IntroductionThe dentinogenesis potential of stem cells during dentin-pulp tissue regeneration may be compromised by microorganism components. Here we aimed to investigate the cell viability and osteo-/odontogenic differentiation of stem cells from apical papilla (SCAP) exposed to bacterial lipopolysaccharide (LPS) and to evaluate the molecular mechanism in vitro. MethodsCCK8 assay was used to assess the SCAP proliferation rate on exposure to different concentrations of LPS in medium. Dentin matrix protein-1 (DMP-1), runt-related transcription factor-2 (Runx-2), and alkaline phosphatase (ALP) expression and mineralized nodule formation were detected by Western blotting and alizarin red S staining to evaluate SCAP osteo-/odontogenic differentiation. Autophagosomes in SCAP and the autophagy-related markers Beclin 1, autophagy-related gene 5 (Atg5), and microtubule-associated proteins light chain 3 (LC3) were detected by transmission electron microscopy and Western blotting, respectively. Effects of the autophagy inhibitor 3-methyladenine on LPS-treated SCAP osteo-/odontogenic differentiation were also examined. ResultsSCAP cell viability was decreased by 5 μg/mL LPS treatment on day 3. LPS (5 μg/mL) inhibited SCAP osteo-/odontogenic differentiation and decreased DMP-1, Runx-2, and ALP expression. Moreover, LC3, Atg5, and Beclin 1 expression and autophagosome number were elevated. Conversely, autophagy inhibition rescued the number of mineralized nodules and DMP-1, Runx-2, and ALP expression in the LPS-treated SCAP. ConclusionsOur findings indicated that autophagy was involved in the suppression of SCAP osteo-/odontogenic differentiation in an LPS-induced inflammatory environment. This study discloses autophagy modulation as a potential new strategy to improve SCAP osteo-/odontogenic differentiation in an inflammatory environment.