Fig. 4
From: Periodontitis impacts on thrombotic diseases: from clinical aspect to future therapeutic approaches
Periodontal infections can lead to bacteremia. Bacteria (eg., P. gingivalis) and their metabolites (e.g., LPS) can activate platelets via TLR2/4. Pro-inflammatory cytokines triggered by periodontitis (e.g., TNF-α and IL-6) promote high endothelial cell expression of P-selectin, which is responsible for neutrophil and monocyte recruitment and activation. Neutrophil extracellular traps (NETs) produced by neutrophil activation bind to platelets and accelerate blood cell aggregation. The mtDNA released from periodontal tissue destruction and the CpG DNA released from periodontal bacterial death can activate immune cells through the intracellular nucleic acid receptor TLR9 and accelerate the formation of platelet monocyte complexes. Meanwhile, Poly P produced by periodontal pathogen activates collagen fiber synthesis and participates in thrombus formation by triggering the factor XII-XI-IX cascade signaling mechanism. The illustration was created by X.Z. using BioRender.com
