Metasurface-enhanced surface plasmon resonance microscopy for long-term label-free monitoring of chondrocyte-biointerface dynamics under mechanical, genetic, and inflammatory perturbations.

Dynamic monitoring of cell-matrix interfacial remodeling remains challenging with conventional endpoint assays, particularly in degeneration-relevant microenvironments. The cartilage endplate (CEP), a key structure for load transmission and solute exchange in the intervertebral disc, provides a model in which early pathological changes involve abnormal cell-matrix adhesion and extracellular matrix remodeling. Here, we established a label-free, long-term monitoring platform based on metasurface-enhanced surface plasmon resonance microscopy (Meta-SPRM) to quantify CEP chondrocyte interfacial dynamics under mechanical, genetic, and inflammatory perturbations. Under perfusion-induced shear, CEP chondrocytes exhibited magnitude-dependent interfacial adaptation, with high shear causing a more sustained reduction in interfacial coupling and contact area. FGFBP1 knockdown further exacerbated this shear-associated loss, supporting a protective role for FGFBP1 in interfacial stability under mechanical stress. Under inflammatory stimulation with M1 macrophage-conditioned medium, interfacial signals increased despite a late decrease in cell spreading, consistent with enhanced interfacial adhesion and matrix remodeling. Axin2 expression increased under shear, was further increased by FGFBP1 knockdown in the shear model, and was also elevated under inflammatory stimulation, supporting its use as an endpoint readout of Wnt/β-catenin-associated transcription across the tested perturbations. Collectively, Meta-SPRM enables continuous live-cell monitoring of CEP chondrocyte interfacial dynamics and relates these changes to endpoint molecular readouts, providing a reproducible platform for comparative biointerface studies and in vitro screening of candidate interventions.