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胶原诱导性关节炎大鼠模型中破坏情况的评估:骨赘形成。

Evaluation of destruction in a collagen-induced arthritis rat model: Bony spur formation.

作者信息

Hu Yiping, Yang Yi, Luo Bin

机构信息

Center for Translational Medicine Research and Development, Shenzhen Institute of Advanced Technology, Chinese Academy of Science, Shenzhen, Guangdong 518055, P.R. China.

Shenzhen College of Advanced Technology, University of Chinese Academy of Sciences, Shenzhen, Guangdong 518055, P.R. China.

出版信息

Exp Ther Med. 2017 Sep;14(3):2563-2567. doi: 10.3892/etm.2017.4817. Epub 2017 Jul 19.

DOI:10.3892/etm.2017.4817
PMID:28962195
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5609218/
Abstract

Over the past 40 years, the collagen-induced arthritis (CIA) animal model has been widely used as a model of rheumatoid arthritis (RA). However, no model is able to completely depict the characteristics of cartilage destruction to date. In the later stage of joint cartilage destruction, bony spurs form in RA. This bony spur formation is an important symptom in the pathological development of RA. In the present study, CIA was used to elucidate the pathological process of bony spur formation. Joint damage and spur formation in the animal model was detected by radiology and histology. Radiology identified bony spurs in the knee and foot joints, which worsened as the disease progressed. Furthermore, following observations of histological sections, fusion and damage of the articular cartilage, as well as a higher number of osteoclasts, were identified. Previous results have determined that bony spurs may be involved in another pathological process that occurs during the later stages of RA. Therefore, further studies investigating this symptom are required to improve the understanding of RA and facilitate the development of an appropriate treatment for RA.

摘要

在过去的40年里,胶原诱导性关节炎(CIA)动物模型已被广泛用作类风湿性关节炎(RA)的模型。然而,迄今为止,没有一种模型能够完全描绘软骨破坏的特征。在关节软骨破坏的后期,RA中会形成骨赘。这种骨赘形成是RA病理发展中的一个重要症状。在本研究中,使用CIA来阐明骨赘形成的病理过程。通过放射学和组织学检测动物模型中的关节损伤和骨赘形成。放射学检查发现膝关节和足部关节出现骨赘,且随着疾病进展而恶化。此外,在观察组织切片后,发现关节软骨融合和损伤,以及破骨细胞数量增多。先前的研究结果已确定,骨赘可能参与RA后期发生的另一种病理过程。因此,需要进一步研究该症状,以增进对RA的了解,并促进开发针对RA的适当治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/5609218/384e4fcb67fd/etm-14-03-2563-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/5609218/ddd22342c40e/etm-14-03-2563-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/5609218/384e4fcb67fd/etm-14-03-2563-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/5609218/ddd22342c40e/etm-14-03-2563-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6128/5609218/384e4fcb67fd/etm-14-03-2563-g02.jpg

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