CORRELATION OF PERIODONTITIS TO STROKE ISCHEMIC IN PATIENT WITH HIPERLIPIDEMIA

FimA

Periodontal TISSUE

Many TNF-α enter systemic circulation achieve brain vascular

TNF-α increased of adhesion molecules (E-selectin, P-selectin, ICAM-1, VCAM-1) in endothelial cell

Hyperlipidemia induced monocyte expression of receptor CCR-2 ad MCP-1.

TNF- α Increased endothelial vascular permeability through activation NADPH-oxidase (NOX) induced by PKC (Protein Kinase C)

High level LDL in blood

Monocyte migrate through th vessel lining via MCP-1, receptor CCR-2, regulated by adhesion molecules (VCAM-1, I-CAM 1, P-selectine, E-selectin, etc.).

Monocyte LDL trapped in an artery brain vascular

TNF- α in circulation and hiperlipidemia increase expression of NADPH oxidase (NOX) -> ROS

TNF- α

LDL + ROS -> OxLDL -> ingested by machrofage through a scavenger receptor -> foam cell

Vascular injury

Platelet activation

Platelet relase growth factors, platelet-derived growth factor (PDGF), TGF-, cytokines IL-1, IL-6 and IL-8, and thrombin.

Proliferation and migration vascular smooth muscle cell from tunica media to tunica intima arteri

BRAIN VESSEL

Pro-inflammatory cytokines

increase the local activity of matrix metalloproteinase-9 (MMP-9)

Unstable plaquePlaque rupture

Tissue factor into circulation blood

Activation coagulation cascade

Blood cloth in plaque

Formed Plug in arterial brain vessel

P. ginggivalis resides and multipliplies in cytosol perinuclear periodontal cell

P. ginggivalis disseminate directly from cell to cell through actine cytoskeleton dependent process. Bacteri spread to host tissue from epithelial to subepithelial tissue with persistent intracellular bacteria spreading mechanism (transcelluler spreading)

P. ginggivalis exit from intracelluler periodontal cell (dependent on polymerization, lipid raft, and microtubule assembly) and spread to periodontal tissue

FimA P. ginggivalis recognized by macrophage cell in periodontal tissue pass through TLR2 and CD14 -> induced macrophage produce proinflammatory cytokines (e.g. TNF-α, etc.)

Adherence and invasion of P. ginggivalis to periodontal epithelial cell (mediated by the binding fimbria (FimA) with beta-1 integrin receptor and by subsequent phosphorylation, activation of the putative integrin signal protein FAK (focal adhesion kinase), paxillin and the concurrent remodeling of the actin cytoskeleton.

P. ginggivalis