The role of RANKL in the pathogenesis of peripheral joint bone destruction in ankylosing spondylitis
- VernacularTitle:细胞核因子?B受体活化因子配基在强直性脊柱炎的表达及意义
- Author:
Wei ZHAO
;
Feng HUANG
- Publication Type:Journal Article
- Keywords:
spondylitis, ankylosing;
arthritis, rheumatoid;
receptor activator of NF-?B ligand (RANKL)
- From:
Medical Journal of Chinese People's Liberation Army
1981;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To determine the protein levels of receptor activator of NF ?B ligand (RANKL) in synovial tissues obtained from ankylosing spondylitis (AS) patients, and compare the expression level and distribution of RANKL protein in AS with that in rheumatoid arthritis (RA), osteoarthritis (OA) and normal synovial tissues, in order to define the role of RANKL expressions in the pathogenesis of arthritis and bone destruction in AS. Methods Immunohistochemical analysis was performed using monoclonal antibodies to determine RANKL expression in 13 AS, 16 RA, 17 OA patients and 6 healthy controls. The protein levels of RANKL in labeled synovial tissue sections were quantified by digital image analysis and semiquantitative analysis to compare the expression of RANKL in positve cells among different patient groups and normal subjects. In addition, RANKL expression was correlated with certain inflammatory indices (including ESR, CRP, blood platelet count) and radiological stage of involved joints, respectively. Results Positive staining of RANKL was seen respectively in all 13 AS patients and 16 patients with RA, and the positive expression was distributed predominantly in the synovial lining layer and at synovium cartilage junctions. There was no significant difference between levels of RANKL expression in tissues from patients with AS and in tissues from RA. No positive staining of RANKL was observed in 6 normal subjects and all OA patients. Positive correlation was found between RANKL protein expression and X ray stage of bone destruction of involved joints in the patients with AS and RA ( r =0 73,0 41, P =0 003,0 021 respectively). Conclusions RANKL plays an important role in the pathogenesis of bone destruction in patients with AS, and its elevated expression level may reflect the degree of bone destruction of peripheral joints in AS patients. Since similar patterns of RANKL expression are found in synovial tissues from AS and RA patients, therefore, we conclude that the pathogenesis of bone destruction in AS may be similar to that in RA
