Department of Orthopaedic Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090 Vienna, Austria.
J Orthop Res. 2012 Feb;30(2):214-20. doi: 10.1002/jor.21521. Epub 2011 Aug 4.
Animal models simulating osteoarthritis are frequently associated with irreversible changes in biomechanics. Although these models successfully induce osteoarthritis, results of experimental repair procedures are impaired by biomechanical problems. The aim of this study was to define the critical size of a chondral lesion to induce unicompartmental osteoarthritis in a stable joint. Sixteen sheep were randomly divided into four treatment groups. A cartilage defect (7- or 14-mm diameter) was created in the weight-bearing zone of the medial femoral condyle. The sheep were mobilized for 6 or 12 weeks. Osteoarthritis was determined by gross assessment, India ink staining, histology (Mankin score), and analysis of COMP in the serum. In the 6-week group, only minor osteoarthritis was registered for either defect size. After 12 weeks, the 14-mm defect induced minor osteoarthritis at the femoral condyle and caused significant degenerative changes at the tibial articular cartilage and the meniscus. The 7-mm defect created focal unicompartmental osteoarthritis at the medial femoral condyle and minor degenerative changes at the corresponding tibia. A 7-mm full-thickness chondral defect with a weight-bearing regimen of 12 weeks induced local osteoarthritis at the medial compartment in an otherwise stable joint as aimed.
动物模型模拟骨关节炎常伴有生物力学的不可逆改变。尽管这些模型成功地诱导了骨关节炎，但实验修复程序的结果因生物力学问题而受到影响。本研究的目的是确定软骨病变的临界大小，以在稳定关节中诱导单间室骨关节炎。16 只绵羊被随机分为四组。在股骨内侧髁的负重区创建软骨缺损（7 或 14mm 直径）。绵羊在 6 或 12 周内进行运动。通过大体评估、印度墨水染色、组织学（Mankin 评分）和血清中 COMP 的分析来确定骨关节炎。在 6 周组中，两种缺损大小均仅记录到轻微的骨关节炎。12 周后，14mm 缺损在股骨髁处引起轻微骨关节炎，并在胫骨关节软骨和半月板处引起明显退行性变化。7mm 缺损在股骨内侧髁处形成局灶性单间室骨关节炎，并在相应的胫骨处引起轻微退行性变化。在其他方面稳定的关节中，采用 12 周的负重方案，7mm 全层软骨缺损可诱导内侧间室的局部骨关节炎。
