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微裂纹导致的流体切应力降低:许莫氏病的一种可能的主要发病机制。

Decreases in fluid shear stress due to microcracks: a possible primary pathogenesis of Kümmell's disease.

机构信息

Department of Orthopaedics, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, #88 Jiefang Road, Hangzhou 310009, PR China.

出版信息

Med Hypotheses. 2011 Nov;77(5):897-9. doi: 10.1016/j.mehy.2011.08.005. Epub 2011 Aug 27.

DOI:10.1016/j.mehy.2011.08.005
PMID:21873000
Abstract

The German doctor Hermann Kümmell described Kümmell's disease as the clinical scenario in which patients suffer a trivial spinal trauma, but develop a symptomatic, progressive, angular kyphosis after a symptom-free period of months to years. Since an intravertebral vacuum phenomenon, which is considered indicative of ischemic osteonecrosis, is often seen in the radiographs of patients with Kümmell's disease, most authors regard ischemic necrosis of the vertebral body as the primary pathogenesis of Kümmell's disease. However, we argue that Kümmell's disease is not commonly associated with typical avascular osteonecrosis of the femoral head and the intravertebral vacuum phenomenon is also present in other diseases. We postulated that even if ischemia plays a role in the pathogenesis of Kümmell's disease, it would not be the proximal cause of Kümmell's disease. In this article, we review the role of fluid shear stress in bone remolding and propose a microcosmic hypothesis in which microcracks lead to decreased fluid shear stress, which acts as the primary cause of Kümmell's disease. This was supported by conclusions drawn from a literature review: (1) fluid shear stress plays a crucial role in bone remodeling, and the osteocyte network is the main sensor of this mechanical stimulus; (2) decreased fluid shear stress will cause disequilibration of bone homeostasis, increasing bone resorption and reducing bone formation; and (3) the fluid flow of lacunar-canalicular porosity (PLC) and fluid shear stress near the microcracks decreases.

摘要

德国医生赫尔曼·库梅勒(Hermann Kümmell)将库梅勒病描述为一种临床情况,即患者遭受轻微的脊柱创伤,但在数月至数年后出现无症状的、进行性的、成角的后凸畸形。由于在库梅勒病患者的 X 光片中经常可见到被认为提示缺血性骨坏死的椎体内真空现象,因此大多数作者认为椎体缺血性坏死是库梅勒病的主要发病机制。然而,我们认为库梅勒病通常与典型的股骨头缺血性坏死无关,并且椎体内真空现象也存在于其他疾病中。我们假设,即使缺血在库梅勒病的发病机制中起作用,它也不是库梅勒病的近端原因。在本文中,我们回顾了流体剪切力在骨重塑中的作用,并提出了一个微观假说,即微裂纹导致流体剪切力降低,这是库梅勒病的主要原因。这一假说得到了文献综述结论的支持:(1)流体剪切力在骨重塑中起着至关重要的作用,骨细胞网络是这种机械刺激的主要传感器;(2)流体剪切力降低会导致骨平衡失调,增加骨吸收并减少骨形成;(3) 微裂纹附近的腔隙-管腔孔隙(PLC)的流体流动和流体剪切力降低。

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