Jove
Visualize
Contact Us
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 Concept Videos

Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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 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...

You might also read

Related Articles

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

Sort by
Same author

Shiga toxin delivery in extracellular vesicles induces high mortality and severe kidney injury in a Gb3-dependent manner.

PLoS pathogens·2026
Same author

Characterizing Meniscal Calcifications with Photon Counting-Based Dual-Energy Computed Tomography.

Annals of biomedical engineering·2026
Same author

Characterization of calcifications in posterior horn of human meniscus using micro-computed tomography.

Osteoarthritis and cartilage open·2026
Same author

Histological analysis of age-related degeneration in human female and male knee cartilage and meniscus.

Osteoarthritis and cartilage open·2026
Same author

Molecular treatments to reduce catabolic effects in human meniscus explant models.

Osteoarthritis and cartilage open·2025
Same author

Anabolic indices of matrix proteins identify regenerative small RNA intrinsic to human cartilage.

Science advances·2025

Related Experiment Video

Updated: Jul 9, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Altered osteoclast development and function in osteopontin deficient mice.

Ahnders Franzén1, Kjell Hultenby, Finn P Reinholt

  • 1Department of Experimental Medical Science, Lund University, BMC C12, SE-22184, Lund, Sweden.

Journal of Orthopaedic Research : Official Publication of the Orthopaedic Research Society
|December 1, 2007
PubMed
Summary

Osteopontin deficiency in mice leads to increased osteoclast numbers but reduced bone resorption, preventing osteoporosis. This highlights osteopontin's role in regulating bone remodeling and osteoclast function.

Related Experiment Videos

Last Updated: Jul 9, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Bone Biology

Background:

  • Osteopontin is a key protein in bone metabolism.
  • Its precise role in bone resorption and osteoporosis remains under investigation.

Purpose of the Study:

  • To investigate the function of osteopontin in bone resorption using a novel knockout mouse model.
  • To elucidate the effects of osteopontin deficiency on bone structure and osteoclast activity.

Main Methods:

  • Generation of osteopontin-null mice via Cre-loxP recombination.
  • Structural and molecular analyses including morphometry and proteomics.
  • Assessment of bone volume, osteoclast characteristics, and osteoporosis development.

Main Results:

  • Osteopontin-null mice exhibited normal bone volume but increased osteoclast number and volume in the lower metaphysis.
  • Osteoclast resorptive capacity was significantly reduced, indicated by decreased ruffled border volume and length.
  • Null mice did not develop age-related bone loss observed in wild-type animals, suggesting protection against osteoporosis.

Conclusions:

  • Osteopontin plays a critical role in regulating osteoclast resorptive capacity, not just their number.
  • Osteopontin deficiency confers protection against osteoporosis development.
  • This study provides quantitative evidence for osteopontin's involvement in bone remodeling and osteoclast function.