Publication: Mechanistic insights into cartilage-sensory nerve crosstalk in osteoarthritis progression

Osteoarthritis (OA) pain arises from dynamic crosstalk between degraded cartilage and sensitized sensory nerves. Cartilage-derived signals, including nerve growth factor (NGF), pro-inflammatory cytokines, and matrix-degrading enzymes, promote nerve sprouting and hyperexcitability. While sensory afferents release neuropeptides that further amplify inflammation and cartilage degeneration. Altered joint mechanics additionally activate mechanosensitive ion channels, linking biomechanical stress to nociceptive signaling. This review summarizes current knowledge on cartilage–sensory nerve interactions in OA and their contribution to pain progression. We discuss key molecular mediators, biomarkers, and therapeutic targets, and provide an overview of in vivo, in vitro, and ex vivo model platforms for studying cartilage–sensory nerve crosstalk, highlighting emerging predictive systems for mechanistic and translational research. Together, these insights support the development of mechanism-based pain phenotyping and personalized therapeutic strategies for OA. (Abstract from the publication)

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Graphical abstract