Induction of S100A7 expression from mechanical stress-induced human dental pulp cells and its effect on osteoclastogenesis

Abstract

Mechanical injuries of dental pulp tissues could lead to root resorption by osteoclast/odontoclast. S100A7 has been demonstrated to involve in inflammatory processes and potentially involved in bone destruction. However, the roles of S100A7 in dental pulp have not been reported. Therefore, this this study aimed to investigate the effect of mechanical stress on S100A7 expression in human dental pulp cells (hDPCs) and to investigate the effect of S100A7 protein on osteoclast differentiation. HDPCs were stimulated with in vitro compressive loading. Cell viability was determined using MTT assay. Real-time PCR (qPCR) and ELISA were utilized to determine the mRNA and protein levels, respectively. Further, osteoclast differentiation assay was performed using primary human monocytes. The differentiation and function of osteoclasts were examined using TRAP staining and resorption pit assay respectively. This study found that compressive mechanical stress did not affect viability of hDPCs while significantly stimulating expression of inflammatory cytokines IL1B, IL6 and VEGF mRNA expression. S100A7 expression in both mRNA and protein levels was significantly increased following mechanical force application of hDPCs. Further, dental pulp tissues from the in vivo mechanical stress treated teeth exhibited higher S100A7 mRNA levels compared with those of the control teeth. S100A7 promoted osteoclast differentiation from primary human monocytes in RANKL- and M-CSF dependent manner. In addition, S100A7 significantly enhanced resorptive pit formation in vitro. RAGE mRNA expression was significantly increased during S100A7-enhanced osteoclast differentiation. In conclusion, mechanical stress induced S100A7 expression in dental pulp and this protein may participate in root resorption via the enhancement of RANKL- and M-CSF- mediated osteoclast differentiation and function.