In chronic inflammation, which leads to tissue destruction and fibrosis, immunocompetent cells migrate through the vascular endothelium to the target tissue. A prototype of these events is synovitis, which occurs in diseases such as rheumatoid arthritis. The hypothesis that cells from the bone marrow could also migrate directly to the synovium through channels interconnecting the two compartments is still under debate. Also, there is no definitive answer regarding the number of cells that result from infiltration of the synovium after migration, or from proliferation at the local site. Furthermore, the survival of the cells in synovitis is being subjected to some scrutiny, because there is some evidence for a lack of apoptosis in pathological conditions.

The interaction between lymphocytes of different subsets and monocyte/macrophages (type A synovial cells) results in the production of proinflammatory cytokines. These include interleukin (IL)-1 and tumour necrosis factor (TNF)-α, which induce connective tissue cells (type B synovial cells or synoviocytes) to produce large amounts of matrix metalloproteinases (MMPs), which in turn degrade extracellular matrix components (eg collagens and proteoglycans).