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股骨头坏死:病理生理学与当前治疗理念

Osteonecrosis of the femoral head: pathophysiology and current concepts of treatment.

作者信息

Petek Daniel, Hannouche Didier, Suva Domizio

机构信息

Clinic of Orthopaedics and Trauma Surgery, HFR-Fribourg District Hospitals, Fribourg, Switzerland.

Clinic of Orthopaedics and Trauma Surgery, Geneva University Hospitals, Geneva, Switzerland.

出版信息

EFORT Open Rev. 2019 Mar 15;4(3):85-97. doi: 10.1302/2058-5241.4.180036. eCollection 2019 Mar.

Abstract

Osteonecrosis of the femoral head is a disabling pathology affecting a young population (average age at treatment, 33 to 38 years) and is the most important cause of total hip arthroplasty in this population. It reflects the endpoint of various disease processes that result in a decrease of the femoral head blood flow.The physiopathology reflects an alteration of the vascularization of the fine blood vessels irrigating the anterior and superior part of the femoral head. This zone of necrosis is the source of the loss of joint congruence that leads to premature wear of the hip.Several different types of medication have been developed to reverse the process of ischemia and/or restore the vascularization of the femoral head. There is no consensus yet on a particular treatment.The surgical treatments aim to preserve the joint as far as the diagnosis could be made before the appearance of a zone of necrosis and the loss of joint congruence. They consist of bone marrow decompressions, osteotomies around the hip, vascular or non-vascular grafts.Future therapies include the use of biologically active molecules as well as implants impregnated with biologically active tissue. Cite this article: 2019;4:85-97. DOI: 10.1302/2058-5241.4.180036.

摘要

股骨头坏死是一种致残性病变,影响年轻人群(治疗时的平均年龄为33至38岁),是该人群全髋关节置换术的最重要原因。它反映了各种导致股骨头血流减少的疾病过程的终点。病理生理学反映了供应股骨头前部和上部的微小血管的血管化改变。这个坏死区域是导致髋关节过早磨损的关节一致性丧失的根源。已经开发出几种不同类型的药物来逆转缺血过程和/或恢复股骨头的血管化。对于特定的治疗方法尚未达成共识。手术治疗旨在在坏死区域出现和关节一致性丧失之前尽可能保留关节。它们包括骨髓减压、髋关节周围截骨术、血管或非血管移植。未来的治疗方法包括使用生物活性分子以及浸渍有生物活性组织的植入物。引用本文:2019;4:85 - 97。DOI:10.1302/2058 - 5241.4.180036。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/02a9/6440301/3f65422afa77/eor-4-85-g001.jpg

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