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Increased Bone Mass Is a Part of the Generalized Lymphoproliferative Disorder Phenotype in the Mouse ^1,2

Vedran Katavi^*, Ivan Kreimir Luki^*, Nataa Kovai^*, Danka Grevi, Joseph A. Lorenzo and Ana Marui^3,*

^* Croatian Institute for Brain Research and Department of Anatomy, Department of Physiology and Immunology, Zagreb University School of Medicine, Zagreb, Croatia; Division of Endocrinology and Metabolism, Department of Medicine, University of Connecticut Health Center, Farmington, CT 06030

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.

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The JI 2003 170: 1129-1130. [Full Text]  

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