Effects of improvement in periodontal inflammation by toothbrushing on serum lipopolysaccharide concentration and liver injury in rats

Acta Odontol Scand. 2009;67(4):200-5. doi: 10.1080/00016350902794818.

Abstract

Objective: Periodontitis increases the serum lipopolysaccharide level, contributing to liver injury. Toothbrushing improves periodontitis and may also affect serum lipopolysaccharide concentration and periodontitis-induced liver injury. The purpose of the present study was to examine whether the improvement in periodontal inflammation by toothbrushing clinically affects the serum lipopolysaccharide level and hepatic pathological changes in rat periodontitis.

Material and methods: Thirty male Wistar rats were divided into 5 groups, 2 groups receiving topical application of pyrogen-free water to the gingival sulcus for 4 or 8 weeks. The next 2 groups received topical application of lipopolysaccharide and proteases for 4 or 8 weeks. The last group received topical application of lipopolysaccharide and proteases for 8 weeks, and the palatal gingiva was brushed with a powered toothbrush once a day for 4 weeks prior to the end of the experimental period.

Results: Topical application of lipopolysaccharide and proteases induced not only periodontal inflammation but also an elevation in the serum lipopolysaccharide concentration, with increasing hepatic inflammation, steatosis and 8-hydroxydeoxyguanosine levels in a time-dependent manner. The rats that received gingival stimulation showed decreased polymorphonuclear leukocyte infiltration and collagen loss levels in the periodontal lesions. Furthermore, this group also showed a decrease in serum lipopolysaccharide concentration and hepatic inflammation, steatosis and 8-hydroxydeoxyguanosine levels, compared with the group receiving no treatment.

Conclusions: Toothbrushing promoted healing of periodontal lesions, decreased serum lipopolysaccharide concentration and suppressed liver injury in a rat periodontitis model.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Alveolar Bone Loss / prevention & control
  • Animals
  • Chemical and Drug Induced Liver Injury / prevention & control
  • Collagen / drug effects
  • Connective Tissue / drug effects
  • Connective Tissue / pathology
  • DNA, Mitochondrial / analysis
  • Deoxyguanosine / analogs & derivatives
  • Deoxyguanosine / blood
  • Epithelial Attachment / drug effects
  • Epithelial Attachment / pathology
  • Escherichia coli
  • Fatty Liver / prevention & control
  • Gingiva / drug effects
  • Gingiva / pathology
  • Leukocyte Count
  • Lipopolysaccharides / adverse effects
  • Lipopolysaccharides / blood*
  • Liver Diseases / blood
  • Liver Diseases / prevention & control*
  • Male
  • Neutrophil Infiltration / drug effects
  • Neutrophils / drug effects
  • Peptide Hydrolases / adverse effects
  • Periodontal Attachment Loss / prevention & control
  • Periodontitis / blood
  • Periodontitis / prevention & control*
  • Random Allocation
  • Rats
  • Rats, Wistar
  • Reactive Oxygen Species / blood
  • Streptomyces griseus / enzymology
  • Toothbrushing*
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • DNA, Mitochondrial
  • Lipopolysaccharides
  • Reactive Oxygen Species
  • Tumor Necrosis Factor-alpha
  • 8-Hydroxy-2'-Deoxyguanosine
  • Collagen
  • Peptide Hydrolases
  • Deoxyguanosine