Fukui Daisuke, Kawakami Mamoru, Cheng Kevin, Murata Koichiro, Yamada Keianne, Sato Rinoka, Yoshida Munehito, Yamada Hiroshi, Inoue Nozomu, Masuda Koichi
Spine Care Center, Wakayama Medical University Kihoku Hospital, 219, Myouji, Katsuragicho, Ito Gun, Wakayama, Japan.
Department of Orthopaedic Surgery, School of Medicine, University of California, 9500 Gilman Dr. MC0863, La Jolla, San Diego, CA, USA.
Eur Spine J. 2017 Aug;26(8):2014-2020. doi: 10.1007/s00586-016-4920-7. Epub 2016 Dec 23.
Intervertebral disc degeneration is thought to contribute to low back pain. However, the pathophysiological mechanisms remain controversial. In a previous study, we developed an animal model that showed delayed gait disturbance after lumbar facetectomy in the rat. We believe that this gait disturbance was caused by low back pain, although the mechanisms of this gait abnormality remain unknown. The purpose of this study was to evaluate structural changes of the lumbar spine after facetectomy in the rat utilizing three-dimensional micro-computed tomography (3DμCT) compared to histology.
Thirty male SD rats were divided into three groups. In the Sham group (n = 13), only exposure of bilateral facet joints at the L4-5 level was performed. In the Experimental group (n = 13), complete resection of bilateral L4-5 facet joints was achieved. Naïve rats (n = 4) were used for controls. At 7-week postoperative, 3DµCT and histological analyses were performed.
On 3DµCT images, increased disc height and endplate irregularities at the L4-5 segment and decreased disc height at adjacent segments were observed in the Experimental group. Histological scores were also higher in the Experimental group than the Sham Group.
Degenerative changes were observed at the facetectomy level. These may correspond with the previously reported delayed gait disturbance after facetectomy. This animal model may be useful to create mechanically induced disc degeneration without direct tissue damage to the disc.
椎间盘退变被认为是导致腰痛的原因之一。然而,其病理生理机制仍存在争议。在先前的一项研究中,我们建立了一种动物模型,该模型显示大鼠腰椎小关节切除术后步态障碍延迟出现。我们认为这种步态障碍是由腰痛引起的,尽管这种步态异常的机制尚不清楚。本研究的目的是利用三维显微计算机断层扫描(3DμCT)并与组织学方法比较,评估大鼠小关节切除术后腰椎的结构变化。
将30只雄性SD大鼠分为三组。假手术组(n = 13)仅暴露L4-5节段的双侧小关节。实验组(n = 13)完成双侧L4-5小关节的完全切除。未处理的大鼠(n = 4)作为对照。术后7周,进行3DμCT和组织学分析。
在3DμCT图像上,实验组L4-5节段椎间盘高度增加、终板不规则,相邻节段椎间盘高度降低。实验组的组织学评分也高于假手术组。
在小关节切除水平观察到退变改变。这些改变可能与先前报道的小关节切除术后延迟出现的步态障碍相对应。这种动物模型可能有助于在不直接损伤椎间盘组织的情况下造成机械性诱导的椎间盘退变。