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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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Changes in the Appendicular Skeleton with Age01:09

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The upper and lower limb initially develops as a small bulge called a limb bud, which appears on the lateral side of the early embryo. The upper limb bud appears near the end of the fourth week of development, with the lower limb bud appearing shortly after.
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Development of the Limb Synovial Joints01:07

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Joints form during embryonic development in conjunction with the formation and growth of the associated bones. The embryonic tissue that gives rise to all bones, cartilage, and connective tissues of the body is called mesenchyme.
The mesenchymal stem cells differentiate into chondrocytes that form the hyaline cartilage, and later the cartilaginous model of the bone. This model further transforms into a bone. This process is known as endochondral ossification.
During development, the limbs...
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Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

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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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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.
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Culturing and Measuring Fetal and Newborn Murine Long Bones
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Achondroplasia: Development, pathogenesis, and therapy.

David M Ornitz1, Laurence Legeai-Mallet2

  • 1Department of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri, USA.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|December 18, 2016
PubMed
Summary
This summary is machine-generated.

Autosomal dominant mutations in fibroblast growth factor receptor 3 (FGFR3) cause achondroplasia and related skeletal dysplasias. This review details FGFR3

Keywords:
FGFFGFR3achondroplasiachondrogenesisendochondral ossificationfibroblast growth factor receptorgrowth platehypochondroplasiaskeletal dysplasiathanatophoric dysplasiatherapy

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Area of Science:

  • Genetics and Molecular Biology
  • Skeletal Biology and Development

Background:

  • Autosomal dominant mutations in fibroblast growth factor receptor 3 (FGFR3) are the primary cause of achondroplasia (Ach), the most common form of human dwarfism.
  • FGFR3 plays a critical role in regulating bone growth, with its expression observed in chondrocytes and mature osteoblasts.

Purpose of the Study:

  • To review the molecular mechanisms underlying growth plate chondrocyte regulation.
  • To elucidate the pathogenesis of achondroplasia and related FGFR3-associated skeletal disorders.
  • To discuss current and emerging therapeutic strategies for improving endochondral bone growth.

Main Methods:

  • Analysis of molecular mechanisms driving increased FGFR3 signaling, including receptor stabilization, enhanced dimerization, and increased tyrosine kinase activity.
  • Review of studies examining the paradoxical effect of elevated FGFR3 signaling on chondrocyte proliferation and maturation.

Main Results:

  • Mutations lead to hyperactive FGFR3 signaling through various mechanisms.
  • Paradoxically, this hyperactivity suppresses chondrocyte proliferation and maturation, leading to reduced growth plate size and bone elongation.
  • Associated conditions include hypochondroplasia, SADDAN, and thanatophoric dysplasia.

Conclusions:

  • Understanding FGFR3 signaling is crucial for comprehending the pathogenesis of achondroplasia and related conditions.
  • Targeting FGFR3 signaling pathways offers potential therapeutic avenues for enhancing endochondral bone growth in affected individuals.