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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...
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.
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
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...
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...

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Related Experiment Video

Updated: May 26, 2026

Drug Treatment and In Vivo Imaging of Osteoblast-Osteoclast Interactions in a Medaka Fish Osteoporosis Model
08:53

Drug Treatment and In Vivo Imaging of Osteoblast-Osteoclast Interactions in a Medaka Fish Osteoporosis Model

Published on: January 1, 2017

Alendronate affects osteoblast functions by crosstalk through EphrinB1-EphB.

E Shimizu1, J Tamasi, N C Partridge

  • 1New York University College of Dentistry, Department of Basic Science and Craniofacial Biology, USA. es152@nyu.edu

Journal of Dental Research
|December 20, 2011
PubMed
Summary

Alendronate, a bisphosphonate, may impair bone healing by altering cell communication. It increases ephrinB1 expression in pre-osteoclasts, which then suppresses osteoblast function via EphB receptors.

More Related Videos

Osteoclast Derivation from Mouse Bone Marrow
06:17

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Related Experiment Videos

Last Updated: May 26, 2026

Drug Treatment and In Vivo Imaging of Osteoblast-Osteoclast Interactions in a Medaka Fish Osteoporosis Model
08:53

Drug Treatment and In Vivo Imaging of Osteoblast-Osteoclast Interactions in a Medaka Fish Osteoporosis Model

Published on: January 1, 2017

Osteoclast Derivation from Mouse Bone Marrow
06:17

Osteoclast Derivation from Mouse Bone Marrow

Published on: November 6, 2014

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Bisphosphonates treat osteoporosis but have unclear mechanisms for side effects like delayed healing.
  • Osteoporosis treatment involves managing bone remodeling, where osteoblasts build bone and osteoclasts resorb it.

Purpose of the Study:

  • To investigate the hypothesis that alendronate inhibits osteoblast function by disrupting osteoclast-osteoblast coupling via ephrinB-EphB signaling.
  • To elucidate the molecular mechanisms behind bisphosphonate-induced bone healing complications.

Main Methods:

  • Adult mice were treated with alendronate for 8 weeks.
  • Gene and protein expression of ephrinB1, EphB1, EphB3, bone sialoprotein (BSP), and osteonectin were analyzed in femurs and bone marrow cells.
  • Osteoblast differentiation was assessed after depleting pre-osteoclasts.

Main Results:

  • Alendronate increased ephrinB1 and EphB1/B3 expression in mouse femurs.
  • Alendronate suppressed bone sialoprotein and osteonectin expression in osteoblasts.
  • Alendronate's effects on osteoblast differentiation were dependent on the presence of pre-osteoclasts.
  • Alendronate upregulated ephrinB1 in pre-osteoclasts and EphB1/B3 in osteoblasts, with ephrinB1 reverse signaling inhibiting osteoblast differentiation.

Conclusions:

  • Alendronate appears to inhibit osteoblast differentiation indirectly by modulating ephrinB1/EphB signaling between pre-osteoclasts and osteoblasts.
  • This pathway provides a potential mechanism for bisphosphonate-associated bone healing impairments.