Fibroblast growth factor 2 involved in the pathogenesis of synovial chondromatosis of temporomandibular joint. (26th December 2013)

• Record Type: Journal Article
• Authors: Li, Yingjie; Cai, Hengxing; Fang, Wei; Meng, Qinggong; Li, Jian; Deng, Mohong; Long, Xing
• Is Part Of: Journal of oral pathology & medicine. Volume 43:Number 5(2014:May)
• Page Start: 388
• Page End: 394
• Publication Date: 2013-12-26
• Subjects: Dentistry -- Periodicals; Teeth -- Diseases -- Periodicals; 617
• DOI: 10.1111/jop.12146
• Languages: English
• ISSNs: 0904-2512

Abstract

<abstract abstract-type="main" id="jop12146-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="jop12146-sec-0001" sec-type="section"> <title>Background</title> <p>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.</p> </sec> <sec id="jop12146-sec-0002" sec-type="section"> <title>Methods</title> <p>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.</p> </sec> <sec id="jop12146-sec-0003" sec-type="section"> <title>Results</title> <p>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 (<italic>Sox9</italic> and <italic>Wnt‐4</italic>), osteogenic genes (<italic>Foxc2</italic>), <italic>FGF‐2, </italic> and <italic>VEGF‐A</italic> 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 (<italic>Sox9</italic>, <italic> Col2</italic>α<italic>1</italic>, and <italic>Aggrecan</italic>), osteogenic genes (<italic>Foxc2</italic>, <italic> osteocalcin</italic>, and <italic>Col1</italic>α<italic>1</italic>), and <italic>VEGF‐A</italic>, but PTX3 inhibited these effects.</p> </sec> <sec id="jop12146-sec-0004" sec-type="section"> <title>Conclusion</title> <p>FGF‐2 was responsible for the formation of cartilaginous loose bodies and involved in the pathogenesis of SC.</p> </sec> </abstract>