Roles of Oral Infections in the Pathomechanism of Atherosclerosis

TY - JOUR

T1 - Roles of Oral Infections in the Pathomechanism of Atherosclerosis

AU - Aarabi, Ghazal

AU - Heydecke, Guido

AU - Seedorf, Udo

PY - 2018/7/6

Y1 - 2018/7/6

N2 - Oral infections occur frequently in humans and often lead to chronic inflammations affecting the teeth (i.e., caries), the gingival tissues surrounding the teeth (i.e., gingivitis and endodontic lesions), and the tooth-supporting structures (i.e., periodontitis). At least four basic pathogenic mechanisms have been proposed that involve oral inflammations in the pathogenesis of atherosclerosis: (1) low level bacteremia by which oral bacteria enter the blood stream and invade the arterial wall; (2) systemic inflammation induced by inflammatory mediators released from the sites of the oral inflammation into the blood stream; (3) autoimmunity to host proteins caused by the host immune response to specific components of oral pathogens; (4) pro-atherogenic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. In this narrative review, we summarize published experimental evidence related to these four mechanisms and discuss their impact on the pathogenesis of atherosclerosis.

AB - Oral infections occur frequently in humans and often lead to chronic inflammations affecting the teeth (i.e., caries), the gingival tissues surrounding the teeth (i.e., gingivitis and endodontic lesions), and the tooth-supporting structures (i.e., periodontitis). At least four basic pathogenic mechanisms have been proposed that involve oral inflammations in the pathogenesis of atherosclerosis: (1) low level bacteremia by which oral bacteria enter the blood stream and invade the arterial wall; (2) systemic inflammation induced by inflammatory mediators released from the sites of the oral inflammation into the blood stream; (3) autoimmunity to host proteins caused by the host immune response to specific components of oral pathogens; (4) pro-atherogenic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. In this narrative review, we summarize published experimental evidence related to these four mechanisms and discuss their impact on the pathogenesis of atherosclerosis.

KW - Journal Article

KW - Review

U2 - 10.3390/ijms19071978

DO - 10.3390/ijms19071978

M3 - SCORING: Review article

C2 - 29986441

VL - 19

SP - 1978

JO - INT J MOL SCI

JF - INT J MOL SCI

SN - 1661-6596

IS - 7

ER -