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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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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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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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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
Nucleosome remodeling complex
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Bone Structure01:55

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Within the skeletal system, the structure of a bone, or osseous tissue, can be exemplified in a long bone, like the femur, where there are two types of osseous tissue: cortical and cancellous.
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Compact Bone01:27

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Most bones contain compact and spongy osseous tissue, but their distribution and concentration vary based on the bone's overall function.
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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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Updated: Feb 13, 2026

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Opening windows for bone remodeling through a SLIT.

Jameel Iqbal1,2, Tony Yuen1, Se-Min Kim1

  • 1Mount Sinai Bone Program, Icahn School of Medicine at Mount Sinai (ISMMS), New York, New York, USA.

The Journal of Clinical Investigation
|March 6, 2018
PubMed
Summary
This summary is machine-generated.

Scientists discovered that SLIT3, a molecule secreted by bone-resorbing cells, promotes bone formation and reduces bone breakdown. This finding offers a new therapeutic target for treating osteoporosis and other bone diseases.

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Area of Science:

  • Bone Biology
  • Cell Signaling
  • Osteoporosis Research

Background:

  • Bone remodeling involves coupled processes of formation and resorption.
  • Dysregulation of bone remodeling leads to diseases like osteoporosis.
  • Current bone-forming agents have limited long-term efficacy due to increased resorption.

Purpose of the Study:

  • To investigate the role of axonal guidance molecules in bone formation-resorption coupling.
  • To explore SLIT3 as a potential therapeutic target for osteoporosis.

Main Methods:

  • Investigated the function of osteoclast-secreted SLIT3.
  • Examined SLIT3/ROBO signaling in ovariectomized mouse models.
  • Assessed effects on osteoblast migration and osteoclast differentiation.

Main Results:

  • Osteoclast-secreted SLIT3 promotes osteoblast migration.
  • SLIT3 suppresses osteoclast differentiation, balancing bone remodeling.
  • Activation of SLIT3/ROBO signaling increased bone mass in mice.

Conclusions:

  • SLIT3 plays a crucial role in regulating bone formation and resorption coupling.
  • SLIT3 represents a promising therapeutic target for osteoporosis.
  • Further exploration of SLIT3 signaling is warranted for bone disease treatment.