Abstract: Objective:?To investigate the effect of LncRNA small nucleolar RNA host genes (SNHG) 8 on osteogenic differentiation of jaw bone marrow mesenchymal stem cells (JBMMSCs). Methods:?LncRNA SNHG8 was eliminated or overexpressed in JBMMSCs by lentivirus transfection; gene expression was detected by qRT-PCR; alkaline phosphatase (ALP) activity detection, alizarinred staining, calcium ion quantification and Western blot were used to determine the osteogenic differentiation ability of JBMMSCs in vitro. JBMMSCs were mixed with HA/TCP materials and subcutaneous transplanted in nude mice, and the osteogenic differentiation ability of JBMMSCs in vivo was detected by hematoxylin-eosin (HE) staining, Masson staining and immunofluorescence staining; reactive oxygen species (ROS) staining was used to detect ROS levels; and the protein expression of the mitogen-activated protein kinase (MAPK) signaling pathway was detected by Western blot. Results: After lncRNA SNHG8 was knocked down, ALP activity and in vitro mineralization ability of JBMMSCs were increased (P＜0.01, and bone sialprotein (BSP) protein expression bands were increased. After lncRNA SNHG8 was overexpressed, ALP activity and in vitro mineralization ability were decreased (P＜0.01), and BSP protein expression bands were decreased. The expression of phosphorylated c-Jun N-terminal kinase (p-JNK) in MAPK pathway was up-regulated by knocking down of lncRNA SNHG8, and overexpression of lncRNA SNHG8 inhibited p-JNK expression. LncRNA SNHG8 deletion can enhance intracellular ROS staining, and overexpression of lncRNA SNHG8 can inhibit intracellular ROS staining. After lncRNA SNHG8 knockout, new bone formation increased in vivo (P＜0.01), and the expression bands of BSP and osteocalcin (OCN) were enhanced. Conclusions:?LncRNA SNHG8 may inhibit the osteogenic differentiation function of JBMMSCs in vitro and in vivo via JNK signaling pathway.