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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 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...
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: May 28, 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

Increased Osteoclast Activity Contributes to Bone Resorption and Osteopenia in a Rett Syndrome Mouse Model.

Nadeem Samee1, Lou Belz1, Nicolas Narboux-Nême1

  • 1CNRS UMR7221, Evolution des Régulations Endocriniennes, MNHN, Cedex 05, F-75231 Paris, France.

Cells
|May 27, 2026
PubMed
Summary

Rett syndrome, caused by MECP2 mutations, leads to osteopenia. This study reveals increased osteoclast activity contributes significantly to bone loss in Mecp2-null mice, progressing from low to high bone turnover.

Keywords:
Mecp2Rett syndromebone resorptionosteoclastsosteoporosis

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Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
08:42

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Related Experiment Videos

Last Updated: May 28, 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

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
08:42

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model

Published on: July 3, 2020

Area of Science:

  • Genetics
  • Bone Biology
  • Neurodevelopmental Disorders

Background:

  • Rett syndrome is a severe neurodevelopmental disorder linked to MECP2 gene mutations.
  • Patients often experience osteopenia and fractures, but the underlying skeletal mechanisms are unclear.
  • Previous studies suggested impaired osteoblast function in Mecp2-null mice.

Purpose of the Study:

  • To investigate the role of osteoclasts in the skeletal defects of Mecp2-null mice.
  • To analyze bone mass, microarchitecture, and remodeling during postnatal development.
  • To understand the age-dependent changes in bone turnover.

Main Methods:

  • Utilized Mecp2-null mouse models.
  • Performed microcomputed tomography and histomorphometric analyses.
  • Analyzed gene expression of bone remodeling markers and osteoclast-associated genes.

Main Results:

  • Mecp2-null mice exhibited reduced bone mineral density, trabecular bone volume, and cortical thickness.
  • Increased osteoclast number, elevated urinary deoxypyridinoline, and higher Cathepsin K expression were observed.
  • Bone remodeling showed an age-dependent shift, with early low turnover followed by increased osteoclast activity.

Conclusions:

  • Increased osteoclast activity is a key factor in Rett syndrome-associated osteopenia.
  • MECP2 deficiency contributes to skeletal pathology through enhanced osteoclast resorption.
  • The findings suggest a progression from low bone turnover to high resorption in Mecp2 deficiency.