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 Disorders01:29

Bone Disorders

8.0K
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...
8.0K
Bone Remodeling01:40

Bone Remodeling

34.4K
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.
34.4K
Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

3.9K
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...
3.9K
Hormones and Bone Tissue01:17

Hormones and Bone Tissue

3.5K
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...
3.5K
Autoimmune Disorders01:29

Autoimmune Disorders

2.4K
Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune...
2.4K
What is the Skeletal System?01:02

What is the Skeletal System?

45.7K
Overview
45.7K

You might also read

Related Articles

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

Sort by
Same author

A model of chronic enthesitis and new bone formation characterized by multimodal imaging.

Disease models & mechanisms·2018
Same author

A comparative analysis of articular bone in large cohort of patients with chronic inflammatory diseases of the joints, the gut and the skin.

Bone·2018
Same author

Effects of ustekinumab versus tumor necrosis factor inhibition on enthesitis: Results from the enthesial clearance in psoriatic arthritis (ECLIPSA) study.

Seminars in arthritis and rheumatism·2018
Same author

Therapeutic benefit of apremilast on enthesitis and dactylitis in patients with psoriatic arthritis: a pooled analysis of the PALACE 1-3 studies.

RMD open·2018
Same author

Physiological effects of modulating the interleukin-6 axis.

Rheumatology (Oxford, England)·2018
Same author

Group 2 Innate Lymphoid Cells Attenuate Inflammatory Arthritis and Protect from Bone Destruction in Mice.

Cell reports·2018
Same journal

Beyond Fracture Probability: Communicating the Full Consequences of Fracture and Contextualization.

Current osteoporosis reports·2026
Same journal

Time-Lapse HR-pQCT: an in Vivo Imaging-Based Assessment of Bone Remodeling Dynamics.

Current osteoporosis reports·2026
Same journal

Cone Beam Computed Tomography of Bonejaws in Patients With Primary Osteoporosis: A Systematic Review.

Current osteoporosis reports·2026
Same journal

Testosterone and Bone Health in Men.

Current osteoporosis reports·2026
Same journal

Stimulant Medications and Bone Health.

Current osteoporosis reports·2026
Same journal

The Innate and Adaptive Immune Functions of Osteoblast-Lineage Cells.

Current osteoporosis reports·2026
See all related articles

Related Experiment Video

Updated: May 4, 2026

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

11.1K

Autoantibody-mediated bone loss.

Ulrike Harre1, Nicolai A Kittan, Georg Schett

  • 1Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany, Ulrike.Harre@uk-erlangen.de.

Current Osteoporosis Reports
|January 11, 2014
PubMed
Summary
This summary is machine-generated.

Autoantibodies, like rheumatoid factor, directly activate bone-resorbing osteoclasts in rheumatoid arthritis (RA), contributing to bone loss. B-cell depletion therapy shows efficacy comparable to TNF-antagonists in RA, underscoring autoantibody significance.

More Related Videos

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
10:35

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Published on: December 26, 2017

7.7K
Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

5.3K

Related Experiment Videos

Last Updated: May 4, 2026

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

11.1K
Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
10:35

Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation

Published on: December 26, 2017

7.7K
Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro
07:51

Effect of Anti-c-fms Antibody on Osteoclast Formation and Proliferation of Osteoclast Precursor In Vitro

Published on: March 18, 2019

5.3K

Area of Science:

  • Immunology
  • Rheumatology
  • Bone Biology

Background:

  • Rheumatoid arthritis (RA) involves autoantibodies (e.g., rheumatoid factor, anti-citrullinated protein antibodies) linked to disease severity and bone loss.
  • Traditionally, autoantibody effects on bone resorption were attributed to inflammation-driven osteoclastogenesis.
  • Emerging evidence suggests autoantibodies directly activate osteoclasts, independent of inflammation.

Purpose of the Study:

  • To investigate the direct role of autoantibodies in osteoclast activation and bone resorption in rheumatoid arthritis.
  • To compare the efficacy of B-cell depletion therapy (rituximab) with established treatments in RA patients.
  • To highlight the significance of autoantibodies in RA pathogenesis and associated bone loss.

Main Methods:

  • Review of recent research on autoantibody mechanisms in rheumatoid arthritis.
  • Analysis of clinical data comparing rituximab and tumor necrosis factor-antagonists in RA patients refractory to methotrexate.
  • Assessment of autoantibody levels and their correlation with disease activity and bone loss.

Main Results:

  • Autoantibodies directly activate osteoclasts and their precursors, a process independent of inflammatory cytokines.
  • B-cell depletion with rituximab, reducing autoantibody levels, demonstrated comparable efficacy to tumor necrosis factor-antagonists in methotrexate-resistant RA.
  • These findings confirm a significant role for autoantibodies in RA-related bone loss.

Conclusions:

  • Autoantibodies play a direct, non-inflammatory role in activating osteoclasts, contributing significantly to bone resorption in rheumatoid arthritis.
  • Targeting autoantibodies through B-cell depletion offers a viable therapeutic strategy for RA patients, particularly those unresponsive to conventional treatments.
  • The study emphasizes the critical importance of addressing autoantibody production for managing RA and preventing bone loss.