 (14.2) 4 (30.7) 4 (28.5)
0 (0.0) 1 (16.6) 3 (21.4) 7 (50) 4 (30.4) 6 (42.8)
0 (0.0) 5 (83.3) 1 (7.1) 2 (14.2) 2 (15.3) 3 (21.4)
al.,31 MTA has 2 specific phases composed of calcium oxide and calcium phosphate after reaction with water. Thus, MTA has calcium oxide on its surface that could react with tissue fluids to form calcium hydroxide. For this reason it is believed that MTA actively promotes hard tissue formation rather than being inert or an irritant like most other materials. New cementum may be derived from either the remaining periodontal ligament or it is derived from the ingrowing connective tissue.26 Cementum deposition was not observed when using amalgam for repair. In the current investigation, ankylosis was seen in 2 specimens associated with MTA without calcium sulfate. This finding is consistent with those reported by Holland et al.24 In addition, Beavers et al.19 observed ankylosis after 7 days from repairing the furcal perforation with calcium hydroxide. Ankylosis is an infrequent complication in the healing of furcal perforation because of the low thermal trauma generated while perforating.2,9,15,22 Although slow speed was used for the perforations in this study, increased temperature may have been generated when inserting the bur into the alveolar bone. This may also have caused resorption and deposition of new bone and cementum. Deposition of bone was found more often than resorption especially with MTA without calcium sulfate. No extrusion of the filling material was noted in the groups that used calcium sulfate compared to those without calcium sulfate. Amalgam extruded into the interradicular area resulted in inflammation, which has been observed in earlier studies.9,13 We used an internal matrix under amalgam repairs as it was reported as advantageous.13 Similar findings were not observed in the present study. This may be attributed to the delayed treatment of the perforated site, which was used here. When the MTA was accidentally extruded into the interradicular area, deposition of hard tissue over the material with the presence of a healthy periodontium was observed. The extrusion of repair materials should be expected in cases of delayed repair of the perforation compared to immediate repair. During immediate repair of modest perforations the periodontal ligament and surrounding hard tissue will act as a barrier.
CONCLUSION Furcation perforation has poor prognosis if the perforation site is not immediately repaired. The healing after delayed repair of furcal perforation shows no statistical significant difference among the 4 test groups. However, placement of MTA alone shows better healing response compared to other groups. The use of calcium sulfate as internal matrix under MTA or amalgam did prevent extrusion of the repaired material into the contaminated perforated area but it caused unfavorable inflammatory reaction. Moreover, uses of calcium sulfate did not aid bone regeneration or prevent epithelium migration into the defected perforation area. Therefore, using calcium sulfate as an internal matrix for MTA is not recommended. REFERENCES 1. Sinai I. Endodontic perforations: their prognosis and treatment. J Am Dent Assoc 1977;95:90-5. 2. Jew R, Weine F, Keen J. A histologic evaluation of periodontal tissues adjacent to root perforations filled with Cavit. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1982;54:124-35. 3. Seltzer S, Sinai I, August D. Periodontal effects of root perforations before and during endodontic procedures. J Dent Res 1970;49:332-9. 4. Meister F, Lommel T, Gerstein H, Davies E. Endodontic perforations which resulted in alveolar bone loss. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1979;47:463-70. 5. Lantz B, Persson P. Periodontal tissue reactions after surgical treatment of root perforations in dog’s teeth: a histologic study. Odont Revy 1970;21:51-62. 6. Lemon R. Nonsurgical repair of perforation defects. Dent Clin North Am 1992;36:349-457. 7. El Deeb ME, El Deeb M, Tabibi A, Jensen J. An evaluation of the use of amalgam, Cavit and calcium hydroxide in the repair of furcation perforation. J Endod 1982;8:459-66. 8. Balla R, LoMonaco C, Skribner J, Lim L. Histological study of furcation perforation treated with tricalcium phosphate, hydroxyapatite, amalgam, and life. J Endod 1991;19:591-5. 9. Pitt Ford T, Torabinejad M, Hong C, Kariyawasam S. Use of mineral trioxide aggregate for repair of furcal perforations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79:756-63. 10. Weldon J, Pashley D, Loushine R, Weller R, Kimbrough W. Sealing ability of mineral trioxide aggregate and Super-EBA when used as furcation repair materials, a longitudinal study. J Endod 2002;28:467-70. 11. Alhadainy H, Himel V. An in vitro evaluation of plaster of Paris
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Reaction of dogs’ teeth to root canal filling with mineral trioxide aggregate or a glass ionomer sealer. J Endod 1999;25:728-30. Holland R, Filho J, Souza V, Nery M, Bernabe P, Junior E. Mineral trioxide aggregate repair of lateral root perforations. J Endod 2001;27:281-4. Apaydin E, Shahrokh S, Torabinejad M. Hard tissue healing after application of fresh or set MTA as root end filling material. J Endod 2004;30:21-4. Torabinejad M, Pitt Ford T, McKendry D, Abedi H, Miller D, Kariyawasam S. Histological assessment of mineral trioxide aggregate as a root end filling in monkeys. J Endod 1997;23:225-8. Koh E, McDonald F, Pitt Ford R, Torabinejad M. Cellular response to mineral trioxide aggregate. J Endod 1998;24:543-7. Holland R. Histochemical response of amputed pulps to calcium hydroxide. Rev Bras Pesq Med Biology 1971;4:83-95. Seux D, Couble M, Hartman D, Gauthier J, Magloire H. Odontoblast like cytodifferentiation of human dental pulp cells in vitro in the presence of a calcium hydroxide containing cement. Arch Oral Biol 1991;36:117-28. Holland R, Souza V, Nery M, Filho J, Bernabe P, Dezan E. Reaction of rat connective tissue to implanted dentin tubes filled with mineral trioxide aggregate or calcium hydroxide. J Endod 1999;25:161-6. Torabinejad M, Hong C, McDonald F, Pitt Ford T. Physical and chemical properties of a new root-end filling material. J Endod 1995;21:349-53.
Reprint requests: Saad Al-Nazhan, BDS, MSD Associate Professor King Saud University, College of Dentistry Division of Endodontics PO Box 60169 Riyadh 11545 Saudi Arabia [email protected]; [email protected]