Simvastatin Promotes Dental Pulp Stem Cell-induced Coronal Pulp Regeneration in Pulpotomized Teeth.

INTRODUCTION: Pulpotomy is a specific treatment used to save root pulp, in which only the inflamed coronal pulp is removed and capping materials are placed. Our study aims to study the effect of simvastatin (1) on the proliferation and differentiation of dental pulp stem cells (DPSCs) and (2) on DPSC-induced pulp regeneration after pulpotomy. METHODS: DPSCs were treated with different concentrations of simvastatin. Cell counting kit-8 activity was examined to test cell proliferation, and alkaline phosphatase assays and alizarin red S staining were conducted to examine differentiation. In addition, DPSCs pretreated with simvastatin were transplanted into the dorsum of CB-17 severe combined immunodeficiency mice. Areas of mineralized tissue were compared. Eighteen immature premolars from 2 beagle dogs were divided into 4 groups and treated by pulpotomy: the mineral trioxide aggregate, absorbable gelatin sponge, canine DPSCs (cDPSCs), and simvastatin groups. The teeth were extracted after 10 weeks, and the areas of regenerated pulp and dentin were calculated and compared. RESULTS: Simvastatin at 1 µmol/L suppressed cDPSCs proliferation but significantly increased alkaline phosphatase activity and mineral nodule formation. In addition, cDPSCs pretreated with 1 µmol/L simvastatin formed significantly more mineralized tissue in CB-17 severe combined immunodeficiency mice. In the in vivo study, the ratios of the areas of pulp and dentin regeneration were 47.3% ± 2.5%, 76.8% ± 4.3%, and 85.8% ± 0.9%, respectively, in the absorbable gelatin sponge, cDPSCs, and simvastatin groups. CONCLUSIONS: Simvastatin stimulates cDPSCs mineralization both in vivo and in vitro. It also promotes DPSC-induced pulp and dentin regeneration after pulpotomy.

Combined effects of mineral trioxide aggregate and human placental extract on rat pulp tissue and growth, differentiation and angiogenesis in human dental pulp cells.

OBJECTIVE: The aim of this study was to evaluate the combined effects of mineral trioxide aggregate (MTA) and human placental extract (HPE) on cell growth, differentiation and in vitro angiogenesis of human dental pulp cells (HDPCs) and to identify underlying signal transduction mechanisms. In vivo dental pulp responses in rats for a pulp-capping agent were examined. MATERIALS AND METHODS: MTS assay. ALP activity test, alizarin red S staining and RT-PCR for marker genes were carried out to evaluate cell growth and differentiation. HUVEC migration, mRNA expression and capillary tube formation were measured to evaluate angiogenesis. Signal transduction was analysed using Western blotting and confocal microscopy. The pulps of rat maxillary first molars were exposed and capped with either MTA or MTA plus HPE. Histologic observation and scoring were performed. RESULTS: Compared to treatment of HDPCs with either HPE or MTA alone, the combination of HPE and MTA increased cell growth, ALP activity, mineralized nodules and expression of marker mRNAs. Combination HPE and MTA increased migration, capillary tube formation and angiogenic gene expression compared with MTA alone. Activation of Akt, mammalian target of rapamycin (mTOR), p38, JNK and ERK MAPK, Akt, and NF-κB were significantly increased by combining HPE and MTA compared with MTA alone. Pulp capping with MTA plus HPE in rats showed superior dentin bridge formation, odontoblastic layers and dentinal tubules and lower inflammatory cell response, compared to the MTA alone group. CONCLUSIONS: This study demonstrates for the first time that the use of MTA with HPE promotes cell growth, differentiation and angiogenesis in HDPCs, which were associated with mTOR, MAPK and NF-κB pathways. Direct pulp capping with HPE plus MTA showed superior results when compared with MTA alone. Thus, the combination of MTA and HPE may be useful for regenerative endodontics.

Promotion of Dental Pulp Cell Migration and Pulp Repair by a Bioceramic Putty Involving FGFR-mediated Signaling Pathways.

Mineral trioxide aggregate is the currently recommended material of choice for clinical pulp repair despite several disadvantages, including handling inconvenience. Little is known about the signaling mechanisms involved in bioceramic-mediated dental pulp repair-particularly, dental pulp cell (DPC) migration. This study evaluated the effects of iRoot BP Plus, a novel ready-to-use nanoparticulate bioceramic putty, on DPC migration in vitro and pulp repair in vivo, focusing on possible involvement of fibroblast growth factor receptor (FGFR)-related signaling, including mitogen-activated protein kinase and Akt pathways. Treatment with iRoot BP Plus extracts enhanced horizontal and vertical migration of DPCs, which was comparable with the effects induced by mineral trioxide aggregate extracts. The DPCs exposed to iRoot BP Plus extracts demonstrated no evident apoptosis. Importantly, treatment with iRoot BP Plus extracts resulted in rapid activation of FGFR, p38 mitogen-activated protein kinase, extracellular signal-regulated kinase (ERK) 1/2, c-Jun-N-terminal kinase (JNK), and Akt signaling in DPCs. Confocal immunofluorescence staining revealed that iRoot BP Plus stimulated focal adhesion formation and stress fiber assembly in DPCs, in addition to upregulating the expression of focal adhesion molecules, including p-focal adhesion kinase, p-paxillin, and vinculin. Moreover, activation of FGFR, ERK, JNK, and Akt were found to mediate the upregulated expression of focal adhesion molecules, stress fiber assembly, and enhanced DPC migration induced by iRoot BP Plus. Consistent with the in vitro results, we observed induction of homogeneous dentin bridge formation and expression of p-focal adhesion kinase, p-FGFR, p-ERK 1/2, p-JNK, and p-Akt near injury sites by iRoot BP Plus in an in vivo pulp repair model. These data demonstrate that iRoot BP Plus can promote DPC migration and pulp repair involving the FGFR-mediated ERK 1/2, JNK, and Akt pathways. These findings provide valuable insights into the signaling mechanisms underlying nanoparticulate bioceramic-mediated pulp repair.

Dentinogenic responses after direct pulp capping of miniature swine teeth with Biodentine.

INTRODUCTION: The aim of this study was to evaluate pulpal responses after experimental direct pulp capping of mechanically exposed teeth with a new calcium silicate-based dentin replacement material. METHODS: Thirty-four anterior and posterior teeth of 3 miniature swine were used. Class V or I cavities were prepared on the buccal or occlusal surfaces, respectively. Pulpal exposures were further performed using a round carbide bur 0.8 mm in diameter. Exposures were treated with white MTA Angelus (Angelus, Londrina, PR, Brazil) or Biodentine (Septodont, Saint Maur des Fosses, France), and the cavities were further restored with Biodentine. The pulpal tissue responses were histologically assessed at postoperative periods of 3 and 8 weeks. Data were statistically analyzed using the Kruskal Wallis and the Mann-Whitney U tests. RESULTS: Inflammatory infiltration or pulp tissue necrosis was not found in any of the specimens. All teeth showed mineralized matrix formation in the form of a complete hard tissue bridge composed of osteodentin or osteodentin followed by a discontinuous or continuous reparative dentin zone. A significantly higher thickness of the hard tissue bridge was found in the group of teeth treated with Biodentine at both 3 and 8 weeks. A number of teeth, which were under root development at the onset of the experimental procedures, exhibited ectopic pulp calcification. CONCLUSIONS: The application of both calcium silicate-based materials in direct contact with the mechanically exposed pulp of healthy miniature swine teeth led to pulp repair with complete hard tissue bridge formation. The thickness of hard tissue bridges was significantly higher after pulp capping with Biodentine.

Initial transient accumulation of M2 macrophage-associated molecule-expressing cells after pulpotomy with mineral trioxide aggregate in rat molars.

INTRODUCTION: M2 (alternatively activated) macrophages are known to participate in wound healing and tissue repair. This study aimed to analyze the temporospatial changes in the distribution and density of M2 macrophage-associated molecule-expressing cells after pulpotomy with mineral trioxide aggregate (MTA) in rat molars to ascertain the role played by M2 macrophages in the healing of MTA-capped pulp tissue. METHODS: The maxillary first molars of 8-week-old Wistar rats were pulpotomized and capped with MTA. After 1-14 days, the teeth were examined after hematoxylin-eosin staining or immunoperoxidase staining of CD68 (a general macrophage marker) and M2 macrophage markers (CD163 and CD204). The density of positively stained cells was enumerated in the surface and inner regions (0-100 µm and 300-400 µm, respectively, from the wound surface). RESULTS: MTA capping initially caused mild inflammatory changes and the formation of a degenerative layer followed by progressive new matrix formation and calcified bridging. At 1-2 days, CD68-, CD163-, and CD204-positive cells started to accumulate beneath the degenerative layer, and the density of these cells was significantly higher in the surface region than in the inner region (P < .05). From 7 days onward, the 3 types of cells displayed an almost normal distribution beneath the newly formed dentinlike matrix. CONCLUSIONS: After the pulpotomy of rat molars with MTA, M2 macrophage-associated molecule-expressing cells transiently accumulated beneath the degenerative layer under the MTA. This suggests that M2 macrophages participate in the initial phases of the healing of MTA-capped pulp tissue.

Iloprost induces tertiary dentin formation.

INTRODUCTION: Prostacyclin (PGI2), a member of the prostaglandin family, can promote angiogenesis and cell proliferation. METHODS: In this study, the effect of the application of a PGI2 analog (iloprost) on dentin repair was examined in vitro and in vivo. RESULTS: Iloprost significantly stimulated the expression of vascular endothelial growth factor and osteo-/odontogenic marker messenger RNA in human dental pulp cells (HDPCs) under osteoinductive conditions in vitro. In addition, iloprost enhanced HDPC alkaline phosphatase enzymatic activity and mineral deposition. An in vivo study was performed using a rat molar mechanical pulp exposure model. After 30 days, histologic analysis revealed that there was a dramatic tertiary dentin formation in the iloprost-treated group compared with the calcium hydroxide and the untreated control groups. Furthermore, vascular endothelial growth factor protein expression in dental pulp tissue was increased in the iloprost-treated group as determined by immunohistochemical staining. CONCLUSIONS: Taken together, the present study, for the first time, shows that iloprost induces the expression of osteo-/odontogenic markers in vitro and promotes angiogenic factor expression and enhances tertiary dentin formation in vivo. This implies the potential clinical usefulness of iloprost in vital pulp therapy.

Odontogenic effect of a fast-setting pozzolan-based pulp capping material.

INTRODUCTION: Mineral trioxide aggregate (MTA) is widely used as a pulp capping material. Recently, a MTA-derived fast-setting pozzolan cement (Endocem; Maruchi, Wonju, Korea) was introduced in the endodontic field. Our aim in this study was to investigate the odontogenic effects of this cement in vitro and in vivo. METHODS: Human dental pulp cells (hDPCs) were cultured, and the effects of Endocem and a previously marketed MTA (ProRoot; Dentsply, Tulsa, OK) on biocompatibility were evaluated by assessing cell morphology and performing a cell viability test. Chemical composition of each material was analyzed by energy-dispersive X-ray spectroscopic analysis. Odontoblastic differentiation was analyzed by alkaline phosphatase activity and alizarin red S staining. The expression of odontogenic-related markers, namely dentin sialophosphoprotein, dentin matrix protein 1, and osteonectin, was evaluated by real-time polymerase chain reaction, Western blotting, and immunofluorescence analysis. Pinpoint pulp exposures were made on rat teeth and then capped with ProRoot or Endocem. After 4 weeks, reparative tertiary dentin formation and inflammatory responses were investigated histologically. RESULTS: The biocompatibility of Endocem was similar to that of ProRoot. Energy-dispersive X-ray spectroscopic analysis showed that ProRoot and Endocem contained similar elemental constituents such as calcium, oxygen, and silicon. Alkaline phosphatase activity and mineralized nodule formation increased in ProRoot- and Endocem-treated cells compared with medium only-treated cells in the control group (P < .05). The expression of odontogenic-related markers was significantly higher in the ProRoot- and Endocem-treated groups than the control group (P < .05), but there was no significant difference in the expression of these markers between the 2 experimental groups (P > .05). Four weeks after the pulp capping procedure, continuous tertiary dentin had formed directly underneath the capping materials and the pulp exposure area in all samples in the 2 treated groups. Furthermore, most specimens either had no inflammation or minor pulpal inflammation. CONCLUSIONS: Our results indicate that ProRoot and Endocem have similar biocompatibility and odontogenic effects. Therefore, Endocem is as effective a pulp capping material as ProRoot.

Application of high-frequency radio waves to direct pulp capping.

INTRODUCTION: In vital pulp therapy such as direct pulp capping, clinical success rates depend on achieving hemostasis in exposed pulp tissue. For hemostasis of exposed pulp tissue, gentle pressure by cotton pellets moistened with sodium hypochlorite is most commonly used. However, more rapid and reliable methods are necessary. Therefore, we focused on high-frequency radio waves (HRW). METHODS: To evaluate reparative dentin induction by HRW, we used a rat direct pulp capping model and performed hemostasis by using HRW of several strengths, covering the pulp with calcium hydroxide as a direct capping agent. After 14 or 28 days, rats were killed, and reparative dentin and pulp inflammation were investigated histologically. RESULTS: Radio wave-induced hemostasis required less time when compared with the control group. Reparative dentin with regularly arranged dentinal tubules was observed in the HRW group. CONCLUSIONS: HRW induce hemostasis and produce high-quality reparative dentin and reduced pulpal inflammation.

Mesenchymal stem cells promote hard-tissue repair after direct pulp capping.

INTRODUCTION: The aim of this study was to investigate the potential of autologous mesenchymal bone marrow stem cells (BMSCs) to promote hard-tissue formation after direct pulp capping procedures. MATERIALS AND METHODS: Bone marrow was aspirated from the iliac crest of healthy dogs of nonspecific race. Mononuclear cells were obtained using the Histopaque (Sigma-Aldrich, St Louis, MO) protocol and cultured for 21 days. Direct pulp capping procedures were performed in posterior teeth, and then mineral trioxide aggregate (MTA), hydroxyapatite/tricalcium phosphate, or BMSCs were used as direct pulp capping agents. After 3 months, animals were sacrificed, and jaw segments were processed for radiographic examination using cone-beam computed tomography scanning and histologic examination to assess the formation of a hard-tissue barrier according to a scoring system. RESULTS: The longitudinal and cross-sectional radiophotographs and histologic sections confirmed the formation of an evident calcific barrier after direct pulp capping with MTA and BMSCs. Statistical analysis of the scores given for radiographic and histologic calcific bridge formation showed that both MTA and BMSCs had a comparable tendency to produce a hard-tissue barrier that was significantly higher than hydroxyapatite tricalcium phosphate (P < .05). CONCLUSIONS: Autologous mesenchymal BMSCs were able to promote hard-tissue formation after direct pulp capping procedures.

Fluocinolone acetonide promotes the proliferation and mineralization of dental pulp cells.

INTRODUCTION: The aim of this study was to investigate the role of the steroid fluocinolone acetonide on the proliferation and mineralization of human dental pulp cells (DPCs). The potential effect of fluocinolone acetonide on reparative dentin formation and the recovery of injured dental pulp were evaluated. METHODS: The proliferative effect of fluocinolone acetonide on DPCs was analyzed by cholecystokinin octapeptide assay and flow cytometry. The mineralized effect of fluocinolone acetonide was investigated by the detection of mineralization-related biomarkers including alkaline phosphatase (ALP), bone sialoprotein, and osteocalcin by using ALP histochemical staining, ALP activity, immunostaining, alizarin red staining, and reverse-transcriptase polymerase chain reaction. The molecules, including dentin sialophosphoprotein and Wnt4, involved in the process of mineralization were detected by real-time polymerase chain reaction and Western blot analysis. RESULTS: Low concentrations of fluocinolone acetonide (0.1-40 µmol/L) promoted the proliferation of DPCs. The flow cytometry results showed that the CD146-positive subpopulation of DPCs was significantly increased after treatment with fluocinolone acetonide at 1 and 10 µmol/L for 48 hours, respectively. The messenger RNA expression and activity of the early-stage mineralization marker ALP were evidently increased in fluocinolone acetonide-treated DPCs compared with the untreated control group, so did the middle-stage mineralization marker bone sialoprotein and the late-stage mineralization marker osteocalcin. Meanwhile, Wnt4 and the dentin-specific marker dentin sialophosphoprotein were obviously up-regulated by fluocinolone acetonide compared with the untreated controls. CONCLUSIONS: Fluocinolone acetonide can promote the proliferation of DPCs, especially for the CD146+ subpopulation. Fluocinolone acetonide can initiate the mineralization of DPCs and has the potential role in repairing injured pulp tissues.

MM-MTA for direct pulp capping: a histologic comparison with ProRoot MTA in rat molars.

AIM: To compare the histomorphological response of rat dental pulps capped with MM-MTA and ProRoot MTA at 1, 2 and 4 weeks postoperatively. MATERIALS AND METHODS: Direct pulp capping with MM-MTA and ProRoot MTA, overlaid with light-cured composite resin, was performed on right and left maxillary first molars of 20 Wistar rats. Animals were killed at 1, 2 and 4 weeks postoperatively. Biopsy samples were stained and viewed by light microscopy to determine dentin bridge formation. Data were statistically evaluated with the Kruskal-Wallis test (p < 0.05). RESULTS: Absence of dentin bridge formation at 1 week, partial dentin bridge formation at 2 weeks and complete dentin bridge formation at 4 weeks are observed with MM-MTA and ProRoot MTA. The results showed no statistically significant difference between both materials at 4 weeks. CONCLUSION: Both materials produced similar responses in the pulp when used for pulp capping in intact, caries-free molars of rats.

Biodentine(TM) induces TGF-ß1 release from human pulp cells and early dental pulp mineralization.

AIM: To assess the ability of a recently developed tricalcium silicate-based cement (Biodentine™) to induce reparative dentine synthesis and to investigate its capacity to modulate pulp cells TGF-ß1 secretion. METHODOLOGY: Biodentine™ was directly applied onto the dental pulp in an entire human tooth culture model. After various culture periods, the interaction of the material with dental pulp tissue was analysed on tissue sections. The effect of increasing surface area of this material on TGF-ß1 secretion was investigated on pulp cell cultures and compared with that of MTA, calcium hydroxide and Xeno(®) III adhesive resin. After performing artificial injuries on pulp cell cultures, the materials eluates were added for 24 h and then TGF-ß1 secretion was quantified by ELISA. Controls were performed by incubating intact cells with the culture medium, while injured cells TGF-ß1 level was used as the baseline value. RESULTS: Biodentine™ induced mineralized foci formation early after its application. The mineralization appeared under the form of osteodentine and expressed markers of odontoblasts. Biodentine™ significantly increased TGF-ß1 secretion from pulp cells (P < 0.03) independently of the contact surface increase. This increase was also observed with calcium hydroxide and MTA, but not with the resinous Xeno(®) III. The statistical analysis showed statistically significant differences between capping materials and the resinous Xeno(®) III (P < 0.001). CONCLUSIONS: When Biodentine™ was applied directly onto the pulp, it induced an early form of reparative dentine synthesis, probably due to a modulation of pulp cell TGF-ß1 secretion.

Direct contact with mineral trioxide aggregate activates and differentiates human dental pulp cells.

INTRODUCTION: Mineral trioxide aggregate (MTA) is routinely used for pulp-capping procedures. However, little is known about its direct interaction with the cells or whether MTA is capable of releasing soluble factors that could help in differentiating cells. There have been no previous studies showing this aspect of MTA. Hence, the aim of this study was to determine whether direct contact of the cells with MTA was necessary to help differentiate the pulp cells into odontoblast-like cells. METHODS: Human dental pulp cells were cultured on gray MTA, either in direct contact or away from the cells on a cell culture insert, and the levels of gene expression, secretion of vascular endothelial growth factor (VEGF), and the rates of cell proliferation were analyzed. RESULTS: MTA when placed in direct contact with the cells promoted up-regulated the expression of important odontoblastic genes like osteocalcin and dentin sialoprotein, thereby showing that direct contact of the cells with the MTA is necessary to promote differentiation of the pulp cells into odontoblast-like cells, which in turn are responsible for dentin bridge formation. MTA also induced an increase in the secretion of VEGF when placed in direct contact with the cells. CONCLUSIONS: Overall, our study supports the fact that direct contact of the cells with the MTA is necessary to help differentiate them into odontoblast-like cells, which in turn will lead to a successful treatment outcome.

Apexification of immature teeth with calcium hydroxide or mineral trioxide aggregate: systematic review and meta-analysis.

OBJECTIVE: The aim of this study was to conduct a quantitative systematic review, including published data, comparing the efficacy of mineral trioxide aggregate and calcium hydroxide as material used for the endodontic management of immature teeth. STUDY DESIGN: Relevant studies published through November 2009 were identified through literature searches using Pubmed (Medline) and Scopus databases. Controlled trials in which calcium hydroxide versus mineral trioxide aggregate were used for the apexification of immature permanent teeth were selected for this study. The evaluation included clinical outcome and apical barrier formation. The principal measure of treatment effect was risk difference. The overall effect was tested by using Z score. Heterogeneity was tested by using the χ(2) statistic and I square (I(2)). A fixed-effect model was used when the studies in the subgroup were sufficiently similar. A random-effects model was used in the summary analysis when there was heterogeneity between the subgroups. RESULTS: Based on reduction of relative risk with 95% confidence intervals we found that the rate of clinical success (P = .29) and apical barrier formation (P = .76) of the 2 interventions had no perceivable discrepancy. Regarding success and apical barrier formation, either calcium hydroxide or mineral trioxide aggregate may be used for the apexification of immature teeth.

TEGDMA reduces mineralization in dental pulp cells.

Direct application of dentin bonding agents onto the exposed pulp has been advocated, but in vivo studies indicate a lack of reparative dentin formation. Our objective was to investigate the role of triethylene glycol dimethacrylate (TEGDMA), a commonly used compound in dentin bonding agents, as a potential inhibitor of mineralization. Human pulp cells were exposed to different concentrations of TEGDMA, and expression of the mineralization-related genes collagen I, alkaline phosphatase, bone sialoprotein, osteocalcin, Runx2, and dentin sialophosphoprotein was analyzed. Gene expression studies by real-time polymerase chain-reaction revealed a concentration- and time-dependent decrease of mineralization markers. A subtoxic TEGDMA concentration (0.3 mM) reduced expression levels by 5 to 20% after 4 hrs and by 50% after 12 hrs. Furthermore, alkaline phosphatase activity and calcium deposition were significantly lower in dental pulp cells treated with TEGDMA over 14 days. These findings indicate that even low TEGDMA concentrations might inhibit mineralization induced by dental pulp cells, thus impairing reparative dentin formation after pulp capping with dentin bonding agents.

Efficacy of polyphasic calcium phosphates as a direct pulp capping material.

OBJECTIVES: Polyphasic calcium phosphates (Poly-CaP), a complex of hydroxyapatite (HAp) and soluble calcium phosphates including alpha-tricalcium phosphate and tetracalcium phosphate, demonstrate promoting effects on hard tissue formation by osteoblasts. We hypothesized that a Poly-CaP block with a soluble calcium phosphates phase on one side and an insoluble HAp phase on the other side is useful for vital pulp therapy as it may promote dentin regeneration and provide the surface effective to achieve sealing. The purpose of this study was to investigate the efficacy of Poly-CaP as a direct pulp capping material by examining the Ca-release profile, the in vivo ability to induce reparative dentinogenesis, and the bonding of HAp surface with adhesive systems. METHODS: Poly-CaP prepared by annealing crude HAp disc was immersed in buffer solution at pH 7.4 or 4.0, and the concentration of Ca released was measured until 15 days. The pulp of 9-week-old Wister rat molar was exposed and capped with Poly-CaP or HAp block, and dentin bridge formation and pulpal inflammation was evaluated histopathologically after 2 or 4 weeks. Etch & rinse or self-etching adhesive was bonded to HAp surface, and the interface was observed using SEM. RESULTS: Poly-CaP exhibited continuous release of Ca with significantly greater amount than HAp at both pH conditions (P<0.05, Student's t-test). Animal tests demonstrated formation of complete dentin bridge at higher rate for Poly-CaP compared with HAp after 4 weeks (P<0.05, Steel-Dwass test). Impregnation of resin into etched HAp surface, with production of intimate contact at the bonding interface, was seen for all adhesives. CONCLUSIONS: Poly-CaP is a potentially useful material for direct pulp capping with the advantages to promote dentin bridge formation and to provide tight sealing by adhesives.

Effects of mineral trioxide aggregate on human dental pulp cells after pulp-capping procedures.

INTRODUCTION: Pulp-capping procedures are routinely performed. The control of infection and biocompatibility of the pulp-capping materials are important factors in determining the treatment outcome. Calcium hydroxide has been considered the gold standard for this procedure. However, previous reports have reported the causes of failures with the use of calcium hydroxide. Mineral trioxide aggregate (MTA) has proved to be effective in the process of pulp capping. METHODS: Human dental pulp stromal cells (DPSCs) were cultured on gray MTA, and the levels of gene expression, secretion of vascular endothelial growth factor, and the surface morphology were analyzed. RESULTS: MTA promoted cell survival and proliferation, which was significantly different from the controls in human DPSCs. MTA up-regulated the expression of transcription factors like Runx2 and genes like osteocalcin, alkaline phosphatase, and dentin sialoprotein, which are important odontoblastic genes, thereby showing the ability to promote differentiation of the pulpal cells into odontoblast-like cells, which, in turn, are responsible for dentin bridge formation. MTA approximately induced a 1.7-fold increase in the secretion of angiogenic factors like vascular endothelial growth factor, which is important in the process of tissue healing and regeneration. The differences between the control and the MTA groups were statistically significant. Scanning electron microscopic studies revealed the differences in the surface morphologies between the control and the MTA groups. CONCLUSION: Overall, this study supports the biocompatible nature of MTA and the possible mechanism of dentin bridge formation along with tissue repair, all of which contribute to a successful treatment outcome.

Response of human dental pulp capped with MTA and calcium hydroxide powder.

OBJECTIVES: To compare the response of human dental pulp capped with a mineral trioxide aggregate (MTA) and Ca(OH)2 powder. METHODS AND MATERIAL: Pulp exposures were performed on the occlusal floor of 40 permanent premolars. The pulp was then capped with either Ca(OH)2 powder (CH) or MTA and restored with resin composite. After 30 days (groups CH30 and MTA30) and 60 days (groups CH60 and MTA60), the teeth were extracted and processed for HE and categorized in a histological score system. The data were subjected to Kruskal-Wallis and Conover tests (alpha = 0.05). RESULTS: In regard to dentin bridge formation, CH30 showed a tendency towards superior performance compared to MTA30 (p > 0.05), although the products showed comparable results at day 60. In the item "Inflammation" and "General State of the Pulp" (p > 0.05), CH showed a tendency towards presenting a higher inflammatory response. In the item "Other Pulpal Findings," MTA and Ca(OH)2 showed equal and excellent performance after 30 and 60 days (p > 0.05). CONCLUSION: After 30 days, Ca(OH)2 powder covered with calcium hydroxide cement showed faster hard tissue bridge formation compared to MTA. After 60 days, Ca(OH)2 powder or MTA materials showed a similar and excellent histological response with the formation of a hard tissue bridge in almost all cases with low inflammatory infiltrate.

Micro-tensile bond strength to bovine sclerotic dentine: influence of surface treatment.

OBJECTIVE: The objective of this study was to evaluate the influence of the surface treatment and acid conditioning (AC) time of bovine sclerotic dentine on the micro-tensile bond strength (micro-TBS) to an etch and rinse adhesive system. MATERIALS AND METHOD: Thirty-six bovine incisors were divided into six groups (n=6): G1 sound dentine submitted to AC for 15s; G2-G6 sclerotic dentine: G2-AC for 15s; G3-AC for 30s; G4-EDTA and AC for 15s; G5-diamond bur and AC for 15s; G6-diamond paste and AC for 15s. An adhesive system was applied to the treated dentine surfaces followed by a hybrid composite inserted in increments and light cured. After 24h storage in water at 37 degrees C, the specimens were perpendicularly cut with a low-speed diamond saw to obtain beams (0.8 mm x 0.8 mm cross-sectional dimensions) for micro-TBS testing. Data was compared by ANOVA followed by Tukey's test (p

Formation of dentin-like particles in dentin defects above exposed pulp by controlled release of fibroblast growth factor 2 from gelatin hydrogels.

The induction of dentin formation on exposed dental pulp is a major challenge in research on the regeneration of the dentin-pulp complex. We examined the effects of fibroblast growth factor 2 (FGF2), which was delivered in either a collagen sponge (noncontrolled release) or incorporated into gelatin hydrogels (controlled release), on the formation of dentin in exposed rat molar pulps. During the early phase of pulp wound healing, pulp cell proliferation and invasion of vessels into dentin defects above exposed pulp were induced in both groups. In the late phase, the induction of dentin formation was distinctly different between the 2 types of FGF2 release. The noncontrolled release of free FGF2 from collagen sponge induced excessive reparative dentin formation in the residual dental pulp, although dentin defects were not noted. In contrast, controlled release of FGF2 from gelatin hydrogels induced the formation of dentin-like particles with dentin defects above exposed pulp. These results suggest the possibility of a novel therapeutic approach for dentin-pulp complex by controlled release of bioactive FGF2.