Periodontitis is an oral chronic inflammatory disease which has been associated with a wide range of systemic disorders some of which include diabetes, inflammatory bowel diseases, cardiovascular diseases, cancer, neurodegeneration, rheumatoid arthritis, and chronic liver diseases. [1][2][3][4][5][6][7] Periodontitis and these systemic conditions all share some degree of similarity in their pathophysiology which is characterized by a long-lasting deregulated inflammatory response.Today it is recognized that genetic predisposition, exposure to acquired risk factors and epigenetic changes throughout life play a decisive role for the development of immune-based disorders by modifying the host's susceptibility. 8,9 Given that time is required for their onset, the inflammatory imbalance resulting from one disease could directly alter the pathophysiology of the other or they could simply occur in a host sharing a similarly disturbed immunological background favorable for the development of general chronic disorders. Regardless of the perspective to be taken into account, periodontitis has an important place, whether as a warning time marker for the predisposition of other chronic diseases, or as an independent factor for their development or clinical worsening with direct effects on patients' uality of life, treatment outcome, and prognosis.The increasing knowledge also suggests that imbalances in the microbiota-immunity interactions may contribute to the onset of a multitude of immune-mediated diseases. 10 While how and when this dysbiosis develops in different organs is still unknown, oral bacteria such as Porphyromonas gingivalis and Fusobacterium nucleatum have been associated with various disorders distant from the oral cavity. [11][12][13] In this context, interactions between oral and gut microbiomes are complex, dynamic, and context-dependent since both sites are part of the multivariate environment of the gastrointestinal tract. Under physiological conditions they can keep a fine-tuned balance across the lifespan, but failures in this crosstalk due to a hostmicrobe disequilibrium have the potential to activate inflammatory networks in different organs. 14 The liver is among the organs that can be more affected by these biological networks and pathogenic disturbances since it maintains anatomical proximity and intense physiological interdependence with the intestine via metabolic exchange and translocation of bacteria. For this reason, interest in the so-called oral-gut-liver axis has emerged, along with the idea that the oral dysbiosis caused by unrestrained inflammation could affect the pathophysiology of chronic liver diseases via blood circulation or enteral route. 1,15,16,17 The activation of a susceptible host immune system by pathogenand damage-associated molecular patterns (PAMPs; DAMPs) in the periodontal milieu could induce the systemic overexpression of an array of pro-inflammatory cytokines and chemokines hence potentially impacting the hepatic metabolism. 11 In parallel, oral bacteria in the contex...