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Studying Orthodontic Tooth Movement in Mice
Published on: August 2, 2024
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Macrophages mediate corticotomy-accelerated orthodontic tooth movement
Yan Wang1,2,3, Hanwen Zhang4, Wen Sun1
1Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China.
Scientific Reports
|November 16, 2018
Summary
Surgical corticotomy accelerates orthodontic tooth movement (OTM) by recruiting macrophages. These immune cells polarize to M1 and M2 phenotypes, promoting osteoclastogenesis and enhancing OTM, with key roles for TNF-α, NF-κB, and JAK/STAT3 signaling pathways.
Area of Science:
- Oral and Maxillofacial Surgery
- Orthodontics
- Immunology
- Cellular and Molecular Biology
Background:
- Surgical corticotomy is known to accelerate orthodontic tooth movement (OTM).
- The precise cellular and molecular mechanisms driving corticotomy-assisted OTM are not fully understood.
- Macrophages are implicated in bone remodeling and inflammation, suggesting a potential role in OTM.
Purpose of the Study:
- To investigate the role of macrophages in corticotomy-assisted orthodontic tooth movement (OTM).
- To elucidate the molecular signaling pathways involved in macrophage recruitment and polarization post-corticotomy.
- To determine the impact of macrophage depletion on corticotomy-enhanced OTM.
Main Methods:
- Orthodontic springs applied to induce OTM in rats/mice, with and without corticotomy.
- Macrophage depletion using liposome-encapsulated clodronate.
- Analysis of macrophage polarization (M1/M2 phenotypes) and signaling pathways (NF-κB, JAK/STAT3) via in vitro co-culture experiments.
Main Results:
- Corticotomy significantly enhanced OTM distance by inducing osteoclastogenesis and macrophage infiltration.
- Macrophages polarized from an M1 to an M2 phenotype during OTM, influenced by TNF-α.
- Depletion of macrophages markedly reduced corticotomy-enhanced OTM, confirming their critical role.
Conclusions:
- Corticotomy promotes OTM by orchestrating macrophage infiltration and polarization.
- Macrophage polarization involves sequential activation of NF-κB (M1) and JAK/STAT3 (M2) signaling pathways.
- These macrophage-mediated processes contribute to OTM by stimulating inflammatory cytokines and osteoclastogenesis.
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