MRI of osteoarthritis the challenges of definition and quantification
膝关节软骨早期退变的MRI表现及临床应用研究
无软骨下 骨硬化 8 20 28
合计
46 22 68
P=0.000,小于0.01
软骨病损 分组 Ⅲ、Ⅳ级 Ⅰ、Ⅱ级 合计
有软骨下 小囊肿 23 3 26
无软骨下 小囊肿 9 33 42
合计
32 36 68
P=0.000,小于0.01
讨
论
正常关节软骨的结构、组成与功能
关节软骨主要有大量细胞外基质与散在
MRI扫描检查
所有患者均行0.2T ARTOSCAN 关节 专用MR扫描仪检查,检查部位为膝关节, 线圈为膝关节专用线圈。采用SE、GE、 STIR及高分辨GE 序列。正常对照组MRI 检查方法同上。隐瞒病史后由两位经验 丰富的影像学专家阅片,关节软骨退变 的MRI分级采用Recht分级法。
统计学方法
结
论
MRI可早期、准确评价关节软骨病变,
与关节镜结合有极高的正确诊断价值。 关节软骨退变的MRI分级有助于弥补早 期OA关节镜诊断的不足,对OA患者早 期及时的治疗有明显的临床意义和卫生 经济学意义。
分布其中的高度特异性细胞——软骨细 胞组成。关节软骨的形成与维持依赖于 软骨细胞。 关节软骨表面至软骨下层,关节软骨的 结构组成依深度而变化,包括细胞的形 状与大小,胶原纤维的粗细与走向,蛋 白多糖的浓度及水含量的多少。
关节软骨可被分为4层:(1)浅表层
(superfical zone) (2)中间或过渡层 (transitional zone)(3)深层或放射带 (radial zone)(4)钙化软骨层(calcified cartilage zone) 关节软骨是组成活动关节面的有弹性的负重组 织,可减轻关节反复滑动中关节面的磨擦,具 有润滑及耐磨损的特性,并且还吸收机械性震 荡,传导重力至软骨下骨。
髌前皮下囊滑囊炎的MRI表现
第23卷 第5期 CT理论与应用研究 Vol.23, No.5 2014年9月(851-856) CT Theory and Applications Sep., 2014丁长青, 潘荣雷, 许若峰, 等. 髌前皮下囊滑囊炎的MRI表现[J]. CT理论与应用研究, 2014, 23(5): 851-856.Ding CQ, Pan RL, Xu RF, et al. MRI findings of the subcutaneous prepatellar bursitis[J]. CT Theory and Applications, 2014, 23(5): 851-856.髌前皮下囊滑囊炎的MRI表现丁长青a,潘荣雷b ,许若峰a,丁爱兰b,刘德海b,孙迎迎b,罗慧b,代兰兰 b(江苏省丰县人民医院 a.影像科;b.骨科,江苏 丰县221700)摘要:目的:探讨髌前皮下囊(SPB)滑囊炎的MRI表现特征和鉴别诊断。
方法:回顾性分析临床随访证实的28例髌前皮下囊滑囊炎的0.35T MRI资料。
结果:27例患者有急慢性膝前损伤史,1例有强直性脊柱炎病史。
以膝前疼痛肿胀为主要临床表现。
MRI表现为髌前皮下紧贴髌骨的扁圆形影,T1WI为中低、T2WI为中高信号。
大小:2.8cm×0.5cm×1.9cm~14.8cm×3.6cm×9.3cm,平均6.6cm×2.0cm×3.7cm。
MRI显示以轴位为佳。
结论:认识髌前皮下囊滑囊炎的临床及MRI表现特征有助于早期正确诊断该病。
关键词:膝关节;滑囊;髌前皮下囊;滑囊炎;膝痛;磁共振成像文章编号:1004-4140(2014)05-0851-06 中图分类号:R445.2 文献标志码:A髌前滑囊由髌前皮下囊(Subcutaneous Prepatellar Bursa,SPB)及髌下皮下囊(Subcutaneous Infrapatellar Bursa,SIB)组成,在膝前急慢性创伤时易受累及,尤以前者多见,临床多表现为前膝肿痛。
MRI的T1ρ成像原理及临床应用
MRI的T1ρ成像原理及临床应用发布时间:2022-12-26T05:46:05.845Z 来源:《医师在线》2022年26期作者:张芳[导读] T1ρ成像技术是近几年新开发的MRI序列,由于其可以无创评估关节软骨早期的退变、损伤、修复,而引起广泛关注张芳内蒙古鄂尔多斯中心医院影像科内蒙古鄂尔多斯市 017000T1ρ成像技术是近几年新开发的MRI序列,由于其可以无创评估关节软骨早期的退变、损伤、修复,而引起广泛关注。
关节软骨是一种特殊的结缔组织,传统的成像技术包括X线平片及常规MRI序列无法早期病变进行评估,量化MRI技术T1ρ序列通过量化关节软骨蛋白多糖PG含量实现了对关节软骨早期疾病的有效评估,本文就T1ρ技术的成像原理及临床应用进展进行综述。
1. T1ρ成像原理自旋锁定T1ρWI技术是指在常规自旋回波或梯度回波序列前,首先施加1个自旋定脉冲簇进行自旋锁定T1ρ的预磁化,然后采用常规自旋回波或梯度回波序列扫描对象的MRI信号来实现自旋锁定T1ρWI。
标准的自旋锁定脉冲簇是由在X轴上1个90°硬脉冲,在Y轴长且弱的自旋定脉冲,以及在X轴上第2个反相90°脉冲所组成的3个连续施加的射频脉冲,来完成自旋锁定T1ρ的预磁化。
自锁定时间即为自旋锁定射频长度。
2. T1ρ在关节软骨中的应用2.1 T1ρ对于正常关节软骨标记物的价值Chun Sing Wong等,对膝关节OA需要进行全关节置换的患者在术前行T1ρ序列扫描,手中获得软骨组织,用蛋白酶K降解关节软骨,测量相对应的软骨组织蛋白多糖PG含量,得出了一个重要的负相关,即T1ρ与PG含量呈负相关。
需要指出的是,同样作为量化MRI技术的T1ρ和T2 mapping(T2图),两者都可以描绘关节软骨组织的生物化学标志物,却存在很大的不同,T1ρ参数描绘为在旋转架中的自旋晶格弛豫,对于细胞外基质ECM中的葡萄糖胺聚糖GAG含量和定位的变化非常敏感。
间充质干细胞治疗膝骨关节炎的临床研究进展
间充质干细胞治疗膝骨关节炎的临床研究进展2.天津博纳戈恩生物科技有限公司,天津 300042;摘要:膝骨关节炎是一种以退行性病理改变为基础的疾患,发病率随年龄增大而升高,因此常见于中老年人群。
目前通常的治疗手段是通过消除炎症或减轻疼痛来缓解症状,从而阻止和延缓疾病的发展,进而保护关节功能,以防功能丧失,然而现有的临床治疗方式远期效果大多并不理想。
近年来随着对间充质干细胞的研究逐步深入,人们发现其可促进软骨再生的特点,因而以间充质干细胞移植为主的治疗方法,在国内外逐渐兴起,并开始进入临床实验阶段。
本文将主要就间充质干细胞治疗膝骨关节炎的原理、以及相关临床研究进行汇总,并为膝骨关节炎相关的研究和间充质干细胞的应用提供参考。
关键词:膝骨关节炎;间充质干细胞;临床研究;自体;同种异体前言膝骨关节炎(Knee Osteoarthritis, KOA)是一种以退行性病理改变为基础的疾患,常见于中老年人群。
该疾病初期症状较轻,临床表现多为膝盖部位肿胀、酸痛、行动不适,坐立姿势改变时疼痛、弹响等,严重时出现活动受限、积液、关节畸形,不及时得到有效治疗病情可能发展为残疾[1]。
KOA常由长期姿势僵化、劳累、外伤、或其它关节退行性病变如软骨退化、半月板磨损等原因导致。
因此该病的治疗关键在于保护软骨,防止进一步受损,同时尽可能使其自我修复和再生。
但由于膝关节部位软骨组织无血管,因此软骨部位自我修复和再生的能力很差,且关节软骨缺损的再生方法很少[2]。
KOA一般采用综合治疗,包括病人教育,药物治疗,理疗或外科手术治疗,现有的治疗方式包括软骨保护剂硫酸氨基葡萄糖、透明质酸关节腔注射、中医针灸推拿、膝关节置换以及间充质干细胞治疗等,其远期效果大多并不理想,而近年来随着对间充质干细胞的研究逐步深入,人们发现其可促进软骨再生的特点,因而以间充质干细胞移植为主的治疗方法,在国内外逐渐兴起,并开始进入临床实验阶段。
本综述将主要就间充质干细胞治疗KOA的原理、以及相关临床研究进行汇总,并为KOA相关的研究和间充质干细胞的应用提供参考。
未分化脊柱关节病的诊断标准
未分化脊柱关节病的诊断标准Ankylosing spondylitis is a form of arthritis that primarily affects the spine. It can cause inflammation, pain, stiffness, and eventually lead to fusion of the vertebrae. However, diagnosing undifferentiated spondyloarthritis (uSpA) can be challenging as the symptoms are often non-specific and can overlap with other conditions.脊柱关节强直是一种主要影响脊柱的关节炎形式。
它可以引起炎症、疼痛、僵硬,最终导致椎体融合。
然而,诊断未分化脊柱关节炎(uSpA)可能具有挑战性,因为症状通常是非特异性的,可能与其他情况重叠。
One of the key aspects in diagnosing uSpA is the presence of inflammatory back pain, which is characterized by gradual onset, improvement with exercise, and waking up at night due to back pain. Imaging studies such as X-rays and MRI may show sacroiliitis, which is inflammation in the sacroiliac joints, supporting the diagnosis of uSpA. Blood tests may also be conducted to check for markers of inflammation, such as C-reactive protein and erythrocyte sedimentation rate.诊断uSpA的一个关键方面是存在炎症性腰背痛,其特征是逐渐出现,运动后得以改善,并因腰背疼痛夜间醒来。
2024髋关节MRI检查及诊断专家共识
2024髓关节MRI检查及诊断专家共识摘要髓关节MRI在临床诊疗中应用广泛,能够评估既关节骨质、关节软骨及周围软组织解剖细节,但当前髓关节MRI的适应证、技术流程及影像评价缺乏规范标准,制约了髓关节疾病的规范化诊疗。
为推动髅关节MRl在我国的规范化应用,中华医学会放射学分会骨关节学组组织专家参阅文献并结合临床实践,经过反复讨论和修订达成能关节MRI检查及诊断共识。
评估能关节的影像学检查方法主要包括X线平片、CT及MRl等。
对于有髓关节症状的患者而言,MRl是对患者管理有重要意义的诊断方法,能够提供额关节解剖细节,包括关节组成骨骨质、关节软骨及其周围软组织信息,相较于X线平片及CT有明显优势[1]。
在临床工作中,髓关节MRI的应用日渐广泛,规范化开展髓关节MRI扫描,了解髓关节相关疾病的影像学特点,对早期诊断和治疗有重要意义[2]。
为推动既关节MRI的规范化应用,中华医学会放射学分会骨关节学组组织专家,参阅国内外最新指南和文献并反复讨论,结合我国临床实际情况起草了本版专家共识,对能关节MRI的检查适应证、扫描技术进行说明,并对常见骸关节疾病的MRl影像表现进行总结,对影像分析要点及诊断报告规范等方面进行规范,旨在更好地为患者诊疗提供支持。
一、检查适应证骸关节常规MRl可用于检查隐匿性骨折、股骨头缺血性坏死等骨质异常,亦适用于检测能臼盂唇病变、骨软骨病变等,也可用于骸关节发育不良(developmentaldysplasiaofthehip,DDH)的术前评估及骸关节术后的随访评估等[3]。
双骸关节MRI的主要适应证包括但不限于髓关节骨关节炎(osteoarthritis,OA\隐匿性骨折或应力性骨折、股骨头缺血性坏死、一过性能关节骨质疏松症、DDH、骨髓浸润性疾病等[4,5,6,7,8]o单骰关节MRI的主要适应证包括但不限于单侧髅部和/或臀部疼痛、髓关节相关腹股沟疼痛,关节活动度下降、跛行,不同种类的髓关节撞击症,髓臼盂唇和/或软骨损伤,大转子疼痛综合征及肌肉肌腱损伤等[9,10,11]o二、MRl技术规范根据检查需求可选择双骰或单髓关节MRI平扫、双骰关节MRI增强检查。
髋关节撞击综合征的影像特征综述
髋关节撞击综合征的影像特征综述熊健;张吉林;易本清【期刊名称】《江西医药》【年(卷),期】2016(051)009【总页数】3页(P987-989)【关键词】髋关节;撞击综合征;FAI;凸轮型;钳夹型;股骨颈疝窝【作者】熊健;张吉林;易本清【作者单位】江西省九江市第一人民医院影像科,九江 332000;江西省九江市第一人民医院影像科,九江 332000;江西省九江市第一人民医院影像科,九江332000【正文语种】中文【中图分类】R816.8髋关节撞击综合征(femoroacetabular impingement,FAI)[1]是瑞士医生Ganz于1999年首先进行了报道,并于2003年正式提出FAI的概念[2]。
FAI 是髋臼盂唇与股骨近端解剖关系出现异常而引起的一种髋关节慢性疼痛并可导致髋关节活动障碍的一种疾病,髋臼损伤及关节软骨退变可发生在股骨头颈与髋臼非正常碰撞后,继而引发相应临床症状,不经过及时合理的治疗最终可导致髋关节退行性骨关节病。
根据发病原因主要来源于髋臼或股骨近端,FAI可分为3种类型:凸轮型撞击(Cam type)、钳夹型撞击(Pincer type)及凸轮钳夹混合型撞击(mixed type)(见图1),近年来,这类疾病数量不断增多,国内外杂志有关于FAI的影像诊断的报道屡见不鲜[3],本综述归纳了我院近年来FAI患者的影像表现并进行总结,为同行在以后的工作中进行经验交流并为临床诊疗提供参考。
FAI的起源是由于股骨近端和髋臼缘的异常接触而引发,可造成包括髋部疼痛,关节软骨的损伤及髋臼盂唇磨损、变性,也可发生于遭受超生理功能的活动范围而导致的剪切力伤害的解剖结构正常的髋关节[4]。
凸轮型FAI常见于经常运动的男性,其特征在于股骨头非球形部分在股骨头颈连接处呈异常之骨赘突出,由于股骨头和颈交界处的异常导致髋关节运动时,股骨头的非半球形部分在屈曲、内旋位对髋臼前上部撞击,臼缘产生间断或持续的关节软骨压力和剪切力,造成由外至内的髋臼软骨磨损,导致软骨从关节盂唇和髋臼上撕裂与凸轮样撞击[5],同时长期刺激可导致相应髋臼硬化。
骨髓水肿是怎么回事?是很严重的病吗?
骨髓水肿是怎么回事?是很严重的病吗?“骨髓水肿”这一词经常出现在医院的检查或诊断结果中,对此,有些临床科的医生也不太知道其意思或疾病的严重程度,当然,病人或家属更不知道什么意思了。
骨髓水肿如何检查才能发现呢?发现骨髓水肿代表什么意思?都见于哪些疾病?是否表示疾病很严重?治疗后能否消失?……类似的问题日常会经常遇到,特别是在网络上会看到很多这类提问。
一些文章或回答大多是从单一某一方面解答或描述,比如外伤性的、缺血性的等,没有做更多方面的解答。
“骨髓水肿”这一词,是随着磁共振成像(MRI)检查技术的应用而出现的,也就是说,只有做MRI检查才能够发现比较早期的骨髓水肿的存在,因为MRI检查对水很敏感,所显示的骨髓水肿比较具有特征,所以直接就可以作出诊断。
即骨髓水肿区在MRI的T2WI压脂像上白,在T1WI上黑。
其他影像检查不能够发现或诊断骨髓水肿(包括X线片、CT、PET-CT、超声等)。
“骨髓水肿”它只是某些疾病中的表现之一,或某一阶段,并不是独立的疾病。
它的出现可以见于:一、骨感染性疾病:细菌性感染,例如骨关节结核、化脓性感染、或其他类型的病菌或病原体感染,这是由于感染时由于炎性细胞的侵润而使得骨组织中的水成分增多,即骨髓水肿。
二、骨关节外伤:由于骨折、骨损伤(虽没有骨干的骨折,但是存在骨小梁的骨折)、疲劳骨折等而使得病骨中水成分增多。
三、肿瘤:在某些骨肿瘤,尤其是恶性骨肿瘤中,由于肿瘤细胞的侵润或或其他伴随的病理因素而导致病变区或邻近骨组织的水成分增多。
四、骨的缺血性疾病:由于缺血造成骨组织的坏死,在进展期:病变区骨小梁中断、破碎,这样使得坏死区或相邻骨组织的水成分增多。
五、骨关节免疫性疾病:最常见的是类风湿性关节炎、强直性脊柱炎等,由于滑膜或肌腱韧带等软组织增生性病变而引起的骨质病变,骨的病变区出现单核细胞、淋巴细胞等炎性细胞侵润而伴水成分增多。
六、退行性骨关节病:由于椎间盘退变或关节软骨的退变与破坏,形成椎体终板炎或软骨下囊变或水肿。
关节镜疗效判定标准和评估方法(一)
关节镜疗效判定标准和评估方法(一)关节镜疗效判定标准和评估方法关节镜手术是一种常见的微创手术,可以用于治疗关节方面的损伤和疾病。
在关节镜手术后,需要对疗效进行判定和评估。
本文将详细介绍关节镜疗效判定标准和评估方法。
1. 关节镜疗效判定标准关节镜疗效判定标准是评估关节镜手术后疗效的指标和标准。
常用的关节镜疗效判定标准包括:•疼痛缓解程度:评估术后关节疼痛的缓解情况,根据疼痛程度分为显著缓解、部分缓解和未缓解等级。
•功能恢复情况:评估术后关节功能的恢复情况,包括活动范围、力量和稳定性等指标。
•影像学改善情况:评估术后关节内部结构的改善情况,包括关节软骨损伤、滑膜炎和骨刺等。
•满意度评定:患者对手术结果的满意程度,通常采用满意度问卷进行评估。
2. 关节镜疗效评估方法关节镜疗效评估方法是对关节镜手术疗效进行量化和客观评价的方法。
常用的关节镜疗效评估方法包括:•功能评估:采用相应的功能评估量表,如VAS评分、Knee Injury and Osteoarthritis Outcome Score (KOOS)、International Knee Documentation Committee (IKDC)评分等,以评估术后关节功能的恢复情况。
•影像学评估:通过关节X线片、MRI或CT等影像学检查,评估术后关节内部结构的改善情况。
•生活质量评估:采用生活质量问卷,如SF-36、EQ-5D等,评估术后患者的生活质量变化情况。
•运动学评估:通过运动学分析系统,评估术后关节运动范围、力量和稳定性等指标。
3. 关节镜疗效判定标准和评估方法的优缺点关节镜疗效判定标准和评估方法各有优缺点,主要包括以下几点:•优点:关节镜疗效判定标准和评估方法能够客观评估术后疗效,为医生和患者提供科学依据,帮助制定有效的治疗方案。
•缺点:由于关节镜手术的复杂性和患者个体差异,不同的标准和方法可能存在一定的主观性和局限性。
结论关节镜疗效判定标准和评估方法对于评估关节镜手术的疗效非常重要。
osteoarthritis and cartilage关节炎与软骨综述
ReviewOsteoarthritis as an in flammatory disease (osteoarthritis is not osteoarthrosis!)F.Berenbaum yz *y University Pierre &Marie Curie,Paris VI,Sorbonne Universités,7quai St-Bernard,75252Cedex 5Paris,France z Department of Rheumatology,AP-HP Saint-Antoine Hospital,75012Paris,Francea r t i c l e i n f oArticle history:Received 25July 2012Accepted 19November 2012Keywords:Osteoarthritis In flammation In flammagingMetabolic syndromeLow-grade in flammation Obesity Synovitis Cytokines AdipokinesInnate immunitys u m m a r yOsteoarthritis (OA)has long been considered a “wear and tear ”disease leading to loss of cartilage.OA used to be considered the sole consequence of any process leading to increased pressure on one particular joint or fragility of cartilage matrix.Progress in molecular biology in the 1990s has profoundly modi fied this paradigm.The discovery that many soluble mediators such as cytokines or prostaglandins can increase the production of matrix metalloproteinases by chondrocytes led to the first steps of an “in flammatory ”theory.However,it took a decade before synovitis was accepted as a critical feature of OA,and some studies are now opening the way to consider the condition a driver of the OA process.Recent experimental data have shown that subchondral bone may have a substantial role in the OA process,as a mechanical damper,as well as a source of in flammatory mediators implicated in the OA pain process and in the degradation of the deep layer of cartilage.Thus,initially considered cartilage driven,OA is a much more complex disease with in flammatory mediators released by cartilage,bone and synovium.Low-grade in flammation induced by the metabolic syndrome,innate immunity and in flam-maging are some of the more recent arguments in favor of the in flammatory theory of OA and high-lighted in this review.Ó2012Osteoarthritis Research Society International.Published by Elsevier Ltd.All rights reserved.Osteoarthritis (OA)has long been considered a “wear and tear ”disease leading to loss of cartilage.OA used to be considered the sole consequence of any process leading to increased pressure on one particular joint (e.g.,overload on weight-bearing joints,anatomical joint incongruency)or fragility of cartilage matrix (genetic alterations of matrix components).This paradigm was mainly based on the observation that chondrocytes,the only cell type present in cartilage,have very low metabolism activity with no ability to repair cartilage.Moreover,unlike all other tissues,articular cartilage,once damaged,cannot respond by a usual in flammatory response because it is non-vascularized and non-innervated.Progress in molecular biology in the 1990s has profoundly modi fied this paradigm.The discovery that many soluble mediators such as cytokines or prostaglandins can increase the production of matrix metalloproteinases (MMPs)by chondrocytes led to the first steps of an “in flammatory ”theory.However,it took a decade before synovitis was accepted as a critical feature of OA,and some studies are now opening the way to consider the condition a driver of theOA process.Recent experimental data have shown that sub-chondral bone may have a substantial role in the OA process,as a mechanical damper,as well as,as a source of in flammatory mediators implicated in the OA pain process and in the degradation of the deep layer of cartilage.Thus,initially considered cartilage driven,OA is a much more complex disease with in flammatory mediators released by cartilage,bone and synovium 1e 3(Fig.1).Interestingly,the source and type of in flammatory mediators may differ by OA phenotype 4.Synovitis (local in flammation)in OAJoint swelling is one clinical feature of OA attributed to in flam-mation and re flecting the presence of synovitis due to thickening of the synovium or to effusion.When patients experience OA flares (night pain,morning stiffness),they usually exhibit in parallel joint effusion,as is seen in classical in flammatory arthropathies such as rheumatoid arthritis (RA)5.Pannus-like synovitis may occur,although much more rarely than in RA 6.Gadolinium-enhanced MRI and ultrasonography are reliable,valid tools for showing OA synovitis 7.Many studies suggest that the presence of synovitis seen by arthroscopy,magnetic resonance imaging (MRI)or ultrasonography may be a surrogate marker of severity and associated with increased risk of radiographic evidence of disease progression 8,9.Systemic high-sensitivity C-reactive protein levels re flect synovial in flammation in*Address correspondence and reprint requests to:F.Berenbaum,Department of Rheumatology,Pierre &Marie Curie University,Assistance Publique-Hôpitaux de Paris,Saint-Antoine Hospital,184rue du Faubourg Saint-Antoine,75012Paris,France.Tel:33-1-49-28-25-20;Fax:33-1-49-28-25-13.E-mail address:francis.berenbaum@sat.aphp.fr.1063-4584/$e see front matter Ó2012Osteoarthritis Research Society International.Published by Elsevier Ltd.All rights reserved./10.1016/j.joca.2012.11.012Osteoarthritis and Cartilage 21(2013)16e 21OA patients and are associated with level of pain 10,11.Interestingly,synovial in flammation frequently occurs in traumatic meniscal injury and is associated with increased pain and dysfunction 12.Why the synovium becomes in flamed in OA remains contro-versial 13.The most accepted hypothesis is that,once degraded,cartilage fragments fall into the joint and contact the synovium.Considered foreign bodies,synovial cells react by producing in flammatory mediators,found in synovial fluid.These mediators can activate chondrocytes present in the super ficial layer of carti-lage,which leads to metalloproteinase synthesis and,eventually,increase cartilage degradation.The mediators can also induce synovial angiogenesis and increase the synthesis of in flammatory cytokines and MMPs by synovial cells themselves (vicious circle).Thus,OA synovitis perpetuates the cartilage degradation.More recently,another theory involves synovial tissue as a primary trigger of the OA process.Indeed,many cell types usually present in immunological processes have been described in OA,as bystanders and as actors 14.Depleting synovial macrophages with clodronate liposome before inducing a collagenase-induced insta-bility model of OA in mice prevented the generation of MMP-induced neoepitopes into cartilage 15,16,which indicates an impor-tant role for synovial macrophages in MMP-mediated cartilage damage.Moreover,osteophyte formation was decreased,which suggests that these cells are pivotal for this feature 16.Synovial In flammation may drive synovial angiogenesis,linked to OA pain,through macrophage activation 17,18.Molecular markers for dendritic cells were detected in the synovium in a post-traumatic rabbit OA model.Interestingly,large numbers of such cells were observed in the early stages after surgery,which suggested their participation in the early stages of OA 19.Suurmond et al.showed anincreased expression of interleukin 17(IL-17)in OA synovial tissue,synovial mast cells being the main IL-17-positive cells 20.Innate immunity as a trigger of local in flammation in OA The innate immune system,also known as non-speci fic immune system,comprises the cells and mechanisms that defend the host from infection by other organisms in a non-speci fic manner.This system is triggered after the binding of pathogen-associated molecular patterns (PAMPs)and danger-associated molecular patterns (DAMPs)on pattern-recognition receptors (PRRs)21,22.Thus,these responses have been studied as predominant features in multiple non-infectious diseases with tissue injury and/or defective repair.PRRs include membrane-associated PRRs (Toll-like receptors [TLRs],the basic signaling receptors of the innate immune system),cytoplasmic PRRs (nucleotide-binding oligomerization domains [NODs],NALPs,RNA helicases)and secreted PRRs (complement receptors,collectins).PAMPs include bacterial and viral ligands and also extracellular matrix molecules.PAMPs are recognized by TLRs and other PRRs.A pioneer study showed that TLRs are increased in level in OA cartilage lesions 23.TLR-2and TLR-4ligands such as low-molecular-weight hyaluronic acid,fibronectin,tenascin-C and alar-mins (S100proteins,high-mobility group protein B1[HMGB1])have been found in OA synovial fluid 24e 26.These factors can induce catabolic responses in chondrocytes and/or in flammatory responses in synoviocytes.For example,S100A8and S100A9proteins are involved in synovial activation and cartilage destruction,and high levels may predict joint destruction in OA 27.These results are corroborated by a proteomic analysis revealing that proteins from OA synovial fluid can induce macrophage production of in flammatoryFig.1.Systemic effects and potential consequences of OA-derived in flammatory mediators.A proposed novel paradigm for the role of low-grade in flammation in OA.Low-grade in flammation is characterized by the release of in flammatory mediators into the blood during MetS (obesity,insulin resistance,lipid abnormalities,hypertension)or aging (secretory senescence,see text).These in flammatory mediators are deleterious for joint tissues,thus initiating and/or perpetuating the OA process.Once activated,OA joint cells in turn release in flammatory mediators into the joint cavity and eventually into the blood.The mediators amplify the low-grade in flammation,which may induce or accelerate other chronic diseases affected by systemic low-grade in flammation.F.Berenbaum /Osteoarthritis and Cartilage 21(2013)16e 2117cytokines via TLR-4signaling28.Interestingly,recent data suggest that these events may occur early in the disease,so innate immunity may be a driver of the OA process.Synovialfluid from patients with early OA cartilage damage showed increasedfibroblast-like syno-viocyte responses to TLR-2and TLR-4ligands28.Increased levels of interleukin-15(IL-15)protein are found in the synovialfluid of early knee OA patients when compared to end-stage OA,and numbers of CD8cells within the synovial membrane is correlated with MMP-129.Another group of proteins involved in innate immunity has recently been highlighted in the context of OA.With proteomic and transcriptomic analyses of synovialfluids and synovial membranes from subjects with OA,Qiang et al.found that the expression and activation of complement is abnormally high in human OA joints30. Moreover,with experimental OA-induced in mice genetically deficient in different complement factors or by using specific pharmacological inhibitors,the authors showed that dysregulation of complement in synovial joints may have a key role in OA pathogenesis.Innate immunity responses may be triggered by crystals31. Calcium pyrophosphate dihydrate and basic calcium phosphate crystals are common in OA jointfluids and tissues32.These crystals, along with uric acid,can interact with the NALP-3inflammasome, an intracellular protein complex involved in IL-1b and IL-18acti-vation by cleaving pro-caspase-1to caspase-133,34.These processes have been well described in gout,but whether they occur in OA remains debatable35.Low-grade systemic inflammation in OALocal production of inflammatory mediators are well known to contribute to cartilage degradation and synovial cell activation,but additional data may link these events to a more systemic pathway. In other words,inflammatory events occurring within joint tissues could be reflected outside the joint in plasma and peripheral blood leukocytes(PBLs)of patients with OA.Levels of several inflamma-tory mediators are higher in OA than healthy sera27,36,37.A remarkable study assessed gene expression profiles in PBLs from patients with OA and found a subset with activated PBLs38.Inter-estingly,cluster analysis revealed two distinct subgroups:one with increased level of IL-1b and one with normal expression.Patients with the inflammatory“IL-1b signature”had higher pain scores and decreased function and were at higher risk of radiographic progression of OA.The risk of hand OA is increased two-fold in obese patients39. This increased risk cannot be explained by the mechanical effect of overload but can certainly be explained by systemic factors released mainly by abdominal adipose tissue and able to reach and then activate joint cells40.These systemic factors,called adipokines,have been extensively studied in OA.Among them,leptin,adiponectin, resistin and visfatin/NAMPT have pro-and/or anti-inflammatory properties in OA41e43.Interestingly,recent epidemiological and clinical data have highlighted that a metabolic syndrome(MetS) rather than obesity itself has the greatest impact on the initiation and severity of OA44e46.In that context,it is noteworthy that there is an independent association between carotid intima medial thick-ness with the prevalence of knee OA(OR1.7,1.1e2.7),and carotid plaque with distal interphalangeal OA(OR 1.4, 1.2e1.7)47.The reasons why there is such a link between atherosclerosis and OA remains elusive.One hypothesis relies on the inflammatory theory of atherosclerosis.Several lines of evidence support the hypothesis that oxidized lipids,including oxidized low-density lipoprotein(ox-LDL),are the most likely triggering factors for cytokine produc-tion48.All these data give strength to the“adipokines theory,”because the concentration of plasma adipokines is known to be associated with MetS49.Not unsurprisingly,a study showed an association of serum adipokine concentration and OA severity50,51. Moreover,systemic adipokines were found associated with local synovial tissue inflammation52.Recently,the infrapatellar fat pad, an adipose tissue localized in the knee,was found to be a potential source of adipokines such as IL-653,54.Whether these discoveries would lead to“anti-adipokine”therapies remain hypothetical since these molecules participate into many other physiological processes.However,some data coming from pre-clinical studies could open opportunities.An inhibitor of visfatin/nicotinamide phosphoribosyltransferase(NAMPT),FK866,has recently demon-strated anti-arthritic properties55.Another result supporting the role of adipokines relates on the clinical efficacy of a dramatic weight loss by bariatric surgery of obese patients on knee OA that parallels a decrease of low-grade inflammatory systemic markers56.A unique study could change the paradigm of the role of inflammation in OA in the near future.Kyrkanides et al.induced OA in mice genetically at risk of Alzheimer disease57.OA exacerbated and accelerated the development of neuroinflammation as assessed by glial cell activation and quantification of inflammation-related mRNAs,as well as A b pathology,assessed by the number and size of amyloid plaques.A likely scenario is that circulating cytokines contribute to brain inflammation and may exacerbate it in the context of Alzheimer disease.Thus,OA could be initiated and/or aggravated by the presence of a systemic low-grade inflammation but this study supports also the hypothesis that OA could be at the initiation of distant age-related diseases via a joint release of inflammatory mediators into the blood stream(Fig.1).Further experimental and epidemiological studies are needed to confirm this provocative hypothesis.Aging,inflammation and OAInflammation is triggered by external mediators such as cyto-kines and proteases,as well as internal cellular mechanisms leading to increased production of inflammatory mediators and lack of elimination of oxidated proteins.These proteins will in turn increase the concentration of reactive oxygen species(ROS)in cells, further adding to the oxidative damage triggering the inflamma-tion58.Interestingly,oxidative stress can promote cell senescence, and in particular chondrocyte senescence59.Although OA is a prototypic age-related disease,the specific mechanisms underlying the process remain largely unknown.At the cellular level,senescence can be divided into two main cate-gories:replicative and secretory.Many human cells in culture have a limited proliferative capacity.After a period of vigorous prolifer-ation,the rate of cell division declines(replicative senescence). However,other cell types like chondrocytes have a lower capacity to divide,which leaves little room for replicative senescence.But these cells have high capacity to synthesize soluble mediators.So, secretory senescence should be predominant with aging.This condition has been called the senescence-associated secretory phenotype(SASP)that includes several inflammatory and prode-gradative mediators driven by oxidative stress60.Interestingly,the SASP is primarily a delayed response to(epi)genomic damage61. Indeed,IL-1b-stimulated MMP-13chondrocyte production increases with age,suggesting that aging chondrocytes acquire a SASP62.Another theory relating inflammation,aging and OA is based on the recent discovery that advanced glycation endproducts(AGEs), produced by a non-enzymatic process in aging tissues,weaken cartilage by modifying its mechanical properties.They can trigger chondrocyte activation by binding to specific receptors present at the surface of the chondrocytes,called RAGE(receptors for AGE). This process can lead to an overproduction of proinflammatory cytokines and MMPs63e65.F.Berenbaum/Osteoarthritis and Cartilage21(2013)16e21 18Post-menopausal OA and in flammationTo understand why the incidence of OA increases greatly after menopause,some groups have investigated estrogen regulation.The estrogen receptor is present in chondrocytes,subchondral osteo-blasts and synoviocytes 66.Its activation by estrogen derivatives has led to controversial results,depending on their concentration.However,the overall effect predominantly leads to inhibition of the expression and secretion of proin flammatory cytokines such as IL-1into the joint 67.Moreover,decreased ovarian function is accompa-nied by a spontaneous increase in level of proin flammatory cyto-kines in plasma 68,which may participate in the low-grade in flammation mentioned here previously.However,this sugges-tion is speculative because the literature is poor on the topic.A direct link between mechanics and in flammation:mechanoreceptor signalingThe controversy about the origin of the OA process,mechanics or in flammation,should be ended soon thanks to recent discoveries in mechanosignaling.Any abnormal mechanical stress applied on a joint (stretch,compression,shear stress,hydrostatic pressure)can be converted into activated intracellular signals in joint cells by mechanoreceptors present at the surface of joint cells (ion chan-nels,integrins)69.These signals may eventually lead to the over-expression of in flammatory soluble mediators such as prostaglandins,chemokines and cytokines when a certain threshold is reached 70.This is the case for chondrocytes and for subchondral bone cells present in subchondral bone 71e 74.Intra-cellularly,the conversion of a mechanical signal to the synthesis of in flammatory mediators is mediated by the activation of inducible signaling pathways.Among them,NF-k B and MAPK pathways seem predominant 75.Therapeutical consequencesIt is noteworthy that despite strong experimental studies described in this review and showing a central role of in flammation in OA,the anti-cytokine approach has not yet proven signi ficative improvement in OA symptoms and structure modi fication.Pilot and controlled studies using anti-IL-1and anti-TNF molecules have not been convincing yet 76,77.However,a very recent open-labeled trial with etanercept is encouraging 78.These disappointing results may be due to the heterogeneity of the OA patients included in these trials,including phenotypes that may have different pathophysiology (Fig.2).ConclusionsThe literature is rich in data suggesting that in flammatory mediators play a pivotal role in the initiation and perpetuation of the OA process.The source of such mediators would be local from joint cells and systemic from other tissues such as adipose tissue released in blood flow and then reaching the joint via the subchondral bone vasculature.These mediators then have a deleterious effect on cartilage,bone and synovium.By extrapolation,more recent data suggest that locally produced mediators may have an impact on the initiation and perpetuation of other age-related and metabolic diseases.Deciphering these in flammatory pathways is critical for the discovery of disease-modifying OA drugs in the future.Author contributionF.Berenbaum is the sole contributor to this review.Con flict of interest No.AcknowledgmentsNo.References1.Kapoor M,Martel-Pelletier J,Lajeunesse D,Pelletier J-P,Fahmi H.Role of proin flammatory cytokines in the pathophysiology of osteoarthritis.Nat Rev Rheumatol 2011Jan;7(1):33e 42.2.Loeser RF,Goldring SR,Scanzello CR,Goldring MB.Osteoar-thritis:a disease of the joint as an organ.Arthritis Rheum 2012Jun;64(6):1697e 707.3.Goldring MB,Otero M.In flammation in osteoarthritis.Curr Opin Rheumatol 2011Sep;23(5):471e 8.4.Bijlsma JWJ,Berenbaum F,Lafeber FPJG.Osteoarthritis:an update with relevance for clinical ncet 2011Jun 18;377(9783):2115e 26.5.Sellam J,Berenbaum F.Clinical features of osteoarthritis.In:Firestein GS,Budd RC,Harris Jr ED,McInnes IB,Ruddy S,Sergent JS,Eds.Kelley ’s Textbook of Rheumatology.Phila-delphia:Elsevier Inc;2008:1547e 61.6.Shibakawa A,Aoki H,Masuko-Hongo K,Kato T,Tanaka M,Nishioka K,et al .Presence of pannus-like tissue on osteoar-thritic cartilage and its histological character.Osteoarthritis Cartilage 2003Feb;11(2):133e 40.7.Guermazi A,Roemer FW,Hayashi D.Imaging of osteoarthritis:update from a radiological perspective.Curr Opin Rheumatol 2011Sep;23(5):484e 91.8.Roemer FW,Guermazi A,Felson DT,Niu J,Nevitt MC,Crema MD,et al .Presence of MRI-detected joint effusion and synovitis increases the risk of cartilage loss in knees without osteoarthritis at 30-month follow-up:the MOST study.Ann Rheum Dis 2011Oct;70(10):1804e 9.9.Ayral X,Pickering EH,Woodworth TG,Mackillop N,Dougados M.Synovitis:a potential predictive factor of struc-tural progression of medial tibiofemoral knee osteoarthritis e results of a 1year longitudinal arthroscopic study in 422patients.Osteoarthritis Cartilage 2005May;13(5):361e 7.10.Stürmer T,Brenner H,Koenig W,Günther K-P.Severity andextent of osteoarthritis and low grade systemic in flammation as assessed by high sensitivity C reactive protein.Ann Rheum Dis 2004Feb;63(2):200e 5.11.Pearle AD,Scanzello CR,George S,Mandl LA,DiCarlo EF,Peterson M,et al .Elevated high-sensitivity C-reactive proteinMetS OAAgeing OAPost-trauma OASystemic release of inflammatory mediatorsLow-grade InflammationSecretory Inflammatory phenotypeOSTEOARTHRITISLocalInflammation (synovitis,mechanoreceptors)Alzheimer ?Atherosclerosis ?Others ?Crystal OAInnate immunityFig.2.An hypothesis for the role of in flammation in the pathogenesis of OA according to the phenotype.For each phenotype,the main pathway leading to the release of in flammatory mediators by the joint is highlighted.However,some pathways are shared between phenotypes.F.Berenbaum /Osteoarthritis and Cartilage 21(2013)16e 2119levels are associated with local inflammatoryfindings in patients with osteoarthritis.Osteoarthritis Cartilage2007 May;15(5):516e23.12.Scanzello CR,McKeon B,Swaim BH,DiCarlo E,Asomugha EU,Kanda V,et al.Synovial inflammation in patients undergoing arthroscopic meniscectomy:molecular characterization and relationship to symptoms.Arthritis Rheum2011Feb;63(2): 391e400.13.Sellam J,Berenbaum F.The role of synovitis in pathophysi-ology and clinical symptoms of osteoarthritis.Nat Rev Rheu-matol2010Nov;6(11):625e35.14.Hussein MR,Fathi NA,El-Din AME,Hassan HI,Abdullah F,Al-Hakeem E,et al.Alterations of the CD4(þ),CD8(þ)T cell subsets,interleukins-1beta,IL-10,IL-17,tumor necrosis factor-alpha and soluble intercellular adhesion molecule-1in rheu-matoid arthritis and osteoarthritis:preliminary observations.Pathol Oncol Res2008Sep;14(3):321e8.15.Blom AB,van Lent PL,Libregts S,Holthuysen AE,van derKraan PM,van Rooijen N,et al.Crucial role of macrophages in matrix metalloproteinase-mediated cartilage destruction during experimental osteoarthritis:involvement of matrix metalloproteinase3.Arthritis Rheum2007Jan;56(1):147e57.16.Blom AB,van Lent PLEM,Holthuysen AEM,van der Kraan PM,Roth J,van Rooijen N,et al.Synovial lining macrophages mediate osteophyte formation during experimental osteoar-thritis.Osteoarthritis Cartilage2004Aug;12(8):627e35.17.Mapp PI,Walsh DA.Mechanisms and targets of angiogenesisand nerve growth in osteoarthritis.Nat Rev Rheumatol2012 Jul;8(7):390e8.18.Haywood L,McWilliams DF,Pearson CI,Gill SE,Ganesan A,Wilson D,et al.Inflammation and angiogenesis in osteoar-thritis.Arthritis Rheum2003Aug;48(8):2173e7.19.E X,Cao Y,Meng H,Qi Y,Du G,Xu J,et al.Dendritic cells ofsynovium in experimental model of osteoarthritis of rabbits.Cell Physiol Biochem2012;30(1):23e32.20.Suurmond J,Dorjée AL,Boon MR,Knol EF,Huizinga TWJ,Toes REM,et al.Mast cells are the main interleukin17-positive cells in anticitrullinated protein antibody-positive and-nega-tive rheumatoid arthritis and osteoarthritis synovium.Arthritis Res Ther2011;13(5):R150.21.Gordon S.Pattern recognition receptors:doubling up for theinnate immune response.Cell2002Dec27;111(7):927e30. 22.Kawai T,Akira S.The role of pattern-recognition receptors ininnate immunity:update on Toll-like receptors.Nat Immunol 2010May;11(5):373e84.23.Kim HA,Cho M-L,Choi HY,Yoon CS,Jhun JY,Oh HJ,et al.Thecatabolic pathway mediated by Toll-like receptors in human osteoarthritic chondrocytes.Arthritis Rheum2006Jul;54(7): 2152e63.24.Scanzello CR,Plaas A,Crow MK.Innate immune system acti-vation in osteoarthritis:is osteoarthritis a chronic wound?Curr Opin Rheumatol2008Sep;20(5):565e72.25.García-Arnandis I,Guillén MI,Gomar F,Pelletier J-P,Martel-Pelletier J,Alcaraz MJ.High mobility group box1potentiates the pro-inflammatory effects of interleukin-1b in osteoar-thritic synoviocytes.Arthritis Res Ther2010;12(4):R165.26.van Lent PLEM,Blom AB,Schelbergen RFP,Slöetjes A,Lafeber FPJG,Lems WF,et al.Active involvement of alarmins S100A8and S100A9in the regulation of synovial activation and joint destruction during mouse and human osteoarthritis.Arthritis Rheum2012May;64(5):1466e76.27.Sohn DH,Sokolove J,Sharpe O,Erhart JC,Chandra PE,Lahey LJ,et al.Plasma proteins present in osteoarthritic synovialfluid can stimulate cytokine production via Toll-like receptor 4.Arthritis Res Ther2012;14(1):R7.28.Nair A,Kanda V,Bush-Joseph C,Verma N,Chubinskaya S,Mikecz K,et al.Synovialfluid from patients with early osteo-arthritis modulatesfibroblast-like synoviocyte responses to toll-like receptor4and toll-like receptor2ligands via soluble CD14.Arthritis Rheum2012Jul;64(7):2268e77.29.Scanzello CR,Umoh E,Pessler F,Diaz-Torne C,Miles T,Dicarlo E,et al.Local cytokine profiles in knee osteoarthritis:elevated synovialfluid interleukin-15differentiates early from end-stage disease.Osteoarthritis Cartilage2009Aug;17(8):1040e8.30.Wang Q,Rozelle AL,Lepus CM,Scanzello CR,Song JJ,Larsen DM,et al.Identification of a central role for comple-ment in osteoarthritis.Nat Med2011Dec;17(12):1674e9. 31.Rosenthal AK.Crystals,inflammation,and osteoarthritis.CurrOpin Rheumatol2011Mar;23(2):170e3.32.MacMullan P,McMahon G,McCarthy G.Detection of basiccalcium phosphate crystals in osteoarthritis.Joint Bone Spine 2011Jul;78(4):358e63.33.Martinon F,Pétrilli V,Mayor A,Tardivel A,Tschopp J.Gout-associated uric acid crystals activate the NALP3inflamma-some.Nature2006Mar9;440(7081):237e41.34.Denoble AE,Huffman KM,Stabler TV,Kelly SJ,Hershfield MS,McDaniel GE,et al.Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation.Proc Natl Acad Sci USA2011Feb1;108(5):2088e93.35.Bougault C,Gosset M,Houard X,Salvat C,Godmann L,Pap T,et al.Stress-induced cartilage degradation does not depend on NLRP3 inflammasome in osteoarthritis.Arthritis Rheum2012Aug29, /10.1002/art.34678[Epub ahead of print]. 36.Attur M,Statnikov A,Aliferis CF,Li Z,Krasnokutsky S,Samuels J,et al.Inflammatory genomic and plasma biomarkers predict progression of symptomatic knee OA(SKOA).Osteo-arthritis Cartilage2012Apr20.Suppl1:S34e S35.37.Fernández-Puente P,Mateos J,Fernández-Costa C,Oreiro N,Fernández-López C,Ruiz-Romero C,et al.Identification ofa panel of novel serum osteoarthritis biomarkers.J ProteomeRes2011Nov4;10(11):5095e101.38.Attur M,Belitskaya-Lévy I,Oh C,Krasnokutsky S,Greenberg J,Samuels J,et al.Increased interleukin-1b gene expression in peripheral blood leukocytes is associated with increased pain and predicts risk for progression of symptomatic knee osteo-arthritis.Arthritis Rheum2011Jul;63(7):1908e17.39.Yusuf E,Nelissen RG,Ioan-Facsinay A,Stojanovic-Susulic V,DeGroot J,van Osch G,et al.Association between weight or body mass index and hand osteoarthritis:a systematic review.Ann Rheum Dis2010Apr;69(4):761e5.40.Pottie P,Presle N,Terlain B,Netter P,Mainard D,Berenbaum F.Obesity and osteoarthritis:more complex than predicted!.Ann Rheum Dis2006Nov1;65(11):1403e5.41.Gabay O,Berenbaum F.Adipokines in arthritis:new kids onthe block.Curr Rheumatol Rev2009;5(4):226e32.42.Gómez R,Conde J,Scotece M,Gómez-Reino JJ,Lago F,Gualillo O.What’s new in our understanding of the role of adipokines in rheumatic diseases?Nat Rev Rheumatol2011Sep;7(9):528e36.43.Gosset M,Berenbaum F,Salvat C,Sautet A,Pigenet A,Tahiri K,et al.Crucial role of visfatin/pre-B cell colony-enhancing factor in matrix degradation and prostaglandin E2synthesis in chondrocytes:possible influence on osteoarthritis.Arthritis Rheum2008May;58(5):1399e409.44.Puenpatom RA,Victor TW.Increased prevalence of metabolicsyndrome in individuals with osteoarthritis:an analysis of NHANES III data.Postgrad Med2009Nov;121(6):9e20.45.Sowers M,Karvonen-Gutierrez CA,Palmieri-Smith R,Jacobson JA,Jiang Y,Ashton-Miller JA.Knee osteoarthritis in obese women with cardiometabolic clustering.Arthritis Rheum2009Oct15;61(10):1328e36.F.Berenbaum/Osteoarthritis and Cartilage21(2013)16e21 20。
关节软骨磁共振分子成像与量化分析新技术
国外医学临床放射学分册ForeignMedicalSciencesClinicalRadiologicalFascicle2007Nov830(6)关节软骨磁共振分子成像与量化分析新技术摘要简述关节软骨组织结构及老年性骨关节炎软骨的生化改变,就磁共振分子成像新技术对老年性骨关节炎在关节软骨形态异常之前的软骨分子结构变化的探测进行总结和比较。
关键词磁共振成像;骨关节炎;关节软骨;蛋白多糖;胶原骨肌放射学中山大学附属第五医院放射科(519000)周智洋邹学农综述单鸿审校=▲=中山大学附属第一医院骨科▲中山大学附属第三医院放射科本课题得到中丹(麦)政府间科技合作项目(AM14:29NNP44)与科技部国际科技合作重点项目计划(2005DFA30570)的资助。
老年性骨关节炎(osteoarthritis,OA)是以关节软骨退变为特征,伴有软骨下骨与关节周围骨质改变的慢性退行性疾病。
20世纪以来,随着人口老龄化和肥胖人数增多,老年性骨关节炎发病率与患病率逐年升高,是导致中老年人生活质量降低和活动功能丧失的常见病与多发病,目前已成为生物和医药技术研究领域中的前沿课题且日益受到重视。
在OA早期,关节软骨退变主要表现为软骨组织内生化成分和结构的改变,即蛋白多糖(proteoglycans,PGs)的丧失、胶原网络结构的破坏与水分的增多,形态学上多无明显变化。
因此,磁共振分子成像和软骨形态学变化之前的生化改变的量化分析已成为OA早期诊断和治疗效果评价的一种无创、有效、敏感的临床新技术,具有重要的临床价值。
一、关节软骨与OA生化改变(一)关节软骨组织结构正常的关节软骨为透明软骨,由软骨细胞和细胞外基质(extracellularmatrix,ECM)组成。
在ECM中,水分占60%~80%,胶原占15%~20%,PGs占3%~10%。
关节软骨不同区域的水含量有所不同,在软骨表层达80%,而深层为65%;其中胶原和PGs的含量也不同。
单源双能量ct检测膝骨关节炎骨髓水肿的价值研究
单源双能量CT检测膝骨关节炎骨髓水肿的价值研究李生虎1ꎬ孟祥鸿1ꎬ刘㊀栋1ꎬ胡云鹏ꎬ尹㊀恒1ꎬ王莉莉21.江苏省无锡市中医医院放射科㊀江苏㊀无锡㊀214071ꎻ2.甘肃省人民医院放射科㊀甘肃㊀兰州㊀730000㊀㊀ʌ摘㊀要ɔ㊀目的㊀探讨单源双能量CT虚拟去钙技术对于膝关节骨关节炎骨髓水肿的诊断价值ꎮ方法㊀回顾性研究2016年~2019年进行单源双能量膝关节检查的患者40例ꎬ同期90天内进行了膝关节MRI检查ꎮ将膝关节图像根据解剖部位分为5区ꎬ由放射诊断医生采用盲法对膝关节磁共振图像和双能量虚拟骨髓显像进行评估ꎮKappa检验评价结果的一致性ꎮROC曲线评估双能量虚拟骨髓显像检测骨髓水肿的效能ꎬ以磁共振图像为金标准计算敏感度㊁特异度ꎮ结果1)两种方法一致性良好ꎬKappa=0.82ꎬP=0.018ꎻ2)敏感度90.43%ꎬ特异度66.98%ꎻ3)ROC曲线下面积为0.883ꎬP=0.000ꎬ95%可信区间为(0.834ꎬ0.932)ꎮ结论㊀单源双能量虚拟骨髓显像和磁共振图像一致性良好ꎬ可用于膝关节骨关节炎骨髓水肿的评估ꎮʌ关键词ɔ㊀骨髓水肿ꎻ骨关节炎ꎬ膝ꎻ体层摄影术ꎬX线计算机ꎻ磁共振成像中图分类号:R744ꎻR814.42㊀㊀㊀文献标识码:A㊀㊀㊀文章编号:1006 ̄9011(2019)11 ̄1959 ̄03ThevalueofsinglesourcedualenergyCTindetectingbonemarrowedemaofkneeosteoarthritisLIShenghu1ꎬMENGXianghong1ꎬLIUDong1ꎬHUYunpeng1ꎬYINHeng1ꎬWANGLili21.DepartmentofRadiologyꎬWuxiCityHospitalofTCMꎬWuxi214000ꎬP.R.China2.DepartmentofRadiologyꎬGansuProvincalHospitalꎬLanzhou730000ꎬP.R.ChinaʌAbstractɔ㊀Objective㊀TostudythevalueofsinglesourceanddualenergyCTvirtualnon ̄calciumtechniqueinthediagnosisofbonemarrowedemainkneeosteoarthritis.Methods㊀Thisretrospectivestudyincluded40patientswhounderwentbothMRIanddual ̄energycomputedtomographyfrom2013to2019within90days.Allimagesweredividedinto5regionsaccordingtotheanatomyandjudgedindependentlybydifferentradiologists.TheconsistencyoftheevaluationresultswastestedbyKappa.Re ̄ceiveroperatingcharacteristiccurvewasusedtoevaluatetheefficacyofdual ̄energyvirtualbonemarrowimagingindetectingbonemarrowedema.MRIwasusedasthegoldstandardtocalculatethesensitivityandspecificity.Results㊀1)ThetwomethodswereingoodagreementwitheachotherꎬKappa=0.82ꎬP=0.018ꎻ2)Thesensitivitywas90.43%andthespecificitywas66.98%.Receiveroperatingcharacteristicanalysisrevealedanareaunderthecurveof0.883ꎬP=0.000ꎬandthe95%confidenceinterval(0.834ꎬ0.932).Conclusion㊀Single ̄sourcedual ̄energyCTvirtualnon ̄calciumtechniqueandmagneticresonanceimaginghaveexcellentconsistencyandfeasibilityforbonemarrowedemaofkneejointinosteoarthritis.ʌKeywordsɔ㊀BonemarrowedemaꎻOsteoarthritisꎬKneeꎻTomographyꎬX ̄raycomputerꎻMagneticresonanceimaging㊀㊀膝关节骨关节炎(kneeosteoarthritisꎬKOA)的研究表明ꎬKOA疼痛与软骨下骨髓水肿相关ꎬ且存在疼痛越重㊁骨髓水肿越严重的趋势[1]ꎮ磁共振成像是目前公认诊断KOA骨髓水肿最可靠的影像检查方法ꎬ但检查时间长ꎬ有检查禁忌的限制[2]ꎬ对于不能安全完成磁共振检查患者ꎬ需要一种替代的方法ꎮ目前双能量CT显示骨髓水肿的研究主要集中在创伤性骨髓水肿方面[2 ̄6]ꎬ对KOA骨髓水肿方面基金项目:江苏省自然科学基金资助项目(编号:BK20180167)作者简介:李生虎(1984 ̄)ꎬ男ꎬ甘肃白银人ꎬ毕业于兰州大学影像医学与核医学专业ꎬ医学硕士ꎬ主治医师ꎬ主要从事医学影像诊断工作通信作者:孟祥鸿㊀副主任医师ꎬ医学硕士㊀E ̄mail:960975141@qq.com的研究甚少ꎮ为此ꎬ本研究初步假设单源双能量CT能够准确诊断KOA引起的骨髓水肿ꎬ以磁共振压脂图像为金标准ꎬ对比分析单源双能量CT虚拟去钙(virtualnon ̄calciumꎬVNCa)技术检测KOA骨髓水肿的可靠性ꎮ1㊀资料与方法1.1㊀临床资料检索医院图像信息传输系统(picturearchivingandcommunicationsystemꎬPACS)ꎬ选取2016年6月~2019年6月进行膝关节单源双能量CT并磁共振检查的患者进行回顾性分析ꎮ入选标准:1)符合«实用骨科学»(第4版)[7]骨关节炎诊断标准ꎻ2)无9591医学影像学杂志2019年第29卷第11期㊀JMedImagingVol.29No.112019明确外伤病史ꎬ无膝关节手术病史ꎬ无膝关节占位性病变ꎻ3)膝关节双能量CT和磁共振检查时间间隔不超过90天ꎻ4)图像能够满足诊断要求无伪影ꎻ5)患者检查前知情同意并签署知情同意书ꎮ最终38例患者40个膝关节符合病例入选标准ꎬ其中男性31例ꎬ女性7例ꎬ年龄35~82岁ꎬ平均(58.75ʃ16 47)岁ꎮ磁共振检查和CT检查时间间隔不超过90天ꎬ平均为(28.82ʃ28.49)天ꎮ1.2㊀检查方法单源双能量CT检查采用德国西门子64排扫描仪(SomatomDefinitionAS)ꎬ患者采取仰卧位ꎬ双膝关节并拢置于扫描野ꎬ局部制动带固定ꎬ避免因运动造成图像匹配异常ꎮ扫描条件:双能量管电压分别为140kV㊁80kVꎬ管电流采用自动管电流技术ꎬ容积扫描模式ꎬ螺距0.7ꎬ层厚3mm㊁层间隔3mmꎮ对所得容积数据进行骨算法重建ꎬ重建间隔0.5mmꎬ层厚0.75mmꎮ所有检查均为非增强扫描ꎮ获得原始图像后导入后处理工作站Syngo.via(版本VB10A)ꎬ通过双能量bonemarrow模块进入软件ꎬ参数设置保持默认值不变ꎬ对所得虚拟骨髓显像(vir ̄tualbonemarrowimageꎬVBMI)标记伪彩加强显示对比ꎬ采用多平面重组(multi ̄planarreformationꎬMPR)技术获得冠状位㊁矢状位等进行全面观察ꎬ对于水肿位置及范围做好记录ꎮ磁共振检查选用飞利浦磁共振扫描仪(Achieva1.5T)ꎬ8通道膝关节专用线圈ꎬ压脂序列(PDW ̄SPAIR)矢状位或冠状位㊁横断位㊁TR2000ms㊁TE50msꎬFOV160mmˑ160mmˑ79mmꎬ层厚4mmꎬ层间距0.4mmꎮ图像评估:事先制定表格ꎬ方便进行观测记录ꎮ对膝关节根据解剖部位划分为5个区域(图1Aꎬ1B)ꎬ区域1:髌骨ꎻ区域2:股骨内侧髁ꎻ区域3:股骨外侧髁ꎻ区域4:胫骨内侧髁ꎻ区域5:胫骨外侧髁ꎮ水肿程度参考RomanGuggenberger等[2]对创伤性骨髓水肿分类方法ꎬ由重到轻分为四类ꎮ1类ꎬ明显水肿ꎻ2类ꎬ很有可能有骨髓水肿ꎻ3类ꎬ很有可能无骨髓水肿ꎻ4类ꎬ没有水肿ꎮ1)VBMI图像数据由有10年工作经验的两位放射科主治医师采用盲法进行评估ꎻ2)磁共振图像判读ꎬ由两位副主任医师采用和VBMI相同的解剖分区㊁分类标准进行判读记录ꎮVBMI和磁共振图像观察过程当中ꎬ可以任意采用适合个人阅片习惯的窗宽窗位和图像放大倍数进行详细观察确定ꎮ当上述图像评估过程中出现结果不一致时协商统一ꎮ1.3㊀统计方法数据分析用SPSS18.0软件包进行ꎮ计量资料以 xʃs表示ꎮ结果一致性采用Kappa检验进行分析ꎮ参考标准:Kappa=1ꎬ认为两次结果完全一致ꎮKappa= ̄1ꎬ认为两次结果完全不一致ꎮKappaȡ0 75认为已经有相当满意的一致程度ꎮKappa<0 4ꎬ认为一致性不理想ꎮ以磁共振为金标准ꎬ计算敏感性㊁特异性以及阳性预测值㊁阴性预测值ꎮ受试者工作特征曲线(receiveroperatingcharacteristiccurvesꎬROC)分析VBMI对骨髓水肿的诊断效能ꎬP<0.05为差异有统计学意义ꎮ2㊀结果㊀㊀38例患者中选取40个膝关节ꎬ共计200个解剖区域ꎬMRI脂肪抑制图像与VBMI对骨性关节炎骨髓水肿1~4类图像检测结果ꎬ见表1ꎬ所得磁共振脂肪抑制图像和VBMIꎬ(图2A~2C)ꎮ1)对磁共振PDW ̄SPAIR序列压脂图像及VBMI进行Kappa检验ꎬKappa=0.82ꎬ表明两种检查方法具有很好的一致性ꎬP=0.018ꎮ评价者间同样具有很好的一致性ꎬVBMI和MRIKappa值分别为0.87和0.88ꎬP=0.001ꎻ2)计算敏感度(90.43%)ꎬ特异度(66 98%)ꎬ阳性预测值(70.83%)ꎬ阴性预测值(88.75%)ꎬ约登指数(0.57)ꎻ3)ROC分析(图3)ꎬ曲线下面积等于0.883ꎬ表明检测准确度较好ꎬ相应的标准误为0.025ꎬP=0.000ꎬ95%可信区间为(0 834ꎬ0.932)ꎮ表1㊀MRI脂肪抑制图像与VBMI对㊀㊀骨性关节炎骨髓水肿1~4类图像检测结果4类3类2类1类合计(单位:个)MRI80154164200VBMI1011821602003㊀讨论㊀㊀双能量CT虚拟去钙技术是一种能够获取特定物质组成成份和物理性质的一种检查技术ꎮ成年人膝关节主要是由黄骨髓㊁软组织和骨质中的钙盐组成ꎮ钙盐成份相对前两种物质具有很高的密度ꎬ可通过140kV和80kV两种能量扫描后ꎬ通过专用软件VNCa技术去除ꎬ从而得到VBMIꎮ再通过窗口技术适当的调整窗宽窗位ꎬ获得骨髓水肿的灰阶图像[3]ꎬ从而判断骨髓水肿的存在与否ꎮ因KOA疼痛与软骨下骨髓水肿相关ꎬ疼痛越重㊁骨髓水肿越严重ꎮ能够明确显示骨髓水肿ꎬ对于KOA疼痛原因的0691医学影像学杂志2019年第29卷第11期㊀JMedImagingVol.29No.112019图1A㊀所示区域1 ̄髌骨㊀图1B㊀2 ̄股骨内侧髁ꎻ3 ̄股骨外侧髁ꎻ4 ̄胫骨内侧髁ꎻ5 ̄胫骨外侧髁㊀图2A~2C㊀男ꎬ57岁ꎮ左膝骨关节炎ꎮ磁共振PDW ̄SPAIR序列冠状位脂肪抑制图像(图2A)显示左股骨外侧髁(3区)有斑片状高信号ꎬ为1类骨髓水肿ꎬ对应双能量虚拟去钙显像(图2Bꎬ2C)显示相同区域骨髓水肿ꎬ分别用箭头标识图3㊀双能量VNCa技术检测KOA骨髓水肿的ROC曲线ꎬ曲线下面积等于0.883ꎬ标准误为0 025ꎬP=0.000ꎬ95%可信区间为(0.834ꎬ0 932)鉴别及治疗方法选择起到重要作用ꎮ本次研究当中ꎬ采用单源双能量CT作为研究设备ꎮ尽管单源双能量CT与双源双能量CT比较ꎬ存在因运动伪影等造成图像匹配异常情况ꎬ但对检测效能方面并无明显差别[8]ꎮKOA骨髓水肿多位于膝关节软骨下骨质ꎬ伴随不同程度软骨退行性病变ꎮ相对创伤性骨髓水肿ꎬKOA骨髓水肿的范围小ꎬ检测的难度增加ꎬ尤其是对于水肿范围小于0.5cm的骨髓水肿ꎬ要准确鉴别更加不易ꎮ本次研究以磁共振为金标准ꎬ对于水肿程度分级ꎬ发现单源双能量CT对KOA骨髓水肿具有较好的诊断价值ꎬROC曲线下面积表明诊断效能中等ꎬ可成为KOA骨髓水肿检测的一种替代检查方法ꎮ研究中评估单源双能量CT检测KOA骨髓水肿的诊断价值ꎬ发现有较高的敏感性和特异性ꎬ阳性预测值和阴性预测值相对较高ꎮ与创伤性关节骨髓水肿相关研究比较[2]ꎬ本次研究敏感性相对较高ꎬ而特异性相对较低ꎬ分析其原因ꎬ可能和纳入病例数量及KOA并发骨髓水肿的程度分级有一定的关系ꎮ针对于研究样本中的单个区域ꎬ存在一定的漏检ꎬ但对于单个膝关节并无漏诊骨髓水肿的情况发现ꎮ磁共振对于创伤㊁炎症及肿瘤等各种原因导致的骨髓水肿的显示起到了非常重要的作用ꎬ但影响因素多[9]ꎬ常导致低年资医生误判而增加了骨髓水肿诊断的假阳性ꎮ另外ꎬ磁共振检查时间长ꎬ存在检查禁忌ꎮ而双能量VNCa技术检查快捷ꎬ空间分辨率高ꎬ对骨质增生等退行性表现显示可靠ꎬ适用于中老年人KOA检测ꎬ并且无检查禁忌ꎬ可成为除磁共振脂肪抑制图像以外的一种可靠补充方法ꎮ不足之处ꎮ首先ꎬ双能量检查在一定程度上增加了辐射剂量需要引起重视ꎬ但已有研究在创伤性膝关节骨髓水肿研究中发现ꎬ适当降低射线剂量并不会造成图像质量的明显下降[10]ꎮ但对于KOA引起的骨髓水肿ꎬ尽可能降低射线剂量是否可以达到诊断要求ꎬ还需要后期进一步研究明确ꎮ另外ꎬ由于两次检查间隔时间的问题ꎬ可能也是出现假阴性的因素之一ꎮ需要后续研究中增加样本量㊁采用前瞻性方法ꎬ并尽可能缩短两种检查方法间隔时间进一步分析ꎮ总之ꎬ采用单源双能量CT获得VBMIꎬ能够很好的检测KOA并发的骨髓水肿ꎬ可用于磁共振检查禁忌的患者ꎬ也能够避免因为磁共振伪影导致误诊ꎬ是一种值得采用的辅助检测手段ꎬ对膝关节疼痛原因的鉴别诊断提供更多的临床参考信息ꎮ参考文献:[1]陆川ꎬ刘海霞ꎬ张国秋ꎬ等.膝骨性关节炎疼痛与骨髓水肿MRI影像学改变的相关性[J].中国中西医结合外科杂志ꎬ2015ꎬ21(3):242 ̄245.[2]GuggenbergerRꎬGnanntRꎬHodlerJꎬetal.Diagnosticperform ̄anceofdual ̄energyCTforthedetectionoftraumaticbonemarrowlesionsintheankle:comparisonwithMRimaging[J].Radiolo ̄gyꎬ2012ꎬ264(1):164 ̄173.(下转1965页)1691剖位置㊁长期接受糖皮质激素治疗及全身炎症水平ꎬ均是肺气肿导致COPD合并骨质疏松症的影响因素ꎬ但具体致病机制尚不明确ꎬ有待进一步研究ꎮ本文的不足:1)因实验组样本量较少ꎬ而未对COPD进行分级分析ꎻ2)本实验仅测量受检者胸椎钙(水)密度ꎬ其它椎体钙(水)密度变化情况尚待进一步研究ꎮ综上所述ꎬ利用GSI图像可初选评估COPD胸椎钙(水)密度与肺通气功能及LAV%变化关系ꎻ肺气肿是加重COPD患者胸椎钙(水)密度减低的重要因素ꎬ监测COPD患者LAV%及胸椎钙(水)密度值对骨质疏松症的预防和治疗有重要临床价值ꎮ参考文献:[1]InoueDꎬWatanabeRꎬOkazakiR.COPDandosteoporosis:linksꎬrisksꎬandtreatmentchallenges[J].InternationalJournalofChronicObstructivePulmonaryDiseaseꎬ2016ꎬ11(5):637 ̄648.[2]陈靖ꎬ郑邵微ꎬ苗延巍ꎬ等.能谱CT定量钙(水)密度技术对腰椎椎体内及椎体间骨密度差异的研究[J].大连医科大学学报ꎬ2015ꎬ37(3):289 ̄292.[3]TanWCꎬBourbeauJꎬAaronSDꎬetal.Globaliitiativeforchro ̄nicobstructivelungdisease2017classificationandlungfunctiondeclineinchronicobstructivepulmonarydisease[J].AmericanJournalofRespiratoryandCriticalCareMedicineꎬ2018ꎬ197(5):670 ̄673.[4]施晓雷ꎬ夏艺ꎬ范丽ꎬ等.慢性阻塞性肺疾病患者肺气肿改变对气道重塑与气流受限相关性的影响[J].临床放射学杂志ꎬ2018ꎬ37(6):931 ̄935.[5]LeeISꎬLeemAYꎬLeeSHꎬetal.Relationshipbetweenpulmo ̄naryfunctionandbonemineraldensityinthekoreannationalhealthandnutritionexaminationsurvey[J].TheKoreanJournalofInternalMedicineꎬ2016ꎬ31(5):899 ̄909. [6]LiangBꎬFengY.TheassociationoflowbonemineraldensitywithsystemicinflammationinclinicallystableCOPD[J].Endo ̄crineꎬ2012ꎬ42(1):190 ̄195.[7]南燕ꎬ王成伟.CT能谱成像技术定量测定羊骨骨密度的可行性[J].医学影像学杂志ꎬ2017ꎬ27(2):327 ̄329. [8]王平ꎬ和建伟ꎬ黄刚ꎬ等.应用双能CT与定量CT对椎体骨密度测量的对照研究[J].中国骨质疏松杂志ꎬ2017ꎬ23(2):159 ̄162.[9]LiLꎬQuYꎬJinXꎬetal.Protectiveeffectofsalidrosideagainstbonelossviahypoxia ̄induciblefactor ̄1αpathway ̄inducedangio ̄genesis[J].ScientificReportsꎬ2016ꎬ6(8):3131 ̄3147. [10]高永炳ꎬ龚波ꎬ武洪林ꎬ等.慢性阻塞性肺疾病肺通气功能与CT肺气肿指数的研究[J].医学影像学杂志ꎬ2016ꎬ26(12):2224 ̄2227.[11]MathioudakisAGꎬAmanetopoulouSGꎬGialmanidisIPꎬetal.Impactoflong‐termtreatmentwithlow‐doseinhaledcorti ̄costeroidsonthebonemineraldensityofchronicobstructivepulmonarydiseasepatients:aggravatingorbeneficial?[J].Respirologyꎬ2013ꎬ18(1):147 ̄153.[12]HenneickeHꎬGaspariniSJꎬBrennan ̄SperanzaTCꎬetal.Glu ̄cocorticoidsandbone:localeffectsandsystemicimplications[J].TrendsinEndocrinology&Metabolismꎬ2014ꎬ25(4):197 ̄211.[13]霍晋ꎬ王蕾ꎬ贾原ꎬ等.老年慢性阻塞性肺疾病合并骨质疏松血清白细胞介素 ̄6及C反应蛋白相关研究[J].中国药物与临床ꎬ2018ꎬ18(12):2104 ̄2106.(收稿日期:2018 ̄09 ̄03)(上接1961页)[3]PacheGꎬKraussBꎬStrohmPꎬetal.Dual ̄energyCTvirtualnon ̄calciumtechnique:detectingposttraumaticbonemarrowlesions ̄feasibilitystudy[J].Radiologyꎬ2010ꎬ256(2):617 ̄624. [4]赵承勇ꎬ罗松ꎬ邓小毅ꎬ等.双能量CT虚拟去钙成像在鉴别急慢性椎体压缩性骨折中的研究[J].医学影像学杂志ꎬ2018ꎬ28(9):1535 ̄1539.[5]章辉庆ꎬ刘海燕ꎬ邱晓辉ꎬ等.双能量CT虚拟去钙图诊断椎体骨髓水肿[J].中国医学影像技术ꎬ2019ꎬ35(2):260 ̄263. [6]WangCKꎬTsaiJMꎬChuangMTꎬetal.Bonemarrowedemainvertebralcompressionfractures:detectionwithdual ̄energyCT[J].Radiologyꎬ2013ꎬ269(2):525 ̄533.[7]胥少汀ꎬ葛宝丰ꎬ徐印坎ꎬ等.实用骨科学[M].北京:人民军医出版社ꎬ2012.1001 ̄1109.[8]DiekhoffTꎬTKꎬAS.Detectionandcharacterizationofcrystalsuspensionsusingsingle ̄sourcedual ̄energycomputedtomo ̄graphy:aphantommodelofcrystalarthropathies[J].InvestRa ̄diolꎬ2015ꎬ50(4):255 ̄260.[9]KrabbeSꎬEshedIꎬPedersenSJꎬetal.Bonemarrowoedemaas ̄sessmentbymagneticresonanceimaginginrheumatoidarthritiswristandmetacarpophalangealjoints:theimportanceoffieldstrengthꎬcoiltypeandimageresolution[J].Rheumatology(Ox ̄ford)ꎬ2014ꎬ53(8):1446 ̄1451.[10]SeoSHꎬSohnYJꎬLeeCHꎬetal.Dual ̄energyCTfordetectionoftraumaticbonebruisesinthekneejoint[J].JKorSocRadiolꎬ2013ꎬ69(6):487 ̄494.(收稿日期:2019 ̄09 ̄16)5691。
中英文的颈椎病
影像学检验:X线示:颈椎椎体及钩椎关节增生,椎 间隙变窄,颈椎生理曲度减小、消失或反弓。
中英文的颈椎病
7/22
Massage Treatment 推拿治疗
Treatment: rely mainly on relieving nerve root constriction,
治疗:以神经根减压为主,以轻柔手法沿放射性神经疼痛部位循 经推拿,缓解疼痛。
手法:患者坐于凳上,颈部肌肉放松。术者立于其背后,两手分 别抵住患者额部及乳突后缘,两手协调将患者头颈上提片刻,再 迟缓屈伸颈部5-10次。
中英文的颈椎病
8/22
2.cervical spondylotic myelopathy 脊髓型颈椎病
Medicalimageology test: X-ray shows: cervical vertebraes and uncovertebral jointhyperplasia, disc space narrow, reduce cervical lordosis, disappear, or anti-bow
体格检验:肌张力增高,腱反射亢进,锥体束征阳性。 影像学检验:X线结果类似于神经根型颈椎病。CT可见颈椎间盘
变性。MRI检验显示受压节段脊髓有信号改变,脊髓受压呈波浪 样压迹。
中英文的颈椎病
10/22
Massage treatment 推拿治疗
Treatment:main purpose is to relieve spinal constriction
影像学检验:椎动脉血流检测及颈动脉造影可 提醒有没有血管压迫、迂曲、变细或阻滞。X 线可显示椎节不稳定及钩椎关节侧方增生。
髌下脂肪垫的MRI定量检测及其在膝关节骨关节炎中的应用进展
国际医学放射学杂志InternationalJournalofMedicalRadiology2021May 鸦44穴3雪:319-323髌下脂肪垫的MRI 定量检测及其在膝关节骨关节炎中的应用进展钟丽洁张晓东*【摘要】髌下脂肪垫(IPFP)是参与膝关节骨关节炎(KOA )发生、发展的重要关节组织。
MRI 可以直接观察和量化IPFP 的变化,包括其形态学表现、信号强度变化及血流灌注变化等,有助于推测IPFP 在KOA 发病及进展中的作用。
就基于MRI 对IPFP 的定量检测方法及其在KOA 中的研究现状和进展予以综述。
【关键词】髌下脂肪垫;膝关节骨性关节炎;磁共振成像;定量检测中图分类号:R684.3;R445.2文献标志码:AQuantitating infrapatellar fat pad with MRI and its application in knee osteoarthritisZHONG Lijie,ZHANGXiaodong.Department of Radiology,Third Affiliated Hospital of Southern Medical University (Orthopaedic Hospital of Guangdong Province),Guangzhou 510631,China.Corresponding author:ZHANG Xiaodong,E-mail:****************【Abstract 】Infrapatellar fat pad (IPFP)is an important joint tissue in the initiation and progression of knee osteoarthritis(KOA).MRI can directly show and quantify the changes of IPFP,including its morphological manifestations,signal intensity changes,blood perfusion parameters,etc.,which is helpful to speculate the role of IPFP in the pathogenesis and progression of KOA.This article reviews the current quantitative detection methods of IPFP based on MRI,also the current research status and progress of its application in KOA.【Keywords 】Infrapatellar fat pad;Knee osteoarthritis;Magnetic resonance imaging;Quantitative detectionIntJMedRadiol,2021,44(3):319-323作者单位:南方医科大学第三附属医院(广东省骨科研究院)影像科,广州510631通信作者:张晓东,E-mail :*****************审校者DOI:10.19300/j.2021.Z18353综述骨肌放射学骨关节炎(osteoarthritis,OA )是最常见的骨关节慢性疾病之一,可以累及全身各关节,其中以膝关节最常见[1]。
儿童青少年与成人前交叉韧带在MRI上的解剖学特征差异
4812|中国组织工程研究|第25卷|第30期|2021年10月儿童青少年与成人前交叉韧带在MRI 上的解剖学特征差异钟锐鑫1,高海燕2,黄浩然2,滕学仁3,戴世友3文题释义:前交叉韧带:又称前十字韧带,位于膝关节内,起自股骨外侧髁的内侧面,斜向前下方,止于胫骨髁间隆起的前部和内、外侧半月板的前角,连接股骨与胫骨,主要作用是限制胫骨向前过度移位,它与膝关节内其他结构共同作用,来维持膝关节的稳定性,使人体能完成各种复杂和高难度的下肢动作。
前交叉韧带重建:即在关节镜微创手术操作下,通过定位制作胫骨、股骨骨道,将自体肌腱移植入骨道并固定的一种手术方式,此手术创伤小、恢复快、并发症少,但因年龄、性别等的不同,重建也具有个体差异性。
摘要背景:儿童和青少年处于生长发育阶段,采用与成人相同的前交叉韧带重建方式,易诱发包括肢体长度差异、移植物失败率高需再次外科手术介入等并发症,同时骨关节炎的发生也会提前。
目的:探讨儿童、青少年与成人前交叉韧带在膝关节MRI 上的解剖学特征差异,为儿童和青少年前交叉韧带的重建提供解剖学基础。
方法:回顾性分析2016年10月至2018年10月在青岛市市立医院行膝关节MRI 检查的受试者,分为儿童青少年组和成人组,两组各入组48例。
分别测量两组受试者前交叉韧带在矢状面上与胫骨及股骨的夹角及前交叉韧带胫骨止点的位置,冠状面上前交叉韧带与胫骨的夹角及前交叉韧带胫骨止点、股骨止点的位置,以及轴位上股骨止点的位置。
并且对儿童、青少年前交叉韧带测量所得数据进行处理,绘制儿童、青少年前交叉韧带形态及位置的生长曲线,分析其生长变化规律。
结果与结论:①儿童青少年组的前交叉韧带矢状面与股骨夹角(t =-2.906,P < 0.05)、前交叉韧带矢状面与胫骨的夹角(t =-10.280,P < 0.05)、前交叉韧带冠状面与胫骨的夹角(t =-5.714,P < 0.05)均小于成人组,差异有显著性意义;②儿童青少年组前交叉韧带胫骨冠状面比值(t =-7.263,P < 0.05)、前交叉韧带股骨轴位面比值(t =-7.378,P < 0.05)均小于成人组,差异有显著性意义;③儿童青少年组前交叉韧带胫骨矢状面比值(t =-1.588,P > 0.05)、前交叉韧带股骨冠状面比值(t =-1.647,P > 0.05)与成人组比较差异无显著性意义;④生长曲线结果显示,在生长发育过程中,儿童青少年组前交叉韧带在矢状面上与股骨和胫骨的夹角及在冠状面上与胫骨的夹角由小变大(P < 0.05);胫骨止点在冠状位上的相对位置由小变大,提示在生长发育过程中,胫骨止点在冠状面上相对胫骨平台内侧来说由内向外移动(P < 0.05);⑤股骨止点在轴位上的相对位置由小变大,提示在生长发育过程中,股骨止点在轴位上相对于股骨外侧髁来说是由外向内移动的(P < 0.05);⑥矢状面上胫骨止点和冠状面上股骨止点儿童青少年组与成人组无明显差异(P ﹥0.05)。
棘上韧带损伤磁共振的文字描述
棘上韧带损伤磁共振的文字描述英文回答:MRI is a very useful tool for diagnosing ligament injuries in the spine. When a ligament is injured, it can cause pain, stiffness, and limited range of motion in the affected area. During an MRI scan, the ligaments appear as dark bands on the images, allowing doctors to see any abnormalities or tears in the ligament.For example, I recently injured my thoracic spine while playing basketball. I was experiencing sharp pain and difficulty moving my upper body. My doctor recommended an MRI to assess the extent of the damage. The MRI revealed a torn supraspinous ligament, which explained my symptoms. The dark band on the image indicated the tear in the ligament, confirming the diagnosis.In addition to detecting ligament injuries, MRI can also show any inflammation or swelling in the surroundingtissues. This information is crucial for determining the best course of treatment for the injury. In my case, theMRI showed inflammation in the ligament, which guided my doctor in recommending rest, physical therapy, and anti-inflammatory medication to help me recover.Overall, MRI is a valuable tool for evaluating ligament injuries in the spine. It provides detailed images thathelp doctors make an accurate diagnosis and develop an effective treatment plan for patients with these injuries.中文回答:磁共振成像对于诊断脊柱韧带损伤非常有用。
臀中肌综合征的磁共振成像诊断价值
臀中肌综合征的磁共振成像诊断价值孙迎迎丁长青丁爱兰王雪璐刘德海王文生【摘要】目的探讨臀中肌综合征(GMS)的磁共振成像(MRI)表现特征及应用价值。
方法收集本院2016—2017年收治并行MRI检查的辽例GMS患者的资料,分析其MRI形态信号特点。
结果急性期MRI可见臀中肌外形存在,肌肉肿胀,臀中肌肌腱信号,肿,T2WI及(STIR)较佳;慢性期可见臀中肌肌纤维局部变薄萎缩,可见信号。
结论MRI可较GMS的病变特征,治。
【关键词】臀中肌综合征;磁共振成像;诊断Diagnosis value of MRI in gluteus medius syndrome Sun Yingying,Ding Chongqing,Ding A Han,.ang Xuelu, Liu Dehai,Wang Wensheng.Department of Imaging,People?Hospital of Fengxian,Jiangsu221700,China [Abstract]Objective T o explore the MRI features and application value of gluteus medius syndrome(GMS). Methods The data of18patients with GMS who underwent MRI examination in our hospital from2016to2017 were collected.The morphology and signal intensity on MRI were analyzed.ResultS In the acute phase,MRI showed the appearance of gluteus medius muscle with swelling and increased signal of gluteus medius muscle tendon mostly accompanied with surrounding edema or hydrops,which showed best on T"WI and STIR sequences.In the chronic phase,local thinning and atrophy of gluteus medius muscle fiber and fat deposition signal were seen.Conclusion MRI can display the lesion characteristics of GMS more accurately and provide evidence support for clinical treatment.【Key words]Gluteus m edius syndrome;Magnetic resonance imaging;Diagnosis臀中肌综合征(GMS)臀中肌变的肌:疼痛综合征,/髓/性。
能谱CT物质分离技术对膝关节骨性关节炎髌下脂肪垫物质的相关性研究
162·中国CT和MRI杂志 2024年1月 第22卷 第1期 总第171期【通讯作者】马春玲,女,主管技师,主要研究方向:骨肌影像学。
E-mail:****************Characterization of Infrapatellar Fat Pad·163CHINESE JOURNAL OF CT AND MRI, JAN. 2024, Vol.22, No.1 Total No.171学差异。
组内数据采用皮尔逊相关性(r)分析,以病例数作为样本量,水基值及脂基值作为变量,当r>0时,两组数据呈正相关,当r<0时,两组数据呈负相关。
用。
然而一旦遭受某些未知诱发条件的影响后,脂肪垫可能会引发非感染性的炎症状况从而造成血液渗漏或者出现积聚现象:这种状况可能进一步引起脂肪垫与髌韧带之间的纤维组织丧失了弹力能力进而使得腿部弯曲活动受限甚至完全无法动弹的情况的发生[5]。
根据 Gallagher等[6,1]人提出的观点IPFP的病变可能是引致疼痛的主要根源之一。
3.2 物质分离技术在宝石能谱CT中的应用 传统的CT使用的是80-140kVp的高频高压发生器产生的混合能量X光,然后经过身体吸收后的计算得出了混合能量影像[7]。
然而,在能谱CT扫描过程中,可以在不到0.5ms的时间里实现80kVp与140kVp之间的瞬间转换,这使我们能够生成两类不同物质的密度映射图,这一过程被称作物质分离技术。
根据研究结果,所有物质的衰减特性都可以用另一种物质的衰减特性来描述,这两种物质则被称为基物质对[8]。
无论哪种结构或物质都可由所对应比例的基物质对的组合来表示。
基物质对并不是所测量组织真实含有的物质,它只是两种物质X线衰减的差异,当基物质对恰好为组织中含有主要成分时,就可以反映组织内该物质的相对含量[9]。
对于膝关节骨性关节炎IPFP的病变情况来说,最主要的表现就是水肿和脂肪两种物质的形成,因此我们可以获得关于水分和脂肪的两个物质密度的投影数据,这样就能够从侧面反映出IPFP的发展变化。
学医遇到困难英语作文高中
学医遇到困难英语作文高中Title: Overcoming Challenges in Pursuit of Medical Education。
In the pursuit of a career in medicine, individualsoften encounter numerous challenges that test their determination and resilience. From rigorous academic requirements to demanding practical experiences, thejourney to becoming a healthcare professional is laden with obstacles. In this essay, we will explore the various difficulties faced by students studying medicine and strategies to overcome them.Firstly, one of the most significant challenges encountered by medical students is the sheer volume of knowledge they must acquire and retain. The medical curriculum is extensive and covers a wide range of subjects, including anatomy, physiology, pharmacology, and pathology. The depth and complexity of these subjects can be overwhelming, especially for those with no prior backgroundin science. Moreover, the rapid pace at which new medical discoveries are made means that students must continually update their knowledge to stay abreast of the latest developments in the field.Another obstacle faced by aspiring doctors is the intense academic pressure associated with medical school. The competitive nature of the admissions process means that only the most academically gifted students gain entry, creating a highly competitive environment where the stakes are high. Additionally, the constant assessments, exams, and evaluations can take a toll on students' mental and emotional well-being, leading to stress, anxiety, and burnout.Furthermore, medical education involves practical training, which presents its own set of challenges.Clinical rotations, where students work under the supervision of experienced physicians, provide invaluable hands-on experience but can also be daunting for novices. The responsibility of caring for patients' health and well-being can be overwhelming, and students must quickly learnto navigate complex medical scenarios while maintaining professionalism and empathy.Despite these challenges, there are several strategies that students can employ to overcome them and succeed in their medical education journey. Firstly, effective time management is essential for staying on top of coursework and exam preparation. By creating a realistic study schedule and prioritizing tasks, students can ensure that they make the most of their time and avoid last-minute cramming.Additionally, seeking support from peers, professors, and mentors can provide invaluable assistance and encouragement during difficult times. Joining study groups, attending review sessions, and participating in extracurricular activities can help students forge meaningful connections with their peers and build a strong support network.Moreover, prioritizing self-care and maintaining a healthy work-life balance is crucial for preventing burnoutand maintaining overall well-being. Engaging in regular exercise, getting enough sleep, and taking breaks to relax and recharge are all important ways to alleviate stress and promote mental health.In conclusion, pursuing a career in medicine is a challenging yet rewarding endeavor that requires dedication, perseverance, and resilience. By acknowledging thedifficulties inherent in medical education and employing effective strategies to overcome them, students can successfully navigate the obstacles they encounter and emerge as competent and compassionate healthcare professionals.This essay is a testament to the tenacity and determination of individuals who choose to embark on this noble profession despite the challenges they may face along the way. Through hard work, perseverance, and a commitmentto lifelong learning, aspiring doctors can fulfill their dreams of making a positive impact on the lives of others and contributing to the advancement of medical science.。
超声弹性成像鉴别膝关节积液与滑膜增生
超声弹性成像鉴别膝关节积液与滑膜增生向醒;张平;杨晶;尹良军;左国庆;郑元义【摘要】目的探讨超声实时弹性成像技术鉴别膝关节积液与滑膜增生的价值.方法对68例MRI检出的同时有滑膜增生和关节积液的患者行超声弹性成像检查,依据弹性成像结果予以弹性分级(Ⅰ~Ⅳ),比较二者的差异.结果共纳入68例患者的72个膝关节,膝关节积液弹性成像评分Ⅰ级32个,Ⅱ级40个,滑膜评分Ⅲ级67个,Ⅳ级5个.弹性成像可清楚观察滑膜及积液的范围及分界,所示积液量低于二维超声所见.结论超声弹性成像技术弹性评分法有助于膝关节积液与增生滑膜的鉴别诊断.【期刊名称】《中国介入影像与治疗学》【年(卷),期】2016(013)009【总页数】4页(P553-556)【关键词】弹性成像技术;关节积液;滑膜【作者】向醒;张平;杨晶;尹良军;左国庆;郑元义【作者单位】重庆医科大学超声影像学研究所,重庆400010;重庆医科大学附属第二医院超声科,重庆400010;重庆医科大学附属第二医院骨科,重庆400010;重庆医科大学超声影像学研究所,重庆400010;重庆医科大学附属第二医院超声科,重庆400010;重庆医科大学附属第二医院骨科,重庆400010;重庆市中医院消化内科,重庆 400021;重庆医科大学超声影像学研究所,重庆400010;重庆医科大学附属第二医院超声科,重庆400010【正文语种】中文【中图分类】R445.1;R684滑膜增生、关节积液是关节的常见病变,也是许多关节疾病共有的表现之一,在关节病变早期即可能出现[1],滑膜病变及关节积液的早期检出对多种关节疾病的诊断及治疗有重要应用价值。
在类风湿肌骨超声分级标准[2]中,需要鉴别增生滑膜与积液,进行相应的分级以制定最优的治疗方案。
较多慢性病变中积液表现为低回声,与增生滑膜区分困难[3],且超声在诊断少量关节积液时存在局限[4]。
目前主要采用探头加压的技术区分增生滑膜与积液,液体可通过探头加压压瘪,但在少量关节积液及积液较深等情况下挤压困难。
- 1、下载文档前请自行甄别文档内容的完整性,平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益,请联系客服反馈,我们会尽快为您处理(人工客服工作时间:9:00-18:30)。
MRI of Osteoarthritis:The Challenges of De finition and Quanti ficationDaichi Hayashi,MD,PhD 1Ali Guermazi,MD,PhD 1,2Frank W.Roemer,MD 1,31Department of Radiology,Boston University School of Medicine,Boston,Massachusetts2Department of Musculoskeletal Imaging,Boston Medical Center,Boston,Massachusetts3Department of Radiology,Klinikum Augsburg,Augsburg,GermanySemin Musculoskelet Radiol 2012;16:419–430.Address for correspondence and reprint requests Ali Guermazi,MD,PhD,Department of Radiology,Quantitative Imaging Center (QIC),Boston University School of Medicine,820Harrison Ave.,FGH Bldg.,3rd Fl.,Boston,MA 02118(e-mail:guermazi@).MRI has become the most important imaging modality for the morphological evaluation of joints in osteoarthritis (OA)research.1–3MRI allows tomographic viewing and depiction of all tissues of the joint,and it enables evaluation of the joint as a whole organ.In this review article,we describe current progress and challenges in OA imaging by focusing on an MRI-based de finition of OA and discussing the different MRI-based research methodologies including semiquantitative,quanti-tative,and compositional/physiologic techniques.Although OA is a disease that can affect any synovial joint of the body,we focus on the knee,which is the most extensively studied joint using MRI.De finition of Knee Osteoarthritis Based on MRICurrently the diagnosis of OA is based on clinical and/or radiographic findings.The American College of Rheumatolo-gy (ACR)classi fication criteria are the mainstay for diagnosing OA both in the clinic and in research (►Table 1).4Clinicalcriteria include a combination of age,signs,and symptoms on physical examination,as well as radiographic and/or labora-tory evidence.When the radiograph is used along with a physical examination,the sensitivity and speci ficity of this combined method for OA diagnosis are 91%and 86%,respec-tively.The clinical diagnosis of OA is the standard against which the classi fication criteria are judged.The ACR classi fi-cation combines clinical and radiographic criteria and re-mains the standard for diagnosis both in the clinic and in research,but it still relies on conventional radiographs that are not sensitive to the early structural changes of OA.The Kellgren Lawrence (KL)grading method is commonly used to de fine OA radiographically for epidemiological study purposes.5The method,established decades ago,takes into account the presence of marginal osteophytes and joint space narrowing in the tibiofemoral joint of the knee using a posteroanterior radiograph.KL grade 0indicates there are no features of OA and represents a normal radiograph;grade 1denotes the presence of equivocal osteophyte(s);grade 2denotes the presence of de finite marginal osteophyte(s),Keywords►osteoarthritis ►MRI ►knee►semiquantitative ►quantitative ►scoringAbstractThe ability of MRI to visualize the joint as a “whole organ ”and to directly and three-dimensionally assess cartilage morphology and composition has given it a crucial role in discovering the natural history of osteoarthritis (OA).Morphological analysis can be semiquantitative or positional analysis such as delayed gadolinium-enhanced MRI of cartilage and T2mapping allows quantitative evaluation of tissue ultrastructure and can detect premorphological changes of cartilage and other tissues.Contrast-enhanced MRI can accurately assess the true extent of synovial in flammation.Most MRI-based studies so far have focused on knee OA,but with the availability of new semiquantitative scoring systems for hand and hip OA,studies of these joints have begun to appear.Because of the technical complexity of MRI and ever increasing number of new and sophisticated imaging sequences and protocols,the speci fic MRI technique in any OA study needs to be carefully tailored to the aims of the study.Issue Theme Advanced Imaging of Arthritis;Guest Editors,Andrew J.Grainger,MRCP,FRCR and Philip J.O ’Connor,MRCP,FRCR,FFSEM (UK).Copyright ©2012by Thieme Medical Publishers,Inc.,333Seventh Avenue,New York,NY 10001,USA.Tel:+1(212)584-4662.DOI /10.1055/s-0032-1329895.ISSN 1089-7860.419D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.which is the de finition of radiographic OA;grade 3denotes the presence of joint space narrowing;and grade 4refers to the presence of “bone-on-bone ”appearance (►Fig.1).6Although radiographic osseous findings are common in OA,radiography cannot directly visualize all of the surround-ing tissues including cartilage with mild damage and menis-cal lesions.In the knee,MRI can visualize most components of the joint including articular cartilage,7,8menisci,9,10intra-articular ligaments,11,12synovium,13,14bone marrow,15–17subchondral cysts,18,19and other peri-and intra-articular lesions 20–22that are not detectable by radiography but that are quite prevalent in joints with no radiographic sign of OA.One MRI study reported the presence of osteophytes in 445knees (72%men,67%women)with normal radiographs (KL grade 0)using a semiquantitative scoring approach.23These results suggest that MRI is indeed much more sensitive than radiography for the detection of early OA structural changes.In a recent effort to de fine OA,the European League Against Rheumatism (EULAR)OA Task Force suggested that a con fident clinical diagnosis of knee OA may be made according to three symptoms —persistent knee pain,morning stiffness,and reduced function —and three signs —crepitus,restricted movement,and bony enlargement.24Part of the research agenda posed by the OA Task Force was to examine the diagnostic signi ficance of MRI for OA.The capacity of MRI to visualize the whole joint as well as structural changes beyond gross changes in bone and in the joint space has resulted in an explosion of research on the use of MRI for assessing diagnostic status,disease severity,and monitoring progression.25MRI is being increasingly used in clinical practice to make diagnostic decisions.Cost concerns,as well as a lack of clarity about diagnostic performance and little standardization of MRI interpretation,make it unclear,however,whether this increased use of MRI in clinical practice is entirely justi fied.These concerns about the use of MRI to facilitate OA diagnosis make rigorous testing necessary,preferably with consistent and well-thought-out MRI protocols.Despite a growing body of MRI literature in OA,there is little uniformity initsTable 1Criteria for classi fication of osteoarthritis of the knee Abbreviations:ESR,erythrocyte sedimentation rate (Westergren);RF,rheumatoid factor;SF OA,synovial fluid signs of osteoarthritis (clear,viscous,or white blood cell count <2000/mm 3).Source:Adapted from Altman,Asch,Bloch et al.4Note:Alternative for the clinical category would be 4of 6,which is 84%sensitive and 89%speci fic.Fig.1Development of radiographic osteoarthritis over a 5-year period in a 28-year-old patient with acute anterior cruciate ligament disruption.(A)Baseline posterior anterior radiograph shows equivocal osteophytes at the medial tibial plateau (arrowhead).No additional osteoarthritic changes are seen.(B)At 5-year follow-up examination,there are de finite osteophytes at the medial tibial plateau (arrow)and the medial femur (arrowhead).Equivocal joint space narrowing is also seen at the medial compartment.A diagnosis of radiographic osteoarthritis (Kellgren Lawrence grade 2)was established at the 5-year visit.Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.420D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.diagnostic application.This lack of uniformity may stem from the absence of criteria for an MRI OA structural diagnosis,as acknowledged by the Osteoarthritis Research Society Inter-national (OARSI)Imaging Working Group.Over the last 3years,the group developed an MRI-based de finition of OA that has been published.26Because most of the research today is focused on the knee,the group also focused on the knee.In the absence of MRI criteria for OA diagnosis,different methods could be used to develop such a consensus-driven de finition.One used commonly in the medical literature is the Delphi process,which is a formal method for reaching consensus.27,28The MRI-based de finition of structural OA was developed using an evidence-driven approach with results of a systematic review provided to an expert group prior to a Delphi exercise.The development of any MRI de finition for OA features will need much validation and testing in the research setting before it is ready for use in the clinical setting.Analysis of an existing data set of 160participants from the progression subcohort of the Osteoarthritis Initiative Study tested the proposed MRI de finition of tibiofemoral OA (►Table 2)against a reference standard of radiographic OA de fined as KL !2.29This modi fied Delphi approach arrived at 11propositions for a de finition of OA on MRI,two of which describe the de fining criteria.The criteria include combinations of the presence of de finite osteophyte formation,full-thickness cartilage loss,subchondral bone marrow lesion or cyst me-niscal subluxation,maceration or degenerative tears,partial-thickness cartilage loss,and bone attrition.►Table 2outlines the suggested de finitions.(Note that the de finition of a “de finite ”osteophyte was not part of the propositions.)Clearly,formal testing of this de finition of OA is needed before the criteria can be more widely used.These attempts to de fine a working de finition of OA from MRI should not be taken as attempts to deny the traditional means of diagnosing OA.MRI can likely detect disease earlier than radiography;in the preliminary analysis of the diagnostic performance of the tibiofemoral OA de finition,good speci ficity but less than optimal sensitivity was observed,likely due to earlier detec-tion.The analysis suggests that further testing should focus on comparisons other than radiographs,which maycaptureTable 2Accepted propositions for de finition of osteoarthritis on MRI after Delphi voting completion Abbreviations:OA,osteoarthritis;PF,patellofemoral.Source:Adapted from Hunter,Arden,Conaghan,et al.26†The de finition of a “de finite osteophyte ”was not delineated in the Delphi process and requires further validation.Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of OsteoarthritisHayashi et al.421D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.later stage disease and thus nullify the potential for detecting early disease that MRI might afford.26Technical Considerations of MRI and Potential PitfallsThe speci fic articular tissues to be investigated will dictate the design of imaging protocols for OA plete ana-tomical coverage is essential,of course.Other qualitative parameters need to be considered carefully including,but not limited to signal homogeneity,correct image orientation,suf ficient spatial resolution,and signal-to-noise ratio.Every effort should be made to minimize technical artifacts that can interfere with the accurate analysis of images.The length of the protocol depends on the number of sequences applied,the number of acquisitions per sequence,type of sequence,and spatial resolution;the “best ”length will be a compromise between patient comfort and tolerance,costs and image quality.Suggestions for MRI protocols to be used with semiquan-titative assessment of knee OA have been published as an OARSI/Outcome Measures in Rheumatoid Arthritis Clinical Trials consensus review.30A more recent publication by Hunter et al gave additional recommendations for pulse sequences to optimize evaluation of different joint tissues.31An optimized protocol that still allows for assessment of most of the articular features included in whole-organ evaluation would consist of proton-density (PD)weighted or T2-weight-ed fat-suppressed sequences in three orthogonal planes.32Additional sequences can add information about speci fic tissues:“cartilage-dedicated ”gradient-echo type sequences,or T1-weighted spin-echo sequences for assessment of scle-rosis or visualization of loose bodies.Individualized angula-tion of sequences can help to delineate speci fic joint structures.For example,a paracoronal T2-weighted sequence depicts the anterior cruciate ligament (ACL)in its full extent,which can help differentiate complete from partial ACL tears (►Fig.2).However,additional sequences take more time and can affect patient comfort.Image preparation also takes more time.The Osteoarthritis Initiative (OAI)published a detaileddescription of their rationale for selecting the protocol for their ongoing OA study,which is the largest of its kind.33Some pulse sequences are better than others for detecting speci fic features,and selection of the appropriate sequence depends on the aim of the study.For example,semiquantita-tive analysis of bone marrow lesions or focal cartilage defects are best done with fluid-sensitive (T2-weighted,PD-weight-ed,or intermediate-weighted)turbo spin-echo sequences with fat saturation.Gradient-echo type sequences should not be used in this case because of their demonstrated inferior sensitivity for these types of lesions (►Fig.3).34–38For synovitis,recent histologic studies have shown that only contrast-enhanced MRI can depict the true extent of the in flamed/thickened synovium (►Fig.4).39,40Adequate image quality is essential.Images need to be acquired in a standardized manner with careful adherence to protocol requirements.30An example of how to acquire optimal image data,an overview of potential problems,and how to resolve the problems is publicly available in the OAI MRI operations manual.41Magnetic field homogeneity,ho-mogeneous fat suppression in fat-saturated sequences,and the absence of motion artifacts are all important for reliable MRI evaluation.Additionally,there are several possible arti-facts to be aware of —susceptibility (including metallic arti-facts and vacuum phenomenon),magic angle,vascular pulsation,and aliasing.30Susceptibility artifacts,for example,can appear in the tibiofemoral joint space,adjacent to or superimposed on the tibiofemoral cartilage and/or a menis-cus.42Because the artifact is depicted as linear hypointensity and fluctuates over time,it can easily be taken for cartilage or meniscal damage.Awareness of this sort of pitfall is essential for accurate diagnosis.43MRI-Based Whole-Joint Evaluation of Osteoarthritis in the KneeSemiquantitative morphological whole-organ scoring was introduced in 1999and has since been applied to numerous knee OA studies.44The knee joint is thought of as an organ in itself,as it is composed of interdependent tissueswhoseFig.2Dedicated angulation of MRI sequences.(A)Sagittal intermediate-weighted fat-saturated image shows thinning and hyperintensity of the anterior cruciate ligament (arrows).A de finite diagnosis cannot be established.(B)Coronal intermediate-weighted fat-saturated image shows hyperintensity of ligament (arrowheads).(C)Paracoronal T2-weighted image con firms an intact continuous ligament that exhibits intraligamentous signal alteration (Kellgren Lawrence grade 2lesion:partial tear).Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.422D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.integrity is essential for the joint to function normally.Analyses based on this methodology have added much to our understanding of the pathophysiology and natural histo-ry of OA,and also of the clinical implications of the morpho-logical alterations.16,45–52Several semiquantitative scoring systems for knee OA assessment have been introduced.A nonexhaustive list includes the Whole-Organ Magnetic Res-onance System (WORMS),53the Knee Osteoarthritis ScoringSystem (KOSS),54the Boston Leeds Osteoarthritis Knee Score (BLOKS),55and the MRI Knee OA Score (MOAKS).31Two recent publications made head-to-head comparisons of the two most commonly used systems,WORMS and BLOKS.These studies highlighted the relative strengths and weak-nesses of the two systems.56,57MOAKS is a recent effort to combine the strengths of existing scoring systems,but little information on its use has been published.Each system evaluates a variety of features relevant to the functional integrity of the knee or potentially involved in the pathophysiology of OA.These features include articular hya-line cartilage integrity,bone marrow abnormalities,subchon-dral cysts,subarticular bone attrition,osteophytes,meniscal integrity and extrusion,cruciate and collateral ligaments integrity,synovitis and effusion,intra-articular loose bodies,periarticular cysts,and bursitides (►Fig.5).In addition to these whole-joint approaches,other scoring systems focus on speci fic OA features such as synovitis 14,58and cartilage.59–61Whole-organ semiquantitative MRI assessment has shown adequate reliability,sensitivity,and speci ficity,as well as an ability to follow the progression of lesions.1,2Several issues affect the choice of a scoring system for a given study.The outcome measures relevant to the study are clearly most important (►Fig.6).Then,available resources need to be taken into account because assessment using a complete whole-organ score is more time consuming and expensive than scoring only selected stly,the available image data set plays an important role because not all features are scorable on all sequences or with any given sequence protocol.Morphological Evaluation Using Low-and High-Field Systems,Extremity MRI,and Weightbearing MRIUse of low-field-strength (0.18to 0.2T)extremity magnets seems inadequate for detailed morphological assessment of knee OA features because they have a lower signal-to-noise ratio and limitations of fat suppression that lead tolowerFig.3The in fluence of sequence choice assessing lesions.(A)Sagittal intermediate-weighted fat-saturated image shows a super ficial focal defect at the lateral femur adjacent to the posterior horn of the lateral meniscus (arrow).(B)Sagittal dual-echo steady state (DESS)image depicts an intact articular surface in this articular region and cannot visualize the defect (arrowhead),despite the higher spatial resolution of the DESSsequence.Fig.4Sagittal T1-weighted fat-saturated image after contrastadministration.Synovitis is depicted as hyperintense linear thickening along the joint cavity (arrows).Joint effusion is visualized asintra-articular hypointensity.Only contrast-enhanced images can differentiate between joint effusion and synovitis.Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.423D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.image quality than with 1.5-or 3-T systems.Dedicated 1.0-T extremity MRI has demonstrated good to excellent intra-and inter-reader reliability for semiquantitative morphological assessment of knee OA features when compared with 1.5-T imaging (►Fig.7).62Recently,3-T systems have demonstrated promising results with optimizing morphological and com-positional cartilage imaging in the knee.37,63The signal-to-noise ratio is about twice as great at 3T as it is at 1.5T,affording improved image quality and spatial resolution,with acquisition times similar to those of a 1.5-T system.A poten-tial downside of 3-T imaging is that the magnetic susceptibil-ity in tissues is exacerbated,the energy deposited in the subjects ’tissues is higher,images are more sensitive to flow,and there is an increase in chemical shift with 3-T compared with 1.5-T imaging.So far,7-T MRI in humans has been applied only in a research setting.64,65In the future,7-T systems may be able to produce higher resolution images with a shorter scan time than 3-T systems.The available protocols for 7-T imaging,however,have not shown any superiority over 3-T protocols for knee cartilage evaluation.66Quantitative Morphological Evaluation of CartilageQuantitative analysis of knee OA features has been applied mainly to cartilage morphology,exploiting thethree-Fig.5Longitudinal bone marrow lesion assessment over 4years.From left to right,top row:Baseline image shows small subchondral bone marrow lesion (BML)adjacent to posterior horn of medial meniscus (arrowhead).At 1year,the BML has increased in size (arrowheads).Bottom row:At 2years,a further increase is noted (small arrow).At 3years,the BML has completely resolved,and at 4years a new BML has developed in the same location (large arrow).Fluctuation in size is characteristic of subchondral bone lesions inosteoarthritis.Fig.6Progression of osteoarthritis.(A)Sagittal intermediate-weighted image at baseline depicts a small horizontal tear in the posterior horn of the medial meniscus (arrow).A small anterior osteophyte at the medial femur is also shown (arrowhead).(B)At 24-month follow-up,there is marked cartilage loss in the medial weightbearing part of the femur (arrowheads).There is also marked joint effusion (asterisk).Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.424D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.dimensional nature of MRI data for assessing tissue param-eters such as volume,thickness,or other continuous vari-ables.67The strengths of quantitative measurements of cartilage or other articular tissues in OA are that they are less observer dependent and more objective than scoring methods and that relatively small changes in cartilage thickness or volume may be detected over time.68Correctly segmenting the cartilage requires well-trained users,work-ing either manually or with segmentation software (►Fig.8).69Most investigations have focused on cartilage volume,but volume has its limitations.Discrimination between patients with OA and healthy subjects is limited because men in general,and anybody with large bones,has larger joint surfaces and more cartilage volume,so there is a wide overlap between groups.70In longitudinal studies,subchondral bone area has been shown to increase with age in general,regardless of OA status.71To overcome these problems,new analytic strategies called “ordered values approach ”and subsequently “extended ordered values ap-proach ”have been proposed.72These analytic methods enable more ef ficient measurement of changes in cartilage thickness,independent of anatomical locations,and they seem to result in improved discrimination be-tween healthy subjects and OA patients.With the extended ordered values approach,changes in subregional thickness in the medial and lateral tibial and femoral cartilage plates are sorted in ascending order.This method showed better sensitivity for detecting differences in longitudinal rates of cartilage loss than anatomical subregions and radiography.72The validity and reproducibility of quantitative cartilage morphometry at 1.5T have been reported previously.68Results based on images acquired with a dedicated 1.0-T extremity unit were consistent with those from a 1.5-T system,albeit less reproducible.73Quantitative cartilage morphometry using a 0.2-T system has been proposed,but has not yet been validated against higher field strengths or external standards.74A study comparing cartilage morphom-etry performed at 3T and 1.5T found poorer precision for the 3T when thin (1.0mm)coronal sections were acquired with a 3-T system.75Results of morphometric assessment from dual-echo steady state images,acquired at 3T in the OAI,were found to be consistent with those from fast low-angle shot (FLASH)images and to display test-retest precision errors similar to FLASH images in the tibiofemoral joint.76,77Compositional/Physiologic MRI of CartilageSome of the advanced MRI techniques enable assessment of biochemical properties of different joint tissues and thus are very sensitive to early premorphological changes.78Most studies applying these compositional/physiologic MRI tech-niques have focused on cartilage,although other tissues such as meniscus and ligaments can also be evaluated.79Fig.7Comparison of dedicated extremity MRI and 1.5-T large-bore MRI.(A)1.0-T extremity MRI (sagittal intermediate-weighted fat-saturated image)shows bone marrow lesions in the medial femur and anterior medial tibia (arrows).(B)A 1.5-T MRI image acquired on the same day con firms the lesions at the same location(arrows).Fig.8Cartilage segmentation.Coronal fast low-angle shot image depicts cartilage as a very hyperintense structure in comparison with subchondral bone and intra-articular fluid.It is excellently suited for segmentation and consequent three-dimensional analysis.Image shows different cartilage plates color coded after segmentation.Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.425D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.Sodium MRI and the delayed gadolinium-enhanced MRI of cartilage (dGEMRIC)techniques are designed to measure the fixed charge density in cartilage,adapting established bio-chemical and histologic approaches for measurement of proteoglycan content.80The techniques are based on the premise that mobile ions will disperse into the cartilage in relation to the concentration of the charged proteoglycan molecules;in the MRI implementation of this principle,the mobile ions are the naturally abundant sodium,or the negatively charged MRI contrast agent gadolinium-diethyle-netriamine penta-acetic acid (Gd[DTPA]2À)(Magnevist,Ber-lex,NJ).Positively charged sodium ions distribute themselves in cartilage in proportion to the concentration of negatively charged glycosaminoglycan molecules.Reproducibility of sodium MRI was found to be similar in both healthy controls and OA subjects.81However,limitations include relatively low resolution,dif ficulty analyzing the thin and curved femoral cartilage,very fast and variable T2,and the need for specialized software.78In the dGEMRIC technique,Gd(DTPA)2Àis injected intra-venously,and images are acquired usually $90minutes after the injection to give the contrast agent time to diffuse into the cartilage before imaging (►Fig.9).The charge on the Gd (DTPA)2Àmolecule disperses into the cartilage inversely to the concentration of negatively charged glycosaminoglycan.Clinical trials of dGEMRIC have demonstrated a correlation between dGEMRIC and the radiographic stage of OA,although a “floor effect ”might be present;dGEMRIC may already be at a relatively low level in moderate and severe disease.82A small clinical trial showed an increase in the dGEMRIC score in tibial cartilage regions of interest in subjects receiving collagen hydrolysate,in comparison with the placebo subjects in which the dGEMRIC score decreased.An interventional study,evaluating the effect of weight loss on articular carti-lage,showed an improvement in articular cartilage quality re flected as an increase in the dGEMRIC index over 12months for the medial but not for the lateral tibiofemoral compart-ment.This finding supports the idea that body weight affects disease progression and emphasizes the role of weight loss in clinical and structural improvement.83Despite some promise,implementation of dGEMRIC has been relatively limited.Although easily applicable on most MRI systems,the gadolinium-based contrast agent has to be injected,and there is a delay between injection and scanning.Ionic and nonionic contrast agents for dGEMRIC were ex-plored in a recent study;the ionic contrast agents seem to offer better discrimination of cartilage status than the non-ionic contrast agents.84T1ρis a time constant that characterizes magnetic relaxa-tion of spins under the in fluence of a radiofrequency field parallel to the spin magnetization.78The resultant contrast is sensitive to the low-frequency interactions between water molecules and their local macromolecular environment,such as glycosaminoglycan and collagen,which constitute most of the extracellular matrix in cartilage.T1ρis complex to implement on MR scanners and limited by radiofrequency power deposition.One recent study demonstrated that acute loading of the knee joint resulted in a signi ficant decrease in T1ρof the medial tibiofemoral compartment,especially in cartilage regions with small focal defects.85This suggests that changes of T1ρvalues under loading may be related to cartilage biomechanical and structural properties.T2mapping has been used to describe the molecular composition of hyaline cartilage in the knee joint on the basis of collagen structure and hydration.86In healthy articular cartilage,T2values increase from deep to super ficial cartilage layers.87It has been shown that T2values are related to age and activity levels,that they vary between tibial and femoral cartilage,and they are associated with OA severity.88–90In addition to the transverse relaxation time (T2)of cartilage,T2Ãrelaxation measures have been tested for depiction of the collagen matrix.T2Ãmapping was shown to be a repeatable process that can differentiate between the OA subjects and control groups.91Systematic ReviewsA systematic review of the responsiveness and reliability of MRI-based measures of knee OA morphological alterations was recently published.The inter-and intra-readerintraclassFig.9Compositional MRI.(A)Sagittal intermediate-weighted fat-saturated image shows a horizontal tear of the posterior horn of the medial meniscus (arrow).(B)Corresponding baseline color-coded T1-weighted image shows normal delayed gadolinium-enhanced MRI of cartilage (dGEMRIC)map.(C)At 24-month follow-up there is a marked decrease in the dGEMRIC index in the medial femoral cartilage coded in red (arrows).Incident partial meniscal maceration can also be seen (arrowhead).Seminars in Musculoskeletal RadiologyVol.16No.5/2012MRI of Osteoarthritis Hayashi et al.426D o w n l o a d e d b y : Y a l e U n i v e r s i t y L i b r a r y . C o p y r i g h t e d m a t e r i a l.。