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Related Concept Videos

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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Bone Formation by Endochondral Ossification01:24

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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Bone Formation by Intramembranous Ossification01:29

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Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
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For transition metal complexes, the coordination number determines the geometry around the central metal ion. Table 1 compares coordination numbers to molecular geometry. The most common structures of the complexes in coordination compounds are octahedral, tetrahedral, and square planar.
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In most main group element compounds, the valence electrons of the isolated atoms combine to form chemical bonds that satisfy the octet rule. For instance, the four valence electrons of carbon overlap with electrons from four hydrogen atoms to form CH4. The one valence electron leaves sodium and adds to the seven valence electrons of chlorine to form the ionic formula unit NaCl (Figure 1a). Transition metals do not normally bond in this fashion. They primarily form coordinate covalent bonds, a...
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The structure of a crystalline solid, whether a metal or not, is best described by considering its simplest repeating unit, which is referred to as its unit cell. The unit cell consists of lattice points that represent the locations of atoms or ions. The entire structure then consists of this unit cell repeating in three dimensions. The three different types of unit cells present in the cubic lattice are illustrated in Figure 1.
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Related Experiment Video

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A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro
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Osteoclast-secreted SLIT3 coordinates bone resorption and formation.

Beom-Jun Kim1, Young-Sun Lee2, Sun-Young Lee2

  • 1Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea.

The Journal of Clinical Investigation
|March 6, 2018
PubMed
Summary

The axon-guidance molecule SLIT3 acts as a clastokine, promoting bone formation and inhibiting resorption. This discovery highlights SLIT3

Keywords:
Bone BiologyCoupling factors

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Area of Science:

  • Bone biology and remodeling
  • Molecular mechanisms of bone metabolism
  • Osteoimmunology

Background:

  • Bone remodeling involves coordinated bone resorption and formation.
  • Osteoclast-derived factors regulate osteoblast activity.
  • Identifying novel regulators of bone metabolism is crucial for treating bone diseases.

Purpose of the Study:

  • To identify novel osteoclast-derived coupling factors.
  • To investigate the role of SLIT3 in bone metabolism.
  • To explore SLIT3 as a therapeutic target for metabolic bone diseases.

Main Methods:

  • Fractionated secretomic analysis to identify SLIT3.
  • In vitro studies on osteoblast migration, proliferation, and osteoclast differentiation.
  • In vivo studies using Slit3-deficient mice and ovariectomized mice.
  • Analysis of circulating SLIT3 levels in postmenopausal women.

Main Results:

  • SLIT3, an axon-guidance molecule, functions as a clastokine stimulating osteoblast migration and proliferation via β-catenin.
  • SLIT3 inhibits osteoclast differentiation in an autocrine manner.
  • Slit3 deficiency in mice leads to osteopenia with reduced bone formation and increased resorption.
  • SLIT3 is crucial for local bone metabolism, with circulating levels correlating positively with bone mass in postmenopausal women.
  • Recombinant SLIT3 administration rescued bone loss in an ovariectomized mouse model.

Conclusions:

  • SLIT3 plays a critical osteoprotective role by simultaneously promoting bone formation and suppressing bone resorption.
  • SLIT3 synchronizes bone remodeling, making it a promising therapeutic target for metabolic bone diseases like osteoporosis.