Extracellular vesicles (EVs) play a crucial role in bone homeostasis and are involved in the pathogenesis of osteoporosis. EVs derived from various sources, such as osteoblasts, osteoclasts, and mesenchymal stem cells (MSCs), regulate the balance between bone formation and resorption. Osteoblast-derived EVs promote bone formation, while osteoclast-derived EVs inhibit it. EVs can also serve as drug carriers to enhance drug targeting and bioavailability in bone tissue, offering a promising strategy for diagnosing and treating osteoporosis. EVs are small membrane-bound structures that can be classified into exosomes (30–150 nm), microvesicles (MVs, 100–1000 nm), and apoptotic bodies (ABs, 1–5 μm). They contain proteins, DNA, mRNAs, miRNAs, and lipids, and play diverse roles in biological processes, including disease pathogenesis. EVs have garnered significant interest in disease diagnosis and treatment, and their potential as therapeutic agents or biomaterials for osteoporosis is promising. The biogenesis of EVs involves different pathways, including ESCRT-dependent and ESCRT-independent mechanisms. EVs can be internalized by cells through various mechanisms, such as membrane fusion, receptor-mediated endocytosis, and macropinocytosis. The fate of EVs after internalization is crucial for their function, as they can be degraded in lysosomes or function within the cell. EVs derived from different sources have distinct roles in osteoporosis. Osteoclast-derived EVs promote bone resorption, while osteoblast-derived EVs promote bone formation. MSC-derived EVs can promote osteoblast activity, inhibit osteoclast differentiation, and regulate immune functions. Macrophage-derived EVs can either promote or inhibit osteogenic differentiation depending on their polarization state. EVs derived from endothelial cells and muscle cells also play roles in bone homeostasis. EVs derived from tumor cells can promote osteoclast differentiation and aggravate bone calcium flow. EVs derived from biological fluids, such as blood, urine, and amniotic fluid, have been shown to play roles in regulating bone homeostasis and can serve as diagnostic markers for osteoporosis. EVs derived from bacteria, such as those from probiotics, have also been shown to have antiosteoporotic effects. EVs derived from plants have been shown to have antiosteoporotic effects. The potential applications of EVs in osteoporosis include diagnostic tools, therapeutic drugs, and engineered optimization. EVs can be modified to improve their targeting and therapeutic efficacy, and can be combined with biomaterials for bone repair. The future perspectives of EVs in osteoporosis include further research on their role in bone homeostasis, their potential as diagnostic and therapeutic agents, andExtracellular vesicles (EVs) play a crucial role in bone homeostasis and are involved in the pathogenesis of osteoporosis. EVs derived from various sources, such as osteoblasts, osteoclasts, and mesenchymal stem cells (MSCs), regulate the balance between bone formation and resorption. Osteoblast-derived EVs promote bone formation, while osteoclast-derived EVs inhibit it. EVs can also serve as drug carriers to enhance drug targeting and bioavailability in bone tissue, offering a promising strategy for diagnosing and treating osteoporosis. EVs are small membrane-bound structures that can be classified into exosomes (30–150 nm), microvesicles (MVs, 100–1000 nm), and apoptotic bodies (ABs, 1–5 μm). They contain proteins, DNA, mRNAs, miRNAs, and lipids, and play diverse roles in biological processes, including disease pathogenesis. EVs have garnered significant interest in disease diagnosis and treatment, and their potential as therapeutic agents or biomaterials for osteoporosis is promising. The biogenesis of EVs involves different pathways, including ESCRT-dependent and ESCRT-independent mechanisms. EVs can be internalized by cells through various mechanisms, such as membrane fusion, receptor-mediated endocytosis, and macropinocytosis. The fate of EVs after internalization is crucial for their function, as they can be degraded in lysosomes or function within the cell. EVs derived from different sources have distinct roles in osteoporosis. Osteoclast-derived EVs promote bone resorption, while osteoblast-derived EVs promote bone formation. MSC-derived EVs can promote osteoblast activity, inhibit osteoclast differentiation, and regulate immune functions. Macrophage-derived EVs can either promote or inhibit osteogenic differentiation depending on their polarization state. EVs derived from endothelial cells and muscle cells also play roles in bone homeostasis. EVs derived from tumor cells can promote osteoclast differentiation and aggravate bone calcium flow. EVs derived from biological fluids, such as blood, urine, and amniotic fluid, have been shown to play roles in regulating bone homeostasis and can serve as diagnostic markers for osteoporosis. EVs derived from bacteria, such as those from probiotics, have also been shown to have antiosteoporotic effects. EVs derived from plants have been shown to have antiosteoporotic effects. The potential applications of EVs in osteoporosis include diagnostic tools, therapeutic drugs, and engineered optimization. EVs can be modified to improve their targeting and therapeutic efficacy, and can be combined with biomaterials for bone repair. The future perspectives of EVs in osteoporosis include further research on their role in bone homeostasis, their potential as diagnostic and therapeutic agents, and