ReviewCureus2024
Role of Nonalcoholic Fatty Liver Disease in Periodontitis: A Bidirectional Relationship.
Review in Cureus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- ZNF143 suppresses mitophagy to drive MASLD progression by regulating SMURF1/TRPV1 axis.Molecular genetics and genomics : MGG · 2026Article
- Melatonin protects liver and periodontal tissues from inflammation exacerbated by metabolic syndrome-periodontitis association.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Peptidylarginine deiminase in Porphyromonas gingivalis-derived outer membrane vesicles exacerbates metabolic dysfunction-associated steatotic liver disease through the NPAS2/CYP4A10 pathway.Journal of nanobiotechnology · 2026Article
- Metabolomic characteristics and mechanisms of subgingival plaque in MASLD patients with periodontitis.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Periodontitis and MASLD: a narrative review of the direct oral-hepatic pathway.Frontiers in cellular and infection microbiology · 2026Review
- Analysis of subgingival microbial community structure in MAFLD patients with periodontitis.Clinical oral investigations · 2025Article
- Lipid Metabolism and Relevance to Chronic Disease.Nutrients · 2025Article
- Interaction Between Periodontitis and MASLD: Pathophysiological Associations and Possibilities of Prevention and Therapy.Biomedicines · 2025Review
- Development of liver disease caused by chronic periodontitis in rats.Journal of applied oral science : revista FOB · 2025Article
- Role of gut-brain axis dysregulation in the pathogenesis of non-alcoholic fatty liver disease: mechanisms and therapeutic implications.American journal of translational research · 2025Review
- The Involvement of Resolvins in Pathological Mechanisms of Periodontal Disease Associated with Type 2 Diabetes: A Narrative Review.International journal of molecular sciences · 2024Review
- The Impact of Type 2 Diabetes Mellitus on Non-Surgical Periodontal Treatment: A Non-Randomized Clinical Trial.Journal of clinical medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) and periodontitis share common risk factors such as obesity, insulin resistance (IR), and dyslipidemia, which contribute to systemic inflammation. It has been suggested that a bidirectional relationship exists between NAFLD and periodontitis, indicating that one condition may exacerbate the other. NAFLD is characterized by excessive fat deposition in the liver and is associated with low-grade chronic inflammation. There are several risk factors for the development of NAFLD, including gender, geriatric community, race, ethnicity, poor sleep quality and sleep deprivation, physical activity, nutritional status, dysbiosis gut microbiota, increased oxidative stress, overweight, obesity, higher body mass index (BMI), IR, type 2 diabetes mellitus (T2DM), metabolic syndrome (MetS), dyslipidemia (hypercholesterolemia), and sarcopenia (decreased skeletal muscle mass). This systemic inflammation can contribute to the progression of periodontitis by impairing immune responses and exacerbating the inflammatory processes in the periodontal tissues. Furthermore, individuals with NAFLD often exhibit altered lipid metabolism, which may affect oral microbiota composition, leading to dysbiosis and increased susceptibility to periodontal disease. Conversely, periodontitis has been linked to the progression of NAFLD through mechanisms involving systemic inflammation and oxidative stress. Chronic periodontal inflammation can release pro-inflammatory cytokines and bacterial toxins into the bloodstream, contributing to liver inflammation and exacerbating hepatic steatosis. Moreover, periodontitis-induced oxidative stress may promote hepatic lipid accumulation and IR, further aggravating NAFLD. The interplay between NAFLD and periodontitis underscores the importance of comprehensive management strategies targeting both conditions. Lifestyle modifications such as regular exercise, a healthy diet, and proper oral hygiene practices are crucial for preventing and managing these interconnected diseases. Additionally, interdisciplinary collaboration between hepatologists and periodontists is essential for optimizing patient care and improving outcomes in individuals with NAFLD and periodontitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.