There is a growing medical understanding that what happens in one part of the body can ripple out to other parts. Now, that idea is being explored in an unexpected place: the mouth. New research from an international team of researchers analyzes the growing evidence linking periodontal disease, commonly known as gum disease, to chronic liver disease, including cirrhosis, metabolic-associated fatty liver disease (MASLD), and alcohol-related liver disease. Despite the distance and functional differences between the mouth and liver, the paper makes strong evidence that the two systems are more closely connected than we thought.
Gum disease, especially its more severe form, periodontitis, is a chronic inflammatory disease caused by bacterial infection in the tooth-supporting tissues. It is one of the most common diseases in the world, and its severity tends to increase with age, smoking, alcohol consumption, and inadequate dental care. For patients who already have liver disease—many of whom share the same risk factors—oral health is often put on the back burner.
But ignoring the mouth can be a mistake. The review outlines a number of ways that periodontitis can worsen liver disease. The first is through the “mouth-gut-liver axis,” a term researchers use to describe the complex interactions between oral bacteria, the gut microbiota, and liver function. Pathogenic bacteria in the mouth may be swallowed or enter the bloodstream during daily activities such as chewing and brushing teeth. Once in the intestine, these microbes may alter the composition of the gut microbiota, leading to dysbiosis and increased intestinal permeability—also known as “leaky gut.” This allows bacterial products such as endotoxins to reach the liver, triggering inflammation and fibrosis.
Animal models further support this theory. Studies have shown that oral administration of specific periodontal pathogens, such as Porphyromonas gingivalis, can exacerbate liver steatosis and inflammation in mice with metabolic diseases. These microbes or their byproducts have even been found in liver tissue, suggesting that the transfer from the mouth to the liver is biologically plausible.
The immune system also plays a central role in this interaction. Chronic periodontal inflammation leads to the release of proinflammatory cytokines such as TNF-α and IL-6, which have long been implicated in the progression of liver disease. In addition, the review highlights the involvement of Th17 cells, a type of immune cell activated by oral pathogens that may migrate to the liver and exacerbate metabolic dysfunction. Together, these pathways form a vicious cycle: liver disease impairs oral health, while oral inflammation accelerates liver damage.
Although clinical data are still accumulating to support this association. Oral health in patients with cirrhosis is consistently worse than in the general population, with higher rates of gingival hyperplasia, attachment loss, and bone loss. The prevalence of periodontitis is as high as 72% in patients awaiting liver transplantation. Studies have also found a link between severe periodontal disease and increased mortality in patients with cirrhosis.
For patients with MASLD, the most common chronic liver disease, the evidence is equally compelling. Population-level studies have found that patients with advanced periodontitis are significantly more likely to develop MASLD, even after adjusting for common risk factors such as obesity and diabetes. One small trial showed that periodontal treatment can improve liver enzyme levels in the short term – suggesting that oral health interventions may affect liver function.
Nevertheless, the review authors caution that this research is still in its early stages. Many clinical data come from observational studies, which cannot clearly prove cause and effect. There are also challenges in disentangling the impact of shared lifestyle and socioeconomic factors on oral and liver health. Nonetheless, the biological plausibility, consistency of findings, and preliminary intervention data make a strong case for greater attention to teeth and gums in patients with liver disease.
The review concludes with a call for multidisciplinary collaboration. Gastroenterologists and hepatologists, who typically manage liver disease, may not think to ask about oral health or refer patients for dental care. Yet the data suggest they should. Similarly, dental professionals may not realize how their work can affect liver disease outcomes. Closer collaboration between these disciplines could lead to earlier detection and better treatment.
Until more definitive evidence is available, one thing is clear: brushing, flossing, and regular visits to the dentist may be more important than we realize, especially for people with chronic liver disease. In the meantime, the researchers are calling for larger, higher-quality trials to test whether treating gum disease can slow liver disease progression or reduce complications. If the link holds, the humble toothbrush could become an unexpected tool in the fight against liver failure.
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