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

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-kappa B) by qRT-PCR and Western blotting; tumor necrosis factor alpha (TNF-alpha), 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-kappa B, TNF-alpha, 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-kappa B pathway may play a role in periodontitis-induced liver inflammation of rats.

Automated summary

This study aimed to clarify the immune mechanism of hepatic injury induced by periodontitis using a rat model. The results showed higher levels of inflammatory response and bone retraction in the periodontitis group, along with elevated levels of immune markers. The study concluded that the TLR4/MyD88/NF-kappa B pathway may play a role in periodontitis-induced liver inflammation in rats.