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Related Concept Videos

Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

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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 Remodeling01:40

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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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Growth of Cartilage and Bone Tissue01:27

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Chondrocytes form a temporary cartilaginous model by dividing and secreting a thick gel-like extracellular matrix. Once the chondrocytes undergo programmed cell death, osteoblasts enter the site of the cartilaginous model. The process of replacing the temporary cartilaginous model with bone in an ordered manner is called endochondral ossification. In endochondral ossification, not all of the cartilage is replaced by bone tissue. Some cartilage that performs a protective and supportive function...
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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.
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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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Updated: Jun 14, 2025

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
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Osteoclasts control endochondral ossification via regulating acetyl-CoA availability.

Daizhao Deng1, Xianming Liu1, Wenlan Huang1

  • 1Department of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou, 510515, Guangdong, China.

Bone Research
|August 28, 2024
PubMed
Summary
This summary is machine-generated.

Mitochondrial respiration, not glycolysis, is vital for cathepsin K (CTSK) production in osteoclasts, regulated by Rheb1. Targeting Rheb1 may improve bone healing, especially after alcohol consumption.

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Area of Science:

  • Cell Biology
  • Metabolism
  • Bone Biology

Background:

  • Osteoclasts are crucial for bone health and fracture repair.
  • The metabolic regulation of osteoclast function, particularly in relation to skeletal development and healing, is not fully understood.

Purpose of the Study:

  • To investigate the role of osteoclast metabolic state in skeletal development and fracture healing.
  • To elucidate the mechanisms by which Rheb1 influences osteoclast function and cathepsin K (CTSK) production.

Main Methods:

  • Utilized osteoclast-specific Rheb1-knockout mouse models.
  • Investigated the impact of Rheb1 on mitochondrial respiration and glycolysis in osteoclasts.
  • Analyzed the relationship between Rheb1, mitochondrial acetyl-CoA generation, and CTSK production.

Main Results:

  • Mitochondrial respiration, not glycolysis, is essential for osteoclast cathepsin K (CTSK) production.
  • Rheb1 regulates CTSK production independently of the mTORC1 pathway.
  • Rheb1 coordinates with mitochondrial acetyl-CoA generation to support CTSK activity.
  • Impaired acetyl-CoA availability in osteoclasts centralizes CTSK elevation.
  • Abnormal endochondral ossification, linked to alcohol consumption, may stem from dysregulated CTSK via acetyl-CoA.

Conclusions:

  • Mitochondrial metabolism, specifically respiration and acetyl-CoA generation regulated by Rheb1, is critical for osteoclast function.
  • Targeting Rheb1 offers a potential therapeutic strategy for bone disorders, including impaired fracture healing associated with alcohol consumption.