Open AccessEnhanced and coordinated in vivo expression of inflammatory cytokines and nitric oxide synthase by chondrocytes from patients with osteoarthritis
Author(s) -
Melchiorri Cinzia,
Meliconi Riccardo,
Frizziero Luigi,
Silvestri Tania,
Pulsatelli Lia,
Mazzetti Ilaria,
Borzì Rosa Maria,
Uguccioni Mariagrazia,
Facchini Andrea
Publication year - 1998
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/1529-0131(199812)41:12<2165::aid-art11>3.0.co;2-o
Subject(s) - nitric oxide synthase , osteoarthritis , in vivo , nitric oxide , inflammatory arthritis , inflammation , proinflammatory cytokine , immunology , chemistry , medicine , microbiology and biotechnology , arthritis , biology , pathology , genetics , alternative medicine
Objective To evaluate the sites of expression of interleukin‐1β (IL‐1β), tumor necrosis factor α (TNFα), and inducible nitric oxide synthase (iNOS) in patients with inflammatory and degenerative joint diseases. Methods Cytokines and iNOS were detected by immunohistochemistry analysis of synovial and cartilage biopsy specimens obtained at knee arthroscopy in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), osteoarthritis (OA), and traumatic knee arthritis. Cytokine and iNOS expression was quantified using computerized image analysis. Results IL‐1β, TNFα, and iNOS were highly expressed by synovial cells (lining layer cells, infiltrating leukocytes, endothelial cells) from patients with inflammatory arthritides and significantly less by synovial cells from patients with OA and traumatic arthritis. In contrast, the latter patients showed high chondrocyte expression of cytokines and iNOS while RA and PsA patients had only minor chondrocyte positivity. In both joint compartments, IL‐1β expression, TNFα expression, and iNOS expression were strongly correlated. Conclusion The enhanced and coordinated expression of IL‐1β, TNFα, and iNOS by chondrocytes strongly supports the hypothesis that chondrocytes are the major site of production of mediators of inflammation in human OA, thus playing a primary role in the pathogenesis of this disease.