Synovial chondromatosis (SC) of temporomandibular joint is rare proliferative disorder featured by the formation of cartilaginous nodules in synovium and joint space.
Transforming growth factor beta 3 (TGF-β3) is closely related to chondrogenic differentiation, and might participate in pathogenesis of SC. We discovered that increased quantity of synoviocytes and blood vessels were observed in SC synovium. The vessel wall and sublining fibroblasts were stained positively by the
antibodies against TGF-β3,
fibroblast growth factor 2 (FGF-2), and CD34. In loose bodies (LBs), TGF-β3 was mainly expressed in chondrocytes and
FGF-2 was expressed in chondrocytes, fibroblasts, and vessel walls. Expressions of TGF-β1, TGF-β3,
FGF-2, Sox9, Wnt-4, Foxc2, and
VEGF-A mRNA were significantly higher in SC synovium. Stimulation of TGF-β3 on synoviocytes increased
alkaline phosphatase (ALP) activity and expressions of chondrogenic genes (Sox9, Col2α1,
Aggrecan, Wnt-4, and Wnt-11), osteogenic genes (Runx2, Foxc2,
osteocalcin, and Col1α1), and
VEGF-A, but failed to influence
FGF-2 expression. However, the addition of
FGF-2 increased TGF-β3 expression. In conclusion, TGF-β3 existed in synovium and LBs of SC, and was responsible for the pathogenesis of SC.