Establishing a new animal model for ankylosing spondylolysis using DCIR deficient mice

强直性脊柱裂（Ankylosing spondylolysis，AS）是脊柱关节病的典型疾病之一，其主要表现为脊柱、骶髂关节等关节的强直。附着点炎是附着点的一种炎症，是强直性脊柱炎的一种原始症状，但其发病机制尚不清楚，治疗方法也不确定。由于DCIR缺陷小鼠自发地发展附着点炎和踝关节强直，我们利用DCIR缺陷小鼠来了解附着点炎症和随后的强直的发病机制，以及产生一种新的动物模型来分析AS。我们发现一种促炎细胞因子参与了关节强直的发展，它具有促进骨形成的能力。因此，本研究表明DCIR缺陷小鼠是一个有用的动物模型，以分析发病机制和评估潜在的试剂来治疗这种疾病。

Ankylosing spondylolysis (AS) is one of typical diseases in spondyloarthlopathy, which develops ankylosis in joints, such as the spines and the sacroiliacs. Although enthesitis, an inflammation of the entheses, is known as a primitive symptom of ankylosisng spondylitis, the pathogenesis remains unclear and the curative treatment isn't yet determined. Since DCIR deficient mice spontaneously developed enthesitis and ankylosing in ankles, we exploited the DCIR deficient mice to understand the pathogenesis of an inflammation in the enthuses and a subsequent ankylosis as well as to generate a new animal mode for analyzing AS. We found that a pro-inflammtory cytokine was implicated in the development of ankylosis, which had the ability to facilitate bone formation. Therefore, this study demonstrates that the DCIR deficient mice are a useful animal model of AS to analyze the pathogenesis and to assess a potential reagent to cure the disease.