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Related Concept Videos

Fractures: Bone Repair01:27

Fractures: Bone Repair

Treatment for a fracture is based on the type of break, the bone affected, and the patient's age.
Minor fractures with no bone displacement are treated by immobilizing the fractured bone using a cast or splint. However, in the case of fractures with displaced bones, the broken bones are repositioned before immobilization to ensure successful healing without deformation and loss of function. The realignment of fractured bone ends is performed through a process called reduction. If the procedure...
Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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 bone...
Bone Formation by Endochondral Ossification01:24

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...
Bone Disorders01:29

Bone Disorders

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...
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

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.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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...

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Related Experiment Video

Updated: Jul 9, 2026

Fracture Apparatus Design and Protocol Optimization for Closed-stabilized Fractures in Rodents
06:59

Fracture Apparatus Design and Protocol Optimization for Closed-stabilized Fractures in Rodents

Published on: August 14, 2018

Genes Associated With Fracture Risk in Thoroughbred Horses Have Novel Roles in Osteogenesis.

Amy C Ross1, Ellison S Lumsden1, Caroline Flood1

  • 1Department of Clinical Sciences and Services, Centre for Vaccinology and Regenerative Medicine, The Royal Veterinary College, Hatfield, Herts, UK.

Animal Genetics
|July 8, 2026
PubMed
Summary
This summary is machine-generated.

Researchers identified novel roles for fracture-associated genes in Thoroughbred horses. These genes impact bone formation and mineralization, potentially explaining genetic fracture risks in racehorses.

Keywords:
bonefracturegeneticshorsemineralisationosteoblastosteogenesis

More Related Videos

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
10:30

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair

Published on: May 23, 2014

Related Experiment Videos

Last Updated: Jul 9, 2026

Fracture Apparatus Design and Protocol Optimization for Closed-stabilized Fractures in Rodents
06:59

Fracture Apparatus Design and Protocol Optimization for Closed-stabilized Fractures in Rodents

Published on: August 14, 2018

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair
10:30

Sequential In vivo Imaging of Osteogenic Stem/Progenitor Cells During Fracture Repair

Published on: May 23, 2014

Area of Science:

  • Genetics
  • Equine Orthopedics
  • Molecular Biology

Background:

  • Bone fractures in Thoroughbred racehorses pose significant welfare concerns.
  • Genetic predisposition is a key factor influencing fracture susceptibility.
  • Previous studies identified 112 differentially expressed genes in osteoblasts from horses with varying genetic fracture risks.

Purpose of the Study:

  • To investigate the novel roles of previously uncharacterized genes in bone formation.
  • To determine the impact of specific genes (ADSSL1, CABP1, ENO2, SPARCL1, UCP2) on osteogenesis in a cell model.
  • To correlate gene expression levels with genetic fracture risk in Thoroughbred horses.

Main Methods:

  • Utilized Saos2 cells cultured under basal and osteogenic conditions.
  • Performed stable overexpression and knockdown of five candidate genes (ADSSL1, CABP1, ENO2, SPARCL1, UCP2).
  • Assessed effects on cell viability, osteogenic gene expression, collagen deposition, and matrix mineralization.

Main Results:

  • Gene overexpression decreased cell viability and osteogenic gene expression under basal conditions.
  • Gene knockdown primarily affected osteogenic gene expression, collagen deposition, and matrix mineralization after osteogenic culture.
  • ADSSL1, CABP1, ENO2, and UCP2 showed significantly lower expression in osteoblasts from genetically high-risk horses.

Conclusions:

  • Novel roles for fracture-associated genes in bone formation and matrix mineralization were identified.
  • Altered expression of these genes may contribute to the increased fracture risk in genetically susceptible Thoroughbreds.
  • This research provides insights into the molecular mechanisms underlying equine bone health and fracture susceptibility.