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Related Concept Videos

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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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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Bone Cells and Tissue01:30

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Bones contain a relatively small number of cells entrenched in a matrix of organic and inorganic components. Although bone cells compose only a small amount of the bone volume, they are crucial to its function. Four types of cells are found within the bone tissue— osteoblasts, osteocytes, osteogenic cells, and osteoclasts.
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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.
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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.
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Related Experiment Video

Updated: Mar 5, 2026

A Simple Pit Assay Protocol to Visualize and Quantify Osteoclastic Resorption In Vitro
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Osteoblast-osteoclast interactions.

Xiao Chen1, Zhongqiu Wang1, Na Duan1

  • 1a Department of Radiology , Affiliated Hospital of Nanjing University of Chinese Medicine , Nanjing , China.

Connective Tissue Research
|March 22, 2017
PubMed
Summary

This review summarizes recent findings on how osteoblasts and osteoclasts communicate to maintain bone health. These cells interact through multiple pathways, including direct contact and cytokines. Osteoblasts influence osteoclast activity via pathways like OPG/RANKL/RANK and Ephrin2/ephB4. Conversely, osteoclasts affect osteoblasts through ATPase isoforms and microRNAs. Cytokines like TGF-β and IGF-1 also play a role. The authors suggest that these interactions could be targeted for drug development. The study highlights the complexity of these signaling mechanisms and their potential for therapeutic use.

Keywords:
Bonebone remodelingcommunicationosteoblastosteoclastBone signaling pathwaysOsteoblast functionOsteoclast regulationBone homeostasis mechanisms

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Osteoclast Derivation from Mouse Bone Marrow
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Area of Science:

  • Bone cell biology within regenerative medicine
  • Cell signaling in skeletal physiology
  • Endocrinology of bone metabolism

Background:

Osteoblasts and osteoclasts regulate bone homeostasis through coordinated activity. Prior research has shown that these cells communicate via multiple pathways. However, recent discoveries have not been fully synthesized. This gap motivated a need to update the literature on osteoblast-osteoclast communication. No prior work had resolved the full scope of signaling mechanisms. Established knowledge includes cytokine and matrix interactions. But recent advances in microRNA and ATPase roles remain underexplored. This paper addresses that uncertainty by compiling recent findings. The synthesis aims to clarify how these interactions may be modulated.

Purpose Of The Study:

This review aimed to summarize recent advances in osteoblast-osteoclast communication. The specific problem is the lack of updated literature on this topic. Bone homeostasis depends on these interactions, yet current summaries are outdated. The motivation is to provide a comprehensive overview of new findings. The authors focused on pathways like OPG/RANKL/RANK and ATPase isoforms. They also examined cytokines and extracellular matrix effects. The goal was to highlight mechanisms that could inform drug development. This work addresses a need for updated knowledge in the field.

Main Methods:

The authors conducted a literature review of recent studies on osteoblast-osteoclast interactions. They analyzed published research on cell signaling pathways and cytokine roles. The approach included synthesizing findings from multiple disciplines. They focused on direct cell-cell contact and soluble factors. The study examined both osteoblast and osteoclast signaling mechanisms. They considered pathways such as Ephrin2/ephB4 and Fas/FasL. The authors also evaluated the role of microRNAs and ATPase isoforms. The synthesis was structured to highlight recent discoveries.

Main Results:

Osteoblasts influence osteoclast activity through several pathways, including OPG/RANKL/RANK and Ephrin2/ephB4. Osteoclasts also affect osteoblasts via ATPase isoforms and microRNAs. Cytokines like TGF-β and IGF-1 from resorbed bone matrix play a role. The RANKL/LGR4/RANK pathway is another key mechanism. Complement component 3a and semaphorin 4D are also involved. These findings suggest multiple points of interaction. The study highlights how these interactions may be modulated. The results indicate potential targets for therapeutic development.

Conclusions:

The authors synthesized recent findings on osteoblast-osteoclast communication. They emphasized the importance of multiple signaling pathways. The study suggests that these interactions could be modulated for therapeutic benefit. The authors propose that drugs may be developed by targeting these pathways. They highlight the role of ATPase isoforms and microRNAs. The review also notes the influence of cytokines like TGF-β and IGF-1. The authors suggest that further research is needed to clarify these mechanisms. Their work provides a foundation for future studies in this area.

The OPG/RANKL/RANK, RANKL/LGR4/RANK, Ephrin2/ephB4, and Fas/FasL pathways are key. These pathways regulate osteoblast and osteoclast activity.

Osteoclasts affect osteoblasts via ATPase isoforms like Atp6v0d2 and microRNAs. These mechanisms modulate bone formation.

Cytokines like TGF-β and IGF-1 from resorbed bone matrix influence osteoblast activity. These molecules are released during bone resorption.

The d2 isoform of the vacuolar ATPase V0 domain (Atp6v0d2) influences osteoblast activity. It is a key component in osteoclast-osteoblast signaling.

MicroRNAs regulate gene expression in osteoblasts and osteoclasts. They are part of the signaling mechanisms between these cells.

The authors suggest that drugs could be developed by modulating these interactions. Targeting specific pathways may lead to new therapies.