Bone resorption and local interleukin-1alpha and interleukin-1beta synthesis induced by Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis lipopolysaccharide

J Periodontal Res. 2001 Feb;36(1):1-8. doi: 10.1034/j.1600-0765.2001.00637.x.

Abstract

Different types of periodontopathic bacterial lipopolysaccharide (LPS) exert various biological activities in vitro. However, whether or not these activities also occur in vivo remains unclear. Thus the present study investigates bone resorption, as well as local IL-1alpha and IL-1beta synthesis induced by Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis LPS in the periodontal tissue of mice. Both types of LPS were injected into mouse gingiva every 48 h and the animals were sacrificed 6 h after the 1st. 4th, 7th, 10th, 13th, 16th, 20th, or 24th injection. Bone resorption in the injected gingiva was histopathologically and histomorphometrically investigated and local concentrations of IL-1alpha and IL-1beta were detected using an enzyme-linked immunosorbent assay. The active resorption ratio was significantly higher in the group given the 10th injection of LPS from A. actinomycetemcomitans than in the group given P. gingivalis LPS. Furthermore, A. actinomycetemcomitans LPS stimulated significantly more synthesis of IL-1alpha than P. gingivalis LPS after the 4th and 10th injections. and of IL-1beta after the 4th, 7th, 10th, 13th, 16th and 20th injections. These results suggest that A. actinomycetemcomitans LPS is a more potent inducer of bone resorption and synthesis of IL-1alpha and IL-1beta in the short term than P. gingivalis LPS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aggregatibacter actinomycetemcomitans / pathogenicity
  • Alveolar Bone Loss / etiology*
  • Alveolar Bone Loss / metabolism
  • Alveolar Bone Loss / microbiology
  • Animals
  • Interleukin-1 / biosynthesis*
  • Lipopolysaccharides / chemistry
  • Lipopolysaccharides / toxicity*
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Porphyromonas gingivalis / pathogenicity

Substances

  • Interleukin-1
  • Lipopolysaccharides