Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Role of Vitamins in Maintaining Bone Health

Role of Vitamins in Maintaining Bone Health

The growth and maintenance of bone are regulated by a combination of nutritional factors, including vitamins, such as vitamin A, B12, C, D, and K.
Vitamin A
Vitamin A is involved in the process of bone remodeling. Retinoic acid, the active metabolite of Vitamin A, has nuclear receptors in osteoblasts and osteoclasts, which are involved in bone remodeling.
Vitamin B12
Vitamin B12 acts as a cofactor during the formation of osteoblast-related proteins, such as osteocalcin. Vitamin B12 plays a role...

Hormones and Bone Tissue

Hormones and Bone Tissue

The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...

Essential Minerals for Bone Health

Essential Minerals for Bone Health

The minerals contained in all of the food we consume are essential for our organ systems. However, certain essential minerals, such as calcium, phosphorus, magnesium, manganese, and fluoride, largely affect bone health.
Calcium and Phosphorus
Calcium is a critical component of bones, especially in the form of calcium phosphate and calcium carbonate. Since the body cannot make calcium, it must be obtained from the diet. However, calcium cannot be absorbed from the small intestine without...

Osteoclasts in Bone Remodeling

Osteoclasts in Bone Remodeling

Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...

Skeleton and Calcium Homeostasis

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.

Bone Disorders

Bone Disorders

Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Butyrate epigenetically licenses sustained epithelial-T cell crosstalk for intestinal immune tolerance.

Nature communications·2026

Same author

Design and validation of a biomechanics device for preclinical arthrofibrosis models.

Bone & joint research·2026

Same author

Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in a <i>Shank3</i> <sup><i>-/-</i></sup> Autism Model.

bioRxiv : the preprint server for biology·2026

Same author

CDCP1 Deletion Protects Against Pressure Overload-Induced Cardiac Dysfunction and Fibrosis in Mice.

Research square·2026

Same author

Genotype epigenome phenotype integration reveals peripheral immune contributions to type I bipolar disorder.

Nature communications·2026

Same author

Inflammation increases the penetrance of behavioral impairment in Shank3 haploinsufficiency mice - can it explain the behavioral regression in Autism?

Molecular psychiatry·2026

Search research articles

Related Experiment Video

Updated: Aug 26, 2025

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 C epigenetically controls osteogenesis and bone mineralization.

Roman Thaler^1,2,3, Farzaneh Khani⁴, Ines Sturmlechner⁵

¹Department of Orthopedic Surgery, Mayo Clinic, Rochester, MN, USA. Thaler.Roman@mayo.edu.

Nature Communications

|October 6, 2022

Summary

Vitamin C epigenetically regulates bone formation by controlling gene expression through DNA and histone modifications. This epigenetic role is crucial for osteoblastogenesis and preventing bone degeneration.

More Related Videos

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Published on: December 3, 2016

Osteoclast Derivation from Mouse Bone Marrow

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Related Experiment Videos

Last Updated: Aug 26, 2025

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

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Published on: December 3, 2016

Osteoclast Derivation from Mouse Bone Marrow

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Area of Science:

Epigenetics
Molecular Biology
Skeletal Biology

Background:

Vitamin C deficiency impairs connective tissue integrity, particularly bone.
Traditionally, Vitamin C's role in bone was linked to collagen synthesis.
The epigenetic mechanisms of Vitamin C in bone formation were unexplored.

Purpose of the Study:

To investigate the epigenetic role of Vitamin C in osteogenic differentiation.
To elucidate how Vitamin C modulates chromatin accessibility and gene expression in bone cells.
To understand the link between Vitamin C, epigenetic modifications, and skeletal integrity.

Main Methods:

Analysis of Vitamin C's effects on histone demethylation (H3K9me3, H3K27me3) and DNA hydroxymethylation (5hmC).
Examination of chromatin accessibility and transcriptional activity near bone-specific genes.
Genetic deletion of Tet1 and Tet2 in murine bone models to assess 5hmC's role.
Comparison of skeletal defects in Vitamin C-deficient and Tet-deficient mice.

Main Results:

Vitamin C epigenetically orchestrates osteoblastogenesis by modulating chromatin.
It regulates histone demethylation and promotes TET-mediated 5hmC at key gene regulatory regions.
This epigenetic regulation is essential for pro-osteogenic gene expression and osteogenic cell differentiation.
Vitamin C is indispensable for osteogenesis but not adipogenesis.
Loss of Tet1/Tet2 in mice phenocopies Vitamin C deficiency-induced skeletal defects.

Conclusions:

Vitamin C's epigenetic functions are central to osteoblastogenesis and bone formation.
These findings reveal a novel mechanism for Vitamin C in maintaining skeletal health.
Targeting Vitamin C's epigenetic pathways could offer new strategies for bone-degenerating conditions.