Objective:To determine the role and molecular mechanism of dexmedetomidine (DEX) in postmenopausal osteoporosis (PMOP) .Methods:Twenty-seven patients with PMOP admitted to Yantai Yantaishan Hospital from Jan. 2020 to Jan. 2021 were selected as PMOP group, and 20 healthy volunteers were selected as Normal group. The differentially expressed miRNAs in PMOP were screened, clinically, the expression of miR-483-3p and catenin beta 1 (CTNNB1) in serum samples of patients with PMOP was detected by qRT-PCR. In vitro experiment, Bone marrow mesenchymal stem cells (BMSCs) were induced into osteoblasts, Dex was used to treat BMSCs and intervene the expression of miR-483-3p, CTNNB1 in BMSCs, the expression level of osteogenesis related indexes (RUNX2、OCN、OPN) was detected. After coculturing Human umbilical vein endothelial cell (HUVECs) with BMSCs, angiogenesis experiment was utilized to detect the angiogenesis ability.Results:Compared with Normal group (1±0.46) (1.03±0.44) , the expression of miR-483-3p (3.23±1.61) was increased in serum of PMOP patients while expression of CTNNB1 (0.50±0.27) was inhibited ( t=5.99, P<0.001) ( t=5.14, P<0.001) . miR-483-3p has a good diagnostic effect on PMOP (AUC=0.86, P<0.001) . After Dex treatment, miR-483-3p level was decreased in BMSCs, CTNNB1 level was increased (all P<0.05) . Dex promoted the expression of RUNX2, OCN, OPN and number of angiogenesis, but this effect was partially reversed by miR-483-3p overexpression (all P<0.05) . CTNNB1 was confirmed as a target gene of miR-483-3p, the inhibition effects of miR-483-3p overexpression on osteogenic differentiation and angiogenesis of BMSCs induced by Dex was partially reversed by CTNNB1 overexpression (all P<0.05) . Conclusion:Dex enhanced CTNNB1 level in PMOP via inhibiting miR-483-3p, subsequently promoted osteogenic differentiation and angiogenesis of BMSCs and inhibited progression of PMOP.