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Serial Ultrasonography Documents New Bone Formation At Entheses in Spondyloarthritis Ralf G. Thiele 1, Bethany A. Marston1, Darren Tabechian2, Allen P. Anandarajah3 and Christopher T. Ritchlin4, 1University of Rochester, Rochester, NY, 2Univ of Rochester Schl of Med, Rochester, NY, 3Univ of Rochester Medical Ctr, Rochester, NY, 4University of Rochester Medical Center, Rochester, NY Presentation Number: 1347 Background/Purpose: Entheseal inflammation is a hallmark feature of spondyloarthritis (SpA). New bone formation is thought to be part of the pathogenesis of joint damage and ankylosis in SpA. A progression from enthesitis to new bone formation and joint damage has been postulated but is difficult to assess as a process in vivo. Conventional radiography cannot visualize tendons, and MRI may be less sensitive in detecting small calcifications than ultrasound (US). The aim of this study was to assess development of enthesitis in vivo using serial high resolution US. Method: 144 images and video clips of 8 clinically symptomatic and sonographically abnormal entheses in 7 patients with SpA (psoriatic arthritis, n=4; reactive arthritis, n=2; ankylosing spondylitis (AS), n=1) were obtained over 2 years (long and short axis views in gray scale and power Doppler, and video clips to document pulsatile flow). The 8 entheses included: origin of patellar ligament: n=3; insertion of Achilles tendon, n=4; insertion of medial collateral ligament of first metatarsophalangeal joint, n=1. US criteria for enthesitis were: 1) cortical irregularity at interface of ligament or tendon and bone; 2) pulse synchronous Doppler signal at interface and within body of tendon or ligament; 3) loss of densely packed fibrillar pattern with decrease of hyperechogenicity and increased thickness of tendon or ligament at insertion or origin (edema). Criterion for entheseal new bone formation was: hyperechoic material within body of tendon or ligament that was not seen on prior studies. All studies were performed by a rheumatologist certified in musculoskeletal ultrasound, with 20 years' experience. Transducer frequencies of 10-18 MHz were used. All patients underwent treatment: NSAIDs alone, n=1; methotrexate and NSAIDs, n=1, methotrexate and TNF-inhibitor, n=5. Result: Inflammatory changes by US criteria decreased in all 8 entheses followed after 15-24 months: No more Doppler signal was seen at the entheses, hypoechogenicity and thickness had decreased in all at the time of the last study. CRP and ESR levels had remained within normal limits in all patients throughout the observation period, and were not suitable as markers of entheseal inflammation in our patients. Clinical entheseal pain was present in all at study entry and none at the time of the last US study. Newly formed hyperechoic material was eventually seen in all entheses (mean time to development 17 months). This calcific appearing material was present at the site of previously seen Doppler signal in all cases (Figure). In the case of AS, enthesitis led to calcification of a collateral ligament. Conclusion: Within entheses, sites of deposition of calcified material correlate with sites of prior hyperemia. In AS, enthesitis preceded collateral ligament calcification in our study. Serial US can document disease development from enthesitis to new bone formation. |
系列超声发现脊柱关节炎附着点处新骨形成 Ralf G. Thiele , et al. ACR 2011. Present No: 1347
背景/目的: 方法:7例SpA患者，其中银屑病关节炎4例，反应性关节炎2例，强直性脊柱炎1例。8处临床和超声异常的附着点炎，2年内共获得144幅图像和视频剪辑(灰阶和能量多普勒的长、短轴视图, 视频剪辑来记录脉动流)。8处附着点包括:髌韧带的起源:n = 3; 跟腱插入处，n = 4; 内侧副韧带插入第一跖趾关节处,n = 1。附着点炎标准是:1) 骨肌腱和韧带表面的不规则或;2) 肌腱或韧带表面和内部有脉冲多普勒信号;3)失去致密的纤维状包裹, 肌腱或韧带插入或起始处回声增强和厚度增加(水肿)。附着点的新骨形成标准是: 在先前检测中未见的肌腱或韧带内高回声物质。由一位有20年经验的具骨骼肌肉超声资质的风湿科医生完成所有的检测。传感器频率为10-18兆赫。所有病人都接受治疗:单用NSAIDS,n = 1;甲氨蝶呤和NSAID,n = 1、甲氨蝶呤和TNF-抑制剂,n = 5。 结果: US对8处附着点炎15-24个月的炎症随访显示：附着点处没有出现更多的多普勒信号，高回声和增厚在末次随访时都有减少。CRP和ESR水平在整个随访期间保持在正常范围，因而不适合在本研究中作为附着点炎症的标记。研究入组时的临床附着点痛在末次随访时都未见。所有附着点处最终都看到新形成的高回声物质(平均时间17个月)。所有患者的这些钙化样物质就出现在以往多普勒信号的部位 (图)。在AS患者,附着点炎导致侧副韧带钙化的发生。 结论:在附着点内，钙化物质沉积部位与既往充血部位相关。本研究中的AS患者， 附着点炎会继发侧副韧带钙化。我们可以从连续US发现，疾病从附着点炎到新骨形成的过程。 |
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