BACKGROUND: Epidemiologic studies suggest a relationship between periodontitis and liver diseases. A rat periodontitis model was used to investigate whether a causal relationship exists between periodontitis and liver diseases. METHODS: Fourteen male Wistar rats (8 weeks old) were divided into two groups: a periodontitis group in which Escherichia coli lipopolysaccharide (LPS) and Streptomyces griseus proteases were applied into the gingival sulcus for 8 weeks, and a control group using pyrogen-free water instead. After blood samples were collected, periodontal tissues and liver specimens were analyzed. RESULTS: Chronic administration of LPS and proteases to the gingival sulcus induced periodontitis and liver injury, including steatosis with inflammation and sinusoidal fibrosis. Apoptosis, enhanced concentration of 8-hydroxydeoxyguanosine, and activated production of tumor necrosis factor-alpha in liver were observed in the periodontitis group, with increased gingival inflammation, serum LPS, and reactive oxygen species. CONCLUSION: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.
BACKGROUND: Epidemiologic studies suggest a relationship between periodontitis and liver diseases. A ratperiodontitis model was used to investigate whether a causal relationship exists between periodontitis and liver diseases. METHODS: Fourteen male Wistar rats (8 weeks old) were divided into two groups: a periodontitis group in which Escherichia colilipopolysaccharide (LPS) and Streptomyces griseus proteases were applied into the gingival sulcus for 8 weeks, and a control group using pyrogen-free water instead. After blood samples were collected, periodontal tissues and liver specimens were analyzed. RESULTS: Chronic administration of LPS and proteases to the gingival sulcus induced periodontitis and liver injury, including steatosis with inflammation and sinusoidal fibrosis. Apoptosis, enhanced concentration of 8-hydroxydeoxyguanosine, and activated production of tumor necrosis factor-alpha in liver were observed in the periodontitis group, with increased gingival inflammation, serum LPS, and reactive oxygen species. CONCLUSION: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.
Authors: Aderonke A Akinkugbe; Gary D Slade; A Sidney Barritt; Stephen R Cole; Steven Offenbacher; Astrid Petersmann; Thomas Kocher; Markus M Lerch; Julia Mayerle; Henry Völzke; Gerardo Heiss; Birte Holtfreter Journal: J Clin Periodontol Date: 2017-09-22 Impact factor: 8.728
Authors: Kati Hyvärinen; Anita M Tuomainen; Saara Laitinen; Igor L Bykov; Liisa Törmäkangas; Kai Lindros; Reijo Käkelä; Georg Alfthan; Irma Salminen; Matti Jauhiainen; Petri T Kovanen; Maija Leinonen; Pekka Saikku; Pirkko J Pussinen Journal: Infect Immun Date: 2009-05-18 Impact factor: 3.441
Authors: Jefferson Soares de Oliveira; Moara E Silva Conceição Pinto; Lucas de Araújo de Bastos Santana; Antonione Santos Bezerra Pinto; David di Lenardo; Daniel Fernando Pereira Vasconcelos Journal: Int J Dent Date: 2016-09-21