Nrf2 activation attenuates both orthodontic tooth movement and relapse

Area of Science:

• Biomedical Science
• Orthodontics
• Cell Biology

Background:

• Osteoclast-mediated bone resorption drives tooth movement in orthodontics.
• Reactive oxygen species (ROS) are key signaling molecules in osteoclastogenesis.
• The Nrf2 pathway regulates cellular antioxidant defenses against oxidative stress.

Purpose of the Study:

• To investigate the effect of Nrf2 activation on osteoclastogenesis.
• To evaluate the impact of Nrf2 activators on orthodontic tooth movement and relapse in vivo.
• To explore Nrf2 activation as a potential therapeutic strategy in orthodontics.

Main Methods:

• In vitro: RAW264.7 cells treated with RANKL and Nrf2 activators (SFN, EGCG) or ROS scavenger (catechin). Assessed osteoclastogenesis, resorption, gene expression, and intracellular ROS.
• In vivo: Mouse model with palatal movement of maxillary first molars using NiTi wire. Weekly injections of SFN or EGCG into palatal gingiva.
• Quantified tooth movement and relapse using stone models.

Main Results:

• SFN and EGCG significantly inhibited RANKL-induced osteoclastogenesis and reduced intracellular ROS in vitro.
• These compounds augmented Nrf2 nuclear translocation and increased antioxidant enzyme expression (HO-1).
• In vivo, SFN and EGCG significantly inhibited orthodontic tooth movement, and SFN also reduced relapse.

Conclusions:

• Nrf2 activation effectively suppresses osteoclastogenesis and oxidative stress.
• Nrf2 activators show potential for enhancing anchorage during orthodontic treatment.
• Pharmacological activation of Nrf2 may serve as a method for retention against orthodontic relapse.