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Updated: Jan 25, 2026

Studying Orthodontic Tooth Movement in Mice
Published on: August 2, 2024
Tooth Movement Modulation and Root Protection via Piezo1-Mediated Production of Superoxide Dismutase 3
Xiaomeng Dong1,2, Yujie Zhu1, Bin Li1
1State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Superoxide dismutase 3 (SOD3) plays a key role in alveolar bone remodeling and cementum repair during orthodontic tooth movement. SOD3 protects roots from resorption by promoting bone and cementum formation while inhibiting bone breakdown.
Area of Science:
- Biomedical Engineering
- Orthodontics
- Cell Biology
Background:
- Alveolar bone remodeling and cementum repair are critical processes during orthodontic tooth movement.
- Superoxide dismutase 3 (SOD3) is an antioxidant enzyme with potential roles in tissue repair and regeneration.
Purpose of the Study:
- To investigate the role of SOD3 in alveolar bone remodeling and cementum repair under orthodontic loading.
- To elucidate the signaling pathways involved in SOD3 production in periodontal ligament cells (PDLCs).
Main Methods:
- Mice models of tooth movement were used with or without adenovirus-mediated SOD3 treatment.
- PDLCs were cultured under mechanical loading and treated with Piezo1 or YAP inhibitors.
- In vitro cell cultures (MC3T3-E1, BMSCs, OCCM-30, BMMs, RAW264.7) were used to assess osteogenic and osteoclastogenic markers with recombinant SOD3 (rmSOD3).
Main Results:
- Orthodontic loading increased SOD3 expression in the periodontal ligament (PDL), potentially mediated by Piezo1 and YAP signaling.
- Exogenous rmSOD3 promoted osteoblastogenesis, enhanced cementoblast differentiation and mineralization, and inhibited osteoclastogenesis.
- SOD3 overexpression in the PDL reduced root resorption and slowed orthodontic tooth movement.
Conclusions:
- Piezo1-mediated SOD3 production in PDLCs protects the root from resorption.
- SOD3 retards orthodontic tooth movement by suppressing osteoclastogenesis and promoting osteoblast and cementoblast differentiation.
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