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Responsable : Cécile Lambert

If the destruction of articular cartilage characterizes the osteoarthritis, inflammation of the synovial membrane is also important in the progression of cartilage damage.

Inflammation of the synovial membrane

In response to cartilage breakdown products and inflammatory mediators released into the joint cavity, the membrane becomes inflamed. This inflammation is secondary to cartilage degradation and moderate. It begins with reference to cartilage damage, and then extends to the whole of the synovial membrane. The hypertrophy and increased number of vessels are among the histological changes characteristic of the inflamed synovium, these changes are often accompanied by infiltration of mononuclear cells (lymphocytes, monocytes/macrophages).

The normal synovium is highly vascularized to provide cartilage nutrients and oxygen. However, in osteoarthritis, the angiogenic process is increased locally. This results in a proliferation of endothelial cells and is attributed to an imbalance between pro- and anti-angiogenic factors. Inflammation and angiogenesis are two processes closely associated with the progression of osteoarthritis.

In our laboratory, we seek to characterize the inflammatory and angiogenic phenotype of fibroblast-like synoviocytes isolated from synovial tissue “normal” or “reaction” (N/R) and osteoarthritis “inflammatory” (I).

Immunohistochemical analysis revealed in the I area a greater number of CD45+ (at the synovial intima and nodular inflammatory infiltrates) and VEGF+ (at the intima).

The diameter of blood vessels identified by von Willebrand factor also appears greater in this area.

In parallel with these results, we observed a significant increased (p<0,001) of IL-6, IL-8 and PGE2 production by synoviocytes from the I area compared to synoviocytes from N/R area.

Finally, in comparison with synoviocytes of N/R area, synoviocytes of I area produced significantly more VEGF (p<0,001) but less than TSP-1 (p<0,001).