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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...
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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.
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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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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.
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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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 bone...

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Related Experiment Video

Updated: Jun 27, 2026

Quantitative [18F]-Naf-PET-MRI Analysis for the Evaluation of Dynamic Bone Turnover in a Patient with Facetogenic Low Back Pain
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NF-kappaB modulators in osteolytic bone diseases.

Jiake Xu1, Hua Fei Wu, Estabelle S M Ang

  • 1Centre for Orthopaedic Research, School of Surgery, University of Western Australia, Nedlands, Australia. jiake.xu@uwa.edu.au

Cytokine & Growth Factor Reviews
|December 3, 2008
PubMed
Summary

Nuclear factor kappa B (NF-kappaB) pathways are crucial for osteoclast function and bone homeostasis. Dysregulation of these pathways contributes to bone diseases, highlighting their therapeutic potential.

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Published on: June 16, 2022

Area of Science:

  • Bone Biology
  • Cell Signaling
  • Immunology

Background:

  • Osteoclasts are key cells in bone resorption and osteolytic disorders.
  • Nuclear factor kappa B (NF-kappaB) signaling is vital for osteoclast formation, survival, and bone homeostasis.
  • Cytokines like RANKL, TNF-alpha, and IL-1 regulate NF-kappaB pathways in osteoclasts.

Purpose of the Study:

  • To explore the role of NF-kappaB signaling pathways in osteoclast biology.
  • To understand the involvement of NF-kappaB mediators in osteoclastogenesis.
  • To investigate the link between abnormal NF-kappaB activation and osteolytic diseases.

Main Methods:

  • Analysis of NF-kappaB signaling pathways in osteoclasts.
  • Investigation of NF-kappaB mediators (TRAF6, aPKC, p62/SQSTM1, CYLD) in RANK-mediated osteoclastogenesis.
  • Evaluation of therapeutic effects of NF-kappaB modulators in mouse models of bone destruction.

Main Results:

  • Abnormal NF-kappaB activation in osteoclasts is associated with excessive bone resorption.
  • NF-kappaB signaling is implicated in osteolytic conditions such as arthritis and periodontitis.
  • NF-kappaB modulators show therapeutic promise in preclinical models of bone destruction.

Conclusions:

  • NF-kappaB pathways are critical regulators of osteoclast function and bone metabolism.
  • Targeting NF-kappaB signaling offers a potential therapeutic strategy for osteolytic bone diseases.
  • Further research into NF-kappaB pathways can lead to novel treatments for bone disorders.