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Related Concept Videos

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...
The Bone Matrix01:18

The Bone Matrix

Bone contains a relatively small number of cells entrenched in a matrix of collagen fibers that provide an adherent surface for inorganic salt crystals. Both components of the matrix, organic and inorganic, contribute to the unusual properties of bone. Without collagen, bones would be brittle and shatter easily. Without mineral crystals, bones would flex and provide little support. This can be observed by an experiment: when the minerals of a bone are dissolved by soaking the bone in acid or...
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...
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.
Essential Minerals for Bone Health01:31

Essential Minerals for Bone Health

The minerals contained in all of the food we consume are essential for our organ systems. However, certain essential minerals, such as calcium, phosphorus, magnesium, manganese, and fluoride, largely affect bone health.
Calcium and Phosphorus
Calcium is a critical component of bones, especially in the form of calcium phosphate and calcium carbonate. Since the body cannot make calcium, it must be obtained from the diet. However, calcium cannot be absorbed from the small intestine without...
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: May 10, 2026

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow
11:11

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

Published on: May 19, 2019

Arrestins in bone.

Brittany N Bohinc1, Diane Gesty-Palmer

  • 1Department of Medicine, Division of Endocrinology and Metabolism, Duke University Medical Center, Durham, North Carolina, USA.

Progress in Molecular Biology and Translational Science
|June 15, 2013
PubMed
Summary
This summary is machine-generated.

Parathyroid hormone (PTH) regulates bone metabolism. A new drug, bPTH(7-34), stimulates bone growth via arrestin signaling, offering a potential osteoporosis treatment with fewer side effects than traditional PTH therapies.

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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts
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Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts

Published on: May 13, 2014

Related Experiment Videos

Last Updated: May 10, 2026

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow
11:11

Isolation, Purification, and Differentiation of Osteoclast Precursors from Rat Bone Marrow

Published on: May 19, 2019

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
09:37

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

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Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts
07:13

Application of Retinoic Acid to Obtain Osteocytes Cultures from Primary Mouse Osteoblasts

Published on: May 13, 2014

Area of Science:

  • Endocrinology
  • Molecular Pharmacology
  • Bone Biology

Background:

  • Parathyroid hormone (PTH) is crucial for calcium-phosphorus balance and bone remodeling.
  • Recombinant human PTH (PTH(1-34)) treats osteoporosis by stimulating bone formation via the PTH type I receptor (PTH1R).
  • PTH1R signaling involves both G protein-coupled pathways and β-arrestin-mediated pathways.

Purpose of the Study:

  • To investigate the role of β-arrestins in PTH1R signaling for bone anabolism.
  • To evaluate the therapeutic potential of β-arrestin-biased agonists for osteoporosis.

Main Methods:

  • In vitro studies using a β-arrestin-selective biased agonist, D-Trp(12), Tyr(34)-bPTH(7-34) [bPTH(7-34)].
  • In vivo studies administering bPTH(7-34) intermittently to mice.
  • Assessment of bone formation, hypercalcemia, and bone resorption markers.

Main Results:

  • bPTH(7-34) activates arrestin-dependent signaling while antagonizing G protein signaling.
  • Intermittent administration of bPTH(7-34) in mice promotes anabolic bone formation independently of G protein pathways.
  • Unlike PTH(1-34), bPTH(7-34) did not induce hypercalcemia or increase bone resorption markers.

Conclusions:

  • β-arrestins act as critical signal transducers for PTH1R, independent of canonical GPCR signaling.
  • β-arrestin-biased agonism represents a novel therapeutic strategy for metabolic bone diseases.
  • Targeting β-arrestin pathways may provide osteoporosis treatments with an improved safety profile.