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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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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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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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The hyoid bone is a small U-shaped bone located in the upper neck at the level of the inferior mandible, with its tips pointing posteriorly. It does not directly articulate with any other bone in the body. The hyoid acts as the attachment site for the tongue, the larynx, and the pharynx. It is held in position by a series of small muscles attached from above or below. These muscles help to move the hyoid up/down or forward/back in coordination with movements of the tongue, larynx, and pharynx...
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Updated: Sep 21, 2025

Visualization of Chondrocyte Intercalation and Directional Proliferation via Zebrabow Clonal Cell Analysis in the Embryonic Meckel&#8217;s Cartilage
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Meckel's Cartilage in Mandibular Development and Dysmorphogenesis.

M Kathleen Pitirri1, Emily L Durham1, Natalie A Romano1

  • 1Department of Anthropology, The Pennsylvania State University, University Park, PA, United States.

Frontiers in Genetics
|June 2, 2022
PubMed
Summary
This summary is machine-generated.

Crouzon syndrome FGFR2 mutation causes craniofacial abnormalities. In mouse models, this mutation alters Meckel's cartilage and mandibular bone development, impacting cell proliferation and signaling pathways.

Keywords:
Crouzon syndromecraniofacial developmentembryonic boneembryonic cartilagefibroblast growth factorlower jawmandibleskull

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Area of Science:

  • Developmental Biology
  • Genetics
  • Craniofacial Development

Background:

  • Crouzon syndrome is a human craniosynostosis disorder caused by mutations in the fibroblast growth factor receptor 2 (FGFR2) gene.
  • The Fgfr2c C342Y mouse model mimics human Crouzon syndrome, exhibiting premature coronal suture closure and craniofacial anomalies.
  • Mandibular malformations in Crouzon syndrome can lead to severe complications, including airway obstruction and malocclusion.

Purpose of the Study:

  • To investigate the relationship between Meckel's cartilage (MC) and mandibular bone development in the Fgfr2c C342Y Crouzon syndrome mouse model.
  • To identify cellular and molecular differences in MC and mandibular bone during embryonic development.

Main Methods:

  • Comparative analysis of Fgfr2c C342Y mutant embryos and their unaffected littermates from embryonic day 13.5 (E13.5) to E17.7.
  • Histological assessment of Meckel's cartilage and mandibular bone morphology.
  • Cellular proliferation assays and analysis of ERK pathway activation.

Main Results:

  • Subtle but distinct differences were observed in MC and mandibular bone between mutant and wild-type embryos.
  • Fgfr2c C342Y embryos showed altered MC length and mandibular bone size, with specific regional differences.
  • Reduced cell proliferation in MC and mandible, and differential ERK pathway activation in MC perichondrium and bone cells were noted.

Conclusions:

  • The Fgfr2c C342Y mutation differentially impacts cell types, locations, and developmental timing within the developing mandible.
  • These findings suggest a complex interplay of cellular changes contributing to mandibular dysmorphogenesis in Crouzon syndrome.
  • Understanding these mechanisms is crucial for developing targeted therapies for craniofacial abnormalities.