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

Yiyun Yue, Xinchan Liu, Li Yan, Boyuan Xia, Weixian Yu

2020Oral Diseases27 citationsDOIOpen Access PDF

Abstract

OBJECTIVES: The aim of this study was to clarify the immune mechanism of hepatic injury induced by periodontitis using a rat model. METHODS: Twenty-four SPF male Wistar rats were randomly divided into two groups: control group (CG) and periodontitis group (PG). In order to induce experimental periodontitis, we tied the wire ligature around bilateral maxillary first molar of rats. After 8 weeks, the following indicators were valued: gingival index, tooth mobility, probing pocket depth; indexes about oxidative stress and circulating biomarkers; bone retraction by micro-CT analysis; Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and nuclear factor kappa B (NF-κB) by qRT-PCR and Western blotting; tumor necrosis factor α (TNF-α), and interleukin-6 (IL-6) by qRT-PCR and immunohistochemical staining; inflammation of periodontal and hepatic tissues by histopathological observation. RESULTS: Periodontal indicators and micro-CT results showed the raised levels of inflammatory response and bone retraction in PG compared with CG. The mRNA and protein levels of TLR4, MyD88, NF-κB, TNF-α, and IL-6 have indicated high values in PG versus CG. Histopathological analysis revealed a correlation between periodontitis and hepatic injury. CONCLUSION: TLR4/MyD88/NF-κB pathway may play a role in periodontitis-induced liver inflammation of rats.

Topics & Concepts

PeriodontitisInflammationMedicineTLR4ImmunohistochemistryPathologyTumor necrosis factor alphaWestern blotInternal medicineChemistryBiochemistryGeneOral microbiology and periodontitis researchImmune Response and InflammationBone Metabolism and Diseases
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