Department of Orthopedic Surgery, Teikyo University Mizonokuchi Hospital, 3-8-3 Mizonokuchi, Takatsu-ku, Kawasaki 213-8507, Japan.
Arch Orthop Trauma Surg. 2011 Nov;131(11):1485-9. doi: 10.1007/s00402-011-1336-z. Epub 2011 Jun 14.
For children and adolescents who are very active athletes, fresh lumbar spondylolysis is the main pathologic cause of lower back pain (LBP). However, regarding the terminal-stage spondylolysis (pars defect), there have been few studies to clarify the pathomechanism of LBP. The purpose of this study is to clarify the cause of LBP associated with pars defects in athletes. This is the first report showing a possible pathomechanism of LBP in active athletes with painful pars defect.
Six pediatric athletes (5 boys and 1 girl) below 18 years old with painful bilateral lumbar spondylolysis were evaluated. In all cases, spondylolysis was identified as terminal stage (pseudoarthrosis) on CT scan. To evaluate the inflammation around the pars defects, short time inversion recovery (STIR) MRI was performed along with the sagittal section. Fluid collection, which is an indicator of inflammatory events, was evaluated in 12 pars defects as well as in 12 cranial and caudal adjoining facet joints.
Inflammation (i.e., fluid collection) was observed in all 12 pars defects in six subjects at the pseudoarthrotic pars defects. In terms of facet joints, 7 of 12 (58%) pars defects showed fluid collection at the cranial and/or caudal adjoining joints on STIR MRI.
The present study showed that inflammation was always present at the pars defects and in some cases at the adjoining facet joints. Thus, it is not difficult to understand how, during sports activity, inflammation may first occur at the pseudoarthrotic site and then spread to the adjoining facet joints. This mechanism could cause LBP associated with terminal-stage (pseudoarthrotics) spondylolysis in athletes.
对于非常活跃的运动员儿童和青少年来说，新鲜的腰椎峡部裂是下腰痛（LBP）的主要病理原因。然而，对于终末期峡部裂（ pars 缺损），很少有研究阐明 LBP 的发病机制。本研究旨在阐明与运动员 pars 缺损相关的 LBP 的病因。这是第一个显示活跃运动员伴疼痛 pars 缺损的 LBP 可能发病机制的报告。
评估了 6 名年龄在 18 岁以下的有双侧腰痛的儿童运动员（5 名男孩和 1 名女孩）。在所有病例中，CT 扫描均确定峡部裂为终末期（假关节）。为了评估 pars 缺损周围的炎症，对 12 个 pars 缺损以及 12 个颅侧和尾侧毗邻关节进行了短反转恢复（STIR）MRI。评估了 12 个 pars 缺损和 12 个颅侧和尾侧毗邻关节中的流体积聚，这是炎症事件的指标。
在 6 名受试者的 12 个 pars 缺损中，所有 12 个 pars 缺损均观察到炎症（即流体积聚）。在关节方面，12 个 pars 缺损中有 7 个（58%）在 STIR MRI 上显示颅侧和/或尾侧毗邻关节的流体积聚。
本研究表明炎症始终存在于 pars 缺损中，在某些情况下也存在于毗邻的关节突关节。因此，不难理解在运动活动中，炎症最初如何首先发生在假关节部位，然后扩散到毗邻的关节突关节。这种机制可能导致与终末期（假关节）峡部裂相关的运动员下腰痛。
