Tachihara Hisayoshi, Kikuchi Shin-ichi, Konno Shin-ichi, Sekiguchi Miho
Department of Orthopaedic Surgery, Fukushima Medical University School of Medicine, Fukushima City, Fukushima, Japan.
Spine (Phila Pa 1976). 2007 Feb 15;32(4):406-12. doi: 10.1097/01.brs.0000255094.08805.2f.
The association between lumbar facet joint inflammation and radiculopathy was investigated using behavioral, histologic, and immunohistochemical testing in rats.
To develop a rat model of lumbar facet joint inflammation and ascertain whether facet joint inflammation induces radiculopathy using this model.
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.
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.
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.
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.
通过对大鼠进行行为学、组织学和免疫组织化学检测，研究腰椎小关节炎症与神经根病之间的关联。
建立腰椎小关节炎症的大鼠模型，并使用该模型确定小关节炎症是否会诱发神经根病。
机械因素和化学因素均被认为是诱发神经根病的重要因素。在腰椎退变疾病中，小关节骨赘可能导致神经根受压，进而诱发神经根病。此外，与其他滑膜关节一样，小关节也可能发生炎症。因此，炎症的滑膜可能释放炎性细胞因子，导致神经根损伤，继而引发神经根病。
将一块含有完全弗氏佐剂的明胶海绵植入大鼠的L5-L6小关节（关节炎组）。对照组使用生理盐水。采用von Frey试验测定机械性异常性疼痛。对硬膜外间隙浸润的炎性细胞进行计数，并通过组织学评估软骨的变化。对L5背根神经节中肿瘤坏死因子（TNF）-α免疫反应阳性细胞进行计数。
关节炎组从第3天开始出现机械性异常性疼痛，在观察期内逐渐恢复。与对照组相比，关节炎组在第3天和第7天硬膜外间隙浸润的炎性细胞数量明显更多。与对照组相比，关节炎组在第1天和第3天TNF-α免疫反应阳性细胞数量显著增加。主要是小型伤害性神经元被染色。
当小关节诱发炎症时，炎症反应会扩散至神经根，并由化学因素诱发腿部症状。这些结果支持小关节炎症诱发神经根病的可能性。
