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Facilitating Reparative Dentin Formation Using Apigenin Local Delivery in the Exposed Pulp Cavity
Yam Prasad Aryal1, Chang-Yeol Yeon1, Tae-Young Kim1
1Department of Biochemistry, School of Dentistry, IHBR, Kyungpook National University, Daegu, South Korea.
Frontiers in Physiology
|December 27, 2021
Summary
Apigenin, a natural flavone, promotes dentin regeneration in mice by reducing inflammation and activating key signaling pathways. This natural compound shows potential for treating exposed pulp injuries.
Area of Science:
- Biomaterials Science
- Regenerative Medicine
- Dental Research
Background:
- Apigenin, a flavone, influences cell signaling, inflammation, and proliferation.
- Dental pulp exposure necessitates effective strategies for pulp repair and dentin regeneration.
- Understanding apigenin's role in modulating pulpal inflammation and tertiary dentin formation is crucial.
Purpose of the Study:
- To investigate the detailed function of apigenin in regulating pulpal inflammation and tertiary dentin formation.
- To examine the effect of apigenin on pulp and dentin regeneration using in vitro and in vivo models.
Main Methods:
- In vitro cultivation of human dental pulp stem cells (hDPSCs) with apigenin.
- In vivo application of apigenin to mechanically exposed mouse molar pulp.
- Histology, immunostainings, and Micro-CT imaging to assess pulpal and dentin changes.
Main Results:
- Apigenin upregulated bone morphogenetic protein (BMP)- and osteogenesis-related signaling molecules in hDPSCs.
- Apigenin modulated inflammatory markers (TNF-α, MPO) and regenerative markers (NESTIN, TGF-β1) in vivo.
- Apigenin treatment facilitated significant dentin-bridge formation and confirmed by Micro-CT.
Conclusions:
- Apigenin promotes reparative dentin formation by modulating inflammation and activating signaling pathways.
- Apigenin is a potential therapeutic agent for regenerating dentin in exposed pulp conditions.
- Further research into apigenin's clinical application for dental caries and traumatic injuries is warranted.
