Fig. 3
From: Roles of extracellular vesicles in periodontal homeostasis and their therapeutic potential
Role of extracellular vesicles (EVs) and bacterial extracellular vesicles (BEVs) in the pathogenesis of periodontitis. A The effects of BEVs on immune invasion. BEVs can serve as decoys that disrupt the complement system, thereby protecting periodontopathogens from complement bactericidal effects. Moreover, BEVs can suppress microbial recognition by macrophages/monocytes by interacting with host cell membrane receptors. B BEVs released from periodontopathogens can bind to the pathogen recognition receptors (PRRs) of host cells, including TLR2, TLR4, and NOD1, triggering the activation of downstream proinflammatory signalling pathways. C BEVs released from periodontopathogens cause periodontal tissue destruction. BEVs can deliver virulence factors, including gingipain and cytolethal distending toxin (CDT), to oral epithelial cells, causing cell dysfunction and detachment. Additionally, BEVs can inhibit the osteogenesis of bone marrow stromal cells (BMSCs) and induce the osteoclastogenesis of osteoclast precursors, leading to bone tissue destruction. BEVs bacterial extracellular vesicles, PRR pathogen recognition receptor, TLR2 Toll-like receptor 2, TLR4 Toll-like receptor 4, NOD1 nucleotide-binding oligomerization domain-containing protein 1, CDT cytolethal distending toxin, BMSCs bone marrow stromal cells. Created with BioRender.com