Koo K H, Jeong S T, Jones J P
Department of Orthopaedic Surgery, Gyeong-Sang National University School of Medicine, Chinju, South Korea.
Clin Orthop Relat Res. 1999 Jan(358):158-65.
To determine whether the histologic lesions classified by the system of Arlet et al as Type 2 (granular necrosis of fatty marrow) and Type 3 (complete medullary and trabecular necrosis) always progress to Type 4 (complete necrosis with marginal medullary fibrosis and appositional new bone formation), 10 femoral heads (nine patients) were monitored for 4 years using serial magnetic resonance images. These femoral heads had been diagnosed histologically as having either Type 2 (seven hips) or Type 3 (three hips) necrosis on initial core biopsies. On the initial magnetic resonance image, none of the femoral heads showed any focal lesions indicative of osteonecrosis. In all instances, superselective angiography showed interruption of the superior retinacular artery, and the bone marrow pressure was elevated. During a followup period of 48 to 54 months, no patient had a reactive low signal intensity band develop on T1 weightings, as evidence of a reparative process around the necrotic portion of the lesion, or any other findings of osteonecrosis on magnetic resonance images. These findings suggest that some Type 2 and 3 lesions of Arlet et al may not develop an obvious reactive interface of reparative revascularization and thus may not progress to definite and classic Type 4 osteonecrosis. This study supports the hypothesis that there is an ischemic threshold between reversible intraosseous hypoxia (bone marrow edema syndrome) and irreversible intraosseous anoxia (classic bone infarction or osteonecrosis) and suggests that borderline necrosis occurs in the transition zone of this ischemic threshold and is nonprogressive.
为了确定按照阿莱特等人的系统分类为2型（脂肪骨髓颗粒性坏死）和3型（完全髓质和小梁坏死）的组织学病变是否总会进展为4型（伴有边缘髓质纤维化和贴附性新骨形成的完全坏死），使用系列磁共振成像对10个股骨头（9名患者）进行了4年的监测。这些股骨头在初次核心活检时经组织学诊断为2型（7髋）或3型（3髋）坏死。在初次磁共振图像上，所有股骨头均未显示任何提示骨坏死的局灶性病变。在所有病例中，超选择性血管造影显示上支持带动脉中断，且骨髓压力升高。在48至54个月的随访期内，没有患者在T1加权像上出现反应性低信号带，作为病变坏死部分周围修复过程的证据，磁共振图像上也没有出现任何其他骨坏死表现。这些发现表明，阿莱特等人分类的一些2型和3型病变可能不会形成明显的修复性血管再生反应界面，因此可能不会进展为明确的经典4型骨坏死。本研究支持这样一种假说，即可逆性骨内缺氧（骨髓水肿综合征）和不可逆性骨内缺氧（经典骨梗死或骨坏死）之间存在一个缺血阈值，并提示临界性坏死发生在这个缺血阈值的过渡区且不会进展。
