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Osteoclasts in Bone Remodeling

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...

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Updated: Jul 3, 2025

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

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

Published on: March 15, 2018

Murine IRF8 Mutation Offers New Insight into Osteoclast and Root Resorption.

A Das¹, S K Yesupatham¹, D Allison¹

¹Division of Periodontology, University of Maryland School of Dentistry, Baltimore, MD, USA.

Journal of Dental Research

|February 12, 2024

Summary

This summary is machine-generated.

A novel mutation in the Interferon regulatory factor 8 (IRF8) gene causes increased osteoclast activity, leading to dental and skeletal issues like root resorption. This study models the mutation in mice, confirming its impact on bone and tooth health.

Keywords:

NFATC Transcription Factors dental biology genetic animal models genetic mutation human association studies osteoclasts

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Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

Published on: May 19, 2019

Area of Science:

Immunology
Genetics
Skeletal Biology

Background:

Interferon regulatory factor 8 (IRF8) is crucial for immune cell function and maintaining skeletal homeostasis.
A specific IRF8 mutation (G388S) is linked to multiple idiopathic cervical root resorption (MICRR), characterized by excessive osteoclast activity.
Understanding the IRF8 G388S variant's role is key to elucidating MICRR pathogenesis and IRF8's function in osteoclastogenesis.

Purpose of the Study:

To investigate the molecular mechanisms underlying MICRR by modeling the human IRF8 G388S mutation in mice.
To determine the specific effects of the IRF8 G388S variant on osteoclastogenesis and skeletal homeostasis.
To explore the impact of this mutation on immune cell development and function.

Main Methods:

Generated Irf8 knock-in (KI) mice using CRISPR/Cas9 to mimic the human IRF8 G388S mutation.
Assessed hematopoietic cell development and macrophage gene signatures in heterozygous (Het) and homozygous (Homo) Irf8 KI mice compared to wild-type (WT) mice.
Evaluated osteoclast formation, resorption activity, root resorption, and alveolar bone loss in vivo and in vitro.

Main Results:

Irf8 KI mice (Het and Homo) exhibited significantly increased osteoclast formation and resorption activity compared to WT mice.
Oral ligature insertion in KI mice led to heightened root resorption and osteoclast-mediated alveolar bone loss.
The IRF8 G388S mutation impaired the inhibition of NFATc1-dependent transcription and affected autophagy pathways crucial for osteoclast differentiation.

Conclusions:

The IRF8 G388S mutation primarily affects osteoclastogenesis, leading to dental and skeletal disorders like MICRR.
Immune cell development and function remain largely unaffected by this specific IRF8 mutation.
This study identifies a critical IRF8 domain for osteoclast regulation and offers insights into skeletal disorders driven by aberrant osteoclast activity.