Dysregulated intracellular Ca2 stores and Ca2 signaling in synovial fluid T lymphocytes from patients with chronic inflammatory arthritis

2000 ◽  
Vol 43 (6) ◽  
pp. 1257-1265 ◽  
Author(s):  
David M. Carruthers ◽  
Helen P. Arrol ◽  
Paul A. Bacon ◽  
Stephen P. Young
Keyword(s):  
T Lymphocytes ◽  
Synovial Fluid ◽  
Inflammatory Arthritis ◽  
Chronic Inflammatory Arthritis

scholarly journals Characterization and Recruitment of Plasmacytoid Dendritic Cells in Synovial Fluid and Tissue of Patients with Chronic Inflammatory Arthritis

2004 ◽  
Vol 173 (4) ◽  
pp. 2815-2824 ◽  
Author(s):  
Roberto Lande ◽  
Elena Giacomini ◽  
Barbara Serafini ◽  
Barbara Rosicarelli ◽  
Gian Domenico Sebastiani ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Synovial Fluid ◽  
Inflammatory Arthritis ◽  
Plasmacytoid Dendritic Cells ◽  
Chronic Inflammatory Arthritis

scholarly journals Mechanisms and Mediators of Pain in Chronic Inflammatory Arthritis

2021 ◽  
Author(s):  
Marco Di Carlo ◽  
Gianluca Smerilli ◽  
Fausto Salaffi
Keyword(s):  
Inflammatory Pain ◽  
Inflammatory Arthritis ◽  
Operational Definition ◽  
Immunosuppressive Drugs ◽  
Therapeutic Strategies ◽  
Future Research ◽  
Common Symptom ◽  
Joint Diseases ◽  
Chronic Inflammatory Arthritis ◽  
Inflammatory Joint Diseases

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.

Aspirin in the Treatment of Chronic Inflammatory Arthritis

JAMA ◽  
1987 ◽  
Vol 257 (10) ◽  
pp. 1331-1331 ◽  
Author(s):  
D. J. McCarty ◽  
M.-E. Csuka
Keyword(s):  
Inflammatory Arthritis ◽  
Chronic Inflammatory Arthritis

scholarly journals Role of Synovial Exosomes in Osteoclast Differentiation in Inflammatory Arthritis

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 120
Author(s):  
Ji Eun Song ◽  
Ji Soo Kim ◽  
Ji Hye Shin ◽  
Ki Won Moon ◽  
Jin Kyun Park ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Inflammatory Arthritis ◽  
Mononuclear Cells ◽  
Osteoclast Differentiation ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tartrate Resistant Acid Phosphatase ◽  
Healthy Donors ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony

This study aimed to investigate the characteristics of exosomes isolated from synovial fluid and their role in osteoclast differentiation in different types of inflammatory arthritis. Exosomes isolated from synovial fluid of rheumatoid arthritis (RA), ankylosing spondylitis (AS), gout, and osteoarthritis (OA) patients were co-incubated with CD14+ mononuclear cells from healthy donors without macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL). Osteoclast differentiation was evaluated via tartrate-resistant acid phosphatase (TRAP) staining and activity and F-actin ring formation. RANKL expression on synovial exosomes was assessed using flow cytometry and an enzyme-linked immunosorbent assay (ELISA). Synovial exosomes were the lowest in OA patients; these induced osteoclastogenesis in the absence of M-CSF and RANKL. Osteoclastogenesis was significantly higher with more exosomes in RA (p = 0.030) than in OA patients, but not in AS or gout patients. On treating macrophages with a specified number of synovial exosomes from RA/AS patients, exosomes induced greater osteoclastogenesis in RA than in AS patients. Synovial exosomal RANKL levels were significantly higher in RA (p = 0.035) than in AS patients. Synovial exosome numbers vary with the type of inflammatory arthritis. Synovial exosomes from RA patients may bear the disease-specific “synovial signature of osteoclastogenesis.”

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