Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats

Takaaki Tomofuji, Daisuke Ekuni, Reiko Yamanaka, Hiroki Kusano, Tetsuji Azuma, Toshihiro Sanbe, Naofumi Tamaki, Tatsuo Yamamoto, Tatsuo Watanabe, Mutsumi Miyauchi, Takashi Takata

Research output: Contribution to journalArticle

51 Citations (Scopus)

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. Conclusion: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.

Original languageEnglish
Pages (from-to)1999-2006
Number of pages8
JournalJournal of Periodontology
Volume78
Issue number10
DOIs
Publication statusPublished - Oct 2007

Fingerprint

Periodontitis
Lipopolysaccharides
Peptide Hydrolases
Inflammation
Liver
Liver Diseases
Streptomyces griseus
Pyrogens
Fatty Liver
Serum
Wistar Rats
Epidemiologic Studies
Reactive Oxygen Species
Fibrosis
Tumor Necrosis Factor-alpha
Apoptosis
Escherichia coli
Control Groups
Water
Wounds and Injuries

Keywords

  • Animals
  • Fatty liver
  • Hepatic steatosis
  • Lipopolysaccharides
  • Periodontitis

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats. / Tomofuji, Takaaki; Ekuni, Daisuke; Yamanaka, Reiko; Kusano, Hiroki; Azuma, Tetsuji; Sanbe, Toshihiro; Tamaki, Naofumi; Yamamoto, Tatsuo; Watanabe, Tatsuo; Miyauchi, Mutsumi; Takata, Takashi.

In: Journal of Periodontology, Vol. 78, No. 10, 10.2007, p. 1999-2006.

Research output: Contribution to journalArticle

Tomofuji, T, Ekuni, D, Yamanaka, R, Kusano, H, Azuma, T, Sanbe, T, Tamaki, N, Yamamoto, T, Watanabe, T, Miyauchi, M & Takata, T 2007, 'Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats', Journal of Periodontology, vol. 78, no. 10, pp. 1999-2006. https://doi.org/10.1902/jop.2007.070056
Tomofuji, Takaaki ; Ekuni, Daisuke ; Yamanaka, Reiko ; Kusano, Hiroki ; Azuma, Tetsuji ; Sanbe, Toshihiro ; Tamaki, Naofumi ; Yamamoto, Tatsuo ; Watanabe, Tatsuo ; Miyauchi, Mutsumi ; Takata, Takashi. / Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats. In: Journal of Periodontology. 2007 ; Vol. 78, No. 10. pp. 1999-2006.
@article{e68fa14e2f67409292cfccc5cacc2964,
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. Conclusion: Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.",
keywords = "Animals, Fatty liver, Hepatic steatosis, Lipopolysaccharides, Periodontitis",
author = "Takaaki Tomofuji and Daisuke Ekuni and Reiko Yamanaka and Hiroki Kusano and Tetsuji Azuma and Toshihiro Sanbe and Naofumi Tamaki and Tatsuo Yamamoto and Tatsuo Watanabe and Mutsumi Miyauchi and Takashi Takata",
year = "2007",
month = "10",
doi = "10.1902/jop.2007.070056",
language = "English",
volume = "78",
pages = "1999--2006",
journal = "Journal of Periodontology",
issn = "0022-3492",
publisher = "American Academy of Periodontology",
number = "10",

}

TY - JOUR

T1 - Chronic administration of lipopolysaccharide and proteases induces periodontal inflammation and hepatic steatosis in rats

AU - Tomofuji, Takaaki

AU - Ekuni, Daisuke

AU - Yamanaka, Reiko

AU - Kusano, Hiroki

AU - Azuma, Tetsuji

AU - Sanbe, Toshihiro

AU - Tamaki, Naofumi

AU - Yamamoto, Tatsuo

AU - Watanabe, Tatsuo

AU - Miyauchi, Mutsumi

AU - Takata, Takashi

PY - 2007/10

Y1 - 2007/10

N2 - 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.

AB - 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.

KW - Animals

KW - Fatty liver

KW - Hepatic steatosis

KW - Lipopolysaccharides

KW - Periodontitis

UR - http://www.scopus.com/inward/record.url?scp=35648939246&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35648939246&partnerID=8YFLogxK

U2 - 10.1902/jop.2007.070056

DO - 10.1902/jop.2007.070056

M3 - Article

C2 - 17916001

AN - SCOPUS:35648939246

VL - 78

SP - 1999

EP - 2006

JO - Journal of Periodontology

JF - Journal of Periodontology

SN - 0022-3492

IS - 10

ER -