Abstract
The purpose of this study was to investigate the effects of calcium carbonate (CaCO3) on the mineralization ability of human dental pulp (HDP) cells and rat molars.in-vivo HDP cellsHDP cells were treated with 1 mM, 100 mM, 10 mM and 1 mM of CaCO3 forupto12days.Nontreated cells served as a control. The cytotoxicity effect on HDP cells were not detected by treatment with each concentration CaCO3. The cell productivity on HDP cells were highest in culture s treated with 10 mM-CaCO3 group. We compared the alkaline phosphatase (ALP) staining and ALP activity of treatment with each concentration CaCO3 group and control. A larger number of 10 mM-CaCO3 group showed positive on ALP staining than other groups. The ALP activity was also highest in cultures treated with 10 mM-CaCO3 group. These results suggested that the mineralization ability of HDP cells were enhanced by treatment with 10 mM-CaCO3 group.in vitro rat molarsThe result of the CaCO3 treatment was then compared with Calvital. Micro computerized tomography (micro CT), hematoxylin and eosin stained (H & E) and immunoreactivity for nestin, dentin matrix protein-1 (DMP-1) and osteopontin (OPN) were also analyzed. The increment of dentine like calcified tissue in the pulp was observed micro CT and H&E stained. Immunoreactivity of nestin was earlier in the moderate inflammation in the CaCO3 groups than the calvital groups.In the CaCO3 groups, immunoreactivity of DMP-1 was identified beneath the amputated site after 7days, and which activity were increasing until 28 days, and OPN was observed in the dentine-like bridge at 28 days, which was also similar to the calvital groups. These findings suggested that primary processes of reparative dentinogenesis after pulpotomy with CaCO3 may involve natural pulpal wound-healing mechanisms that are similar to the restitution processes observed during pulpotomy with calvital. However, CaCO3 may prove to be less irritation and more calcified tissue formation than traditional Ca(OH)2 based materials when used as pulpotomy agent.