强直性脊柱炎（AS）患病率高，误诊误治常见，现有治疗手段对慢性炎症控制较好，但对病理性成骨疗效甚微。探索AS病理性成骨的机制一直是该领域研究的热点和难点。我们前期已证实AS患者MSC成骨能力增强，进一步研究发现AS患者破骨前体细胞分化为破骨细胞的能力明显减弱，我们推测病变局部成骨与破骨的失衡可能是AS病理性成骨的重要原因，但AS破骨细胞分化障碍的机制尚不清楚。基因芯片结果提示AS患者破骨前体细胞内长链非编码RNA-OC（LncRNA-OC）表达明显上调,且敲减LncRNA-OC后其分化为破骨细胞的能力恢复正常。预实验结果提示LncRNA-OC可能通过募集TRIM8调控TAK1的泛素化。本课题拟以此为切入点在体外深入研究LncRNA-OC调控TAK1泛素化的具体机制并在体内探讨其在AS病理性成骨中的作用，阐明其在AS病理性成骨中的诊疗价值，为AS早期诊断和治疗提供新思路。

The prevalence of ankylosing spondylitis (AS) is high, which is common in misdiagnosis and misdiagnosis. The existing treatment methods are better for chronic inflammation, but have little effect on pathological osteogenesis. Exploring the mechanism of pathological osteogenesis in AS has been a hot and difficult topic in this field. We previously demonstrated that AS MSC possessed a greater capacity for osteogenic differentiation than normal MSC. Further research found that osteoclastogenesis was weaken in AS than normal. We supposed that the imbalance between osteogenesis and osteoclastogenesis may be the main reason for pathological osteogenesis in AS. However, the mechanism why osteoclastogenesis was abnormal in AS remains unclear. Gene microarray showed that long non-coding RNA-OC (LncRNA-OC) was up-regulated in osteoclast precursors from AS patients. Besides, osteoclastogenesis was restored to normal in AS after knocking down LncRNA-OC. Further study found that LncRNA-OC may regulate the ubiquitination of TAK1 through raising TRIM8. Therefore, we mainly investigate the mechanism of the ubiquitination of TAK1 regulated by LncRNA-OC and the role in the pathological osteogenesis of AS. Moreover, we estimate the value of LncRNA-OC in the diagnosis and treatment for the pathological osteogenesis of AS, which may provide new ideas for early diagnosis and treatment of AS.