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Xylitol Down-Regulates 1α,25-Dihydroxy Vitamin D3-induced Osteoclastogenesis via in Part the Inhibition of RANKL Expression in Osteoblasts

TLDR
Xylitol Down-Regulates 1α,25-Dihydroxy Vitamin D3-induced Osteoclastogenesis via in Part the Inhibition of RANKL Expression in Osteoblasts
Abstract
This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License(http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited. Xylitol Down-Regulates 1α,25-Dihydroxy Vitamin D3-induced Osteoclastogenesis via in Part the Inhibition of RANKL Expression in Osteoblasts

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Citations
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A review on osteoclast diseases and osteoclastogenesis inhibitors recently developed from natural resources.

TL;DR: Osteoclast-related diseases, such as osteoporosis, rheumatoid arthritis, Paget's disease, osteoclastoma, and periprosthetic osteolysis, are currently the most common reasons for bone inflammation, pain and fractures, resulting in low quality of life.

Bumetanide, the specific inhibitor of Na+-K+-2C1- cotransport, inhibits 1α,25-dihydroxyvitamin D3-induced osteoclastogenesis in a mouse co-culture system

TL;DR: In this article, a co-culture system was used to investigate the mechanism by which bumetanide inhibits osteoclastogenesis, and the mRNA expressions of the receptor activator of nuclear factor (NF)−κB ligand (RANKL) and osteoprotegerin (OPG) were analysed by RT-PCR.
References
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The Ligand for Osteoprotegerin (OPGL) Directly Activates Mature Osteoclasts

TL;DR: Findings indicate that, in addition to their effects on OC precursors, OPGL and OPG have profound and direct effects on mature OCs and indicate that the OC receptor, RANK, mediates OPGl's effects.
Journal ArticleDOI

Cellular mechanisms of bone remodeling

TL;DR: Bone remodeling is a tightly regulated process securing repair of microdamage (targeted remodeling) and replacement of old bone with new bone through sequential osteoclastic resorption and osteoblastic bone formation.
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