Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Bone Formation by Endochondral Ossification

Bone Formation by Endochondral Ossification

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...

Growth of Cartilage and Bone Tissue

Growth of Cartilage and Bone Tissue

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...

Development of the Limb Synovial Joints

Development of the Limb Synovial Joints

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Does the neutral zone quantification method matter? Efficacy of evaluating neutral zone during destabilization and restabilization in human spine implant testing.

Journal of biomechanics·2021

Same author

Prenatal muscle forces are necessary for vertebral segmentation and disc structure, but not for notochord involution in mice.

European cells & materials·2021

Same author

Balancing biological and biomechanical performance in intervertebral disc repair: a systematic review of injectable cell delivery biomaterials.

European cells & materials·2020

Same author

Crosslinker concentration controls TGFβ-3 release and annulus fibrosus cell apoptosis in genipin-crosslinked fibrin hydrogels.

European cells & materials·2020

Same author

Functional cell phenotype induction with TGF-β1 and collagen-polyurethane scaffold for annulus fibrosus rupture repair.

European cells & materials·2020

Same author

Short-term foetal immobility temporally and progressively affects chick spinal curvature and anatomy and rib development.

European cells & materials·2019

Search research articles

Related Experiment Video

Updated: Mar 11, 2026

Optical Sectioning and Visualization of the Intervertebral Disc from Embryonic Development to Degeneration

Optical Sectioning and Visualization of the Intervertebral Disc from Embryonic Development to Degeneration

Published on: July 8, 2021

AGEs induce ectopic endochondral ossification in intervertebral discs

S Illien-Jünger¹, O M Torre, W F Kindschuh

¹Leni and Peter W. May Department of Orthopaedics, Box 1188, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, NY 10029, New York, USA.Svenja.illien-junger@mssm.edu.

European Cells & Materials

|November 19, 2016

Summary

This summary is machine-generated.

Ectopic calcifications in intervertebral discs (IVDs) are linked to advanced glycation end products (AGEs). This AGE/RAGE pathway drives IVD cell hypertrophy and osteogenic differentiation, accelerating degeneration.

More Related Videos

A Proinflammatory, Degenerative Organ Culture Model to Simulate Early-Stage Intervertebral Disc Disease.

A Proinflammatory, Degenerative Organ Culture Model to Simulate Early-Stage Intervertebral Disc Disease.

Published on: February 14, 2021

Author Spotlight: Enhancing Bone Regeneration with Vascularized Artificial Cartilage Integration

Author Spotlight: Enhancing Bone Regeneration with Vascularized Artificial Cartilage Integration

Published on: July 14, 2023

Related Experiment Videos

Last Updated: Mar 11, 2026

Optical Sectioning and Visualization of the Intervertebral Disc from Embryonic Development to Degeneration

Optical Sectioning and Visualization of the Intervertebral Disc from Embryonic Development to Degeneration

Published on: July 8, 2021

A Proinflammatory, Degenerative Organ Culture Model to Simulate Early-Stage Intervertebral Disc Disease.

A Proinflammatory, Degenerative Organ Culture Model to Simulate Early-Stage Intervertebral Disc Disease.

Published on: February 14, 2021

Author Spotlight: Enhancing Bone Regeneration with Vascularized Artificial Cartilage Integration

Author Spotlight: Enhancing Bone Regeneration with Vascularized Artificial Cartilage Integration

Published on: July 14, 2023

Area of Science:

Biomedical Science
Orthopedics
Cell Biology

Background:

Ectopic calcifications in intervertebral discs (IVDs) are linked to degeneration and potential structural failure.
The role of advanced glycation end products (AGEs) in this calcification process is not well understood.

Purpose of the Study:

To investigate the hypothesis that ectopic calcifications in the IVD are associated with AGEs.
To explore the role of AGEs in inducing hypertrophy and osteogenic differentiation in IVD cells via the AGE/RAGE axis.

Main Methods:

Histological analysis of human IVDs at various degeneration stages.
Cell culture of bovine nucleus pulposus and cartilaginous endplate cells treated with AGEs.
Inhibition of the receptor for AGE (RAGE) to assess its involvement.

Main Results:

Ectopic calcifications were found in human IVDs, co-localizing with AGEs (MG-H1), Collagen 10 (COL10), and Osteopontin (OPN).
AGE treatment in cell culture increased ectopic calcifications and upregulated COL10 and OPN expression.
RAGE inhibition reduced COL10 and OPN expression, indicating its role in the differentiation process.

Conclusions:

AGE accumulation is associated with endochondral ossification in IVDs.
The AGE/RAGE axis likely induces hypertrophy and osteogenic differentiation in IVD cells, contributing to degeneration.
Targeting the AGE/RAGE pathway may offer a novel therapeutic strategy for IVD degeneration.