Department of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada.
Department of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Bone and Joint Institute, University of Western Ontario, London, Ontario, Canada.
Spine (Phila Pa 1976). 2017 Oct 1;42(19):1440-1446. doi: 10.1097/BRS.0000000000002132.
Basic science study of the relationship between the structural properties of the spine and its surrounding musculature.
To determine whether an increase in spine stiffness causes an inverse compensatory change in the passive stiffness of the adjacent paraspinal muscles.
Intervertebral disc degeneration causes an increase in multifidus passive stiffness; this was hypothesized to compensate for a decrease in spine stiffness associated with disc degeneration. Mice lacking equilibrative nucleoside transporter 1 (ENT1) develop progressive ectopic calcification of the fibrous connective tissues of the spine, which affects the lumbar spine by 6 months of age and likely creates a mechanically stiffer spine.
Experiments were conducted on four groups of mice (n = 8 mice/group): wild-type (WT) and ENT1 knockout (KO) at 2 or 8 months of age. Lumbar spines were removed and tested in cyclic axial compression to determine neutral zone length and stiffness. Single muscle fibers and bundles of fibers were isolated from lumbar multifidus and erector spinae, as well as tibialis anterior (a non-spine-related control) and tested to determine elastic modulus (passive stiffness).
At 2 months of age, neither spine nor muscle stiffness was different between KO and WT. At 8 months of age, compared with WT the lumbar spines of ENT1 KO mice had a stiffer and shorter neutral zone, and the paraspinal muscle fibers were less stiff; however, fiber bundles were not different. In addition, tibialis anterior was not different between KO and WT.
This work has confirmed that calcification of spinal connective tissues in the ENT1 KO mouse results in a stiffened spine, whereas the concurrent decrease in muscle fiber elastic modulus in the adjacent paraspinal muscles suggests a direct compensatory relationship between the stiffness of the spine and the muscles that are attached to it.
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脊柱结构特性与其周围肌肉之间关系的基础科学研究。
确定脊柱刚度的增加是否会导致相邻脊柱旁肌肉的被动刚度产生反向补偿性变化。
椎间盘退变导致多裂肌被动刚度增加；这被假设为补偿与椎间盘退变相关的脊柱刚度降低。缺乏平衡核苷转运蛋白 1 (ENT1) 的小鼠会出现脊柱纤维连接组织的进行性异位钙化，这种情况在 6 月龄时就会影响到腰椎，并可能使脊柱在机械上变得更僵硬。
在四组小鼠（每组 8 只小鼠）上进行了实验：2 月龄和 8 月龄的野生型（WT）和 ENT1 敲除（KO）小鼠。取出腰椎进行循环轴向压缩试验，以确定中立区长度和刚度。从腰椎多裂肌和竖脊肌以及胫骨前肌（非脊柱相关对照）中分离出单个肌纤维和肌纤维束，并进行弹性模量（被动刚度）测试。
在 2 月龄时，KO 和 WT 之间的脊柱和肌肉刚度均无差异。在 8 月龄时，与 WT 相比，ENT1 KO 小鼠的腰椎具有更硬和更短的中立区，脊柱旁肌肉纤维的刚度降低；然而，纤维束没有差异。此外，KO 和 WT 之间的胫骨前肌没有差异。
这项工作证实了 ENT1 KO 小鼠脊柱连接组织的钙化导致脊柱僵硬，而相邻脊柱旁肌肉中肌纤维弹性模量的同时降低表明脊柱刚度与附着其上的肌肉之间存在直接的补偿关系。
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