非创伤性成人股骨头缺血性坏死股骨头塌陷的预测

股骨头缺血性坏死特别是非创伤性股骨头缺血性坏死高发于中青年[1] ,发病机理尚不十分清楚 ,尽管导致股骨头缺血性坏死的原因不同 ,但却有相似的病理过程和结果 ,多数患者在出现症状后如不经治疗 ,将不可避免地出现股骨头塌陷[1] 。股骨头塌陷是导致髋关节骨性关节炎和关节功能受损的重要原因。患者因此常需接受全髋关节置换治疗。由于多数患者年青且累及双侧髋关节等因素 ,人工关节置换术后远期疗效较其他疾病差[1] 。本病具有很高的塌陷率 ,但目前对股骨头缺血性坏死自然病程尚不十分清楚[1,2 ] 。通常所认为的股骨头塌陷的发生率为 6 8%…     

非创伤性股骨头坏死的国外研究进展

非创伤性股骨头坏死在国内外均被列为尚未解决的难治性疾病之一,本文中作者综合近几年的研究对非创伤性股骨头坏死的病因及手术和非手术治疗方法进行最新的阐述.非创伤性股骨头坏死的发病有遗传学基础,各种危险因素及遗传易感性的相互作用将决定病情的转归.早期诊断及在股骨头出现塌陷之前进行干预是关节保留治疗能否得到良好结果的关键.关节是否保留取决于放射影像学表现.对于股骨头已经塌陷的患者,行关节置换术的满意度优于关节保留治疗.最新的药物治疗方法如生长分化因子可能会改变作者目前的治疗方法,但是有待于临床研究结果及长期的随访.     

不典型非创伤性股骨头坏死的诊断

目的探讨不典型非创伤性股骨头坏死的影像表现及诊断方法。方法回顾性分析8例(8髋)非创伤性股骨头坏死的不典型影像表现,并按照年龄、性别、病灶大小与典型非创伤性股骨头坏死对照比较临床表现及影像特点。结果8例(8髋)病理结果与非创伤性股骨头坏死相符。8例(8髋)不典型非创伤性股骨头坏死MRI均无典型T1WI的带样征,无明显T2WI双线征;X线平片及CT无典型硬化带,仅有针尖样钙化。临床表现与典型非创伤性股骨头坏死无明显差异。结论少数非创伤性股骨头坏死出现不典型影像特点,诊断应结合病理。     

非创伤性股骨头缺血坏死血浆内皮素水平的临床研究

目的：探讨非创性股骨头缺血坏死患者血浆内皮素（ＥＴ）水平的变化及临床意义。方法：对５８例非创伤性股骨头缺血坏死患者血浆内皮素水平进行测定，并与２０例长骨骨折患者比较。结果：非创伤性股骨头缺血坏死组血浆内皮素水平显著升高。结论：内皮素可能与非创性股骨头缺血坏死有关。     

非创伤性股骨头缺血性坏死的临床病因分析

目的：探讨非创伤性股骨头缺血性坏死的临床病因构成及特点，方法：对成人非创伤性股骨头缺血坏死306例（504髋），按病因分组并行统计学处理，结果：306例中酒精性139例（46％），激素性105例（34％），酒精＋激素性40例（13％），非酒精非激素性22例（7%），酒精性高于激素性（P＜0．05）。酒精＋激素性平均饮酒数小于酒精性（P＜0．05），酒精＋激素性的激素用量小于激素性（P＜0．05），酒精＋激素性双髋坏死率高于酒精性和激素性（P＜0．05）。结论：酒精和激素是非创伤性股骨头缺血性坏死的主要致病原因，酒精性有上升趋势，酒精和激素具有协同致病作用。     

非创伤性股骨头坏死的基因多态性研究进展

非创伤性股骨头坏死(non-traumatic osteonecrosis of femoral head,NONFH)是一类以髋关节疼痛、功能障碍进行性加重为主的疾病,严重危害人体健康,全世界的发病人数呈逐年上升趋势,但其具体发病机制仍不清楚。近年的研究表明,基因多态性分析有助于破解这一难题。本文综述了与NONFH相关的热点基因,旨在为NONFH的预防和治疗找到新的方法和途径。     

MicroRNA表达对非创伤性股骨头坏死的影响研究进展

MicroRNA是具有调控功能的内源性非编码RNA,广泛参与人体发育、细胞增殖、脂质代谢等过程,并对上述生命过程起到一定的调控作用。部分学者认为,非创伤性股骨头坏死的发生可能与脂质代谢紊乱、内皮细胞损伤、干细胞分化异常、骨细胞凋亡和机体高凝状态等因素有关,上述过程均有microRNA的广泛参与,提示microRNA对股骨头坏死的发生、发展可能起着至关重要的作用,近年来,microRNA在非创伤性股骨头坏死的作用机制研究中得以深入。研究发现:前列腺癌、胰腺癌、乳腺癌等患者循环血中microRNA表达谱呈现特异性变化,部分学者提出循环microRNA可作为一种潜在的新型标志物,有望实现疾病的早期诊断。本文综述了非创伤性股骨头坏死相关microRNA的研究进展,同时对其在本疾病中的应用进行展望。     

细胞因子治疗非创伤性股骨头缺血坏死的研究进展

股骨头缺血性坏死是以骨的活性成分死亡为主要改变的病理过程，其发生与多种疾病、药物及髋关节创伤有关。其中，非创伤性股骨头坏死（nontraumatic osteonecrosis of femoral head，NONFH）的发病率逐年增加，但其病因及发病机理至今尚未完全阐明，国内外学者提出了许多病因学假说，诸如脂肪代谢紊乱、骨髓内压力升高、血管内凝血学说、骨质疏松学说等等，其常用的治疗方法有药物治疗、     

Endothelial nitric oxide synthase gene polymorphisms in patients with nontraumatic femoral head osteonecrosis.

As endothelial nitric oxide synthase (eNOS) has beneficial effects on skeletal, vascular, and thrombotic systems, the association between nontraumatic femoral head osteonecrosis (FHON) and eNOS gene polymorphisms was investigated in Korean patients with FHON. Genomic DNA from 103 patients with nontraumatic FHON (idiopathic in 50, steroid-induced in 29, and alcohol abuse in 24) and 103 control subjects matched for gender and age (3-year range) was analyzed for the 27-bp repeat polymorphism in intron 4 and Glu298Asp polymorphism in exon 7. The frequencies of alleles and genotypes were compared between patients and control subjects. The frequency of 4a allele was significantly higher in total patients than control subjects [6.8% vs. 2.4%, p = 0.0345, odds ratio (OR) 2.931]. In subgroup analysis, the 4a allele significantly increased in patients with idiopathic FHON versus control subjects (9.0% vs. 2.4%, p = 0.0297, OR 3.976). The frequency of the 4a/b genotype in total patients (13.6% vs. 4.9%, p = 0.0302, OR 3.083) as well as patients with idiopathic FHON (18.0% vs. 4.9%, p = 0.0246, OR 4.302) was higher than control subjects. The distribution of Glu298Asp polymorphisms was not significantly different between patients and control subjects. Microstellate polymorphism in intron 4 of eNOS polymorphism was significantly associated with idiopathic FHON in Korean patients. Because 4a allele is associated with lower synthesis of eNOS, these results suggest that carrier state of 4a allele in intron 4 might be a genetic risk factor of FHON and could provide insight into the protective role of nitric oxide in the pathogenesis of FHON.     

股骨头坏死误诊现状及分析

探讨股骨头坏死误诊的主要原因,有利于减少其误诊及漏诊的发生率,提高股骨头坏死的诊断水平。本文分析近15年国内有关股骨头坏死误诊文献。对易与股骨头坏死混淆的9种疾病进行鉴别分析。股骨头坏死早期易误诊为其它疾病;而股骨头坏死中晚期的一些症状、体征及影像表现与一些疾病相似,易将这些疾病误诊为股骨头坏死。髋关节疾病病理改变的不同始发部位,在相应的影像异常表现有各自不同的特异性表现。     

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.     

Alterations in the differentiation ability of mesenchymal stem cells in patients with nontraumatic osteonecrosis of the femoral head: comparative analysis according to the risk factor.

It has been suggested that decreased replication capacity of mesenchymal stem cells (MSCs) or decreased MSCs activity in the bone marrow is related to nontraumatic osteonecrosis (ON). However, little is known about differentiation ability of MSCs according to the risk factor of nontraumatic ON. We hypothesize that differentiation abnormalities in MSCs of the bone marrow of the proximal femurs might be related to nontraumatic ON of the femoral head. The purpose of this study was to investigate the osteogenic and adipogenic differentiation ability of MSCs in patients with nontraumatic ON of the femoral head. We examined the differentiation ability of MSCs in cultures derived from the bone marrow of the proximal femurs obtained from 10 patients with hip osteoarthritis (OA) and 37 patients with nontraumatic ON of the femoral head undergoing hip replacement surgery. We analyzed the osteogenic and adipogenic differentiation ability of MSCs according to the risk factor [alcohol-induced (15 patients), idiopathic (12 patients) and steroid-induced (10 patients)] of nontraumatic ON of the femoral head separately and compared it with patients with hip OA. The osteogenic activity was measured as the extracellular matrix calcification by alizarin red S staining and the alkaline phosphatase activity, and the adipogenic activity was measured as the accumulation of Oil red O-positive lipid vacuoles. The osteogenic differentiation ability of MSCs in patients with alcohol-induced and idiopathic ON was significantly reduced compared with that in patients with OA (p < 0.05 and p < 0.05, respectively). In patients with steroid-induced ON, the osteogenic differentiation ability was found to be increased, but the difference was not statistically significant. The adipogenic differentiation ability of MSCs was not significantly changed in patients with alcohol-induced, idiopathic, and steroid-induced ON compared to patients with OA. Our results indicate that altered osteogenic differentiation ability in MSCs is related to nontraumatic ON of the femoral head and the differentiation potential of MSCs in patients with nontraumatic ON differs according to its risk factor.     

激素性和酒精性股骨头坏死组织形态学的对比分析

目的比较分析激素性股骨头坏死和酒精性股骨头坏死的组织形态学特点。方法选取自2012-12—2013-12诊治的股骨头坏死26例,激素性股骨头坏死14例(激素组),酒精性股骨头坏死12例(酒精组),将同期行THA的6例股骨颈骨折(股骨头正常)作为对照组。将26例坏死股骨头及6例正常股骨头制备成病理切片标本进行HE染色、改良Masson染色,通过光学显微镜进行组织形态学定量分析。结果与对照组相比,激素组和酒精组同源软骨细胞数减少、骨小梁面积减小,而空骨陷窝率、骨陷窝面积及长径、软骨成骨指数、脂肪细胞长径、血管形成量及新生骨小梁面积等均高于正常水平,差异有统计学意义(P0.05)。激素组空骨陷窝率、骨小梁面积、新生骨小梁面积及脂肪细胞长径等均低于酒精组,而软骨成骨指数高于酒精组,差异有统计学意义(P0.05);2组在骨陷窝面积及长径、有效血管及无效血管数、同源软骨细胞数方面差异无统计学意义(P0.05)。结论酒精性股骨头坏死在组织形态学表现上更为复杂,坏死程度更加严重,在修复过程中也不同于激素性股骨头坏死。     

Unique plasma metabolomic signature of osteonecrosis of the femoral head

Metabolomic analysis was performed to determine the metabolomic signature of osteonecrosis of the femoral head (ONFH), and to investigate the underlying relationship between the metabolomic signature and the pathogenesis of ONFH. Plasma samples were collected from 30 ONFH patients and 30 normal subjects. The global metabolomic profile was obtained through a combination of high‐throughput liquid‐ and gas‐chromatography‐based mass spectrometry analyses. All statistical analyses were conducted using the R software. The results showed clear differences in the metabolomic signature between the plasma of ONFH patients compared with normal subjects. Among the 354 identified metabolites, the expression of 123 metabolites were significantly changed in ONFH patients compared with normal subjects (p < 0.05, q < 0.10). Bioinformatics analysis revealed that these abnormal metabolites were mainly involved in lipid‐, glutathione‐, nucleotide‐, and energy‐associated pathways, which might be related to enhanced inflammation, oxidative stress, and energy deficiency due to ONFH. This study provides the first metabolomic analysis of ONFH, and identifies a previously unrecognized metabolic signature in ONFH plasma. The results offer new insights into the pathological mechanisms of ONFH through its influence on metabolic pathways, providing the requisite framework for identifying biomarkers or novel targets for therapeutic intervention. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 34:1158–1167, 2016.     

Superelastic cage implantation: a new technique for treating osteonecrosis of the femoral head with mid-term follow-ups

We developed a device for the treatment of Ficat and Arlet stage II and III osteonecrosis of the femoral head. This device, which we named the “super-elastic cage,” was designed to provide mechanical support for the necrotic weight-bearing area of the femoral head to prevent its collapse. The cage was used in combination with surgical removal of necrotic bone, insertion of vascularized pedical bone graft, or impacted autologous cancellous bone graft. A total of 93 hips in 62 patients at Ficat stage II to III were included in a 8-year study. Implantations were performed by 2 different approaches: Smith-Peterson approach and minimal invasive approach by the lateral side of great trochanter. The follow-up period was between 72 and 107 months. Of the femoral heads in this study, 82.7% survived. The superelastic cage implantation technique may offer an alternative treatment to the early and middle stages of osteonecrosis of the femoral head.     

钽棒治疗早期非创伤性股骨头坏死的回归性研究

[目的]分析钽棒治疗早期股骨头坏死的临床疗效,探讨影响钽棒治疗早期股骨头坏死临床疗效的因素.[方法]钽棒治疗早期股骨头坏死病例149例(168髋),男96例,女53例;平均年龄32.36岁.Ⅰ期和Ⅱ期(塌陷前)88髋,Ⅲ期(塌陷后)80髋,其中双侧19例.根据ARCO分期,进行Harris评分和影像学评估.将Harris评分70分以下、再次手术、影像学病变进展(股骨头由非塌陷变塌陷或塌陷加重,关节间隙狭窄加重)视为钽棒失败.[结果]共随访到130例138髋,平均随访时间(31.47±5.78)(8～61)个月,术前平均Harris评分为62.65,术后为79.50(P<0.05).优良率为68.12%.Cox风险模型分析显示大病灶、外侧病灶、植骨与否是手术失败的风险因素,病因、性别、年龄、病灶是否在股骨头骺板内,对钽棒治疗早期股骨头坏死的临床疗效无明显影响.[结论]影响钽棒治疗早期股骨头坏死临床疗效的因素是病灶大小(大于30%)、坏死灶位置(外侧型)、植骨与否,钽棒治疗早期股骨头坏死需要清除死骨、联合植骨.