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Related Concept Videos

Roles of Electrolytes: Calcium and Phosphate01:27

Roles of Electrolytes: Calcium and Phosphate

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Calcium and phosphate are essential electrolytes in the human body, with calcium being the most abundant mineral. Around 99% of the body's calcium is stored in the skeleton and teeth, forming a crystal lattice of mineral salts in combination with phosphates. Calcium plays crucial roles in various bodily functions such as blood clotting, neurotransmitter release, muscle tone maintenance, and nervous and muscle tissue excitability.
The calcium concentration in blood plasma is primarily...
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Bone Disorders01:29

Bone Disorders

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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...
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What is the Skeletal System?01:02

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Overview
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Bone Remodeling01:40

Bone Remodeling

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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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Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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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...
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Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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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...
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Updated: Dec 25, 2025

Analysis of Minerals Produced by hFOB 1.19 and Saos-2 Cells Using Transmission Electron Microscopy with Energy Dispersive X-ray Microanalysis
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FGF23-Related Hypophosphataemic Bone Disease.

Antonio González-Meneses López1

  • 1Unidad de Dismorfología, Unidad de Gestión Clínica de Pediatría, Hospital Universitario Virgen del Rocío, Sevilla, Spain. antonio.gonzalezmeneses.l.sspa@juntadeandalucia.es.

Advances in Therapy
|April 3, 2020
PubMed
Summary

X-linked hypophosphataemic rickets is a rare metabolic bone disease causing skeletal deformities. Advances in genetic diagnosis and understanding fibroblast growth factor 23 (FGF23) offer new treatment possibilities beyond symptom management.

Keywords:
FGF23KlothoMetabolic skeletal dysplasiasRenal failureX-linked hypophosphataemic rickets

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Area of Science:

  • Medical Genetics
  • Endocrinology
  • Bone Metabolism

Background:

  • Metabolic skeletal dysplasias are rare, hereditary bone disorders often misdiagnosed.
  • X-linked hypophosphataemic rickets exemplifies these conditions, causing phosphaturia, skeletal deformities, and short stature due to phosphate-calcium imbalance.

Discussion:

  • Recent genetic advances enable more accurate diagnosis and differentiation from similar conditions.
  • Understanding phosphate-calcium metabolism highlights the role of fibroblast growth factor 23 (FGF23) and Klotho imbalances.

Key Insights:

  • Targeting FGF23 excess with monoclonal antibodies offers a potential alternative to symptomatic treatment.
  • Genetic testing and multi-gene panels are crucial for diagnosing rare renal and skeletal diseases.

Outlook:

  • Future treatments may focus on rebalancing FGF23 levels.
  • Conventional radiology, surgery, and animal models remain important for diagnosis and managing bone deformities.