Non-alcoholic fatty liver disease (NAFLD) has a chronic and progressive characteristic, being characterized by the accumulation of fat in liver, without alcoholic or autoimmune disease, with defined steatosis of varying degrees that can evolve to non-alcoholic steatohepatitis in which the presence of fibrosis and lobular inflammation can be observed, being considered one of the main risk factors for liver cirrhosis and hepatocellular carcinoma [1], [2].

Periodontal disease (PD) is an inflammatory condition that progressively may affect the tooth's supporting structures, causing inflammation, gingival bleeding, injury to the periodontal ligament and bone loss [3], [4]. In 2018, the new classification of periodontal and peri-implant diseases and conditions reinforced that systemic conditions impact the course of periodontitis [4]. Some authors describe the pathophysiology association between systemic conditions [5] and periodontal disease as coronary heart disease, chronic kidney disease, diabetes mellitus, and liver transplantation [6], [7], [8], [9], as well as chronic use of medications, including corticosteroid use, is associated with the incidence of PD [10].

Periodontitis affects the supporting structures of the teeth, and the periodontal tissues, mainly causing the loss of permanent teeth. The onset and extent of the inflammatory process, initiated by the supporting periodontal tissue, characterized by inflammation of the gums, subgingival pathogenic plaque, clinical attachment loss with periodontal pocket, and loss of adjacent supporting bone, results in the diagnosis of periodontal disease [11]. Thus, we understand how periodontitis is considered a multifactorial disease. In addition, systemic diseases predispose individuals to present physiological changes triggered by the disease mechanism or the use of medications, which can contribute to the progression of periodontal disease.

Several risk factors can be associated with the emergence and progression of NAFLD, such as insulin resistance, obesity, diet, genetic factors, and infections by certain types of intestinal bacteria [12]. Although, until then, oral infections are not related to the emergence of NAFLD, some studies show that they can be more aggressive in this group of patients [13], [14], [15]. In addition, other studies have already shown that oral infections, especially those involving the bacteria Porphyromonas gingivalis, can have an important impact on the progression of NAFLD [16], [17].

NAFLD is the hepatic manifestation of the metabolic syndrome, and therefore, we can establish an association between the systemic inflammatory state observed in PD and the metabolic syndrome since there is an increase in the levels of inflammatory cytokines harming both pathologies [18], [19]. Thus, the metabolic imbalance may impact the development and progression of NAFLD, as well as the progression of PD [20].

This review aimed to evaluate the association between PD e NAFLD.