PURPOSE The precise mechanism and pathological role of postlaminectomy/laminotomy fibrosis (PLF) in postoperative neurological deficits have not been established. Many studies use magnetic resonance imaging (MRI) to prove that there is no consistent correlation between PLF and postoperative neurological deficits and back pain (PNDBP). Therefore, we assumed that the direct-compression effect may not be the only factor but that other neurological deficits associated with pathological mechanisms should exist and need more investigation. The purpose of this study was to compare over time the differences and changes in histopathological properties of PLF in rats. METHODS We used a rat model with walking-track analysis for neurologic evaluation, grading scale to evaluate PLF, histomorphometric measurements of dura sac diameter, and histological tissue reactions (dura mater and spinal rootlets) juxtaposed to the postlaminectomy/laminotomy defect. The 54 adult Sprague-Dawley rats were divided into laminotomy (n = 18), laminectomy (n = 18), and sham-operation groups (n = 18). All groups were subdivided into three equal subgroups based on different postoperative time points (1, 2, and 3 months). All sections of vertebral column were stained with hematoxylin and eosin and with Masson's trichrome. RESULTS The results showed that only a slight compression effect reflected by nonsignificant changes in the maximum anterior-posterior diameters within the dura sac, in the walking tract test, and increased grades of PLF over time. In addition, significant pathological inflammatory changes, such as thickening of the dura mater, axonal swelling, and neovascularization, were found in the post-laminectomy/laminotomy groups at each time point. CONCLUSION Laminectomy-/laminotomy-related inflammation may lead to PLF, and these pathological changes may be the main cause of postoperative neurological deficits. These findings show that research on preventing PLF should include perioperative modulation of inflammatory reactions induced by laminectomy/laminotomy.

中文翻译：

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椎板切除术/椎板切开术纤维化对大鼠硬脑膜和马尾神经根的组织学改变的大规模压缩作用的意义：一项在大鼠中的实验研究。

目的尚未确定椎板切除术/椎板切开术纤维化（PLF）在术后神经功能缺损中的确切机制和病理学作用。许多研究使用磁共振成像（MRI）来证明PLF与术后神经功能缺损和背痛（PNDBP）之间没有一致的相关性。因此，我们认为直接压缩作用可能不是唯一的因素，而是应该存在与病理机制相关的其他神经系统缺陷，需要进一步研究。这项研究的目的是随着时间的推移比较大鼠PLF组织病理学特性的差异和变化。方法我们使用具有步行轨迹分析的大鼠模型进行神经系统评估，分级量表以评估PLF，硬膜囊直径的组织形态学测量，并与椎板切除术/椎板切开术缺损并列的组织学反应（硬脑膜和脊柱小根）。将54只成年Sprague-Dawley大鼠分为开腹手术（n = 18），椎板切除术（n = 18）和假手术组（n = 18）。根据不同的术后时间点（1、2和3个月）将所有组细分为三个相等的亚组。脊柱的所有切片均用苏木精和曙红以及Masson三色染色。结果结果表明，在步行道试验中，硬膜囊内最大前后直径的无显着变化反映了轻微的压迫作用，并且随着时间的推移，PLF等级增加。此外，重大的病理性炎症变化，例如硬脑膜增厚，轴突肿胀和新血管形成，在每个时间点的椎板切除术后/剖宫术组中均发现了这种情况。结论椎板切除术/椎板切开术相关的炎症可能导致PLF，这些病理变化可能是术后神经功能缺损的主要原因。这些发现表明，预防PLF的研究应包括围手术期调节椎板切除术/截肢术引起的炎症反应。