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Related Concept Videos

Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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.
The Parathyroid Glands00:59

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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Related Experiment Video

Updated: Jul 13, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
03:57

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Published on: July 14, 2023

Can hyperparathyroid bone disease be arrested or reversed?

Klaus Olgaard1, Ewa Lewin

  • 1University of Copenhagen, Department of Nephrology, P2132, Rigshospitalet, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark. olgaard@rh.dk

Clinical Journal of the American Society of Nephrology : CJASN
|August 21, 2007
PubMed
Summary

Chronic kidney disease causes parathyroid hyperplasia and bone disease. Treatments that lower parathyroid hormone (PTH) levels can improve bone health in uremia, but oversuppression may cause adynamic bone disease.

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Last Updated: Jul 13, 2026

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy
03:57

Generation of Hypoparathyroid Rats via Carbon-Nanoparticle-Assisted Parathyroidectomy

Published on: July 14, 2023

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
07:13

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation

Published on: March 14, 2017

Area of Science:

  • Nephrology
  • Endocrinology
  • Bone Metabolism

Background:

  • Chronic uremia is associated with parathyroid hyperplasia, excessive parathyroid hormone (PTH) secretion, and progressive hyperparathyroid bone disease.
  • These conditions develop early in the course of chronic kidney disease.

Purpose of the Study:

  • To review the potential for arresting or reversing hyperparathyroid-induced bone disease in chronic uremia.
  • To focus on studies utilizing bone histology to assess skeletal changes.

Main Methods:

  • Review of investigations employing bone histology to evaluate hyperparathyroid bone disease.
  • Exclusion of studies relying solely on bone mineral density or indirect laboratory markers of bone turnover (excluding PTH).

Main Results:

  • Significant suppression of PTH secretion or reversal of hyperparathyroidism is necessary for regression of hyperparathyroid bone disease.
  • Paired bone biopsy studies demonstrate that diminished PTH levels can improve or normalize bone histology in patients with established hyperparathyroid bone disease.

Conclusions:

  • Treatment strategies aimed at reducing PTH levels can lead to improvements in hyperparathyroid bone disease in uremic patients.
  • Caution is advised as excessive suppression of PTH may result in the development of adynamic bone disease.