Abstract
Inflammatory bone disease is a general term for a series of diseases caused by chronic inflammation, which leads to the destruction of bone homeostasis, that is, theosteolytic activity of osteoclastsincreases,andthe osteogenicactivity ofosteoblasts decreases, leading toosteolysis. Macrophages areinnate immunecell with plasticity,andtheirpolarization is related to inflammatory bone diseases. The dynamic balanceof macrophagesbetween theM1 phenotype and theM2 phenotypeaffectsthe occurrence and development ofdiseases. In recent years, an increasing number of studies have shown that extracellular vesicles existing in the extracellular environment can act on macrophages, affecting the progress of inflammatory diseases. This process is realized by influencing the physiological activity or functional activity of macrophages, inducing macrophages to secrete cytokines, and playing an anti-inflammatory or pro-inflammatory role. In addition, by modifying andediting extracellularvesicles, thepotentialof targeting macrophagescan beused to provide new ideasfordeveloping newdrug carriersforinflammatory bone diseases.
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