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Although suppressing ROS\u2010driven oxidative stress is essential for limiting inflammatory injury, impaired clearance of accumulated apoptotic cells may perpetuate local inflammation and hinder regenerative repair. Here, single\u2010cell RNA sequencing identifies macrophages as the dominant immune population in TMJOA and reveals a redox\u2010inflammatory phenotype accompanied by elevated apoptotic burden but insufficient macrophage efferocytosis, indicating a pathological mismatch between oxidative stress and efferocytic clearance. To correct this mismatch, this study develops MCP@CD\u2010MOF, a macrophage\u2010targeting cyclodextrin metal\u2013organic framework nanoplatform co\u2010loaded with curcumin and pioglitazone. In vitro, MCP@CD\u2010MOF reduces macrophage ROS accumulation and inflammatory cytokine production, enhances efferocytic uptake of apoptotic chondrocytes, and promotes matrix\u2010regenerative macrophage\u2013chondrocyte crosstalk. In vivo, intra\u2010articular administration of MCP@CD\u2010MOF preferentially accumulates in synovial macrophages, alleviates local inflammation, reduces apoptotic burden, and preserves osteochondral architecture without detectable systemic toxicity. Mechanistically, MCP@CD\u2010MOF coordinates the FOXO1\u2013GPX4\/ERK1\/2\u2013NOX2 redox network with the FAK\u2013DOCK1\u2013PAK1 efferocytosis pathway. Collectively, MCP@CD\u2010MOF integrates redox regulation with efferocytosis\u2010driven macrophage reprogramming, providing a disease\u2010modifying biomaterial strategy that couples inflammation resolution with osteochondral repair in TMJOA.<\/jats:p>","DOI":"10.1002\/adhm.71698","type":"journal-article","created":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T04:37:10Z","timestamp":1789360630000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Macrophage\u2010Targeted Cyclodextrin\u2010Based Metal\u2013Organic Frameworks Restore Redox\u2013Efferocytosis Coupling to Promote Osteochondral Repair in Temporomandibular Joint Osteoarthritis"],"prefix":"10.1002","volume":"15","author":[{"given":"Jinyang","family":"Wang","sequence":"first","affiliation":[{"name":"Guanghua School of Stomatology Hospital of Stomatology Sun Yat\u2010sen University  Guangzhou China"},{"name":"Guangdong Provincial Key Laboratory of 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