Shapiro Frederic, Connolly Susan, Zurakowski David, Menezes Nina, Olear Elizabeth, Jimenez Mauricio, Flynn Evelyn, Jaramillo Diego
Department of Orthopaedic Surgery, Children's Hospital Boston, Boston, MA 02115, USA.
J Bone Joint Surg Am. 2009 Dec;91(12):2903-14. doi: 10.2106/JBJS.H.01464.
Ischemic necrosis of the femoral head can be induced surgically in the piglet. We used this model to assess femoral head deformation and repair in vivo by sequential magnetic resonance imaging and by correlating end-stage findings with histologic assessments.
Ischemic necrosis of the femoral head was induced in ten three-week-old piglets by tying a silk ligature around the base of the femoral neck (intracapsular) and cutting the ligamentum teres. We used magnetic resonance imaging with the piglets under general anesthesia to study the hips at forty-eight hours and at one, two, four, and eight weeks. Measurements on magnetic resonance images in the midcoronal plane of the involved and control sides at each time documented the femoral head height, femoral head width, superior surface cartilage height, and femoral neck-shaft angle. Histologic assessments were done at the time of killing.
Complete ischemia of the femoral head was identified in all involved femora by magnetic resonance imaging at forty-eight hours. Revascularization began at the periphery of the femoral head as early as one week and was underway in all by two weeks. At eight weeks, magnetic resonance imaging and histologic analysis showed deformation of the femoral head and variable tissue deposition. Tissue responses included (1) vascularized fibroblastic ingrowth with tissue resorption and cartilage, intramembranous bone, and mixed fibro-osseous or fibro-cartilaginous tissue synthesis and (2) resumption of endochondral bone growth. At eight weeks, the mean femoral head measurements (and standard error of the mean) for the control compared with the ligated femora were 10.4 +/- 0.4 and 4.8 +/- 0.4 mm, respectively, for height; 26.7 +/- 0.8 and 31.2 +/- 0.8 mm for diameter; 1.1 +/- 0.1 and 2.3 +/- 0.1 mm for cartilage thickness; and 151 degrees +/- 2 degrees and 135 degrees +/- 2 degrees for the femoral neck-shaft angle. Repeated-measures mixed-model analysis of variance revealed highly significant effects of ligation in each parameter (p < 0.0001).
Magnetic resonance imaging allows for the assessment of individual hips at sequential time periods to follow deformation and repair. There was a variable tissue response, and histologic assessment at the time of killing was shown to correlate with the evolving and varying magnetic resonance imaging signal intensities. Femoral head height on the ischemic side from one week onward was always less than the initial control value and continually decreased with time, indicating collapse as well as slowed growth. Increased femoral head width occurred relatively late (four to eight weeks), indicating cartilage model overgrowth concentrated at the periphery.
可通过手术诱导仔猪发生股骨头缺血性坏死。我们利用该模型，通过连续磁共振成像以及将终末期结果与组织学评估相关联，在体内评估股骨头的变形和修复情况。
对10只3周龄仔猪，通过在股骨颈基部（关节囊内）结扎丝线并切断圆韧带，诱导股骨头缺血性坏死。在全身麻醉下对仔猪进行磁共振成像，分别于术后48小时、1周、2周、4周和8周对髋关节进行研究。每次在患侧和对照侧的正中矢状面进行磁共振图像测量，记录股骨头高度、股骨头宽度、上表面软骨高度和股骨颈干角。处死时进行组织学评估。
磁共振成像显示，术后48小时所有患侧股骨的股骨头均出现完全缺血。股骨头周边最早在1周时开始血管再生，至2周时全部开始血管再生。8周时，磁共振成像和组织学分析显示股骨头变形及不同的组织沉积。组织反应包括：（1）血管化的成纤维细胞长入，伴有组织吸收以及软骨、膜内骨和混合性纤维骨或纤维软骨组织合成；（2）软骨内骨生长恢复。8周时，对照侧与结扎侧股骨的平均股骨头测量值（及均值标准误）分别为：高度，10.4±0.4和4.8±0.4mm；直径，26.7±0.8和31.2±0.8mm；软骨厚度，1.1±0.1和2.3±0.1mm；股骨颈干角，151°±2°和135°±2°。重复测量混合模型方差分析显示，结扎对各参数均有高度显著影响（p<0.000１）。
磁共振成像可在连续时间段内对个体髋关节进行评估，以跟踪其变形和修复情况。存在不同的组织反应，处死时的组织学评估显示与不断变化的磁共振成像信号强度相关。缺血侧股骨头高度从1周起始终低于初始对照值，并随时间持续下降，表明出现塌陷以及生长减缓。股骨头宽度增加相对较晚（4至8周），表明软骨模型过度生长集中在周边。
