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Related Concept Videos

Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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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
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
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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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Bone Disorders01:29

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.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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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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Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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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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Related Experiment Video

Updated: Apr 15, 2026

Semiautomated Longitudinal Microcomputed Tomography-based Quantitative Structural Analysis of a Nude Rat Osteoporosis-related Vertebral Fracture Model
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Bone Organoids as Advanced Models for Osteoporosis: Development, Application, and Future Prospects.

Chao Liu1, Xueliang Zhang1, Rui Yu1

  • 1The First Clinical College of Shenyang Campus, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China.

International Journal of Molecular Sciences
|April 14, 2026
PubMed
Summary

Bone organoids offer a complex 3D model for studying osteoporosis, mimicking human bone better than traditional methods. Further refinement is needed for reliable drug screening and regenerative medicine applications in skeletal disorders.

Keywords:
bone organoidsbone remodelingosteoporosisstem cell technologytranslational medicine

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Area of Science:

  • Biomaterials Science
  • Regenerative Medicine
  • Skeletal Biology

Background:

  • Osteoporosis is a major global health issue, characterized by low bone mass and increased fracture risk.
  • Traditional research models (animal, 2D cultures) lack the complexity of human bone's microenvironment, limiting translational relevance.
  • Bone organoids represent a promising 3D biomimetic system for modeling skeletal diseases.

Purpose of the Study:

  • To critically review advances in bone organoid technology for osteoporosis modeling.
  • To differentiate validated capabilities from aspirational claims in current bone organoid research.
  • To identify methodological gaps hindering the clinical translation of bone organoids.

Main Methods:

  • Synthesis of recent literature on bone organoid development and applications.
  • Focus on stem cell biology, tissue engineering, and 3D culture systems.
  • Integration of osteogenic and endothelial cells within biomimetic matrices.

Main Results:

  • Bone organoids can replicate key features of bone physiology and pathology, including osteoporosis models (estrogen deficiency, glucocorticoid use, aging, genetic factors).
  • These 3D systems support mechanistic studies and pharmacological testing.
  • Current limitations include incomplete vascularization, poor mechanical fidelity, instability, and lack of standardization.

Conclusions:

  • Bone organoids show significant potential for modeling osteoporosis and advancing skeletal research.
  • Technological refinement, quantitative metrics, and regulatory standardization are crucial for clinical readiness.
  • Overcoming current barriers will enable reliable drug screening, regenerative medicine, and precision treatments for osteoporosis.