The effects of enoxaparin on the reparative processes in experimental osteonecrosis of the femoral head of the rat

The blood supply of one femoral head of 6-month-old rats was severed by incising the periosteum of the neck and cutting the ligamentum teres. The rats were killed on the 30th postoperative day and the femoral bones were obtained for semiquantification of the reparative processes in the necrotic heads. Fourteen rats were treated with enoxaparin and 14 untreated animals served as controls. Statistically, the amounts of necrotic bone in the epiphysis were less, the extent of remodeling of the femoral heads was milder, and the articular cartilage degeneration was slighter in the enoxaparin-treated than untreated rats. There was no significant difference in the quantities of newly formed bone in femoral heads of treated and untreated rats. These findings are in agreement with the known effects of unfractionated and low-molecular-weight heparins which enhance osteoclastic bone resorption and angiogenesis and decrease osteoblastic bone formation. The former activities, operative in minimizing the structural distortion of the femoral head, oppose the crucial event in the pathogenesis of post-osteonecrotic osteoarthritis.     

Computer-assisted image analysis of the rat postosteonecrotic remodeled femoral head.

Osteonecrosis of rat femoral heads was induced by stripping the periosteum of the neck and cutting the ligamentum teres. The epiphyseal marrow and bone were necrotic on the 5th postoperative day. Specimens obtained 18 and 36 days postoperatively showed fibrous and hematopoietic-fatty tissue in the intertrabecular spaces, osteoclastic bone resorption, osteogenesis, and degeneration of the joint cartilage. Morphometrically, the means of the height-to-length ratios of the control, 6-day, 18-day, and 36-day femoral heads were 0.26, 0.28, 0.48, and 0.29, respectively. The shape factor of the femoral heads of the control rats was higher than 0.81 in 80% of the cases, while those of rats killed on the 6th, 18th, and 36th postoperative day were higher than 0.81 in 65, 60, and 50% of cases, respectively. Statistically, the means of the height-to-length ratios and the values of the shape factors of the femoral heads of the rats killed 18 days postoperatively differed significantly from those of the other three groups of rats. The quantitatively gauged data of the remodeled epiphyses negate the authors' subjective impression concerning early flattening of the femoral heads after surgically produced osteonecrosis.     

Osteoarthritis-like disorder in rats with vascular deprivation-induced necrosis of the femoral head.

The reparative processes following vascular deprivation-induced necrosis of the femoral head were studied histologically in rats sacrificed 2, 7, 14, 21, 42 and 92 days postoperatively. The blood supply was severed by incision of the periosteum at the neck of the femoral head and transection of the ligamentum teres. Granulation tissue and a well-vascularized fibrous tissue originating from the joint capsule invaded the necrotic marrow spaces. With progressive resorption of the necrotic tissues and osteoneogenesis, both appositional and intramembranous, within the fibrotic intertrabecular spaces, the remodeling process led to a shift of the normal spongy architecture of the femoral head to a compacta-like one. In a few cases, osseous bridges bisected a necrotic physeal cartilage at the latest time intervals. The remodeling was associated with flattening of the femoral heads as well as with degenerative, regenerative and reparative alterations of the articular cartilage. In one of the two femoral heads obtained three months postoperatively, cystic spaces developed in the fibrous subchondral zone. Our findings are consistent with the view that ineffective attempts at restoring the prenecrotic state of the femoral head by replacing the necrotic with viable tissue triggers the collapse of the femoral head. Thickening and condensation of the subchondral bone, leading to increased stiffness of the subchondral zone, result in the osteoarthritis-like disorder. Mimicking the well-known phases of human osteonecrosis, the model readily allows for preclinical studies of therapeutic regimens.     

Localization of vascular endothelial growth factor during the early reparative phase of the rats' vessels deprivation-induced osteonecrosis of the femoral heads

The expedited revascularization of the rats' avascular, necrotic femoral heads suggests the operation of angiogenic factor(s). The blood circulation of the epiphysis was interrupted by cutting the cervical periosteum and the ligamentum teres of rats' femoral heads. Three days postoperatively, the marrow was necrotic. Seven days postoperatively, the subchondral bony plate and trabecular bone were necrotic as well. The joint capsule was distended by myriad, so-called synovial fibroblasts, all of which were virtually immunoreactive with an antibody to vascular endothelial growth factor. The expression of this factor in the synovial membrane of non-operated rats was limited to preexisting blood vessels. Revascularization of necrotic, avascular femoral heads makes up the essential step in the chain of events terminating in the repair processes, that is, resorption of the necrotic debris and its substitution by newly formed bony and hematopoietic-fatty tissues. Synthesis and release of excessive amounts of vascular endothelial growth factor by these fibroblasts explain the lively angiogenesis in the necrotic intertrabecular spaces of the femoral heads.     

Postosteonecrotic osteoarthritis-like disorder of the femoral head of rats

The femoral heads of 15 rats were studied histologically 3 months after the induction of ischaemic necrosis by incising the cervical periosteum and cutting the ligamentum teres. The epiphyses consisted of immature disorganized subchondral and trabecular bone. The inter-trabecular spaces contained fibrous or haematopoietic tissue. Residual necrotic bone was rare. There was marked osteoblastic and osteoclastic activity. The articular aspect of the heads showed a spectrum of changes, ranging from cartilaginous degeneration with fibrillation and loss of glycosaminoglycans to an eburnated and polished bony surface. In seven rats, transphyseal bridges connected the epiphyseal and metaphyseal bony trabeculae to each other. It is suggested that the postnecrotic reparative processes, including the resorption of the necrotic debris and its replacement by newly formed, weak bone, led to an osteoarthritis-like disorder. This healing pattern of the necrotic femoral head was reminiscent of the progressive remodelling that occurs in rings in femoral capital osteonecrosis of adult human patients and in Perthes's disease of children.     

Experimentally gained insight - based proposal apropos the treatment of osteonecrosis of the femoral head

An impeded blood flow through the femoral head is incriminated in the etiopathogenesis of osteonecrosis of the femoral head. The disorder is either primary (idiopathic avascular osteonecrosis) or secondary to one condition or another, say, corticosteroid medication, fracture of the neck, coagulation defects, physical or thermal damage, storage disorders, alcoholism, and infectious, autoimmune as also marrow infiltrating diseases. In the wake of the necrosis, several mediators are released in increased amounts, prime among which is the vascular endothelial growth factor. The intermediates recruit endothelial progenitor cells, macrophages, osteoclasts, fibroblasts, and osteoblasts, which, pervading throughout the necrotic areas, initiate the reparative processes. The dead, soft and hard tissular debris is substituted by fibrous - later on by hematopoietic-fatty tissue - and bone. The newly formed, appositional and intramembranous bone is deficient in its mechanical properties. The ordinary load-carrying functions suffice to deform these weakened femoral heads so that osteoarthritic changes develop. Considering contemporary assumptions of the causes of osteonecrosis, oxygenation, revascularization, and core decompression are the realistic therapeutic interventions. Necrosis of rats' femoral heads is studied as a model of osteonecrosis in both adults and children. In view of rodents' lifelong persisting physeal cartilage, vascular deprivation-induced osteonecrosis in rats mimics children's Perthes disease. The experimental model, which is well suited to test treatment modalities, has been used to investigate the effects of exposure to hyperbaric oxygen with and without non-weight bearing, medication of enoxaparin, and creation of an intraosseous conduit on the remodeling of the avascular necrotic femoral head. Intriguingly, the shape of treated rats' femoral heads is disfigured to a greater degree than that of untreated animals. This is most likely due to the reduced yield strength and elastic modulus as well as the raised strain-to-failure of the recently formed bone making up the post-necrotic femoral heads. It follows that expedited osteogenesis is, counter intuition, detrimental to maintaining the hemispherical shape of the femoral head, and thus to an articulation with congruent load-bearing surfaces. If this is indeed the case, the remodeling of the necrotic femoral head should be delayed, rather than sped up, as the present day paradigm would have it. Bearing in mind that the dead osseous structures keep their mechanical attributes for quite a while, a slowed down new bone formation would favor the gradual replacement of the necrotic by living bone. Therefore, management of the adult patients with osteonecrosis and children with Perthes disease should focus on a slowly progressive substitution so that the decline of the bone's mechanical properties is kept to a minimum. One viable therapeutic mode is a medication of inhibitors of the vascular endothelial growth factor.     

骨髓间充质干细胞移植联合氯化锂治疗兔股骨头缺血坏死疗效

BACKGROUND: Lithium chloride can promote the proliferation and osteogenic capacity of bone marrow mesenchymal stem cells in the necrotic region after avascular necrosis of the femoral head, which has become an issue of concern. OBJECTIVE: To compare the advantages and disadvantages of bone marrow stem cell transplantation combined with lithium chloride in the treatment of rabbit femoral head necrosis. METHODS: Passage 2 bone marrow mesenchymal stem cells from 1-week-old New Zealand rabbits were cultured in 0, 5, 10, 20, 40 mmol/L lithium chloride. Forty-eight healthy adult New Zealand rabbits were selected to make femoral head necrosis models in the right femoral head using liquid nitrogen freezing method and then randomized into four groups: model group with no implantation; lithium chloride group given lithium chloride treatment at 3 days after modeling; cell transplantation group given gelatin sponge implantation and bone marrow mesenchymal stem cell suspension injection into the femoral head after modeling; combined group given bone marrow mesenchymal stem cell suspension injection and lithium chloride treatment. Intraperitoneal injection of lithium chloride (45.2 mg/kg) was given daily beginning at the postoperative 3rd day, and the treatment duration was 4 weeks. RESULTS AND CONCLUSION: Lithium chloride at 10 mmol/L had the maximum effect on the proliferation of rabbit bone marrow mesenchymal stem cells, and if the concentration of lithium chloride was > 10 mmol/L, the promotion role of lithium chloride began to decline. After combined treatment, the morphology of the femoral head was restored a little, with increased bone density and thickened trabecular bone; the level of β-catenin in the femoral head was significantly increased in the combined group compared with the cell transplantation group or the lithium chloride group. These findings show that bone marrow stem cell transplantation combined with lithium chloride treatment can promote the recovery from femoral head necrosis by increasing bone mass of the trabecular bone and bone density of the femoral head in the necrotic region.      

Intravenous transplantation of allogeneic bone marrow mesenchymal stem cells and its directional migration to the necrotic femoral head

In this study, we investigated the feasibility and safety of intravenous transplantation of allogeneic bone marrow mesenchymal stem cells (MSCs) for femoral head repair, and observed the migration and distribution of MSCs in hosts. MSCs were labeled with green fluorescent protein (GFP) in vitro and injected into nude mice via vena caudalis, and the distribution of MSCs was dynamically monitored at 0, 6, 24, 48, 72 and 96 h after transplantation. Two weeks after the establishment of a rabbit model of femoral head necrosis, GFP labeled MSCs were injected into these rabbits via ear vein, immunological rejection and graft versus host disease were observed and necrotic and normal femoral heads, bone marrows, lungs, and livers were harvested at 2, 4 and 6 w after transplantation. The sections of these tissues were observed under fluorescent microscope. More than 70 % MSCs were successfully labeled with GFP at 72 h after labeling. MSCs were uniformly distributed in multiple organs and tissues including brain, lungs, heart, kidneys, intestine and bilateral hip joints of nude mice. In rabbits, at 6 w after intravenous transplantation, GFP labeled MSCs were noted in the lungs, liver, bone marrow and normal and necrotic femoral heads of rabbits, and the number of MSCs in bone marrow was higher than that in the, femoral head, liver and lungs. Furthermore, the number of MSCs peaked at 6 w after transplantation. Moreover, no immunological rejection and graft versus host disease were found after transplantation in rabbits. Our results revealed intravenously implanted MSCs could migrate into the femoral head of hosts, and especially migrate directionally and survive in the necrotic femoral heads. Thus, it is feasible and safe to treat femoral head necrosis by intravenous transplantation of allogeneic MSCs.     

股骨头坏死术前术后DSA评价

目的：通过对股骨头坏死病例术前术后行DSA检查,了解其术前股骨头血供情况,评价术后疗效。方法：对55例股骨头坏死病例行DSA检查。手术前病例25例,其中FicatⅡ期10例、Ⅲ-Ⅳ期15例,均伴髋关节异常。手术后30例,其中大转子转移股骨头成形术15例,带血管蒂髂骨骨瓣移植髓腔减压术15例。所有患者均选择旋股内外血管造影。结果：术前25例患者中20例旋股内动脉终末支中断、消失,3例股骨头染色良好,2例支持带动脉正常;25例均未见髋部静脉显影。术后30例髋部动脉造影示全部病例随手术方式不同出现髋部动脉发生解剖性变化,股骨头圆韧带动脉均未见显示。结论：股骨头坏死术前DSA造影可准确判断病侧股骨头动脉供血情况,对确定手术方式具有指导意义。手术后DSA造影对判断疗效具有重要价值。     

实验性肝坏死后再生肝窦内皮细胞的形态学观察及机制探讨

目的探讨肝坏死后再生过程中肝窦内皮细胞的形态学变化及其再生机制。方法Wistar雄性大白鼠60只,其中实验组为50只,非处理组及生理盐水组各5只作为对照组。实验组分10个小组,在一次性注射二甲基亚硝胺（DMN）50mg／kg后,分别于第12、24、36小时和第2、3、5、7、8、10及14天乙醚麻醉下处死,迅速取肝组织、骨髓及外周血。采用HE、免疫组织化学、双重免疫荧光标记方法通过光镜、电镜予以观察。结果注射DMN后12h肝组织内开始出现小灶状坏死,第24小时逐渐明显。第36小时坏死最明显,并且坏死灶内浸润大量的ED-1（大白鼠单核细J彬吞噬细胞标记物）阳性细胞。注射后第2天和第3天,坏死组织碎片和红细胞被ED-1阳性的吞噬细胞吞噬消除。第5天,在肝组织坏死灶内一些单核细胞其形态由圆形转变成梭形。第7天,细胞与残存的网织纤维接触,并表达SE-1（大白鼠肝窦内皮细胞标记物）及Tie-1（内皮细胞特异性受体）,此时常见ED-1／SE-1及ED-1／Tie-1双重阳性的梭形细胞。第8天,除了病变范围变小外,其肝组织形态相似于第7天。到第10天,增生的肝组织数量增加,充填坏死区。第14天坏死组织几乎完全被再生的肝及纤维组织所取代。注射DMN后12h骨髓中ED-1阳性的单核细胞开始增生,其中部分细胞表达5-溴-2-脱氧尿苷（BrdU）／ED-1,并在36h其数量达高峰。而这些细胞形态相似于骨髓中圆形单核细胞,其在第24小时至第10天出现于外周血中,高峰时间与骨髓相同。外周血中这些细胞的形状与肝组织坏死区内的ED-1阳性细胞相似。结论注射DMN后圆形ED-1阳性单核细胞首先在骨髓内增殖,通过血液循环到达肝坏死区域,再分化为肝窦内皮细胞,即DMN介导的坏死区域的肝窦重建可能部分通过血管新生来完成。     

介入导向溶栓治疗股骨头缺血坏死──附12例报告

目的：探索股骨头缺血坏死的介入治疗方法。方法：采用Seldinger穿刺超选择插管至旋股外、内动脉，灌入溶栓药物，治疗12例14个股骨头缺血坏死。洁果：介入治疗后，髋关节疼痛明显缓解或消失，活动自如，骨质逐步修复。结论：股骨头缺血坏死是由微循环障碍引起，介入导向溶栓对治疗股骨头缺血坏死有明显的疗效。     

液氮冷冻兔股骨头坏死模型制备新方法及可靠性评价

目的 建立一种可靠的并可用于治疗和研究新的液氮冷冻法制成的兔股骨头坏死动物模型。方法 采用成年新西兰大白兔21只,无菌条件下手术分离臀肌,切断股骨头圆韧带,显露股骨头。用医用棉签蘸取液氮,对股骨头进行3次冷冻3次复温,制备兔双侧股骨头坏死模型。于术后3、7d及2、4、6、8周进行X线摄片,股骨头大体形态和组织病理学观察。结果 X线摄片结果显示,制模2周时股骨头密度增高;4周时出现密度不均影像;6周时外形出现不规则变化,边缘有透亮区;8周时开始塌陷,关节间隙增大,骺板模糊。股骨头大体形态随时间推移,其受损程度呈加重演变特点。制模3 d的股骨头组织切片可见软骨细胞和骨细胞坏死;2周见骨小梁断裂、排列紊乱;4周见髓腔脂肪细胞坏死,内有新生血管及增生纤维组织;6周时出现匍行附着;而8周可见新骨沉积性生长,骺板处细胞挤压、变形。结论 本实验中建立的液氮冷冻股骨头坏死模型新方法具有创伤性小、贴近人股骨头坏死病理演变规律的优点,为干细胞移植等治疗和研究提供了一种新的模型制备方法。     

生脉成骨胶囊治疗股骨头坏死后股骨生物力学特性研究

目的：探讨生脉成骨胶囊治疗股骨头坏死后的股骨生物力学特性,评判药物的有效性,为临床提供科学依据。方法：采用２０只成年大白兔股骨分为模型组、治疗组与正常组进行生物力学实验应力分析,对股骨的强度、刚度进行系统检测。结果：（１）激素诱导的兔股骨头坏死模型组其股骨的强度和刚度明显下降,低于正常组和治疗组（Ｐ＜０．０５）。（２）生脉成骨胶囊治疗的兔股骨其强度和刚度明显高于正常组和模型组（Ｐ＜０．０５）;（３）生脉成骨胶囊对股骨头坏死治疗具有重要作用,能改善血运,促进愈合,加速骨化过程。结论：生脉成骨胶囊对股骨头坏死治疗在改善血运,促进坏死骨修复,恢复股骨头的力学性能上有积极的影响,十分安全有效。     

有限元分析髓芯减压并同种异体植骨治疗股骨头缺血性坏死的生物力学改变

目的:分析髓芯减压并同种异体植骨治疗早期股骨头缺血性坏死的临床应用。方法:选取收治的1例早期股骨头缺血坏死男性患者,入院后术前对患侧股骨头行多层螺旋CT扫描,然后将CT扫描的图片资料导入专业的有限元分析软件,建立股骨头缺血坏死的有限元模型,在有限元模型上模拟进行髓芯钻孔减压术,隧道植入骨块到软骨下骨约0~6 mm处,自体松质骨夯实。双足站立位为股骨头的模拟受力体位,髋关节的负荷条件为:外展肌合力M、髂胫束力T以及髋关节接触力J分别为1 060、1 721、1 621 N,选取90°、120°以及150°的坏死角度,分别计算未处理过的股骨头坏死模型的塌陷值、行单纯髓芯减压以及行髓芯减压加植骨时的塌陷值。结果:股骨头的正常骨质杨氏模量高于坏死骨的杨氏模量,正常骨质的横向变形系数低于坏死骨。行股骨头髓芯钻孔减压术后,股骨头的塌陷值显著增加,而减压隧道植入同种异体骨后,其塌陷值显著减低,但高于正常的股骨头。同时,由于股骨头坏死角度的增加,其塌陷值也明显增加。结论:髓芯钻孔减压并同种异体植骨术能有效增进坏死区的骨质修复,加强减压通道所致股骨头支撑结构的改变,防止股骨头关节面的塌陷。     

股骨头缺血性坏死多层螺旋CT三维构筑及介入治疗的临床意义

目的:探讨采用多层螺旋CT对股骨头缺血性坏死进行三维立体构筑的技术方法及介入治疗的临床价值.方法:使用Siemens Somatom Definition 64层螺旋CT对31例股骨头缺血性坏死患者共36髋进行薄层扫描,利用Inspace软件和NeuroDSA软件进行影像重组和三维立体构筑,并在X、Y和Z轴上旋转,观察股骨头的解剖形态.对I期坏死患者采用单纯经股骨头供血动脉灌注扩张血管及溶栓药物进行介入治疗;对II期及股骨头外形完整的III期患者首先采用介入治疗,然后经环钻剜出坏死骨植入混合自体骨髓间充质干细胞的自体松质骨.结果:容积重组图像显示早期缺血坏死的股骨头解剖形态基本正常,股骨头表面可见凹凸不平.股骨头坏死区的体积I期(8髋)为(1218.97±449.93)mm3,II期(22髋)为(3671.19±1316.83)mm3,股骨头完整的III期(6髋)为(7874.18±2381.22)mm3.根据HHS评分,疗效优23髋(63.89%),良10髋(27.78%),可3髋(8.33%),差0髋.结论:多层螺旋CT三维重组技术能够立体构筑股骨头的解剖形态,并在不同层面上对坏死区的大小进行测量,对股骨头缺血性坏死患者治疗方法的选择具有重要的临床指导意义.     

三足负重犬股骨头坏死模型的生物力学相关性研究

目的研究股骨头坏死病程各阶段的生物力学改变,探讨其生物力学发生作用的机制。方法取杂种犬24只,固定一侧前肢建立三足负重犬模型。随机取三足负重犬一侧后肢为实验侧,在股骨头内注射无水酒精,致股骨头坏死;对侧为对照侧,在股骨头内注入等量生理盐水。造模后1、3、6及12周处死动物,每组6只,分别对两组股骨头行大体观察以及放射学、组织学、生物力学检测。结果术后3周股骨头坏死侧点压硬度及中部松质骨弹性模量相对对照侧分别下降29%和32.9%,此时仅MRI可见股骨头出现低密度坏死区,组织学主要表现为骨坏死。术后6、12周股骨头坏死侧点压硬度相对对照侧分别下降了45.5%和48.7%,中部松质骨弹性模量相对对照侧分别下降了34.1%和32.4%。6周时坏死侧X线可见股骨头内密度不均,组织学表现为坏死和修复反应并存,坏死区向软骨下骨区进展。12周时坏死侧X线可见股骨头负重区下出现局部骨密度减低区,组织学出现关节软骨面塌陷和关节间隙狭窄。结论生物力学是股骨头病程进展的重要影响因素;病程进展中,特别是修复期力学性能的显著下降可能是后期塌陷的最直接原因。治疗股骨头坏死不仅应促进骨修复,更应提供病变区一个有利、稳定的生物力学环境。     

酒精性股骨头缺血坏死大鼠模型的制备

BACKGROUND:The relationship between long-term heavy drinking and alcohol-induced necrosis of the femoral head has long been clear, but the pathogenesis of alcohol-induced necrosis of the femoral head is currently not fully understood. OBJECTIVE:To establish a rat model of alcohol-induced avascular necrosis of femoral head and to study its pathogenesis. METHODS:Eighty Wistar rats were randomly divided into experimental and control groups (40 rats per group). Rats in the experimental group were intragastrically administered strong wine 10 mL/kg, once a day, for 6 consecutive days. Rats in the control group were given physiological saline 10 mL/kg, once a day, for 6 consecutive days. Bilateral femoral heads were randomly collected from six rats every month for histomorphological observation. RESULTS AND CONCLUSION:(1) Osteonecrosis: in the experimental group, at 3 months, trabecular bone became thin, arranged disorderly, and the number of empty lacuna began to increase. At 6 months, typical osteonecrosis appeared, and vacant lacunaes increased significantly. In the control group, trabecular bone was complete and neatly arranged. Osteocytes were visible in bone lacuna, and normal morphology of cells was seen. (2) Injury of blood vessels: in the experimental group, at 3 months, micro-intimal hyperplasia was observed. Elastic fibers of partial vascular endothelium were reduced. Elastic fiber and middle-layer smooth muscle breakage and proliferation were found. At 6 months, above manifestations were more remarkable. In the control group, arteriole film was not thickened, and vessel wall was normal. (3) Formation of microthrombus, in the experimental group, the number of microthrombus was increased at 3 months, and became significant at 6 months. In the control group, the number of microthrombus was not altered. (4) Results indicated that chronic alcohol intake can lead to microvascular endothelial injury in the rat femoral head. Abnormal blood microcirculation was detected in local region, and resulted in avascular necrosis of the femoral head. The degree of necrosis was associated with alcohol intake.     

3D打印导航模板辅助髓芯减压植骨治疗ARCOⅡ期非创伤性股骨头坏死

文题释义：3D打印导航模板：即3D打印技术与计算机虚拟导航相结合的技术,依据CT或者MRI成像的三维模型,结合快速成型的3D打印技术将虚拟三维导航模板打印成实体用于设计手术方案或引导术中操作。髓芯减压植骨：股骨头坏死非塌陷期常用的保髋术式之一,通过钻孔降低股骨头内的高压,改善静脉回流,促进毛细血管再生,同时通过减压通道对股骨头内坏死区域植入人工骨或自体骨,分散股骨头局部应力集中,避免股骨头进一步塌陷。 背景：髓芯减压植骨是治疗ARCOⅡ期非创伤性股骨头坏死的主要术式,但是存在定位不准确,坏死骨清除不彻底或过多的风险。 目的：观察3D打印导航模板辅助髓芯减压植骨治疗ARCOⅡ期非创伤性股骨头坏死的精确性和安全性。方法：收集2017年1至11月西安交通大学附属红会医院收治的80例(96髋)ARCOⅡ期非创伤性股骨头坏死患者,将其随机分为2组,3D组40例(48髋)行3D打印导航模板辅助髓芯减压植骨;对照组40例(48髋)行传统髓芯减压植骨,即未使用导航模板。2组患者对治疗方案均知情同意,且得到医院伦理委员会批准。分别记录2组手术时间、术中透视次数、术中失血量,观察术后第3,6,12,24个月X射线片复查结果,评估股骨头存活率、髋关节Harris评分、疼痛目测类比评分等指标,进行疗效对比。结果与结论：①3D组与对照组比较,手术时间由(132.57±14.86) min缩短至(82.63±10.31) min,术中透视次数由(16.80±2.15)次降低至(4.93±1.36)次,失血量由(143.23±17.98)mL降低至(75.64±16.23)mL,3D组在手术时间、透视次数、失血量方面均优于对照组(P < 0.05);②术后24个月影像学随访结果显示,3D组仅2例股骨头发生塌陷,但髋关节功能尚可,未行人工髋关节置换,股骨头存活率为96%;对照组中有9例股骨头发生塌陷,其中4例因髋关节活动受限行人工全髋置换,股骨头存活率为81%;3D组股骨头存活率高于对照组(P=0.024);③与对照组比较,3D组在Harris评分、目测类比评分方面均有所改善(P < 0.05);④提示将3D 打印导航模板应用于髓芯减压植骨治疗ARCOⅡ期非创伤性股骨头坏死,可减少手术时间、术中透视次数及出血量,提高术中定位的精确性和安全性。 ORCID: 0000-0001-8758-1626(陈冬冬) 中国组织工程研究杂志出版内容重点：人工关节;骨植入物;脊柱;骨折;内固定;数字化骨科;组织工程     

早中期继发性膝关节骨坏死手术疗效的临床体会

目的探讨手术治疗早中期继发性膝关节骨坏死的临床疗效。方法我院2009年6月至2013年6月收治23例早中期继发性膝关节骨坏死住院患者,共35个膝关节,其中27例膝关节有手术适应证。27例膝关节术前膝关节HSS评分59~84分,平均(63.4±3.8)分。根据膝关节不同情况选用不同的手术方法,12例坏死区髓心减压术,5例死骨刮除打压植骨术,7例关节镜下探查清理术及5例自体软骨移植术。结果术后随访3年,HSS评分73~94分,平均(77.6±4.8)分。有2例坏死区髓心减压术临床症状无明显改善;1例死骨刮除打压植骨术软骨下骨塌陷,关节坏死面进一步扩大;1例关节镜探查清理关节破坏进一步加重;其余患者临床症状均有明显改善。结论早中期继发性膝关节骨坏死患者手术治疗可推迟或组织膝关节的进一步坏死。     

激素性和酒精性股骨头坏死局部BMP表达强度的比较研究

目的 比较研究激素性和酒精性股骨头坏死（ONFH）修复期股骨头内BMP表达强度并进行比较分析，进一步认识不同病因造成ONFH表现不同的分子生物学基础。方法 取13例股骨头坏死，其中7例激素性（男5例，女2例），6例酒精性（均为男性），另取新鲜股骨颈骨折3天内行全髋置换术的2例作为对照组。分别按照负重区软骨面、软骨下坏死中心、修复区和相对正常区取材，并制成石蜡切片，做BMP的免疫组织化学染色，分析其结果。结果 三组之间在积分光密度和数密度上，酒精组明显高于激素组和正常股骨颈骨折组（P〈0．05），而激素组在数值上小于正常组，但无显著性差异（P〉0．05）。结论 激素性ONFH和酒精性ONFH具有不同的BMP表达强度。且激素性ONFH的BMP表达强度弱于酒精性ONFH。