scholarly journals Membrane-Associated IL-1 Contributes to Chronic Synovitis and Cartilage Destruction in Human IL-1α Transgenic Mice

2003 ◽  
Vol 172 (1) ◽  
pp. 577-584 ◽  
Author(s):  
Yasuo Niki ◽  
Harumoto Yamada ◽  
Toshiyuki Kikuchi ◽  
Yoshiaki Toyama ◽  
Hideo Matsumoto ◽  
...  
2021 ◽  
Vol 10 (6) ◽  
pp. 1241
Author(s):  
Yoshiya Tanaka

In rheumatoid arthritis, a representative systemic autoimmune disease, immune abnormality and accompanying persistent synovitis cause bone and cartilage destruction and systemic osteoporosis. Biologics targeting tumor necrosis factor, which plays a central role in the inflammatory process, and Janus kinase inhibitors have been introduced in the treatment of rheumatoid arthritis, making clinical remission a realistic treatment goal. These drugs can prevent structural damage to bone and cartilage. In addition, osteoporosis, caused by factors such as menopause, aging, immobility, and glucocorticoid use, can be treated with bisphosphonates and the anti-receptor activator of the nuclear factor-κB ligand antibody. An imbalance in the immune system in rheumatoid arthritis induces an imbalance in bone metabolism. However, osteoporosis and bone and cartilage destruction occur through totally different mechanisms. Understanding the mechanisms underlying osteoporosis and joint destruction in rheumatoid arthritis leads to improved care and the development of new treatments.


Arthritis ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Mohammad Javad Fattahi ◽  
Abbas Mirshafiey

Rheumatoid arthritis (RA) is a chronic, autoimmune, and complex inflammatory disease leading to bone and cartilage destruction, whose cause remains obscure. Accumulation of genetic susceptibility, environmental factors, and dysregulated immune responses are necessary for mounting this self-reacting disease. Inflamed joints are infiltrated by a heterogeneous population of cellular and soluble mediators of the immune system, such as T cells, B cells, macrophages, cytokines, and prostaglandins (PGs). Prostaglandins are lipid inflammatory mediators derived from the arachidonic acid by multienzymatic reactions. They both sustain homeostatic mechanisms and mediate pathogenic processes, including the inflammatory reaction. They play both beneficial and harmful roles during inflammation, according to their site of action and the etiology of the inflammatory response. With respect to the role of PGs in inflammation, they can be effective mediators in the pathophysiology of RA. Thus the use of agonists or antagonists of PG receptors may be considered as a new therapeutic protocol in RA. In this paper, we try to elucidate the role of PGs in the immunopathology of RA.


2011 ◽  
Vol 70 (Suppl 2) ◽  
pp. A76-A76
Author(s):  
A. Stratis ◽  
C. Wehmeyer ◽  
C. Cromme ◽  
C. Wunrau ◽  
G. Kollias ◽  
...  

2005 ◽  
Vol 52 (12) ◽  
pp. 3713-3717 ◽  
Author(s):  
Jukka Morko ◽  
Riku Kiviranta ◽  
Kirsi Joronen ◽  
Anna-Marja Säämänen ◽  
Eero Vuorio ◽  
...  

2001 ◽  
Vol 159 (6) ◽  
pp. 2309-2320 ◽  
Author(s):  
Peter L.E.M. Van Lent ◽  
Karin Nabbe ◽  
Arjen B. Blom ◽  
Astrid E.M. Holthuysen ◽  
Annet Sloetjes ◽  
...  

2008 ◽  
Vol 41 ◽  
pp. S189
Author(s):  
Kathryn Stok ◽  
Danièle Noël ◽  
Florence Apparailly ◽  
David Gould ◽  
Yuti Chernajovsky ◽  
...  

2007 ◽  
Vol 73 (1) ◽  
pp. 136-146 ◽  
Author(s):  
Na Lin ◽  
Chunfang Liu ◽  
Cheng Xiao ◽  
Hongwei Jia ◽  
Keisuke Imada ◽  
...  

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