Estrogen modulates cytokine expression in human periodontal ligament cells

Although systemic bone loss accompanying estrogen deficiency has been proposed as a risk factor for periodontal disease in post-menopausal women, the mechanisms involved remain unclear. The objective of this study was to elucidate the potential bone-sparing effect of estrogen (17 beta-estradiol, E-2) via modulation of inflammatory cytokine production in human periodontal ligament (hPDL) cells. E. coli lipopolysaccharide (LPS) increased the production of proinflammatory cytokines TNF-alpha, IL-1 beta, IL-6, and receptor activator of NF-kappa B ligand (RANKL) by hPDL cells at both mRNA and protein levels. E 2 treatment reversed the stimulatory effects of LPS on pro-inflammatory cytokine expression by hPDL cells. Moreover, E-2 up-regulated osteoprotegerin (OPG) expression and therefore attenuated the reduction of the OPG vs. RANKL ratio. Our results suggested that estrogen may play a significant role in modulating periodontal tissue responses to LPS, and may exert its bone-sparing effects on periodontal tissues via altering the expression of inflammatory cytokines in hPDL cells.