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Related Experiment Video

Updated: Nov 1, 2025

Author Spotlight: Comparing Alveolar and Long Bone Remodeling to Explore OTM Model Potential
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FOXO3 Mediates Tooth Movement by Regulating Force-Induced Osteogenesis.

A Jin1, Y Hong1, Y Yang1

  • 1Center of Craniofacial Orthodontics, Department of Oral and Craniomaxillofacial Science, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, College of Stomatology, Shanghai Jiao Tong University, National Center for Stomatology, National Clinical Research Center for Oral Diseases, Shanghai Key Laboratory of Stomatology, Shanghai, China.

Journal of Dental Research
|June 23, 2021
PubMed
Summary
This summary is machine-generated.

Forkhead box O3 (FOXO3) is crucial for orthodontic tooth movement (OTM). This protein responds to mechanical force, promoting bone remodeling and osteogenesis essential for effective orthodontic treatments.

Keywords:
bone remodelingcell differentiationforkhead box protein O3mechanotransductionmesenchymal stem cellsorthodontics

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Area of Science:

  • Biomedical Engineering
  • Orthodontics
  • Cell Biology

Background:

  • Increasing demand for orthodontic treatments due to high malocclusion prevalence.
  • Understanding mechanical force-induced alveolar bone remodeling in orthodontic tooth movement (OTM) is key.
  • Bone mesenchymal stem cells (BMSCs) are vital for bone remodeling and sensing mechanical forces.

Purpose of the Study:

  • To identify the key factor mediating mechanical force-induced osteogenesis during OTM.
  • To investigate the role of forkhead box O3 (FOXO3) in mechanical force-induced osteoblastic differentiation of BMSCs.

Main Methods:

  • Reverse-phase protein arrays on BMSCs exposed to mechanical force.
  • In vivo inhibition of FOXO3 using repaglinide.
  • In vitro knockdown and overexpression of FOXO3 in BMSCs.
  • Analysis of FOXO3 cooperation with RUNX2 in osteocalcin transcription.

Main Results:

  • FOXO3 expression significantly upregulated during mechanical force-induced osteoblastic differentiation of BMSCs.
  • FOXO3-positive cells were higher on the OTM side, correlating with enhanced osteogenesis.
  • Inhibiting FOXO3 delayed OTM and impaired bone formation; FOXO3 knockdown inhibited differentiation, while overexpression enhanced it.
  • FOXO3 promotes osteocalcin transcription by cooperating with RUNX2.

Conclusions:

  • FOXO3 is critical for OTM, responding to mechanical force.
  • FOXO3 directly regulates downstream osteoblastic differentiation.
  • FOXO3 plays a significant role in mechanical force-induced osteogenesis during OTM.