骨性关节炎软骨下骨病变机制研究进展

长期以来对骨性关节炎(osteoarthritis,OA)中关节软骨的改变进行较为深入的研究,但对软骨下骨的改变研究相对较少,而软骨下骨的改变是OA进程中所必需的病理变化.近年研究发现软骨下骨改变在OA发病过程中起着积极作用,软骨下骨硬化或软化不仅是OA发生的结果,而且与其发生发展密切相关,提示OA治疗既应关注软骨变化,又要预防软骨下骨退变.该文从软骨下骨的生物力学、骨重塑、分子生物学等方面就软骨下骨在骨性关节炎发病中的病变机制研究进展作一综述.     

胫骨高位截骨钢板置入联合关节镜治疗伴下肢力线不良的内侧半月板后角退变性损伤北大核心

背景:既往研究发现,胫骨高位截骨和胫骨高位截骨联合关节镜手术均能够有效治疗合并下肢力线不良的内侧间室骨关节炎,但对比二者治疗效果的研究较少。目的:对比胫骨高位截骨与胫骨高位截骨后钢板置入联合关节镜手术治疗伴下肢力线不良的内侧半月板后角退变性损伤的临床疗效。方法:选择2015年7月至2019年1月遵义医科大学附属医院收治的膝关节骨关节炎患者48例,均伴下肢力线不良的内侧半月板退变性损伤,其中24例接受胫骨高位截骨钢板置入联合关节镜手术(试验组),另24例接受单纯的胫骨高位截骨钢板置入手术(对照组)。比较两组患者术后不同时间点的膝关节功能评分及影像学检测指标。结果与结论:(1)试验组患者术后6,12个月的纽约特种外科医院膝关节评分、膝关节Lysholm评分均高于对照组(P <0.05),两组术后24,36个月的纽约特种外科医院膝关节评分、膝关节Lysholm评分比较差异无显著性意义(P> 0.05);试验组患者术后6个月的目测类比评分低于对照组(P <0.05),两组术后12,24,36个月的目测类比评分比较差异无显著性意义(P> 0.05);(2)术后12个月的影像学检查显示,两组患者的下肢力线与股胫角均得到有效改善,两组间股胫角、下肢力线通过胫骨平台的相对位置、胫骨平台后倾角比较差异均无显著性意义(P>0.05);(3)结果表明,胫骨高位截骨钢板置入及联合关节镜手术均能有效治疗伴下肢力线不良的内侧半月板后角退变性损伤,有效改善患者关节功能、缓解疼痛症状,其中胫骨高位截骨联合关节镜手术治疗的早期临床疗效更好。     

脉冲电磁场可抑制老年大鼠膝关节软骨退变

背景：脉冲电磁场作为一种重要的物理治疗方法对骨关节炎的疗效确切，但其作用机制尚未完全明确。目的：观察脉冲电磁场对老年大鼠膝关节软骨退变的影响。方法：选取8只6月龄SD大鼠作为青年组，正常饲养8周，不做任何处理；将16只22月龄SD大鼠随机分为老年组(n=8)和脉冲电磁场组(n=8)，对脉冲电磁场组大鼠进行脉冲电磁场干预，1次/d，每周5 d，连续干预8周，老年组正常饲养8周，不做任何处理。8周后麻醉处死所有大鼠，进行相关指标的检测。结果与结论：(1)与青年组相比，老年组大鼠血清Ⅱ型胶原C端肽水平升高(P <0.05)；与老年组相比，脉冲电磁场组大鼠血清Ⅱ型胶原C端肽水平降低(P <0.05)；(2)显微CT显示，与青年组相比，老年组大鼠胫骨的骨体积分数、骨密度、骨小梁数量均降低(P <0.05)，骨小梁间隙增大(P <0.05)；与老年组相比，脉冲电磁场组大鼠胫骨的骨体积分数、骨密度、骨小梁数量均升高(P <0.05)，骨小梁间隙减少(P <0.05)；(3)胫骨平台番红O-固绿染色显示，老年组大鼠关节软骨结构紊乱，软骨细胞明显减少，无法区分潮线；脉...     

骨质疏松与骨关节炎患者松质骨的显微结构

目的:通过显微计算机断层扫描(micro-computed tomography,Micro-CT)检测股骨头松质骨显微结构,研究骨质疏松与骨关节炎的关系。方法:绝经后妇女骨质疏松性股骨颈骨折和原发性髋关节骨关节炎患者各20名,以Micro-CT扫描检测股骨头软骨下松质骨标本,对2组患者的松质骨显微结构参数进行比较。结果:骨质疏松与骨关节炎松质骨显微结构参数:骨体积分数(bone volume fraction,BV/TV)、骨表面积体积比(bone surface/bone volume,BS/BV)、骨小梁厚度(trabecular thickness,Tb.Th)、骨小梁间距(trabecular separation,Tb.Sp)、结构模型指数(structure model index,SMI)、连接密度(connectivity density,Conn.D)比较差异有统计学意义,BV/TV,SMI与Tb.N,TbTh,BS/BV,Tb.Sp呈相关关系。结论:骨质疏松与骨关节炎的显微结构存在差异,这些差异可能导致相反的骨缺陷;BV/TV,SMI是评价显微结构参数的2个重要指标。     

依降钙素干预膝骨关节炎模型大鼠软骨下骨的变化

文题释义： 依降钙素：为人工合成的鳗鱼降钙素多肽衍生物,其主要作用是抑制破骨细胞活性,减少骨的吸收,防止骨钙丢失,同时可降低正常动物和高钙血症动物血清钙,对实验性骨质疏松有改善骨强度、骨皮质厚度、骨钙质含量、骨密度等作用。 p38丝裂原活化蛋白激酶(p38 MAPK)：p38 MAPK是MAPK亚族中的一员,它以转录因子为作用目标,通过对转录因子的磷酸化来调节许多转录因子的活性,进而介导炎症反应和细胞凋亡,参与体内细胞的应激反应。研究认为p38 MAPK是调节膝关节骨关节炎发病机制中炎症产生的关键上游信号,影响骨关节炎的发生与发展,是近年来研究的热点。 背景：骨关节炎存在软骨下骨吸收和骨形成失去平衡,课题组前期研究发现膝骨关节炎大鼠关节软骨改变前软骨下骨就已经发生改变。 目的：通过观察膝骨关节炎大鼠膝关节软骨下骨的变化,探讨依降钙素对软骨下骨p38 MAPK表达及软骨下骨吸收的影响。 方法：雌性3月龄SD大鼠随机分为3组：假手术组(n=6)不切除卵巢,切除同卵巢等体积大小的脂肪组织,切开双侧膝关节,但不损伤交叉韧带;模型组(n=6)切除双侧卵巢后,再切断双侧膝关节前交叉韧带,建立卵巢切除+前交叉韧带切断模型,不进行药物干预;依降钙素组(n=6)建立卵巢切除+前交叉韧带切断模型后,依降钙素5 IU/kg,每周2次肌肉注射。12周后分析软骨下骨的骨密度、软骨下骨p38蛋白表达水平以及血清Ⅰ型胶原交联C-末端肽、Ⅱ型胶原交联C-末端肽、白细胞介素1、白细胞介素6、骨特异性碱性磷酸酶、抗酒石酸酸性磷酸酶5b水平。实验方案经南华大学动物实验伦理委员会批准。 结果与结论：①依降钙素组软骨下骨的骨体积分数、骨小梁数量显著高于模型组(P < 0.05),骨小梁分离度显著低于模型组(P < 0.05);②模型组的骨体积分数、骨小梁数量、骨小梁厚度显著低于假手术组(P < 0.01或< 0.05)、骨小梁分离度显著高于假手术组(P < 0.01);③依降钙素组血清Ⅰ型胶原交联C-末端肽、白细胞介素1、白细胞介素6、抗酒石酸酸性磷酸酶5b显著低于模型组(P < 0.05),模型组Ⅰ型胶原交联C-末端肽、Ⅱ型胶原交联C-末端肽、白细胞介素1、白细胞介素6、抗酒石酸酸性磷酸酶5b明显高于假手术组(P < 0.05);④软骨下骨p38蛋白表达水平依降钙素组显著低于模型组(P < 0.01)、模型组显著高于假手术组(P < 0.01);⑤结果说明,依降钙素可能通过下调p38 MAPK表达,抑制骨关节炎促炎因子分泌及软骨下骨吸收。 ORCID: 0000-0002-2108-9820(伍琦) 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     

个体化开放楔形胫骨高位截骨治疗内侧间室膝骨关节炎的优势

文题释义：开放楔形胫骨高位截骨：是一种治疗内侧间室膝骨关节炎合并膝内翻的保膝术式。通过胫骨近端内侧切口,在水平面、冠状面双截骨后,进行楔形撑开、钢板固定。其治疗意义在于将内翻的下肢力线转移至相对正常的膝外侧,以缓解内侧症状,延长关节寿命,延缓骨关节炎进展,甚至避免关节假体置换。 个体化力线矫形：根据膝骨关节炎的多阶段性,针对不同退变程度的膝内侧间室,施行不同的力线矫形方案。通过术前规划截骨后的楔形撑开角度或距离,可以将内翻的下肢力线矫正至中线或偏外侧,以达到临床治疗效果。 背景：开放楔形胫骨高位截骨对于内侧间室膝骨关节炎合并膝内翻患者疗效明确,但目前关于力线矫正点的选择仍以Fujisawa点作为参考,个体化力线矫形是否能获得更优越的临床疗效？ 目的：探讨开放楔形胫骨高位截骨术中个体化下肢力线矫形治疗内侧间室膝骨关节炎的短期疗效。 方法：选择2016年6月至2018年5月无锡市人民医院骨科因内侧间室膝骨关节炎行开放楔形胫骨高位截骨治疗的46例患者。根据X射线片、MRI综合评估患膝并划分退变等级(Ⅰ-Ⅲ级),其中Ⅰ,Ⅱ级患者随机分为个体化组及对照组,每组16例;14例Ⅲ级患者作为Fujisawa组。个体化组轻度退变Ⅰ级矫正下肢力线至胫骨平台50%点,中度退变Ⅱ级矫正至胫骨平台外侧55%点;对照组、Fujisawa组均矫正力线至62.5%点。测量评估术后下肢力线,比较术前、术后膝关节活动度、股胫角、胫骨近端内侧角;随访术前及术后3,6,12个月患膝的美国特种外科医院评分、西安大略和麦克马斯特大学骨关节炎指数,比较患者术后综合满意度的自评分。结果与结论：①所有患者均获得12个月随访;②3组下肢力线矫形结果满意,术后膝关节活动度、胫骨近端内侧角较术前明显增加,股胫角明显减少(P < 0.05);③随着随访时间延长,3组患者的美国特种外科医院评分显著增加,西安大略和麦克马斯特大学骨关节炎指数显著减少,组内不同时点差异有显著性意义(P < 0.05);个体化组术后3,6个月美国特种外科医院评分高于对照组,西安大略和麦克马斯特大学骨关节炎指数低于对照组,差异有显著性意义(P < 0.05);个体化组及对照组术后12个月美国特种外科医院评分、西安大略和麦克马斯特大学骨关节炎指数差异无显著性意义(P > 0.05);④所有患者对手术矫形效果满意,个体化组术后综合满意评分高于对照组,差异有显著性意义(P < 0.05);⑤结果表明,个体化开放楔形胫骨高位截骨通过准确地力线矫形,有利于膝关节早期功能恢复,提升患者满意度。 ORCID: 0000-0003-0566-2858(俞颖豪) 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     

骨保护素基因敲除小鼠腰椎间盘退变与腰椎骨质疏松

背景：骨保护素基因敲除小鼠已被证明会表现出明显的骨质疏松及骨关节炎表型。 目的：观察骨保护素基因敲除小鼠随年龄增长腰椎间盘退变和骨质疏松的动态变化关系。 方法：分别取出生后4,8,12周的骨保护素基因敲除纯合子小鼠及正常对照组小鼠的L3椎体和L4/5椎间盘,运用Micro-CT检测L3椎体松质骨微结构指标;用苏木精-伊红染色法观察L4/5椎间盘形态学,测量椎间盘及软骨终板高度。 结果与结论：骨保护素基因敲除纯合子小鼠组L3椎体骨小梁数量、骨小梁厚度、骨体积分数较正常组均明显下降(P < 0.05),而骨小梁分离度、结构模型指数较正常小鼠增高(P < 0.05)。8周及12周的骨保护素基因敲除纯合子小鼠的L4/5椎间盘软骨终板出现退变征象,软骨终板排列不规则,并有骨髓腔组织进入软骨终板及外层纤维环。提示骨保护素基因在维持椎间盘正常的结构和功能方面起到重要作用,骨保护素基因缺失后可导致椎间盘退变和椎体骨质疏松。     

高负荷运动抑制鼠软骨细胞自噬并促进其凋亡

目的 探讨不同负重跑步训练对大鼠膝关节软骨细胞的影响,以及静水压加载对ATDC5小鼠成软骨细胞自噬和凋亡的作用.方法 8周龄SD雄性大鼠随机分为安静组、运动组、低负荷运动组、高负荷运动组,应用大鼠跑台训练6周.收集大鼠膝关节行显微CT (Micro-CT)分析胫骨平台骨体积分数(BV/TV)、骨表面积组织体积比(BS/...     

RhoA/ROCK信号通路在异常应力下关节软骨中的表达

背景：RhoA/ROCK信号通路在活体内关节软骨退变或者骨性关节炎的病理过程中是否发挥着作用,为此设计了该实验。 目的：探索RhoA/ROCK信号通路在软骨退变过程中的作用。 方法：采用家兔右膝关节伸直位制动模型,对制动2,4,6 周及对照组家兔的右膝关节胫骨平台负重面全层软骨进行苏木精-伊红染色、番红O染色及RhoA、ROCK免疫组织化学染色,比较制动前后软骨组织学、病理积分及RhoA、ROCK表达变化情况。 结果与结论：随着制动时间的延长,关节软骨退变程度逐渐加重,Mankin评分逐渐增加,且各组评分之间差异有显著性意义(P < 0.05)。免疫组织化学提示RhoA、ROCK表达变化主要集中在切线层及中间层软骨,且二者在关节软骨退变过程中表达变化趋势一致,均为先增多后减少。结果表明,在关节软骨退变过程中,RhoA/ROCK信号通路表达先递增后逐渐降低,RhoA/ROCK信号通路在异常应力所致的关节软骨退变过程中发挥了效应。     

软骨下骨病理骨重建过程中骨细胞的代谢机制

背景：骨性关节炎一直被认为是关节软骨的退变和降解。现已逐步认识到软骨下骨结构及分子代谢的病理变化在关节退变的过程中发挥了重要的作用。 目的：观察软骨下骨在骨性关节炎进程中结构及细胞、相关因子和信号通道的变化,分析软骨下骨的病理改变对关节软骨退变的影响。 方法：使用骨性关节炎、软骨下骨、软骨退变、骨重建、骨代谢等关键词,检索中国知识资源总库与PubMed、Medline、Embase数据库中的相关研究论文,了解骨性关节炎进程中软骨下骨骨代谢平衡破坏后在结构及分子信号机制的病理变化,分析这些病理改变与关节软骨退变的关系。 结果与结论：纳入 54篇符合标准的文献。软骨下骨的病理骨重建贯穿骨性关节炎的始终,局部骨细胞的代谢及干细胞分化异常与软骨退变相互影响。通过对软骨下骨病理骨重建过程中骨细胞代谢机制的深入了解,为骨性关节炎提供了新的治疗靶点。     

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.     

Enhancement of subchondral bone quality by alendronate administration for the reduction of cartilage degeneration in the early phase of experimental osteoarthritis

To evaluate the effects of alendronate (ALN) on the subchondral bone quality and cartilage degeneration in the early phase of experimental model of osteoarthritis after anterior cruciate ligament transaction (ACLT). Thirty male adult healthy Japanese white rabbits after right ACLT or sham operation were divided into three groups (n = 10 per group): Sham; ACLT + ALN [after ACLT, the rabbits were treated with ALN daily starting from 4 days after surgery (10 μg/kg/d subcutaneously)]; and ACLT + NS group (after ACLT, the rabbits were injected saline as a placebo). At 60 days postsurgery, specimens from the affected knees were harvested. Histological analysis (HE and Safranin-O staining) as well as Mankin score were carried out to assess the cartilage degradation. BMP-2 and MMP-13 immunohistochemistry were also performed to demonstrate the alterations of cartilage molecular metabolism. Subchondral bone quality was evaluated by bone mineral density (BMD) and microstructure histomorphometry assay. For bone mineral density evaluation, 1/4 distal femurs, medial and lateral regions of femoral condylus were scanned with dual X-ray absorptiometry to assess the subchondral bone mass. Giemsa, von Kossa stain, and fluorescence technique for undecalcified bone section were carried out to examine the morphometry of the subchondral trabecular bone and subchondral plate. Histological and Mankin score analyses displayed that ALN treatment markedly reduced cartilage lesions and delayed the cartilage degeneration in OA joints. Immunohistochemistry assay further indicated that this cartilage-protective role of ALN was associated with elevating BMP-2 while inhibiting MMP-13 expression. BMD assessment demonstrated that ALN treatment significantly suppressed subchondral bone resorption. The results from histomorphometry assay of subchondral bone revealed that ALN treatment markedly increased the percent trabecular area (BV/TV), trabecular thickness (Tb.Th), and trabecular number (Tb.N). Moreover, both thickness and the porosity of the subchondral plate in ACLT + ALN group presented significantly higher than that in ACLT + NS group, while no significant difference was found between ACLT + ALN and Sham group. ALN plays an important role in cartilage protection in OA joints that is associated with the improvement of subchondral bone quality through reduction of subchondral bone resorption. ALN could be potentially used as a disease-modifying strategy to limit the progression of OA.     

Subchondral osteopenia and accelerated bone remodelling post‐ovariectomy – a possible mechanism for subchondral microfractures in the aetiology of spontaneous osteonecrosis of the knee?

Osteopenia and subchondral microfractures are implicated in the aetiology of spontaneous osteonecrosis of the knee (SPONK). The ovine tibia shows significant alterations of the trabecular architecture within the subchondral bone of the medial tibial plateau post‐ovariectomy (OVX), including reduced trabecular bone volume fraction. We hypothesise that accelerated subchondral bone resorption may also play a role in increasing microfracture risk at this site. Twenty‐two sheep were examined in this study; 10 of the sheep underwent OVX, while the remainder (n = 13) were kept as controls (CON). Five fluorochrome dyes were administered intravenously at 12‐week intervals via the jugular vein to both groups, to label sites of bone turnover. These animals were then killed at 12 months post‐operatively. Bone turnover was significantly increased in the OVX group in both trabecular bone (2.024 vs. 1.047 no. mm^?2; P = 0.05) and within the subchondral bone plate (4.68 vs. 0.69 no. mm^?2; P < 0.001). In addition to the classically described turnover visible along trabecular surfaces, we also found visual evidence of intra‐trabecular osteonal remodelling. In conclusion, this study shows significant alterations in bone turnover in both trabecular bone and within the subchondral bone plate at 1 year post‐OVX. Remodelling of trabecular bone was due to both classically described hemi‐osteonal and intra‐trabecular osteonal remodelling. The presence of both localised osteopenia and accelerated bone remodelling within the medial tibial plateau provide a possible mechanism for subchondral microfractures in the aetiology of SPONK. Further utilisation of the OVX ewe may be useful for further study in this field.     

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.     

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.     

膝骨性关节炎患者胫骨软骨下骨超微结构改变的CT评价

文题释义： 膝骨性关节炎：是一种以渐进性的关节损伤为主要特征,并最终导致患者关节疼痛甚至残疾,极大地降低患者生活质量。 CT：利用精确准直的X射线束、γ射线、超声波等,与灵敏度极高的探测器一同围绕人体的某一部位作一个接一个的断面扫描,具有扫描时间快、图像清晰等特点。 背景：软骨下骨的改变在膝骨性关节炎的作用得到了越来越多的重视,但是既往研究主要以动物为观察对象,由于动物与人存在差异,因而直接在人体关节内获得相关数据是非常必要的。 目的：通过CT技术评价非膝骨性关节炎患者与膝骨性关节炎患者软骨下骨板及软骨下骨超微结构的区别,来探讨软骨下骨在膝骨性关节炎疾病的发生和发展中的作用。 方法：于2016年7月至2018年7月在郑州市骨科医院影像科就诊患者中,收集30例膝骨性关节炎患者(膝骨性关节炎组)及30例非膝骨性关节炎患者(非膝骨性关节炎组)的CT扫描数据,使用MIMICS软件比较2组胫骨平台内外侧软骨下骨板以及软骨下骨小梁超微结构。试验于2016-06-10经郑州市骨科医院伦理委员会审批通过,审批号为2016医院伦审第004号。 结果与结论：①与非膝骨性关节炎组相比,膝骨性关节炎组软骨下骨板在外侧部位和内侧部位骨密度都明显增加,孔隙率则出现显著的下降,而软骨下骨板厚度内侧部分较非膝骨性关节炎组显著增厚;②膝骨性关节炎软骨下骨小梁同样存在明显变化,表现为膝骨性关节炎组内外侧软骨下骨骨小梁厚度较非膝骨性关节炎组均明显增加,同时内侧松质骨分离度也较非膝骨性关节炎组低;膝骨性关节炎组结构模型指数和连接密度值低于非膝骨性关节炎组;③结果表明,膝骨性关节炎患者胫骨软骨下骨板及软骨下骨松质骨的改变主要在于超微结构稳态的破坏,这一改变可能是膝骨性关节炎发病原因之一。 ORCID: 0000-0002-9805-3084(白玉) 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     

Bone density of the human talus does not increase with the cartilage degeneration score

Osteoarthritis (OA) is a common, disabling condition of synovial joints that can eventually lead to reduced, or lost, mobility. It is characterized by both articular cartilage degeneration and subchondral bone changes. However, a cause‐and‐effect relationship between the two tissues remains controversial. Increased subchondral bone density has been associated with early degenerative changes in the cartilage of knee, hip, and finger joints—joints in which progressive changes to OA are common. In contrast, the ankle joint is known to exhibit early cartilage changes, but is not prone to the development of OA. In the present study, it was found that cartilage degeneration on the talus is not associated with an increase in bone density, as assessed through peripheral quantitative computed tomography (pQCT). Anat Rec 266:81–86, 2002. © 2002 Wiley‐Liss, Inc.     

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.     

Subchondral trabecular structural changes in the proximal tibia in an ovine model of increased bone turnover

Ovariectomized (OVX) sheep are now considered to be useful models for a variety of metabolic bone disorders. The specific aim of this study was to determine the effects of ovariectomy on the structural parameters and material density of the subchondral bone of the ovine tibial plateau as measured by microcomputed tomography (MicroCT). Twenty-three sheep were examined in this study; 10 of the sheep underwent ovariectomy (OVX), and the remainder (n=13) were kept as controls (CON). These animals were then sacrificed at 12 months post-operatively. Three-dimensional analyses were performed of osteochondral samples (15 mm deep) which were obtained from the medial tibial plateau using MicroCT. Bone volume fraction of the subchondral trabecular bone was reduced in the ovariectomized sheep as compared to control animals (0.439 vs. 0.483, P=0.038). Trabeculae were also significantly thinner in the OVX group (0.220 vs. 0.252 mm, P=0.010), with reduced connectivity density (7.947 vs. 11.524 mm(-3) , P=0.014). There was a trend towards lower numbers of individual trabeculae present in the OVX group as compared to controls, but this did not reach significance (2.817 vs. 3.288 mm(-1) , P=0.1). There was also increased trabecular separation in the OVX group, which again fell short of significance (0.426 vs. 0.387 mm, P=0.251). There was no difference in hydroxyapatite concentration (HA) between the two groups (929 vs. 932 mgHA cm(-3) , P=0.687). In conclusion, significant alterations of the trabecular architecture under the tibial plateau were observed following 12 months of oestrogen-deficiency in this ovine model. Despite these marked morphological and structural density differences, the material densities were equal in the two groups.     

膝关节软骨下立柱式自体骨移植后软骨的变化

目的 通过观察兔膝关节软骨下立柱式自体骨移植的软骨的变化,探讨移植后关节软骨塌陷及软骨退变的原因。方法 ４２只大耳白兔为实验对象,随机分为Ａ、Ｂ两组。分别建立保留不同厚度的关节软骨下大块骨缺损的动物模型,采用立柱式自体额骨移植。分别于术后第１、１２周处死１０只、３２只动物,切取标本。应用光镜、透射电镜,对实验动物的软骨进行形态学观察。结果 Ａ组平均残留软骨下骨的厚度为１．４２ｍｍ,１周时软骨下骨未