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Back pain is extremely common in clinical setting. In the history, back pain has been believed to be seldom associated with clearly identifiable tissue damage or anatomical defect, but it is rather a normal part of life and aging. 1  Back pain is also considered to have multifactorial etiology involving biological (age, sex, and genetic), psychosocial (stress), and environmental (food, toxins, infection, and trauma) factors. More recent epidemiological investigation has revealed that cooccurring pain sites in the body are linearly increased with age, suggesting important roles of age in pain. In this report, I will highlight the roles of normal age-related axonal degeneration in the nervous system that may predispose to the chronicity of pain in general and of back pain in specific conditions. First, across the lifespan, aging process results in development of polyneuropathies along the whole somatosensory system characterized by damage of both large myelinated and unmyelinated C fibers. The age-related polyneuropathies are a predisposing factor to chronicity of mechanical pain hypersensitivity (hyperalgesia and allodynia) under both inflammatory and nerve injury conditions. For example, in aged rats, mechanical pain hypersensitivity lasts much longer relative to young cohorts in a rat model of experimental inflammatory pain as well as in a rat model of radiculopathy caused by chronic compression of dorsal root ganglia/dorsal roots by placing a steel rod into intervertebral foramen. Second, age-related polyneuropathies are initiated by myelin breakdown that is likely to be caused by decline of NGF receptors and myelin proteins, subsequently leading to axonal degeneration and loss of sensory receptors. Third, age-related polyneuropathies that are characterized by myelin breakdown and axonal degeneration are accompanied by activations of both astrocytes and microglial cells in the central somatosensory system. Together, myelin breakdown and axonal degeneration in the nervous system are common features of aged spinal cord that are likely to be a predisposing factor to chronicity of back pain due to widespread neuropathies and angiopathies which normally supply the spine. Targeting and unraveling the pathogenesis of age-related myelin breakdown and axonal degeneration would shed new light on the underlying mechanisms of chronic back pain in specific and chronic pain in general.    Acknowledgments The article is supported by grants (2011CB504100, 2013BAI04B04, and 81171049). I am grateful to Fang Xie and Han Fu for performing the experiments and to our team members for collaborations.    Disclosure of Interest    None declared    Reference    Fordyce WE. Back Pain in Workplace. Seattle, WA: IASP Press; 1995

Chronicity of Back Pain: Predisposing Factor of Normal Age-Related Axonal Degeneration