Fundamentals of intervertebral disc degeneration and related discogenic pain.

IF 2 Q2 ORTHOPEDICS
Bao-Gan Peng
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引用次数: 0

Abstract

Lumbar intervertebral disc degeneration is thought to be the main cause of low back pain, although the mechanisms by which it occurs and leads to pain remain unclear. In healthy adult discs, vessels and nerves are present only in the outer layer of the annulus fibrosus and in the bony endplate. Animal models, and histological and biomechanical studies have shown that annulus tear or endplate injury is the initiating factor for painful disc degeneration. Injury to the disc triggers a local inflammatory repair response that activates nociceptors and promotes the synthesis of neuropeptides such as substance P and calcitonin gene-related peptide, by dorsal root ganglion neurons. These neuropeptides are transported to injured discs and act as pro-inflammatory molecules, promoting the production of an "inflammatory soup" by inducing vasodilatation and plasma extravasation as well as by promoting the release of chemical mediators from disc cells and infiltrating immune cells, causing neurogenic inflammation that leads to progressive disc degeneration and discogenic pain.

椎间盘退变的基本原理和相关的椎间盘源性疼痛。
腰椎间盘退变被认为是腰痛的主要原因,尽管其发生和导致疼痛的机制尚不清楚。在健康成人椎间盘中,血管和神经仅存在于纤维环的外层和骨终板中。动物模型、组织学和生物力学研究表明,椎间盘环撕裂或终板损伤是疼痛性椎间盘退变的起始因素。椎间盘损伤触发局部炎症修复反应,激活伤害感受器,促进背根神经节神经元合成P物质和降钙素基因相关肽等神经肽。这些神经肽被运送到受损的椎间盘,充当促炎分子,通过诱导血管扩张和血浆外渗,以及通过促进椎间盘细胞释放化学介质和浸润免疫细胞,促进“炎症汤”的产生,引起神经源性炎症,导致进行性椎间盘退变和椎间盘源性疼痛。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
3.10
自引率
0.00%
发文量
814
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