TABLE 2.

Overview of key regulated cell death (RCD) pathways involved in osteomyelitis.

Pathway	Core molecular features/mediators	Major cellular effects in osteomyelitis	References
Apoptosis	Activation of caspase family; formation of apoptotic bodies	Loss of osteoblasts; regulation of immune cell function; resolution (or delay) of inflammation	Josse et al. (2015), Wen et al. (2024), Robinson et al. (2018)
Pyroptosis	Inflammasomes (e.g., NLRP3); Caspase-1/4/5/11; GSDMD; release of IL-1β/IL-18	Intense inflammatory response; cytokine release; enhanced bone resorption and tissue damage	Gao et al. (2025a), Vasudevan et al. (2023), Chen et al. (2024d), Wu et al. (2021)
Ferroptosis	Iron accumulation; lipid peroxidation; dysfunction of GPX4/SLC7A11	Plasma membrane damage; release of inflammatory mediators; impaired function of osteoblasts and BMSCs	Wang et al. (2023b), Zhou et al. (2025a), Chen et al. (2021a), Bell et al. (2024)
Necroptosis	RIPK1–RIPK3–MLKL signaling axis	Pro-inflammatory cell death; tissue injury	Ni et al. (2021), Ai et al. (2024)
PANoptosis	PANoptosome complex (e.g., ZBP1, AIM2, NLRP12); coordinated activation of multiple death pathways	Highly inflammatory and synergistic programmed cell death; potential driver of severe immunopathology	Yang et al. (2025a), Samir et al. (2020), He et al. (2025)