Roles of Oral Infections in the Pathomechanism of Atherosclerosis
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Roles of Oral Infections in the Pathomechanism of Atherosclerosis. / Aarabi, Ghazal; Heydecke, Guido; Seedorf, Udo.
in: INT J MOL SCI, Jahrgang 19, Nr. 7, 06.07.2018, S. 1978.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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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 -