internal prostaglandin synthesis augments osteoprotegerin production in human gingival fibroblasts stimulated by lipopolysaccharide periodontitis is an inflammatory bone disease caused by gramnegative anaerobic bacteria osteoclast differentiation is regulated by the balance between receptor activator of nuclear factor kappa b ligand rankl and osteoprotegerin opg the purpose of this study was to examine the mechanism of opg production in human gingival fibroblasts hgf stimulated by lipopolysaccharide lps from periodontopathic bacteria the expressions of tolllike receptor 2 tlr2 and tlr4 in hgf were examined using flowcytometry hgf were stimulated with whole cell extracts or lps from actinobacillus actinomycetemcomitans and porphyromonas gingivalis with or without polymyxin b a lps inhibitor in addition hgf were stimulated with lps prostaglandin e2 pge2 various agonists of pge receptors ep1 ep2 ep3 and ep4 agonists with or without indomethacin ind a prostaglandin synthesis inhibitor opg and pge2 production was measured using an enzymelinked immunosorbent assay elisa hgf expressed both tlr2 and tlr4 both a actinomycetemcomitans and p gingivalis lps augmented opg expression in hgf whole cell extracts from a actinomycetemcomitans and p gingivalis augmented opg production by hgf the augmentation was suppressed by polymyxin b ind suppressed opg production in lpsstimulated hgf pge2 stimulated hgf to produce opg ep1 and ep2 agonists but not ep3 and ep4 agonists increased opg production by hgf these results suggest that lpsinduced opg production by hgf is regulated via ep1 andor ep2 receptors by endogenously generated pge2