Li Yingjie, Cai Hengxing, Fang Wei, Meng Qinggong, Li Jian, Deng Mohong, Long Xing
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.
J Oral Pathol Med. 2014 May;43(5):388-94. doi: 10.1111/jop.12146. Epub 2013 Dec 26.
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.
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.
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.
FGF-2 was responsible for the formation of cartilaginous loose bodies and involved in the pathogenesis of SC.
颞下颌关节滑膜软骨瘤病（SC）是一种罕见的增殖性疾病，其特征是在滑膜和关节间隙形成软骨或骨软骨结节。成纤维细胞生长因子2（FGF-2）常用于软骨形成分化试验。因此，我们推测FGF-2可能参与SC的发病机制。
采用组织学和免疫组织化学方法观察SC滑膜和游离体（LB）标本。进行实时聚合酶链反应以比较SC和正常滑膜中的基因表达。在有或没有其拮抗剂长五聚素3（PTX3）的情况下，用FGF-2刺激SC滑膜细胞6天。进行实时聚合酶链反应和碱性磷酸酶（ALP）活性检测，以研究FGF-2和PTX3的作用。
SC滑膜，无论面向关节腔还是覆盖LB，其特征均为滑膜细胞和血管数量增加。FGF-2在LB的软骨细胞和成纤维样细胞以及血管壁中表达。SC滑膜中软骨形成基因（Sox9和Wnt-4）、成骨基因（Foxc2）、FGF-2和VEGF-A mRNA的表达明显高于对照组。FGF-2对SC滑膜细胞的刺激增加了ALP活性以及软骨形成基因（Sox9、Col2α1和聚集蛋白聚糖）、成骨基因（Foxc2、骨钙素和Col1α1）和VEGF-A的表达，但PTX3抑制了这些作用。
FGF-2促成了软骨游离体的形成并参与了SC的发病机制。
