Osteoporotic Bone Metabolism in Rodent Models
Summary
Osteoporotic bone metabolism in rodent models centres on the disruption of the normal balance between bone resorption and formation. In experimental settings, removal of ovarian hormones through ovariectomy reliably induces an osteoporotic phenotype characterised by trabecular thinning, cortical porosity and declines in bone mineral density. These changes are monitored using imaging modalities such as micro-CT, histomorphometric analysis of bone microarchitecture and biochemical markers of bone turnover in serum and urine. Key cellular processes involve enhanced osteoclastogenesis driving excessive bone resorption, alongside impaired osteoblastogenesis limiting new bone formation. Rodent models have been instrumental in elucidating the molecular pathways influenced by oestrogen deficiency, including alterations in the RANK–RANKL–OPG axis, Wnt signalling and local growth factor responses. This work underpins the preclinical assessment of novel therapeutic strategies, contributes to a deeper understanding of fracture risk and informs translational approaches for human osteoporosis management.
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Osteoporotic Bone Metabolism in Rodent Models publication trend
The graph below shows the total number of articles in osteoporotic bone metabolism in rodent models across all publications each year (not limited to Nature Index journals).
Technical terms
Osteoblastogenesis: differentiation of osteoblasts responsible for new bone formation.
Osteoclastogenesis: generation of osteoclasts which resorb bone tissue.
Trabecular bone: spongy, porous bone found at the ends of long bones and in vertebrae.
Cortical bone: dense outer layer of bone that provides structural strength.
Bone mineral density (BMD): quantitative measure of mineral content in a given volume of bone.
RANKL: cytokine that binds to RANK to stimulate osteoclast differentiation and activity.
Wnt signalling: molecular pathway that regulates osteoblast activity and bone formation.
References
- Recombinant Human Peptide Growth Factors, Bone Morphogenetic Protein-7 (rhBMP7), and Platelet-Derived Growth Factor-BB (rhPDGF-BB) for Osteoporosis Treatment in an Oophorectomized Rat Model. Biomolecules (2024).
- ZEB1 regulates bone metabolism in osteoporotic rats through inducing POLDIP2 transcription. Journal of Orthopaedic Surgery and Research (2022).
- The crucial role of beta-catenin in the osteoprotective effect of semaglutide in an ovariectomized rat model of osteoporosis. Naunyn-Schmiedeberg's Archives of Pharmacology (2024).
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