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Nerve growth factor (NGF), released by osteoblasts, endothelial cells, and infiltrating immune cells, plays a key role in promoting this ectopic innervation, establishing a direct link between structural bone changes and pain signaling ( via its receptor DCC, has been shown to drive the sprouting of calcitonin gene-related peptide (CGRP)+ nociceptive fibers in the subchondral bone, thereby contributing directly to pain hypersensitivity associated with OA (Zhu et al., 2019)