scholarly journals Cr1, CD35 IN synovial fluid from patients with inflammatory joint diseases

1997 ◽  
Vol 40 (3) ◽  
pp. 520-526 ◽  
Author(s):  
Salima Sadallah ◽  
Estelle Lach ◽  
Hans U. Lutz ◽  
Sibylle Schwarz ◽  
Pierre-André Guerne ◽  
...  
Rheumatology ◽  
2010 ◽  
Vol 49 (4) ◽  
pp. 671-682 ◽  
Author(s):  
A. Baillet ◽  
C. Trocme ◽  
S. Berthier ◽  
M. Arlotto ◽  
L. Grange ◽  
...  

Rheumatology ◽  
1998 ◽  
Vol 37 (7) ◽  
pp. 773-778 ◽  
Author(s):  
M. A. Iniguez ◽  
J. L. Pablos ◽  
P. E. Carreira ◽  
F. Cabre ◽  
J. J. Gomez-Reino

2011 ◽  
Vol 52 (3) ◽  
pp. 169-175 ◽  
Author(s):  
Eric Röhner ◽  
Georg Matziolis ◽  
Carsten Perka ◽  
Bernd Füchtmeier ◽  
Timo Gaber ◽  
...  

1994 ◽  
Vol 37 (3) ◽  
pp. 342-348 ◽  
Author(s):  
Alicia Humbría ◽  
Federico Díaz-González ◽  
Miguel R. Campanero ◽  
Alicia G. Arroyo ◽  
Armando Laffón ◽  
...  

2000 ◽  
Vol 206 (2) ◽  
pp. 85-100 ◽  
Author(s):  
Renate Claus ◽  
Thomas Bittorf ◽  
Hermann Walzel ◽  
Josef Brock ◽  
Robert Uhde ◽  
...  

Author(s):  
Marco Di Carlo ◽  
Gianluca Smerilli ◽  
Fausto Salaffi

Abstract Purpose of the review Pain in chronic inflammatory joint diseases is a common symptom reported by patients. Pain becomes of absolute clinical relevance especially when it becomes chronic, i.e., when it persists beyond normal healing times. As an operational definition, pain is defined chronic when it lasts for more than 3 months. This article aims to provide a review of the main mechanisms underlying pain in patients with chronic inflammatory joint diseases, discussing in particular their overlap. Recent findings While it may be intuitive how synovial inflammation or enthesitis are responsible for nociceptive pain, in clinical practice, it is common to find patients who continue to complain of symptoms despite optimal control of inflammation. In this kind of patients at the genesis of pain, there may be neuropathic or nociplastic mechanisms. Summary In the context of chronic inflammatory joint diseases, multiple mechanisms generally coexist behind chronic pain. It is the rheumatologist’s task to identify the mechanisms of pain that go beyond the nociceptive mechanisms, to adopt appropriate therapeutic strategies, including avoiding overtreatment of patients with immunosuppressive drugs. In this sense, future research will have to be oriented to search for biomarkers of non-inflammatory pain in patients with chronic inflammatory joint diseases.


Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 902
Author(s):  
Susanne N. Wijesinghe ◽  
Mark A. Lindsay ◽  
Simon W. Jones

Osteoarthritis (OA) and rheumatoid arthritis (RA) are two of the most common chronic inflammatory joint diseases, for which there remains a great clinical need to develop safer and more efficacious pharmacological treatments. The pathology of both OA and RA involves multiple tissues within the joint, including the synovial joint lining and the bone, as well as the articular cartilage in OA. In this review, we discuss the potential for the development of oligonucleotide therapies for these disorders by examining the evidence that oligonucleotides can modulate the key cellular pathways that drive the pathology of the inflammatory diseased joint pathology, as well as evidence in preclinical in vivo models that oligonucleotides can modify disease progression.


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