![]() Initially, the development of novel therapeutic approaches for patients experiencing nociceptive and/or neuropathic chronic pain was driven by the necessity to avoid long-term side effects resulting from the chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) and opioid therapies. However, the impact of these neuroimmune and neuroinflammatory responses on the onset of acute pain and its transition to chronic entities in humans is yet to be determined. 6 Both mechanisms have been widely studied in animals laying the groundwork for specific pain therapies in humans. 4, 5 Preclinical evidence has identified neuroimmune and inflammatory neuromodulatory responses in the nervous system (eg pathological activation of microglia and astrocytes in the spinal cord) as two of the major contributors to pain pathogenesis and persistence. Glial cells such as microglia, oligodendrocytes, astrocytes, and ependymal cells have shown to alter activity and gene expression when exposed to physiological stressors, including nerve damage. Neuroinflammation, including alteration of glial cells function following nerve injury or gliosis, has emerged as a promising mechanism triggering the transition to chronic back pain. Chronic low back pain (LBP) comprises a heterogeneous group of disorders including, but not limited to, persistent spinal pain syndrome and radicular pain. ![]() 1, 2 Undoubtedly, chronic pain results in a significant physical, psychological, emotional and economic burden for patients. Chronic pain is a well-known clinical entity affecting a substantial proportion of the general population.
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