强直性脊柱炎继发骨质疏松症的机制研究进展

强直性脊柱炎是临床的常见病、多发病，极易导致脊柱关节的进行性退变和脆性骨折的发生，给患者的身心健康和生活质量带来严重影响。骨质疏松症作为强直性脊柱炎的主要并发症，其本质还是机体内环境紊乱引起的骨代谢失衡，免疫紊乱、激素失调参与其发病的整个过程，细胞因子、激素和信号通路在强直性脊柱炎继发骨质疏松症中的作用极其重要。从分子生物学层面揭示强直性脊柱炎继发骨质疏松症的具体机制，可为临床强直性脊柱炎诊疗中积极配合抗骨质疏松治疗提供理论依据。

Progress in the study of the mechanism of osteoporosis secondary to ankylosing spondylitis

Ankylosing spondylitis is a common and frequent clinical disease, which is highly susceptible to progressive degeneration of the spinal joints and the occurrence of fragility fractures, causing serious impact on the physical and mental health and quality of life of the patients. As a major complication of ankylosing spondylitis, osteoporosis is essentially an imbalance of bone metabolism caused by disorders of the body''s internal environment, with immune disorders and hormonal imbalances involved in its pathogenesis. Exploration of the mechanism of osteoporosis secondary to ankylosing spondylitis at the molecular biology level provides a theoretical basis for clinical treatment of ankylosing spondylitis with active anti-osteoporosis therapy.