Estrogen deficiency has been proposed as a risk factor for periodontal disease in postmenopausal women, the mechanisms involved remain unclear. Now estrogen deficiency-triggered changes in inflammatory cytokines are beginning to emerge as a common theme that may have a significant impact on bone resorption. The present study was designed to explore the modulatory effect of estrogen on the bone-resorbing cytokines such as TNF-a, IL-1b and IL-6 in the hPDL cells and to elucidate the potential bone-sparing effects of estrogen in periodontal tissues via altering the pro-inflammatory cytokines expression.
Methods:
The hPDL cells were stimulated by E. coli LPS (Sigma, 20ug/ml)) with or without estrogen (17b-estradiol, E2, Sigma) (10-7, 10-8 or 10-9 M). The untreated hPDL cells served as normal control. To confirm the specificity of the estrogen effects, we employed ICI 182,780 (Tocris Cookson, 10-6 M), a specific estrogen receptor antagonist, as negative control. Secreted TNF-a, IL-1b and IL-6 in conditioned culture media were measured by commercially available ELISA kits. And the effects of E2 on mRNA expression of TNF-a, IL-1b and IL-6 were determined by semi-quantitative RT-PCR.
Results:
E. coli lipopolysaccharide (LPS) significantly increased the production of pro-inflammatory cytokines TNF-a, IL-1b and IL-6 by hPDL cells at both mRNA and protein level. E2 treatment reversed LPS-induced TNF-a, IL-1b and IL-6 expression. Pretreatment of hPDL cells with ICI 182,780 resulted in a reversal of E2's influence on the cytokine production. Furthermore, no change of TNF-a, IL-1b and IL-6 expression had been detected in hPDL cells incubated with E2 alone.
Conclusions:
Our results suggested that estrogen may play significant roles in modulating the periodontal tissue responses to LPS, and may exert its bone-sparing effects on periodontal tissues via altering the inflammatory cytokines expression in hPDL cells.