Related Experiment Videos
Compressive force induces osteoblast apoptosis via caspase-8
1Division of Orthodontics and Dentofacial Orthopedics, Department of Oral Health and Development Sciences, School of Dentistry, Tohoku University, 4-1 Seiryo-cho, Aoba-ku, Sendai 980-8575, Japan. goga@mail.tains.tohoku.ac.jp
Journal of Dental Research
|February 25, 2006
Summary
Excessive orthodontic force causes cell death. Compressive force induces apoptosis in human osteoblast-like cells via caspase-8 signaling, impacting periodontal remodeling during tooth movement.
Area of Science:
- Biomedical Engineering
- Cell Biology
- Orthodontics
Background:
- Periodontal remodeling is essential for orthodontic tooth movement.
- Excessive orthodontic forces can lead to cell death in periodontal tissues.
- The specific mechanisms of cell death induced by compressive forces are not fully understood.
Purpose of the Study:
- To investigate whether continuous compressive force induces apoptosis in human osteoblast-like cells (MG-63 cells) in vitro.
- To elucidate the signaling pathway involved in compressive force-induced apoptosis.
Main Methods:
- Application of continuous compressive force to MG-63 cells in vitro.
- Assessment of cell viability and morphology.
- TUNEL assay to quantify apoptosis.
- Measurement of caspase-3 activity and evaluation of inhibitor effects (caspase-8 and caspase-9 inhibitors).
Main Results:
- Compressive force caused irregular cell alignment and decreased cell viability.
- TUNEL analysis revealed a time- and force-dependent increase in apoptotic cells.
- Caspase-3 activity increased with compressive force magnitude.
- Caspase-8 inhibition significantly reduced caspase-3 activity, while caspase-9 inhibition had no effect.
Conclusions:
- In vitro application of compressive force induces apoptosis in MG-63 cells.
- Apoptosis is mediated through the activation of caspase-3 via the caspase-8 signaling cascade.
- Findings provide insights into the cellular mechanisms underlying orthodontic force-induced tissue remodeling and potential cell death.