Non-alcoholic fatty liver disease is becoming the leading cause of chronic liver disease with a prevalence of 20% worldwide. The prognosis depends on the degree of fibrosis: patients with a low degree of fibrosis (F0-F2) have a good prognosis unlike those with severe fibrosis or cirrhosis (F3-F4), exposed to excess mortality from cardiovascular diseases , cancers, and complications of cirrhosis. The diagnosis of the fibrosis stage is histological but the worsening of the fibrosis remains unknown.~The intestinal microbiota is an etiological factor in NAFLD and dysbiosis is associated with the severity of fibrosis. There is also a physiopathological rationale between oral bacterial microbiota and NAFLD. The oral microbiota is very rich, it corresponds to a reservoir of 1010 bacteria of Gram-negative bacteria (BGN). Its dysbiosis causes oral infections like periodontal diseases, immuno-infectious pathologies linked to an imbalance between the bacterial etiological factor and the host's immune defenses.~Many studies suggest that Porphyromonas gingivalis, a virulent periodontopathogenic bacterium, is associated with many systemic diseases such as cardiovascular diseases. In addition, a recent study showed the impact of Porphyromonas gingivalis on Non-Alcoholic Steatosis Liver Disease (NASH). It would be responsible for aggravation of non-alcoholic fatty liver disease (NAFLD) by stimulating inflammation in the damaged liver tissue.~the hypothesis that the salivary levels of Porphyromonas Gingivalis could be associated with the degree of severity of fibrosis in NAFLD patients, and would constitute a new therapeutic target for the evaluation of fibrosis. This work would open new perspectives in treatment strategies.
Many studies suggest that Porphyromonas gingivalis, a virulent periodontopathogenic bacterium, is associated with many systemic diseases such as cardiovascular diseases. In addition, a recent study showed the impact of Porphyromonas gingivalis on Non-Alcoholic Steatosis Liver Disease (NASH). It would be responsible for aggravation of non-alcoholic fatty liver disease (NAFLD) by stimulating inflammation in the damaged liver tissue.