Journal of Material Sciences & Engineering

Magnesium Chloride Mediates Dentinogenesis in Normal Human Dental Pulp Cells via Activation of the p38 Mitogen-activated Protein Kinase/BMP-2/SMADs Signaling Pathways: An In Vitro Study

Abstract

Rania M Salem, Chang Zhang , Laisheng Chou

Up-regulation of odontogenic differentiation and dentin formation in dental pulp are key factors in vital pulp therapy. In previous work, magnesium chloride (MgCl2 ) has been contemplated for its potentiality of enhancing cell attachment, proliferation rate and expression of dentin matrix proteins of normal human dental pulp cells (HDPCs). However, the mechanism by which MgCl2 stimulates p38 mitogen-activated protein kinase (p38MAPK)/bone morphogenic protein (BMP-2)/SMADS signaling pathways in dental repair remains rather obscure. This study was designed to study and compare the stimulatory effect of different concentrations of MgCl2 on expression of BMP-2, SMADs 1/5/9, phosphorylated p38 (p-p38), and non-phosphorylated p38 MAPK in signal transduction pathways of HDPCs. HDPCs were cultured with 0.5 mm, 1 mm, 2 mm, 4m m, 8mm concentrations of supplemental MgCl2 , 0 mm as the negative control group. Statistical analysis using Multi-Way Analysis of Variance (MANOVA) with Wilks’ lambda test. Results showed that 0.5, 1 mm, and 2mm supplemental MgCl2 concentrations elicited the highest up regulatory effect on expression of BMP-2, phosphorylated SMADs 1/5/9, p-p38 compared to the negative control all time points (P<0.0001). However, 4 mm and 8 mm supplemental MgCl2 concentrations downregulated BMP-2, phosphorylated SMADs 1/5/9, p-p38 expression at all-time intervals (P<0.0001). This is the first study to report that MgCl2 at the optimal concentrations of 0.5 mm-2 mm might stimulate the differentiation of HDPCs via p38 mitogenactivated protein kinase (p38MAPK)/bone morphogenic protein (BMP-2)/SMADS signaling pathways.