钛合金支撑架植入治疗股骨头缺血性坏死的动物实验研究

[目的]通过动物模型,观察支撑架置入治疗狗股骨头缺血性坏死的疗效。[方法]本研究设计一种中空多孔圆柱状带螺纹的钛合金支撑架,选用成年杂种狗15只,用液氮冷冻法制造股骨头坏死模型,通过中心减压钻隧道至股骨头坏死区软骨下骨,然后沿隧道拧入支撑架。术后分期处死,取标本观察相关指标。[结果]术后无1例发生股骨头塌陷,X线片显示支撑架位置良好,组织学观察显示术后坏死股骨头得以逐步重建,再生的松质骨小梁能够长入支撑架中并改建、修复、替代股骨头内坏死的骨组织,形成穿越支撑架网孔的网状松质骨结构。[结论]利用多孔中空支撑架给股骨头坏死区软骨下骨板提供支撑,防止股骨头塌陷。多孔网状结构容许松质骨的长入和爬行替代,对治疗狗股骨头坏死有明显疗效。提示钛合金支撑架可用于股骨头坏死的治疗。     

开窗病灶清除植骨术治疗股骨头缺血性坏死

目的　寻求治疗股骨头缺血性坏死的简便而有效的手术方法。方法　设计一种于股骨头颈交界处开窗、坏死骨清除减压、髂骨松质骨填充植骨术 ,术后配合牵引髋关节 ,早期持续被动功能锻炼的方法 ,治疗股骨头缺血性坏死 2 0例 2 9个股骨头。结果　 2 0例 2 9个股骨头经 1～ 3年随访 ,效果满意。髋痛消失 ,髋关节功能良好 ,行走及下蹲正常或基本正常。结论　此术式可彻底清除坏死骨 ,消除血供障碍因素 ,为重建血运修复骨质创造条件 ,在病灶清除后的股骨头空腔内 ,填充大量松质骨支撑软骨面 ,为骨修复提供成骨条件。早期髋关节持续被动功能锻炼对关节软骨的修复和预防关节粘连是极为有利的。此法操作简便 ,创伤小 ,效果好。     

多孔钽金属植入治疗早期股骨头坏死研究进展

股骨头坏死主要在年轻人中发病,PennsylvaniaⅣ期以上患者只能行人工关节置换术,这对患者生活有较大影响,还需面临翻修问题。预防性手术治疗股骨头和软骨下骨板塌陷前的早期坏死,可有效阻止和限制坏死继续进展,进而推迟行人工关节置换术时间。有研究表明,股骨头坏死病因不仅有生物因素,还有部分生物力学因素。近几年发明的多孔钽金属植入物具有良好生物相容性,手术操作简单、微创,对股骨头和软骨下骨板可提供安全、有效的力学支撑,早期治疗股骨头坏死的临床效果令人满意,为治疗早期股骨头坏死提供了一种新选择。该文就多孔钽金属植入物研究背景、生物力学性能、使用方法及临床疗效作一综述。     

实验性股骨颈骨折修复过程的生物力学研究

目的：探索股骨颈骨折引起股骨头坏死塌陷的发病机理。方法：在犬股骨头颈交界处截断股骨颈,术后分5周组（5条）。20周组（5条）及各组的对照组,对其修复过程进行病理学,计量组织学、四环素标记及生物力学的研究。结果：（1）病理学检查：5周组,股骨头内骨小梁坏死,其框架结构不变;20周组,股骨头关节面塌陷,头内纤维组织、软骨痂及骨痂形成。（2）计量组织学分析示20周组的股骨头骨小梁体积及软骨下骨厚度较对照组及5周组低。（3）四环素标记示20周组的荧光带比对照组及5周组宽。5周组的最窄。（4）生物力学测定：20周组的软骨下骨及松质骨的生物力学强度较对照组及5周组低。结论：股骨颈骨折可致股骨头坏死,后者引起修复及血供重建,修复则可导致塌陷,股骨头塌陷与软骨下骨及松质骨的生物力学特性关系密切。     

植入型丹参缓释剂治疗股骨头坏死的实验研究

目的研究丹参缓释剂植入股骨头内治疗股骨头坏死的效果.方法参照Rich等方法,用马血清、醋酸强的松龙复制家兔股骨头坏死的动物模型,造模8周后实验组(A组)将丹参缓释剂40 mg植入到右侧股骨头内.对照组(B组)用同样方法植入赋形剂40 mg.正常对照(C组).术后不同时间做X线摄片、ECT扫描、组织学及扫描电镜检查.结果 X线片示A组右侧股骨头骨密度增高,透光区较小,B组骨密度减低,有大小不等透光区;ECT扫描示A组静态放射性分布中等浓聚,而B组静态图像放射性分布呈炸面包圈样改变,欠均匀;组织学检查显示A组骨空陷窝率、血管数、骨髓腔内脂肪细胞直径较B组明显改善(P＜0.01);扫描电镜检查显示A组松质骨结构较规则,骨陷窝结构完整,部分骨板断裂,骨小管可见.B组结构紊乱不清,骨板断裂,骨陷窝少,骨小管消失.结论丹参缓释剂植入到坏死的股骨头模型内,能改善股骨头血供,促进坏死骨的吸收、修复与重建.为股骨头坏死这种新的治疗方法提供实验依据.     

股骨头不同区域囊变对力学承载的影响

目的探索股骨头不同部位囊变对股骨头力学承载的影响。方法取新鲜人体股骨上段标本,行螺旋CT断层扫描,得到CT数据二维图像,采用Efilm软件系统处理,人工识别股骨头边缘轮廓,将数据输入计算机,利用Ansys-5.7大型计算机软件建立股骨上段三维有限元异物同构模型,模拟股骨头内不同部位直径1cm的囊变灶。施加3种不同载荷,分析股骨头内应力分布情况及应力/强度比值,预测股骨头塌陷的危险性。结果所构建股骨头三维有限元异物同构模型共有21852个节点,10472个单元。囊变区强度降低导致应力下传受限,在其边缘区产生应力集中。股骨头负重区下方及其内侧和外侧的囊变应力集中最明显,表现为张力集中,其上方骨板下松质骨应力/强度比值明显升高,易引起股骨头塌陷。当囊变位于股骨头的前方、后方或下方时,塌陷风险小。结论股骨头囊变灶位于股骨头负重区的下方或其内、外侧时,可行带血运的髂骨瓣植入,骨瓣应与软骨下骨板接触。如果坏死范围较大,负重区下方及其内外侧均受累,髂骨瓣应位于负重区的下方。     

同种异体骨支撑架结合自体骨和DBM治疗股骨头坏死

目的探讨同种异体骨支撑架植入结合自体松质骨和脱钙骨基质（DBM）治疗成人股骨头坏死初步疗效。方法采用经大转子下通过股骨颈钻隧道至股骨头骨坏死区,将装有自体松质骨和DBM的同种异体骨支撑架经隧道置入骨坏死区直至软骨下骨约5mm处,隧道远端用自体髂骨填塞。结果经临床应用23例24个髋关节,随访12～27个月,并按成人股骨头缺血性坏死疗效百分评价法进行评价,优良率为95.8％。结论同种异体骨支撑架植入结合自体松质骨和DBM治疗成人股骨头坏死具有以下优点：①手术操作简单,不破坏患者股骨头本身的血液供应,创伤小,且不增加日后行人工关节置换的困难;②将具有骨诱导活性的DBM直接放入骨坏死区,成骨作用强;③增加股骨头负重区软骨下骨的机械支撑,降低局部应力,有利于股骨头坏死的修复及重建。     

钛合金支撑架结合自体骨和DBM治疗股骨头坏死

【目的】探讨空心钛合金支架植入结合自体松质骨和脱钙骨基质（DBM）治疗成人股骨头坏死初步疗效。【方法】采用经大转子下通过股骨颈钻隧道至股骨头骨坏死区，将装有自体松质骨和DBM的空心钛合金支架经隧道置入骨坏死区直至软骨下骨约5mm处，髓道远端用自体髂骨填塞。【结果】经临床应用13例。15个髋关节，随访14-36个月，并按成人股骨头缺血性坏死疗效百分评价法进行评价，优良率为93．3％。【结论】空心钛合金支架植入结合自体松质骨和DBM治疗成人股骨头坏死具有以下优点：（1）手术操作简单，不破坏患者股骨头本身的血液供应，创伤小。（2）将具有骨诱导活性的DBM直接放入骨坏死区，成骨作用强。（3）增加股骨头负重区软骨下骨的机械支撑，降低局部应力，有利于股骨头坏死的修复及重建。     

丹参酮Ⅱ-a磺酸钠结合髓芯减压打压植骨治疗犬股骨头坏死的研究

目的：研究丹参酮Ⅱ-a磺酸钠结合打压植骨治疗犬股骨头坏死的疗效。方法：以液氮冷冻法制作犬单侧股骨头缺血性坏死模型,随机分为两组,实验组采用将浸泡过丹参酮Ⅱ-a磺酸钠的松质骨植入到股骨头内,对照组将松质骨植入股骨头内,术后进行x线摄片、标本组织学及扫描电镜检查。结果：实验组股骨头骨密度较术前增高,透光区较小,组织学显示实验组骨空陷窝数和脂肪细胞直径较对照组明显改善（P〈0．05）。术后12周,扫描电镜可见再生软骨表面与正常透明软骨极为相似,成骨细胞增殖活跃,骨细胞成圆形,核膜清晰,趋于成熟。结论：丹参酮Ⅱ-a磺酸钠能改善股骨头血供,促进坏死骨的吸收、修复与重建。     

多孔钽块置入治疗股骨头缺血性坏死的生物力学及三维有限元分析

[目的]对比研究三种治疗成人股骨头缺血性坏死的生物力学方法;探讨髓芯减压对股骨头机械支撑力的影响及钽块置入治疗股骨头缺血性坏死的独特优势.[方法]选择健康成人右侧股骨为研究对象,经层厚2.0mm的螺旋CT扫描得各断面图像,输入计算机识别和提取股骨轮廓并行三维重建.按生理状态下股骨力载荷的三维空间分布,施加髋关节接触力1620N,外展肌合力1061N,髂胫束力1720N.对股骨头三维有限元模型进行计算,求出股骨头受力模型在不同坏死角度,不同减压位置股骨头负重区表面的塌陷值.[结果]股骨头髓芯减压后的塌陷值明显增大,以负重区最为明显(P＞0.05),且随着坏死角度的增大股骨头的塌陷值也随着增大.[结论]髓芯减压虽能清除死骨,但减压本身则进一步降低了股骨头的力学性能,单纯的植骨并不能增加股骨头的机械支撑力;髓芯减压基础上以多孔钽金属块为股骨头及软骨下骨板提供安全而有效的力学支撑,能有效防止塌陷,并为骨组织的修复提供条件.     

Structural consequences of subchondral bone involvement in segmental osteonecrosis of the femoral head.

Appearance of a crescent sign usually marks the onset of necrotic femoral head collapse, but very little is known about which local factors contribute most critically to avoiding or postponing fracture of at-risk juxtaarticular cancellous bone. A three-dimensional finite element model was used to test the hypothesis that an initially mechanically uncompromised subchondral plate could provide a substantial degree of stress protection to a weakened underlying segmental infarction. The computational simulation of osteonecrosis showed that the principal stress distribution for an assumption of subchondral plate weakening (given also an underlying, comparably weakened segmental infarction) differed inappreciably from that of a normal femoral head. However, the tendency for local structural failure, as reflected in the ratio of stress to strength, was substantially higher in the former instance. If, instead, the mechanical integrity of the subchondral plate overlying the weakened segmental infarction was assumed to be preserved, computed stress levels in the at-risk subjacent necrotic cancellous bone were still over 70% as high as for the weakened-plate case. The data thus indicate that even a fully normal subchondral plate can provide only modest stress protection of a weakened underlying segmental infarction, whereas weakening of the necrotic cancellous bone throughout the infarction induces marked stress increase in the overlying subchondral plate. These findings suggest that the onset of collapse is probably dominated much more strongly by the degree of structural degradation of the cancellous bone within the main infarct body, than by the degree of structural degradation within the subchondral plate.     

Magnetic resonance imaging and histology of repair in femoral head osteonecrosis

Different repair processes affect the clinical course of nontraumatic avascular femoral head osteonecrosis, not just necrotic lesion size and location. Fourteen femoral heads were retrieved at total hip arthroplasty after core decompression treatment, or after conservative treatment was done on 13 male patients diagnosed with different stages of femoral head osteonecrosis. To determine repair types, features of coronal magnetic resonance images were correlated with light microscopy findings on corresponding coronal undecalcified sections and microradiographs of the retrieved femoral heads. In five femoral heads, repair of necrotic bone and marrow remained restricted to the reactive interface for as many as 63 months, producing the diagnostic osteosclerotic rim with adjacent hypervascularity (limited repair). Nine femoral heads showed extension of the repair process into the necrosis. In five femoral heads, predominant resorption of necrotic bone led to femoral head breakdown within 2 to 50 months (destructive repair). In four femoral heads, reparative bone formation had started from subchondral fractures and/or the reactive interface, definitely reducing the size of the necrotic area (reconstructive repair). In the latter, the disease progressed slowly or stopped for as many as 45 months, irrespective of treatments, but elimination of risk factors seemed beneficial. Although core decompression did not always reach the necrotic area and improve repair, it reduced accompanying bone marrow edema and could delay the disease progress. Osteonecrosis with limited repair can be identified on magnetic resonance images obtained at followup, but the similar signal changes of destructive and reconstructive repair cannot be distinguished on magnetic resonance images alone. The evidence of reconstructive repair in nontraumatic osteonecrosis, however, gives hope for treatments that can improve repair to a sufficient creeping substitution of the affected femoral head.     

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.     

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.     

人股骨头坏死微观结构及成骨、破骨细胞活性的区域性分布特征

 目的 比较人股骨头坏死标本不同区域的骨微观结构及成、破骨细胞活性。方法 收集2011年3月至2013年5月行全髋关节置换的非创伤性股骨头坏死患者术后的股骨头标本10例（Ficat Ⅳ期）,男6例,女4例;年龄40～57岁,平均47.7岁。Micro-CT扫描后,根据影像学识别骨质密度不同,将每个标本分为软骨下骨区、坏死区、硬化区、健康区,通过病理学检测、纳米压痕、实时荧光定量PCR、免疫组化染色等方法对不同区域的骨微观结构、微观力学性能及成骨、破骨细胞活性进行比较。结果 Micro-CT结果显示,股骨头坏死标本软骨下骨区及坏死区的骨小梁连续性破坏;硬化区的骨小梁数目增多,间隙变窄;正常区域骨小梁结构完整,厚度分布均匀。软骨下骨区、坏死区、硬化区和健康区骨小梁的弹性模量分别为（13.808±4.22） GPa、（13.999±3.816） GPa、（17.266±3.533） GPa和（11.927±1.743） GPa;硬度分别为（0.425±0.173） GPa、（0.331±0.173） GPa、（0.661±0.208） GPa和（0.423±0.088） GPa。抗酒石酸酸性磷酸酶（Trap）染色结果显示,软骨下骨区和坏死区可见Trap染色阳性细胞,硬化区及健康区未见Trap染色阳性细胞。免疫组化染色结果显示,骨形成相关因子Runx2和BMP2在硬化区及健康区表达高于其他区域;骨吸收相关因子RANK和RANKL在软骨下骨区及坏死区表达高于其他区域。结论 股骨头坏死塌陷过程中,骨微观结构发生明显改变,而坏死区骨小梁微观力学强度较健康区无显著降低。股骨头坏死标本中软骨下骨区及坏死区破骨细胞活性增强,硬化区成骨细胞活性增强。     

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.     

The cause of subchondral bone cysts in osteoarthrosis: a finite element analysis

BACKGROUND: The etiology of subchondral bone cysts in arthrotic joints is unclear. MATERIALS AND METHODS: We used two-dimensional finite element analysis to evaluate the hypothesis that subchondral bone cysts in the osteoarthrotic hip joint may be the result of microfractures caused by localized cartilage defects or a thinned layer of cartilage. We evaluated the equivalent bone stress (von Mises (VM) stress) in the cancellous bone as an indicator of potential microfractures and further development of cystic lesions. RESULTS: Cartilage defects induced stress peaks in the subchondral bone. This peak stress distribution corresponded to the clinical observation of development of acetabular and femoral subchondral cysts in a "kissing" position. A femoral subchondral bone cyst induced a stress peak at the corresponding acetabular site, whereas subchondral acetabular cysts did not increase stress in the femoral head. Acetabular cysts showed an increased level of stress at the lateral and medial border of the lesion which was much higher than the stress levels in the femoral head, indicating a tendency to faster growth. INTERPRETATION: Our study supports the theory that stress-induced bone resorption may cause development of subchondral bone cysts in osteoarthrosis.