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Updated: Aug 11, 2026
06:17
Osteoclast Derivation from Mouse Bone Marrow
Published on: November 6, 2014
Bone stromal cells in pagetic bone and Paget's sarcoma express RANKL and support human osteoclast formation
1Department of Orthopaedics, Tangdu Hospital, The Fourth Military Medical University, Xian, China.
The Journal of Pathology
|February 17, 2006
Summary
Paget
Area of Science:
- Bone Biology and Disease
- Cell Signaling and Communication
- Oncology and Sarcoma Research
Background:
- Paget's disease is characterized by abnormal bone remodeling and increased osteoclast activity.
- Osteoclast formation is regulated by factors like RANKL and OPG.
- Paget's disease can rarely lead to sarcoma, such as osteosarcoma.
Purpose of the Study:
- To investigate the role of bone stromal cells in Paget's disease and Paget's sarcoma.
- To determine the mechanism by which pagetic bone stromal cells influence osteoclast formation.
- To explore the potential therapeutic target of RANKL/OPG pathway in Paget's disease.
Main Methods:
- Co-culture of monocytes with pagetic bone stromal cells and Paget's sarcoma stromal cells.
- Assessment of osteoclast formation via cell-cell contact and soluble factors.
- Evaluation of the effect of osteoprotegerin (OPG) on osteoclastogenesis.
Main Results:
- Pagetic bone stromal cells express RANKL and promote osteoclast formation via a RANKL-dependent mechanism.
- Osteoclast formation was induced by both contact-dependent and soluble factors released by pagetic stromal cells.
- Stromal cells from morphologically normal bone in a Paget's patient also stimulated osteoclast formation, which was inhibited by OPG.
Conclusions:
- Paget's bone stromal cells actively support osteoclast formation through a RANKL-dependent pathway.
- This process involves both direct cell-cell contact and the secretion of soluble RANKL.
- Targeting the RANKL/OPG pathway may offer a therapeutic strategy for Paget's disease.
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