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Pathogenesis of RA

- Discussion:
    - combination of genetic and environmental factors in its etiology;
    - an important early event may result from the interaction of antigen presenting macrophages w/ T cells (helper/inducer);
    - HLA-D allele DR4 is associated w/ RA patients;
    - although clinical laboratories measure IgM rheumatoid factor, other classes of RF have been described;
           - it is generally believed that complexes of IgG rheumatoid factor w/ IgG can deposit in blood vessels and lead to vasculitis;
    - celluar inflammation:
           - inflammation in the joint cavity can be intense;
           - it is likely that the monocyte is most reponsible for mediating tissue destruction;
           - in addition to this, more than one billion neutrophils enter moderately inflamed rheumatoid knee joint each day;
           - this leads to degradation of articular cartilage, menisci, and ligaments without restriction;
    - inciting causes:
           - hepatitis B vaccine: rare but reported complication (most of these patients have MHC II genes as a risk factor);
                  - ref: The development of rheumatoid arthritis after recombinant hepatitis B vaccination.
           - patients w/ RA have higher titers than normal individuals of antibodies to antigens of the Epstein-Barr (EB) virus, and rheumatoid peripheral blood lymphocytes undergo transformation into EB virus-containing cells;

- Synovitis:
    - in RA, normally delicate synovial membrane becomes infiltrated with macrophages, lymphocytes, plasma cells, and granulocytes;
    - synovitis in RA behaves much like localized neoplasia, w/ increases in cell number & increase in synovial destructive potential as it invades cartilage, ligaments, and subchondral bone

NIH conference. Rheumatoid arthritis: evolving concepts of pathogenesis and treatment.