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Related Concept Videos

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.
Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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 Structure01:55

Bone Structure

Within the skeletal system, the structure of a bone, or osseous tissue, can be exemplified in a long bone, like the femur, where there are two types of osseous tissue: cortical and cancellous.
Bone Formation by Intramembranous Ossification01:29

Bone Formation by Intramembranous Ossification

Intramembranous ossification is one of the two processes involved in the development of bones within an embryo. The flat bones of the face, most of the cranial bones, and the clavicles are formed via this process. During intramembranous ossification, the bones develop directly from sheets of undifferentiated mesenchymal connective tissue.
The process begins when mesenchymal cells in the embryonic skeleton gather together and differentiate into osteogenic cells, which then develop into...
Bone Formation by Endochondral Ossification01:24

Bone Formation by Endochondral Ossification

Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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...

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Related Experiment Video

Updated: Jun 3, 2026

Half-segmental Diaphyseal Bone Defect Model in Rats for Evaluating Bone Substitute Performance in Load-bearing Regions
04:32

Half-segmental Diaphyseal Bone Defect Model in Rats for Evaluating Bone Substitute Performance in Load-bearing Regions

Published on: December 30, 2025

FGF23 in skeletal modeling and remodeling.

Yongbo Lu1, Jian Q Feng

  • 1Department of Biomedical Sciences, Baylor College of Dentistry Texas A & M University Health Science Center, 3302 Gaston Avenue, Dallas, TX 75246, USA.

Current Osteoporosis Reports
|March 16, 2011
PubMed
Summary

Fibroblast growth factor 23 (FGF23) regulates phosphate balance and vitamin D synthesis. This review explores FGF23

Area of Science:

  • Biochemistry
  • Endocrinology
  • Genetics

Background:

  • Fibroblast growth factor 23 (FGF23) is a bone-derived hormone regulating phosphate homeostasis and vitamin D metabolism.
  • Dysregulation of FGF23 causes inherited disorders like hypophosphatemic rickets and impacts skeletal mineralization.
  • FGF23 influences phosphate excretion and vitamin D synthesis, maintaining phosphate balance.

Purpose of the Study:

  • To review recent findings on FGF23 regulation.
  • To elucidate the roles of FGF23 in bone modeling and remodeling.
  • To summarize current understanding of FGF23 in human genetic disorders and animal models.

Main Methods:

  • Review of human genetic disorder studies.
  • Analysis of genetically engineered mouse models.

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Establishing a Diaphyseal Femur Fracture Model in Mice

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Last Updated: Jun 3, 2026

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  • In vitro experimental approaches.

    • Main Results:

    • Excess FGF23 leads to phosphate wasting and impaired bone mineralization.
    • FGF23 deficiency causes hyperphosphatemia, elevated vitamin D, and ectopic ossification.
    • Recent research clarifies FGF23 regulation and its functions in bone.

    Conclusions:

    • FGF23 is a critical regulator of phosphate and vitamin D metabolism.
    • Altered FGF23 levels are implicated in various skeletal and mineral disorders.
    • Further research clarifies FGF23's complex roles in bone health.