In the context of T. forsythia infection, macrophage-derived CEVs are rich in proinflammatory cytokines and inflammatory mediators, such as TNF, IL-1β, HLA class I histocompatibility antigen B-7 alpha chain (HLA-B) and matrix metalloproteinase-9 (MMP9), which contribute to an exaggerated inflammatory response during the progression of periodontitis.23 Under normal conditions, periodontal ligament stem cells (PDLSCs) can mitigate the inflammatory microenvironment via the T helper 17 (Th17) cell/regulatory T-cell (Treg)/miR-155-5p/Sirtuin-1 (SIRT1) regulatory network. The gene discussed is IL1B; the disease is periodontitis.