骨免疫微环境中炎症因子诱导骨丢失的机制及免疫治疗研究进展  

Advances on the mechanism of inflammatory cytokine-induced bone loss in bone immune-microenvironment and immunotherapy

作　　者：王志凌 郭源源[2] 张浩[3] 傅德皓 WANG Zhi-ling;GUO Yuan-yuan;ZHANG Hao;FU De-hao(Orthopedics Department,Yantai Affiliated Hospital of Binzhou Medical University.Yantai,Shandong,264003,China)

机构地区：[1]滨州医学院烟台附属医院手足外科,山东省264003 [2]华中科技大学同济医学院附属梨园医院药剂科,湖北省430061 [3]华中科技大学同济医学院附属梨园医院老年病科,湖北省430061 [4]上海市第六人民医院创伤骨科,200080

出　　处：《中国骨与关节杂志》2023年第12期943-948,共6页Chinese Journal of Bone and Joint

基　　金：国家自然科学基金(82370889)。

摘　　要：骨是一个动态器官,通过不断的骨构塑和骨重建来维持其正常的结构和功能[1-2]。在骨重建过程中,成骨细胞的骨形成和破骨细胞的骨吸收是紧密耦合的动态平衡过程,可以保证骨的强度和骨矿物质稳定[3]。干扰成骨细胞和破骨细胞的活性和功能,可以导致这种平衡遭到破坏,可能导致骨丢失[2]。造成骨丢失的原因往往与性别。Inflammation induced-bone loss is an universal phenomenon in chronic inflammatory diseases and age-related diseases.However,its mechanism is still not clear.Following the development of osteoimmunology,the effects of inflammatory cytokines in bone immune-microenvironment on osteoclasts and osteoblasts through osteoprotegerin/receptor activator of nuclear factor kappa-B(NF-κB)ligand/receptor activator of NF-κB(OPG/RANKL/RANK)pathway have been researched widely.Meanwhile,immunotherapy aiming at chronic inflammation hasbeen already applied in treating immunoporosis.This article will review the essential signaling mechanism of pro-inflammatory cytokines,including the suppression of osteoblastogenesis and promotion of osteoclastogenesis,as well as the current therapies based on cytokines and lymphocytes for inflammatory bone loss.

关 键 词：骨质吸收 细胞因子类 信号传导 破骨细胞 骨质疏松 综述 

分 类 号：R681[医药卫生—骨科学]