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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

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 bone...
Role of Vitamins in Maintaining Bone Health01:25

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...
Bone Disorders01:29

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...
Essential Minerals for Bone Health01:31

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...
Bone Remodeling01:40

Bone Remodeling

Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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Related Experiment Video

Updated: Jun 18, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Ascorbic acid accelerates osteoclast formation and death.

Damien Le Nihouannen1, Jake E Barralet, Jenna E Fong

  • 1Faculty of Dentistry, McGill University, 740 Dr. Penfiled Ave., Montreal, Quebec, Canada.

Bone
|November 26, 2009
PubMed
Summary
This summary is machine-generated.

Ascorbic acid (AA) initially stimulates osteoclast formation by acting as an oxidant, increasing cell number and size. However, AA later accelerates osteoclast death, ultimately limiting bone resorption.

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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
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A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

Related Experiment Videos

Last Updated: Jun 18, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

Area of Science:

  • Cell Biology
  • Biochemistry
  • Bone Metabolism

Background:

  • Ascorbic acid (AA) is crucial for bone formation, but its role in osteoclast activity remains debated.
  • Osteoclasts are key cells responsible for bone resorption.

Purpose of the Study:

  • To investigate the dual effect of ascorbic acid (AA) on osteoclastogenesis.
  • To elucidate the role of oxidative stress and cellular metabolism in AA-mediated osteoclast modulation.

Main Methods:

  • Primary mouse bone marrow cultures and RAW 264.7 cells were used.
  • Cells were treated with osteoclastogenic factors RANKL and MCSF, with and without AA.
  • Osteoclast number, size, nucleation, oxidative stress markers (GSH/GSSG, H2O2), mitochondrial activity (JC-1), and ATP levels were assessed.

Main Results:

  • AA significantly increased osteoclast number, size, and nucleation.
  • AA exhibited pro-oxidant effects, decreasing glutathione levels and increasing H2O2 production.
  • AA enhanced mitochondrial activity and ATP levels during early osteoclastogenesis but accelerated cell death in the late stage.

Conclusions:

  • Ascorbic acid acts as an oxidant during osteoclastogenesis, initially promoting osteoclast formation.
  • AA subsequently limits osteoclast lifespan, leading to an overall attenuation of bone resorption.
  • This dual action reconciles in vitro stimulation with in vivo bone resorption findings.