Abstract: Background　Despite the prevalence of mandibular osseous defects, their underlying pathological mechanisms remain incompletely elucidated. The emerging concept of the "brain-bone" axis implies a significant regulatory crosstalk between neural and skeletal tissues. However, the potential contribution of astrocytes—crucial glial support cells within the central nervous system—and their secreted exosomes to the regenerative repair of jaw bone defects remains unexplored.Objective　The primary aim of this investigation was to delineate the regulatory effects of astrocyte-derived exosomes on the cellular proliferation and osteogenic lineage commitment of Jaw Bone Marrow Mesenchymal Stem Cells.Methods　Primary JBMSCs were harvested and purified from C57BL/6N mice, with third-passage cells selected for subsequent assays. Concurrently, exosomes were isolated from the C8-D1A astrocyte cell line and subjected to characterization. JBMSCs were stratified into a blank control group (0 μg/mL) and experimental groups exposed to varying concentrations of AD-Exos (10, 50, and 100 μg/mL) for a 24-hour incubation period. Quantitative Real-Time PCR (qRT-PCR) was employed to assess the mRNA transcription levels of the proliferation marker Mcm2 and osteogenic markers Runx2, Alp, and OCN. Furthermore, Western blot analysis was utilized to quantify the protein expression of Mcm2, Bmp2, Runx2, Alp, and OCN. Results　Both JBMSCs and AD-Exos were successfully isolated and exhibited typical phenotypic characteristics. Comparative analysis revealed that, relative to the control group, intervention with 10 μg/mL AD-Exos significantly upregulated the mRNA expression of Mcm2, Runx2, Alp, and OCN. Consistent with genetic findings, Western blotting confirmed that the 10 μg/mL concentration notably enhanced the protein synthesis of Mcm2, Bmp2, Runx2, Alp, and OCN in JBMSCs.Conclusion　AD-Exos exert a positive regulatory influence on the proliferation and osteogenic differentiation of JBMSCs. Specifically, a concentration of 10 μg/mL was identified as the optimal dosage for maximizing these biological responses. Collectively, these findings provide robust experimental evidence and establish a theoretical framework for developing novel biotherapies targeting jaw bone defect repair.