The single feature most characteristic of rheumatoid arthritis is tumorlike proliferation of the synovium. During the past year, we have obtained further evidence implicating platelet-derived growth factor and fibroblast growth factor-1 in the disease process. In brief, we have demonstrated high level expression of tyrosine phosphorylated proteins in RA synovia that colocalized with PDGF and FGF-1. Upregulation of synovia from patients with osteoarthritis was minimal. In addition, further evidence was also obtained implicating upregulated expression of cyclooxygenase, uteroglobin and corticocotropin releasing hormone in the pathobiology of RA synovitis. The data showing secretion of corticotropin releasing hormone in rheumatoid joint fluids and tissue further support our view that complex interactions between the neuroendocrine system and the immune system are involved in regulating synovitis.
