Key result
Oral inflammation may promote AF through bacteremia, systemic inflammation, autoimmunity, autonomic activation, and toxins.
Why the study?
Does oral inflammation contribute to the pathogenesis of atrial fibrillation?
This narrative review outlines five potential mechanisms by which oral inflammation and infections may contribute to the pathogenesis of atrial fibrillation.
Supports potential oral inflammation-AF link; hypothesis-generating and requires prospective trials before clinical relevance.
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.
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Aarabi et al. (2018) conducted a review in Atrial fibrillation. Oral inflammations was evaluated. Oral inflammations may contribute to the pathogenesis of atrial fibrillation through five basic mechanisms including bacteremia, systemic inflammation, autoimmunity, autonomic activation, and toxins.
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