Persistent inflammatory pain induces neuroplastic changes that sustain nociceptive processing. As a dynamic structural and functional component of nervous tissue, the extracellular matrix (ECM) and perineuronal nets (PNNs) can modulate pain sensitivity by regulating synaptic plasticity. We hypothesized that ECM remodeling in the spinal cord and primary somatosensory cortex (S1) correlates with nociceptive alterations during chronic pain. To test this, we employed an inflammatory pain model and evaluated mechanical allodynia (electronic Von Frey) and thermal hyperalgesia (Hargreaves apparatus). Spinal cord and S1 samples were processed for triple immunofluorescence targeting ECM components, NeuN, and parvalbumin, followed by confocal microscopy. Behavioral assays revealed sex differences: females exhibited smaller threshold reduction and faster recovery. Preliminary analyses of ECM and PNN expression demonstrated regional differences: while S1 showed changes at day 13 post-injection, no alterations were detected in the spinal cord. These findings suggest a complex temporal pattern of ECM remodeling in the CNS during inflammatory pain. Such modifications may promote maladaptive plasticity and central sensitization, pointing to potential therapeutic targets for persistent pain. Ongoing studies aim to further dissect sex-related mechanisms in ECM regulation during pain.