上、下坡跑台训练膝骨关节炎模型大鼠关节软骨及炎症因子的变化

BACKGROUND: Different training methods have different effects on primary knee osteoarthritis. OBJECTIVE: To compare the effects of uphill or downhill running on articular cartilage degeneration and inflammatory responses of knee osteoarthritis rats.   METHODS: 108 female Sprague-Dawley rats were randomly divided into six groups: normal control group, ovariectomized group, uphill running group (run & up), downhill running group (run & down), uphill running model group (model & up), downhill running model group (model & down). The rats in the normal control group were raised routinely with no treatment; rats in the ovariectomized group were ovarientomized and raised in routine way; rats in the run & up group and run & down group were subjected to uphill running training on the slop +15° or downhill running training on the slop -15°; rats in the model & up group and model & down group were subjected to uphill running training on the slop +15°or downhill running training on the slop -15° after ovarientomized. Training programs were as follows: 28 m/min, 60 minutes per day, 6 days per week. RESULTS AND CONCLUSION: Compared with the other five groups, in the model & up group, the Mankin’s score was significantly increased, indicating that articular cartilage degeneration occurred, and the peak of carboxy-terminal telopeptide of type II collagen contained in the urine had passed, at 4 weeks after modeling. At 6 weeks, the Mankin’s score of the model & down group was increased to reach the degeneration standard, but it was still lower than that of the model & up group; the expression levels of tumor necrosis factor-α and interleukin-1β in the synovial fluid were significantly higher in the model & up and model & down groups than the other four groups. At 8 weeks, the Mankin’s score and the expression levels of tumor necrosis factor-α and interleukin-1β were further increased in the model & up and model & down groups, especially in the model & up group. These results indicate that treadmill running exercise after ovariectomized can result in articular cartilage injury and local inflammatory responses; compared with the downhill running training, the uphill running training can cause cartilage injury earlier and more efficiently.      

姜黄素保护关节软骨抑制骨关节炎的作用和机制

背景：研究证实姜黄素具有抗炎抗氧化抗凋亡作用。 目的：综合阐述姜黄素保护关节软骨及抑制骨关节炎等方面的机制和作用。 方法：作者检索 1973至2014 年 PubMed、Embase、Elseveir数据库文献。检索词为“Osteoarthritis,curcumin,chondrocyte,articular cartilage”,按照事先制定的标准逐一评价纳入研究的文献,提取有效资料进行综合分析。 结果与结论：姜黄素可通过抑制氧化作用酶,清除自由基,完成抗氧化作用,从而防止骨关节炎的发生和进展。姜黄素抑制基质金属蛋白酶的对软骨基质的消耗,增加Ⅱ型胶原的产生。姜黄素通过抑制胞浆型磷脂酶A2,环氧化酶2,脂氧合酶5,从而完成抗炎反应。姜黄素抑制白细胞介素1β导致的线粒体肿胀和凋亡,完成抗凋亡作用。临床研究提示,姜黄素或者其衍生物骨关节炎患者膝关节功能、关节疼痛等均有改善。高浓度姜黄素对体外培养的细胞和组织有毒性作用。 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;组织工程全文链接：     

木瓜蛋白酶诱导膝关节骨关节炎模型兔滑膜病理变化与药物注射时间的关系

背景：木瓜蛋白酶诱导兔膝关节骨性关节炎的造模方法可获得稳定的退行性关节炎模型。 目的：观察兔膝关节腔内注射木瓜蛋白酶诱导骨关节炎后,滑膜炎性病理改变与药物注射时间的关系。 方法：将木瓜蛋白酶水溶液分别在实验开始的第1,4,7天分别注射入15只西兰大白兔右膝关节腔内,建立膝关节骨性关节炎兔模型,于首次注射后第2,4,6周分别观察膝关节滑膜大体及组织病理学变化,每个时间点5只。 结果与结论：木瓜蛋白酶首次注射后第2周,兔膝关节滑膜炎性反应最严重,表现为滑膜细胞增生最明显,下层疏松纤维及血管组织明显增生,可见较多淋巴浆细胞浸润,第4,6周时炎性反应逐渐减轻。说明兔膝关节首次注射木瓜蛋白酶后2周时滑膜炎性反应最严重。     

木瓜蛋白酶诱导早期膝骨关节炎模型大鼠软骨超微结构的动态变化

背景:木瓜蛋白酶诱导大鼠膝关节骨性关节炎是常用造模方法,能获得稳定的骨关节炎模型。目的:观察木瓜蛋白酶诱导大鼠膝早期骨关节炎进程中透射电镜下关节软骨细胞超微结构的变化规律。方法:将18只SD大鼠随机分为3组,2只为正常对照组不做干预;16只大鼠右膝关节腔注射木瓜蛋白酶和L-半胱氨酸混合液诱导骨关节炎模型(骨关节炎模型组),左侧注射生理盐水(生理盐水对照组)。注射后第1,2,4,6周后分别取材,使用透射电镜观察股骨内侧髁关节软骨超微结构变化。结果与结论:正常对照组和生理盐水对照组胞质内有丰富的粗面内质网、线粒体。骨关节炎模型组注射1周后,线粒体空泡化,可见轻度扩张的粗面内质网;2周后,出现脂滴,线粒体变性明显,空泡化严重,数目减少,粗面内质网扩张明显;4周后,脂滴增多,线粒体数目明显减少,大部分粗面内质网高度扩张,部分粗面内质网溶解断裂;6周后,胞质内见数个脂滴,大部分线粒体消失,仅有少量线粒体存在,大部分粗面内质网断裂溶解。说明木瓜蛋白酶诱导大鼠膝早期骨关节炎进程中透射电镜下软骨超微结构呈渐进性变化。     

组织工程软骨研究进展

组织工程学是 2 0世纪 80年代末期发展起来的一门新兴边缘学科。它是综合应用工程学和生命科学的基本原理、理论和技术 ,在体外预先构建有生命的种植体 ,然后植入体内修复组织缺损 ,替代组织器官的一部分或全部功能。软骨为单一细胞 (软骨细胞 )构成组织 ,透明软骨、弹性软骨和纤维软骨组成人体重要结构 ,具有十分重要的生理功能。组织工程软骨是第一个组织工程化组织 ,在矫形外科和整形外科领域 ,组织工程软骨研究受到高度重视 ,发展迅速。本文介绍矫形外科领域中组织工程软骨研究发展。1　种子细胞1 1　软骨细胞多数研究以软骨细胞为种子…     

手术诱导膝骨关节炎兔模型的制备方法

背景：目前常用的膝骨关节炎动物模型制备方法主要有手术创伤和关节腔内注射蛋白酶诱导两大类。关节腔内注射药物诱导模型并不稳定,传统的手术造模方法对膝关节损伤较大,且成模过程与临床膝骨关节炎的发展过程差异较大。目的：通过不同手术方式损伤膝关节制备兔膝骨关节炎模型,探讨膝骨关节炎动物模型的最佳制备方法。方法：将16只雄性五六月龄新西兰大白兔随机分为假手术组、模型A组、模型B组、模型C组,每组4只。假手术组切开右侧膝关节内侧后立即缝合;模型A组磨损右侧膝关节半月板、磨损前交叉韧带;模型B组摘除右侧膝关节半月板、磨损前交叉韧带;模型C组摘除右侧膝关节半月板、切断前交叉韧带。术后连续3 d注射抗生素,记录一般情况。4周后通过X射线片观察关节情况,苏木精-伊红染色观察软骨组织变化,酶联免疫吸附法检测右侧膝滑膜液和血清中炎症因子水平。结果与结论：(1)模型组右侧膝关节明显出现红肿热痛情况,皮温明显高于假手术组;(2)术后模型组右侧膝关节皮温较假手术组明显升高,差异有显著性意义(P <0.05);(3)X射线片显示假手术组膝关节未见异常,模型组出现不同程度的关节面破坏及关节间隙狭窄,其中模型C组最为...     

骨吸收抑制剂降钙素对骨关节炎大鼠软骨组织形态及蛋白多糖的影响

背景：近年来有报道指出降钙素在临床上治疗骨关节炎有较好的临床疗效,但关于其对骨关节炎的作用机制却少有报道。目的：观察降钙素对实验性骨关节炎模型大鼠软骨组织形态及蛋白多糖的影响。方法：将30只SD大鼠随机均分为3组,模型组与给药组均切断右肢前交叉韧带制作骨关节炎模型,假手术组仅打开关节腔,不做韧带切断,给药组于造模后成功后第2天开始皮下注射降钙素15 IU/(kg•d),模型组与假手术组均皮下注射等量生理盐水,连续给药6周。造模后10周,观察各组大鼠胫骨关节面,X射线检查股骨远端和内外侧踝软骨下骨骨密度,苏木精-伊红染色观察骨组织形态,甲胺苯蓝染色观察软骨组织中蛋白多糖含量。结果与结论：假手术组大鼠胫骨关节面光滑,有光泽;模型组大鼠胫骨关节面无光泽,关节软骨暗红色,有较大溃疡面形成;给药组大鼠软骨面无光泽,局部溃疡,表面粗糙不平。与假手术组比较,模型组内外侧踝软骨下骨骨密度、骨体积、骨小梁数目升高(P < 0.05),骨小梁分离度及蛋白多糖含量降低(P < 0.05);给药组内外侧踝软骨下骨骨密度、骨体积、骨小梁数目低于模型组(P < 0.05),骨小梁分离度及蛋白多糖含量高于模型组(P < 0.05)。表明降钙素对骨关节炎大鼠软骨有较好的保护作用,并能促进骨组织分泌蛋白多糖。 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     

红姜提取物保护早期膝骨关节炎模型大鼠的关节软骨

BACKGROUND: Studies have reported that the combined use of ginger extract to reduce the levels of serum pro-inflammatory cytokines, including interleukin-1β, interleukin-6, tumor necrosis factor-α, is related to the reduction of cartilage injury in knee osteoarthritis. OBJECTIVE: To observe the protective effect of red ginger extract on articular cartilage and the expression of serum interleukin-1β, interleukin-6, tumor necrosis factor-α and cartilage tissue type II collagen α1 mRNA in rats with early knee osteoarthritis, and to explore the protective effect of red ginger extract on articular cartilage of rats with early knee osteoarthritis and its possible mechanism. METHODS: Fifty SPF Sprague-Dawley rats were randomly divided into blank group, model group, low-dose red ginger, high-dose red ginger and positive control group (n=10 per group). Except for the blank group, the rats in the other four groups were used to prepare knee osteoarthritis models by intraarticular injection of 4% papain 0.2 mL+0.03 mol/L L-cysteine mixed solution. The rats in the blank and model groups were fed routinely, and the low-dose red ginger, high-dose red ginger and positive control groups were given 50 mg/kg red ginger extract aqueous solution, 100 mg/kg red ginger extract aqueous solution and 18 mg/kg celecoxib capsule aqueous solution respectively. All the interventions were conducted once a day, for 4 continuous weeks. Four weeks after treatment, the rats in each group were killed and the knee joints were stained with safranin O-fast green. The articular cartilage was scored by Mankin scoring. The expression levels of interleukin-1β, interleukin-6, tumor necrosis factor-α in serum and type II collagen α1 mRNA in cartilage were detected. The study protocol was approved by the Animal Ethics Committee of Guangzhou University of Chinese Medicine, with an approval No. 20190917002. RESULTS AND CONCLUSION: The pathological section of knee cartilage showed that there was cartilage matrix loss in the model and each treatment group, and the Mankin score of each treatment group was significantly higher than that of the blank group (P < 0.05) and lower than that of the model group (P < 0.05). There was no significant difference between the high-dose group and the positive control group (P > 0.05), but the scores of the two groups were lower than that of the low-dose group. The levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α were upregulated in the positive control group, high-dose red ginger group and low-dose red ginger group compared with the blank group and down-regulated compared with the model group (P < 0.05). Moreover, and the levels of these cytokines were ranked as follows: positive control group < high-dose red ginger group < low-dose red ginger group (P < 0.05). The level of type II collagen α1 mRNA in cartilage showed no significant difference between the blank group and the high-dose red ginger group and the positive control group (P > 0.05), whereas the expression of type II collagen α1 mRNA was significantly increased in the model group and low-dose red ginger group compared with the other three groups (P < 0.05). To conclude, red ginger extract may protect the articular cartilage of knee osteoarthritis by inhibiting interleukin-1β, interleukin-6, and tumor necrosis factor-α, thereby delaying the development of knee osteoarthritis. Compared with the low-dose group, high-dose red ginger extract has better anti-inflammatory effect. © 2021, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.     

软骨下骨量变化与软骨退变的相关性

背景：关节软骨与软骨下骨在骨关节炎病变进程中的相互作用机制目前尚未完全阐明。软骨下骨量改变在骨关节炎病理进程中亦发挥重要作用。 目的：分析2种手术方式及2种蛋白酶诱导建立兔膝关节骨关节炎动物模型的效果,以及软骨下骨量变化与关节软骨退变的相关性。 方法：32只新西兰大白兔随机分为4组：Hulth模型组、前交叉韧带切断模型组、Ⅱ型胶原蛋白酶组及木瓜蛋白酶组,每组8只,右膝关节造模,左膝关节作为自身对照。造模后0,4,8周行DXA扫描,8周行MRI扫描后处死实验动物,取双侧膝关节制作病理组织学切片,比较各组膝关节影像学表现、大体形态及病理变化,并采用Mankin评分进行定量分析。 结果与结论：造模后0,4,8周实验侧膝关节骨密度进行性降低,骨量降低程度Hulth模型组>前交叉韧带切断模型组>Ⅱ型胶原蛋白酶组>木瓜蛋白酶组。MRI显示实验侧股骨内外髁关节软骨厚度变薄,厚度Hulth模型组<前交叉韧带切断模型组<Ⅱ型胶原蛋白酶组<木瓜蛋白酶组。大体标本、组织切片观察及Mankin评分显示手术建模组骨关节炎程度较药物组重,Hulth模型组病变最重,木瓜蛋白酶组最轻。结果说明关节内手术及关节腔内注射蛋白酶均能建立骨关节炎动物模型;手术造模可复制出中晚期骨关节炎,药物诱导可产生骨关节炎早期改变。骨关节炎病变严重程度与软骨下骨骨密度呈负相关;关节软骨退变和软骨下骨改变相互关联,病变进行性发展。     

常山酮阻止早期骨性关节炎的关节软骨退变北大核心

背景:研究证实,常山酮能够减弱骨性关节炎病程发展的进程。目的:进一步验证常山酮对早期骨性关节炎的防治作用。方法:健康C57BL6J雄性小鼠45只,随机分为3组,每组15只,假手术组只打开小鼠右膝关节囊不损伤其他部位,术后不做处理;其余小鼠均切断小鼠右膝前交叉韧带造骨性关节炎模型,安慰剂组造模后第3天开始给予蒸馏水灌胃每天1次;常山酮组造模后第3天开始按0.5 mg/kg剂量灌胃,每天1次,28 d后处死小鼠取右膝关节,做苏木精-伊红染色和番红固绿染色观察关节组织的形态和结构;免疫组织化学检测转化生长因子β1的表达量。结果与结论:(1)组织学观察,假手术组关节软骨结构正常,潮线清晰,细胞排列整齐,未有软骨表面磨损痕迹;安慰剂组关节软骨层明显变薄,甚至部分损伤至潮线,软骨表面磨损严重并有碎裂现象,细胞排列紊乱;常山酮组软骨细胞分层较清晰且排列较整齐,潮线清晰,细胞形态较规则;(2)3组透明软骨厚度假手术组>山酮组>安慰剂组,钙化软骨厚度假手术组<常山酮组<安慰剂组,透明软骨厚度/钙化软骨假手术组>常山酮组>安慰剂组;(3)OARSI评分常山酮组显著低于安慰剂组,转化生长因子β1阳性细胞/软骨细胞值常山酮组显著低于安慰剂组,2项指标3组间比较差异均有显著性意义(P<0.05);(4)结果表明,常山酮灌胃能部分阻止小鼠早期骨性关节炎关节软骨退变,其作用机制可能是降低转化生长因子β1的表达,从而延缓骨性关节炎的进展。     

The electron microscope appearance of the subchondral bone plate in the human femoral head in osteoarthritis and osteoporosis

The subchondral bone plate supports the articular cartilage in diarthrodial joints. It has a significant mechanical function in transmitting loads from the cartilage into the underlying cancellous bone and has been implicated in the destruction of cartilage in osteoarthritis (OA) and its sparing in osteoporosis (OP), but little is known of its composition, structure or material properties. This study investigated the microscopic appearance and mineral composition of the subchondral bone plate in femoral heads from patients with OA or OP to determine how these correspond to changes in composition and stiffness found in other studies. Freeze-fractured full-depth samples of the subchondral bone plate from the femoral heads of patients with osteoarthritis, osteoporosis or a matched control group were examined using back scattered and secondary emission scanning electron microscopy. Other samples were embedded and polished and examined using back-scattered electron microscopy and electron probe microanalysis. The appearances of the samples from the normal and osteoporotic patients were very similar, with the subchondral bone plate overlayed by a layer of calcified cartilage. Osteoporotic samples presented a more uniform fracture surface and the relative thicknesses of the layers appeared to be different. In contrast, the OA bone plate appeared to be porous and have a much more textured surface. There were occasional sites of microtrabecular bone formation between the trabeculae of the underlying cancellous bone, which were not seen in the other groups, and more numerous osteoclast resorption pits. The calcified cartilage layer was almost absent and the bone plate was apparently thickened. The appearance of the osteoarthritic subchondral bone plate was, therefore, considerably different from both the normal and the osteoporotic, strongly indicative of abnormal cellular activity.     

Exercise protects against insulin-dependent diabetes-induced osteoarthritis in rats: A scanning electron microscopy study

We tested the hypothesis that swim exercise can protect the articular cartilage from damages induced secondary to insulin-dependent diabetes mellitus in rats using the scanning electron microscopy and to monitor the blood levels of oxidative and antioxidative stress biomarkers that are known to be modulated in osteoarthritis (OA). A profound damage to the cartilage was observed in the diabetic rats. Our findings also show that swim exercise protects the knee joints from damage induced by diabetes as well as significantly inhibiting OA-induced upregulation of thiobarbituric acid reactive substances (TBARS) and tumor necrosis factor alpha (TNF-α) and augmented superoxide dismutase (SOD) inhibition by OA. Thus, we demonstrated an effective protection by swim exercise against diabetes-induced OA in a rat model of the disease.     

Diacerein protects against iodoacetate-induced osteoarthritis in the femorotibial joints of rats

The present study was undertaken to investigate the effect of diacerein on the histopathology of articular cartilage and subchondral bone of the femorotibial joint in rats. Osteoarthritis was induced in rats after single intra-articular injection of sodium iodoacetate. Rats were sacrificed 1, 2, 4, and 8 weeks post intra-articular injection to evaluate the progression of histopathogenesis of osteoarthritis. Diacerein was orally administered (15 mg/kg) once daily post 1 and 2 weeks of iodoacetate injection in two groups, respectively, for up to 12 weeks. Articular cartilage and subchondral bone of the rats of both groups were examined after 8 and 12 weeks, respectively. Quantitative histological analyses were performed by scoring these sections as per the OARSI system. Chondroitin sulfate was also estimated in articular cartilage by decrease in absorbance of methylene blue on complexation with chondroitin sulfate using a spectrophotometer. Intra-articular injection of iodoacetate induced loss of articular cartilage with progressive subchondral bone sclerosis and degeneration. Based on histopathological and biochemical findings, diacerein treatment showed chondroprotective effect. Furthermore, the chondroprotective effect of diacerein was found to be more pronounced after 12 weeks as compared to 8 weeks in both cases (i.e., post 1 and 2 weeks of iodoacetate injection). Similar results were observed by investigation of chondroitin sulfate during biochemical study, showing the chondroprotective effect. In conclusion, diacerein exhibits chondroprotective effect in rats with late onset of action.     

The bovine patella as a model of early osteoarthritis

The bovine patella model has been used extensively for studying important structure–function aspects of articular cartilage, including its degeneration. However, the degeneration seen in this model has, to our knowledge, never been adequately compared with human osteoarthritis (OA). In this study, bovine patellae displaying normal to severely degenerate states were compared with human tissue displaying intact cartilage to severe OA. Comparisons of normal and OA features were made with histological scoring, morphometric measurements, and qualitative observations. Differential interference contrast microscopy was used to image early OA changes in the articular cartilage matrix and to investigate whether this method provided comparable quality of visualisation of key structural features with standard histology. The intact bovine cartilage was found to be similar to healthy human cartilage and the degenerate bovine cartilage resembled the human OA tissues with regard to structural disruption, cellularity changes, and staining loss. The extent of degeneration in the bovine tissues matched the mild to moderate range of human OA tissues; however, no bovine samples exhibited late‐stage OA. Additionally, in both bovine and human tissues, cartilage degeneration was accompanied by calcified cartilage thickening, tidemark duplication, and the advancement of the cement line by protrusions of bony spicules into the calcified cartilage. This comparison of degeneration in the bovine and human tissues suggests a common pathway for the progression of OA and thus the bovine patella is proposed to be an appropriate model for investigating the structural changes associated with early OA.     

Autophagy in osteoarthritis

Osteoarthritis is characterized by continuous degeneration of articular cartilage resulting in disability. The death of chondrocytes and the loss of the extracellular matrix are the central peculiarities in cartilage degeneration during osteoarthritis pathogenesis. Autophagy is an essential cellular homeostasis mechanism whereby cellular organelles and macromolecules are recycled to maintain cellular metabolism. Autophagy is reported to be cytoprotective effects for articular cartilage, and osteoarthritis is associated with decreased autophagy. While autophagy is known to be cytoprotective to chondrocytes, its role may vary with differing stages and models of osteoarthritis. Therefore, more in-depth studies on autophagy are needed to determine its impact on cell survival and death in articular cartilage under various in vitro and in vivo conditions. Application of autophagy on osteoarthritis therapeutics will be possible after a profound understanding is established on the role of autophagy in osteoarthritis pathogenesis.     

Early Cartilage Degeneration in a Rat Experimental Model of Developmental Dysplasia of the Hip

Osteoarthritis (OA) is a common long-term complication of developmental dysplasia of the hip (DDH) that is associated with a higher incidence of OA. In addition, the age of onset of OA in DDH patients is significantly younger than in the general population. In order to investigate the early degeneration in DDH cartilage, we used a rat DDH model that was established by the straight-leg swaddling position. The hips were isolated from the DDH model rats and an untreated control group at postnatal weeks 2, 4, 6, and 8. Histology and proteoglycan levels were observed in articular cartilage using Safranin O staining. Biomarkers of cartilage degeneration, including type X collagen and matrix metalloproteinase (MMP)-13, were assessed using immunohistochemistry and quantitative real-time polymerase chain reaction. In addition, expressions of ADAMTS-4 and ADAMTS-5 were studied using quantitative real-time polymerase chain reaction at different ages. DDH rats showed decreased proteoglycans and derangement of chondrocytes when compared with the control group. Collagen X and MMP-13 expressions were higher in the superficial zone of DDH rats than in that of controls (p < 0.05), and the increase was age-dependent. mRNA expression of Collagen X and MMP-13 showed similar results (p < 0.05). A significant increase in mRNA expression of ADAMTS-5 was found in the DDH model cartilage at 8 weeks (p < 0.05). However, no change was observed in ADAMTS-4 expression. This study shows that degenerative cartilage changes occur at an early stage in the rat DDH model and become aggravated with age.     

SOX Trio Decrease in the Articular Cartilage with the Advancement of Osteoarthritis

SOX trio (SOX-5, SOX-6, and SOX-9) maintain the chondrocytic phenotypes and are vital for chondrogenesis in embryonic development. The purpose of this study is to investigate the change in the expression of SOX trio with the advancement of osteoarthritis (OA) in human articular cartilage (AC). Human OA samples from eight patients were obtained from the distal femoral condyles during total knee arthroplasty. Minimally OA cartilage taken from areas with no obvious surface defects on lateral condyles was compared with advanced OA cartilage obtained from areas within 1 cm of overt lesion located on medial condyle surface. SOX-5, SOX-6, and SOX-9 gene expressions significantly decreased by 41% (p = 0.047), 46% (p = 0.047), and 56% (p = 0.029) in advanced OA area compared with the minimally OA area. There was a significant decrease in aggrecan and type II collagen (COL2A1) gene expressions by 73% (p = 0.029) and 65% (p = 0.029), respectively, in advanced OA area compared with the minimally OA area. From Western blotting and immunohistochemistry, SOX-5, SOX-6, SOX-9, type II collagen, and aggrecan protein expressions also significantly decreased in advanced OA cartilage compared with minimally OA cartilage. DNA methylation study of SOX-9 promoter regions revealed no difference in the epigenetic status between the two areas. It is concluded that SOX trio gene and protein decreased with advancement of OA in human articular cartilage.     

关节软骨力学特征研究进展

骨关节炎(osteoarthritis OA)是一种以关节疼痛和僵硬为特征的慢性退行性关节疾患,好发于老年人群。OA发病缓慢,病程较长,早期临床表现和组织学改变均不明显,限制了疾病的早期诊断与治疗。关节软骨微观结构决定了软骨宏观力学特性。软骨微观结构具有区域差异性,导致软骨的力学性能也具有区域依赖性,从软骨浅表区到深区软骨抗负荷、抗形变能力逐渐增加。然而,在OA病程发展过程中,软骨微观构成改变导致OA软骨抗负荷、抗形变能力降低。通过检测关节软骨的微观构成可以推测软骨的力学特性,反之检测软骨的力学指标可以了解软骨早期的微观改变,从而有助于了解OA的病程发展,便于疾病的早期诊断。综述近年来关节软骨在正常和急慢性损伤状态下力学性能的相关研究文献,阐述软骨结构与力学性能之间的关系,为OA的病程发展、早期诊断与治疗提供进一步理论依据。     

关节软骨力学特性间接预测方法的研究进展

关节软骨具有非常优异的力学特性,是影响人体运动、载荷传递的关键因素之一.随着人们参与体育运动的增多以及老龄化程度的加剧,出现关节软骨损伤及其相关病症的人数显著增多.实现关节软骨力学特性的有效表征,是对关节软骨进行损伤评估和功能评价的核心环节.总结当前国内外关于关节软骨力学特性间接测量方法的研究进展,并对关节软骨力学特性...     

Mild degenerative changes of hip cartilage in elderly patients: an available sample representative of early osteoarthritis

This study investigated the cellular and molecular changes which occur in cartilage from adults with femoral neck fracture (FNF) and osteoarthritis (OA), and explored the similarities in hip cartilage obtained from elderly patients and patients with early OA. Femoral heads were retrieved from 23 female patients undergoing total hip arthroplasty (THA). This group included 7 healthy patients with FNF (hFNF), 8 elderly adults with FNF (eFNF), and 8 elderly patients with hip OA (OA). After high-field MRI T2 mapping, osteochondral plugs were harvested from the weight-bearing area of femoral heads for subsequent macroscopic, histologic, and immunochemical evaluation. Additionally, the contents of cartilage matrix were analyzed, and gene expression was detected. The surface of cartilage from hFNF and eFNF patients appeared smooth, regular, and elastic, whereas it showed irregularities, thinning, and defects in OA patients. Elevated T2 values and decreased accumulation of glycosaminoglycans (GAGs) were detected in cartilage from eFNF patients. Furthermore, type I collagen accumulation was slightly increased and type X collagen concentration was obviously elevated in eFNF patients; however, type II collagen distribution and the contents and anisotropy of collagen fibrils in eFNF patients showed no significant changes. Consistent with histology and immunohistochemical results, aggrecan was downregulated and type X collagen was upregulated, while collagens types I and II showed no significant changes in eFNF patients. The cellular and molecular characteristics of hip cartilage in eFNF patients who showed no symptoms of OA were similar to those in patients with mild OA. Thus, eFNF cartilage can serve as a comparative specimen for use in studies investigating early OA.