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RESEARCH REPORT |
1 Department of Orthodontics and
2 Department of Oral Biology, School of Stomatology, the Fourth Military Medical University, Xian, 710032, China
* corresponding author, yinding2005{at}yahoo.com.cn
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 (17β-estradiol, E2) via modulation of inflammatory cytokine production in human periodontal ligament (hPDL) cells. E. coli lipopolysaccharide (LPS) increased the production of pro-inflammatory cytokines TNF-
, IL-1β, IL-6, and receptor activator of NF- B ligand (RANKL) by hPDL cells at both mRNA and protein levels. E2 treatment reversed the stimulatory effects of LPS on pro-inflammatory cytokine expression by hPDL cells. Moreover, E2 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.
KEY WORDS: 17β-estradiol cytokine periodontal ligament cells
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