Heparin is biocompatible and can induce differentiation of human dental pulp cells.

AIM: To investigate the biocompatibility, osteogenic bioactivity and mRNA expression of the osteo/odontogenic markers bone morphogenetic protein 2 (BMP-2), osteocalcin (OC) and alkaline phosphatase (ALP), induced by heparin in human dental pulp cells (hDPCs). METHODOLOGY: hDPCs were exposed to the heparin, and cell viability was assessed by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT), and cell death was evaluated by flow cytometry. Osteogenic bioactivity was evaluated by the alkaline phosphatase (ALP) assay, and the detection of calcium deposits by alizarin red staining (ARS). The gene expression of BMP-2, OC and ALP was quantified with real-time PCR. Statistical analysis was performed with ANOVA and Bonferroni or Tukey post-test and t-test (α = 0.05). RESULTS: Heparin had no cytotoxic effect and did not induce apoptosis. After 3 days, heparin had significantly higher ALP activity in comparison with the control (P < 0.05). Heparin had a significant (P < 0.05) stimulatory effect on the formation of mineralized nodules. BMP-2 and OC mRNA expressions were significantly higher in cells exposed to heparin than control group after 1 day (P < 0.05). CONCLUSIONS: Heparin was biocompatible in hDPCs, induced osteogenic bioactivity and enhanced mRNA expression of osteo/odontogenic markers BMP-2 and OC. These results suggest that heparin has potential to induce osteo/odontogenic cell differentiation of hDPCs.

Human dental pulp cells response to mineral trioxide aggregate (MTA) and MTA Plus: cytotoxicity and gene expression analysis.

AIM: To investigate the cytotoxicity, osteogenic bioactivity and mRNA expression of osteogenic markers of bone morphogenetic protein 2 (BMP-2), osteocalcin (OC) and alkaline phosphatase (ALP) induced by the extracts of set MTA Plus (MTA P) (Avalon Biomed Inc. Bradenton, FL, USA) in comparison with MTA (Angelus, Londrina, PR, Brazil) on human dental pulp cells (hDPCs). METHODOLOGY: Cell viability was assessed by mitochondrial dehydrogenase enzymatic (MTT) assay, and the mechanism of cell death was evaluated by flow cytometry. Bioactivity was evaluated by alkaline phosphatase (ALP) assay and detection of calcium deposits with alizarin red staining (ARS). The gene expression of BMP-2, OC and ALP was quantified with real-time PCR. Statistical analysis was performed with analysis of variance and Bonferroni or Tukey post-test (α = 0.05). RESULTS: MTA and MTA P were not cytotoxic and did not induce apoptosis. MTA P had significant higher ALP activity in relation to MTA and the control (P < 0.05). MTA had a significantly higher percentage of mineralized area than MTA P (P < 0.05). The expression of BMP2 and OC mRNA was significantly higher in cells exposed to MTA than MTA P after 1 day (P < 0.05). At day 3, the mRNA expression of ALP was significantly higher in MTA P compared with MTA (P < 0.05). CONCLUSIONS: MTA and MTA Plus were noncytotoxic, increased mineralization processes in vitro and induced the expression of osteogenic markers.