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骨骼对损伤的反应机制。

Mechanisms of bone response to injury.

作者信息

Dittmer Keren E, Firth Elwyn C

机构信息

Institute of Veterinary, Animal and Biomedical Sciences, Massey University, Palmerston North, New Zealand (Dittmer).

Department of Sport and Exercise, Faculty of Science, University of Auckland, Auckland, New Zealand (Firth).

出版信息

J Vet Diagn Invest. 2017 Jul;29(4):385-395. doi: 10.1177/1040638716679861. Epub 2017 Jan 6.

DOI:10.1177/1040638716679861
PMID:28061633
Abstract

Bone, despite its relatively inert appearance, is a tissue that is capable of adapting to its environment. Wolff's law, first described in the 19th century, describes the ability of bone to change structure depending on the mechanical forces applied to it. The mechanostat model extended this principle and suggested that the amount of strain a bone detects depends on bone strength and the amount of muscle force applied to the bone. Experimental studies have found that low-magnitude, high-frequency mechanical loading is considered to be the most effective at increasing bone formation. The osteocyte is considered to be the master regulator of the bone response to mechanical loading. Deformation of bone matrix by mechanical loading is thought to result in interstitial fluid flow within the lacunar-canalicular system, which may activate osteocyte mechanosensors, leading to changes in osteocyte gene expression and ultimately increased bone formation and decreased bone resorption. However, repetitive strain applied to bone can result in microcracks, which may propagate and coalesce, and if not repaired predispose to catastrophic fracture. Osteocytes are a key component in this process, whereby apoptotic osteocytes in an area of microdamage promote targeted remodeling of the damaged bone. If fractures do occur, fracture repair can be divided into 2 types: primary and secondary healing. Secondary fracture repair is the most common and is a multistage process consisting of hematoma formation and acute inflammation, callus formation, and finally remodeling, whereby bone may return to its original form.

摘要

尽管骨骼外观相对无活性,但它是一种能够适应其环境的组织。沃尔夫定律于19世纪首次被描述,它描述了骨骼根据施加于其上的机械力改变结构的能力。机械稳态模型扩展了这一原理,并表明骨骼检测到的应变大小取决于骨骼强度和施加于骨骼的肌肉力量大小。实验研究发现,低强度、高频机械负荷被认为在增加骨形成方面最有效。骨细胞被认为是骨骼对机械负荷反应的主要调节者。机械负荷导致骨基质变形被认为会引起腔隙-小管系统内的组织液流动,这可能激活骨细胞机械传感器,导致骨细胞基因表达发生变化,最终增加骨形成并减少骨吸收。然而,施加于骨骼的重复性应变会导致微裂纹,微裂纹可能会扩展并合并,如果不修复则易引发灾难性骨折。骨细胞是这一过程的关键组成部分,在微损伤区域凋亡的骨细胞会促进受损骨骼的靶向重塑。如果确实发生骨折,骨折修复可分为两种类型:一期愈合和二期愈合。二期骨折修复最为常见,是一个多阶段过程,包括血肿形成和急性炎症、骨痂形成,最后是重塑,在此过程中骨骼可能恢复到其原始形态。

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