Abstract
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.
Highlights
Transforming growth factor beta 3 involved in the pathogenesis of synovial chondromatosis of temporomandibular joint Yingjie Li1, Loaye Abdelaziz El.Mozen[2], Hengxing Cai[1], Wei Fang[1], Qinggong Meng[1], Jian Li1, Mohong Deng1 & Xing Long[1]
This study focused on the role of Transforming growth factor beta 3 (TGF-b3) in the pathogenesis of Synovial chondromatosis (SC), because TGF-b3 was potent mediator for inducing chondrogenesis of MSCs7,8,16 and had a higher chondrogenic potential of a more rapid differentiation than TGF-b117
The cartilaginous nodules were observed in both synovium and joint space[4,5,18], and made of cartilaginous extracellular matrix (ECM) and chondrocytes which are absent in normal synovium[19,20]
Summary
Transforming growth factor beta 3 involved in the pathogenesis of synovial chondromatosis of temporomandibular joint Yingjie Li1, Loaye Abdelaziz El.Mozen[2], Hengxing Cai[1], Wei Fang[1], Qinggong Meng[1], Jian Li1, Mohong Deng1 & Xing Long[1]. 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-b3) is closely related to chondrogenic differentiation, and might participate in pathogenesis of SC. Synovial chondromatosis (SC) of temporomandibular joint (TMJ) is a rare proliferative disorder of synovium accompanied by formation of cartilaginous nodules in synovium and joint space[1,2,3], as well as secondary calcification and ossification[4]. We hypothesized that TGF-b3 might be responsible for chondrogenic differentiation of TMJ synoviocytes and the pathogenesis of SC. Our group previously discovered that fibroblast growth factor 2 (FGF-2) was responsible for the formation of loose bodies (LBs) and increased blood vessels of synovium. The relation between TGF-b3 and FGF-2 was investigated in this research
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