胸椎黄韧带骨化（TOLF）是导致胸椎管狭窄的主要病理因素，严重影响患者生活质量。炎症环境是影响细胞成骨分化的重要因素，巨噬细胞（Mφ）及其分泌的抑瘤素M（OSM）能促进细胞成骨分化。炎症反应在TOLF中的作用机制未明，Mφ和OSM是否参与黄韧带细胞的成骨分化尚无报道。我们预实验发现Mφ存在于骨化前缘的黄韧带组织且M1型Mφ刺激后黄韧带细胞内OSM/JAK2/STAT3通路激活。因此我们提出假说：M1型Mφ分泌OSM激活黄韧带细胞OSM/JAK2/STAT3通路，促进黄韧带细胞成骨分化。本课题拟检测Mφ及OSM/JAK2/STAT3通路在骨化的黄韧带组织和细胞中的表达，并在细胞水平深入探讨M1型Mφ及OSM/JAK2/STAT3通路对黄韧带细胞成骨分化的作用方式和分子机制。进一步揭示TOLF发病的分子机制，阐明Mφ介导的炎症反应在黄韧带骨化中的作用，为TOLF的临床诊疗提供新的理论依据。

Thoracic ossification of ligamentum flavum (TOLF) is the main pathological factor leading to thoracic spinal stenosis, which seriously affects the quality of life of the patients. Inflammatory environment is an important factor affecting cell osteogenic differentiation. Macrophages and Macrophage-derived Oncostatin M (OSM) can promote the osteogenic differentiation. However, the mechanism of inflammation in TOLF remains unclear. Whether macrophages and OSM participate in the osteogenic differentiation of ligamentum flavum cells has not been reported. We previously found that macrophages were present in the ligamentum flavum tissue at the ossification front and the OSM/JAK2/STAT3 pathway in ligamentum flavum cells was activated after M1 macrophage stimulation. Therefore, we hypothesized that OSM derived from M1 macrophage could activate the OSM/JAK2/STAT3 pathway of ligamentum flavum cells and promote the osteogenic differentiation of ligamentum flavum cells. In this study, we intend to further detect the expression of macrophage and OSM/JAK2/STAT3 in ossified ligamentum flavum tissues and cells; explore the role and molecular mechanism of M1 macrophage and OSM/JAK2/STAT3 in the osteogenic differentiation of ligamentum flavum cells at the cellular level. These studies further reveal the molecular regulatory mechanism of TOLF, clarify the role of inflammation in the ossification of ligamentum flavum, and provide a new theoretical basis for clinical diagnosis and treatment of TOLF.