Dental Pulp Stem Cells Orchestrate Macrophage Polarisation in Pulpitis via Mitochondrial Transfer
Xiaoqian Gong1, Lisha Zhu1, Can Wang1
1Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Tongji Research Institute of Stomatology, Department of Implantology, Shanghai Tongji Stomatological Hospital and Dental School, Tongji University, Shanghai, China.
International Endodontic Journal
|January 11, 2026
Summary
Mitochondrial transfer from dental stem cells to macrophages reduces inflammation and promotes healing in pulpitis. Enhancing this transfer alleviates pulpal inflammation and aids tissue repair.
Area of Science:
- Immunology
- Stem Cell Biology
- Dental Research
Background:
- Pulpitis is a common dental condition involving macrophages and dental pulp stem cells (DPSCs).
- Mesenchymal stem cells regulate immunity via mitochondrial transfer, a mechanism unexplored in pulpitis.
- DPSCs are crucial for pulp repair and immune regulation.
Purpose of the Study:
- To investigate the role of mitochondrial transfer between DPSCs and macrophages in pulpitis.
- To determine how mitochondrial transfer influences macrophage polarization and pulpitis progression/resolution.
Main Methods:
- Lipopolysaccharide-stimulated cocultures of DPSCs and macrophages were used to study mitochondrial transfer.
- Macrophage polarization, mitochondrial function, and immunometabolic profiles were analyzed.
- Inhibition and enhancement of mitochondrial transfer were performed using pharmacological agents.
- Experiments utilized human dental pulp explants and rat pulpitis models.
Main Results:
- Mitochondrial transfer from DPSCs to macrophages decreased during inflammation.
- Inhibiting transfer worsened M1 macrophage polarization; enhancing it promoted M2 polarization.
- Mitochondria-receiving macrophages showed enhanced M2 polarization and improved function.
- Augmenting mitochondrial transfer alleviated pulpitis and promoted repair in preclinical models.
Conclusions:
- Mitochondrial transfer via tunnelling nanotubes improves macrophage metabolic profiles.
- Enhanced DPSC-to-macrophage mitochondrial transfer promotes M2 polarization, reducing inflammation and aiding pulp repair.
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