Table 1.

Therapeutic targets for ferroptosis in osteoporosis and periodontitis.

Drugs	Mechanism for the treatment of osteoporosis	RCD	Drugs	Mechanism for the treatment of periodontitis
tFNA-Cur	A nanoparticle formulation. Activates the Nrf2/GPX4, enhances curcumin bioavailability and stability, and mitochondrial function. Inhibits ferroptosis in BMSCs. Promotes osteogenic differentiation.Stimulates bone formation.	Ferroptosis	Ssa	Promotes E lipid peroxidation and mitochondrial damage. Inhibits osteoclast differentiation and function. Includes the Nrf2/SCL7A11/GPX4, which regulates the cellular antioxidant response and ferroptosis.
FtMt	Mitigates ROS accumulation and protects osteoblasts.	Ferroptosis	Liproxstatin-1	Alleviates bone resorption and inflammation.
Metformin	Inhibits osteoblast ferroptosis. Runx2/Cbfa1 and AMPK activate metformin.	Ferroptosis	Ferrostatin-1	Stimulates osteogenesis.
2ME2	HIF-1α inhibitor. Induces osteoclast ferroptosis and delays bone mass loss.	Ferroptosis	Resveratrol	Restores SLC7A11/GPX4 axis. Reduces pro-inflammatory expression.
EC-Exos	Rescue osteoblasts、protect bone microstructure.	Ferroptosis	IL-17	Involve the interaction of pSTAT3(with nuclear factor NRF2).
ATF3	Suppresses system Xc-.	Ferroptosis
Melatonin	Activates the Nrf2/HO-1 pathway. Protects bone microarchitecture.	Ferroptosis
ICA	Reduces iron deposition, ROS, geneBax, and SLC7A1-1 and upregulates the Nrf2, GPX4, Nrf2, and Runx2. Increases trabecular bone density, accelerates callus formation, and facilitates the transition from fibrous to osseous callus.