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Updated: Jun 16, 2026

Practical Considerations for the Design, Execution, and Interpretation of Studies Involving Whole-Bone Bending Tests of Rodent Bones
Published on: September 1, 2023
Characterization of mandibular bone in a mouse model of chronic kidney disease
Melissa M Lee1, Emily Y Chu, Mohga M El-Abbadi
1Department of Periodontics, University of Washington School of Dentistry, Seattle, WA 98195-6365, USA.
Background:
Chronic kidney disease (CKD) is a worldwide health problem with increasing prevalence and poor outcomes, including severe cardiovascular disease and renal osteodystrophy. With advances in medical treatment, patients with CKD are living longer and require oral care. The aim of this study is to determine the effects of CKD and dietary phosphate on mandibular bone structure using a uremic mouse model.
Methods:
Uremia (U) was induced in female dilute brown agouti/2 mice by partial renal ablation. Uremic mice received a normal-phosphate (NP) or a high-phosphate (HP) diet. sham surgeries were performed in a control group of mice; half received an NP diet, and the other half was fed an HP diet. At termination, animals were sacrificed, and mandibles were collected for microcomputed tomography (micro-CT) and histologic analysis.
Results:
Sera levels of blood urea nitrogen, parathyroid hormone, and alkaline phosphatase were significantly increased in U/NP and U/HP mice versus sham controls, whereas serum calcium was increased in the U/HP group, and no differences were noted in serum phosphate levels among groups. Micro-CT analyses revealed a significant reduction in cortical bone thickness and an increase in trabecular thickness and trabecular bone volume/tissue volume in U/NP and U/HP groups compared to the sham/NP group. A significant reduction in cortical bone thickness was also found in the sham/HP group versus the sham/NP group. Histologic evaluation confirmed increased trabeculation in the U groups.
Conclusion:
CKD in mice, especially under conditions of HP feeding, results in marked effects on alveolar bone homeostasis.

