IADR Abstract Archives
A Road to Tubular Dentin Regeneration: CPNE7 and Functional Peptides
Objectives: Aged odontoblasts at resting phase do not actively react to external stimuli by mineral deposition. Our previous study demonstrated that CPNE7, identified in preameloblast-conditioned medium, induces odontoblast differentiation and mineralization in vitro, and promoted tertiary dentin formation in beagle dog indirect pulp capping model. In this study, we investigated the role of CPNE7 in stimulating physiologic dentin formation using few different tooth defect models, and gauged its weight as a component of dentin matrix proteins.
Methods: Artificial tooth defects in varying depths were generated in beagle premolars. For shallow and deep cavity models, the dentin exposures were capped with GI cement after treating rhCpne7, while for pulp exposure model, GIC filling followed treating rhCPNE7 and MTA. Tertiary dentin formation was histologically evaluated 3 weeks after the experiment. The state of the underlying cells were checked by Tunnel assay. Lastly, the effects of EDTA-soluble dentin matrix proteins (DMPs) with and without neutralizing CPNE7 were also assessed in cavity models.
Results: We observed tertiary dentin formation in both the dentin and pulp exposure models. The regenerated dentin showed the characteristics of physiologic dentin, regardless of the cavity depths. Dentinal tubule structure was clearly observed beneath the remaining dentin, instead of bone-like osteodentin commonly formed in MTA capping. Much less cell death was observed when rhCPNE7 was treated. In the case of DMPs treatment, tubular dentin was regenerated as previously reported. However, the number of dentinal tubules decreased remarkably when CPNE7 was neutralized.
Conclusions: CPNE7 seems to induce both the odontoblast differentiation and reactivation. The depth of cavities, in other words, the extent of the external stimuli determines whether CPNE7 induces pulp stem cells to differentiate into new odontoblasts, or simply reactivates the underlying odontoblasts at resting phase. In both cases, physiologic dentin retaining dentinal tubules were regenerated in vivo.
Methods: Artificial tooth defects in varying depths were generated in beagle premolars. For shallow and deep cavity models, the dentin exposures were capped with GI cement after treating rhCpne7, while for pulp exposure model, GIC filling followed treating rhCPNE7 and MTA. Tertiary dentin formation was histologically evaluated 3 weeks after the experiment. The state of the underlying cells were checked by Tunnel assay. Lastly, the effects of EDTA-soluble dentin matrix proteins (DMPs) with and without neutralizing CPNE7 were also assessed in cavity models.
Results: We observed tertiary dentin formation in both the dentin and pulp exposure models. The regenerated dentin showed the characteristics of physiologic dentin, regardless of the cavity depths. Dentinal tubule structure was clearly observed beneath the remaining dentin, instead of bone-like osteodentin commonly formed in MTA capping. Much less cell death was observed when rhCPNE7 was treated. In the case of DMPs treatment, tubular dentin was regenerated as previously reported. However, the number of dentinal tubules decreased remarkably when CPNE7 was neutralized.
Conclusions: CPNE7 seems to induce both the odontoblast differentiation and reactivation. The depth of cavities, in other words, the extent of the external stimuli determines whether CPNE7 induces pulp stem cells to differentiate into new odontoblasts, or simply reactivates the underlying odontoblasts at resting phase. In both cases, physiologic dentin retaining dentinal tubules were regenerated in vivo.