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Updated: Jun 24, 2026

Studying Orthodontic Tooth Movement in Mice
Published on: August 2, 2024
Orthodontic force stimulates eNOS and iNOS in rat osteocytes.
S D Tan1, R Xie, J Klein-Nulend
1Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam and VU University Amsterdam, Research Institute MOVE, Amsterdam, The Netherlands.
Nitric oxide synthases, endothelial (eNOS) and inducible (iNOS), play key roles in bone remodeling during orthodontic tooth movement. eNOS is linked to bone formation under tension, while iNOS is associated with bone resorption under compression.
Area of Science:
- Orthodontics
- Bone Biology
- Cell Signaling
Background:
- Mechanosensitive osteocytes are crucial for bone remodeling.
- Nitric oxide (NO), produced by osteocytes via eNOS and iNOS, regulates bone remodeling.
- The specific roles of eNOS and iNOS in response to orthodontic forces are not fully understood.
Purpose of the Study:
- To investigate the expression of eNOS and iNOS in osteocytes during orthodontic force application.
- To determine the distinct roles of eNOS and iNOS in mediating bone tissue responses to orthodontic forces.
Main Methods:
- Orthodontic force (10 cN) was applied to rat molars using NiTi coil springs for 120 hours.
- Immunohistochemistry was used to detect eNOS and iNOS expression in osteocytes in tension and compression areas.
- A split-mouth design was employed for the study.
Main Results:
- In the tension area, eNOS-positive osteocytes increased from 24 hours, while iNOS remained constant.
- In the compression area, iNOS-positive osteocytes increased after 6 hours, and eNOS-positive osteocytes increased after 24 hours.
- Differential expression patterns suggest distinct roles for eNOS and iNOS in response to mechanical stress.
Conclusions:
- eNOS appears to mediate bone formation in the tension zone during orthodontic tooth movement.
- iNOS seems to mediate inflammation-induced bone resorption in the compression zone.
- Both eNOS and iNOS are important regulators of osteocyte-mediated bone remodeling under orthodontic forces.
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