The clarification of mechanism regulating reparative dentin formation via SIBLING proteins

2018 Fiscal Year Final Research Report

• Project/Area Number: 17K17082
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Morphological basic dentistry
• Research Institution: Niigata University
• Principal Investigator: Saito Kotaro 新潟大学, 医歯学系, 助教 (10733719)
• Project Period (FY): 2017-04-01 – 2019-03-31
• Keywords: 象牙芽細胞 / オステオポンチン / 窩洞形成 / マウス / 器官培養 / DMP1

Outline of Final Research Achievements

This study aimed to elucidate the role of DMP1 and OPN in regulating odontoblast-like cell differentiation following tooth injury. Once preexisting odontoblasts died, Nestin-positive newly differentiated odontoblast-like cells were arranged along the pulp-dentin border and began to express DMP1/Dmp1. In Opn KO mice, the expression of DMP1/Dmp1 was upregulated compared to that of wild-type mice. In vitro assay demonstrated that the gene suppression of Dmp1 by siRNA showed a tendency to decrease the differentiation rate of odontoblast-like cells from 70.1% to 52.2% in wild-type teeth. In addition, the suppression of Dmp1 in Opn KO teeth tended to lead to the inhibition of odontoblast-like cell differentiation. These results suggest that the expression of Dmp1 is upregulated in Opn KO mice both in vivo and in vitro and DMP1 compensate for lack of OPN in regulating odontoblast-like cell differentiation following tooth injury.

Free Research Field

口腔解剖学

Academic Significance and Societal Importance of the Research Achievements

歯の損傷後に新たな象牙質を形成する象牙芽細胞の分化機構の解明は、将来の歯髄再生治療を実現するのに必須の課題である。本研究では、オステオポンチンおよびdentin matrix protein 1(DMP1)に着目し、これらを抑制するマウスモデルおよび培養実験系を用いて、象牙芽細胞の分化率を比較検討した。オステオポンチンおよびDMP1のいずれも、抑制した系において、有意差はないものの、象牙芽細胞の分化率が低下する傾向を示した。この結果から、DMP1およびオステオポンチンは歯の損傷後の象牙芽細胞の分化を制御する重要な因子である可能性が示唆された。