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Related Concept Videos

Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

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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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Bone Formation by Endochondral Ossification01:24

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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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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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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 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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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
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Jagged1 is essential for osteoblast development during maxillary ossification.

Cynthia R Hill1, Masato Yuasa2, Jonathan Schoenecker3

  • 1Department of Otolaryngology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

Bone
|February 5, 2014
PubMed
Summary

Jagged1 (Jag1) signaling in cranial neural crest cells is crucial for maxillary bone development. Its deletion causes maxillary hypoplasia, impacting bone formation and osteoblast differentiation.

Keywords:
Cranial neural crestJagged1Maxillary hypoplasiaMesenchymal cellsOssificationOsteoblasts

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Area of Science:

  • Craniofacial development
  • Bone biology
  • Molecular signaling

Background:

  • Maxillary hypoplasia, resulting from inadequate bone formation, causes dental, respiratory, and cosmetic issues.
  • Jagged1 (Jag1) is a key signaling molecule in embryonic development.

Purpose of the Study:

  • To investigate the role of Jagged1 (Jag1) in cranial neural crest (CNC) cells during maxillary bone development.
  • To understand the molecular mechanisms underlying Jag1-mediated osteoblast differentiation.

Main Methods:

  • Conditional deletion of Jagged1 (Jag1) in CNC cells using Wnt1-cre; Jagged1(f/f) mice (Jag1CKO).
  • Micro-computed tomography (μCT) evaluation of bone morphology and density.
  • In vitro culture of Jag1CKO mouse embryonic maxillary mesenchymal (MEMM) cells.
  • Analysis of collagen deposition, ossification markers, and osteoblast gene expression.
  • Treatment with JAG1-Fc to assess rescue effects.

Main Results:

  • Jag1CKO mice exhibited maxillary hypoplasia with altered bone morphology and density.
  • Reduced collagen deposition and delayed ossification were observed in Jag1CKO maxillas.
  • Jag1CKO MEMM cells showed decreased mineralization and impaired osteoblast differentiation.
  • Dysregulated BMP receptor expression in Jag1CKO MEMM cells indicated impaired BMP signaling response.
  • JAG1-Fc treatment rescued in vitro mineralization and osteoblast gene expression.

Conclusions:

  • Jagged1 (Jag1) signaling within CNC-derived MEMM cells is essential for proper osteoblast development and differentiation.
  • Disruption of Jag1 signaling impairs maxillary ossification through mechanisms involving BMP signaling pathways.
  • Targeting Jag1 signaling may offer therapeutic potential for conditions involving maxillary hypoplasia.