title: Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats.
abstract: 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.
  
  
  CONCLUSIONS
  Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.
authors.affiliation: Department of Oral Health, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
authors.forename: Takaaki
authors.initials: T
authors.lastname: Tomofuji
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ekuni
authors.forename: Reiko
authors.initials: R
authors.lastname: Yamanaka
authors.forename: Hiroki
authors.initials: H
authors.lastname: Kusano
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Azuma
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Sanbe
authors.forename: Naofumi
authors.initials: N
authors.lastname: Tamaki
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Watanabe
authors.forename: Mutsumi
authors.initials: M
authors.lastname: Miyauchi
authors.forename: Takashi
authors.initials: T
authors.lastname: Takata
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D053938:DNA Fragmentation; D004272:DNA, Mitochondrial / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D005234:Fatty Liver / Q000209:etiology* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000097:blood / Q000494:pharmacology; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism; D010447:Peptide Hydrolases / Q000494:pharmacology; D010518:Periodontitis / Q000139:chemically induced / Q000150:complications*; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D004272:DNA, Mitochondrial; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D010447:Peptide Hydrolases; D003849:Deoxyguanosine