Fig. 1.

Stimulation by oral pathogenic bacteria induce dysfunctional PDLFs. a Toxic products, secreted by pathogenic bacteria, lead to the production of inflammatory factors and the activation of multiple signaling pathways through pattern recognition receptors. b Metabolites and virulence factors produced by pathogenic bacteria induce inflammatory death in PDLFs, resulting in the release of inflammatory factors. The black arrows indicate activation. Gram⁻ gram-positive bacteria, Gram +  gram-negative bacteria, TD Treponema denticola, LPS lipopolysaccharide, PG peptidoglycan, MSP major surface protein, MDP muramyl dipeptide MurNAc-L-Ala-D-isoGln, TLR toll-like receptor, panx1 Pannexin-1, P2XR7 P2RX7 receptor, MyD88 myeloid differentiation factor 88, TRIF6 Tumor necrosis factor receptor associated factor 6, NLR NOD-like receptor, NLRP3 NLRP3 inflammasome, ROS Reactive oxygen species, NCOA4 cargo receptor nuclear receptor coactivator 4, HIF-1α Hypoxia-inducible factor-1 α, DAMPs death-associated molecular patterns, RIPK3 receptor-interacting protein serine-threonine kinases-3, MLKL mixed lineage kinase domain-like protein, VCAM-1 vascular cellular adhesion molecule-1, RANKL receptor activator of nuclear factor-kappa B ligand, MMP Matrix metalloproteinase, NOD nucleotide-binding oligomerization domain, ECSIT, evolutionarily conserved signaling intermediate in Toll pathways, NOX NADPH Oxidases, ERK Extracellular signal-regulated kinases, COX-2 cyclooxygenase-2, GP130 Glycoprotein 130, sIL-6R soluble interleukin-6 receptor, TNF-α Tumor necrosis factor α, IL-1 interleukin-1, IL-1β interleukin-1β, RASA4 RAS p21 protein activator 4, MCP-1 Monocyte chemoattractant protein-1