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KMID : 0848120130380030127
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International Journal of Oral Biology
2013 Volume.38 No. 3 p.127 ~ p.134
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Xylitol Down-Regulates 1α,25-Dihydroxy Vitamin D3-induced Osteoclastogenesis via in Part the Inhibition of RANKL Expression in Osteoblasts
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Lee Syng-Ill
Ohk Seung-Ho
Jeong Hyun-joo
Kim Jong-Pill
Yoo Yun-Jung
Seo Jeong-Taeg
Shin Dong-Min
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Abstract
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Xylitol is a sugar alcohol with a variety of functionsincluding bactericidal and anticariogenic effects. However,the cellular mechanisms underlying the role of xylitol in bonemetabolism are not yet clarified. In our present study, weexploited the physiological role of xylitol on osteoclast differentiationin a co-culture system of osteoblastic and RAW264.7 cells. Xylitol treatment of these co-cultures reducedthe number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells induced by 10 nM 1α,25(OH)2D3 in a dose?dependent manner. A cell viability test revealedno marked cellular damage by up to 100 mM of xylitol.Exposure of osteoblastic cells to xylitol decreased RANKL,but not OPG, mRNA expression in the presence of 10-8 M1α,25(OH)2D3 in a dose?dependent manner. Furthermore,bone resorption activity, assessed on bone slices in the coculturesystem, was found to be dramatically decreased withincreasing xylitol concentrations. RANKL and OPG proteinswere assayed by ELISA and the soluble RANKL (sRANKL)concentration was decreased with an increased xylitol concentration.In contrast, OPG was unaltered by any xylitol concentrationin this assay. These results indicate that xylitolinhibits 1α,25(OH)2D3-induced osteoclastogenesis by reducingthe sRANKL/OPG expression ratio in osteoblastic cells.
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KEYWORD
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xylitol, bone resorption, osteoclastogenesis, RANKL
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