Gamada Hisanori, Funayama Toru, Setojima Yusuke, Ogata Yosuke, Sunami Takahiro, Sakashita Kotaro, Okuwaki Shun, Miura Kousei, Noguchi Hiroshi, Takahashi Hiroshi, Yamazaki Masashi, Koda Masao
Department of Orthopaedic Surgery, Institute of Medicine, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, 305-8575, Ibaraki, Japan.
Eur Spine J. 2025 Mar 3. doi: 10.1007/s00586-025-08750-y.
Pyogenic spondylodiscitis is a significant health concern, particularly in older individuals. Minimally invasive surgical techniques, such as posterior fixation, are promising for infection control; however, their mechanisms remain unclear. This study aimed to clarify how posterior fixation promotes infection control in an animal model.
Thirty female Wistar rats were used to create a pyogenic spondylodiscitis model by injecting methicillin-sensitive Staphylococcus aureus into the intervertebral space between the 6th and 7th coccygeal vertebrae. Three days post-injection, rats were divided into fixation and control groups. The fixation group underwent posterior fixation with an external fixator, whereas the control group underwent screw insertion alone. Bone destruction was assessed via microcomputed tomography on postoperative days (POD) 7, 14, and 21. Immunohistochemistry for cathepsin K and receptor activator of nuclear factor-kappa B ligand (RANKL) was performed on POD 7 samples to assess osteoclast activity.
The fixation group showed less bone destruction than the control group at POD 14 (35% vs. 56%, p = 0.0007) and POD 21 (30% vs. 52%, p < 0.0001). The cathepsin K-positive area was significantly reduced in the fixation group (p = 0.027). RANKL expression was localized within the intervertebral disc in the fixation group, whereas RANKL was strongly expressed on the bone surface adjacent to the disc in control. The RANKL-positive area was also reduced in the fixation group (p = 0.041).
Our combined model of pyogenic spondylodiscitis and posterior fixation supports the theory that posterior fixation stability suppresses RANKL and osteoclast expression, promoting infection control.
化脓性脊椎椎间盘炎是一个重大的健康问题，尤其在老年人中。诸如后路固定等微创外科技术在控制感染方面颇具前景；然而，其作用机制仍不清楚。本研究旨在阐明后路固定在动物模型中是如何促进感染控制的。
30只雌性Wistar大鼠通过向第6和第7尾椎之间的椎间隙注射对甲氧西林敏感的金黄色葡萄球菌来建立化脓性脊椎椎间盘炎模型。注射后3天，将大鼠分为固定组和对照组。固定组采用外固定器进行后路固定，而对照组仅进行螺钉植入。在术后第7、14和21天通过微型计算机断层扫描评估骨质破坏情况。对术后第7天的样本进行组织蛋白酶K和核因子κB受体激活剂配体（RANKL）的免疫组织化学检测，以评估破骨细胞活性。
在术后第14天（35%对56%，p = 0.0007）和第21天（30%对52%，p < 0.0001），固定组的骨质破坏比对照组少。固定组中组织蛋白酶K阳性区域显著减少（p = 0.027）。RANKL表达在固定组局限于椎间盘内，而在对照组中RANKL在椎间盘相邻的骨表面强烈表达。固定组中RANKL阳性区域也减少（p = 0.041）。
我们的化脓性脊椎椎间盘炎与后路固定联合模型支持以下理论，即后路固定稳定性抑制RANKL和破骨细胞表达，从而促进感染控制。
