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Osteoporosis animal model

Osteoporosis animal model

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Osteoporosis
Bone-related disease model

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Experimental results

Experimental results

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Osteoporosis

Introduction to Osteoporosis Animal Models

Osteoporosis animal models are essential research tools that mimic key pathological features, including reduced bone mass, disrupted bone microarchitecture, and diminished bone strength, and are widely used to investigate the mechanisms of bone metabolism and to evaluate anti‑osteoporotic therapeutics. Depending on the underlying etiological factors, these models can be classified into postmenopausal osteoporosis models (ovariectomy‑induced OVX models), age‑related osteoporosis models, glucocorticoid‑induced models, unloading‑induced models, and nutrition‑deficiency models. Among them, the OVX rat model is the most extensively employed classic model, as it effectively replicates the increased bone resorption and loss of bone mass associated with estrogen deficiency. Glucocorticoid‑induced models are well suited for studying secondary osteoporosis, whereas aging‑related models more closely resemble the natural aging process. Comprehensive assessments—based on parameters such as bone mineral density (BMD), bone histomorphometry, bone biomechanics, and bone metabolic markers—enable a thorough characterization of the onset and progression of osteoporosis.

Service Advantages of the Aniphe BioLablogical Osteoporosis Animal Model Platform

Ailinfei’s osteoporosis animal models offer a variety of well-established modeling protocols, accompanied by comprehensive bone‑related assays, providing end-to-end support for preclinical efficacy evaluation of anti‑osteoporotic drugs.

Comprehensive model coverage

Complete range of model types

We offer various osteoporosis models, including ovariectomized (OVX) models, hormone‑induced models, and low‑calcium diet‑induced models.

Standardization of the modeling process

Model establishment is stable and uniform.

Standardized surgical and administration protocols were employed, resulting in minimal intergroup differences in bone mineral density and bone microstructural parameters, with excellent experimental reproducibility.

Multidimensional Evaluation System

Complete bone-related testing suite

CT, bone biochemistry, bone histopathology, and mechanical strength testing can be performed concurrently, with complete data delivered directly.

Adapted for multi-cycle studies

Supports personalized customization

The modeling duration and dosing schedule are adjustable, making it suitable for combination therapies and studies involving complex bone injuries.

Adapted for multi-cycle studies

Quality control standards have been refined.

Bone density was assessed by sampling in each batch to validate the modeling efficacy; the raw data are complete and meet the requirements for drug registration.

Adapted for multi-cycle studies

One-stop, hassle-free delivery

We provide end-to-end services spanning model establishment, animal housing, regular blood sampling, and terminal tissue collection and analysis, thereby shortening your R&D timeline.

Modeling cycle

12 weeks

1  Laboratory animals

C57 female mice

1  Positive drug

Commonly used agents such as sodium alendronate and estradiol benzoate can increase bone mineral density and improve trabecular bone architecture, serving as experimental controls.

1  Application areas

It is primarily used in research on bone metabolism mechanisms, screening for anti‑osteoporotic drugs and natural products, evaluating biologics and bone‑repair materials, and conducting basic and translational studies on postmenopausal, age‑related, and secondary osteoporosis and other related conditions.

Experimental results

Construction of an osteoporosis animal model

01 Ovariectomy (OVX) model

Bilateral ovariectomy is performed in female rats or mice to induce estrogen deficiency, leading to increased bone resorption, reduced bone mass, and disruption of bone microarchitecture. A stable osteoporotic phenotype develops 4 to 12 weeks post‑operation. This model effectively mimics postmenopausal osteoporosis and is the most widely used system for evaluating therapeutic efficacy and investigating pathogenic mechanisms.

02 Glucocorticoid-Induced Model

By repeatedly administering glucocorticoids such as dexamethasone and prednisolone, osteoblast activity is suppressed and bone resorption is promoted, leading to a decrease in bone mineral density and reduced bone strength. The modeling period typically ranges from 4 to 12 weeks. This model is primarily used to simulate secondary osteoporosis resulting from long-term clinical glucocorticoid therapy.

03 OPG-KO mouse model

By employing gene knockout technology to delete the OPG gene, the RANKL/RANK signaling pathway is activated, promoting osteoclast differentiation and bone resorption, resulting in pronounced bone mass loss and trabecular destruction in mice even during early postnatal development. This model exhibits a stable phenotype and high genetic consistency, making it well suited for studies of bone metabolism mechanisms and the development of targeted therapeutics.

Micro-CT examination

This figure presents the quantitative analysis results of bone microarchitecture obtained by micro-CT. The results show:

Trabecular bone volume fraction (Tb.BV/TV): The value in the model group was significantly lower than that in the control group, indicating a reduced proportion of trabecular bone and marked bone loss.

Trabecular separation (Tb.Sp): The value in the model group was significantly higher than that in the control group, indicating increased trabecular spacing and a more porous bone architecture.

Together, these two indicators confirm that the bone microarchitecture of the mice has deteriorated following model induction, thereby validating the successful establishment of an osteoporosis model.

 

 

Comparative treatment data for sodium alendronate, raloxifene, and 17β-estradiol

HE staining results showed that in the Sham OVX sham‑surgery group (a), the trabeculae were densely and neatly arranged, with narrow intertrabecular spaces and normal microarchitectural integrity; whereas in the untreated OVX model group (b), the trabeculae were sparse, with a marked increase in fractures, markedly enlarged medullary cavities, and typical signs of bone microstructural disruption characteristic of postmenopausal osteoporosis.

Both the two alendronate sodium dose groups (c and d) and the two raloxifene dose groups (e and f) improved bone damage: trabecular bone density increased, trabecular gaps decreased, medullary spaces narrowed, and the bone architecture was restored. Moreover, the higher the drug dose, the more pronounced the restoration of bone microarchitecture, thereby confirming that these two positive‑control drugs can ameliorate ovariectomy‑induced trabecular bone loss in the femur.

 

References: Effects of genistein aglycone in osteoporotic,ovariectomized rats: a comparison with

alendronate, raloxifene and oestradiol.