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Research

Knowledge on the impact of endogenous mechanisms, such as hormones, on the periodontitis and atherosclerosis disease process is limited. Both periodontitis and atherosclerosis are aggravated by estrogen deficiency, as occurs after menopause. We show recently, using the NHANES cohort, that post-menopausal women on hormone replacement therapy (HRT) have more teeth and less inflammation compared to those not on HRT and, furthermore, that the beneficial effect of HRT is dependent on sufficient plasma levels of vitamin D. Thus, we conclude that estrogen in combination with vitamin D has a protective effect on periodontal health, but the mechanisms are not understood. Importantly, we show vitamin D down-regulates pro-inflammatory cytokine expression, suggesting that it possess anti-inflammatory properties. We propose that vitamin D both potentiates estrogen-evoked anti-inflammation and promotes estrogen-induced stimulation of bone formation, i.e. preserves bone tissue and tooth attachment otherwise lost in periodontitis. We are intrigued by the dramatic up-regulation of the antimicrobial peptide LL-37 in response to treatment with vitamin D representing an alternative mechanism of action. The objective of this project is to unravel biological mechanisms explaining the protective effect of estrogen and vitamin D on periodontitis and atherosclerosis.  

Research

UKÄ subject classification

  • Medical and Health Sciences

Keywords

  • Inflammation
  • Estrogen
  • Vitamin D
  • Antimicrobial peptides
  • Apoptosis
  • Proliferation
  • LL-37
  • Polyamines
  • Periodontitis
  • Endothelial cells

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