USING MINERAL TRIOXIDE AGGREGATE AS A PULP-CAPPING MATERIAL

USING MINERAL TRIOXIDE AGGREGATE AS A PULP-CAPPING MATERIAL

ARTICLE 1 USING MINERAL TRIOXIDE AGGREGATE AS A PULP-CAPPING MATERIAL THOMAS R. PITT FORD, B.D.S., PH.D.; MAHMOUD TORABINEJAD, D.M.D., M.S.D., PH.D.;...

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ARTICLE 1

USING MINERAL TRIOXIDE AGGREGATE AS A PULP-CAPPING MATERIAL THOMAS R. PITT FORD, B.D.S., PH.D.; MAHMOUD TORABINEJAD, D.M.D., M.S.D., PH.D.; HAMID R. ABEDI, B.D.S.; LEIF K. BAKLAND, D.D.S.; STALIN P. KARIYAWASAM

Gentists have long recognized that traumatic exposures of the dental pulp can be successfully capped with calcium hydroxide preparations that produce calcific bridges across the wound surface.'4 Several investigators have demonstrated that the exposed dental pulp has the capacity to heal when microleakage and bacterial contamination are prevented.356 Therefore, it appears that an effective pulpcapping material should be biocompatible, provide a biological seal and prevent bacterial leakage. An experimental material, mineral trioxide aggregate, or MTA (Loma Linda University), has recently been shown in a series of investigations to be biocompatible and to seal pathways of communication between the root canal system and the external surface of the teeth.7'-4 Dye and bacterial leakage studies78 have shown the sealing ability of MTA to be superior to that of amalgam- or zinc oxideeugenol-, or ZOE, based materials. The biocompatibility of MTA is equal or superior to that of these materials.1011 Furthermore, the use of MTA as a root-end filling material in dogs and monkeys, as well as furcation repair material in dogs, has led to superior results compared with amalgam.12-'4

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This study examined the dental pulp responses in monkeys to mineral trioxide aggregate, or

MTA, and a calcium hydroxide preparation when used as pulp-

capping materials. After the pulps of 12 mandibular incisors were exposed with a No. I round

mentum over MTA when it was used as a root-end filling material'2"13 or as a repair material in experimentally perforated furcation of mandibular premolars of dogs.'4 The purpose of this study was to compare the dental pulp responses in monkeys after MTA or a calcium hydroxide preparation (Dycal, L.D. Caulk) was applied as a pulp-capping material.

bur, they were capped with either MTA or the calcium hydrox-

ide preparation. After five

months, the authors noted no pulpal inflammation in five of six samples capped with MTA, and all six pulps in this group had a

complete dentin bridge. In contrast, all of the pulps capped with the calcium hydroxide prepara-

tion showed pulpal inflammation, and bridge formation occurred in

only two samples. Based on these results, it appears that MTA has the potential to be used as a pulp-capping material during

vital pulp therapy.

Histologic examination of specimens in these experiments showed formation of new ce-

MIVATERIALS AND METHODS

We used 12 mandibular incisors in four healthy 4-year-old cynomolgus monkeys in this experiment. General anesthesia was achieved with an intramuscular injection of 20 milligrams per kilogram of ketamine. We isolated the teeth with a rubber dam and, using a No. 1 round bur in a high-speed handpiece with copious water spray, created standardized pulp exposures (1 millimeter in diameter) through a lingual access opening. We controlled bleeding with sterile cotton pellets before placing the pulp-capping materials. The materials used were either a calcium hydroxide preparation or MTA. The calcium hydroxide preparation was mixed according to the manufacturer's directions and applied to the exJADA, Vol. 127, October 1996 1491

RESEARCHposure site; the remainder of the cavity was filled with amalgam. The MTA powder was mixed with sterile saline (at a 3:1 powder-saline ratio) and packed into the entire access cavity. Five months later, we surgically removed the teeth and their surrounding tissues from the jaws after killing the animals and perfusing them with formalin. The specimens were processed for histologic examination. The sections were stained with hematoxylin and eosin as well as by the Brown and Brenn method for identification of bacteria in the samples. Two of the investigators (T.P.F. and H.A.) assessed the sections jointly for the presence of dentin bridge, inflammation and bacteria on the cavity walls.

walls in any tooth filled with MTA, but did detect bacteria in one sample filled with the calcium hydroxide preparation and amalgam.

RESULTS

DISCUSSION

All of the pulps capped with MTA showed dentin bridge formation (Figure 1), and all but one were free of inflammation. The bridge that formed adjacent to the MTA was thick and continuous with the original

The favorable tissue responses to MTA as a pulp-capping material mirror those observed in the cuspids of beagle dogs.15 Abedi and associates15 created standardized pulp exposures in the cuspids of six beagle dogs

dentin. In contrast, only two dental pulps capped with the calcium hydroxide preparation had dentin bridges, and all six had pulpal inflammation (Figure 2), which was severe and dominated by polymorphonuclear leukocytes. We did not observe bacteria on cavity

All of the pulps capped with MTA showed dentin bridge formation and all but one were free of inflammation.

Figure 1. Histologic section demonstrating the pulpal response to pulp capping with mineral trioxide aggregate (Loma Linda University). A dentin bridge has formed a complete barrier at the exposure site and the pulp is free of inflammation (original magnification X50, hematoxylin and eosin stain).

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and examined the amount of hard tissue formation and degree of inflammation adjacent to the MTA and calcium hydroxide preparation. Histomorphometric analysis of their data after two months showed a significantly higher frequency of calcific bridge formation and less inflammation in the MTA group compared with the calcium hydroxide group.

We observed a thick dentin bridge in all pulps capped with MTA. The bridge was continuous with the adjacent dentin, and dentinal tubules were observed in the bridge, particularly close to the pulp. The dentin bridge under the MTA showed irregularities in some sections, although no tunnel defects or soft-tissue inclusions were noted. Cox and associates6 and Pitt Ford and Roberts4 reported the presence of tunnel defects in the dentin bridge after direct pulp capping with various calcium hydroxide preparations. These authors speculated that these defects can act as pathways for microleakage and inflammatory changes in pulp.

Figure 2. Histologic section demonstrating the pulpal response to pulp capping with a calcium hydroxide preparation (Dycal, L.D. Caulk). The pulp is inflamed and no dentin bridge has formed (original magnification X50, hematoxylin and eosin stain).

RBES[ARCH11 The formation of dentin adjacent to MTA could be due to its sealing ability,7'8 biocompatibility,""1 alkalinity9 or other properties associated with this material. Recent in vitro investigation has demonstrated the ability of MTA to stimulate cytokine release from bone cells,16 indicating that it actively promotes hard tissue formation rather than being inert, as are many dental materials.17 The unsatisfactory pulpal responses to the calcium hydroxide preparation covered by amalgam could be due to the fact that amalgam did not provide a bacterial-tight seal, and not the result of the preparation's lack of biocompatibility. The lack of chronic inflammatory cells and presence of polymorphonuclear leukocytes in pulps capped with the calcium hydroxide preparation indicate active microleakage through the interface between amalgam and tooth structure. Many investigators have implicated bacterial microleakage at restoration margins as the cause of pulpal inflammation.'1120 However, staining bacteria in histologic sections is often difficult and may not show the bacteria despite their presence in the samples.21 Pitt Ford and Roberts4 have shown that the calcium hydroxide preparation produces dentin bridge successfully in the absence of infection. The importance of avoiding bacterial contamination after pulp capping was shown by Cox and associates,17 who used ZOE cement to prevent bacterial leakage. Translating these findings to clinical practice has always been difficult because ZOE-based cements cannot be used as permanent restorative materials. In addition, use of a

ZOE-based cement under composite resin is contraindicated.22 MTA appears to meet the requirements for pulp-capping materials. It stimulates dentin bridge formation and prevents microleakage.7' The material sets slowly9 but, far from being a disadvantage, this slow setting time prevents setting shrinkage, which is a feature of most dental cements and could be one of the reasons for leakage associated with these materials.

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It appears that MTA seals the pathways of communication between the root canal system and the external surfaces of the teeth. Therefore, it is suitable as a pulpcapping material during vital pulp therapy.

Once set, MTA has a compressive strength that equals some of the fortified ZOE bases,9 and it can be trimmed back with a bur to place a permanent overlying restoration. Unlike calcium hydroxide cement bases, which may dissolve, MTA has negligible solubility.9 An in vitro study by Rehfeld and associates23 and clinical observations of Barnes and Kidd24 and Lewin25 indicate that calcium hydroxide dissolves under amalgam restorations. These investigators24'25 attributed the disappearance of calcium hydroxide to microleakage of restorative materials placed over the calcium hydroxide preparations. Because MTA sets hard and has neglible solu-

bility, its use as a pulp-capping material should prevent recontamination of dental pulp, which can occur with calcium hydroxide preparations, as shown by Cox and associates.6 CONCLUSION

Based on the results of this study and the properties demonstrated when MTA was used as a root-end filling material and for repair of iatrogenic root perforation,12"'4 it appears that MTA seals the pathways of communication between the root canal system and the external surfaces of the teeth. Therefore, it is suitable as a pulp-capping material during vital pulp therapy. Future studies with larger sample sizes are needed to confirm the results of the present investigation. . Dr. Pitt Ford is a senior lecturer in the Department of Conservative Dentistry, United Medical and Dental Schools of Guy's and St. Thomas' Hospitals, University of London, England. Dr. Torabinejad is a professor of endodontics and director, Graduate Endodontics, Department of Endodontics, School of Dentistry, Loma Linda University, Loma Linda, Calif. 92350. Address reprint requests to Dr. Torabinejad. Dr. Abedi is an assistant professor, Department of Endodontics, School of Dentistry, Loma Linda University, Loma Linda, Calif. Dr. Bakland is an associate dean and chairman, Department of Endodontics, School of Dentistry, Loma Linda University, Loma Linda, Calif. Mr. Kariyawasam is a member of Anatomy and Cell Biology, United Medical and Dental Schools of Guy's and St. Thomas' Hospitals, University of London, England.

None of the authors has any financial interest in the materials tested. Loma Linda University will receive general research sup-

port from royalties generated. 1. Stanley HR, Lundy T. Dycal therapy for pulp exposures. Oral Surg Oral Med Oral

Pathol 1972;34(5):818-27. 2. Tronstad L. Reaction of the exposed pulp to Dycal treatment. Oral Surg Oral Med Oral Pathol 1974;38(6):945-53. 3. Cvek M, Granath L, Cleaton-Jones P, Austin J. Hard tissue barrier formation in pulpotomized monkey teeth capped with

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RESEARCHcyanoacrylate or calcium hydroxide for 10 and 60 minutes. J Dent Res 1987;66(6):1166-74. 4. Pitt Ford TR, Roberts GJ. Immediate and delayed direct pulp capping with the use of a new visible light-cured calcium hydroxide preparation. Oral Surg Oral Med Oral Pathol 1991;71(3):338-42. 5. Cox CF, Bergenholtz G, Fitzgerald M, et al. Capping of the dental pulp mechanically exposed to the oral microflora-a 5-week observation of wound healing in the monkey. J Oral Pathol 1982;11(4):327-39. 6. Cox CF, Bergenholtz G, Heys DR, Syed SA, Fitzgerald M, Heys RJ. Pulp capping of dental pulp mechanically exposed to oral microflora: a 1-2 year observation of wound healing in the monkey. J Oral Pathol 1985;14(2):156-68. 7. Torabinejad M, Watson TF, Pitt Ford TR. Sealing ability of a mineral trioxide aggregate when used as a root end filling material. J Endod 1993;19(12):591-5. 8. Torabinejad M, Rastegar AF, Kettering JD, Pitt Ford TR. Bacterial leakage of mineral trioxide aggregate as a root-end filling material. J Endod 1995;21(3):109-12. 9. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. J Endod 1995;21(7):349-53.

10. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Cytotoxicity of four root end filling materials. J Endod 1995;21(10):489-92. 11. Torabinejad M, Hong CU, Pitt Ford TR, Kariyawasam SP. Tissue reaction to implanted SuperEBA and mineral trioxide aggregate in the mandible of guinea pigs: a preliminary report. J Endod 1995;21(11):569-71. 12. 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(12):603-8. 13. Torabinejad M, Pitt Ford TR, McKendry DJ, Abedi HR, Miller DA, Kariyawasam SP. Histologic assessment of mineral trioxide aggregate as root end filling in monkeys. J Endod (In press). 14. Pitt Ford TR, Torabinejad M, McKendry DJ, Hong CU, Kariyawasam SP. Use of mineral trioxide aggregate for repair of furcal perforations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1995;79(6):756-62. 15. Abedi HR, Torabinejad M, Pitt Ford TR, Bakland LK. The use of mineral trioxide aggregate cement (MTA) as a direct pulp capping agent (Abstract no. 44). J Endod 1996;22(4):199. 16. Koh ET, Pitt Ford TR, Torabinejad M, McDonald F. Mineral trioxide aggregate stimulates cytokine production in human os-

teoblasts. J Bone Min Res 1995;10S:S406. 17. Cox CF, Keall CL, Keall HJ, Ostro E, Bergenholtz G. Biocompatibility of surface sealed dental materials against exposed pulps. J Prosthet Dent 1987;57(1):1-8. 18. Watts A. Bacterial contamination and the toxicity of silicate and zinc phosphate cements. Br Dent J 1979;146(1):7-13. 19. Cox CF. Biocompatibility of dental materials in the absence of bacterial infection. Oper Dent 1987;12(4):147-52. 20. Browne RM, Tobias RS, Crombie IK, Plant CG. Bacterial miocroleakage and pulpal inflammation in experimental cavities. Int Endod J 1983;16(4):147-55. 21. Mjor IA. Histologic demonstration of bacteria subjacent to dental restorations. Scand J Dent Res 1977;85(3):169-74. 22. Smith BGN, Wright TS, Brown D. The clinical handling of dental materials. 2nd ed. Oxford, England: Butterworth-Heinemann; 1994:139-40. 23. Rehfeld RL, Mazer RB, Leinfelder KF, Russell CM. Evaluation of various forms of calcium hydroxide in the monitoring of microleakage. Dent Mater 1991;7(3):202-5. 24. Barnes IE, Kidd EAM. Disappearing Dycal: an opinion. Br Dent J 1979;147(5):111. 25. Lewin DA. Disappearing Dycal. Br Dent J 1980;148(2):32.

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