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Related Concept Videos

Bone Formation by Endochondral Ossification01:24

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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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Osteoclasts in Bone Remodeling01:31

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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...
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Bone Remodeling01:40

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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.
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Bone Formation by Intramembranous Ossification01:29

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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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Fractures: Bone Repair01:27

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Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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Related Experiment Video

Updated: Feb 26, 2026

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

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Unexpected Bone Formation Produced by RANKL Blockade.

Sergio Portal-Núñez1, Aranzazu Mediero1, Pedro Esbrit1

  • 1Bone and Joint Research Unit, Instituto de Investigación Sanitaria, Fundación Jiménez Díaz, Universidad Autónoma de Madrid (UAM), Avenida de los Reyes Católicos 2, 28040 Madrid, Spain.

Trends in Endocrinology and Metabolism: TEM
|July 23, 2017
PubMed
Summary

Denosumab, an antibody blocking RANKL, increases bone mass. Emerging research suggests it may also have anabolic effects by influencing osteoblasts and bone marrow adipocytes, a mechanism requiring further study.

Keywords:
RANKLantiresorptivebone formationdenosumabosteoporosis

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Area of Science:

  • Bone biology
  • Pharmacology
  • Endocrinology

Background:

  • Denosumab (Dmab) is a monoclonal antibody inhibiting RANKL, a key regulator of bone resorption.
  • Dmab treatment significantly increases bone mass, but the underlying mechanisms remain debated.
  • Potential for intrabone dystrophic mineralization and controversial anabolic effects are under investigation.

Purpose of the Study:

  • To explore potential pathways mediating the anabolic action of Denosumab.
  • To discuss the role of RANKL-dependent reverse signaling in osteoblasts.
  • To examine the influence of bone marrow adipocytes on osteoclastogenesis and Dmab's effects.

Main Methods:

  • Review and commentary on existing research regarding Denosumab's mechanism of action.
  • Analysis of proposed pathways involving osteoblast signaling and bone marrow adipocyte interactions.
  • Discussion of the implications of RANKL inhibition beyond antiresorption.

Main Results:

  • Denosumab's potent bone antiresorptive action is well-established.
  • Evidence suggests a potential anabolic role for Denosumab via osteoblast reverse signaling.
  • Bone marrow adipocytes' modulation of osteoclastogenesis via RANKL production is highlighted.

Conclusions:

  • The anabolic potential of Denosumab, possibly mediated by RANKL-dependent reverse signaling, warrants further investigation.
  • Understanding these pathways is crucial for fully elucidating Denosumab's impact on bone mass.
  • Future research should focus on validating these proposed mechanisms and their clinical significance.