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Related Concept Videos

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...
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...
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...
Bone Remodeling01:40

Bone Remodeling

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.

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Related Experiment Video

Updated: Jun 13, 2026

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

MASH-induced elevation of FGF23 promotes hepatic osteodystrophy.

Yuki Okamoto1, Yoshiharu Tsuru2, Yuma Nonoshita1

  • 1Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, 113-8657, Japan.

Bone
|June 11, 2026
PubMed
Summary

Metabolic dysfunction-associated steatohepatitis (MASH) causes bone weakness by increasing fibroblast growth factor 23 (FGF23). Elevated FGF23 disrupts bone remodeling, leading to hepatic osteodystrophy and increased fracture risk.

Keywords:
Bone remodelingFGF23Hepatic osteodystrophyMASHPhosphorus

Related Experiment Videos

Last Updated: Jun 13, 2026

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

Area of Science:

  • Hepatology
  • Bone Biology
  • Endocrinology

Background:

  • Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease.
  • MASH can lead to hepatic osteodystrophy, characterized by bone weakness and fractures.
  • Current treatments like calcium supplementation are often ineffective for MASH-related bone issues.

Purpose of the Study:

  • Investigate the role of fibroblast growth factor 23 (FGF23) in MASH-induced hepatic osteodystrophy.
  • Determine the impact of elevated FGF23 on bone mineral density and remodeling in MASH.
  • Explore the mechanisms by which FGF23 affects osteoblast and osteoclast activity.

Main Methods:

  • Generated MASH mouse models using a choline- and methionine-deficient high-fat diet.
  • Performed histological and biochemical analyses to assess liver steatosis and inflammation.
  • Utilized micro-computed tomography to evaluate bone mineral density and structure.
  • Measured serum FGF23 and phosphorus levels.
  • Assessed the effects of FGF23 on osteoblast and osteoclast differentiation in vitro.

Main Results:

  • MASH mice exhibited severe hepatic steatosis, inflammation, and weakened bones (decreased bone mineral density, trabecular number; increased trabecular separation).
  • Serum FGF23 levels were significantly elevated in MASH mice, while serum phosphorus remained unchanged.
  • FGF23 promoted osteoclast differentiation and suppressed osteoblast differentiation, indicating a role in bone remodeling imbalance.

Conclusions:

  • Elevated FGF23 in MASH contributes to hepatic osteodystrophy by disrupting bone remodeling.
  • FGF23 may be a key mediator linking MASH to bone disease.
  • Targeting FGF23 could offer a novel therapeutic strategy for MASH-related bone complications.