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Does facet joint inflammation induce radiculopathy?: an investigation using a rat model of lumbar facet joint inflammation.

机译：小关节炎症会诱发神经根病吗？：一项使用大鼠腰小关节炎症模型的研究。

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STUDY DESIGN: The association between lumbar facet joint inflammation and radiculopathy was investigated using behavioral, histologic, and immunohistochemical testing in rats. OBJECTIVES: To develop a rat model of lumbar facet joint inflammation and ascertain whether facet joint inflammation induces radiculopathy using this model. SUMMARY OF BACKGROUND DATA: Both mechanical and chemical factors have been identified as important for inducing radiculopathy. In lumbar spondylosis, facet joint osteophytes may contribute to nerve root compression, which may induce radiculopathy. Furthermore, inflammation may occur in the facet joint, as in other synovial joints. Inflamed synovium may thus release inflammatory cytokines and induce nerve root injury with subsequent radiculopathy. METHODS: A piece of gelatin sponge containing complete adjuvant was inserted into the L5-L6 facet joint in rats (arthritis group). Saline was used in the control group. Mechanical allodynia was determined using the von Frey test. Inflammatory cells infiltrating the epidural space were counted, and changes in cartilage were assessed histologically. Tumor necrosis factor (TNF)-alpha-immunoreactive cells in the L5 dorsal root ganglion were counted. RESULTS: Mechanical allodynia was observed in the arthritis group from day 3, gradually recovering during the observation period. Significantly larger numbers of inflammatory cells had infiltrated the epidural space by days 3 and 7 in the arthritis group than in controls. Numbers of TNF-alpha-immunoreactive cells were significantly increased at days 1 and 3 in the arthritis group compared with controls. Predominantly small nociceptive neurons were stained. CONCLUSIONS: When inflammation was induced in a facet joint, inflammatory reactions spread to nerve roots, and leg symptoms were induced by chemical factors. These results support the possibility that facet joint inflammation induces radiculopathy.
机译：研究设计：使用行为，组织学和免疫组化试验对大鼠腰椎小关节炎症和神经根病之间的关系进行了研究。目的：建立大鼠腰椎小关节炎症模型，并使用该模型确定小关节炎症是否诱发神经根病。背景数据概述：机械和化学因素均已被认为对诱发神经根病很重要。在腰椎病中，小关节骨赘可能会导致神经根受压，从而诱发神经根病。此外，与其他滑膜关节一样，发炎可能会在小关节中发生。因此，发炎的滑膜可能释放出炎性细胞因子并引起神经根损伤，继而发生神经根病。方法：将一块含有完全佐剂的明胶海绵插入大鼠（关节炎组）的L5-L6小关节中。在对照组中使用盐水。机械性异常性疼痛使用冯·弗雷（von Frey）测试确定。计数渗入硬膜外腔的炎性细胞，并通过组织学评估软骨的变化。计数L5背根神经节中的肿瘤坏死因子（TNF）-α-免疫反应性细胞。结果：关节炎组从第3天开始观察到机械性异常性疼痛，并在观察期间逐渐恢复。与对照组相比，关节炎组在第3天和第7天，大量的炎性细胞浸润了硬膜外腔。与对照组相比，在关节炎组的第1天和第3天，TNF-α免疫反应性细胞的数量显着增加。主要是小的伤害感受神经元被染色。结论：当小关节发炎时，发炎反应扩散到神经根，而腿部症状则由化学因素引起。这些结果支持了小关节炎症引起神经根病的可能性。

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