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Here, we show that excessive accumulation of neutrophil extracellular traps (NETs) in infected bone tissues contributes to osteomyelitis\u2010associated apoptosis and impaired osteogenesis. NETs disrupt PINK1\/Parkin\u2010mediated mitochondrial quality control in osteoblast lineage cells, thereby promoting apoptosis, whereas inhibition of NET formation alleviates these pathological changes and improves bone repair in mice. Bone defects are aggravated in\n                    <jats:italic>Prkn<\/jats:italic>\n                    \u2010knockout mice upon the induction of osteomyelitis, supporting the functional role of PINK1\/Parkin\u2010dependent mitophagy in the repair of infected bone. As a therapeutic strategy, gallium\u2013selenium nanoparticles (GaSe\n                    <jats:sub>x<\/jats:sub>\n                    ) exert potent antibacterial activity, redirect neutrophils from NET formation toward phagocytosis, preserve osteoblast mitochondrial homeostasis, attenuate excessive mitophagy, and ultimately promote the repair of infected bone defects in rats. Collectively, these findings support NET\u2010driven osteoblast mitochondrial injury as a critical repair\u2010limiting mechanism in osteomyelitis and establish GaSe\n                    <jats:sub>x<\/jats:sub>\n                    as a redox\u2010regulating platform that modulates this mechanism while preserving neutrophil antibacterial defense.\n                  <\/jats:p>","DOI":"10.1002\/adma.75457","type":"journal-article","created":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T10:56:20Z","timestamp":1792666580000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["GaSe\n                    <sub>x<\/sub>\n                    Nanoparticles Modulate Neutrophil Function and Mitigate NET\u2010Driven Osteogenic Impairment in Osteomyelitis 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