Yingjie Li1, Hengxing Cai, Wei Fang, Qinggong Meng, Jian Li, Mohong Deng, Xing Long. 1. Department of Oral and Maxillofacial Surgery, The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.
Abstract
BACKGROUND: Synovial chondromatosis (SC) of temporomandibular joint (TMJ) is a rare proliferative disorder characterized by the formation of cartilaginous or osteocartilaginous nodules in synovium and joint space. Fibroblast growth factor 2 (FGF-2) is frequently applied in chondrogenic differentiation assays. Therefore, we hypothesized that FGF-2 might involved in the pathogenesis of SC. METHODS: SC synovium and loose bodies (LBs) specimens were observed by histological and immunohistochemical methods. Real-time PCR was conducted for comparing genes expressions in SC and normal synovium. SC synoviocytes were stimulated by FGF-2 in the presence or absence of its antagonist long pentraxin-3 (PTX3) for 6 days. Real-time PCR and alkaline phosphatase (ALP) activity were performed to examine the effects exerted by FGF-2 and PTX3. RESULTS: SC synovium, no matter facing the articular cavity or covering LB, was characterized by increased quantity of synoviocytes and blood vessels. FGF-2 was expressed in chondrocytes and fibroblast-like cells of LBs, and the wall of blood vessels. Expressions of chondrogenic genes (Sox9 and Wnt-4), osteogenic genes (Foxc2), FGF-2, and VEGF-A mRNA were significantly higher in SC synovium than that of the control group. The stimulation of FGF-2 on SC synoviocytes increased ALP activity and expressions of chondrogenic genes (Sox9, Col2α1, and Aggrecan), osteogenic genes (Foxc2, osteocalcin, and Col1α1), and VEGF-A, but PTX3 inhibited these effects. CONCLUSION: FGF-2 was responsible for the formation of cartilaginous loose bodies and involved in the pathogenesis of SC.
BACKGROUND:Synovial chondromatosis (SC) of temporomandibular joint (TMJ) is a rare proliferative disorder characterized by the formation of cartilaginous or osteocartilaginous nodules in synovium and joint space. Fibroblast growth factor 2 (FGF-2) is frequently applied in chondrogenic differentiation assays. Therefore, we hypothesized that FGF-2 might involved in the pathogenesis of SC. METHODS: SC synovium and loose bodies (LBs) specimens were observed by histological and immunohistochemical methods. Real-time PCR was conducted for comparing genes expressions in SC and normal synovium. SC synoviocytes were stimulated by FGF-2 in the presence or absence of its antagonist long pentraxin-3 (PTX3) for 6 days. Real-time PCR and alkaline phosphatase (ALP) activity were performed to examine the effects exerted by FGF-2 and PTX3. RESULTS: SC synovium, no matter facing the articular cavity or covering LB, was characterized by increased quantity of synoviocytes and blood vessels. FGF-2 was expressed in chondrocytes and fibroblast-like cells of LBs, and the wall of blood vessels. Expressions of chondrogenic genes (Sox9 and Wnt-4), osteogenic genes (Foxc2), FGF-2, and VEGF-A mRNA were significantly higher in SC synovium than that of the control group. The stimulation of FGF-2 on SC synoviocytes increased ALP activity and expressions of chondrogenic genes (Sox9, Col2α1, and Aggrecan), osteogenic genes (Foxc2, osteocalcin, and Col1α1), and VEGF-A, but PTX3 inhibited these effects. CONCLUSION:FGF-2 was responsible for the formation of cartilaginous loose bodies and involved in the pathogenesis of SC.