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Related Concept Videos

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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...
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Related Experiment Video

Updated: Jul 10, 2026

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

Published on: March 15, 2018

Activated platelets positively regulate RANKL-mediated osteoclast differentiation.

Barbara Weicht1, Philipp Maitz, Barbara Kandler

  • 1Department of Oral Surgery, Medical University Vienna, Vienna, Austria.

Journal of Cellular Biochemistry
|October 25, 2007
PubMed
Summary

Activated platelets enhance osteoclastogenesis, the formation of bone-resorbing osteoclasts, through platelet releasates (PRS). These PRS activate key signaling pathways, promoting bone cell differentiation.

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Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

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Published on: February 28, 2017

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Last Updated: Jul 10, 2026

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

Published on: March 15, 2018

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

Area of Science:

  • Hematology
  • Immunology
  • Cell Biology

Background:

  • Platelets are known to influence bone marrow cultures containing stromal cells.
  • The direct role of activated platelets in promoting osteoclast differentiation from hematopoietic cells is not fully understood.

Purpose of the Study:

  • To investigate whether platelet releasates (PRS) directly promote osteoclastogenesis in hematopoietic cells.
  • To elucidate the underlying molecular mechanisms involved in PRS-mediated osteoclast formation.

Main Methods:

  • Utilized stroma-depleted, M-CSF-dependent bone marrow cells cultured with RANKL and PRS.
  • Assessed osteoclastogenesis by counting tartrate-resistant acid phosphatase-positive multinucleated cells (MNCs) and measuring osteoclast-specific gene expression.
  • Investigated the role of transforming growth factor-beta (TGF-beta) and downstream signaling pathways (Smad-2, p38, JNK).

Main Results:

  • PRS significantly increased osteoclastogenesis and osteoclast-specific gene expression.
  • Osteoclastogenesis was observed even in B-cell and T-cell depleted hematopoietic cells.
  • Neutralization of TGF-beta in PRS reduced osteoclastogenic capacity.
  • PRS induced phosphorylation of Smad-2, p38, and JNK; blocking p38, but not JNK, suppressed osteoclastogenesis.

Conclusions:

  • Activated platelets directly enhance osteoclastogenesis via PRS.
  • TGF-beta within PRS and activation of the p38 signaling pathway are crucial for this effect.
  • Platelets represent a significant modulator of osteoclast differentiation and bone remodeling.