Ludwig Boltzmann Institute of Osteology at Hanusch Hospital of WGKK and AUVA, Trauma Centre Meidling, 4(th) Medical Department, Hanusch Hospital, Vienna, Austria.
Bone. 2010 Feb;46(2):379-85. doi: 10.1016/j.bone.2009.10.006. Epub 2009 Oct 13.
Traditionally, it is believed that structural failure of the ischemic epiphysis as well as changes in radiodensity seen in the early stage of Legg-Calvé-Perthes disease is due to the repair process. However, little is known if matrix properties are altered following ischemic injury of the juvenile femoral head. The purpose of this study was to determine the matrix mineralization density, an important determinant of material quality and strength, of the proximal femoral epiphysis in an experimental animal model of Perthes disease. Ten piglets were surgically induced with femoral head ischemia and euthanized at 4 and 8 weeks following surgery. Contralateral, unoperated femoral heads were used as controls. Bone and calcified cartilage mineralization density distribution parameters were determined using quantitative backscattered electron imaging (qBEI) in the epiphyseal calcified articular cartilage, subchondral bone and central trabecular bone region. Histological as well as radiographic assessment was also performed. In the necrotic calcified epiphyseal cartilage matrix, a significant increase in the mean degree of mineralization (CaMean: +24%, p<0.0001) as well as the homogeneity of mineralization (CaWidth: -21%, p<0.05) and a significantly reduced amount of low mineralized matrix (CaLow: -49%, p<0.0001) were already present at 4 weeks post-ischemia induction. Similar changes, but more moderate, were also seen in the subchondral bone region. In contrast, in the necrotic central trabecular region, significant changes in matrix mineralization were found at 8 weeks (CaMean: +4%, p<0.05; CaWidth: -22%, p<0.05; CaLow: -8%, p<0.05) but not at 4 weeks post-ischemia induction. Our findings indicate that the process of matrix mineralization continues in necrotic calcified articular cartilage and bone following femoral head ischemia, which leads to a higher and more homogenous mineralized tissue matrix altering its intrinsic material properties. This may also explain the increased radiodensity seen in the early stage of Perthes disease prior to the initiation of the repair process.
传统上,人们认为缺血性骨骺的结构失效以及莱格-卡尔维-佩尔特斯病早期所见的放射密度变化是修复过程的结果。然而,对于少年股骨头缺血性损伤后基质特性是否发生改变,人们知之甚少。本研究的目的是确定实验性佩尔特斯病动物模型中股骨头缺血后近侧股骨骨骺的基质矿化密度,这是材料质量和强度的重要决定因素。10 头小猪通过手术诱导股骨头缺血,并在手术后 4 周和 8 周时安乐死。对侧未手术的股骨头用作对照。使用定量背散射电子成像(qBEI)在骨骺钙化关节软骨、软骨下骨和中央小梁骨区域确定骨和钙化软骨矿化密度分布参数。还进行了组织学和放射学评估。在坏死的钙化骺软骨基质中,矿化程度的平均值(CaMean:+24%,p<0.0001)以及矿化均匀度(CaWidth:-21%,p<0.05)显著增加,而低矿化基质的量明显减少(CaLow:-49%,p<0.0001),在缺血诱导后 4 周即可观察到。在软骨下骨区域也观察到类似但更温和的变化。相比之下,在坏死的中央小梁区域,基质矿化在缺血后 8 周时(CaMean:+4%,p<0.05;CaWidth:-22%,p<0.05;CaLow:-8%,p<0.05)发生显著变化,但在缺血诱导后 4 周时未发生变化。我们的研究结果表明,股骨头缺血后,坏死的钙化关节软骨和骨中的基质矿化过程仍在继续,这导致矿化组织基质的更高和更均匀,改变其固有材料特性。这也可以解释在修复过程开始之前,佩尔特斯病早期所见的放射密度增加。