Influences of the depth-dependent material inhomogeneity of articular cartilage on the fluid pressurization in the human knee

The material properties of articular cartilage are depth-dependent, i.e. they differ in the superficial, middle and deep zones. The role of this depth-dependent material inhomogeneity in the poromechanical response of the knee joint has not been investigated with patient-specific joint modeling. In the present study, the depth-dependent and site-specific material properties were incorporated in an anatomically accurate knee model that consisted of the distal femur, femoral cartilage, menisci, tibial cartilage and proximal tibia. The collagen fibers, proteoglycan matrix and fluid in articular cartilage and menisci were considered as distinct constituents. The fluid pressurization in the knee was determined with finite element analysis. The results demonstrated the influences of the depth-dependent inhomogeneity on the fluid pressurization, compressive stress, first principal stress and strain along the tissue depth. The depth-dependent inhomogeneity enhanced the fluid support to loading in the superficial zone by raising the fluid pressure and lowering the compressive effective stress at the same time. The depth-dependence also reduced the tensile stress and strain at the cartilage–bone interface. The present 3D modeling revealed a complex fluid pressurization and 3D stresses that depended on the mechanical contact and relaxation time, which could not be predicted by existing 2D models from the literature. The greatest fluid pressure was observed in the medial condyle, regardless of the depth-dependent inhomogeneity. The results indicated the roles of the tissue inhomogeneity in reducing deep tissue fractures, protecting the superficial tissue from excessive compressive stress and improving the lubrication in the joint.     

股四头肌肌力对前十字韧带重建术后髌股关节软骨损伤的影响

 目的 探讨股四头肌肌力对前十字韧带重建术后髌股关节软骨损伤的影响。方法 2009年12月至2013年8月前十字韧带断裂重建术后1年以上行内固定取出术的患者76例,男51例,女25例;前十字韧带重建术时患者年龄16~44岁,平均27.6岁。取内固定术前行双侧股四头肌、腘绳肌等速肌力测试,取内固定的同时行二次关节镜检查,观察髌骨和滑车软骨损伤情况,分析股四头肌、腘绳肌肌力与髌股关节软骨损伤分级的关系。结果 前十字韧带重建术至二次关节镜检查的时间为12~51个月,平均25.3个月。前十字韧带重建术后34例患者（45%）患侧与健侧股四头肌肌力比值≤80%,17例患者（22%）患侧与健侧腘绳肌肌力比值≤80%。将患者分为患侧与健侧股四头肌肌力比值＞80%组（42例）与肌力比值≤80%组（34例）。两组分别有9例（21%）和16例（47%）出现术后髌骨软骨损伤分级增加,髌骨软骨损伤加重发生率的差异有统计学意义;两组髌骨软骨损伤分级平均增加0.10和0.68级,差异有统计学意义。两组分别有11例（26%）和11例（32%）出现术后滑车软骨损伤分级增加,滑车软骨损伤加重发生率的差异无统计学意义;两组滑车软骨损伤分级平均增加0.55和0.71级,差异无统计学意义。结论 前十字韧带重建术后股四头肌肌力恢复到健侧的80%以上,可明显减少髌骨软骨损伤的发生和加重。     

CD105+滑膜间充质干细胞成软骨能力

目的 分选CD105+滑膜间充质干细胞(SMSCs),观察其增殖和向软骨细胞分化的能力.方法 酶消化滑膜组织分离SMSCs,流式细胞仪分选CD105+ SMSCs;第3、7天采用WST-1测定SMSCs的增殖能力;软骨诱导21 d进行免疫组织化学染色,检测蛋白聚糖和Ⅱ型胶原.结果 酶消化获取的SMSCs为星形或梭形,分选后SMSCs形态无明显变化.免疫荧光显示分选组CD105+细胞较未分选组明显增多.WST-1增殖检测提示两组细胞吸光度值3 d(0.376±0.012、0.329±0.012)、7 d(0.581±0.009、0.524±0.007)比较差异有统计学意义(P＜0.05).成软骨诱导培养21 d后,分选组甲苯胺蓝和Ⅱ型胶原染色均较未分选组多且深,说明CD105+ SMSCs合成更多软骨细胞外基质.结论 CD105+ SMSCs具有较强的增殖和成软骨能力,CD105+ SMSCs可成为软骨组织工程良好的种子细胞.     

The effects of dexamethasone in vitro on the production of collagenase and inhibitor by synovial and cartilage explants from the joints of rabbits with a proliferative arthritis

Summary Using a rabbit model arthritis we have investigated the ability of dexamethasone to alter the production of collagenase and the specific metallo-proteinase inhibitor TIMP by explants of synovium and cartilage in vitro. The patterns of collagenase and TIMP production by untreated explants from arthritic joint tissues in culture were similar to those described previously [1, 2]. Dexamethasone dramatically altered the patterns of production of collagenase and TIMP. At a dose of 10 nM, or above, the patterns of production by treated synovium resembled those of normal rabbit synovium: collagenase production was suppressed and TIMP increased compared with untreated arthritic synovium. The levels of latent collagenase in cartilage also fell with increasing doses of dexamethasone and TIMP levels were higher, although normal levels were not reached.These experiments have been conducted as a prelude to testing the effects of various anti-rheumatic drugs in vivo, and attempting to correlate changes in clinical parameters with the subsequent production of collagenase and TIMP in vitro. The data are discussed in relation to the therapeutic use of corticosteroids and to their mode of action on joint tissues.     

大骨节病区儿童血清硒与硫酸化因子活性关系的初步研究

为进一步阐明大骨节病患儿血清硫酸化因子活性降低的原因,本文在牛关节软骨稳态培养的基础上,加入服硒与未服硒大骨节病患儿血清及正常儿童对照组血清进行培养。培养5天后测定硫酸化因子活性及血清硒的水平。结果表明,服硒后能明显提高血清硒的水平,而血清硫酸化因子活性无改善。初步显示出,服硒不能有效地改善大骨节病区患儿硫酸化因子的活性。     

肌骨关节系统磁共振成像临床应用及进展

近年来,MRI技术的不断发展为肌骨系统疾病诊断提供了多种无创性活体成像新方法,包括软骨成分定量分析、短T2组织结构显示及骨微观结构成像,为临床早期诊断及治疗监测提供依据。不同MRI技术的临床应用与进展将逐步提高骨关节系统影像诊断水平,为肌骨关节系统MRI研究开辟新的途径。     

骨髓间充质干细胞复合多肽凝胶及成软骨生成因子修复兔关节软骨缺损

背景：多肽水凝胶因为其具有良好的可塑型性,能够与损伤部位很好的无缝隙结合,所以采用该材料作为支架是骨、软骨组织工程中一种可行的探索。目的：骨髓间充质干细胞联合新型可注射多肽凝胶及成软骨生成因子修复兔关节软骨缺损,观察其修复效果。方法：首先分离培养兔骨髓间充质干细胞,兔左侧膝关节处制备直径5 mm,深3 mm的全层骨-软骨缺损模型;右侧造模后空置作为对照。实验分为3组,单纯自组装多肽凝胶移植组,自组装多肽凝胶+成软骨因子组和自组装多肽凝胶+成软骨因子+骨髓间充质干细胞组。采用的成软骨因子包括转化生长因子β1,地塞米松和胰岛素样生长因子1,三者混合后加入到自组装多肽凝胶或骨髓间充质干细胞中。于处理后12周时处死动物行大体及组织学观察、X射线摄片、免疫组织化学法进行组织学评分评估修复情况。结果与结论：单纯自组装多肽凝胶移植在12周后显示出非常好的修复效果,可见番红O染色,Ⅱ型胶原蛋白免疫组织化学染色强度以及组织学评分明显高于其他组(P <0.05)。自组装多肽凝胶+成软骨因子组修复效果较好,与自组装多肽凝胶组相似,但其修复区域蛋白聚糖表达比对照组明显升高(P <0.01)。自组装多肽凝胶+成软骨因子+骨髓间充质干细胞组修复效果不佳,12周未能完全修复缺损区域,与单纯自组装多肽凝胶组比较骨赘的形成有所增加。结果表明,单纯自组装多肽凝胶能够在原位修复骨软骨缺损并促进软骨修复,提示以自组装多肽凝胶支架移植有望提高目前修复软骨缺损的效果。     

过量氟与软骨代谢

氟中毒与软骨组织代谢有着密切的联系，过量氟对软骨有明显的损害作用，可造成钙、磷等无机元素代谢异带．导致软骨蛋白多糖合成与分解失调，干扰软骨基质胶原代谢及改变软骨组织酶的活性。     

滑膜间充质干细胞的生物学特性及其在软骨组织工程中应用的研究进展

滑膜间充质干细胞(Synovium-derived mesenchymal stem cells,SMCSs)的增殖能力强,分离方法简便,具有多向分化潜能。其中SMSCs的成软骨分化能力尤为突出,被广泛应用于软骨缺损修复的实验中,因此SMSCs可能成为软骨组织工程领域中新的种子细胞,为关节软骨疾病治疗提供了新的可能性。本文对SMSCs的组织来源、生物学特性以及在软骨组织工程中的应用展开综述。     

Bone formation in axial spondyloarthritis

The success of targeted therapies directed against tumor necrosis factor for patients with spondyloarthritis has shifted the focus of physicians and scientists towards the prevention of structural damage to the involved structures, in particular the sacroiliac joints and the spine, to avoid loss of function and disability. Structural damage to the skeleton as witnessed by radiography mainly consists of new bone formation potentially progressively leading to spine or joint ankylosis. This important long-term outcome parameter has been difficult to study, not alone because the time window for change may be long but also because human tissues with direct translational relevance are rarely available. Data from rodent models have identified growth factor signaling pathways as relevant targets. Both human and animal studies have tried to understand the link between inflammation and new bone formation. At the current moment, most evidence points towards a strong link between both but with the question still lingering about the sequence of events, disease triggers, and the interdependence of both features of disease. New discoveries such as a masterswitch T cell population that carries the IL23 receptor and the analysis of auto-antibodies directed again noggin and sclerostin are contributing to innovative insights into the pathophysiology of disease. Long-term data with tumor necrosis factor (TNF) inhibitors also suggest that some window of opportunity may exist to inhibit structural disease progression. All these data provide support for a further critical analysis of the available datasets and boost research in the field. The introduction of novel disease definitions, in particular the characterization of non-radiographic axial spondyloarthritis patients, will likely be instrumental in our further understanding of structural damage.