![]() Then, the initial fracture pain signal is emitted by activated mechanosensors expressed by nerve fibers densely innervating the periosteum. įracture pain often originates from mechanical distortion of somatosensory nerve terminals innervating bones and muscles. Patients with CFP not only have poor musculoskeletal functional recovery but also experience depression, anxiety, cognitive impairments, and complex regional pain syndrome (CRPS), which have been identified as related to worsening pain perception and a serious threat to quality of life. Notably, the incidence rate of chronic pain is 61.7% after ankle and knee fractures and 55.1% after tibial fractures. Chronic fracture pain is one of the common clinical chronic pains, which is characterized by severe pain during exercise, mechanical allodynia, and cold hyperalgesia. Ĭhronic pain is considered to be pain that persists beyond the normal healing time, usually referring to pain lasting >3 months. According to statistics, the annual number of patients who experience a traumatic fracture is over 4,400,000 in China, and about 9,000,000 people per year experience an osteoporotic fracture worldwide. We also review the mechanisms of action of analgesics in the clinic and their side effects as well as promising therapeutic candidates (e.g., specialized pro-resolving mediators, a caspase-6 inhibitor, and a STING agonist) for pain relief by the attenuation of neuroinflammation with the aim of better managing patients undergoing CFP in the clinical setting.īone fractures, resulting from orthopedic trauma or osteoporosis, contribute to increasing rates of morbidity, disability, mortality, and medical expenditures worldwide. ![]() This review summarizes current literature on the excitatory synaptic plasticity, microgliosis, and microglial activation-associated signaling molecules and discusses the unconventional modulation of caspases and stimulator of interferon genes (STING) in the pathophysiology of CFP. ![]() Recent progress has deepened our understanding of the emerging properties of chemokine production, proinflammatory mediator secretion, caspase activation, neurotransmitter release, and neuron-glia interaction in initiating and sustaining synaptogenesis, synaptic strength, and signal transduction in central pain sensitization, indicating the possibility of targeting neuroinflammation to prevent and treat CFP. The typical physiopathological characteristics of CFP are a neuroinflammatory response and excitatory synaptic plasticity, but the specific molecular mechanisms involved remain poorly elucidated. Analgesics available for CFP in clinics not only have poor curative potency but also have considerable side effects therefore, it is important to further explore the pathogenesis of CFP and identify safe and effective therapies. Chronic fracture pain (CFP) after orthopedic repairs is considered one of the most critical contributors to interference with the physical rehabilitation and musculoskeletal functional recovery. Fracture pain often originates from mechanical distortion of somatosensory nerve terminals innervating bones and muscles and is maintained by central sensitization. Bone fracture following traumatic injury or due to osteoporosis is characterized by severe pain and motor impairment and is a major cause of global mortality and disability.
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