Osteoporosis

Osteoporosis is a disease characterized by reduced bone mass and structural deterioration of bone tissue, leading to increased susceptibility to fractures. GemPharmatech's preclinical osteoporosis platform includes estrogen-deficient OVX and humanized RANKL mice that enable rigorous evaluation of antiresorptive and bone-forming therapeutics.

2
Validated Models
50+
Studies Completed

Advantages

Our Advantages

GemPharmatech's core capabilities for preclinical osteoporosis research.

Clinically Relevant Bone-Loss Models

OVX-induced estrogen deficiency in female C57BL/6JGpt mice produces increased body weight, reduced uterine ratio, and trabecular bone loss relevant to postmenopausal osteoporosis.

Quantitative Bone Assessment

Micro-CT provide BMD/BMC and trabecular endpoints including BV/TV, Tb.Th, Tb.N, and Tb.Sp, supported by histology of the femur.

Human Target–Oriented Application

The B6-hRANKL-Tg + OVX platform supports evaluation of human specific biologic therapies

Model Library

Validated models for preclinical osteoporosis bone-loss research .

Case Studies

Case Studies & Validation Data

Explore our studies demonstrating the efficacy of various therapeutic interventions.

OVX-Induced Osteoporosis Mouse Model

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Female C57BL/6JGpt mice were ovariectomized at 8 weeks of age. Ten weeks after surgery, OVX mice showed increased body weight and decreased uterine weight ratio compared with the sham group. Micro-CT analysis of the femur and tibia showed significant reductions in BV/TV, Tb.Th, Tb.N, BMD, and BMC, along with increased Tb.Sp. These results support the establishment of a stable estrogen deficiency-induced bone loss phenotype in this model.

(A) Quantitative analysis of bone volume fraction (BV/TV). (B) Quantitative analysis of trabecular number (Tb.Th). (C) Quantitative analysis of trabecular thickness(Tb.Sp). (D) Quantitative analysis of trabecular separation (Tb.N). (E) Quantitative analysis of bone mineral density (BMD). (F) Quantitative analysis of Bone mineral content (BMC). (G) Representative three-dimensional micro-CT reconstruction images of bone tissues from G1-sham and G2-OVX mice. Compared with the sham group, OVX mice exhibited reduced bone mass, sparse trabecular architecture, impaired trabecular connectivity, and enlarged trabecular spaces, indicating successful induction of osteoporosis-like bone microstructural deterioration after ovariectomy. Data presented as mean ± SEM.

B6-hRANKL-Tg + OVX Osteoporosis Model

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Denosumab treatment increased BV/TV, Tb.N, and BMC and improved Tb.Sp versus model. These data show that the B6-hRANKL-Tg-based osteoporosis platform is responsive to bone-protective intervention and is suitable for evaluation of agents relevant to human RANKL biology.

(A) Quantitative analysis of bone volume fraction (BV/TV). (B) Quantitative analysis of trabecular thickness (Tb.Th). (C) Quantitative analysis of trabecular separation (Tb.Sp). (D) Quantitative analysis of trabecular number (Tb.N). (E) Quantitative analysis of bone mineral density (BMD). (F) Quantitative analysis of Bone mineral content (BMC). Female B6-hRANKL-Tg mice were ovariectomized at 8 weeks of age. After surgery, micro-CT analysis of bone tissues showed that B6-hRANKL-Tg + OVX mice exhibited significant reductions in BV/TV, Tb.N, BMD, and BMC, along with increased Tb.Sp, compared with the control group. These results support the establishment of a stable estrogen deficiency-induced bone loss phenotype in this model. After denosumab intervention, several bone microarchitecture- and bone density-related parameters showed improving trends, suggesting that denosumab may alleviate B6-hRANKL-Tg + OVX-induced bone loss and structural deterioration. Data presented as mean ± SEM.

Models

All Product Lines

Browse our comprehensive catalog of over 30,000 mouse models covering various gene families, signaling pathways, and disease models. Use advanced filters to find the perfect model for your research.