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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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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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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.
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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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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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Related Experiment Video

Updated: Apr 21, 2026

Visualization of Chondrocyte Intercalation and Directional Proliferation via Zebrabow Clonal Cell Analysis in the Embryonic Meckel’s Cartilage
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Cdc42 is critical for cartilage development during endochondral ossification.

Wataru Suzuki1, Atsushi Yamada, Ryo Aizawa

  • 1Departments of Biochemistry (W.S., A.Y., R.A., D.S., M.N., R.N., R.K.), Prosthodontics (W.S., K.B.), Periodontology (R.A., M.Y.), and Orthodontics (M.N., R.N., K.M.), School of Dentistry, Showa University, Tokyo 142-8555, Japan; Laboratory of Animal Resources (H.K., T.H., A.A.), Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo 113-0033, Japan; and Department of Physiology and Cell Biology (S.T.), Tokyo Medical and Dental University Graduate School and Faculty of Medicine, Tokyo 101-0062, Japan.

Endocrinology
|October 25, 2014
PubMed
Summary

Cdc42 protein is crucial for normal skeletal development. Loss of Cdc42 in cartilage cells leads to shorter limbs and impaired bone formation, highlighting its essential role in endochondral ossification.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Skeletal Biology

Background:

  • Cdc42, a Rho GTPase, regulates diverse cellular processes.
  • Its role in cartilage development and endochondral ossification is not fully understood.

Purpose of the Study:

  • To investigate the physiological functions of Cdc42 in chondrocytes during cartilage development.
  • To determine the impact of Cdc42 deficiency on endochondral bone formation.

Main Methods:

  • Generation of chondrocyte-specific Cdc42 knockout mice (Cdc42(fl/fl); Col2-Cre).
  • Gross morphological analysis, skeletal preparations (Alcian blue/Alizarin red staining).
  • Histological analysis of femur growth plates and gene expression analysis of chondrocyte markers.

Main Results:

  • Mutant mice exhibited shorter limbs and body length compared to controls.
  • Growth plate defects included reduced proliferation zone, expanded hypertrophic zone, and disorganized chondrocytes.
  • Decreased expression of chondrocyte markers (Col2, Col10, Mmp13) and impaired bone mineralization were observed.

Conclusions:

  • Cdc42 is essential for normal chondrocyte proliferation, differentiation, and organization in growth plates.
  • Disruption of Cdc42 function leads to abnormal endochondral bone formation.
  • Cdc42 plays a critical role in skeletal development.