摘要
糖皮质激素广泛应用于治疗各种变态反应性和自身免疫性疾病，但长期应用会导致糖皮质激素性骨质疏松症(GIOP)。炎性细胞因子：肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)在骨代谢中起重要调节作用，但其在骨代谢中的作用尚不清楚。骨细胞可以通过缝隙连接直接调节成骨细胞和破骨细胞的形成和功能，也可以通过传递分子信号间接调节成骨细胞和破骨细胞的形成和功能。凋亡的成骨细胞释放RANKL、HMGB 1和促炎细胞因子刺激破骨细胞发生.此外，骨细胞还能分泌FGF 23来调节骨代谢。高水平的GCs暴露可导致骨细胞凋亡，影响骨间隙连接，导致骨丢失。GCS治疗可产生更多的FGF 23来抑制骨矿化。GCS还破坏血管，降低骨细胞的可行性和矿物质沉积率，导致骨强度下降。GCs诱导的骨细胞凋亡小体可促进TNF-α和IL-6的产生.另一方面，肿瘤坏死因子-α和IL-6通过改变成骨细胞向破骨细胞和成骨细胞的信号而发挥协同作用。此外，肿瘤坏死因子-α还可诱导骨细胞凋亡，并导致骨质量恶化。IL-6和骨细胞可能相互作用。因此，我们推测GCs通过肿瘤坏死因子-α和IL-6来调节成骨细胞的生成，这些细胞在发生凋亡的骨细胞周围高度表达。本文综述了骨细胞在调节成骨细胞和破骨细胞中的作用。此外，GCs改变了骨细胞与成骨细胞/破骨细胞之间的关系。此外，我们还讨论了肿瘤坏死因子-α和IL-6通过调节骨细胞在眼压中的作用。最后，我们讨论了用促炎信号通路作为治疗靶点的可能性。
关键词: TNF-α，IL-6，骨细胞，破骨细胞，成骨细胞，GIOP.
图形摘要
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