强直性脊柱炎新骨形成机制研究进展  

Progress on Mechanism of New Bone Formation in Ankylosing Spondylitis

作　　者：扶忠超 叶志中[1] 尹志华[1] 曾惠琼[1] 黄进贤[2] 

机构地区：[1]广东医学院附属福田医院香蜜湖风湿病分院广东医学院风湿病研究所,广东广州518000 [2]香港大学深圳医院,广东深圳518040

出　　处：《现代生物医学进展》2015年第35期6997-7000,共4页Progress in Modern Biomedicine

基　　金：国家自然科学基金项目(81102266;81301529);广东省自然科学基金博士启动项目(S2013040012296);福田区科技计划项目(FTWS201308);深圳市医学重点学科建设资助项目(2005C10)

摘　　要：强直性脊柱炎(Ankylosing spondylitis,AS)是以骶髂关节和脊柱病变为主的炎性疾病。其特征性病理表现为炎症和新骨形成。近年来使用肿瘤坏死因子(Tumor necrosis factor,TNF)抑制剂控制AS炎症已卓有成效,却无法阻止影像学进程,其病理性新骨形成可致残,严重影响患者健康生活,但其机制尚不完全清楚。目前研究认为复杂的新骨形成机制与Wnt/β-catenin信号通路及其调控因子、炎症介质密切相关。本文结合当前国内外的研究就AS新骨形成机制进展展开综述,为深入研究新骨形成机制提供新思想。Ankylosing spondylitis is a kind of inflammatory diseases major involved sacroiliac joint and spine lesions. Its characteristic pathological symptoms is new bone formation and inflammation. For the past few years, we can effective reduce inflammation of AS by tumour necrosis factor （TNF） inhibitor treatment, but did not inhibit radiographic progression. The pathologic new bone formation may even lead to disability, which is seriously affect healthy life of the patients. However, the mechanism of new bone formation is not fully understood. Current studies show that the complex mechanism of new bone formation is closely related to Wnt/β-catenin signaling pathway, its regulatory factors and Inflammatory mediators. This paper reviews domestic and foreign current researchers on progress in new bone formation mechanism of AS. The purpose of this review is to provide new ideas for further study of new bone formation mechanlsm.

关 键 词：强直性脊柱炎 WNT/Β-CATENIN信号通路 新骨形成 炎症 

分 类 号：R593.23[医药卫生—内科学]