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

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.

You might also read

Related Articles

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

Sort by
Same author

CMIP as a novel candidate gene for neurodevelopmental and neuropsychiatric disorders.

European journal of human genetics : EJHG·2026
Same author

The genetics and outcomes of an altered FGF23-1,25D-PTH axis in diseases of mineral metabolism.

Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research·2026
Same author

Systemic Phosphate Elevations Induce Fibroblast Growth Factor 23 Production in Skeletal Muscle to Reduce Renal Phosphate Reabsorption in Mice.

Journal of the American Society of Nephrology : JASN·2026
Same author

Characterization of CTNND2-related neurodevelopmental disease, phenotype-genotype spectrum and WNT dynamics in early neurogenesis.

Research square·2026
Same author

Multi-tissue spatial transcriptomics identified simultaneous responses to oxidative stress and apoptosis in parallel with tissue-specific reprogramming in modeled chronic kidney disease-mineral and bone disorder.

JBMR plus·2025
Same author

A proposed path to explaining the unexplained anemia of aging.

The journals of gerontology. Series A, Biological sciences and medical sciences·2025

Related Experiment Video

Updated: Jun 15, 2026

Modeling Primary Bone Tumors and Bone Metastasis with Solid Tumor Graft Implantation into Bone
06:53

Modeling Primary Bone Tumors and Bone Metastasis with Solid Tumor Graft Implantation into Bone

Published on: September 9, 2020

Tumor-induced osteomalacia.

Emily G Farrow1, Kenneth E White

  • 1Department of Medical & Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA.

Expert Review of Endocrinology & Metabolism
|March 16, 2010
PubMed
Summary
This summary is machine-generated.

Tumor-induced osteomalacia involves tumors causing kidney phosphate wasting via phosphatonins. Fibroblast growth factor-23 (FGF-23) is a key phosphatonin, impacting phosphate homeostasis and linking skeleton-kidney endocrine interactions.

More Related Videos

Models of Bone Metastasis
08:49

Models of Bone Metastasis

Published on: September 4, 2012

Related Experiment Videos

Last Updated: Jun 15, 2026

Modeling Primary Bone Tumors and Bone Metastasis with Solid Tumor Graft Implantation into Bone
06:53

Modeling Primary Bone Tumors and Bone Metastasis with Solid Tumor Graft Implantation into Bone

Published on: September 9, 2020

Models of Bone Metastasis
08:49

Models of Bone Metastasis

Published on: September 4, 2012

Area of Science:

  • Endocrinology
  • Nephrology
  • Oncology

Background:

  • Tumor-induced osteomalacia (TIO) is an acquired disorder characterized by renal phosphate wasting.
  • TIO shares clinical and biochemical similarities with genetic hypophosphatemic disorders like ADHR and X-linked hypophosphatemia.
  • The discovery of circulating tumor-derived factors, or 'phosphatonins', was prompted by TIO studies.

Purpose of the Study:

  • To review the significance of TIO in understanding phosphate homeostasis.
  • To highlight the role of phosphatonins, particularly FGF-23, in TIO pathogenesis.
  • To explore the endocrine interplay between the skeleton and kidneys in phosphate regulation.

Main Methods:

  • Literature review of TIO, phosphatonins, and FGF-23.
  • Analysis of biochemical and skeletal phenotypes in TIO and related disorders.
  • Discussion of current understanding of phosphate handling and endocrine regulation.

Main Results:

  • Tumors in TIO produce phosphatonins that induce renal phosphate wasting.
  • FGF-23 is identified as a major phosphatonin and the causative factor in ADHR.
  • TIO research has significantly advanced the understanding of phosphate homeostasis.

Conclusions:

  • TIO serves as a critical model for studying phosphate metabolism and phosphatonin function.
  • FGF-23 plays a central role in TIO and other hypophosphatemic conditions.
  • Understanding TIO elucidates complex endocrine interactions governing phosphate balance.