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Structural consequences of subchondral bone involvement in segmental osteonecrosis of the femoral head

 

作者: Thomas D. Brown,   Kelly J. Baker,   Richard A. Brand,  

 

期刊: Journal of Orthopaedic Research  (WILEY Available online 1992)
卷期: Volume 10, issue 1  

页码: 79-87

 

ISSN:0736-0266

 

年代: 1992

 

DOI:10.1002/jor.1100100110

 

出版商: Wiley Subscription Services, Inc., A Wiley Company

 

关键词: Femoral head;Osteonecrosis;Subchondral plate;Finite element;Stress

 

数据来源: WILEY

 

摘要:

AbstractAppearance of a crescent sign usually marks the onset of necrotic femoral head collapse, but very little is known about which local factors contribute most critically to avoiding or postponing fracture of at‐risk juxtaarticular cancellous bone. A three‐dimensional finite element model was used to test the hypothesis that an initially mechanically uncompromised subchondral plate could provide a substantial degree of stress protection to a weakened underlying segmental infarction. The computational simulation of osteonecrosis showed that the principal stress distribution for an assumption of subchondral plate weakening (given also an underlying, comparably weakened segmental infarction) differed inappreciably from that of a normal femoral head. However, the tendency for local structural failure, as reflected in the ratio of stress to strength, was substantially higher in the former instance. If, instead, the mechanical integrity of the subchondral plate overlying the weakened segmental infarction was assumed to be preserved, computed stress levels in the at‐risk subjacent necrotic cancellous bone were still over 70% as high as for the weakened‐plate case. The data thus indicate that even a fully normal subchondral plate can provide only modest stress protection of a weakened underlying segmental infarction, whereas weakening of the necrotic cancellous bone throughout the infarction induces marked stress increase in the overlying subchondral plate. These findings suggest that the onset of collapse is probably dominated much more strongly by the degree of structural degradation of the cancellous bone within the main infarct body, than by the degree of structural degradation within the subchondra

 

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