Evaluation Of Mineral Trioxide Aggregate And Calcium Hydroxide Cement .

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Clinical Research Evaluation of Mineral Trioxide Aggregate and Calcium Hydroxide Cement as Pulp-capping Agents in Human Teeth Maria de Lourdes R. Accorinte, DDS, MS, PhD,* Roberto Holland, DDS, MS, PhD,† Alessandra Reis, DDS, PhD,‡§ Marcelo C. Bortoluzzi, DDS, PhD,‡ Sueli S. Murata, DDS, MS, PhD,† Eloy Dezan, Jr, DDS, MS, PhD,† Valdir Souza, DDS, MS, PhD,† and Loguercio Dourado Alessandro, PhD‡§ Abstract This study evaluated the histomorphologic response of human dental pulps capped with mineral trioxide aggregate (MTA) and Ca(OH)2 cement (CH). Pulp exposures were performed on the occlusal floor of 40 human permanent premolars. After that, the pulp was capped either with CH or MTA and restored with composite resin. After 30 and 60 days, teeth were extracted and processed for histologic exam and categorized in a histologic score system. The data were subjected to Kruskal-Wallis and Conover tests ( .05). All groups performed well in terms of hard tissue bridge formation, inflammatory response, and other pulpal findings. However, a lower response of CH30 was observed for the dentin bridge formation, when compared with MTA30 and MTA60 groups. Although the pulp healing with calcium hydroxide was slower than that of MTA, both materials were successful for pulp capping in human teeth. (J Endod 2008;34:1– 6) Key Words Biocompatibility, calcium hydroxide, human pulp, mineral trioxide aggregate, pulp capping, pulp therapy From the *Department of Dental Materials, School of Dentistry, University Brás Cubas, São Paulo, SP, Brazil; †Department of Endodontics, School of Dentistry, São Paulo State University, UNESP-Araçatuba, São Paulo, SP, Brazil; ‡Dental Materials and Operative Dentistry, School of Dentistry, University of Oeste de Santa Catarina, Joaçaba, SC, Brazil; and § Dental Materials and Operative Dentistry, School of Dentistry, University of Ponta Grossa, PR, Brazil. Address requests for reprints to Dr Alessandro Dourado Loguercio, Universidade do Oeste de Santa Catarina, Faculdade de Odontologia, Av Getúlio Vargas, 2225, Bairro Flor da Serra, 89600-000, Joaçaba, SC, Brazil. E-mail address: aloguercio@hotmail.com. 0099-2399/ 0 - see front matter Copyright 2008 by the American Association of Endodontists. doi:10.1016/j.joen.2007.09.012 JOE — Volume 34, Number 1, January 2008 T he aim of conservative pulp therapy is to maintain the coronal and radicular pulp tissue in a viable condition. To accomplish this goal, living pulp tissue exposed to the oral environment should be protected to preserve its vitality (1). Many studies indicated that calcium hydroxide and calcium hydroxide compounds are the gold standard in human teeth (2– 4), against which new materials should be tested. However, several disadvantages have been listed with the use of calcium hydroxide material. Presence of tunnels in dentin barrier, extensive dentin formation obliterating the pulp chamber, high solubility in oral fluids, and lack of adhesion and degradation after acid etching are some of the limitations reported (5–7). Because of the aforementioned disadvantages, a variety of materials have been proposed as candidates for direct pulp capping during recent years such as mineral trioxide aggregate (MTA). Initially, MTA was used in endodontics to seal off all pathways of communication between the root canal system and the external surface of the tooth (8). Pitt Ford et al. (9) were the first to evaluate the performance of MTA for pulp capping in monkey’s teeth, and they demonstrated superior performance of MTA compared with calcium hydroxide. After testing both materials in dogs’ pulp, Faraco and Holland (10) showed that MTA achieved the most favorable results. Although several case reports and clinical studies have evaluated the effect of MTA for pulp capping in permanent human teeth (11, 12), few histologic studies have been conducted to evaluate the histologic response of MTA in human teeth (13, 14). In a recent literature review, Roberts et al. (15) reported that there are still insufficient clinical studies evaluating the performance of MTA for pulp capping. Therefore, the purpose of this clinical study was to compare the histomorphologic features of MTA and calcium hydroxide cement after 30 and 60 days. The null hypothesis to be tested was that no significant difference will be observed in pulps capped with MTA and calcium hydroxide during the 2 periods of evaluation. Materials and Methods Forty healthy human premolars scheduled to be extracted for orthodontic reasons were selected from patients ranging from 15–30 years old. All teeth were examined clinically and radiographically to ensure absence of proximal caries and periapical lesions. The patients and/or their parents signed consent forms after receiving a detailed explanation about the experimental rationale, clinical procedures, and possible risks. The parents and the adult volunteers were asked to read and sign a consent form allowing the clinical procedure. Both the consent form and the research protocol were reviewed and approved by the Human Subject Review Committee from the University of Oeste of Santa Catarina, SC, Brazil. The vitality of all teeth was tested with thermal testing. ENDO-ICE frozen gas (Coltène/Whaledent Inc, Mahwah, NJ) was applied for 5 seconds on the buccal surface of the teeth scheduled for the pulp therapy and adjacent teeth. After local anesthesia (Citanest 3%; Merrel Lepetit, São Paulo, Brazil) the rubber dam isolation was installed, and each tooth was pumiced with a rubber cup at low speed. Occlusal cavities were prepared by means of sterile diamond burs (#1095; KG Sorensen, Barueri, São Paulo, Brazil) at high speed under water/spray coolant. The dimensions of the cavity were MTA and Calcium Hydroxide Cement as Pulp-capping Agents 1

Clinical Research Figure 1. Experimental design. occlusal depth, 3.0 0.2 mm; mesiodistal width, 4.0 0.5 mm; and faciolingual width, 3.0 0.2 mm. The cavity dimensions were checked with a digital caliper in an attempt to standardize the cavity size. Pulp exposure was performed in the center of the pulpal floor by means of a round diamond bur under water cooling (#1014, 1.2; KG Sorensen). One bur was used for each cavity. The teeth were then divided into 4 experimental groups (n 10). Homeostasis was established with a sterile cotton pellet soaked in saline solution. In groups 1 (CH30) and 2 (CH60), calcium hydroxide cement (Life, Kerr, Romulus, MI) was applied in the occlusal floor. In groups 3 (MTA30) and 4 (MTA60), MTA (Dentsply Caulk, Milford, DE) was applied in the occlusal floor (Fig. 1). After that, a thin layer of resin-modified glass ionomer cement (Vitrebond; 3MESPE, St Paul, MN) was applied. A total of 10 teeth were used for each experimental condition. Scotchbond Multi Purpose Plus (3M ESPE, St Paul, MN), a 3-step, etch-and-rinse adhesive system, was used for all groups. Enamel and dentin were conditioned with 35% phosphoric acid for 20 seconds. The TABLE 1. Scores Used during Histologic Exams: Hard Tissue Bridge Scores Continuity 1 2 Complete Little communication of the capping material with dental pulp Only lateral deposition of hard tissue on the walls of the cavity of pulp exposition Absence of hard tissue bridge and absence of lateral deposition of hard tissue 3 4 Scores 1 2 3 4 Morphology Dentin or dentin associated an irregular hard tissue Only irregular hard tissue deposition Only a slight layer of hard tissue deposition No hard tissue deposition Scores Thickness* Up to 250 m 150–249 m 1–149 m Partial or absent bridge 1 2 3 4 Scores Localization 1 Closure to the exposition area without invading the pulp space Bridge invading pulp space next to the opposite dentin wall Bridge reached the opposite dentin wall No bridge or only hard tissue deposition on the walls of the exposition cavity 2 3 4 *Evaluated with a micrometric ocular in 3 different points of the bridge. 2 Accorinte et al. acidic agent was rinsed out, and the dentin was slightly dried in such way that the surface stayed visibly moist with a shiny appearance. One coat of the primer was applied and air-dried for 20 seconds. The bonding resin was subsequently applied and light-cured for 10 seconds. Increments of Z-100 (3M ESPE) were used to restore the cavities. Each increment ( 2 mm) was light-cured for 40 seconds at 450 mW/cm2 (Ultralux electronic; Dabi Atlante, Ribeirão Preto, SP, Brazil). A radiometer (Model 100P; Demetron Research Corp, Kerr, Danbury, CT) was used to check the light intensity immediately before each clinical appointment. When necessary, the material excesses were removed by using an ultra-fine diamond bur at high speed under water cooling (KG Sorensen). Teeth from groups 1 and 3 were extracted after 30 days, whereas teeth from groups 2 and 4 were extracted after 60 days. The patients were asked about the presence or absence of postoperative sensitivity after 30 and 60 days. The extraction was performed under local anesthesia. The apical third of all roots was sectioned in 5 mm to facilitate fixation in 10% buffered formalin solution for 72 hours. The teeth were decalcified in 50% formic acid–sodium citrate for 6 – 8 weeks, prepared according to normal histologic techniques and embedded in paraffin. Six-micrometer-thick sections were cut with a microtome parallel to the main vertical axis of the tooth. The number of sections obtained per tooth was not fixed. On the average, 10 –12 slides containTABLE 2. Scores Used during Histologic Exams of Dental Pulp: Inflammatory Response Scores 1 2 3 4 Scores 1 2 Intensity of inflammatory reaction* (acute and chronic processes) Absent or very few inflammatory cells Mild: average number less than 10 inflammatory cells Moderate: average number 10-25 inflammatory cells Severe: average number greater than 25 inflammatory cells Extension of the inflammatory reaction (acute and chronic processes) 4 Absent Mild: inflammatory cells only next to dentin bridge or area of pulp exposition Moderate: inflammatory cells are observed in part of coronal pulp Severe: all coronal pulp is infiltrated or necrotic Scores General state of the pulp 3 1 2 3 4 No inflammatory reaction With inflammatory reaction Abscess Necrosis *Evaluated in different areas with a magnification of 400 . JOE — Volume 34, Number 1, January 2008

Clinical Research TABLE 3. Scores Used during Histologic Exams of Dental Pulp: Other Pulpal Findings Scores Giant cells 1 2 3 4 Absent Mild Moderate Pulp necrosis Scores Particles of capping materials 1 2 3 4 Absent Mild Moderate Large number Scores Presence of microorganisms 1 4 Absent Present ing 4 –5 six-micrometer-thick sections were obtained. The sections, mounted on glass slides, were stained with hematoxylin-eosin. Brown and Brenn technique was used to evaluate the presence of bacteria. The sections were blindly evaluated by an experienced and calibrated pathologist according to the criteria described in Tables 1, 2, and 3 (1). Regarding inflammatory response of dental pulp, the area of counting the cells was near the exposure pulp and capping material. Each histomorphologic event was evaluated in a 1– 4 score system, with 1 being the best result and 4 the worst result. The multiple sections were used to achieve an overall assessment for each tooth. The scores attributed to each group were subjected to nonparametric Kruskal-Wallis analysis. This test was performed separately for each histologic exam (hard tissue bridge, inflammatory response of dental pulp and general state of the pulp, and other pulpal findings) (Tables 1, 2, and 3). The comparisons between averages were performed by comparing the ranks with appropriately computed critical values ( .05) by using the Conover U test. This test is considered very powerful for several independent samples (16). Results The percentage of scores for each group is shown in Tables 4, 5, and 6. All groups performed well in terms of hard tissue bridge formation, inflammatory response, and other pulpal findings. However, an inferior response of group CH30 was observed for the hard tissue bridge formation, when compared with MTA30 and MTA60 groups (Table 4) (P .05). In other pulpal findings, CH30 was also inferior to MTA30 (P .05), particularly as a result of the high percentage of calcium hydroxide particles inside the pulp tissue (Table 6). No postoperative sensitivity was reported by patients throughout the study period. Histomorphologic Features Group CH30 Sixty percent of the specimens exhibited either total (20%) or partial (40%) dentin bridge formation (Fig. 2A and B). No hard tissue bridge was observed in 40% of the cases. In these cases, a chronic inflammatory infiltrate was observed in the pulp tissue near capping material or hard tissue bridge (Fig. 2B). In 70% of the cases, little black-colored particles of Ca(OH)2 surrounded by macrophages were found. In 10% of the specimens, gram-negative microorganisms were observed, probably as a result of coronal infiltration. In these cases, no hard bridge formation occurred, and there was an acute and chronic inflammatory infiltrate. Group CH60 Sixty percent of the specimens exhibited completely hard tissue bridges, and in 30% of the cases, hard tissue bridge was partial (Fig. 2C). Only in 10% of the cases, no hard tissue bridge was formed. The hard tissue bridge was usually thin and near to the exposure site (70%), with aspect of normal pulp (Fig. 2C and D). In 60% of the specimens, a chronic inflammatory infiltrate was observed, whereas in 40% of the sample no inflammatory infiltrate was observed. Presence of the capping material associated to macrophages was observed in 60% of the specimens. Giant cells were present in 10% of the cases, and no microorganisms were found in this group. Group MTA30 Thirty percent of the specimens exhibited completely hard tissue bridges, and in 70% of the cases, the hard tissue bridges were partial (Fig. 2E and F). In 70% of the specimens, a chronic inflammatory infiltrate with different intensities and extensions was observed (Fig. 2F), and only in 10% of the cases there was an acute inflammatory infiltrate (Fig. 2E). Presence of capping particles or dentin fragments was observed in 20% of the specimens (Fig. 2F). Giant cells and microorganisms were not detected in this group. Group MTA60 Fifty percent of the specimens exhibited complete hard tissue bridges (Fig. 2G and H), and in 40% of the specimens the hard tissue bridges were partial, and the capping material communicated with the pulpal tissue. No hard tissue bridge was observed in 10% of the specimens. The hard tissue bridge was usually thin (70%) and near to the exposure site (70%). In 80% of the specimens, a chronic inflammatory infiltrate was observed (Fig. 2G). Presence of the capping material associated to macrophages and particles of capping material inside pulpal tissue were rarely found. In 10% of the specimens, gram-negative microorganisms were observed, probably as a result of coronal infiltration or failure in the seal provided by the rubber dam isolation. TABLE 4. Percentage of Scores (%) Attributed for Each Group in Each Criterion of Hard Tissue Bridge as Well as Multiple Comparisons Groups CH30 CH60 MTA30 MTA60 Continuity 1 2 3 4 20 60 30 50 40 10 60 20 — 20 10 20 40 10 — 10 * 2.6 1.8 1.8 1.9 Morphology 1 2 3 4 60 60 70 60 — 10 20 30 — — 10 — 40 30 — 10 * 2.2 2.0 1.4 1.6 Thickness 1 2 3 4 — 20 — 30 — — 10 — 60 50 80 50 40 30 10 20 * 3.4 2.9 3.0 2.6 Localization 1 2 3 4 60 40 90 70 — 30 — 10 — — — — 40 30 10 20 * † 2.2 2.2 1.3 1.7 2.6 b 2.2 a,b 1.9 a 2.0 a Different superscripted letters indicate significant differences (P .05). *Means for each group in each subitem of the criteria of hard tissue bridge. †Overall means for the criteria. JOE — Volume 34, Number 1, January 2008 MTA and Calcium Hydroxide Cement as Pulp-capping Agents 3

Clinical Research TABLE 5. Percentage of Scores (%) Attributed for Each Group in Each Criterion of Dental Pulp as Well as Multiple Comparisons Acute inflammation Groups CH30 CH60 MTA30 MTA60 Intensity 1 2 3 4 80 80 90 80 10 10 10 — 10 10 — — — — — 20 * 1.3 1.3 1.1 1.6 Chronic inflammation Extension 1 2 3 4 80 80 90 80 20 20 10 — — — — 10 — — — 10 * 1.2 1.2 1.1 1.5 Intensity 1 2 3 4 10 10 30 20 60 60 50 60 20 20 10 10 10 10 10 10 * 2.2 2.3 2.0 2.1 General state of pulp Extension 1 2 3 4 10 10 30 20 60 60 30 60 20 20 40 10 10 10 — 10 * 2.3 2.3 2.1 2.1 † 1 2 3 4 * 10 40 30 20 90 60 70 60 — — — 10 — — — 10 1.9 1.6 1.7 2.1 1.8 a 1.7 a 1.6 a 1.9 a Different superscripted letters indicate significant differences (P .05). *Means for each group in each subitem of the criteria. †Overall means for the criteria. calcium hydroxide after 30 days. Thus, it seems that MTA takes advantage in producing healing in a shorter period of time (9), because in the 60-day evaluation both pulp-capping agents yielded similar results. This finding corroborates with previous studies conducted in animals (9, 10). On the other hand, Iwamoto et al. (14) reported no significant difference between MTA and calcium hydroxide regarding hard tissue bridge formation or inflammatory cell response. Whereas Iwamoto et al. (14) used white MTA, the present investigation used the grey one. The composition of both materials is rather different. A significantly higher amount of iron is present in the grey MTA compared with the white, besides the fact that the latter does not contain aluminum and dicalcium silicate (23, 24). Although one study has demonstrated that the white MTA is not as biocompatible as the grey version (25), no significant difference was observed between both MTA versions when used for pulp capping (14). Thus, this matter still deserves further evaluations to elucidate the concerns raised. Another finding that deserves attention is the fact that in 70% of the cases, little black-colored particles of Ca(OH)2 surrounded by macrophages were found in the calcium hydroxide group after 30 days, which was not observed in the MTA groups. Because these particles might induce calcification similar to what occurs with dentin chips, their presence could have been responsible for retarding the healing process of Ca(OH)2, although controversy exists as to whether these particles that have been accidentally forced into the pulp promote or retard healing (26). No significant difference regarding the presence of microorganisms was found among the groups evaluated. This means that the bacteriostatic action of calcium hydroxide and MTA per se (27–29) was enough to reduce the number of viable bacteria near the pulp exposure. On the other hand, the low sensibility of the histochemical staining technique for the detection of bacteria makes their identification difficult, mainly when there is a small number of such microorganisms (21). Moreover, bacteria are easily removed from dental tissue during histologic preparation (30, 31). Discussion If we consider the formation of complete or partial hard tissue bridge, with no or little communication between capping material and dental pulp as clinical success of pulp capping (13, 14), we can ensure that all groups achieved pulp healing, because in most of the teeth either a complete or partial hard tissue bridge was formed. Although the exact mechanism by which MTA induces hard tissue bridge formation is not completely understood, there are indications that the mechanism of initiation of reparative dentinogenesis in capping with MTA and Ca(OH)2 cement is similar (10, 17). Tziafas et al. (17) observed a homogenous zone of crystalline structures that was initially found along the pulp-MTA interface, whereas pulp cells, showing changes in their cytologic and functional state, were arranged in close proximity to the crystals. Although MTA does not contain calcium hydroxide, calcium oxide is formed after MTA hardening, which can react with tissue fluids to produce calcium hydroxide (18). According to Seux et al. (19), after contact with pulp tissue, MTA presents some structures that are similar to calcite crystals found in calcium hydroxide. They attract fibronectin, which is generally responsible for cellular adhesion and differentiation, as do calcium hydroxide. According to Faraco and Holland (10), the presence of necrotic tissue nearest to the hard tissue bridge suggests that MTA, similar to calcium hydroxide, initially causes necrosis by coagulation in contact with pulp connective tissue. This reaction might occur because of the high alkalinity of the product, whose pH is near to 9 –10 (20, 21). Recently, Min et al. (22) compared the cellular effects of Portland cement (the base of MTA) with other materials, including calcium hydroxide cement, on cultured human pulp cells. The results suggested that Portland cement is biocompatible and allows the expression of mineralization-related genes on cultured human pulp cells. These genes are responsible for inductive process on hard tissue bridge formation with MTA cement. Despite the similarity in the responses of MTA and calcium hydroxide, one cannot deny that a faster hard tissue bridge formation occurred when MTA was used. A significant difference was observed between MTA and TABLE 6. Percentage of Scores (%) Attributed for Each Group in Each Criterion of Other Pulpal Findings as Well as Multiple Comparisons Giant cells Groups CH30 CH60 MTA30 MTA60 Particles of capping materials * 1 2 3 4 90 90 100 90 10 10 — — — — — — — — — 10 1.1 1.1 1.0 1.3 Presence of microorganisms * 1 2 3 4 30 40 80 80 50 50 20 10 10 10 — — 10 — — 10 1 2.0 1.7 1.2 1.4 90 100 100 90 * † 1.3 1.0 1.0 1.3 1.5 b 1.3 a,b 1.1 a 1.3 a,b 4 — — — — — — — — 10 — — 10 Different superscripted letters indicate significant differences (P .05). *Means for each group in each subitem of the criteria. †Overall means for the criteria. 4 Accorinte et al. JOE — Volume 34, Number 1, January 2008

Clinical Research testing these procedures under the aforementioned condition to verify the reproducibility of the findings reported in this clinical evaluation. However, although the use of vital healthy teeth for this kind of study has limitations, it still has the benefit of standardization and can be regarded as acceptable in respect to material selection and handling. The histomorphologic features of this study support the fact that MTA can be safely used for pulpal capping of human teeth. MTA seemed to heal the pulp tissue at a faster rate than Ca(OH)2 cement, although after 60 days both materials reached similar and excellent results for pulp capping in human teeth. Acknowledgments This study was partially supported by CNPq Grants (551049/ 2002-2, 350085/2003-0, 302552/2003-0, and 474225-2003-8). References Figure 2. (A) Ca(OH)2, 30 days. Incomplete hard tissue bridge is shown. Observe that the hard tissue bridge is near dentin (white arrows), and there is an intense and acute inflammatory infiltrate with different intensity and extension below the hard tissue bridge (hematoxylin-eosin; original magnification, 40 ). (B) Ca(OH)2, 30 days. Higher magnification of (A). No hard tissue bridge was formed in the the center of the exposure site. There is also no contact between calcium hydroxide cement (above) and the pulp tissue (below) (white arrow). One can also observe an intense and acute inflammatory infiltrate with hyperemic vessels (black arrow) (hematoxylin-eosin; original magnification, 100 ). (C) Ca(OH)2, 60 days. There is a partial, irregular, and thin hard tissue bridge with a communication of the capping material with dental pulp (white arrow) (hematoxylin-eosin; original magnification, 40 ). (D) Ca(OH)2, 60 days. Higher magnification of (C). Observe a partial hard tissue bridge with a communication of the capping material in same points ( black arrow). Observe a chronic inflammatory infiltrate with different intensity and extension (hematoxylin-eosin; original magnification, 100 ). (E) MTA, 30 days. There is a complete and irregular hard tissue bridge (white arrow). Observe irregular hard tissue bridge and chronic inflammatory infiltrate with different intensity and extension (hematoxylin-eosin; original magnification, 40 ) (F) MTA, 30 days. Higher magnification of (E). Although there are irregularities in the hard tissue bridge, a complete hard tissue bridge was formed (white arrow). Observe a chronic inflammatory infiltrate around the exposure site (hematoxylin-eosin; original magnification, 100 ). (G) MTA, 60 days. In this case, complete hard tissue bridge is shown (white arrow). Only chronic inflammatory infiltrate with different intensity and extension can be seen near to dentin walls (black arrow) (hematoxylin-eosin; original magnification, 40 ). (H) MTA, 60 days. Higher magnification of (G). Observe hard bridge tissue (white arrow), new odontoblast layer in contact with hard bridge (black arrow), and normal pulpal tissue near hard bridge tissue (black *) (hematoxylin-eosin; original magnification, 100 ). The results of this study should be carefully evaluated because the capping procedure was accomplished in sound teeth. In most clinical scenarios, the pulp exposure frequently occurs by a carious process in which the level of inflammation is much higher. The ideal would be JOE — Volume 34, Number 1, January 2008 1. Mestrener SR, Holland R, Dezan E Jr. Influence of age on the behavior of dental pulp of dog teeth after capping of an adhesive system or calcium hydroxide. Dent Traumatol 2003;19:255– 61. 2. Pereira JC, Segala AD, Costa CAS. Human pulpal response to direct pulp capping with an adhesive system. Am J Dent 2000;13:139 – 47. 3. Costa CAS, Nascimento ABL, Teixeira HM, Fontana UF. Response of human pulps capped with a self-etching adhesive system. Dent Mater 2001;17:230 – 40. 4. Accorinte MLR, Loguercio AD, Reis A, Muench A, Araújo VC. Response of human pulps capped with a bonding agent after bleeding control with menostatic agents. Oper Dent 2005;30:147–55. 5. Cox CF, Subay RK, Ostro E, Suzuki S, Suzuki SH. Tunnel defects in dentin bridges: their formation following direct pulp capping. Oper Dent 1996;21:4 –11. 6. Cox CF, Hafez AA, Akimoto N, Otsuki M, Suzuki S, Tarim B. Biocompatibility of primer, adhesive and resin composite systems on non-exposed and exposed pulps of non-human primate teeth. Am J Dent 1998;11:S55– 63. 7. Cox CF, Tarim B, Kopel H, Gurel G, Hafez A. Technique sensitivity: biological factors contributing to clinical success with various restorative materials. Adv Dent Res 1998;5:85–90. 8. Torabinejad M, Chivian N. Clinical applications of mineral trioxide aggregate. J Endod 1999;25:197–205. 9. Pitt Ford TR, Torabinejad M, Abedi HR, Bakland LK, Kariyawasam SP. Using mineral trioxide aggregate as a pulp-capping materials. J Am Dent Assoc 1996;127:1491– 4. 10. Faraco Junior IM, Holland R. Response of the pulp of dogs to capping with mineral trioxide aggregate or calcium hydroxide cement. Dent Traumatol 2001;17:163– 6. 11. Aeinehchi M, Eslami B, Ghanbariha M, Saffar AS. Mineral trioxide aggregate (MTA) and calcium hydroxide as pulp-capping agents in human teeth: a preliminary report. Int Endod J 2003;36:225–31. 12. Whitherspoon DE, Small JC, Harris GZ. Mineral trioxide aggregate pulpotomies: a case series outcomes assessment. J Am Dent Assoc 2006;137:610 – 8. 13. Chacko V, Kurikose S. Human pulpal response to mineral trioxide aggregate (MTA): a histological study. J Clin Pediatr Dent 2006;30:203–9. 14. Iwamoto CE, Erika A, Pameijer CH, Barnes D, Romberg EE, Jefferies S. Clinical and histological evaluation of white ProRoot MTA in direct pulp capping. Am J Dent 2006;19:85–90. 15. Roberts HW, Toth JM, Berzins DW, Charlton DG. Mineral trioxide aggregate material use in endodontic treatment: a review of the literature. Dent Mater (in press). 16. Conover WJ. Practical nonparametric statistics. New York: John Willey, 1980: 229 –39. 17. Tziafas D, Pantelidou O, Alvanou A, Belibasakis G, Papadimitriou S. The dentinogenesis effect of mineral trioxide aggregate (MTA) in short-term capping experiments. Int Endod J 2002;35:245–54. 18. Koh ET, McDonald F, Pitt Ford TR, Torabinejad M. Cellular response to mineral trioxide aggregate. J Endod 1998;24:543–7. 19. Seux D, Coulbe ML, Hartmann DJ, Gauthier JP, Magloire H. Odontoblast-like cytodifferentiation of human dental pulp cells in vitro in the presence of a calcium hydroxide-contain cement. Arch Oral Biol 1991;36:117–28. 20. Torabinejad M, Hong CU, McDonald F, Pitt Ford TR. Physical and chemical properties of a new root-end filling material. J Endod 1995;21:349 –53. 21. Stanley HR. Criteria for standardizing and increasing credibility of direct pulp capping studies. Am J Dent 1998;11:S17–34. 22. Min KS, Kim HI, Park HJ, Pi SH, Hong CU, Kim EC. Human pulp cells response to Portland cement in vitro. J Endod 2007;33:163– 6. MTA and Calcium Hydroxide Cement as Pulp-capping Agents 5

Clinical Research 23. Camilleri J, Montesin FE, Brady K, Sweeney R, Curtis RV, Pitt Ford TR. The constitution of mineral trioxide aggregate. Dent Mater 2005;21:297–303. 24. Song J-S, Mante FK, Romanow WJ, Kim S. Chemical analysis of powder and set forms of Portland cement, gray ProRoot MTA, white ProRoot MTA, and gray MTA-Angelus. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006; 102:809 –15. 25. Perez AL, Spears R, Gutmann JL, Opperman LA. Osteoblasts and MG63 osteosarcoma cells behave differently when in contact with ProRoot MTA and white MTA. Int Endod J 2003;36:564 –70. 26. Stanley HR. Pulp capping: conserving the dental pulp— can it be done? is it worth it? Oral Surg Oral Med Oral Pathol 1989;68:628 –39. 6 Accorinte et al. 27. Forsten L, Soderling E. The alkaline and antibacterial effect of seven Ca(OH)2 liners in vitro. Acta Odontol Scand 1984;42:93– 8. 28. Torabinejad M, Hong CU, Pitt Ford TR, Kettering JD. Antibacterial effects of some root end filling materials. J Endod 1995;21:403– 6. 29. Estrela C, Bammann LL, Estrela CR, Silva RS, Pecora JD. Antimicrobial and chemical study of

with calcium hydroxide was slower than that of MTA, both materials were successful for pulp capping in human teeth. (J Endod 2008;34:1-6) Key Words Biocompatibility, calcium hydroxide, human pulp, min-eral trioxide aggregate, pulp capping, pulp therapy T he aim of conservative pulp therapy is to maintain the coronal and radicular pulp

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