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Chondral Defects Cause Kissing Lesions in a Porcine Model.
CARTILAGE ( IF 2.8 ) Pub Date : 2020-08-22 , DOI: 10.1177/1947603520951636
Wenqiang Yan 1 , Xingquan Xu 1 , Qian Xu 1 , Ziying Sun 1 , Zhongyang Lv 1 , Rui Wu 1 , Wenjin Yan 1 , Qing Jiang 1, 2 , Dongquan Shi 1
Affiliation  

Objective

To assess the development of kissing lesions 12 months after the generation of full-thickness chondral defects.

Design

Eight minipigs were randomized into 2 groups: the Φ8.5 mm full-thickness chondral defect group (8.5FT group) and the Φ6.5 mm full-thickness chondral defect group (6.5FT group). The Φ8.5 mm or Φ6.5 mm full-thickness chondral defects were prepared in the medial femoral condyle. Knee magnetic resonance imaging (MRI) was performed before sacrifice. India ink staining was performed to macroscopically assess kissing lesions. Histologic staining (hematoxylin-eosin [HE], safranin O/fast green, toluidine blue staining) and immunohistochemistry (collagen I, collagen II, collagen X, MMP-3) were performed. Microcomputed tomography analysis was completed to assess subchondral bone alterations.

Results

Obvious kissing lesions were observed on the tibial plateau. Knee MRI demonstrated high cartilage signal intensity in the medial femoral condyle and opposite tibial plateau. HE staining demonstrated cartilage fibrillation and prominent cell death. The depletion of safranin O, toluidine blue staining, and collagen II was observed in the kissing lesion areas. The kissing lesion areas demonstrated increased collagen I, Collagen X, and MMP-3 expression. The 8.5FT group showed a significantly lower mean trabecular number (2.80 1/mm) than the control group (3.26 1/mm). The 6.5FT group showed a significantly increased mean trabecular thickness (0.54 mm) and a decreased mean trabecular number (2.71 1/mm) compared to the control group (0.32 mm; 3.26 1/mm).

Conclusions

Obvious kissing lesions were observed on the tibial plateau. Knee MRI demonstrated high cartilage signal The presented findings support the development of kissing lesions caused by full-thickness chondral defects.



中文翻译:

软骨缺陷导致猪模型中的接吻损伤。

客观的

评估全层软骨缺损产生后 12 个月后接吻损伤的发展情况。

设计

将8只小型猪随机分为2组:Φ8.5 mm全层软骨缺损组(8.5FT组)和Φ6.5 mm全层软骨缺损组(6.5FT组)。在股骨内侧髁处制备Φ8.5mm或Φ6.5mm全层软骨缺损。处死前进行膝关节磁共振成像(MRI)。进行印度墨水染色以宏观评估接吻损伤。进行组织学染色(苏木精-伊红 [HE]、番红 O/固绿、甲苯胺蓝染色)和免疫组织化学(胶原蛋白 I、胶原蛋白 II、胶原蛋白 X、MMP-3)。完成显微计算机断层扫描分析以评估软骨下骨的改变。

结果

胫骨平台处观察到明显的接吻损伤。膝关节 MRI 显示股骨内侧髁和相对的胫骨平台软骨信号强度较高。HE染色显示软骨纤维颤动和显着的细胞死亡。在接吻病变区域观察到番红 O、甲苯胺蓝染色和胶原蛋白 II 的消耗。接吻病变区域显示 I 型胶原蛋白、X 型胶原蛋白和 MMP-3 表达增加。8.5FT 组的平均小梁数量 (2.80 1/mm) 显着低于对照组 (3.26 1/mm)。与对照组(0.32 mm;3.26 1/mm)相比,6.5FT 组的平均小梁厚度显着增加(0.54 mm),平均小梁数量显着减少(2.71 1/mm)。

结论

胫骨平台处观察到明显的接吻损伤。膝关节 MRI 显示出高软骨信号 所提出的结果支持由全层软骨缺陷引起的接吻损伤的发展。

更新日期:2020-08-23
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