摘要

The German doctor Hermann Kummell described Kummell'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 Kummell's disease, most authors regard ischemic necrosis of the vertebral body as the primary pathogenesis of Kummell's disease. However, we argue that Kummell'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 Kummell's disease, it would not be the proximal cause of Kummell'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 Kummell'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.

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