SpA/AS滑膜-附着端复合体炎生物力学因素的影像学研究

SpA/AS is a common disabling autoimmune disease. Synovial - entheseal complex is the main inflammatory target of early SpA/AS. Biomechanical factors can induce the inflammation of this functional area. The biomechanical factors is how to influence the occurrence and development of synovial - entheseal complex inflammation in SpA/AS, is the current scientific problem to be solved..This project will choose the VG1 induced HLA - B27 positive rat model as the research object. It will use the control study methods of magnetic resonance imaging, micro – CT and finite element analysis and histopathological results, respectively research the relationship between inflammation and new bone formation in synovial - entheseal complex and different stress conditions, and the relationship between the biomechanical function form and the MAPK/ERK pathway, and study the relationship between progress and prognosis of the synovial - entheseal complex inflammation and the strength of exercise and traction.. It aims to build a set of comprehensive evaluation of synovial - entheseal complex structure and function by imaging and histopathological imaging technology; to understand the biomechanical factors how to act on the enthesitis in SpA/AS, to study the relationship between MAPK/ERK pathway and synovial - entheseal complex inflammation; to predict the strength of exercise and traction benefiting the prognosis of SpA/AS.

SpA/AS是一种常见的致残性自身免疫性疾病，滑膜-附着端复合体是早期SpA/AS的主要炎症靶区。生物力学因素能够诱发该功能区的炎症。生物力学因素是如何影响SpA/AS滑膜-附着端复合体炎的发生和发展，是当前亟待解决的科学问题。.该项目通过VG1诱导HLA-B27阳性大鼠模型作为研究对象，采用磁共振功能成像、micro-CT有限元分析等影像学技术与组织病理学进行对照的方法，分别研究滑膜-附着端炎及新骨形成与不同应力的关系，以及生物力学作用形式与力学通路MAPK/ERK间的关系。并研究滑膜-附着端炎的发展及预后与运动及牵引强度的关系。旨在建立一套综合评价滑膜-附着端复合体结构和功能的影像学和组织病理学成像技术；探索生物力学因素对SpA/AS附着端炎的作用形式；明确力学通路MAPK/ERK与SpA/AS滑膜-附着端复合体炎的关系；预测有利于SpA/AS预后的运动和牵引强度。

SpA/AS是一种常见的致残性自身免疫性疾病，滑膜-附着端复合体是早期SpA/AS的主要炎症靶区。生物力学因素能够诱发该功能区的炎症。生物力学因素是如何影响SpA/AS滑膜-附着端复合体炎的发生和发展，是当前亟待解决的科学问题。该项目通过VG1诱导HLA-B27阳性大鼠模型作为研究对象，采用磁共振功能成像、micro-CT有限元分析等影像学技术与组织病理学进行对照的方法，分别研究滑膜-附着端炎及新骨形成与不同应力的关系，以及生物力学作用形式与力学通路MAPK/ERK间的关系。并研究滑膜-附着端炎的发展及预后与运动及牵引强度的关系。该研究发现:滑膜附着端的运动损伤会引起附着端炎症，机械应力通过ERK1/2信号通路诱发SPA附着端的炎症反应。阻断ERK1/2信号通路后，AS小鼠附着端炎症较对照组减轻。尾吊小鼠后肢负重1/10至1/6体重组AS小鼠存在明显骨质疏松，但附着端炎症较1/4及1/3体重负重组减少。运动生物力学因素在强直性脊柱炎疾病的发生发展中起到重要作用，机械应力通过ERK1/2信号通路诱发附着端炎症发生。