Metal–Organic Framework-Integrated Nanoplatform Orchestrates Osteochondral-Synovial Homeostasis for Osteoarthritis Therapy

released from CLKM reprogrammed synovial macrophages toward a reparative phenotype, mitigating inflammation-driven cartilage matrix degradation and inhibiting osteoclastogenesis. Furthermore, KGN cooperated with the ionic microenvironment to enhance stem cell recruitment and chondrogenesis, driving structural cartilage repair. In surgery-induced OA mice, CLKM effectively preserved cartilage integrity, reduced synovitis, normalized subchondral bone remodeling, and restored gait symmetry. In loading-induced post-traumatic OA (PTOA) mice, a single intra-articular injection of CLKM counteracted PTOA progression. This study establishes CLKM as a versatile nanoplatform that orchestrates chondroprotection, immunomodulation, and tissue remodeling, disrupting the vicious cycle and offering a promising strategy for OA management.