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Related Experiment Video

Updated: May 2, 2026

Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells

Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells

Published on: May 4, 2018

Vitamin D endocrine system and osteoclasts.

Naoyuki Takahashi¹, Nobuyuki Udagawa², Naoyuki Udagawa²

¹Institute for Oral Science, Matsumoto Dental University , Nagano, Japan.

Bonekey Reports

|March 8, 2014

Summary

Active vitamin D compounds like eldecalcitol paradoxically increase bone mineral density by suppressing bone resorption in osteoporosis. Eldecalcitiol reduces osteoclast formation by suppressing RANKL in osteoblasts, unlike in vitro studies.

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Isolation of Mesenchymal Stem Cells from Human Alveolar Periosteum and Effects of Vitamin D on Osteogenic Activity of Periosteum-derived Cells

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Area of Science:

Endocrinology
Bone Biology
Pharmacology

Background:

Vitamin D's active form (1α,25(OH)2D3) stimulates bone resorption via RANKL.
Active vitamin D compounds are used to treat osteoporosis by increasing bone mineral density (BMD).
The mechanism by which these compounds suppress bone resorption in vivo remains unclear.

Purpose of the Study:

To investigate the in vivo mechanism of bone resorption suppression by eldecalcitol.
To clarify the discrepancy between in vitro and in vivo effects of active vitamin D on bone resorption.

Main Methods:

Daily administration of eldecalcitol to mice.
Assessment of osteoclast precursors and osteoclast formation in bone marrow and ex vivo cultures.
Measurement of RANKL expression in osteoblasts.

Main Results:

Eldecalcitiol administration did not affect osteoclast precursor numbers or ex vivo osteoclast formation.
Eldecalcitiol suppressed RANKL expression in osteoblasts in vivo.
The in vivo suppression of bone resorption is linked to reduced RANKL expression.

Conclusions:

Active vitamin D compounds suppress bone resorption in vivo through mechanisms distinct from their in vitro effects.
Eldecalcitiol's therapeutic effect in osteoporosis involves suppressing RANKL expression in osteoblasts, leading to reduced bone resorption and increased BMD.
Further research is needed to fully elucidate the complex interplay between vitamin D, RANKL, and bone metabolism.