| First Author | Hentunen TA | Year | 2000 |
| Journal | Bone | Volume | 26 |
| Issue | 2 | Pages | 183-8 |
| PubMed ID | 10678414 | Mgi Jnum | J:105410 |
| Mgi Id | MGI:3614964 | Doi | 10.1016/s8756-3282(99)00247-1 |
| Citation | Hentunen TA, et al. (2000) A murine model of inflammatory bone disease. Bone 26(2):183-8 |
| abstractText | We have recently reported the identification of a new recessive mutation on murine chromosome 18 that results in tail kinks and deformity in the lower extremities of mice. Preliminary examination of the bones of these mice showed that there are abnormalities present that resembled chronic recurrent multifocal osteomyelitis. Accordingly, this new mutation was named "CMO." In this report, we describe the histology of bones in CMO mice, as well as the capacity of the bone marrow cells from these animals to form osteoclasts (OCLs). In addition, we tested conditioned media from non-adherent marrow cells and total marrow cells from CMO mice for their capacity to induce OCL formation in normal murine marrow cultures. These studies demonstrated that the bone disease in these animals is inflammatory in nature, and a soluble factor(s) that is not IL-1alpha, IL-6 or TNF-alpha is released by marrow cells from CMO animals and enhances OCL formation in normal murine marrow cultures. |
