Introduction: CPoint is a polymeric endodontic point that takes advantage of water-induced, non-isotropic radial expansion to adapt to canal irregularities. This study evaluated the effects of CPoint on the viability and mineralization potential of odontoblast-like cells.
Methods: The biocompatibility of CPoint and commercially available gutta-percha points was evaluated by using a rat odontoblast-like cell line (MDPC-23). Cell viability was evaluated with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and confocal laser scanning microscopy. The mineralization potential of MDPC-23 cells, in the presence of the root-filling materials, was evaluated by examining the changes in osteogenic gene marker expression (quantitative real-time polymerase chain reaction), alkaline phosphatase activity, alizarin red S assay, and transmission electron microscopy.
Results: CPoint showed higher initial cytotoxicity compared with gutta-percha and Teflon (P < .05), which became nonsignificant after 4 immersion cycles. Significant differences were also found between eluents from CPoint and gutta-percha at 1:1 concentration (P < .05) but not at 1:10 or 1:100 concentration. Both materials induced minimal apoptosis-induced alteration in plasma membrane permeability, as evidenced by flow cytometry and confocal laser scanning microscopy. Compared with the Teflon negative control, CPoint and gutta-percha groups showed up-regulation of most osteogenic gene markers except for dentin sialophosphoprotein, which was down-regulated. Alkaline phosphatase activity and alizarin red assay for CPoint and gutta-percha were both significantly higher than for Teflon but not significantly different from each other (P > .05). Transmission electron microscopy showed discrete nodular electron-dense mineralization foci in all 3 groups.
Conclusions: The in vitro biocompatibility of CPoint is comparable to gutta-percha with minimal adverse effects on osteogenesis after elution of potentially toxic components.
Published by Elsevier Inc.