PT  - JOURNAL ARTICLE
AU  - Y T Konttinen
AU  - V Bergroth
AU  - D Nordström
AU  - K Koota
AU  - B Skrifvars
AU  - G Hagman
AU  - C Friman
AU  - M Hämäläinen
AU  - P Slätis
TI  - Cellular immunohistopathology of acute, subacute, and chronic synovitis in rheumatoid arthritis.
AID  - 10.1136/ard.44.8.549
DP  - 1985 Aug 01
TA  - Annals of the Rheumatic Diseases
PG  - 549--555
VI  - 44
IP  - 8
4099  - http://ard.bmj.com/content/44/8/549.short
4100  - http://ard.bmj.com/content/44/8/549.full
SO  - Ann Rheum Dis1985 Aug 01; 44
AB  - Cellular inflammation in rheumatoid arthritis (RA) synovial membrane was studied in biopsy specimens taken at different stages of synovitis and disease. Patients were classified into three subgroups: acute RA, subacute RA, and chronic RA. Inflammatory cells were characterised by a histochemical esterase method and immunohistochemical peroxidase-antiperoxidase (PAP) and avidin-biotin-peroxidase (ABC) staining. The amounts and distribution of inflammatory cells were different in various stages of the synovitis. In acute onset RA monocytes and granulocytes predominated, suggesting that the beginning of rheumatoid inflammation is similar to inflammatory reaction in general. The presence of T cells and also of plasma cells in subacute RA suggests underlying subclinical changes also in apparently healthy joints in RA. The most typical feature of prolonged synovitis in chronic RA was its intensity, characterised by the presence of large T cell and plasma cell infiltrates. Our findings suggest that the immunological mechanisms are secondary to the tissue damage caused by the initial inflammatory events of unknown cause. However, the immunological mechanisms may still play a central role in the aetiopathogenesis, because findings in chronic RA suggest a defective down-regulation of the immune response.