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Pain 

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date: 03 June 2020

Significant advances in our understanding of the neurobiology of pain in osteoarthritis (OA) have occurred in the last decade and are herein summarized. Pain is the predominant symptom of OA and occurs at multiple levels from non-cartilage peripheral tissues to spinal cord, and brain and back. At each level, nerve function is regulated by complex ionic channels, neuropeptide expression, and cytokine and chemokine activity. Previously considered a non-inflammatory condition, it is now recognized that cell proliferation and inflammatory cytokine production occurs in OA synovium, contributing to peripheral sensitization. Genetic profile influences nociceptive neuropeptide expression and thus, pain perception. Both peripheral and central sensitizing factors, including increased neuropeptide and microglial activity, lead to pain augmentation and persistence. Pain processing in brain centres such as the somatosensory cortex and insula are influenced by affective areas such as the amygdala. Descending receptor pathways through the midbrain to the dorsal horn, such as norepinephrine, serotonin, opioid, and cannabinoid, normally provide pain inhibitory function but this function may be diminished in chronic pain states such as OA, leading to allodynia and hyperalgesia. Functional neuroimaging has contributed to our understanding of the complex interplay of peripheral and central mechanisms. Recent evidence that grey matter volume decrease in chronic pain states may be reversible (e.g. after pain relief post OA hip arthroplasty) illuminates the potential for central neuroplasticity. Greater understanding of the neurobiology of OA pain provides evidence for therapeutic approaches that address peripheral and/or central pain mechanisms and provides a guide for future targeted pain therapeutics.

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