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(ii) Cu 2+ induces the secretion of acidic SMase from leukocytes which in turn leads to accumulation of erythrocytic ceramide [131] and (iii) treatment of erythrocytes with extracellular SMase resulted in ceramide-associated alterations in membrane-cytoskeleton interactions and membrane organization [125]
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
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