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Related Concept Videos

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...
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.
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...
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...
Hormones and Bone Tissue01:17

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...

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Related Experiment Video

Updated: Jun 3, 2026

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

Homocysteine mediated decrease in bone blood flow and remodeling: role of folic acid.

Neetu Tyagi1, Madhavi Kandel, Charu Munjal

  • 1Department of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, Kentucky 40202, USA. n0tyag01@louisville.edu

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|April 7, 2011
PubMed
Summary
This summary is machine-generated.

Folic acid (FA) supplementation improved bone blood flow and density in mice with hyperhomocysteinemia (HHcy). FA ameliorated HHcy-induced bone loss by reducing oxidative stress and improving nitric oxide bioavailability.

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Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

Area of Science:

  • Biochemistry
  • Bone Biology
  • Nutritional Science

Background:

  • Hyperhomocysteinemia (HHcy), characterized by elevated homocysteine (Hcy) levels, is linked to bone disorders.
  • Homocysteine accumulation in bone matrix may impair bone strength, but the precise mechanisms of Hcy-induced bone loss and remodeling remain unclear.

Purpose of the Study:

  • To investigate the role of folic acid (FA) in mitigating genetically HHcy-associated reductions in bone blood flow and remodeling.
  • To elucidate the molecular mechanisms underlying Hcy-induced bone alterations and the protective effects of FA.

Main Methods:

  • Utilized wild-type (WT) and cystathionine-β-synthase heterozygous (CBS+/-) mice, with or without FA supplementation (300 mg/kg).
  • Assessed tibial bone blood flow using laser Doppler and ultrasonic flow probes.
  • Measured tibial bone density (BD) via dual-energy X-ray absorptiometry.
  • Analyzed bone homogenates for oxidative stress markers (NOX-4, Trx-1), bone remodeling (MMP-9), and nitric oxide bioavailability (eNOS/iNOS/NO) using Western blot.

Main Results:

  • CBS+/- mice exhibited decreased tibial blood flow and reduced bone density compared to WT mice.
  • Elevated levels of NOX-4, iNOS, and MMP-9, along with decreased Trx-1 and eNOS, were observed in CBS+/- mice, indicating increased oxidative stress and altered bone remodeling.
  • FA supplementation ameliorated these detrimental effects in CBS+/- mice, improving blood flow, bone density, and molecular markers.

Conclusions:

  • Genetically induced hyperhomocysteinemia impairs bone blood flow and density, associated with oxidative stress and altered bone remodeling.
  • Folic acid supplementation demonstrates therapeutic potential in counteracting HHcy-induced bone loss by restoring vascular function and reducing oxidative damage.