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A murine model of inflammatory bone disease
T A Hentunen1, S J Choi, B F Boyce
1Department of Medicine/Hematology, University of Texas Health Science Center, San Antonio, USA.
Bone
|March 25, 2000
Summary
A new mouse mutation, chronic recurrent multifocal osteomyelitis (CMO), causes bone deformities. Marrow cells from CMO mice release a factor that enhances osteoclast formation, indicating an inflammatory bone disease.
Area of Science:
- Genetics
- Immunology
- Skeletal Biology
Background:
- A novel recessive mutation on mouse chromosome 18 causes tail kinks and limb deformities.
- Preliminary bone examination revealed abnormalities resembling chronic recurrent multifocal osteomyelitis (CMO).
Purpose of the Study:
- To investigate the bone histology in CMO mice.
- To assess the osteoclast (OCL) formation capacity of bone marrow cells from CMO mice.
- To identify soluble factors from CMO marrow cells that influence OCL formation.
Main Methods:
- Histological analysis of bones from CMO mice.
- In vitro culture of bone marrow cells to assess osteoclastogenesis.
- Testing conditioned media from CMO marrow cells for osteoclast-inducing activity in normal murine marrow cultures.
Main Results:
- CMO mouse bone histology shows inflammatory bone disease.
- Marrow cells from CMO mice exhibit enhanced osteoclast formation capacity.
- Conditioned media from CMO marrow cells contain soluble factor(s) that promote osteoclastogenesis in normal marrow cultures.
Conclusions:
- The bone disease in CMO mice is inflammatory.
- A novel soluble factor, distinct from IL-1α, IL-6, or TNF-α, is released by CMO marrow cells.
- This factor contributes to enhanced osteoclast formation, driving the observed bone pathology.