Schaible Hans-Georg, Richter Frank, Ebersberger Andrea, Boettger Michael K, Vanegas Horacio, Natura Gabriel, Vazquez Enrique, Segond von Banchet Gisela
Institute of Physiology 1/Neurophysiology, University Hospital Jena, Teichgraben 8, 07740 Jena, Germany.
Exp Brain Res. 2009 Jun;196(1):153-62. doi: 10.1007/s00221-009-1782-9. Epub 2009 Apr 11.
Both inflammatory and degenerative diseases of joints are major causes of chronic pain. This overview addresses the clinical problem of joint pain, the nociceptive system of the joint, the mechanisms of peripheral and central sensitization during joint inflammation and long term changes during chronic joint inflammation. While the nature of inflammatory pain is obvious the nature and site of origin of osteoarthritic pain is less clear. However, in both pathological conditions mechanical hyperalgesia is the major pain problem, and indeed, both joint nociceptors and spinal nociceptive neurons with joint input show pronounced sensitization for mechanical stimulation. Molecular mechanisms of mechanical sensitization of joint nociceptors are addressed with an emphasis on cytokines, and molecular mechanisms of central sensitization include data on the role of excitatory amino acids, neuropeptides and spinal prostaglandins. The overview will also address long-term changes of pain-related behavior, response properties of neurons and receptor expression in chronic animal models of arthritis.
关节的炎症性疾病和退行性疾病都是慢性疼痛的主要原因。本综述探讨了关节疼痛的临床问题、关节的伤害感受系统、关节炎症期间外周和中枢敏化的机制以及慢性关节炎症期间的长期变化。虽然炎症性疼痛的性质很明显，但骨关节炎疼痛的性质和起源部位尚不清楚。然而，在这两种病理状态下，机械性痛觉过敏都是主要的疼痛问题，事实上，关节伤害感受器和接受关节传入的脊髓伤害感受神经元对机械刺激均表现出明显的敏化。文中将探讨关节伤害感受器机械敏化的分子机制，重点是细胞因子，中枢敏化的分子机制包括兴奋性氨基酸、神经肽和脊髓前列腺素作用的数据。本综述还将探讨关节炎慢性动物模型中疼痛相关行为、神经元反应特性和受体表达的长期变化。
