Conclusions
This study helped elucidate the potential reason for the difficulty in forming pulp-dentin complex.
Results
After isolating and culturing PDLSCs and SCAPs from human third molars, we compared the migration of PDLSCs and SCAPs. Then we investigated the role of SDF-1α-CXCR4/CXCR7 axis in PDLSC migration. We further investigated the impact of Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) on PDLSC migration and the potential mechanism. PDLSCs showed better migration under both noninflammatory and inflammatory conditions than SCAPs. SDF-1α can promote the migration of PDLSCs by elevating the expression of CXCR4 and CXCR7, increasing the interaction between them, promoting expression of β-arrestin1 and activating the ERK signaling pathway. P. gingivalis LPS can promote the migration of PDLSCs toward SDF-1α through increasing the expression of CXCR4 via the NF-κB signaling pathway, promoting the expression of β-arrestin1, and activating the ERK signaling pathway. Conclusions: This study helped elucidate the potential reason for the difficulty in forming pulp-dentin complex.