Table 2.

Therapeutic targets for RCD in osteoporosis and periodontitis.

Drugs	Mechanism for the treatment of osteoporosis	RCD	Drugs	Mechanism for the treatment of periodontitis
COX19, MAP-2K2, FDX1	Strongly correlated with immune cell infiltration and associated with osteoporosis prognosis.	Cuproptosis	ME-344, NV-128, RILUZOLE	Demonstrated good affinity for target genes(SLC7A11, SLC3A-2, RPN1, NCKAP1, LRPPRC, NDUFS1).
TXNRD1 inhibitors	Increases bone cystine content, reduces osteoclast numbers, and mitigates bone loss.	disulfidptosis	Target molecules	MLKL, DCN, IL1B, and IL18. Reduce inflammation and tissue destruction.
PGRMC2	Modulates the differentiation of monocytes into macrophages and influences BM-MSC behavior.	disulfidptosis	ZBP1 Inhibitor	Reduces inflammatory cytokine secretion and cell death.
BMDMs	Essential cells in macrophage activation and osteolysis.	PANoptosis	Caspase-1 Inhibitor	Alleviate inflammation and tissue damage.
Apelin-13	Regulates autophagy, apoptosis, and inflammation, exerting multifaceted protective effects on bone.	PANoptosis	RIPK1/3 Blockor	Prevents necroptotic cell death and subsequent inflammation.
		PANoptosis	CEBPG, TFA-P2C, BNIP3	Tissue biomarkers for periodontitis.
		PANoptosis	TTM	Promotes autophagosome formation and enhances mitophagy-related gene expression, while counteracting LPS-induced suppression of autophagic flux. Mitigates LPS-induced lysosomal dysfunction. Increases lysosomal membrane permeability and the secretion of cathepsin B. Enhances autophagic flux and lowers cathepsin B levels.