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Godište 35 supplement 2 - Institut za reumatologiju

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23. Lam J, Abu-Amer Y, Nelson CA, Fremont DH, Ross FP, Teitelbaun SL. Tumour necrosis factor<br />

super family cytokines and the pathogenesis of inflammatory osteolyses. Ann Rheum Dis 2002;<br />

61 (suppl II): ii82-ii83<br />

24. Shimizo S, Shio<strong>za</strong>wa S, Shio<strong>za</strong>wa K, Imura S, Fugita T: Quantitative histological studies on the<br />

pathogenesis of periarticular osteoporosis in rheumatoid arthritis. Arthritis Rheum 1985; 28:25–3<br />

___________________________<br />

SUMMARY<br />

Clinical of Rheumatology, Military Medical Academy Belgrade<br />

MEHANICAL DEMAGE OF JOINTS IN RHEUMATOID ARTHRITIS<br />

DUŠAN STEFANOVIĆ<br />

Rheumatoid arthritis is a chronic, inflammatory, systemic disease characterized by joint pain and<br />

swelling, joint destruction and pannus formation. The RA pannus consists of a hypertrophic synovial<br />

membrane composed of hyperplastic synoviocytes and inflammatory cells that infiltrate synovial<br />

membrane. T cells, B cells, macrophage-like cells, mast cells and endothelial cells are all-present in the<br />

RA synovium and contribute to the inflammatory processes. T cells play pivotal role in RA. Abnormal Tcell<br />

immunity in RA is not limited to the joint. RA is characterized by massive abnormalities in the<br />

composition of the T-cell pool. T cells recognize arthritogenic antigen on the surface of antigenpresenting<br />

cells in the joint. Activated T cells in the synovium provide mediators that regulate the<br />

functional ability of macrophages, fibroblasts and B cells. B cells produce auto antibodies that may be<br />

pathogenic; fibroblasts secrete cytokines and metalloproteinases that have harmful effects on tissue; and<br />

endothelial cells control the influx of inflammatory cells into the synovium.<br />

K e y w o r d s: rheumatoid arthritis, T cells, pathogenesis

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