Tóth Ferenc, David Frédéric H, LaFond Elizabeth, Wang Luning, Ellermann Jutta M, Carlson Cathy S
Department of Veterinary Population Medicine, College of Veterinary Medicine, University of Minnesota, 435 AnSci/VetMed, 1988 Fitch Avenue, St. Paul, Minnesota, 55108.
Department of Veterinary Clinical Sciences, University of Minnesota, St. Paul, Minnesota.
J Orthop Res. 2017 Apr;35(4):868-875. doi: 10.1002/jor.23332. Epub 2016 Jun 19.
In vivo visualization of subclinical osteochondrosis (OC) lesions, characterized by necrosis of epiphyseal growth cartilage, is necessary to clarify the pathogenesis of this disease. Hence, our objectives were to demonstrate induced necrosis of the epiphyseal cartilage in vivo using MRI and to monitor progression or resolution of resulting lesions. We also aimed to improve the goat model of OC by introducing controlled exercise. Vascular supply to the epiphyseal cartilage was surgically interrupted in four 5-day-old goats to induce ischemic cartilage necrosis in a medial femoral condyle. Starting 3 weeks postoperatively, goats underwent daily controlled exercise until euthanasia at 6, 10, 11 (n = 2) weeks postoperatively. T maps of operated and control femora were obtained in vivo at 3 (n = 4), 6 (n = 4), 9 (n = 3), and 11 (n = 2) weeks postoperatively using a 3 T MR scanner. In vivo MRI findings were validated against MRI results obtained ex vivo at 9.4 T in three goats and compared to histological results in all goats. Surgical interruption of the vascular supply caused ischemic cartilage necrosis in three out of four goats. T maps obtained in vivo at 3 T identified regions of increased relaxation time consistent with discrete areas of cartilage necrosis 3-11 weeks postoperatively and demonstrated delayed progression of the ossification front at 9 (n = 1) and 11 (n = 2) weeks postoperatively. In vivo MRI findings were confirmed by ex vivo MRI at 9.4 T and by histology. Identification of cartilage necrosis in clinical patients in the early stages of OC using T maps may provide valuable insight into the pathogenesis of this condition. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:868-875, 2017.
亚临床骨软骨病(OC)病变以骨骺生长软骨坏死为特征,对其进行体内可视化对于阐明该疾病的发病机制至关重要。因此,我们的目标是利用磁共振成像(MRI)在体内证实骨骺软骨的诱导性坏死,并监测由此产生的病变的进展或消退情况。我们还旨在通过引入控制性运动来改进OC山羊模型。对4只5日龄山羊的骨骺软骨血管供应进行手术阻断,以诱导股骨内侧髁的缺血性软骨坏死。术后3周开始,山羊每天进行控制性运动,直至术后6、10、11周(n = 2)实施安乐死。术后3周(n = 4)、6周(n = 4)、9周(n = 3)和11周(n = 2)时,使用3T MR扫描仪在体内获取手术侧和对照侧股骨的T图。体内MRI结果与3只山羊在9.4T下的体外MRI结果进行验证,并与所有山羊的组织学结果进行比较。手术阻断血管供应导致4只山羊中的3只出现缺血性软骨坏死。在3T下体内获取的T图显示,术后3 - 11周弛豫时间增加的区域与软骨坏死的离散区域一致,并在术后9周(n = 1)和11周(n = 2)显示骨化前沿进展延迟。体内MRI结果通过9.4T的体外MRI和组织学得到证实。使用T图在OC临床患者早期识别软骨坏死可能为该疾病的发病机制提供有价值的见解。© 2016骨科研究协会。由威利期刊公司出版。《矫形外科学研究》35:868 - 875,2017。