AKT1 and periodontitis: Exosomes from inflamed PDLSCs promote pro-inflammatory M1 macrophage polarization via transferring miR-143-3p, which regulates the PI3K/AKT/NF-κB pathway. This increases pro-inflammatory cytokines (IL-12, IL-1β) and markers (CCR7, MINCLE) while reducing anti-inflammatory M2 markers (CD163, IL-10, MRC1), contributing to inflammatory progression in periodontitis [25].