Intracapsular hip fracture: Increased cortical remodeling in the thinned and porous anterior region of the femoral neck
Intracapsular hip fracture: Increased cortical remodeling in the thinned and porous anterior region of the femoral neck
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DOI：
10.1007/s001980050223
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发表时间：
1999-01-01
影响因子：
4
通讯作者：
Reeve, J
中科院分区：
文献类型：
--
作者：
Bell, KL;Loveridge, N;Reeve, J
先前已经表明，在跌落到大粗隆上时，前下皮质承受最大的拉应力。我们最近发现，在股骨颈骨折的病例中，股骨颈前部和前下部的皮质变薄和孔洞最大。为了研究这是否与髋关节囊内骨折患者和尸检对照女性股骨颈组织哈弗氏重塑相关的表面参数有关，我们对此进行了研究。冰冻切片进行抗酒石酸酸性磷酸酶(TRAP)或碱性磷酸酶(ALP)活性检测。在股骨颈的每个象限(下、前、上、后)确定活跃的管子的比例。然后将活检组织包埋于甲基丙烯酸酯中，以便使用Goldner‘s和SoloChrome切片进行组织形态计量学。在所有病例中，大脑皮层根管改建的比例没有显著增加(p=0.846)，但改建的区域分布与对照组明显不同。在前皮质，进行根管重塑的比例增加了56%(p=0.0087)，而在上侧区域则相对减少了35%(p=0.0047)。在病例的前皮质中，侵蚀(p=0.019)和类骨质(p=0.041)根管的比例分别增加了76%和42%。在上部区域，重塑部位的比例下降是由于具有骨样表面的根管显著减少(51%；p=0.0031)。以皮质孔隙度为因变量的协方差分析表明，孔隙度显著依赖于侵蚀的区域分布(p=0.033)，而与形成的渠道的分布(p=0.153)无关(R(2)adj=0.51)。病例组前部TRAP和碱性磷酸酶细胞水平显著高于对照组(TRAP 55%，p=0.006；碱性磷酸酶36%，p=0.003)。对于后部和下部，细胞陷阱和碱性磷酸酶水平与对照组相比没有明显差异。这些数据表明，我们以前在髋部骨折病例中观察到的前皮质皮质变薄和孔洞增加与哈弗斯重塑指数的增加有关。这些发现与假设一致，即在髋部骨折病例中，前皮质的重塑失衡是一个持续到骨折时的过程，是由于与成骨反应相关的破骨细胞活动增加，而成骨反应不足以防止骨丢失。
It has been shown previously that the anteroinferior cortex is subjected to maximal tensile stress during a fall onto the greater trochanter. We have recently shown that in cases of femoral neck fracture, cortical thinning and porosity is greatest in the anterior and antero-inferior region of the femoral neck. To investigate whether this is due to increased remodeling, we have quantified surface-based parameters associated with Haversian remodeling in femoral neck biopsies from women with intracapsular hip fracture and postmortem controls. Cryostat sections of chilled biopsies were reacted for either tartrate-resistant acid phosphatase (TRAP) or alkaline phosphatase (ALP) activity. Proportions of active canals were determined in each quadrant (inferior, anterior, superior, posterior) of the femoral neck. The biopsies were then embedded in methacrylate to permit histomorphometry using Goldner's and Solochrome sections. In the cases there was no significant increase in the proportion of canals undergoing remodeling in the cortex as a whole (p = 0.846), but the regional distribution of remodeling was markedly different from that in the controls. In the anterior cortex, the proportion of canals undergoing remodeling was increased by 56% (p = 0.0087); in contrast there was a relative decrease of 35% in the superior region (p=0.0047). In the anterior cortex of cases there were 76% and 42% increases in the proportions of eroded (p=0.019) and osteoid-bearing (p = 0.041) canals, respectively. In the superior region, the decrease in the proportion of remodeling sites was due to a marked decrease in canals with an osteoid surface (51%; p=0.0031). Covariance analysis with cortical porosity as the dependent variable showed that porosity was significantly dependent on the regional distribution of eroded (p = 0.033) but not on the distribution of forming (p =0.153) canals (R(2)adj = 0.51). Cellular levels of TRAP and ALP were significantly elevated in the anterior region of cases compared with the controls (TRAP 55%, p=0.006; ALP 36%, p=0.003). For the posterior and inferior regions there were no marked differences in cellular TRAP and ALP levels compared with control values. These data show that the increased cortical thinning and increased porosity we have previously observed in the anterior cortex in cases of hip fracture are associated with increased indices of Haversian remodeling. These findings are consistent with the hypothesis that, in cases of hip fracture, remodeling imbalance in the anterior cortex is a continuing process up to the time of fracture and is due to increased osteoclastic cellular activity associated with an osteoblastic response that is inadequate to prevent bone loss.