股骨头骨坏死样本空间结构的Micro-CT评估

目的以股骨头骨坏死样本的Micro-CT断层图像为基础，对其进行空间结构评估。方法2003年11月～2005年6月，收集股骨头骨坏死患者行全髋关节置换术时取出的股骨头样本6个，对样本进行Micro-CT断层扫描，获取股骨头骨坏死样本的计算机三维图像，图像空间分辨率为36μm×36μm×36μm。手工选取兴趣区，随后采用骨体积分数（BV／TV）、骨小梁间隙（Tb．Sp）、骨小梁厚度（Tb，Th）、骨小梁数目（Tb．N）、骨表面积体积比（BS／BV）、结构模型指数（SMI）、骨小梁模型因子（Tb．Pf）等三维空间参数分别对股骨头骨坏死标本的正常区域、硬化带和塌陷区进行评价。结果晚期股骨头骨坏死硬化区和塌陷区的骨小梁空间结构明显改变：硬化区Bv／Tv明显增加，Tb．Th明显增厚，Tb，Sp变窄，SMI与正常区域的骨小梁无差别；而塌陷区Bv／Tv明显减少，BS／BV增大，Tb．N和Tb．Pf增加，Tb，Th改变不明显。结论Micro-CT作为一种新的检测手段，能够在不损伤样本的条件下快速获取股骨头骨坏死样本断层图像，具有精度高、检测快、可进行三维重建分析的优点。晚期股骨头骨坏死不同区域的骨三维结构呈现出不同的空间结构特征。     

影像学预测股骨头坏死塌陷的研究进展

<正>股骨头坏死塌陷的发生主要为坏死股骨头机械及生物力学性能下降所致。坏死的早期髓腔造血细胞开始死亡,骨母细胞、骨细胞及破骨细胞发生坏死,骨陷窝中的骨细胞消失。此时,骨小梁的结构仍维持原态,密度及骨的坚韧度还未受到影响。其后逐步开始产生修复反应,坏死区域的一侧破骨细胞、骨质发生吸收,而另一侧出现成骨细胞形成新骨,由正常区向坏死区伸展,但修复过程不完全平衡,处在死骨与活骨交界处即修复带的坏死骨小梁已进入修复期,但位于坏死中心部位的骨小梁未行修复,此时即出现因修复不全而致的骨结构损害及力学性能降低,最终发生股骨头塌陷。目     

激素性与酒精性股骨头坏死患者骨标本坏死区域病理与显微结构特点分析北大核心CSCD

目的观察激素性和酒精性股骨头坏死(osteonecrosis of the femoral head,ONFH)患者骨标本坏死区域的病理和显微结构特点。方法收集2015年8月—2016年4月因ONFH行人工全髋关节置换术的股骨头标本30个,其中男22例,女8例;酒精性15例,激素性15例;两组国际骨循环协会(ARCO)分期构成比较差异无统计学意义(Z=2.143,P=0.143)。取激素性与酒精性ONFH患者骨标本不同区域(坏死区、硬化区、正常区)骨组织,行大体观察、HE染色并计算空骨陷窝率。将完整股骨头标本行Micro-CT扫描,并进行骨微结构定量分析以下参数:骨小梁相对体积(bone volume to total volume,BV/TV)、骨表面积与骨骼体积比(bone surface area to bone volume ratio,BS/BV)、骨矿密度(bone mineral density,BMD)、骨矿容量(bone mineral content,BMC)、结构模型指数(structure model index,SMI)、骨小梁数目(trabecular plate number,Tb.N)、骨小梁厚度(trabecular plate thickness,Tb.Th)、骨小梁间隙(trabecular spacing,Tb.Sp)。结果大体观察示激素性和酒精性ONFH均有骨小梁连续性中断,骨小梁吸收区域有囊变被肉芽组织取代,激素性ONFH肉芽组织内有血管新生的痕迹,酒精性ONFH肉芽组织内血管新生痕迹不明显。HE染色示激素性和酒精性ONFH坏死区均有骨质结构紊乱、骨髓坏死、骨陷窝空虚,其中激素性ONFH骨小梁结构和连续性破坏更严重,酒精性ONFH骨小梁更粗,连续性较激素性ONFH好。激素性ONFH坏死区的空骨陷窝率明显高于酒精性ONFH(P<0.05),但两种ONFH硬化区和正常区空骨陷窝率比较差异无统计学意义(P>0.05)。激素性与酒精性ONFH坏死区与硬化区之间区域在Micro-CT图像中均是低密度区,但前者形态不规则,对应部位大体标本可见富含血运的肉芽组织形成,后者对应部位大体标本见无血运的纤维肉芽组织形成。骨微结构定量分析显示,激素性ONFH坏死区和硬化区BV/TV、BMD、BMC、Tb.N、Tb.Th明显低于酒精性ONFH,BS/BV、SMI、Tb.Sp显著高于酒精性ONFH,差异均有统计学意义(P<0.01);两种ONFH正常区上述各指标比较差异均无统计学意义(P>0.05)。结论激素性和酒精性ONFH标本坏死区的骨小梁连续性均破坏。但两种ONFH有不同的坏死表现形式,激素性ONFH以多发灶性溶骨性骨质破坏为特点,酒精性ONFH是以凝固性骨质坏死为特点。     

小鼠激素性股骨头坏死的组织学演变

目的通过激素性股骨头坏死小鼠模型，了解其组织学变化过程及其规律。方法选用2个月龄FVB小鼠，分为6组，每组5只，A、B、C、D组行甲基强的松龙每日21mg／kg体重皮下注射，分别持续1、2、3、4周，在处死前10和3d以30mg／kg体重腹腔注射盐酸四环素，E组为对照组；F组母鼠行双侧卵巢切除。股骨头行苏木素-伊红（HE）染色、甲苯胺蓝染色、四环素标记、TUNEL和Micro-CT。结果4周时股骨头软骨下骨板和骨小梁出现坏死和空的骨陷窝；有跨越骨骺的骨桥形成；部分骨小梁见双荧光标记带，其中大量骨细胞和成骨细胞TUNEL阳性。Micro-CT发现1～3周骨量逐步下降，股骨头三维重建可见桔皮样改变。结论FVB小鼠作为激素性股骨头坏死的早期病理过程的动物模型有其一定应用价值。     

激素性与酒精性股骨头坏死患者骨标本坏死区域病理与显微结构特点分析

目的观察激素性和酒精性股骨头坏死(osteonecrosis of the femoral head,ONFH)患者骨标本坏死区域的病理和显微结构特点。方法收集2015年8月—2016年4月因ONFH行人工全髋关节置换术的股骨头标本30个,其中男22例,女8例;酒精性15例,激素性15例;两组国际骨循环协会(ARCO)分期构成比较差异无统计学意义(Z=2.143,P=0.143)。取激素性与酒精性ONFH患者骨标本不同区域(坏死区、硬化区、正常区)骨组织,行大体观察、HE染色并计算空骨陷窝率。将完整股骨头标本行Micro-CT扫描,并进行骨微结构定量分析以下参数:骨小梁相对体积(bone volume to total volume,BV/TV)、骨表面积与骨骼体积比(bone surface area to bone volume ratio,BS/BV)、骨矿密度(bone mineral density,BMD)、骨矿容量(bone mineral content,BMC)、结构模型指数(structure model index,SMI)、骨小梁数目(trabecular plate number,Tb.N)、骨小梁厚度(trabecular plate thickness,Tb.Th)、骨小梁间隙(trabecular spacing,Tb.Sp)。结果大体观察示激素性和酒精性ONFH均有骨小梁连续性中断,骨小梁吸收区域有囊变被肉芽组织取代,激素性ONFH肉芽组织内有血管新生的痕迹,酒精性ONFH肉芽组织内血管新生痕迹不明显。HE染色示激素性和酒精性ONFH坏死区均有骨质结构紊乱、骨髓坏死、骨陷窝空虚,其中激素性ONFH骨小梁结构和连续性破坏更严重,酒精性ONFH骨小梁更粗,连续性较激素性ONFH好。激素性ONFH坏死区的空骨陷窝率明显高于酒精性ONFH(P0.05),但两种ONFH硬化区和正常区空骨陷窝率比较差异无统计学意义(P0.05)。激素性与酒精性ONFH坏死区与硬化区之间区域在Micro-CT图像中均是低密度区,但前者形态不规则,对应部位大体标本可见富含血运的肉芽组织形成,后者对应部位大体标本见无血运的纤维肉芽组织形成。骨微结构定量分析显示,激素性ONFH坏死区和硬化区BV/TV、BMD、BMC、Tb.N、Tb.Th明显低于酒精性ONFH,BS/BV、SMI、Tb.Sp显著高于酒精性ONFH,差异均有统计学意义(P0.01);两种ONFH正常区上述各指标比较差异均无统计学意义(P0.05)。结论激素性和酒精性ONFH标本坏死区的骨小梁连续性均破坏。但两种ONFH有不同的坏死表现形式,激素性ONFH以多发灶性溶骨性骨质破坏为特点,酒精性ONFH是以凝固性骨质坏死为特点。     

高位股骨头颈开窗植骨支撑术治疗早期股骨头坏死

 目的 探讨高位股骨头颈开窗植骨支撑术治疗早期股骨头坏死的近期疗效。方法 2009 年 1 月至 2011 年12月采用高位股骨头颈开窗植骨支撑术治疗早期股骨头坏死 26例（35髋）,男 11例,女 15例;年龄 18~65岁,平均 37.4岁。股骨头坏死 ARCO分期ⅡA期 6髋、ⅡB期 13髋、ⅡC期 16髋。采用高位股骨头颈开窗植骨支撑术治疗,开窗位置位于股骨头颈交界处靠近股骨头方向,累及部分股骨头软骨。术后第 1个月及以后每 3个月定期门诊随访,依据 Harris髋关节评分及优良率评估疗效。结果 25例 33髋获得随访,失访 1例 2髋。随访时间 18~32个月,平均 24个月。随访期间未出现感染及神经损伤等并发症。总体 Harris 髋关节评分由术前（73.42±7.30）分提高至末次随访的（85.85±11.63）分;其中ⅡA 期患者由（74.50±1.76）分提高至（91.17±1.60）分;ⅡB 期患者由（73.92±8.03）分提高至（86.00±10.49）分;ⅡC 期患者由（72.60±8.29）分提高至（83.60±14.29）分。总体优良率由术前 36.4%提高至 84.9%;ⅡA 期患者由 33.3%提高至 100.0%;ⅡB 期患者由 41.7%提高至 91.7%;ⅡC 期患者由 33.3%提高至 73.3%。手术前后 Harris 髋关节评分及优良率的差异均有统计学意义。结论 高位股骨头颈开窗植骨支撑术治疗早期股骨头坏死近期疗效好,能促进坏死修复,改善髋关节症状。     

创伤性股骨头坏死中骨细胞凋亡初探

[目的]初步探索骨细胞凋亡与创伤性股骨头坏死的关系。[方法]采用光镜观察（HE）、Hoeehest33258荧光染色及Bcl-2蛋白免疫组化染色对股骨颈骨折和创伤性股骨头坏死患者共30例（分为早、中、晚期组）和10例正常对照的股骨头标本进行组织学观察、骨细胞凋亡和Bcl-2蛋白检测。[结果]与对照组相比，30例标本中均可见不同程度的空骨陷窝化。其中，早期组骨细胞凋亡活性强于其它组，中期标本的骨细胞的凋亡活性降低、Bcl-2表达增强，而晚期标本几乎不能检测到骨细胞凋亡和Bcl-2表达，差异均有显著性意义（P〈0．05）。[结论]骨细胞凋亡参与了创伤性股骨头坏死的早期发病过程，适当的干预可能是改善患者预后的关键。     

骨内微血管和骨的同步三维显像及定量评价

[目的]评价基于显微CT(Micro-CT)骨内微血管造影进行骨内微血管显影和三维重建在缺血性股骨头坏死(osteonecrosis of femoral head,ONFH)研究中的应用价值,实现在三维空间内同时定量评价骨显微结构及骨矿物量和骨内微血管。[方法]采用局部液氮冷冻和射频加热交替的方法建立鸸鹋塌陷性股骨头坏死动物模型,右侧为手术侧,左侧为对照侧。术后定期进行核磁检查,证实造模成功后自鸸鹋腹主动脉注入亚纳米级硫酸钡明胶混悬液进行下肢血管造影,取下肢股骨标本进行Micro-CT扫描,通过软件进行骨内微血管的二维及三维重建,同时结合Micro-CT骨显微结构研究,并将标本常规HE染色进行组织学检查。[结果]在术后12周证实出现股骨头塌陷,至16周16只动物出现股骨头塌陷。Micro-CT图像骨小梁结构及骨内血管显示清晰,与对照侧相比鸸鹋股骨头坏死塌陷后股骨头部的骨小梁厚度、骨体积分数增加,骨矿物量及骨小梁间距减小,血管体积分数减小,且差异均具有统计学意义。[结论]以亚纳米级硫酸钡作为造影剂,Micro-CT骨内微血管造影可以在不破坏骨标本的基础下清晰的显示骨内微血管,不干扰影像及组织学检查,并实现骨内...     

脂质代谢及破骨细胞活性在激素性股骨头坏死塌陷发生过程中的作用研究

目的:通过诱导激素性股骨头坏死的动物模型并观测模型的相关指标,研究脂质代谢及破骨细胞活性在激素性股骨头坏死塌陷发生过程中的作用.方法:将雄性SD大鼠40只(150 g左右),随机分为空白对照组和激素实验组,腹腔注射大肠杆菌内毒素后,实验纽每周1次臀肌注射醋酸强的松龙35.5 mg/kg,对照组每周1次臀肌注射生理盐水2 ml,于第12周用药结束后处死动物,进行血清抗酒石酸酸性磷酸酶5b(Trap-5b)、总胆固醇(TC)、甘油三酯(TG)、软骨下骨生物力学、股骨骨密度测定,制作HE染色病理切片,进行茜红素和抗酒石酸酸性磷酸酶(TRACP)染色,并进行统计分析.结果:实验组的血清总胆固醇、甘油三酯、抗酒石酸酸性磷酸酶5b含量显著升高(P<0.01),局部骨髓内出现大量破骨细胞,骨质丢失严重(P<0.01),软骨下骨生物力学性能显著下降(P<0.01).结论:脂质代谢紊乱是激素性股骨头坏死重要的发病机制;破骨细胞活性增强、数量增加,引起骨质严重丢失导致的软骨下骨生物力学性能下降是股骨头塌陷的直接原因.     

淫羊藿苷干预兔早期激素性股骨头坏死的实验研究

目的探讨淫羊藿苷对激素诱导的兔早期激素性股骨头坏死干预效果。方法50只成年新西兰兔(体质量2.5~3.0 kg)随机分为对照组(n=10)、模型组(n=20)及实验组(n=20)。模型组和实验组采用脂多糖联合甲泼尼龙注射制备早期激素性股骨头坏死模型;实验组首次注射甲泼尼龙开始每日灌服淫羊藿苷药液1次,对照组及模型组灌服等量生理盐水,连续6周。于6周后取左侧股骨头行大体观察;Micro-CT扫描观察骨小梁微结构,测量骨小梁相对体积(bone volume to total volume,BV/TV)、骨小梁数量(trabecular number,Tb.N)、骨小梁厚度(trabecular thickness,Tb.Tn)及骨小梁分离度(trabecular separation,Tb.Sp),并构建三维图像观察;HE染色观察骨小梁结构、骨细胞及骨髓脂肪细胞形态变化,按照病理学诊断标准检测股骨头坏死模型造模是否成功,计算空骨陷窝率。结果实验期间共7只动物死亡,最终对照组9只、模型组16只、实验组18只纳入研究。大体及Micro-CT扫描、三维重建显示,与对照组相比,模型组股骨头塌陷明显,骨小梁断裂、排列紊乱稀疏;实验组股骨头表面皱褶,塌陷不明显,骨小梁结构轻度退变。与对照组相比,模型组和实验组Tb.N、Tb.Tn、BV/TV下降、Tb.Sp升高;与模型组相比,实验组Tb.N、Tb.Tn、BV/TV升高、Tb.Sp降低;组间比较差异均有统计学意义(P<0.05)。HE染色示模型组骨小梁中骨细胞减少,空骨陷窝较多,骨小梁间脂肪细胞堆积,部分呈囊状融合;实验组骨小梁形态较模型组完整,骨细胞坏死及脂肪细胞肥大不明显。按照股骨头坏死病理学诊断标准,对照组无骨坏死发生,模型组骨坏死发生率为81.3%(13/16),实验组为66.7%(12/18),差异无统计学意义(P=0.448)。模型组和实验组发生坏死的股骨头标本其空骨陷窝率分别为33.1%±1.4%及18.9%±0.8%,均高于对照组12.7%±1.5%,且模型组明显高于实验组,差异均有统计学意义(P<0.05)。结论淫羊藿苷对激素诱导的兔早期激素性股骨头坏死具有保护作用,可以降低骨细胞凋亡,改善骨微结构,延缓骨坏死发生。     

Subchondral fracture after ischemic osteonecrosis of the immature femoral head in piglet model

This experimental investigation was performed to study the development of a subchondral fracture after ischemic osteonecrosis of the immature femoral head using a piglet model. Forty-eight male piglets were studied after placing a ligature tightly around the femoral neck to disrupt the blood supply to the femoral head. Animals were euthanized 2-8 weeks after the induction of ischemia. Radiographic, histologic, and histomorphometric assessments were made. A subchondral fracture was seen in 12 out of 32 infarcted femoral heads (38%) that were in the initial radiographic stage of ischemic osteonecrosis. The fracture was seen mainly in those femoral heads that had a prolonged period of the initial stage where the initiation of revascularization and repair was delayed. Histomorphometric assessment showed decreased trabecular thickness and volume in the subchondral region of the infarcted femoral heads compared with the contralateral normal heads. After ischemic osteonecrosis, the trabecular bone in the subchondral region is thinner and less bone volume is present because of a lack of new bone formation. The results of this study support the hypothesis that a subchondral fracture in the immature femoral head develops as a result of mechanic failure of the trabecular bone in the subchondral region.     

Microcrack density and nanomechanical properties in the subchondral region of the immature piglet femoral head following ischemic osteonecrosis

Development of a subchondral fracture is one of the earliest signs of structural failure of the immature femoral head following ischemic osteonecrosis, and this eventually leads to a flattening deformity of the femoral head. The mechanical and mineralization changes in the femoral head preceding subchondral fracture have not been elucidated. We hypothesized that ischemic osteonecrosis leads to early material and mechanical alterations in the bone of the subchondral region. The purpose of this investigation was to assess the bone of the subchondral region for changes in the histology of bone cells, microcrack density, mineral content, and nanoindentation properties at an early stage of ischemic osteonecrosis in a piglet model. This large animal model has been shown to develop a subchondral fracture and femoral head deformity resembling juvenile femoral head osteonecrosis. The unoperated, left femoral head of each piglet (n = 8) was used as a normal control, while the right side had a surgical ischemia induced by disrupting the femoral neck vessels with a ligature. Hematoxylin and eosin (H&E) staining and TUNEL assay were performed on femoral heads from 3 piglets. Quantitative backscattered electron imaging, nanoindentation, and microcrack assessments were performed on the subchondral region of both control and ischemic femoral heads from 5 piglets. H&E staining and TUNEL assay showed extensive cell death and an absence of osteoblasts in the ischemic side compared to the normal control. Microcrack density in the ischemic side (3.2 ± 0.79 cracks/mm²) was significantly higher compared to the normal side (0.27 ± 0.27 cracks/mm²) in the subchondral region (p < 0.05). The weighted mean of the weight percent distribution of calcium (CaMean) also was significantly higher in the ischemic subchondral region (p < 0.05). Furthermore, the nanoindentation modulus within localized areas of subchondral bone was significantly increased in the ischemic side (16.8 ± 2.7 GPa) compared to the normal control (13.3 ± 3.2 GPa) (p < 0.05). Taken together, these results support the hypothesis that the nanoindentation modulus of the subchondral trabecular bone is increased in the early stage of ischemic osteonecrosis of the immature femoral head and makes it more susceptible to microcrack formation. We postulate that continued loading of the hip joint when there is a lack of bone cells to repair the microcracks due to ischemic osteonecrosis leads to microcrack accumulation and subsequent subchondral fracture.     

Pathology of femoral head collapse following transtrochanteric rotational osteotomy for osteonecrosis

We investigated the pathology of femoral head collapse following transtrochanteric anterior rotational osteotomy. Six femoral heads were obtained during total hip arthroplasty some 2–12 years after osteotomy. In all cases, the preoperatively necrotic lesions exhibited mostly osteonecrosis with accumulation of bone marrow cell debris and trabecular bone with empty lacunae, although repair tissue such as granulation tissue and appositional bone formation were observed in limited areas in some cases. In the transposed intact articular surface of the femoral head, osteoarthritic changes such as fissure penetration to the subchondral bone and osteophyte formation were commonly observed. In newly created subchondral areas at weight-bearing sites, trabecular thickness and the number of trabecular bones had decreased, with few osteoblasts, osteoclasts, and osteocytes being present, resulting in a coarse lamellar structure of the trabecular bone. These findings suggest that transposed areas in cases of failure consist mostly of low-turnover osteoporotic lesions which could cause collapse of the femoral head. Received: 5 October 1999     

股骨头缺血性坏死新月征的形成机制

目的对发生股骨头缺血性坏死出现x线片上“新月征”股骨头的结构改变及与所受应力的对应关系进行研究,探讨“新月征”的形成机制。方法收集1998年3月-2003年4月全髋关节置换术前X线片显示有“新月征”的股骨头16例18髋,进行大体和冠状位断面观察。应用有效压应力原理和应力集中理论对发生在缺血性坏死股骨头上的结构改变原因进行解释和说明。结果松质骨内的骨小梁形成三维立体交互连接的网格结构,孔隙率50％～90％,髓内压20～30mmHg。股骨头内松质骨的构造符合多孔介质的定义,是一种多孔介质。松质骨的变形机制与多孔介质材料变形机制相同。软骨下骨板与松质骨间的断面结构改变使应力易在二者交界处集中。有效压应力原理和应力集中理论可对发生在缺血坏死股骨头上的一些现象及彼此之间的关系进行明确的解释和说明。结论导致“新月征”骨折线正发生在软骨下骨板下的原因是由于在坏死灶外侧软骨下骨板局灶性被吸收发生后,软骨下骨板与未被修复坏死松质骨交界处发生应力集中,集中的应力导致骨折线正位于软骨下骨板下,施加在未被修复坏死松质骨上增加的有效压应力引起未被修复坏死松质骨的体积减小,从而导致新月形空腔在软骨下骨板下形成,新月形空腔在X线片上显示出“新月征”。     

Abnormal subchondral bone microstructure following steroid administration is involved in the early pathogenesis of steroid-induced osteonecrosis

Summary

Loss of bone microstructure integrity is thought to be related to osteonecrosis. But the relationship between the time when bone microstructure integrity loss appears and the onset of osteonecrosis has not yet been determined. Our study demonstrated abnormal changes of subchondral bone microstructure involved in the early pathogenesis of osteonecrosis.

Introduction

Using a rabbit model, we investigated the changes of subchondral bone microstructure following steroid administration to identify the onset of abnormal bone microstructure development in steroid-induced osteonecrosis.

Methods

Fifty-five adult female Japanese White rabbits (mean body weight 3.5 kg; mean age 24 months) were used and randomly divided among three time points (3, 7, and 14 days) consisting of 15 rabbits each, received a single intramuscular injection of methylprednisolone acetate (MP; Pfizer Manufacturing Belgium NV) at a dose of 4 mg/kg, and a control group consisting of 10 rabbits was fed and housed under identical conditions but were not given steroid injections. A micro-CT scanner was applied to detect changes in the trabecular region of subchondral bone of excised femoral head samples. Parameters including bone volume fraction (BV/TV), bone surface (BS), trabecular bone pattern factor (Tb.Pf), trabecular thickness/number/separation (Tb.Th, Tb.N, and Tb.Sp), and structure model index (SMI) were evaluated using the software CTAn (SkyScan). After micro-CT scans, bilateral femoral heads were cut in the coronal plane at a thickness of 4 μm. The sections were then stained with haematoxylin-eosin and used for the diagnosis of osteonecrosis and the rate of development of osteonecrosis.

Results

The BV/TV, BS, Tb.Th and Tb.N demonstrated a time-dependent decline from 3, 7, and 14 days compared with the control group, while the Tb.Pf, Tb.Sp and SMI demonstrated an increase at 3, 7, and 14 days compared with the control group. For the histopathology portion, osteonecrosis was not seen 3 days after steroid treatment, but was present 7 days after treatment and was obvious 14 days after treatment. Furthermore, the rate of osteonecrosis appearing between 7 and 14 days was not significantly different. In addition, the presence and variation of BV/TV, BS, Tb.Pf, Tb.Th, Tb.N, and SMI demonstrated significant changes at 7 days compared with the control group except Tb.Sp (at 14 days) and this is the time when osteonecrosis is thought to occur in this model.

Conclusion

This study demonstrated that osteonecrosis in rabbits is chronologically associated with changes in subchondral bone microstructure.

     

Mechanics of femoral head osteonecrosis using three-dimensional finite element method

A three-dimensional finite element model of a femoral head was developed using a surface modeling technique. The distribution of the stress index S (S = effective stress / yield strength, sigma/sigmaY) in various sizes of segmental osteonecrosis was assessed. The stress index of the femoral head was within physiological limits when the necrotic angle was less than 110 degrees. Within both the subchondral region and the deep necrotic region adjacent to the necrotic-viable interface, values of the stress index significantly higher than the normal physiological level (>0.1) appeared when the necrotic angle was 110 degrees or more. In the analysis of 28 osteonecrotic femoral head specimens, fracture appeared in two major locations: the deep necrotic region near the underlying necrotic-viable interface (19 femoral heads) and the subchondral region (7 femoral heads). In 2 femoral heads, the fracture involved both regions. Both sites of fracture coincided with the region of stress index greater than 0.1 in the finite element model study. These results may provide baseline information for predicting the collapse of the femoral head and determining the treatment modality of early stage osteonecrosis.     

Morphological analysis of collapsed regions in osteonecrosis of the femoral head

In order to investigate the mechanisms of collapse in osteonecrosis of the femoral head, we examined which part of the femoral head was the key point of a collapse and whether a collapsed region was associated with the size of the necrotic lesion. Using 30 consecutive surgically removed femoral heads we retrospectively analysed whole serial cut sections, specimen photographs, specimen radiographs and histological sections. In all of the femoral heads, collapse consistently involved a fracture at the lateral boundary of the necrotic lesion. Histologically, the fractures occurred at the junction between the thickened trabeculae of the reparative zone and the necrotic bone trabeculae. When the medial boundary of the necrotic lesion was located lateral to the fovea of the femoral head, 18 of 19 femoral heads collapsed in the subchondral region. By contrast, when the medial boundary was located medial to the fovea, collapse in the subchondral region was observed in four of 11 femoral heads (p = 0.0011). We found that collapse began at the lateral boundary of the necrotic lesion and that the size of the necrotic lesion seemed to contribute to its distribution.     

Relationship between microstructure and degree of mineralization in subchondral bone of osteoarthritis: a synchrotron radiation μCT study

We analyzed the microstructure and degree of mineralization of the subchondral trabecular bone in hip osteoarthritis (OA) using synchrotron radiation computed tomography (SRCT) to identify the relationship between bone structure and bone turnover. Subchondral bone samples were extracted from femoral heads of 10 terminal-staged hip OA patients. The SRCT scan was performed at 30 keV energy and 5.9 μm voxel size. Trabecular bone structure, bone cyst volume, and the degree of trabecular bone mineralization were measured, and correlations between bone structure and the degree of mineralization were analyzed. In addition, the trabecular bone was divided into the area immediately surrounding the bone cyst and the remaining area, and they were compared. The average cyst volume fraction in the whole region was 31.8%, and the bone volume fraction in the bone region was 55.6%. Cyst volume was the only structural parameter that had a significant correlation with the degree of mineralization. The degree of mineralization was diminished when the bone cyst was larger (r = -0.81, p = 0.004). The trabecular bone immediately surrounding the bone cyst had a lower degree of mineralization when compared with the remaining trabecular bone (p = 0.008). In the bone sclerosis of OA subchondral bone, there are many large and small bone cysts, which are expected to play a significant part in the high bone turnover of OA.     

Subcapital fractures associated with extensive osteonecrosis of the femoral head

The authors reviewed 10 patients with subcapital fractures associated with extensive osteonecrosis of the femoral head and distinguished these fractures from traumatic femoral neck fractures The mean age of the patients was 52 years (range, 36-68 years). Nine patients were younger than 60 years. Eight patients had risk factors for osteonecrosis. Necrosis was extensive and involved nearly the whole femoral head. Fracture occurred at the junction between a necrotic bone and reparative bone and extended downward through the reparative interface to the healthy inferior cortex of the femoral neck. Patients experienced hip pain that was aggravated gradually during a period of 1 to 24 weeks before diagnosis of the fracture. In all patients, the opposite femoral head was involved with osteonecrosis. In two femoral heads, slight collapse or subchondral fracture (crescent sign) also was observed. No patient had a history of precipitating trauma. In patients younger than 60 years with a subcapital fracture, fracture associated with extensive osteonecrosis of the femoral head should be suspected when a history of trauma is not obvious, when the opposite hip shows findings of osteonecrosis, and when the patient has a risk factor of osteonecrosis. In these fractures, osteosynthesis rarely should be considered because of the high failure rate caused by additional progression of extensive osteonecrosis and the probability of nonunion.     

Biophysical stimulation in osteonecrosis of the femoral head

Osteonecrosis of the femoral head is the endpoint of a disease process that results from insufficient blood flow and bone-tissue necrosis, leading to joint instability, collapse of the femoral head, arthritis of the joint, and total hip replacement. Pain is the most frequent clinical symptom. Both bone tissue and cartilage suffer when osteonecrosis of the femoral head develops. Stimulation with pulsed electromagnetic fields (PEMFs) has been shown to be useful for enhancing bone repair and for exerting a chondroprotective effect on articular cartilage. Two Italian studies on the treatment of avascular necrosis of the femoral head with PEMFs were presented in this review. In the first study, 68 patients suffering from avascular necrosis of the femoral head were treated with PEMFs in combination with core decompression and autologous bone grafts. The second one is a retrospective analysis of the results of treatment with PEMFs of 76 hips in 66 patients with osteonecrosis of the femoral head. In both studies clinical information and diagnostic imaging were collected at the beginning of the treatment and at the time of follow up. Statistical analysis was performed using chi-square test. Both authors hypothesize that the short-term effect of PEMF stimulation may be to protect the articular cartilage from the catabolic effect of inflammation and subchondral bone-marrow edema. The long-term effect of PEMF stimulation may be to promote osteogenic activity at the necrotic area and prevent trabecular fracture and subchondral bone collapse. PEMF stimulation represents an important therapeutic opportunity to resolve the Ficat stage-I or II disease or at least to delay the time until joint replacement becomes necessary.