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疲劳微损伤是骨力学和生物学的基本要素。

Fatigue microdamage as an essential element of bone mechanics and biology.

作者信息

Martin R Bruce

机构信息

Orthopaedic Research Laboratories, University of California at Davis Medical Center, Sacramento, CA 95817, USA.

出版信息

Calcif Tissue Int. 2003 Aug;73(2):101-7. doi: 10.1007/s00223-002-1059-9.

Abstract

The fossil record shows that bone remodeling has existed since the earliest large vertebrates became weight-bearing on land, but the functions of remodeling have long been debated. The principal protagonists in this debate have been those favoring a mechanical function and those asserting that remodeling serves to move calcium in and out of the skeleton. In recent years the arguments of the former school have included not only the adaptation of internal structure to specific kinds of stresses, but the need to remove fatigue damage. It has become clear that (1) physiologic strains continually produce fatigue damage in bone; (2) this damage weakens bone and is associated with both osteocyte apoptosis and the activation of remodeling; and (3) remodeling is the only means by which this damage can be removed. The significance of these observations is increased by the fact that fatigue failure is more likely in larger structures. This "volume effect," along with the advantages of enhanced mobility and metabolic efficiency, may have selected for bone remodeling as a means of controlling fatigue damage as it occurs, allowing larger vertebrates to maintain a relatively light skeleton over an extended lifetime. In this view, bone remodeling is not primarily a mechanism for calcium transport, but is intimately related to other inflammatory repair responses.

摘要

化石记录表明,自最早的大型脊椎动物在陆地上开始负重以来,骨骼重塑就已存在,但重塑的功能长期以来一直存在争议。这场争论的主要参与者是那些支持机械功能的人以及那些断言重塑的作用是使钙进出骨骼的人。近年来,前一派的观点不仅包括内部结构对特定类型应力的适应,还包括消除疲劳损伤的必要性。已经很清楚的是:(1)生理应变会持续在骨骼中产生疲劳损伤;(2)这种损伤会削弱骨骼,并与骨细胞凋亡和重塑激活相关;(3)重塑是消除这种损伤的唯一途径。这些观察结果的重要性因以下事实而增加:较大结构中更可能发生疲劳失效。这种“体积效应”,连同增强的机动性和代谢效率的优势,可能促使选择骨骼重塑作为一种在疲劳损伤发生时进行控制的手段,使大型脊椎动物能够在延长的生命周期内维持相对较轻的骨骼。按照这种观点,骨骼重塑主要不是一种钙运输机制,而是与其他炎症修复反应密切相关。

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