Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation
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Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation. / Aarabi, Ghazal; Schnabel, Renate B; Heydecke, Guido; Seedorf, Udo.
In: BIOMOLECULES, Vol. 8, No. 3, 01.08.2018, p. 66.Research output: SCORING: Contribution to journal › SCORING: Review article › Research
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TY - JOUR
T1 - Potential Impact of Oral Inflammations on Cardiac Functions and Atrial Fibrillation
AU - Aarabi, Ghazal
AU - Schnabel, Renate B
AU - Heydecke, Guido
AU - Seedorf, Udo
PY - 2018/8/1
Y1 - 2018/8/1
N2 - Inflammation may be a risk factor for atrial fibrillation (AF). Oral infections frequently lead to chronic inflammation, such as gingivitis, periodontitis, and endodontic lesions. In this narrative review, we consider five basic pathogenic mechanisms that involve oral infections and inflammations in the pathogenesis of AF: (1) low level bacteremia by which oral bacteria enter the blood stream at inflamed sites of the oral cavity and invade the heart; (2) Systemic inflammation induced by inflammatory mediators, which are released from the sites of oral inflammation into the blood stream, affecting cardiac remodeling; (3) autoimmunity against molecular structures expressed in the heart caused by the host immune response to specific components of oral pathogens; (4) potentially arrhythmic effects mediated by activation of the autonomous nervous system triggered by oral inflammations; and (5) arrhythmic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. A number of studies support the involvement of all five mechanisms, suggesting a potentially complex contribution of oral inflammations to the pathogenesis of AF.
AB - Inflammation may be a risk factor for atrial fibrillation (AF). Oral infections frequently lead to chronic inflammation, such as gingivitis, periodontitis, and endodontic lesions. In this narrative review, we consider five basic pathogenic mechanisms that involve oral infections and inflammations in the pathogenesis of AF: (1) low level bacteremia by which oral bacteria enter the blood stream at inflamed sites of the oral cavity and invade the heart; (2) Systemic inflammation induced by inflammatory mediators, which are released from the sites of oral inflammation into the blood stream, affecting cardiac remodeling; (3) autoimmunity against molecular structures expressed in the heart caused by the host immune response to specific components of oral pathogens; (4) potentially arrhythmic effects mediated by activation of the autonomous nervous system triggered by oral inflammations; and (5) arrhythmic effects resulting from specific bacterial toxins that are produced by oral pathogenic bacteria. A number of studies support the involvement of all five mechanisms, suggesting a potentially complex contribution of oral inflammations to the pathogenesis of AF.
KW - Journal Article
KW - Review
U2 - 10.3390/biom8030066
DO - 10.3390/biom8030066
M3 - SCORING: Review article
C2 - 30071583
VL - 8
SP - 66
JO - BIOMOLECULES
JF - BIOMOLECULES
SN - 2218-273X
IS - 3
ER -