Could inflammatory arthritis be triggered by progenitor cells in the joints?

Morphogenesis genes are tightly regulated during fetal life, where they are responsible for limb bud initiation, patterning processes of the limb, cartilage development, and joint formation. These genes are highly conserved across species and include Wnt (wingless), BMP (bone morphogenetic protein), noggin, chordin, FGF (fibroblast growth factor), and hedgehog gene families. Recent studies report that these morphogenesis genes are de novo expressed in rheumatoid synovitis. The presence and potential activity of these genes in adult joints may reflect a new situation: the migration of undifferentiated stromal mesenchymal progenitor cells into the injured joints attracted by the continuing repair process. Another hypothesis would be that the continued persistence of undifferentiated/immature fetal cells in the joints may result in cell activation and immune responses.