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Related Experiment Videos

Association between periodontitis and hyperlipidemia: cause or effect?

C W Cutler1, E A Shinedling, M Nunn

  • 1Department of Periodontics and Biomedical Sciences, Baylor College of Dentistry, Dallas, TX 75266-0677, USA. ccutler@tambcd.edu

Journal of Periodontology
|January 13, 2000
PubMed
Summary
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Periodontitis is linked to hyperlipidemia and antibodies against Porphyromonas gingivalis lipopolysaccharides (LPS). Elevated triglycerides modulate inflammatory responses in immune cells stimulated by P. gingivalis LPS.

Area of Science:

  • Oral Health and Systemic Disease
  • Immunology
  • Cardiovascular Health

Background:

  • Epidemiological studies suggest a link between periodontitis and coronary artery disease.
  • Animal studies indicate endotoxin exposure can cause hyperlipidemia and myeloid cell hyperactivity.
  • The human association between periodontitis, Porphyromonas gingivalis, LPS, and hyperlipidemia remains unclear.

Purpose of the Study:

  • To investigate the association between periodontitis, systemic exposure to Porphyromonas gingivalis, and hyperlipidemia in humans.
  • To explore the effect of triglycerides on inflammatory responses in polymorphonuclear leukocytes (PMNs) stimulated by P. gingivalis LPS.

Main Methods:

  • Serum samples from 26 periodontitis patients and 25 controls were analyzed for antibodies against P. gingivalis and its LPS using ELISA and Western blotting.

Related Experiment Videos

  • Serum triglyceride and cholesterol levels were measured.
  • Logistic regression examined associations between periodontitis and lipid levels/antibodies.
  • PMNs were incubated with triglycerides and stimulated with P. gingivalis LPS to measure IL-1beta release.

    • Main Results:

    • Periodontitis was significantly associated with age, elevated triglycerides, elevated cholesterol, and higher antibody titers against P. gingivalis and its LPS.
    • P. gingivalis LPS stimulation of PMNs induced modest IL-1beta release.
    • Triglyceride addition significantly increased IL-1beta secretion from LPS-stimulated PMNs.

    Conclusions:

    • A significant relationship exists between periodontitis, hyperlipidemia, and antibodies to P. gingivalis LPS, meriting further research.
    • Elevated triglycerides can modulate IL-1beta production by PMNs in response to P. gingivalis LPS stimulation.