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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...
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Related Experiment Video

Updated: May 13, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Dynamic visualization of RANKL and Th17-mediated osteoclast function.

Junichi Kikuta1, Yoh Wada, Toshiyuki Kowada

  • 1Laboratory of Cellular Dynamics, WPI–Immunology Frontier Research Center, Osaka University, Osaka, Japan.

The Journal of Clinical Investigation
|January 17, 2013
PubMed
Summary

Mature osteoclasts switch between static, bone-resorbing (R) and moving, non-resorbing (N) states. The osteoclast-activating factor RANKL and Th17 cells rapidly convert N osteoclasts to R, impacting bone destruction.

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Area of Science:

  • Cell Biology
  • Immunology
  • Bone Biology

Background:

  • Osteoclasts are crucial for bone resorption, originating from hematopoietic precursors.
  • In vivo control mechanisms governing mature osteoclast function remain incompletely understood.
  • Previous research identified molecular signals but lacked in situ functional insights.

Purpose of the Study:

  • To visualize and characterize mature osteoclast behavior and function in living mouse bone tissue.
  • To investigate the dynamic regulation of osteoclast resorptive activity in vivo.
  • To elucidate the role of RANKL and Th17 cells in modulating osteoclast function.

Main Methods:

  • Intravital multiphoton microscopy of fluorescently labeled mature osteoclasts in intact mouse bone.
  • Observation of osteoclast motility and function under varying pathophysiological conditions.
  • Experimental manipulation using RANKL and Th17 cells to assess osteoclast conversion.

Main Results:

  • Mature osteoclasts exhibit distinct motility patterns, categorized as static-resorptive (R) or moving-nonresorptive (N).
  • The ratio of R to N osteoclasts fluctuates with bone's pathophysiological state.
  • RANKL and Th17 cell-cell contact rapidly induce N-to-R conversion of osteoclasts.

Conclusions:

  • Osteoclast function is dynamically regulated in vivo, with distinct mobile and static phenotypes.
  • RANKL acts as a rapid modulator of mature osteoclast resorptive capacity.
  • RANKL-expressing Th17 cells directly induce osteoclast activation, contributing to inflammatory bone destruction.