首页> 外文期刊>European spine journal >Lumbar posterolateral fusion inhibits sensory nerve ingrowth into punctured lumbar intervertebral discs and upregulation of CGRP immunoreactive DRG neuron innervating punctured discs in rats
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Lumbar posterolateral fusion inhibits sensory nerve ingrowth into punctured lumbar intervertebral discs and upregulation of CGRP immunoreactive DRG neuron innervating punctured discs in rats

机译:腰椎后外侧融合抑制大鼠感觉神经向穿刺腰椎间盘内生长和上调CGRP免疫反应性DRG神经元支配穿刺椎间盘

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Degeneration of lumbar intervertebral discs is thought to be a cause of low back pain. Studies have found that a cause of discogenic low back pain is intervertebral disc inflammation and axonal growth of afferent fibers innervating the disc. Lumbar spine fusion for chronic discogenic low back pain is considered an effective procedure. However, no study has investigated the mechanism of pain relief. We did this by applying Fluoro-Gold (FG) to the ventral aspect of the L4–L5 intervertebral discs of 40 rats. We exposed the nucleus pulposus to the annulus fibrosus in a disc punctured model. Rats were divided into 4 groups. Group A: Punctured intervertebral disc with sham posterolateral fusion (PLF) (n?=?10), Group B: Punctured intervertebral disc with PLF (n?=?15), Group C: Normal intervertebral disc (no puncture) with PLF (n?=?10), and Group D: Normal disc (no disc puncture) with sham PLF (n?=?5). Four weeks after surgery, bilateral L1–L5 dorsal root ganglia (DRGs) were stained with growth-associated protein 43 (GAP43), a marker of axonal growth, and calcitonin gene-related peptide (CGRP), a neuropeptide marker of pain. Bone union was evaluated using X-ray imaging. Of the FG-labeled neurons, the proportions of GAP43- and CGRP-immunoreactive (IR) neurons in Group A were significantly higher than in Group D (P??0.05). The proportions of GAP43- and CGRP-IR neurons in bone union rats in Group B were significantly lower than in nonunion rats in Group B and in the rats in Group A (P??0.05). No significant differences in GAP43- and CGRP-IR neurons were observed between bone union and nonunion rats in Group C and the rats in Group D (P??0.05). PLF is strongly related to the downregulation of GAP43 and CGRP expression. Therefore, PLF may suppress the increase of inflammatory neuropeptides and the process of axonal growth. Moreover, these results may explain, in part, the mechanism of pain relief following lumbar spinal fusion for chronic discogenic low back pain in humans...
机译:腰椎间盘退变被认为是腰痛的原因。研究发现,椎间盘源性下腰痛的原因是椎间盘发炎和支配椎间盘的传入纤维的轴突生长。腰椎融合治疗慢性椎间盘源性下腰痛被认为是一种有效的方法。但是,尚无研究研究缓解疼痛的机制。我们通过在40只大鼠的L4–L5椎间盘的腹侧应用氟金(FG)来实现此目的。我们在椎间盘穿刺模型中将髓核暴露于纤维环。将大鼠分为4组。 A组:假性后外侧融合(PLF)的穿刺椎间盘(n?=?10),B组:PLF的穿刺椎间盘(n?=?15),C组:PLF的正常椎间盘(无穿刺)( n?=?10),D组:正常盘(无盘穿刺),假PLF(n?=?5)。手术后四周,双侧L1-L5背根神经节(DRG)被轴突生长的标志物生长相关蛋白43(GAP43)和疼痛的神经肽标志物降钙素基因相关肽(CGRP)染色。使用X射线成像评估骨结合。在FG标记的神经元中,A组的GAP43和CGRP免疫反应(IR)神经元的比例显着高于D组(P <0.05)。 B组骨结合大鼠中GAP43-和CGRP-IR神经元的比例显着低于B组骨不连和A组大鼠(P <0.05)。 C组骨结合和不愈合大鼠与D组大鼠的GAP43-和CGRP-IR神经元差异无统计学意义(P> 0.05)。 PLF与GAP43和CGRP表达的下调密切相关。因此,PLF可抑制炎症性神经肽的增加和轴突生长的过程。此外,这些结果可能部分解释了腰椎融合术后疼痛的缓解机制,可解决人类慢性椎间盘源性下腰痛...

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