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Pathophysiology and treatment of pain in joint disease.

机译:关节疾病疼痛的病理生理学和治疗。

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摘要

Deep somatic pain originating in joints and tendons is a major therapeutic challenge. Spontaneous pain and mechanical hypersensitivity can develop as a consequence of sensitization of primary afferents directly involved in the inflammatory process, but also following sensitization of neuronal processing in the spinal cord (central sensitization) or higher centres. Inflammatory pain is linked to sensitization of sensory proteins at the nociceptive endings whereas pain originating from nerve damage (neuropathic pain) has been linked to changes in axonal ion channels producing ectopic discharge in nociceptors as a source of pain. New targets for analgesic therapy include sensory proteins at the nociceptive nerve endings such as the activating TRPV and ASIC channels, but also inhibitory opioid and cannabinoid receptors. Therapeutic targets are also found among the axonal channels that set membrane potential and modulate discharge frequency such as voltage sensitive sodium channels and various potassium channels.
机译:源于关节和肌腱的深部躯体疼痛是主要的治疗挑战。自发性疼痛和机械性超敏反应可能是由于直接参与炎症过程的初级传入者敏化的结果,也可能是由于脊髓中神经元加工的敏化(中央敏化)或更高中心引起的。炎症性疼痛与伤害性感受器末端的感觉蛋白敏化有关,而源于神经损伤(神经性疼痛)的疼痛与轴突离子通道的变化有关,在伤害性感受器中产生异位放电。镇痛药的新目标包括伤害性神经末梢的感觉蛋白,例如激活的TRPV和ASIC通道,以及抑制性阿片和大麻素受体。还可以在设置膜电位并调节放电频率的轴突通道(例如电压敏感的钠通道和各种钾通道)中找到治疗靶标。

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