Jove
Visualize
Contact Us

Related Concept Videos

Growth of Cartilage and Bone Tissue01:27

Growth of Cartilage and Bone Tissue

4.9K
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...
4.9K
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

16.0K
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...
16.0K
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

4.3K
The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
4.3K
Bone Disorders01:29

Bone Disorders

8.7K
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.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
8.7K
Nature and Nurture01:10

Nature and Nurture

23.1K
Many human characteristics, like height, are shaped by both nature—in other words, by our genes—and by nurture, or our environment. For example, chronic stress during childhood inhibits the production of growth hormones and consequently reduces bone growth and height. Scientists estimate that 70-90% of variation in height is due to genetic differences among individuals, and 10-30% of variation in height is due to differences in the environments that individuals experience,...
23.1K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

4.9K
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...
4.9K

You might also read

Related Articles

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

Sort by
Same author

Murine model of high bone mass osteogenesis imperfecta exhibits bone matrix hyper-mineralization, misaligned mineral crystals, and altered osteoblast differentiation.

Bone research·2026
Same author

Elevated <i>MMP9</i> Expression-A Potential In Vitro Biomarker for COMPopathies.

International journal of molecular sciences·2025
Same author

Genetic identification of three CITES-listed sharks using a paper-based Lab-on-a-Chip (LOC).

PloS one·2024
Same author

Modeling human skeletal development using human pluripotent stem cells.

Proceedings of the National Academy of Sciences of the United States of America·2023
Same author

Exploration of Social Proximity and Behavior in Captive Malayan Tigers and Their Cubs.

Animals : an open access journal from MDPI·2023
Same author

Curcumin Reduces Pathological Endoplasmic Reticulum Stress through Increasing Proteolysis of Mutant Matrilin-3.

International journal of molecular sciences·2023
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: Apr 17, 2026

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
07:23

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Published on: December 3, 2016

12.6K

Increased classical endoplasmic reticulum stress is sufficient to reduce chondrocyte proliferation rate in the growth

Louise H W Kung1, M Helen Rajpar1, Richard Preziosi2

  • 1Wellcome Trust Centre for Cell-Matrix Research, Faculty of Life Sciences, The University of Manchester, Manchester, United Kingdom.

Plos One
|February 19, 2015
PubMed
Summary

Endoplasmic reticulum (ER) stress contributes to bone growth reduction in skeletal dysplasias like MED and PSACH. This study shows ER stress alone can impair bone growth without affecting growth plate structure.

More Related Videos

Culturing and Measuring Fetal and Newborn Murine Long Bones
06:58

Culturing and Measuring Fetal and Newborn Murine Long Bones

Published on: April 26, 2019

8.8K
A Microfluidic Platform for Stimulating Chondrocytes with Dynamic Compression
07:23

A Microfluidic Platform for Stimulating Chondrocytes with Dynamic Compression

Published on: September 13, 2019

7.2K

Related Experiment Videos

Last Updated: Apr 17, 2026

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification
07:23

Culture of Murine Embryonic Metatarsals: A Physiological Model of Endochondral Ossification

Published on: December 3, 2016

12.6K
Culturing and Measuring Fetal and Newborn Murine Long Bones
06:58

Culturing and Measuring Fetal and Newborn Murine Long Bones

Published on: April 26, 2019

8.8K
A Microfluidic Platform for Stimulating Chondrocytes with Dynamic Compression
07:23

A Microfluidic Platform for Stimulating Chondrocytes with Dynamic Compression

Published on: September 13, 2019

7.2K

Area of Science:

  • Skeletal biology
  • Molecular genetics
  • Cellular pathology

Background:

  • Mutations in COMP and MATN3 cause multiple epiphyseal dysplasia (MED) and pseudoachondroplasia (PSACH).
  • These conditions often involve endoplasmic reticulum (ER) stress and unfolded protein response (UPR) activation due to protein misfolding.
  • The specific role of ER stress in disease pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the role of ER stress and UPR in the pathogenesis of MED and PSACH.
  • To determine if ER stress is a sufficient factor in causing disease phenotypes.

Main Methods:

  • Generated a transgenic mouse line (ColIITgcog) expressing an ER stress-inducing protein (Tgcog) in chondrocytes.
  • Characterized skeletal and histological phenotypes of the mice.
  • Assessed ER stress markers (BiP, eIF2α, Xbp1) and chondrocyte proliferation.

Main Results:

  • Tgcog expression induced ER stress and UPR activation in chondrocytes.
  • ColIITgcog mice showed reduced long bone growth and chondrocyte proliferation rates.
  • No significant disruption in chondrocyte morphology, growth plate architecture, or apoptosis was observed.

Conclusions:

  • Targeted induction of ER stress in chondrocytes is sufficient to reduce bone growth, a key feature of MED and PSACH.
  • ER stress is a pathogenic factor in MED and PSACH.
  • Additional intra- and extra-cellular factors likely contribute to the overall pathology of these diseases.