Institute of Physiology/Neurophysiology 1, Jena University Hospital-Friedrich Schiller University Jena, Teichgraben 8, 07740, Jena, Germany.
Curr Rheumatol Rep. 2012 Dec;14(6):549-56. doi: 10.1007/s11926-012-0279-x.
Pain is a major clinical problem of osteoarthritis (OA). Recently, OA has been thought to be a disease of the whole joint with both destruction of cartilage and inflammatory components such as synovitis and bone marrow lesions. Clinical studies have documented a significant inflammatory soft tissue contribution to the severity and frequency of OA pain. Both clinical and experimental studies have provided evidence for the sensitization of pain pathways during OA, involving pronounced changes in joint nociceptors and changes of the nociceptive processing in the spinal cord, brainstem, and thalamocortical system. Additionally, evidence has been provided for neuropathic pain components in OA models. Concerning molecular mechanisms of OA pain and potential options for pain therapy, studies on nerve growth factor, cytokines, sodium channel blockers, hyaluronic acid preparations, and others are addressed in this review.
疼痛是骨关节炎（OA）的一个主要临床问题。最近，OA 被认为是一种整个关节的疾病，既有软骨破坏，也有滑膜炎和骨髓病变等炎症成分。临床研究记录了炎症性软组织对 OA 疼痛的严重程度和频率有显著贡献。临床和实验研究都为 OA 期间痛觉通路的敏化提供了证据，包括关节伤害感受器的明显变化以及脊髓、脑干和丘脑皮质系统中伤害感受处理的变化。此外，OA 模型中也有神经病理性疼痛成分的证据。关于 OA 疼痛的分子机制和疼痛治疗的潜在选择，本文综述了神经生长因子、细胞因子、钠离子通道阻滞剂、透明质酸制剂等方面的研究。
