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Updated: Apr 8, 2026
Polarization and Characterization of M1 and M2 Human Monocyte-Derived Macrophages on Implant Surfaces
Published on: December 6, 2024
M1-like Macrophage Polarization Promotes Orthodontic Tooth Movement
1Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, P.R. China Center for Craniofacial Stem Cell Research and Regeneration, Peking University School and Hospital of Stomatology, Beijing, P.R. China.
Abstract:
Macrophages play a crucial role in inflammatory-mediated bone loss. Orthodontic tooth movement (OTM) is associated with inflammatory bone remodeling. However, whether and how macrophages contribute to mechanical force-induced OTM remains unknown. In this study, we hypothesized that polarization of M1-like macrophages may contribute to the OTM. Orthodontic nickel-titanium springs were applied to the upper first molars of rats or mice to induce OTM. The distance of OTM gradually increased after mechanical force was applied to the rats for 5 and 10 d. M1-like macrophage polarization and expression of M1 cytokine tumor necrosis factor (TNF)-α also increased after force application. More importantly, monocyte/macrophage depletion in mice by injection of clodronate liposomes decreased the distance of OTM and the number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts and CD68(+) macrophages, accompanied by reduced expressions of M1 markers TNF-α and inducible nitric oxide synthase (iNOS), whereas systemic transfusion of M1 macrophages in mice increased them. Further experiments showed that injection of recombinant TNF-α increased the distance of OTM and the number of TRAP-positive osteoclasts and CD68(+) macrophages, as well as upregulated the expression of TNF-α and iNOS. Blockage of TNF-α by etanercept injection reduced the distance of OTM and the number of TRAP-positive osteoclasts and CD68(+) macrophages, as well as decreased the levels of TNF-α and iNOS. These data suggest that M1-like macrophage polarization promotes alveolar bone resorption and consequent OTM after mechanical force application.
Insights
M1-like macrophage polarization drives bone loss during orthodontic tooth movement. Inhibiting tumor necrosis factor-alpha (TNF-α) reduces this effect, suggesting a therapeutic target for orthodontic treatment.
Area of Science:
- Immunology
- Orthodontics
- Bone Biology
Background:
- Macrophages are key players in inflammatory bone loss.
- Orthodontic tooth movement (OTM) involves inflammatory bone remodeling, but the role of macrophages is unclear.
Purpose of the Study:
- To investigate the role of M1-like macrophage polarization in mechanical force-induced OTM.
- To explore the involvement of tumor necrosis factor-alpha (TNF-α) in this process.
Main Methods:
- Mechanical force was applied to induce OTM in rats and mice.
- Monocyte/macrophage depletion and M1 macrophage transfusion were performed.
- Levels of M1 markers (TNF-α, iNOS) and osteoclast activity (TRAP) were assessed.
- Recombinant TNF-α and etanercept (TNF-α inhibitor) were administered.
Main Results:
- OTM distance, M1 macrophage polarization, and TNF-α expression increased with mechanical force.
- Macrophage depletion reduced OTM and osteoclast formation, while M1 transfusion exacerbated it.
- TNF-α administration increased OTM, and etanercept treatment reduced it.
Conclusions:
- M1-like macrophage polarization promotes alveolar bone resorption and OTM.
- TNF-α signaling is a critical mediator in this process, representing a potential therapeutic target.
