1984 VOLVO AWARD IN BIOMECHANICS - MECHANISM OF FACET LOAD TRANSMISSION AS A HYPOTHESIS FOR LOW-BACK-PAIN
1984 VOLVO AWARD IN BIOMECHANICS - MECHANISM OF FACET LOAD TRANSMISSION AS A HYPOTHESIS FOR LOW-BACK-PAIN
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DOI：
10.1097/00007632-198409000-00005
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发表时间：
1984-01-01
期刊：
影响因子：
3
通讯作者：
KING, AI
中科院分区：
文献类型：
--
作者：
YANG, KH;KING, AI
下背痛有一个复杂和多方面的病因。关节面已被证明是承重结构，可能是腰痛的一个部位。本文的目的是建立轴向载荷通过小关节传递的机制，并提出下腰痛的小关节相关假说。用两种方法研究了荷载传递机理。腰椎节段用椎间负荷传感器（IVLC）测量椎间盘负荷，以便推断小关节负荷。施加的载荷从椎体中心向前移动10 mm，向后移动12.5 mm。然后将关节面从身体上分离并轴向加载，以确定它们在拉伸和压缩下的刚度，并观察关节的失效模式。从光学上看，孤立小关节的压缩载荷相当于脊柱的伸展，拉伸载荷相当于脊柱的屈曲。最后，建立了一个腰椎运动节段的有限元模型，以模拟小关节载荷的传递，并研究椎间盘退变对小关节载荷的影响。六个腰椎节段的研究结果显示，正常小关节占3- 25%。如果小关节有关节炎，载荷可高达47%。对孤立小关节的实验表明，它们在压缩时表现为刚性弹簧，在拉伸时表现为弱。关节囊韧带所提供的阻力比受压时小一个数量级。当加压至失效时，腰椎下关节面相对于下方椎骨的上级关节面向后旋转，导致关节囊在约6 kN时破裂，但无骨折。压缩性关节面载荷的传递是通过下关节面尖端与下方椎骨峡部的接触发生的。数据还表明，过载的小关节将导致下小关节向后旋转，导致关节囊拉伸。有限元模型预测，由于椎间盘高度降低，关节突载荷增加。提出了以下假设：关节突负荷过大会拉伸关节囊，可能是导致腰痛的原因。需要进一步的研究来证明这一假设。
Low-back pain has a complex and multi-faceted etiology. The articular facets have been shown to be load-bearing structures and may be a site for low-back pain. The aim of this paper is to establish the mechanism for the transmission of axial load across a facet joint and to propose a facet-related hypothesis for low-back pain. The mechanism of load transmission was studied by two methods. Lumbar segments were instrumented with an intervertebral load cell (IVLC) to measure disc load so that facet load could be deduced. The applied load was moved 10 mm anteriorly and 12.5 mm posteriorly from the center of the vertebral body. The facets then were separated from the body and loaded axially to determine their stiffness in tension and compression and to observe the fallure mode of the joint. It was shown optically that compressive loading of the isolated facet joints was equivalent to spinal extension and tensile loading to spinal flexion. Lastly, a finite element model of a lumbar motion segment was developed to simulate the transmission of facet load and to study the effects of disc degeneration on facet loads. Results of the study on six lumbar segments revealed that the normal facets carried 3–25%. If the facet joint was arthritic, the load could be as high as 47%. Experiments on isolated facet joints revealed that they behaved as a stiffening spring in compression and were weak in tension. The resistance supplied by the capsular ligaments was an order of magnitude less than that in compression. When loaded to failure in compression, the inferior lumbar facets rotated posteriorly relative to the superior facets of the vertebra below and caused the capsule to rupture at about 6 kN without bony fracture. The transmission of compressive facet load occurs through contact of the tip of the inferior facet with the pars of the vertebra below. The data also show that an overloaded facet joint will cause rearward rotation of the inferior facet, resulting in the stretching of the joint capsule. The finite element model predicted an increase in facet load due to a decrease in disc height. The following hypothesis is proposed: Excessive facet loads stretch the joint capsule and can be a cause for low-back pain. Further study is needed to prove this hypothesis.