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- Title
骨性关节炎发病机制研究进展.
- Authors
袁普卫; 杨威; 康武林; 李珣; 刘德玉
- Abstract
Osteoarthritis (OA) is a chronic progressive disease. The most common clinical manifestation is chronic joint pain, with limited activity,severe joint swelling and stiffness,even deformity. The main pathological changes are articular cartilage degeneration and its local bone sclerosis,but its specific pathogenesis is unknown. It is widely believed that the increase in bone internal pressure plays an important role in the pathogenesis of OA. However,with the urgent need in the clinic and the rapid development of molecular biology,immunology and other related disciplines,the pathogenesis research has new progress. It is gradually believed that the degradation of matrix metalloproteinases,cell apoptosis,cytokines (CK) ,and aquaporins (AQPs) are also involved in the development of OA,especially the latter two. Cytokines are polypeptide molecules that are produced by a variety of cells,which have the function of regulating immune response. Among others,interleukin 1 (IL-1) and insulin like growth factors (IGFs) play a significant role in OA. IL-1 inhibits the synthesis of glucosamine and collagen and promotes their hydrolysis. IGFs promote the proliferation of chondrocytes and synthesis of cartilage matrix. AQPs regulates micro environment by regulation of water flow of the chondrocytes,and maintains the stability of cellular osmolarity and the balance of synthesis and degradation of the extracellular matrix. The subtypes of AQPs in cartilage are AQP1 and AQP3,which are closely related to articular cartilage degeneration. However,further research is needed for the specific pathological mechanism.
- Publication
Chinese Journal of Osteoporosis, 2016, Vol 22, Issue 7, p902
- ISSN
1006-7108
- Publication type
Article
- DOI
10.3969/j.issn.1006-7108.2016.07.023