Alleviation of osteoarthritis progression through far-infrared therapy targeting osteoclast cytoskeleton and MAPK/c-Fos/NFATc1 signaling inhibition

This study investigated the anti-osteoclastic and chondroprotective effects of far-infrared (FIR) therapy in osteoarthritis (OA), focusing on its ability to modulate pathological osteoclast (OC) activation and subchondral bone remodeling. A monosodium iodoacetate (MIA)-induced OA rat model was used, and FIR's therapeutic potential was evaluated through longitudinal assessment of nociception (von Frey test), cartilage integrity (histomorphometry: H P < 0.05). (2) Cellular studies showed FIR inhibited RANKL-mediated OC differentiation, as evidenced by reduced TRAP activity and downregulation of OC-specific markers (P < 0.05). (3) Transcriptomic analysis identified actin cytoskeleton reorganization and OC differentiation pathways as primary targets of FIR intervention. This finding was supported by disrupting F-actin ring formation and modulating key regulatory proteins via MAPK/c-Fos/NFATc1 signaling (P < 0.05). Our findings establish FIR therapy as an effective physical pharmacology strategy for OA management. It simultaneously addresses nociception, cartilage degeneration, and pathological bone remodeling through selective targeting of OC cytoskelet.