Xylitol Down-Regulates 1alpha,25-Dihydroxy Vitamin D3-induced Osteoclastogenesis via in Part the Inhibition of RANKL Expression in Osteoblasts.
- Author:
Seung Ho OHK
1
;
Hyunjoo JEONG
;
Jong Pill KIM
;
Yun Jung YOO
;
Jeong Taeg SEO
;
Dong Min SHIN
;
Syng Ill LEE
Author Information
1. Department of Oral Biology, Yonsei University, Seoul 120-749, Korea. lsi@yuhs.ac
- Publication Type:Original Article
- Keywords:
xylitol;
bone resorption;
osteoclastogenesis;
RANKL
- MeSH:
Acid Phosphatase;
Bone Resorption;
Cell Survival;
Coculture Techniques;
Enzyme-Linked Immunosorbent Assay;
Isoenzymes;
Osteoblasts;
Osteoclasts;
Proteins;
RNA, Messenger;
Vitamins;
Xylitol
- From:International Journal of Oral Biology
2013;38(3):127-134
- CountryRepublic of Korea
- Language:English
-
Abstract:
Xylitol is a sugar alcohol with a variety of functions including bactericidal and anticariogenic effects. However, the cellular mechanisms underlying the role of xylitol in bone metabolism are not yet clarified. In our present study, we exploited the physiological role of xylitol on osteoclast differentiation in a co-culture system of osteoblastic and RAW 264.7 cells. Xylitol treatment of these co-cultures reduced the number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells induced by 10 nM 1alpha,25(OH)2D3 in a dose-dependent manner. A cell viability test revealed no 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) M 1alpha,25(OH)2D3 in a dose-dependent manner. Furthermore, bone resorption activity, assessed on bone slices in the co-culture system, was found to be dramatically decreased with increasing xylitol concentrations. RANKL and OPG proteins were assayed by ELISA and the soluble RANKL (sRANKL) concentration was decreased with an increased xylitol concentration. In contrast, OPG was unaltered by any xylitol concentration in this assay. These results indicate that xylitol inhibits 1alpha,25(OH)2D3-induced osteoclastogenesis by reducing the sRANKL/OPG expression ratio in osteoblastic cells.
