Oral-Hepatic Axis in Liver Toxicity: The Emerging Role of Dental Infections in Hepatic Dysfunction

Introduction and Clinical Significance

The clinical presentation of liver toxicity secondary to dental pathology represents an underappreciated yet mechanistically plausible phenomenon that bridges multiple fields of medicine—from dentistry and oral surgery to hepatology and functional medicine. While conventional hepatology often focuses on viral hepatitis, alcohol-related liver disease, and metabolic dysfunction, an emerging body of evidence reveals that chronic oral infections, particularly those associated with periodontitis, root canal infections, and cavitations (ischemic osteonecrosis of the jawbone), can contribute significantly to systemic inflammation and hepatic injury through what has been termed the "oral-gut-liver axis."

The connection between oral health and liver disease is not merely correlative but appears to be mechanistically driven by several interconnected pathways: bacterial translocation from oral sites to the liver via the bloodstream, the production and systemic dissemination of bacterial endotoxins (particularly lipopolysaccharide, or LPS), chronic low-grade systemic inflammation, and disruption of the intestinal barrier function that normally protects the liver from enteric bacterial products. Recent research has established that periodontitis and metabolic dysfunction-associated steatotic liver disease (MASLD) share common pathophysiological mechanisms, with chronic inflammation and oral bacteria from periodontal disease triggering systemic inflammatory responses that directly impact hepatic function [12]. This relationship is sufficiently robust that hepatologists and dentists are now being called upon to collaborate more closely in managing patients with liver disease [12].

The gut-liver axis has been extensively studied and is now recognized as a critical determinant of hepatic health [1]. However, the oral cavity represents the first point of contact with the external environment and serves as a reservoir for potentially pathogenic bacteria that can influence both intestinal and hepatic homeostasis. When dental infections persist—whether from failed root canals, cavitations, or advanced periodontitis—they create a continuous source of bacterial antigens and inflammatory mediators that can overwhelm the body's natural detoxification and immune regulatory systems. This chronic antigenic load places particular stress on the liver, which must process and detoxify these bacterial products while simultaneously managing its metabolic, synthetic, and immunological functions.

Mechanistic Pathways: From Oral Infection to Hepatic Injury

The pathophysiology linking oral infections to liver toxicity involves several overlapping and synergistic mechanisms that collectively create a perfect storm for hepatic dysfunction.

Bacterial Translocation and Endotoxemia

The primary mechanism through which oral infections influence hepatic function is through bacterial translocation—the passage of viable bacteria or their products from the oral cavity into the systemic circulation. Unlike the intestinal tract, which has multiple barrier mechanisms including tight junctions, mucus layers, and secretory IgA, the oral mucosa is relatively permeable, particularly in areas of active inflammation or infection. When periodontitis or periapical infections are present, the integrity of the gingival epithelium is compromised, creating portals of entry for oral bacteria into the bloodstream [8].

Once in circulation, these bacteria and their products—particularly LPS from gram-negative organisms commonly found in periodontal pockets and infected root canals—trigger a systemic inflammatory cascade. The liver, receiving approximately 75% of its blood supply from the portal vein (which drains the intestinal tract) and 25% from the hepatic artery, is continuously exposed to these circulating bacterial products. Hepatic Kupffer cells, the resident macrophages of the liver, recognize LPS through toll-like receptor 4 (TLR4), initiating the production of pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) [8][12].

The Gut-Liver Axis Disruption

Critically, oral dysbiosis does not remain confined to the oral cavity but can significantly impact the composition and function of the intestinal microbiome. Research has demonstrated that oral bacteria can travel to and colonize the intestinal tract, where they may disrupt the normal commensal bacterial populations [8]. This oral-to-gut bacterial translocation has been particularly well documented in the context of periodontitis, where pathogenic oral bacteria such as Porphyromonas gingivalis, Fusobacterium nucleatum, and Aggregatibacter actinomycetemcomitans have been detected in intestinal tissue and fecal samples [12].

The intestinal dysbiosis resulting from oral bacterial seeding has profound implications for hepatic health. The gut microbiome plays a central role in maintaining intestinal barrier integrity, regulating bile acid metabolism, modulating systemic inflammation, and producing metabolites that influence hepatic function [1][17]. When this delicate ecosystem is disrupted, several pathological processes ensue. First, intestinal barrier function deteriorates—a phenomenon known as "leaky gut"—allowing increased translocation of bacteria and bacterial products from the intestinal lumen into the portal circulation [11][19]. This increased bacterial translocation delivers a heightened antigenic load directly to the liver, overwhelming its capacity for detoxification and immune regulation.

Second, dysbiosis alters the production of bacterial metabolites that normally support hepatic health. Short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate are produced by commensal bacteria and serve critical functions including maintaining intestinal barrier integrity, regulating inflammation, and modulating hepatic lipid metabolism [1][17]. When dysbiosis reduces SCFA production, these protective effects are lost, predisposing to both intestinal permeability and hepatic metabolic dysfunction.

Third, dysbiosis disrupts bile acid metabolism, a critical function of the gut-liver axis. Bile acids are synthesized in the liver, stored in the gallbladder, secreted into the intestine to facilitate fat digestion, and then partially reabsorbed and returned to the liver via enterohepatic circulation. The gut microbiome performs essential modifications of bile acids through deconjugation and dehydroxylation reactions [1][16]. When these microbial processes are disrupted, the composition of the bile acid pool changes, potentially leading to accumulation of toxic bile acid species that can directly injure hepatocytes [6]. Furthermore, bile acids serve as signaling molecules that activate nuclear receptors such as the farnesoid X receptor (FXR), which regulates glucose and lipid metabolism, inflammation, and hepatic regeneration [16]. Dysbiosis-induced alterations in bile acid signaling can therefore have wide-ranging effects on hepatic function.

Chronic Systemic Inflammation

Perhaps the most clinically significant mechanism linking oral infections to liver toxicity is the establishment of chronic, low-grade systemic inflammation. Both periodontitis and endodontic infections create persistent inflammatory foci that continuously release pro-inflammatory cytokines into the circulation [12]. This chronic inflammatory state has been implicated in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD), the most common liver disorder worldwide [8][12].

The relationship between periodontitis and MAFLD is bidirectional and self-reinforcing. Chronic oral inflammation drives hepatic inflammation and metabolic dysfunction, while metabolic syndrome (which is closely associated with MAFLD) impairs immune function and wound healing, predisposing to more severe periodontal disease [12]. The inflammatory mediators produced in response to oral infections—including C-reactive protein (CRP), IL-6, and TNF-α—have direct hepatotoxic effects. IL-6, in particular, has been shown to play a central role in the inflammatory cascade associated with alcoholic liver disease, and probiotics that reduce IL-6 levels have demonstrated hepatoprotective effects [20].

At the cellular level, chronic inflammation promotes hepatic stellate cell activation, the key step in hepatic fibrogenesis [11][16]. When hepatic stellate cells are activated by inflammatory signals, they transform from quiescent, vitamin A-storing cells into proliferative, collagen-producing myofibroblasts that deposit extracellular matrix and drive progressive liver fibrosis. The inflammatory milieu also promotes hepatocyte apoptosis and necrosis, further perpetuating the cycle of inflammation and injury.

Oxidative Stress and Mitochondrial Dysfunction

Chronic infection and inflammation generate reactive oxygen species (ROS) that contribute to oxidative stress in hepatocytes. The liver is particularly vulnerable to oxidative damage due to its high metabolic activity and rich blood supply. Oxidative stress leads to lipid peroxidation, protein oxidation, and DNA damage, all of which impair hepatocellular function [5][7]. Mitochondria, the powerhouses of the cell, are especially susceptible to oxidative damage. When mitochondrial function is compromised, hepatocytes lose their capacity for fatty acid oxidation, leading to intracellular lipid accumulation—a hallmark of fatty liver disease [5]. Additionally, damaged mitochondria release damage-associated molecular patterns (DAMPs) that further activate inflammatory pathways, creating a vicious cycle of inflammation, oxidative stress, and cellular injury.

Dental infections liver toxicity: Clinical Evidence and Key Studies

The clinical evidence linking oral infections to liver disease spans multiple research domains, from epidemiological studies demonstrating associations between periodontitis and liver disease to mechanistic studies elucidating the biological pathways involved.

Periodontitis and Liver Disease

Multiple studies have established a robust association between periodontitis and metabolic dysfunction-associated liver disease. A comprehensive review emphasized the clinical interplay between gum disease and MASLD, noting that chronic inflammation and oral bacteria from periodontal disease can spread systemically, reaching and affecting the liver [12]. The review called for enhanced collaboration between hepatologists and dentists, recognizing that effective management of liver disease may require addressing underlying oral infections.

A Chinese-language review published in the Journal of Sichuan University Medical Science Edition further explored this connection, describing how oral dysbiosis leads to hepatic metabolic dysregulation [8]. The authors detailed how bacteria from diseased gums can travel to the liver via the bloodstream, where they trigger inflammatory responses and disrupt normal metabolic processes. This direct bacterial translocation from oral sites to hepatic tissue represents a critical mechanism that is often overlooked in conventional hepatology practice.

The Gut-Microbiota-Liver Axis in Hepatic Disease

The broader context of gut-liver axis dysfunction provides important insights into how oral infections might precipitate or exacerbate liver disease. A comprehensive review in Frontiers in Immunology explored how the gut-microbiota-liver axis drives MAFLD [1]. The authors emphasized that gut microbial dysbiosis leads to increased intestinal permeability, enhanced translocation of bacterial products to the liver, and altered production of microbial metabolites that influence hepatic metabolism and inflammation. While this review focused primarily on intestinal dysbiosis, the mechanisms described are directly applicable to oral infection-induced liver disease, as oral bacteria can seed the intestinal microbiome and thereby influence the entire gut-liver axis.

Supporting this concept, research has demonstrated that various environmental toxins and dietary factors can disrupt the gut-liver axis and precipitate hepatic injury. For instance, a study on the fungicide fluazinam showed that this compound causes liver metabolism disorders and intestinal inflammation by disrupting gut bacteria and bile acid metabolism [3]. Similarly, research on bisphenol P revealed that this chemical triggers hepatic injury via gut microbiota dysbiosis-induced intestinal barrier disruption [19]. While these studies focused on chemical toxins rather than infections, they illustrate a critical principle: disruption of the gut-liver axis, regardless of the initial insult, can lead to significant hepatic pathology. Oral infections represent another such insult that can initiate this cascade.

Small Intestinal Bacterial Overgrowth and Liver Disease

The connection between bacterial overgrowth and liver disease has been particularly well studied in the context of cirrhosis. A cross-sectional study examined the association between small intestinal bacterial overgrowth (SIBO) and portal hypertension in patients with hepatitis C-related cirrhosis [15]. The researchers found that SIBO was significantly more common in cirrhotic patients with portal hypertension, suggesting that altered gut bacterial populations contribute to disease progression. While this study focused on intestinal overgrowth rather than oral infections per se, it demonstrates that bacterial dysbiosis—whether originating from the intestine or seeded from oral sources—can worsen liver disease and its complications.

Furthermore, research on the intestinal LGR4 signaling pathway revealed how gut barrier dysfunction influences liver fibrosis [11]. The study found that alterations in intestinal barrier function affect bacterial translocation, intrahepatic microbiota composition, and hepatic immune responses, all of which contribute to progressive liver scarring. This provides direct mechanistic evidence that bacterial translocation from any source—including oral infections—can drive hepatic fibrogenesis.

Therapeutic Interventions Targeting the Gut-Liver Axis

The therapeutic potential of modulating the microbiome-gut-liver axis has been extensively investigated, providing further evidence of the causal relationship between dysbiosis and liver disease. A systematic review and network meta-analysis evaluated gut microbiome-modulating therapies in patients with liver cirrhosis [2]. The researchers found that probiotics, prebiotics, and synbiotics significantly improved liver function and reduced disease severity. These benefits were attributed to restoration of gut microbial balance, reduced bacterial translocation, and modulation of inflammatory responses. While these interventions were administered to the intestinal tract, their efficacy in treating liver disease underscores the importance of addressing bacterial dysbiosis at all levels—including its potential oral sources.

Specific studies on probiotics in liver disease have yielded promising results. Research on probiotics in alcoholic liver disease found that probiotic supplementation significantly reduced inflammatory cytokines, particularly IL-6, while increasing the anti-inflammatory cytokine IL-10 [20]. These findings suggest that interventions aimed at restoring microbial balance can directly mitigate the inflammatory processes that drive liver injury.

The potential of fermented foods to modulate the gut-liver axis has also been explored, with evidence suggesting that fermented foods improve gut microbial diversity, enhance intestinal barrier function, and reduce hepatic inflammation [17]. The therapeutic effects of these dietary interventions support the concept that modulating microbial populations—whether through diet, probiotics, or addressing sources of pathogenic bacteria such as oral infections—can meaningfully impact liver health.

Natural Compounds and Hepatoprotection via the Gut-Liver Axis

Several studies have demonstrated that natural compounds with anti-inflammatory and microbiome-modulating properties can ameliorate liver disease through effects on the gut-liver axis. Research on black sesame pigment showed that it significantly improved non-alcoholic fatty liver disease by modulating gut microbiota composition, enhancing intestinal barrier integrity, and suppressing hepatic inflammation through the HIF-1 signaling pathway [5]. Similarly, anthocyanins from purple highland barley bran demonstrated hepatoprotective effects in NAFLD through restoration of gut microbial balance and reduction of inflammatory signaling [7]. Safflower polysaccharides improved alcoholic liver fibrosis by targeting the FXR receptor, regulating intestinal flora, and modulating bile acid metabolism [16].

These studies collectively demonstrate that compounds which restore microbial balance and reduce inflammation can reverse liver disease, even in advanced cases with established fibrosis. This suggests that addressing the root causes of dysbiosis and inflammation—including chronic oral infections—should be a therapeutic priority.

Advanced Diagnostic Approaches

Recent advances in machine learning and multi-omics analysis have revealed the profound influence of the microbiome on liver disease staging and progression. A study published in Computers in Biology and Medicine developed a machine learning tool that integrates clinical data, biochemical markers, and microbiome insights to non-invasively stage liver fibrosis in NASH patients [14]. The success of this approach highlights the central role that microbial dysbiosis plays in liver disease pathogenesis and suggests that comprehensive assessment of microbial status—including oral microbial populations—should be part of the evaluation of patients with unexplained liver disease.

A comprehensive review in Critical Reviews in Oncology/Hematology explored the microbiome-gut-liver axis in chronic inflammation and cancer, emphasizing how this axis profoundly impacts health and disease trajectories [13]. The authors advocated for a multi-omics approach and personalized medicine strategies that account for individual variations in microbial composition and host-microbe interactions. This precision medicine framework is particularly relevant for patients with liver toxicity secondary to oral infections, as individual variation in oral and gut microbiome composition, immune function, and genetic susceptibility likely influences disease risk and therapeutic response.

Fecal Microbiota Transplantation in Liver Disease

The most direct evidence that microbial dysbiosis drives liver disease comes from studies of fecal microbiota transplantation (FMT). Research has shown that FMT can help various liver diseases by restoring gut health and rebalancing the microbiome [18]. FMT has demonstrated benefits in patients with hepatic encephalopathy, alcoholic hepatitis, and NAFLD. The mechanism appears to involve restoration of beneficial bacterial populations, reduction of pathogenic bacteria, enhancement of intestinal barrier function, and modulation of bile acid metabolism. While FMT addresses intestinal dysbiosis rather than oral infections directly, its efficacy provides proof-of-concept that correcting dysbiosis—wherever it originates—can reverse liver disease.

Functional Medicine Implications and Clinical Management

The evidence linking oral infections to liver toxicity has profound implications for functional medicine practice and demands an integrated, systems-based approach to patient care. For the patient presenting with liver toxicity secondary to cavitations or infected root canals, several clinical interventions should be considered.

Dental Intervention as Primary Treatment

The most critical intervention is addressing the source of infection through appropriate dental treatment. This may involve surgical exploration and remediation of cavitations, retreatment or extraction of failed root canals, and comprehensive periodontal therapy for active gum disease. Cavitations, or areas of ischemic bone necrosis in the jaw, are particularly problematic as they harbor anaerobic bacteria in a protected environment that is difficult for the immune system to access. These sites can serve as chronic sources of bacterial antigens and inflammatory mediators. Surgical debridement of cavitational lesions, often guided by cone beam computed tomography (CBCT) imaging, may be necessary to eliminate the infectious nidus.

For infected root canals, the decision between retreatment and extraction should be made carefully, considering the extent of periapical pathology, the structural integrity of the tooth, and the patient's overall systemic health. In patients with significant liver dysfunction or systemic inflammatory disease, extraction may be preferable to avoid ongoing antigenic exposure. Following extraction, meticulous socket management and possibly adjunctive therapies such as platelet-rich fibrin (PRF) or ozone therapy may promote optimal healing and reduce the risk of developing new cavitations.

Restoring Gut Microbial Balance

Given the central role of gut dysbiosis in mediating the effects of oral infections on liver health, interventions aimed at restoring intestinal microbial balance are essential. High-quality, multi-strain probiotics containing species such as Lactobacillus, Bifidobacterium, and Saccharomyces boulardii have demonstrated benefits in liver disease [2][20]. The optimal probiotic regimen should provide adequate colony-forming units (typically 25-100 billion CFU daily) and include strains with documented anti-inflammatory and barrier-protective properties.

Prebiotics—non-digestible fibers that selectively promote the growth of beneficial bacteria—should also be incorporated, either through supplementation or through dietary sources such as vegetables, fruits, legumes, and whole grains [2]. Synbiotics, which combine probiotics and prebiotics, may offer synergistic benefits [2]. Additionally, fermented foods such as sauerkraut, kimchi, kefir, and traditionally fermented vegetables provide both live beneficial organisms and bioactive compounds that support gut and liver health [17].

Enhancing Intestinal Barrier Function

Restoration of intestinal barrier integrity is critical to prevent ongoing bacterial translocation to the liver. Several nutrients and compounds have demonstrated efficacy in supporting barrier function:

• L-glutamine: An amino acid that serves as the primary fuel source for enterocytes and supports tight junction integrity
• Zinc: Essential for maintaining epithelial barrier function and immune competence
• Vitamin D: Modulates tight junction proteins and supports immune regulation
• Butyrate: A short-chain fatty acid that nourishes colonocytes and enhances barrier function (can be supplemented directly or promoted through prebiotic fiber intake)
• Quercetin: A flavonoid with anti-inflammatory properties that supports barrier integrity

Anti-Inflammatory and Hepatoprotective Interventions

Given the role of chronic inflammation in mediating liver injury, targeted anti-inflammatory interventions are warranted. Natural compounds with documented hepatoprotective and anti-inflammatory properties include:

• Silymarin (milk thistle): Contains silybinin and other flavonolignans that protect hepatocytes from oxidative damage, support glutathione production, and modulate inflammatory signaling
• N-acetylcysteine (NAC): A glutathione precursor with direct antioxidant effects and ability to reduce hepatic inflammation
• Curcumin: The active compound in turmeric, with potent anti-inflammatory and antioxidant properties; lipidated or nano-formulations enhance bioavailability
• Omega-3 fatty acids: EPA and DHA from fish oil reduce hepatic inflammation and improve metabolic parameters in NAFLD
• Anthocyanins and polyphenols: Found in berries, purple vegetables, and certain whole grains, these compounds modulate the gut-liver axis and reduce hepatic oxidative stress [5][7]

Supporting Bile Acid Metabolism

Given the importance of bile acid signaling in hepatic health and the role of dysbiosis in disrupting bile acid metabolism, interventions to support this pathway should be considered. These may include:

• Bile acid sequestrants or binders: In cases of bile acid accumulation or dysregulation (though these must be used judiciously and monitored carefully)
• Taurine: An amino acid involved in bile acid conjugation
• Fiber: Soluble fiber binds bile acids in the intestine and promotes their excretion, helping to regulate the bile acid pool
• FXR agonists: While pharmaceutical FXR agonists are in development, natural compounds such as those found in safflower may support FXR signaling [16]

Comprehensive Detoxification Support

The liver's detoxification capacity may be overwhelmed in the context of chronic bacterial antigen exposure. Supporting hepatic detoxification pathways can help reduce toxic burden:

• Phase I support: B vitamins (especially B2, B3, B6, B12, and folate) serve as cofactors for cytochrome P450 enzymes
• Phase II support: Sulfur-containing amino acids (cysteine, methionine), glycine, glutathione, and cruciferous vegetables support conjugation reactions
• Phase III support: Adequate hydration and fiber intake support the elimination of conjugated toxins

Monitoring and Follow-Up

Patients with liver toxicity secondary to oral infections require careful monitoring to assess response to treatment and adjust interventions accordingly. Laboratory assessment should include:

• Liver function tests: ALT, AST, alkaline phosphatase, GGT, bilirubin, albumin
• Inflammatory markers: CRP, IL-6 (if available)
• Metabolic markers: Fasting glucose, insulin, lipid panel
• Intestinal barrier markers: Zonulin, LPS antibodies, or other markers of intestinal permeability (if available)
• Advanced fibrosis markers: Fibrosis-4 (FIB-4) score, NAFLD fibrosis score, or direct assessment via elastography or imaging

Clinical reassessment should occur at regular intervals (typically every 4-8 weeks initially, then every 3-6 months) to evaluate symptom improvement, normalize laboratory abnormalities, and prevent disease progression.

Lifestyle and Dietary Interventions

Beyond supplements and dental treatment, fundamental lifestyle and dietary modifications are essential:

• Anti-inflammatory diet: Emphasis on whole foods, vegetables, fruits, legumes, nuts, seeds, and fatty fish; minimization of processed foods, refined sugars, and inflammatory fats
• Avoidance of alcohol: Complete abstinence is advisable during active liver disease
• Weight management: If metabolic syndrome or obesity is present, gradual weight loss improves hepatic function
• Regular physical activity: Exercise improves insulin sensitivity, reduces hepatic fat, and modulates inflammation
• Stress management: Chronic stress impairs immune function and gut barrier integrity; mind-body practices such as meditation, yoga, or deep breathing support healing
• Sleep optimization: Adequate, restorative sleep is essential for immune function and hepatic regeneration

Conclusion and Clinical Takeaways

The emerging understanding of the oral-gut-liver axis reveals that chronic oral infections—including periodontitis, failed root canals, and cavitations—can contribute significantly to liver toxicity through multiple interconnected mechanisms. Bacterial translocation from oral sites to the systemic circulation and liver, seeding of the intestinal microbiome with pathogenic oral bacteria, chronic systemic inflammation, disruption of intestinal barrier function, and perturbation of bile acid metabolism collectively create a cascade of events that can precipitate or exacerbate hepatic dysfunction.

For the clinician managing a patient with liver toxicity secondary to oral infections, a comprehensive, systems-based approach is essential. This must begin with definitive treatment of the oral infection through appropriate dental intervention—whether surgical remediation of cavitations, retreatment or extraction of infected root canals, or comprehensive periodontal therapy. However, dental treatment alone is insufficient; restoration of gut microbial balance, enhancement of intestinal barrier function, reduction of systemic inflammation, support of hepatic detoxification pathways, and optimization of bile acid metabolism are all critical components of a complete therapeutic strategy.

The evidence reviewed here underscores several key clinical principles: First, the oral cavity should be considered a potential source of systemic inflammation and liver disease in patients with unexplained hepatic dysfunction. Second, collaboration between dentists, oral surgeons, and functional medicine practitioners is essential for optimal patient outcomes. Third, interventions targeting the microbiome—through probiotics, prebiotics, fermented foods, and natural compounds—have demonstrated efficacy in improving liver function and should be incorporated into treatment protocols. Fourth, restoration of intestinal barrier integrity is critical to prevent ongoing bacterial translocation and hepatic injury. Fifth, comprehensive support of hepatic detoxification and anti-inflammatory pathways accelerates healing and prevents disease progression.

As our understanding of the microbiome-gut-liver axis continues to evolve, it becomes increasingly clear that optimal liver health requires attention to the entire digestive tract—from the oral cavity through the intestines. For patients with liver toxicity secondary to oral infections, addressing the root cause through integrated dental and functional medicine interventions offers the best hope for meaningful clinical improvement and long-term health restoration.

References

[1] Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis. Frontiers in Immunology (2026). https://pubmed.ncbi.nlm.nih.gov/41716420/

[2] The Efficacy of Gut Microbiome-Modulating Therapies on Liver Cirrhosis: A Systematic Review and Network Meta-Analysis. Clinical and Translational Gastroenterology (2026). https://pubmed.ncbi.nlm.nih.gov/41778620/

[3] Fluazinam Caused Liver Metabolism Disorders and Intestinal Inflammation by Affecting Gut-Liver Axis in Mice. Journal of Agricultural and Food Chemistry (2026). https://pubmed.ncbi.nlm.nih.gov/41848155/

[5] Black Sesame Pigment Ameliorates Non-Alcoholic Fatty Liver Disease via Modulation of the Gut-Liver Axis and HIF-1 Signaling Pathway. Antioxidants (Basel, Switzerland) (2026). https://pubmed.ncbi.nlm.nih.gov/41750558/

[6] The secretory protein, CLCF1, improves cholestatic liver disease by inhibiting hepatic bile acid synthesis and promoting bile acid excretion. Communications Biology (2026). https://pubmed.ncbi.nlm.nih.gov/41840139/

[7] Hepatoprotective potential of anthocyanins from purple highland barley bran against non-alcoholic fatty liver disease through gut-liver axis. Food Research International (Ottawa, Ont.) (2026). https://pubmed.ncbi.nlm.nih.gov/41794448/

[8] [Periodontitis and Metabolic Dysfunction-Associated Fatty Liver Disease: From Oral Dysbiosis to Hepatic Metabolic Dysregulation]. Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical Science Edition (2026). https://pubmed.ncbi.nlm.nih.gov/41834959/

[11] Intestinal LGR4 Signalling Alters Bacterial translocation, Intrahepatic Microbiota composition, and Type 1 Interferon Expression in Murine Liver Fibrosis. Inflammation (2025). https://pubmed.ncbi.nlm.nih.gov/41420724/

[12] Periodontitis and Metabolic Dysfunction-Associated Steatotic Liver Disease: emphasizing the clinical interplay between hepatologists and dentists. Odontology (2025). https://pubmed.ncbi.nlm.nih.gov/40954401/

[13] Microbiome-gut-liver axis in chronic inflammation and cancer immunotherapy: Multi-omics Insights and a translational roadmap toward personalized medicine. Critical Reviews in Oncology/Hematology (2026). https://pubmed.ncbi.nlm.nih.gov/41707756/

[14] Revolutionizing hepatic fibrosis staging: A machine learning approach combining clinical, biochemical, and microbiome insights. Computers in Biology and Medicine (2026). https://pubmed.ncbi.nlm.nih.gov/41806697/

[15] Association of small intestinal bacterial overgrowth with portal hypertension in HCV-related cirrhosis: a cross-sectional study. Clinical and Experimental Medicine (2026). https://pubmed.ncbi.nlm.nih.gov/41838205/

[16] Safflower Polysaccharides Target FXR to Regulate Intestinal Flora and Metabolic Disorders, Affecting FGFR4/FGF15 to Improve Alcoholic Liver Fibrosis in Mice. Phytotherapy Research : PTR (2026). https://pubmed.ncbi.nlm.nih.gov/41844399/

[17] Fermented Foods and the Gut-Liver Axis: Modulation of MASLD Through Gut Microbiota. Nutrients (2026). https://pubmed.ncbi.nlm.nih.gov/41683364/

[18] Fecal microbiota transplantation in liver diseases: Therapeutic potential and associated risks. Progress in Molecular Biology and Translational Science (2026). https://pubmed.ncbi.nlm.nih.gov/41714079/

[19] Bisphenol P triggers hepatic injury via gut microbiota dysbiosis-Induced intestinal barrier disruption. Journal of Environmental Management (2026). https://pubmed.ncbi.nlm.nih.gov/41707419/

[20] Evaluating the Efficacy of Probiotics on Inflammatory Cytokines in Alcoholic Liver Disease: A Focus on IL-6 and IL-10. Nutrients (2026). https://pubmed.ncbi.nlm.nih.gov/41754184/

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