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[股骨头缺血性坏死中“新月征”形成的机制]

[Mechanism of "crescent sign" formation in avascular necrosis of femoral head].

作者信息

Zhang Nianfei, Qi Shengwen, Chai Jianfeng

机构信息

Department of Orthopedic Surgery, China-Japan Friendship Hospital, 100029, Beijing, P. R. China.

出版信息

Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi. 2008 Mar;22(3):303-6.

PMID:18396707
Abstract

OBJECTIVE

To investigate corresponding relation between structure change of the femoral head with "crescent sign" and stress exerted on the avascular necrosis of femoral head, to explore the mechanism of the "crescent sign" formation.

METHODS

From March 1998 to April 2003, the femoral heads of 18 hips in 16 cases having osteonecrosis and "crescent sign" in X-ray film before total hip arthroplasty, were collected. General and coronal section plane morphology of the femoral heads were observed. The principle of effective stress and stress concentration theory were used to explain the phenomena and structure changes in osteonecrosis of the femoral head.

RESULTS

Cancellous bone existed as a three-dimensional, interconnected network of trabeculae rods and plates, with 50%-90% of porosity and 20-30 mmHg bone marrow pressure. According to the definition of porous media, bones especially cancellous bone was a kind of solid and liquid two phases porous media. Cross-sectional structure changes in the junction between subchondral plate and cancellous were the place where stress concentrated. The principle of effective stress and stress concentration theory could explain the phenomena and their relationship that occurred in avascular necrosis of the femoral head.

CONCLUSION

The "crescent sign" starts in an area of very focal resorption in the subchondral plate laterally and peripherally. The focal resorption in the subchondral plate breaks the continuity of subchondral plate and causes stress concentration in the resorption region. The concentrated stress accumulates in the junction between subchondral plate and unrepaired necrotic cancellous bone brings on the fracture right below the subchondral plate. The focal resorption of the subchondral plate also provides a pathway for the pore water in the unrepaired necrotic bone skeleton to outflow, therefore cause effective stress increase and unrepaired necrotic bone skeleton be compacted by increased effective stress applied on unrepaired necrotic cancellous bone skeleton, and results in the volume decrease of unrepaired necrotic cancellous bone and the formation of cavum below the subchondral plate. The cavum shows "crescent sign" in the X-ray film.

摘要

目的

探讨具有“新月征”的股骨头结构改变与股骨头缺血性坏死所受应力之间的对应关系,以探寻“新月征”的形成机制。

方法

收集1998年3月至2003年4月间16例全髋关节置换术前X线片存在骨坏死且有“新月征”的18个股骨头。观察股骨头大体及冠状切面形态。应用有效应力原理和应力集中理论解释股骨头坏死中的现象及结构变化。

结果

松质骨呈三维相互连接的小梁杆和板的网络结构,孔隙率为50% - 90%,骨髓压力为20 - 30 mmHg。根据多孔介质的定义,骨尤其是松质骨是一种固液两相多孔介质。软骨下板与松质骨交界处的横截面结构变化是应力集中的部位。有效应力原理和应力集中理论能够解释股骨头缺血性坏死中发生的现象及其关系。

结论

“新月征”起始于软骨下板外侧及周边非常局限的吸收区域。软骨下板的局限性吸收破坏了软骨下板的连续性,并导致吸收区域的应力集中。集中的应力积聚在软骨下板与未修复的坏死松质骨交界处,致使软骨下板下方发生骨折。软骨下板的局限性吸收也为未修复的坏死骨骨架中的孔隙水提供了流出通道,从而导致有效应力增加,未修复的坏死骨骨架因施加在未修复的坏死松质骨骨架上的有效应力增加而被压实,导致未修复的坏死松质骨体积减小以及软骨下板下方空洞形成。该空洞在X线片上表现为“新月征”。

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