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Updated: Jun 15, 2026
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Trabecular Bone Microarchitecture Evaluation in an Osteoporosis Mouse Model
Published on: September 8, 2023
Increased trabecular bone formation in mice lacking the growth factor midkine.
Claudia Neunaber1, Philip Catala-Lehnen, F Timo Beil
1Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Summary
Midkine (Mdk) deficiency in mice leads to increased bone formation and density, suggesting Mdk antagonists could treat osteoporosis.
Area of Science:
- Cell Biology
- Bone Biology
- Endocrinology
Background:
- Midkine (Mdk) and pleiotrophin (Ptn) are heparin-binding growth factors primarily known for neuronal effects.
- Previous studies on Ptn-deficient mice did not reveal skeletal abnormalities.
- Mdk expression increases during osteoblast differentiation, suggesting a role in bone formation.
Purpose of the Study:
- To investigate the role of Midkine (Mdk) in bone formation and remodeling.
- To determine the skeletal phenotype of Mdk-deficient mice.
- To explore the molecular mechanisms underlying Mdk's effect on bone.
Main Methods:
- Analysis of Mdk-deficient mice at 12 and 18 months of age.
- Histomorphometric quantification of trabecular and cortical bone.
- Genome-wide expression analysis of primary osteoblasts.
- Ovariectomy in Mdk-deficient and wild-type mice.
Main Results:
- Mdk-deficient mice exhibited increased trabecular bone volume and cortical porosity.
- Bone formation rate was elevated in Mdk-deficient mice, with differential effects on bone resorption.
- Genome-wide analysis identified Ank and Enpp1 as Mdk-induced genes.
- Mdk-deficient mice showed resistance to bone loss after ovariectomy.
Conclusions:
- Mdk deficiency results in increased trabecular bone formation in mice.
- Mdk plays a significant role in regulating bone remodeling.
- Mdk-specific antagonists may offer a therapeutic strategy for osteoporosis.
