Articular calcified cartilage canals in the third metacarpal bone of 2-year-old thoroughbred racehorses

We describe morphological aspects of the articular calcified cartilage mineralizing front 'tidemark' in the distal joint surface of the third metacarpal bone from 14 horses. Compositional backscattered electron scanning electron microscopy and confocal scanning light microscopy were conducted on polymethylmethacrylate (PMMA)-embedded medio-lateral slices. After maceration, scanning electron microscopy (SEM) was used to study the calcified cartilage surface in the 'wedges' intervening between the slices. An anatomically reproducible clustering of canals in the calcified cartilage was found at one site on the sagittal ridge in all the horses. The site is one that is relatively less loaded during joint function. These canals through calcified cartilage result from osteoclastic resorption (cutting cones) penetrating from bone through to the non-mineralized hyaline articular cartilage. Their presence may indicate a pathway for connection between bone and cartilage extracellular fluid. In one horse, repair of such canals by plugging with new calcified cartilage was demonstrated. Differences in the degree of mineralization of regions of cartilage were seen in the combined compositional-cum-topographical backscattered SEM images of the macerated 'tidemark' front. More-or-less circular patches of lower mineralization density were frequently centred on (and may possibly originate from) canals. These microanatomical features should be searched for in other joints, at other ages and in other species to discover their frequency and significance.     

Quantitative ultrasound imaging detects degenerative changes in articular cartilage surface and subchondral bone

Previous studies have suggested that quantitative ultrasound imaging could sensitively diagnose degeneration of the articular surface and changes in the subchondral bone during the development of osteoarthrosis (OA). We have recently introduced a new parameter, ultrasound roughness index (URI), for the quantification of cartilage surface roughness, and successfully tested it with normal and experimentally degraded articular surfaces. In this in vitro study, the applicability of URI was tested in bovine cartilage samples with spontaneously developed tissue degeneration. Simultaneously, we studied the sensitivity of quantitative ultrasound imaging to detect degenerative changes in the cartilage-bone interface. For reference, histological degenerative grade of the cartilage samples was determined. Mechanical reference measurements were also conducted. Cartilage surface roughness (URI) was significantly (p<0.05) higher in histologically degenerated samples with inferior mechanical properties. Ultrasound reflection at the cartilage-bone interface was also significantly (p<0.05) increased in degenerated samples. Furthermore, it was quantitatively confirmed that ultrasound attenuation in the overlying cartilage significantly affects the measured ultrasound reflection values from the cartilage-bone interface. To conclude, the combined ultrasound measurement of the cartilage surface roughness and ultrasound reflection at the cartilage-bone interface complement each other, and may together enable more sensitive and quantitative diagnosis of early OA or follow up after surgical cartilage repair.     

股骨近端主压力骨小梁生物力学特性

目的股骨头坏死是一种常见病,导致其发病的原因有很多,其中股骨颈骨折后股骨头坏死的原因尚不清楚,机制不明,由于其局部解剖结构特殊,根据其内部结构特点,对骨小梁结构进行研究,为解释股骨颈骨折后股骨头坏死的发生原因提供实验依据。方法对正常中国人(45～60岁)尸体股骨近端主压力骨小梁系统从上到下分成3个区,分别在Endura TEC ELF3200生物力学材料动态力学性能测试系统上,从主压力骨小梁方向及与其垂直方向上进行拉伸、压缩性能实验研究。结果得出了股骨近端主压力骨小梁系统3个区在主压力骨小梁系统方向及与其垂直方向的压缩、拉伸屈服强度、极限强度、弹性模量等测试指标的实验结果。从上到下3个区的弹性模量等生物力学性能依次递增,主压力方向的压缩生物力学性能要明显高于拉伸生物力学性能,并且生物力学性能在主压力系统方向及与其垂直方向有明显差异。结论股骨近端主压力骨小梁的主要力学性能是承受压应力,并且具有明显的各向异性。     

Morphological,biochemical and mechanical properties of articular cartilage and subchondral bone in rat tibial plateau are age related

The purpose of this study was to investigate age‐related changes in the morphological, biochemical and mechanical properties of articular cartilage (AC) and subchondral bone in the rat tibial plateau. Female Wistar rats were grouped according to age (1, 3, 5, 7, 9, 11, 13, 15, 16 and 17 months, with 10 rats in each group). The ultrastructures, surface topographies, and biochemical and mechanical properties of the AC and subchondral bone in the knee joints of the rats were determined through X‐ray micro‐tomography, histology, immunohistochemistry, scanning electron microscopy (SEM), atomic force microscopy and nanoindentation. We found that cartilage thickness decreased with age. This decrease was accompanied by functional condensation of the underlying subchondral bone. Increased thickness and bone mineral density and decreased porosity were observed in the subchondral plate (SP). Growth decreased collagen II expression in the tibial cartilage. The arrangement of trabeculae in the subchondral trabecular bone became disordered. The thickness and strength of the fibers decreased with age, as detected by SEM. The SP and trabeculae in the tibial plateau increased in roughness in the first phase (1–9 months of age), and then were constant in the second phase (11–17 months of age). Meanwhile, the roughness of the AC changed significantly in the first phase (1–9 months of age), but the changes were independent of age thereafter. This study gives a comprehensive insight into the growth‐related structural, biochemical and mechanical changes in the AC and subchondral bone. The results presented herein may contribute to a new understanding of the pathogenesis of age‐related bone diseases.     

Topographical variations in articular cartilage and subchondral bone of the normal rat knee are age-related

In osteoarthritis animal models the rat knee is one of the most frequently investigated joint. However, it is unknown whether topographical variations in articular cartilage and subchondral bone of the normal rat knee exist and how they are linked or influenced by growth and maturation. Detailed knowledge is needed in order to allow interpretation and facilitate comparability of published osteoarthritis studies. For the first time, the present study maps topographical variations in cartilage thickness, cartilage compressive properties and subchondral bone microarchitecture between the medial and lateral tibial compartment of normal growing rat knees (7 vs. 13 weeks). Thickness and compressive properties (aggregate modulus) of cartilage were determined and the subchondral bone was analyzed by micro-computed tomography. We found that articular cartilage thickness is initially homogenous in both compartments, but then differentiates during growth and maturation resulting in greater cartilage thickness in the medial compartment in the 13-week-old animals. Cartilage compressive properties did not vary between the two sites independently of age. In both age-groups, subchondral plate thickness as well as trabecular bone volume ratio and trabecular thickness were greater in the medial compartment. While a high porosity of subchondral bone plate with a high topographical variation (medial/lateral) could be observed in the 7-week-old animals, the porosity was reduced and was accompanied by a reversion in topographical variation when reaching maturity. Our findings highlight that there is a considerable topographical variation in articular cartilage and subchondral bone within the normal rat knee in relation to the developmental status.     

Rapid decalcification of articular cartilage and subchondral bone using an ultrasonic cleaner with EDTA

Articular cartilage and subchondral bones were used to be the samples for studying effects of drugs in the joint degenerative diseases such as osteoarthritis. Because of the deposition of mineral salts, articular cartilage and subchondral bones require decalcification process to soften the tissues. EDTA is a chelating agent that is commonly used to remove mineral salts, but this step is time-consuming and can take as long as 45 days. Commercial ultrasonic cleaner and microwave oven were reported to reduce the decalcification timing. The aim of this study is to determine and compare the decalcification of human articular cartilage and subchondral bone using EDTA together with ultrasonic cleaner or microwave oven. Hundred pieces of articular cartilage and subchondral bones obtained from osteoarthritis patients undergone total-knee-replacement were divided into 10 groups according to decalcification method (ultrasonic cleaner or microwave) and timing (2, 4, 6, 8, and 10 h). In each group, all cartilage and subchondral bone pieces were decalcified and sectioned, and subsequently stained with haematoxylin and eosin, Von Kossa, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, or caspase-3 immunohistochemistry. The optimal timing of decalcification of articular cartilage and subchondral bones using EDTA together with ultrasonic cleaner was at 8 and 10 h, while the timing using EDTA together with microwave oven was more than 10 h. Clear TUNEL and caspase-3 signals were obtained from samples decalcified using EDTA together with ultrasonic cleaner for 8 h. In summary, to our knowledge, this is the first study that compared EDTA decalcification between ultrasonic cleaner and microwave oven. Here, we report a new methodology for decalcification for articular cartilage and subchondral bones that reduces decalcification time from weeks to hours and is suitable for further pathological analyses.     

髋关节软骨高、低负重区微纳结构的力学性质对比

文题释义：微纳层面：相对于宏观层面而言,是对宏观层面的一个补充,由肉眼可见的毫米级别到肉眼不可见的微米、纳米级别。分别使用微米级、纳米级原子力显微镜探针测量软骨微纳弹性模量,以揭示软骨在微纳层面力学性能的特点,以及与宏观层面力学性能的关系。 负重区：在日常活动运动中,由于机体力线等不同,势必造成软骨不同区域负重出现不同,不同的负重也会影响到胶原纤维等物质的重塑重构,引起软骨力学性能的改变。 背景：髋关节软骨具有高、低负重区域,既往研究表明2个区域的宏观弹性模量是不同的。然而在微米和纳米水平上的弹性模量尚不清楚,这些信息对于进一步理解软骨微米和纳米力学性质至关重要。此外,影响软骨2个区域机械性能的微纳结构至今仍有待阐明。 目的：探究微纳层面髋关节软骨高、低负重区力学性质与结构。 方法：取新鲜正常猪股骨头软骨,使用原子力显微镜直径为5 μm的球形尖端测量不同负重区微米级压缩弹性模量,使用曲率半径为5 nm的ScanAsyst-Air探针测量其纳米级压缩弹性模量、纳米结构和胶原纤维直径。扫描电子显微镜用于识别软骨不同负重区微米结构。 结果与结论：①股骨头软骨高负重区微米级弹性模量为(433.05±146.52) kPa,低负重区微米级弹性模量为(331.19±84.88) kPa,高负重区域在微米水平上的压缩弹性模量显著高于低负重区域(P=0.029 8);②股骨头软骨高负重区纳米级弹性模量为(1.24±0.42) GPa,低负重区纳米级弹性模量为(1.28±0.41) GPa,在纳米水平上2个区域的胶原纤维的压缩弹性模量差异无显著性意义(P=0.846 2);③在微米水平上,股骨头软骨高负重区域的胶原纤维排列更规则;在纳米水平上,2个负重区域的胶原纤维直径差异无显著性意义(P=0.926 4);④以上结果表明,股骨头软骨高负重区胶原纤维较低负重区交联更规则,使软骨高负重区微米级压缩弹性模量高于低负重区,与宏观上压缩弹性模量趋势一致,但高负重并没有影响到纳米层面单个胶原纤维。 ORCID: 0000-0001-7971-5372(郭江博) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Evaluation of enzymatic proteoglycan loss and collagen degradation in human articular cartilage using ultrashort echo time-based biomarkers: A feasibility study

The objective of the current study was to investigate the feasibility of quantitative 3D ultrashort echo time (UTE)-based biomarkers in detecting proteoglycan (PG) loss and collagen degradation in human cartilage. A total of 104 cartilage samples were harvested for a trypsin digestion study (n = 44), and a sequential trypsin and collagenase digestion study (n = 60), respectively. Forty-four cartilage samples were randomly divided into a trypsin digestion group (tryp group) and a control group (phosphate-buffered saline [PBS] group) (n = 22 for each group) for the trypsin digestion experiment. The remaining 60 cartilage samples were divided equally into four groups (n = 15 for each group) for sequential trypsin and collagenase digestion, including PBS + Tris (incubated in PBS, then Tris buffer solution), PBS + 30 U col (incubated in PBS, then 30 U/ml collagenase [30 U col] with Tris buffer solution), tryp + 30 U col (incubated in trypsin solution, then 30 U/ml collagenase with Tris buffer solution), and tryp + Tris (incubated in trypsin solution, then Tris buffer solution). The 3D UTE-based MRI biomarkers included T₁, multiecho T₂*, adiabatic T_1ρ (AdiabT_1ρ), magnetization transfer ratio (MTR), and modeling of macromolecular proton fraction (MMF). For each cartilage sample, UTE-based biomarkers (T₁, T₂*, AdiabT_1ρ, MTR, and MMF) and sample weight were evaluated before and after treatment. PG and hydroxyproline assays were performed. Differences between groups and correlations were assessed. All the evaluated biomarkers were able to differentiate between healthy and degenerated cartilage in the trypsin digestion experiment, but only T₁ and AdiabT_1ρ were significantly correlated with the PG concentration in the digestion solution (p = 0.004 and p = 0.0001, respectively). In the sequential digestion experiment, no significant differences were found for T₁ and AdiabT_1ρ values between the PBS + Tris and PBS + 30 U col groups (p = 0.627 and p = 0.877, respectively), but T₁ and AdiabT_1ρ values increased significantly in the tryp + Tris (p = 0.031 and p = 0.024, respectively) and tryp + 30 U col groups (both p < 0.0001). Significant decreases in MMF and MTR were found in the tryp + 30 U col group compared with the PBS + Tris group (p = 0.002 and p = 0.001, respectively). It was concluded that AdiabT_1ρ and T₁ have the potential for detecting PG loss, while MMF and MTR are promising for the detection of collagen degradation in articular cartilage, which could facilitate earlier, noninvasive diagnosis of osteoarthritis.     

Recent advances in the understanding of molecular mechanisms of cartilage degeneration,synovitis and subchondral bone changes in osteoarthritis

Osteoarthritis (OA), the most common form of degenerative joint disease, is linked to high morbidity. It is predicted to be the single greatest cause of disability in the general population by 2030. The development of disease-modifying therapy for OA currently face great obstacle mainly because the onset and development of the disease involve complex molecular mechanisms. In this review, we will comprehensively summarize biological and pathological mechanisms of three key aspects: degeneration of articular cartilage, synovial immunopathogenesis, and changes in subchondral bone. For each tissue, we will focus on the molecular receptors, cytokines, peptidases, related cell, and signal pathways. Agents that specifically block mechanisms involved in synovial inflammation, degeneration of articular cartilage, and subchondral bone remodeling can potentially be exploited to produce targeted therapy for OA. Such new comprehensive agents will benefit affected patients and bring exciting new hope for the treatment of OA.     

淫羊藿苷治疗骨性关节炎过程中对关节软骨、软骨下骨、滑膜等影响的机制

文题释义： 淫羊藿苷：为淫羊藿干燥茎叶的提取物,呈淡黄色针状结晶粉末, 相对分子质量为676.65, 属黄铜类化合物,现代药理学研究发现其具有很强的生物活性, 对骨组织、免疫系统、肿瘤组织、神经系统、生殖系统、内分泌系统和心血管系统等具有显著作用。 滑膜：是关节囊的内层。滑膜呈淡红色,平滑闪光,薄而柔润,由疏松结缔组织组成,其功能是制造和调节滑液等。滑膜直接附着于关节软骨的边缘并向内贴附在关节囊内的非关节区域,覆盖在关节囊、关节内韧带、骨与肌腱表面。滑膜分泌滑液,在关节活动中起重要作用。背景：淫羊藿苷是具有补肾强筋健骨功效的淫羊藿的主要有效成分,近年来大量的研究发现淫羊藿苷在治疗骨性关节炎方面有着显著作用。 目的：综述淫羊藿苷治疗骨性关节炎的分子机制研究进展。 方法：第一作者应用计算机以“Icariin、Osteoarthritis、Cartilage、Subchondral bone、Synovial membrane 、Synovium、Inflammation”及“淫羊藿苷、骨关节炎、骨性关节炎、软骨、软骨下骨、滑膜、炎症”作为主题词检索PubMed、中国知网、万方、维普等数据库相关文献,按入选标准及排除标准进行筛选,最终纳入42篇文献进行分析。 结果与结论：淫羊藿苷通过促进骨髓间充质干细胞的成软骨分化及增强软骨细胞和成骨细胞的增殖,抑制软骨细胞外基质的降解、降低破骨细胞的活性和减轻炎症因子所致的滑膜炎症反应来有效的治疗骨性关节炎。但其最佳有效剂量及浓度安全性仍需要大量实验研究,目前绝大部分实验仍停留在动物及组织细胞等基础实验,尚需要大量临床研究,继续完善其具体机制,以期为淫羊藿苷治疗骨关节炎提供循证医学证据。ORCID:0000-0002-2013-743X(余绍涌)中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Topographical variations of the strain-dependent zonal properties of tibial articular cartilage by microscopic MRI

The topographical variations of the zonal properties of canine articular cartilage over the medial tibia were evaluated as the function of external loading by microscopic magnetic resonance imaging (µMRI). T2 and T1 relaxation maps and GAG (glycosaminoglycan) images from a total of 70 specimens were obtained with and without the mechanical loading at 17.6?µm depth resolution. In addition, mechanical modulus and water content were measured from the tissue. For the bulk without loading, the means of T2 at magic angle (43.6?±?8.1?ms), absolute thickness (907.6?±?187.9?µm) and water content (63.3?±?9.3%) on the meniscus-covered area were significantly lower than the means of T2 at magic angle (51.1?±?8.5?ms), absolute thickness (1251.6?±?218.4?µm) and water content (73.2?±?5.6%) on the meniscus-uncovered area. However GAG (86.0?±?15.3?mg/ml) on the covered area was significantly higher than GAG (70.0?±?8.8?mg/ml) on the uncovered area. Complex relationships were found in the tissue properties as the function of external loading. The tissue parameters in the superficial zone changed more profoundly than the same properties in the radial zone. The tissue parameters in the meniscus-covered areas changed differently when comparing with the same parameters in the uncovered areas. This project confirms that the load-induced changes in the molecular distribution and structure of cartilage are both depth-dependent and topographically distributed. Such detailed knowledge of the tibial layer could improve the early detection of the subtle softening of the cartilage that will eventually lead to the clinical diseases such as osteoarthritis.     

Mono-iodoacetate-induced histologic changes in subchondral bone and articular cartilage of rat femorotibial joints: an animal model of osteoarthritis

Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain and a progressive loss of articular cartilage. Studies to elucidate the pathophysiology of OA have been hampered by the lack of a rapid, reproducible animal model that mimics both the histopathology and symptoms associated with the disease. Injection of mono-iodoacetate (MIA), an inhibitor of glycolysis, into the femorotibial joint of rodents promotes loss of articular cartilage similar to that noted in human OA. Here, we describe the histopathology in the subchondral bone and cartilage of rat (Wistar) knee joints treated with a single intra articular injection of MIA (1 mg) and sacrificed at 1, 3, 5, 7, 14, 28, and 56 days postinjection. Histologically, the early time points (days 1-7) were characterized by areas of chondrocyte degeneration/necrosis sometimes involving the entire thickness of the articular cartilage in the tibial plateaus and femoral condyles. Changes to the subchondral bone, as evidenced by increased numbers of osteoclasts and osteoblasts, were noted at by day 7. By 28 days, there was focal fragmentation and collapse of bony trabeculae with fibrosis and increased osteoclastic activity. By 56 days there were large areas of bone remodeling evidenced by osteoclastic bone resorption and newly formed trabeculae with loss of marrow hematopoietic cells. Subchondral cysts and subchondral sclerosis were present in some rats. In conclusion, intra-articular injection of MIA induces loss of articular cartilage with progression of subchondral bone lesions that mimic those of OA. This model offers a rapid and minimally invasive method to reproduce OA-like lesions in a rodent species.     

Isorhamnetin ameliorates inflammatory responses and articular cartilage damage in the rats of monosodium iodoacetate-induced osteoarthritis

Abstract

Context: Osteoarthritis (OA) is a degenerative joint disease with damage to the articular cartilage. Active production of inflammatory cytokine/chemokine and matrix metalloproteinases may be found during the progression of OA. Isorhamnetin had the effects of anti-inflammatory, antioxidant, anti-ischemia, anti-atherosclerotic hepatoprotective and anticancer activities.

Objective: Our study was focused on the effects of isorhamnetin treatment in OA.

Materials and methods: We used monosodium iodoacetate (MIA)-induced OA rats to evaluate the effects of isorhamnetin related anti-inflammatory process. The rats in all groups were sacrificed on four weeks post-MIA injection. The measurements of knee joint swelling, histological analysis, serum inflammatory biomarkers and western blot were evaluated.

Results: We found that isorhamnetin may reduce MIA-induced knee swelling by significantly reduction of articular cartilage damage.in rats. Suppression of pro-inflammatory cytokines production was found after isohamnetin treatment. Isorhamnetin inhibited the production of NO and PGE2, and the expression of iNOS and COX-2. The production of COMP, CTX-II and osteopontin (OPN) were also inhibited in MIA-induced OA rats.

Discussion and conclusions: Isorhamnetin may modulate the inflammatory progression of OA in MIA-induced OA rats. The prevention of cartilage damage was found in OA after adequate isorhamnetin treatment. Isorhamnetin may serve as a potential agent for the management of OA.     

IGF-1在股骨头再造关节软骨化生中的作用

目的观察分析大转子骨瓣表面骨膜及腱膜等纤维结缔组织向关节软骨转化的规律及胰岛素样生长因子-1(IGF-1)在软骨化生过程中的作用。方法制备液氮冷冻双侧股骨头缺血性坏死(Osteonecrosis of femoral head,ONFH)的动物模型。左侧股骨头造模后即缝合关节囊,右侧股骨头根据分组不同采用不同的处理方式:A组(骨瓣治疗组):带血管蒂大转子骨瓣进行股骨头再造;B组(骨瓣加Ad-IGF-1基因治疗治疗组):带血管蒂大转子骨瓣股骨头再造,关节内注入表达IGF-1的腺病毒载体(Ad-IGF-1);两组动物分别于3,6,12,18,24周每批4只处死,对骨瓣进行大体观察,组织病理学观察,免疫组化检测。结果所有动物左侧冷冻区组织坏死,纤维状物覆盖,碎片样组织修复。组织病理切片及免疫组化证实A组右侧骨瓣区自6周出现透明软骨细胞,B组右侧骨瓣区自3周出现透明软骨细胞,B组较A组修复效果好。结果经统计学处理有统计学意义。结论大转子表面的骨膜及腱膜能够向关节软骨化生,IGF-1对大转子表面的骨膜及腱膜向关节软骨化生有促进作用,为ONFH的外科治疗及生长因子的应用提供基础。     

Simultaneous regeneration of articular cartilage and subchondral bone induced by spatially presented TGF-beta and BMP-4 in a bilayer affinity binding system

Subchondral defect repair is a multitask challenge requiring the simultaneous regeneration of cartilage and bone. Herein, we describe the features of a hydrogel system designed to simultaneously induce the endogenous regeneration of hyaline cartilage and subchondral bone. The system was constructed as two layers, spatially presenting the chondroinductive transforming growth factor-β1 (TGF-β1) in one layer and the osteoinductive bone morphogenetic protein-4 (BMP-4) in a second layer, via affinity binding to the matrix. Human mesenchymal stem cells seeded in the bilayer system differentiated into chondrocytes and osteoblasts in the respective layers, confirming the spatial presentation and prolonged activity of TGF-β1 and BMP-4. Administration of the bilayer system with affinity-bound TGF-β1 and BMP-4 (with no cells) into a subchondral defect in rabbits induced endogenous regeneration of articular cartilage and the subchondral bone underneath within 4weeks. Cartilage extracellular matrix proteoglycans were found in the top layer, with no mineralization, whereas the layer underneath consisted of newly formed woven bone. The results indicate that stem cells migrating into the defect are able to sense the biological cues spatially presented in the hydrogel and respond by differentiation into the appropriate cell lineage. The strategy has a real translational potential for repairing osteochondral defects in humans as it is acellular and can be implanted via a minimally invasive method.     

Ultrastructural change of the subchondral bone increases the severity of cartilage damage in osteoporotic osteoarthritis of the knee in rabbits

Osteoporotic osteoarthritis is a phenotype of osteoarthritis (OA) manifested as fragile and osteoporotic subchondral bone. However, the ultrastructural features of subchondral bone in osteoporosis OA have not been determined. The study was aimed to investigate the ultrastructural dynamic changes of subchondral bone in osteoporotic OA model and how the ultrastructural damage in the subchondral bone caused by osteoporosis deteriorated the cartilage damage in OA. Eighteen rabbits were equally randomized to three groups, including the control, the OA and the osteoporotic OA groups. The structural changes of cartilage were evaluated by HE and safranin-O fast green staining, the Mankin’s grading system was used to assess the stage of OA progression. And microstructural or ultrastructural changes in subchondral bone were assessed by micro-computed tomography or by scanning electron microscopy. According to the changes of cartilage histopathology, the OA group was in the early pathological stage of OA while the osteoporotic OA group was in the middle stage of OA based on Mankin’s grading system. In addition, the damage of cartilage surface, reduction in the number of chondrocytes and the matrix staining were more increased in the osteoporotic OA group compared to the OA group. Compared to the OA group, the subchondral bone in the microstructure and ultrastructure in the osteoporotic OA group showed more microfracture changes in trabecular bone with more destructions of the tree-like mesh. Moreover, the collagen fibers were random rough with a fewer amount of bone lacunae in subchondral cortical plate in the osteoporotic OA group compared to the OA group. These findings indicated that the subchondral bone ultrastructure in the osteoporotic OA model was characterized by the destruction of the network structure and collagen fibers. The subchondral bone ultrastructural damage caused by osteoporosis may change mechanical properties of the upper cartilage and aggravate OA cartilage. Therefore, early diagnosis and treatment of osteoporosis is of great significance to prevent early OA from further developing osteoporotic OA.     

VEGF-A is associated with early degenerative changes in cartilage and subchondral bone

Paired cartilage and subchondral bone of subjects with no clinical history of joint disorders were analyzed to determine whether antioxidant enzymes, inflammatory cytokines and growth factors can be linked to a pre-osteoarthritis. Tissue explants were phenotyped according to Osteoarthritis Research Society International grading and micro-computed tomography, and also screened for the expression of several markers using quantitative polymerase chain reaction. The expression of these same genes was measured in SW1353 cells treated with hydrogen peroxide, to gain insight into the pathways involved with oxidative stress responses. Vascular endothelial growth factor A (VEGF-A) was up-regulated in the cartilage samples that showed early cartilage or bone degeneration. Oxidative stress in chondrocytes provoked up-regulation of interleukin-1β, interleukin-6, aggrecan, and SRY-box containing gene 9. Our results confirm the hitherto evidence of the deteriorating effects of the oxidative stress on cartilage and suggest the link between VEGF-A and pre-osteoarthritis.     

Osteochondritis dissecans of the elbow: histopathological assessment of the articular cartilage and subchondral bone with emphasis on their damage and repair

Osteochondritis dissecans (OCD) of the elbow is a localized injury of the articular cartilage and subchondral bone that is commonly seen in the young athlete. In the present study, the extent of damage and repair on the articular cartilage and subchondral bone was examined histologically using specimens of 25 osteochondral cylinders and seven loose bodies obtained from 25 young athletes who had undergone osteochondral autograft surgery. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) assays for detecting apoptotic cells and immunohistochemistry of matrix metalloproteinases (MMP) were performed on the osteochondral cylinder specimens. The histological findings of the OCD of the elbow showed that the articular cartilage exhibited degenerative change, mimicking osteoarthritis, and was markedly damaged as the lesion progressed. TUNEL-positive cells and MMP-3- and -13-expressing cells were distributed in the degenerative articular cartilage and reparative fibrocartilage tissue. Separation occurred at either the deep articular cartilage or the subchondral bone, with the former being dominant in the early OCD lesions. The present results suggest that the primary pathological changes in OCD of the elbow were due to damage of articular cartilage induced by repeated stress following degenerative and reparative process of articular cartilage and subchondral fracturing, and separation subsequently occurred on the cartilage and developed onto the subchondral bone in its advanced stages.     

The mechanical and material properties of elderly human articular cartilage subject to impact and slow loading

The mechanical properties of articular cartilage vary enormously with loading rate, and how these properties derive from the composition and structure of the tissue is still unclear. This study investigates the mechanical properties of human articular cartilage at rapid rates of loading, compares these with measurements at slow rates of loading and explores how they relate to the gross composition of the tissue. Full-depth femoral head cartilage biopsies were subjected to a slow, unconfined compression test followed by an impact at an energy of 78.5 mJ and velocity 1.25 m s⁻¹. The modulus was calculated from the slope of the loading curve and the coefficient of restitution from the areas under the loading and unloading curves.Tissue composition was measured as water, collagen and glycosaminoglycan contents. The maximum dynamic modulus ranged from 25 to 150 MPa. These values compared with 1–3 MPa measured during quasi-static loading. The coefficient of restitution was 0.502 (0.066) (mean (standard deviation)) and showed no site variation. Water loss was not detectable. Composition was not strongly associated with modulus; water and collagen contents together predicted about 25% of the variance in modulus.     

带股方肌蒂骨瓣移位治疗成人股骨头缺血性坏死的疗效及安全性分析

目的　研究分析带股方肌蒂骨瓣移位治疗成人股骨头缺血性坏死的疗效及安全性。 方法　选取2013年1月-2016年1月于我院接受带股方肌蒂骨瓣移植手术的患者96例作为研究对象,参照世界骨循环研究学会分期标准将患者分为Ⅰ期、Ⅱ期、Ⅲ期3个分期,并分别研究对比3个分期疗效及安全性情况。 结果　3个不同分期的患者治疗后Harris评分均要显著高于治疗前,差异有统计学意义（P＜0.05）。随着年龄的增长,愈合速度呈明显的延长趋势,差异有统计学意义（P＜0.05）。随着患者临床分期的加深,患者治疗的优良率呈明显的下降趋势,差异有统计学意义（P＜0.05）。观察不同分期患者并发症情况,结果无明显差异,证明带股方肌蒂骨瓣移植较为安全有效,差异有统计学意义（P＜0.05）。 结论　带股方肌蒂骨瓣移位治疗股骨头缺血性坏死具有十分显著的疗效,患者恢复时间较快,是一种值得肯定的手术方法。