| First Author | Katavić V | Year | 2003 |
| Journal | J Immunol | Volume | 170 |
| Issue | 3 | Pages | 1540-7 |
| PubMed ID | 12538719 | Mgi Jnum | J:126902 |
| Mgi Id | MGI:3762289 | Doi | 10.4049/jimmunol.170.3.1540 |
| Citation | Katavic V, et al. (2003) Increased bone mass is a part of the generalized lymphoproliferative disorder phenotype in the mouse. J Immunol 170(3):1540-7 |
| abstractText | We investigated the bone phenotype of mice with generalized lymphoproliferative disorder (gld) due to a defect in the Fas ligand-mediated apoptotic pathway. C57BL/6-gld mice had greater whole body bone mineral density and greater trabecular bone volume than their wild-type controls. gld mice lost 5-fold less trabecular bone and had less osteoclasts on bone surfaces after ovariectomy-induced bone resorption. They also formed more bone in a model of osteogenic regeneration after bone marrow ablation, had less osteoclasts on bone surfaces and less apoptotic osteoblasts. gld and wild-type mice had similar numbers of osteoclasts in bone marrow cultures, but marrow stromal fibroblasts from gld mice formed more alkaline phosphatase-positive colonies. Bone diaphyseal shafts and bone marrow stromal fibroblasts produced more osteoprotegerin mRNA and protein than wild-type mice. These findings provide evidence that the disturbance of the bone system is a part of generalized lymphoproliferative syndrome and indicates the possible role of osteoprotegerin as a regulatory link between the bone and immune system. |
