Their results, published today in The Journal of Clinical Investigation , provide evidence for a central pathogenic contribution of angiogenic blood vessels to the maintenance and severity of arthritic disease, and the potential viability of anti-angiogenic therapy for the treatment of rheumatoid arthritis. Moreover, it appears that the same anti-angiogenesis strategy that impacts tumor growth may also impact the progression of rheumatoid arthritis. While rheumatoid arthritis has been classified as an angiogenesis-associated disease, scientists have not yet determined whether angiogenesis the growth of new blood vessels directly participates in arthritic disease or is a consequence of ongoing inflammation. This paper provides evidence that angiogenesis contributes to arthritic disease. A joint affected by rheumatoid arthritis is characterized by the proliferation of the synovial lining forming excessive folds of inflamed tissue, termed pannus.
Pannus formation is thought to be central to the process of joint destruction.
Angiogenesis appears to be required for pannus development, and plays a role in inflammation as a source of cytokine and protease activity. Although the specific factors that promote angiogenesis in rheumatoid arthritis have not been identified, synovial tissue and fluid contain angiogenesis-promoting molecules. Joint swelling synovial infiltrate, pannus formation and the incidence of cartilage erosions were all significantly reduced in animals treated early with this integrin antagonist. Inhibition of neovascularization in this model may influence many parameters of disease, including inflammation, protease production and tissue metabolism. Previous studies conducted in the Cheresh lab for the past several years suggested targeting alpha v beta 3 on blood vessel cells within malignant tumors as a way to cut off the source of nourishment to the tumors.