Despite the prevalence of low back pain (LBP) in society, the pathomechanism of LBP continues to elude researchers. LBP patients have demonstrated morphological and material property changes to their lumbar soft tissues, potentially leading to irregular load sharing within the lumbar spine. This study aims to analyze potential stress shielding consequential of augmented soft tissue properties via the comparison of a healthy and LBP finite element models. The models developed in this study include the vertebrae, intervertebral discs and soft tissues from L1–S1. Soft tissue morphology and material properties for the LBP model were augmented to reflect documented clinical findings. Model validation preceded testing and was confirmed through comparison to the available literature. Relative to the healthy model, the LBP model demonstrated an increase in stress by 15.6%, with 99.8% of this stress increase being distributed towards the thoracolumbar fascia. The majority of stress skewed towards the fascia may indicate a potential stress allocation bias whereby the lumbar muscles are unable to receive regular loading, leading to stress shielding. This load allocation bias and subsequent stress shielding may potentially contribute to the progression and pathomechanism of LBP but prospective studies would be required to make that link.

Graphical abstract

中文翻译：

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包括胸腰筋膜在内的有限元腰椎应力屏蔽检查

尽管腰痛 (LBP) 在社会中普遍存在，但研究人员仍不了解 LBP 的发病机制。LBP 患者的腰椎软组织已表现出形态和材料特性的变化，可能导致腰椎内不规则的负荷分配。本研究旨在通过比较健康和 LBP 有限元模型来分析增强软组织特性的潜在应力屏蔽结果。本研究中开发的模型包括来自 L1-S1 的椎骨、椎间盘和软组织。增强了 LBP 模型的软组织形态和材料特性，以反映记录的临床发现。模型验证先于测试，并通过与现有文献的比较得到确认。相对于健康模型，LBP 模型显示压力增加了 15.6%，其中 99.8% 的压力增加分布到胸腰筋膜。大部分压力偏向筋膜可能表明存在潜在的压力分配偏差，由此腰部肌肉无法正常承受负荷，从而导致压力屏蔽。这种负荷分配偏差和随后的压力屏蔽可能有助于 LBP 的进展和病理机制，但需要前瞻性研究来建立这种联系。

图形概要