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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

The identification of a SIRT6 activator from brown algae Fucus distichus

Neuropsychopharmacol 33 , 21872199 (2008)