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Pain in OA is influenced by multiple interconnected mechanisms: Peripheral sensitization lowering the activation threshold of nociceptors Inflammatory mediators and adipokines amplifying pain signals Neurovascular remodeling increasing nerve density within the joint Synovial immune dysregulation creating a pro-inflammatory microenvironment Joint acidosis activating proton-sensitive pain pathways Persistent peripheral input leading to **central sensitization** and chronic pain This explains why: Some patients experience severe pain despite mild X-ray changes

doi: 10.3390/biom5010194 26

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Sterigmatocystin-induced oxidative DNA damage in human liver-derived cell line through lysosomal damage