Pathogenesis of temporomandibular disorder induced by matrix degradation

基质降解引起的颞下颌关节紊乱的发病机制

• 批准号: 25893216
• 负责人: KATAOKA Yoshihiro
• 金额: $ 0.92万
• 依托单位: Kyushu Dental College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Research Activity Start-up
• 财政年份: 2013
• 资助国家: 日本
• 起止时间: 2013-08-30 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-25893216/
• 关键词: 細胞外マトリックス; 関節破壊; 滑膜; 軟骨; マトリックスメタロプロテアーゼ; 炎症性サイトカイン

In the present study, we examined the effects of inflammatory cytokines on synovial fibroblasts and chondrocytes in vitro. Tumor necrosis factor-alpha (TNF-alpha) enhanced matrix metalloproteinase-13 (MMP-13) mRNA expression in chondrocytes. Pre-treatment with high molecular weight hyaluronic acid suppressed TNF-alpha-mediated enhancement of MMP-13.On the other hand, interleukin-17 (IL-17) stimulates MMP-3 mRNA expression in synovial sarcoma cells. Immunofluorescent staining in synovial fibroblasts derived from human temporomandibular joints (TMJ) revealed that expression of IL-17 receptor (IL-17RA) that was primarily localized on the cell surface, whereas no immunofluorescent staining was seen in chondroyctes. Thesse results suggest that the main target of IL-17 in TMJ is synovial tissue.

在本研究中，我们研究了炎性细胞因子对滑膜成纤维细胞和软骨细胞在体外的影响。肿瘤坏死因子-α（TNF-α）增强软骨细胞基质金属蛋白酶-13（MMP-13）mRNA的表达。高分子量透明质酸预处理可抑制TNF-α介导的MMP-13的表达，而白细胞介素-17（IL-17）可刺激滑膜肉瘤细胞MMP-3 mRNA的表达。免疫荧光染色显示，来自人颞下颌关节（TMJ）的滑膜成纤维细胞的IL-17受体（IL-17 RA）的表达，主要定位于细胞表面，而没有免疫荧光染色被视为软骨细胞。提示IL-17在TMJ中的主要作用靶点是滑膜组织。

项目成果

Clinical comparison between arthrocentesis and conventional conservative treatment with maxillomandibular fixation for unilateral high condylar fractures

关节穿刺术与常规上下颌骨固定保守治疗单侧高髁骨折的临床比较

• DOI: 10.1111/joor.12124
• 发表时间: 2014
• 期刊: J Oral Rehabil
• 影响因子: 2.9
• 作者: Nogami S;Yamauchi K;Kataoka Y;Takano H;Yamashita Y;Takahashi T
• 通讯作者: Takahashi T