AKT1 and periodontitis: Based on these findings, we speculated that lncRNA MEG3 may participate in this system of periodontitis PDLSCs and act as a ceRNA, and searched for potential interactions between lncRNA MEG3 and IGF1. As expected, we found that lncRNA MEG3 could sponge miR-27a-3p, resulting in IGF1 up-regulation, and PI3K/Akt signaling pathway was activated, all which promoted PDLSC osteogenic differentiation ultimately.