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Related Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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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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Hormones and Bone Tissue01:17

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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
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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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Role of Vitamins in Maintaining Bone Health01:25

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The growth and maintenance of bone are regulated by a combination of nutritional factors, including vitamins, such as vitamin A, B12, C, D, and K.
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Bone Disorders

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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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Bone contains a relatively small number of cells entrenched in a matrix of collagen fibers that provide an adherent surface for inorganic salt crystals. Both components of the matrix, organic and inorganic, contribute to the unusual properties of bone. Without collagen, bones would be brittle and shatter easily. Without mineral crystals, bones would flex and provide little support. This can be observed by an experiment: when the minerals of a bone are dissolved by soaking the bone in...
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Related Experiment Video

Updated: Aug 26, 2025

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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A20 controls RANK-dependent osteoclast formation and bone physiology.

Arne Martens1,2, Pieter Hertens1,2, Dario Priem1,2

  • 1Center for Inflammation Research VIB, Ghent, Belgium.

EMBO Reports
|October 4, 2022
PubMed
Summary
This summary is machine-generated.

The protein A20 regulates bone formation by controlling osteoclast differentiation. A20 deficiency in osteoclasts leads to osteoporosis, highlighting its role in bone turnover.

Keywords:
A20boneosteoclast - inflammationosteoporosis

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Area of Science:

  • Molecular Biology
  • Immunology
  • Bone Biology

Background:

  • The anti-inflammatory protein A20 (TNFAIP3) inhibits NF-κB signaling and inflammation.
  • A20 gene variations are linked to inflammatory diseases like rheumatoid arthritis (RA).
  • Myeloid-specific A20 deficiency in mice causes severe polyarthritis and promotes osteoclastogenesis.

Purpose of the Study:

  • To investigate the role of A20 in osteoclast differentiation and bone formation.
  • To determine if A20 specifically regulates osteoclast function independently of its anti-inflammatory role.

Main Methods:

  • Generated and analyzed osteoclast-specific A20 knockout mice.
  • Performed in vitro studies using osteoclast precursor cells from A20-deficient mice.
  • Investigated the molecular mechanism of A20 action at the RANK receptor complex.

Main Results:

  • Osteoclast-specific A20 knockout mice exhibit severe osteoporosis but not inflammatory arthritis.
  • A20-deficient osteoclast precursor cells show enhanced responsiveness to RANKL-induced differentiation.
  • A20 binds to the RANK receptor complex, inhibiting NF-κB activation via its zinc finger domains (ZnF 4 and 7).

Conclusions:

  • A20 is a critical regulator of RANK-induced NF-κB signaling specifically in osteoclasts.
  • A20 controls osteoclast differentiation, essential for maintaining proper bone development and turnover.
  • These findings reveal a distinct role for A20 in bone homeostasis separate from its inflammatory functions.