Abstract
Periodontal disease is an inflammatory disease caused by pathogenic oral microorganisms that leads to the destruction of alveolar bone and connective tissues around the teeth. Although many studies have shown that periodontal disease is a risk factor for systemic diseases, such as type 2 diabetes and cardiovascular diseases, the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease has not yet been clarified. Thus, the purpose of this review was to reveal the relationship between NAFLD and periodontal disease based on epidemiological studies, basic research, and immunology. Many cross-sectional and prospective epidemiological studies have indicated that periodontal disease is a risk factor for NAFLD. An in vivo animal model revealed that infection with periodontopathic bacteria accelerates the progression of NAFLD accompanied by enhanced steatosis. Moreover, the detection of periodontopathic bacteria in the liver may demonstrate that the bacteria have a direct impact on NAFLD. Furthermore, Porphyromonas gingivalis lipopolysaccharide induces inflammation and accumulation of intracellular lipids in hepatocytes. Th17 may be a key molecule for explaining the relationship between periodontal disease and NAFLD. In this review, we attempted to establish that oral health is essential for systemic health, especially in patients with NAFLD.
Highlights
Periodontal disease, especially chronic periodontitis, is an infectious disease induced by oral bacteria that can lead to the destruction of soft tissues surrounding the teeth, bones, and ligaments [1]
This review summarizes the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease (Figure 1) and shows the possibility that periodontal disease aggravates NAFLD
An in vivo animal model showed a piece of the mechanism by which periodontal disease affects NAFLD
Summary
Periodontal disease, especially chronic periodontitis, is an infectious disease induced by oral bacteria that can lead to the destruction of soft tissues surrounding the teeth, bones, and ligaments [1]. There are three hypotheses for how periodontitis affects systemic diseases. Local periodontal infection leads to an increase in systemic inflammatory mediators [12,13]. Some studies have shown that increased inflammatory mediator levels were decreased after successful periodontal treatment [14]. Alterations in the oral microbiome due to periodontal disease may affect the gut microbiome. The gastrointestinal tract begins with the mouth and proceeds to the intestines; ingested bacteria travel through the tract; affect gut microbiota composition [17]. Dysbiosis of the gut microbiota can lead to several diseases, including diabetes, rheumatoid arthritis, and inflammatory bowel disease [18]
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