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椎间盘退变的病理机制及神经营养因子和所选元素浓度在腰痛发生中的作用。

Pathomechanism of the IVDs Degeneration and the Role of Neurotrophic Factors and Concentration of Selected Elements in Genesis of Low Back Pain.

机构信息

Department of Neurosurgery, 5th Military Clinical Hospital with the SP ZOZ Polyclinic in Krakow, 30-901, Krakow, Poland.

Department of Histology, Cytophysiology and Embryology, Faculty of Medicine in Zabrze, Academy of Silesia in Katowice, 41-800, Zabrze, Poland.

出版信息

Curr Pharm Biotechnol. 2023;24(9):1164-1177. doi: 10.2174/1389201024666221021142904.

DOI:10.2174/1389201024666221021142904
PMID:36281863
Abstract

Degenerative disc disease of the lumbosacral spine is a very common medical problem. An episode of sciatica occurs at least once in the life of 60-90% of the human population. A phenomenon that is closely related to the process of lowering the pH of the extracellular matrix degenerating the intervertebral disc (IVD) is the precipitation of calcium salts, especially pyrophosphate dehydrate and hydroxyapatite. In such an altered environment of the IVD, we can observe an increased influx of monocytes, macrophages, T-lymphocytes, as well as non-immunocompetent cells, which are a source of cytokines, e.g., tumor necrosis alpha (TNF-α), interleukin- (IL-1β, IL-8). The above-mentioned mediators of an inflammatory condition contribute to an increase in the expression of Brain-Derived Neurotrophic Factor (BDNF) and Glial cell Derived Neurotrophic Factor (GDNF) in mast cells and chondrocytes, as well as to the descending transport of these mediators along the nerve endings. In the process of degeneration of the IVD as a result of repeated and even slight injuries, there is damage to the connections of the endplate of the vertebral bodies with the IVD, which results in an impairment of the penetration of nutritional substances and water into the disc. As a consequence, there is an overexpression of the brain-derived neurotrophic factor GDNF, as well as neuromodulin (GAP-43) in the mast cells and chondrocytes of the IVDs, while descending transport of these mediators along the nerve fibers is also observed.

摘要

腰椎骶椎退行性椎间盘疾病是一种非常常见的医学问题。至少有 60-90%的人群一生中会经历一次坐骨神经痛。与椎间盘(IVD)细胞外基质 pH 值降低导致的退化过程密切相关的现象是钙盐的沉淀,特别是焦磷酸盐脱水物和羟磷灰石。在这种改变的 IVD 环境中,我们可以观察到单核细胞、巨噬细胞、T 淋巴细胞以及非免疫细胞的大量涌入,这些细胞是细胞因子的来源,例如肿瘤坏死因子-α (TNF-α)、白细胞介素- (IL-1β、IL-8)。上述炎症条件的介质有助于增加肥大细胞和软骨细胞中脑源性神经营养因子 (BDNF) 和胶质细胞源性神经营养因子 (GDNF) 的表达,并沿着神经末梢向下运输这些介质。在 IVD 退化的过程中,由于反复甚至轻微的损伤,椎体终板与 IVD 的连接受到损伤,这导致营养物质和水渗透到椎间盘的能力受损。结果,IVD 中的肥大细胞和软骨细胞中脑源性神经营养因子 GDNF 以及神经调节素 (GAP-43) 的过度表达,同时也观察到这些介质沿着神经纤维向下运输。

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