Pathogenesis of RA
- 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;
- 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.
Original Text by Clifford R. Wheeless, III, MD.
Last updated by Data Trace Staff on Tuesday, August 21, 2012 2:36 pm