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[从骨髓水肿到骨坏死。新概念]

[From bone marrow edema to osteonecrosis. New concepts].

作者信息

Fernandez-Canton Guillermo

机构信息

Centro OSATEK, Unidad de Dr. Areilza, Bilbao, País Vasco, España.

出版信息

Reumatol Clin. 2009 Sep-Oct;5(5):223-7. doi: 10.1016/j.reuma.2008.02.004. Epub 2009 May 20.

DOI:10.1016/j.reuma.2008.02.004
PMID:21794615
Abstract

The widespread use of MRI in the diagnosis of articular pathology has allowed for an improved knowledge of a series of disturbances that occur with epiphyseal bone edema as a main radiological sign, featured as low signal intensity of the bone marrow on T1 and high signal on STIR and fat saturated T2 sequences. The new etiopathogenic theories postulate a clear differentiation between primary and secondary osteonecrosis. While secondary osteonecrosis is related to risk factors, primary osteonecrosis is a result of a subcondral insufficiency fracture. Both have different characteristic and MRI criteria. The pathogenesis of transient bone edema syndrome (BMES) is currently under discussion, divided between the biomechanic theory and the more classic one that relates to the complex and poorly understood mechanisms associated with complex regional pain syndrome type I (reflex sympathetic dystrophy). The BMES, classically considered a reversible form of osteonecrosis, has enough differentiated features to be considered as a distinct disease. Bone marrow edema can be as extensive in either insufficiency or fatigue stress fractures than in BMES. The diagnostic key is the display of a subcondral bone fracture. These can be resolved or occasionally evolve into a primary osteonecrosis.

摘要

磁共振成像(MRI)在关节病理学诊断中的广泛应用,使人们对一系列以骨骺骨髓水肿为主要影像学表现的病变有了更深入的认识,其特征为在T1加权像上骨髓呈低信号强度,在短T1反转恢复序列(STIR)和脂肪抑制T2加权序列上呈高信号。新的病因学理论明确区分了原发性和继发性骨坏死。继发性骨坏死与危险因素有关,而原发性骨坏死是软骨下不全骨折的结果。两者具有不同的特征和MRI标准。目前,短暂性骨髓水肿综合征(BMES)的发病机制仍在讨论中,存在生物力学理论和与I型复杂性区域疼痛综合征(反射性交感神经营养不良)相关的更为经典但复杂且理解不足的机制两种观点。BMES传统上被认为是骨坏死的一种可逆形式,具有足够独特的特征,可被视为一种独立的疾病。骨髓水肿在不全骨折或疲劳应力性骨折中可能与BMES一样广泛。诊断的关键在于显示软骨下骨折。这些骨折可以愈合,偶尔也会发展为原发性骨坏死。

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