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

Bone Remodeling01:40

Bone Remodeling

41.2K
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.
41.2K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

4.8K
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...
4.8K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

14.1K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
14.1K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

11.0K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
11.0K
Inflammatory Response01:28

Inflammatory Response

19.6K
An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
19.6K
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

You might also read

Related Articles

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

Sort by
Same author

Pharmacokinetic and biodistribution (PK/BD) study of ProGel-Dex, a thermoresponsive dexamethasone prodrug for sustained joint pain relief in a mouse model of osteoarthritis.

Nanomedicine : nanotechnology, biology, and medicine·2025
Same author

Joint damage is more severe following a single bout than multiple bouts of high magnitude loading in mice.

Osteoarthritis and cartilage·2025
Same author

Intradermal Injection of a Thermoresponsive Polymeric Dexamethasone Prodrug (ProGel-Dex) Ameliorate Dermatitis in an Imiquimod (IMQ)-Induced Psoriasis-like Mouse Model.

Molecular pharmaceutics·2024
Same author

Identification of formulation parameters that affect the analgesic efficacy of ProGel-Dex - A thermoresponsive polymeric dexamethasone prodrug for chronic arthritis pain relief.

Nanomedicine : nanotechnology, biology, and medicine·2024
Same author

PTH treatment before cyclic joint loading improves cartilage health and attenuates load-induced osteoarthritis development in mice.

Science advances·2024
Same author

Thermoresponsive Polymeric Hydromorphone Prodrug Provides Sustained Local Analgesia without Apparent Adverse Effects.

Molecular pharmaceutics·2024

Related Experiment Video

Updated: Apr 11, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.5K

Inflammatory signaling induced bone loss.

Steven R Goldring1

  • 1Research Division, Hospital for Special Surgery, Weill Cornell Medical College, New York, NY, USA.

Bone
|June 2, 2015
PubMed
Summary
This summary is machine-generated.

Systemic inflammatory disorders like rheumatoid arthritis can harm bones, leading to bone loss and fracture risk. This review examines how these conditions disrupt bone remodeling and skeletal health.

Keywords:
BoneBone remodelingRheumatoid arthritisSpondylitisSystemic lupus

More Related Videos

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

12.2K

Related Experiment Videos

Last Updated: Apr 11, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.5K
A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders
11:47

A Novel in vivo Gene Transfer Technique and in vitro Cell Based Assays for the Study of Bone Loss in Musculoskeletal Disorders

Published on: June 8, 2014

12.2K

Area of Science:

  • Rheumatology and Bone Biology
  • Skeletal Pathophysiology

Background:

  • Systemic inflammatory disorders frequently impact skeletal integrity.
  • Inflammation disrupts normal bone remodeling processes, affecting articular and peri-articular tissues.
  • These conditions can lead to systemic bone loss and increase the risk of osteoporotic fractures.

Purpose of the Study:

  • To review the effects of systemic inflammatory rheumatologic disorders on bone remodeling.
  • To focus on rheumatoid arthritis (RA) as a model, while also discussing systemic lupus erythematosus (SLE) and seronegative spondyloarthropathies (SpAs).
  • To highlight differential impacts of inflammation on bone remodeling across various conditions.

Main Methods:

  • Literature review focusing on inflammatory rheumatologic disorders and their skeletal manifestations.
  • Analysis of the mechanisms by which inflammation affects bone remodeling.
  • Comparative review of rheumatoid arthritis, SLE, and SpAs (including ankylosing spondylitis, reactive arthritis, inflammatory bowel disease arthritis, juvenile onset spondyloarthropathy, and psoriatic arthritis).

Main Results:

  • Rheumatoid arthritis serves as a key model for inflammation-induced bone remodeling dysregulation.
  • Systemic inflammatory conditions commonly cause bone loss and elevate fracture risk.
  • Differential effects on bone remodeling are observed across various inflammatory arthropathies.

Conclusions:

  • Inflammatory rheumatologic disorders pose a significant threat to skeletal health through bone remodeling disruption.
  • Understanding these effects is crucial for managing bone loss and fracture risk in affected patients.
  • Further research into "Muscle Bone Interactions" is warranted given the interconnectedness of these systems.