Propofol-induced osteogenic differentiation in dental pulp stem cells: Modulation of MAPK signaling under inflammatory conditions.

Background/purpose: Bone regeneration in an inflammatory environment remains a significant challenge in the field of regenerative dentistry. Previous studies have demonstrated that inflammation inhibits osteogenic differentiation, necessitating the development of novel therapeutic approaches to counteract these effects. We investigated the effects of propofol on the osteogenic differentiation of dental pulp stem cells (DPSCs) under inflammatory conditions and explored the underlying signaling mechanisms. Materials and methods: DPSCs were cultured in the presence of lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-α) to mimic inflammatory conditions. Propofol (10, 50, and 100 μM) was administered, and its effects on cell viability, alkaline phosphatase (ALP) activity, and mineralization were assessed. In addition, the expression of osteogenic markers was analyzed and activation of the mitogen-activated protein kinase (MAPK) signaling pathway was examined by western blotting. Results: Propofol significantly enhanced ALP activity and mineralization in DPSCs under inflammatory conditions. In addition, it upregulated the expression of osteogenic marker genes and proteins. Functionally, propofol treatment activated p38 phosphorylation and suppressed extracellular signal regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) phosphorylation. Conclusion: Propofol promotes the osteogenic differentiation of DPSCs under inflammatory conditions by activating the p38/MAPK signaling while modulating the ERK and JNK pathways. This suggests that propofol has potential therapeutic applications in bone regeneration and regenerative dentistry, particularly in inflammatory environments.