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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...
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.
Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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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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Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...

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Related Experiment Video

Updated: May 30, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
09:37

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Expression of RANKL/OPG during bone remodeling in vivo.

H Tanaka1, T Mine, H Ogasa

  • 1Department of Orthopedic Surgery, Yamaguchi Grand Medical Center, Hofu, Japan. tnk@ymghp.jp

Biochemical and Biophysical Research Communications
|July 21, 2011
PubMed
Summary
This summary is machine-generated.

The study reveals that receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) expression links bone formation to resorption. Increased RANKL/OPG ratio during bone remodeling indicates heightened osteoclastogenic stimulation.

Related Experiment Videos

Last Updated: May 30, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
09:37

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Area of Science:

  • Bone Biology
  • Skeletal Physiology
  • Cell Signaling

Background:

  • Receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) interactions are crucial for osteoclastogenesis.
  • These proteins, produced by osteoblasts, link bone formation and resorption processes.
  • Understanding their dynamic expression during bone remodeling is key to skeletal health.

Purpose of the Study:

  • To investigate the in vivo expression patterns of RANKL and OPG during bone remodeling.
  • To determine the relationship between osteoclastogenic stimulation and osteoblastic differentiation.
  • To elucidate the role of RANKL and OPG as molecular links between bone formation and resorption.

Main Methods:

  • Rat femurs underwent marrow ablation, with RNA extraction on days 0, 3, 6, and 9.
  • Northern blot analysis assessed temporal gene expression of osteoblast markers (procollagen α1 (I), alkaline phosphatase, osteopontin, osteocalcin).
  • Real-time PCR quantified OPG and RANKL mRNA levels; RANKL/OPG ratio was calculated. Histological analysis examined immunoreactivity.

Main Results:

  • Osteoblast markers increased by day 3, peaking on day 6.
  • OPG mRNA expression upregulated on day 6, decreasing by day 9.
  • RANKL mRNA expression increased over 20-fold by day 9, leading to a peak RANKL/OPG ratio.
  • RANKL and OPG immunoreactivity localized to bone marrow cells.

Conclusions:

  • Osteoblast differentiation markers are upregulated during the bone formation phase.
  • RANKL and OPG expression is subsequently stimulated, indicating the bone resorption phase.
  • The RANKL/OPG ratio serves as a critical index linking bone formation to resorption during remodeling.