Periodontal disease may induce liver fibrosis in an experimental study on Wistar rats

Meşter, Alexandru; Ciobanu, Lidia; Taulescu, Marian; Apostu, Dragoș; Lucaciu, Ondine; Filip, Gabriela Adriana; Feldrihan, Vasile; Licărete, Emilia; Ilea, Aranka; Piciu, Doina; Oltean‐Dan, Daniel; Scurtu, Iuliu; Berce, Cristian; Câmpian, Radu Septimiu

doi:10.1002/jper.18-0585

Cited by 22 publications

(24 citation statements)

References 40 publications

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“…One animal study showed that periodontitis induced by virulent periodontal factors determined oxidative damage of the liver in rats (Tomofuji et al, 2007). A previous study confirmed that experimental periodontitis induced the increasing level of the oxidative stress parameters and liver fibrosis in rats (Mester et al, 2019). In this study, a significant relationship was observed between CAL and liver fibrosis, while no association was found in PD.…”

Section: Discussionsupporting

confidence: 73%

“…These contributors act in a coordinated and cooperative manner to promote hepatic inflammation and fibrosis (Tilg & Moschen, 2010). Periodontitis could promote hepatic injury by increasing systemic inflammation and oxidative stress (Alazawi et al, 2017; Mester et al, 2019). One animal study showed that periodontitis induced by virulent periodontal factors determined oxidative damage of the liver in rats (Tomofuji et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

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Association between periodontitis and fibrotic progression of non‐alcoholic fatty liver among Japanese adults

Kuroe

Furuta

Takeuchi

et al. 2021

J Clinic Periodontology

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Aim Non‐alcoholic fatty liver (NAFL) is known to develop into liver fibrosis, which increases the risk of liver cirrhosis and liver cancer. The association between periodontal condition and fibrotic progression of NAFL is unclear. This study aimed to clarify this longitudinal association. Materials and Methods Among 4812 participants aged 35–64 years undergoing annual health check‐ups between 2003 and 2004, and follow‐up 5 years later, 392 participants were diagnosed with NAFL. After excluding participants with liver fibrosis at baseline, 341 participants were followed up for 5 years. NAFL disease fibrosis score of ≥−1.455 was used to evaluate the probability of the presence of liver fibrosis. Results During the follow‐up period, 10.6% of participants progressed to liver fibrosis. A higher clinical attachment level (CAL) tended to be associated with the incidence of liver fibrosis in the logistic regression analysis (odds ratio [OR] 1.82, 95% confidence interval [CI], 0.94–3.49, p = .074). The stratified analysis by obesity revealed a significant association with higher CAL in obese participants (OR 2.87, 95% CI, 1.23–6.69, p = .015), but not in non‐obese participants. Conclusion Higher CAL was associated with an increased probability of liver fibrosis in obese adults with NAFL.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 99%

Association between periodontitis and fibrotic progression of non‐alcoholic fatty liver among Japanese adults

Kuroe

Furuta

Takeuchi

et al. 2021

J Clinic Periodontology

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“…Micro-CT images of the right halves were taken with Skyscan (Bruker MicroCT, Kontich, Belgium) after macroscopic examination. Three-dimensional reconstructions were made and analyzed by NRecon 1.6.3 (Brucker MicroCT) [ 48 ].…”

Section: Methodsmentioning

confidence: 99%

Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS

Sun

et al. 2020

Molecules

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Conventional treatments for chronic periodontitis are less effective in controlling inflammation and often relapse. Therefore, it is necessary to explore an immunomodulatory medication as an adjuvant. Ginsenoside Rb3 (Rb3), one of the most abundant active components of ginseng, has been found to possess anti-inflammatory and immunomodulatory properties. Here, we detected the anti-inflammatory effect of Rb3 on Porphyromonas gingivalis LPS-stimulated human periodontal ligament cells and experimental periodontitis rats for the first time. We found that the expression of pro-inflammatory mediators, including IL-1β, IL-6 and IL-8, upregulated by lipopolysaccharide (LPS) stimulation was remarkably downregulated by Rb3 treatment in a dose-dependent manner at both transcriptional and translational levels. Network pharmacological analysis of Rb3 showed that the mitogen-activated protein kinase (MAPK) signaling pathway had the highest richness and that p38, JNK, and ERK molecules were potential targets of Rb3 in humans. Western blot analysis revealed that Rb3 significantly suppressed the phosphorylation of p38 MAPK and p65 NF-κB, as well as decreased the expression of total AKT. In experimental periodontitis rat models, reductions in alveolar bone resorption and osteoclast generation were observed in the Rb3 treatment group. Thus, we can conclude that Rb3 ameliorated Porphyromonas gingivalis LPS-induced inflammation by inhibiting the MAPK/AKT/NF-κB signaling pathways and attenuated alveolar bone resorption in experimental periodontitis rats.

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“…Tooth mobility (TM) was elevated according to the following scale: 0 = physiological mobility; 1 = slight mobility in buccolingual direction; 2 = moderate mobility in buccolingual and mesiodistal directions; and 3 = severe mobility in buccolingual, mesiodistal, and vertical directions (Mester et al., 2019).…”

Section: Methodsmentioning

confidence: 99%

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

et al. 2020

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Periodontitis is an inflammatory oral disease characterized by periodontal pathogenic bacteria as the initiating factor and the destruction of periodontal supporting tissues, that are gingiva, periodontal membrane, and alveolar bone resorption (Kinane, Stathopoulou, & Papapanou, 2017), affecting most of the adults worldwide (Bellentani, 2017; Eke et al., 2015). One of the pathogenic factors of periodontitis is imbalance in the host reactions caused by the appearance and persistence of dysbiotic oral microbiota and other metabolites that cause the overproduction of inflammatory mediators. In addition, periodontitis can induce an imbalance between oxidant and antioxidant agents, ultimately causes the periodontal tissue damages (Hajishengallis, 2015).

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Periodontal disease may induce liver fibrosis in an experimental study on Wistar rats

Cited by 22 publications

References 40 publications

Association between periodontitis and fibrotic progression of non‐alcoholic fatty liver among Japanese adults

Association between periodontitis and fibrotic progression of non‐alcoholic fatty liver among Japanese adults

Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response to Porphyromonas gingivalis LPS

The role of TLR4/MyD88/NF‐κB pathway in periodontitis‐induced liver inflammation of rats

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