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骨下骨囊肿生长中加压流体的作用。

The role of pressurized fluid in subchondral bone cyst growth.

机构信息

Department of Biomedical Engineering, Eindhoven University of Technology, PO Box 513, 5600 MB, Eindhoven, The Netherlands.

出版信息

Bone. 2011 Oct;49(4):762-8. doi: 10.1016/j.bone.2011.06.028. Epub 2011 Jun 30.

Abstract

Pressurized fluid has been proposed to play an important role in subchondral bone cyst development. However, the exact mechanism remains speculative. We used an established computational mechanoregulated bone adaptation model to investigate two hypotheses: 1) pressurized fluid causes cyst growth through altered bone tissue loading conditions, 2) pressurized fluid causes cyst growth through osteocyte death. In a 2D finite element model of bone microarchitecture, a marrow cavity was filled with fluid to resemble a cyst. Subsequently, the fluid was pressurized, or osteocyte death was simulated, or both. Rather than increasing the load, which was the prevailing hypothesis, pressurized fluid decreased the load on the surrounding bone, thereby leading to net bone resorption and growth of the cavity. In this scenario an irregularly shaped cavity developed which became rounded and obtained a rim of sclerotic bone after removal of the pressurized fluid. This indicates that cyst development may occur in a step-wise manner. In the simulations of osteocyte death, cavity growth also occurred, and the cavity immediately obtained a rounded shape and a sclerotic rim. Combining both mechanisms increased the growth rate of the cavity. In conclusion, both stress-shielding by pressurized fluid, and osteocyte death may cause cyst growth. In vivo observations of pressurized cyst fluid, dead osteocytes, and different appearances of cysts similar to our simulation results support the idea that both mechanisms can simultaneously play a role in the development and growth of subchondral bone cysts.

摘要

已有研究提出,高压流体在软骨下骨囊肿的发展中起重要作用。然而,确切的机制仍存在推测。我们使用已建立的计算性机械调节骨适应模型来研究两个假设:1)高压流体通过改变骨组织的受力条件引起囊肿生长,2)高压流体通过破骨细胞死亡引起囊肿生长。在骨微结构的二维有限元模型中,骨髓腔充满了液体以模拟囊肿。随后,对流体进行加压,或模拟破骨细胞死亡,或同时进行这两种操作。加压而不是增加负荷,这是目前的主流假设,反而会降低周围骨的负荷,从而导致净骨吸收和囊腔生长。在这种情况下,形成了一个不规则形状的囊腔,在去除加压流体后,该囊腔变得圆形,并获得了硬化骨的边缘。这表明囊肿的发展可能是分阶段进行的。在破骨细胞死亡的模拟中,囊腔也发生了生长,囊腔立即呈现出圆形和硬化骨的边缘。同时结合这两种机制会增加囊腔的生长速度。总之,高压流体引起的应力屏蔽和破骨细胞死亡都可能导致囊肿生长。对囊肿内高压流体、死骨细胞以及与我们的模拟结果相似的不同表现形式的囊肿的体内观察结果支持这样一种观点,即这两种机制可以同时在软骨下骨囊肿的发展和生长中发挥作用。

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