Rodent Osteoporosis (OP) Models

Osteoporosis (OP) is a systemic skeletal disorder characterized by decreased bone mass, microarchitectural deterioration, and increased fracture risk. Glucocorticoid-induced osteoporosis is the most common form of secondary OP, resulting from long-term glucocorticoid therapy. HKeyBio offers two well-validated rodent osteoporosis models induced by dexamethasone (Dex), a potent glucocorticoid: SD rat model and C57BL/6 mouse model. Dexamethasone inhibits bone formation and enhances bone resorption, leading to cortical and trabecular bone loss. These models recapitulate key human OP features including body weight changes, elevated serum alkaline phosphatase (ALP), reduced bone mineral density, and histopathological alterations. They provide robust platforms for preclinical efficacy testing of novel anti-osteoporotic agents such as bisphosphonates, SERMs, and anabolic therapies.

Quantity:
Availability:





Inquire Add to Basket

Product Description

Key Features & Benefits

Clinically relevant – Recapitulates human glucocorticoid-induced osteoporosis with suppressed bone formation, enhanced resorption, and microarchitectural deterioration.

Multiple species – Rat and mouse models available to suit different experimental needs (larger size vs. genetic manipulation).

Comprehensive endpoints – Body weight, serum ALP, X-ray imaging, histopathology (H&E, TRAP staining), bone histomorphometry, micro-CT (optional).

Translational value – Ideal for testing bisphosphonates (alendronate), SERMs (raloxifene), anabolic agents (teriparatide), and RANKL inhibitors.

IND-ready data packages – Studies can be conducted in accordance with GLP principles.

Technical Data & Validation

Dex Induced C57BL/6 Osteoporosis Model

64ced60a61166799157f1c5fe01bc08f

Dex Induced SD Osteoporosis Model

7bbb6f12961910a6627747bd33bb3682

Applications

• Efficacy testing of anti-osteoporotic agents: bisphosphonates (alendronate, zoledronic acid), SERMs (raloxifene), anabolic agents (teriparatide, romosozumab), and RANKL inhibitors (denosumab)

• Evaluation of novel therapies targeting bone formation or resorption pathways

• Target validation for glucocorticoid-induced osteoporosis mechanisms

• Biomarker discovery (bone turnover markers, ALP, osteocalcin, CTX-I)

• IND-enabling pharmacology and toxicology studies

Model Specifications

Parameter	SD Rat OP Model	C57BL/6 Mouse OP Model
Species/Strain	Sprague-Dawley rat	C57BL/6 mouse
Induction method	Dexamethasone (1–2.5 mg/kg) administered intramuscularly or subcutaneously, 2–3 times/week for 4–8 weeks
Study duration	4–10 weeks (induction + treatment phase)
Key endpoints	Body weight, serum ALP, X-ray imaging, histopathology (H&E, TRAP), bone histomorphometry, micro-CT (optional)	Body weight, serum ALP, histopathology, micro-CT (optional)
Positive control	Alendronate or teriparatide available as reference compounds
Data package	Raw data, analysis reports, X-ray images, histology slides, micro-CT data (optional), bioinformatics (optional)

❓ Frequently Asked Questions

Q1: What osteoporosis model do you provide?

A1: We offer dexamethasone (Dex)-induced osteoporosis models using SD rats and C57BL/6 mice for preclinical research on secondary osteoporosis.

Q2: What is the modeling mechanism?

A2: Dexamethasone, a glucocorticoid, inhibits bone formation and disrupts bone metabolism. It reduces bone mass and damages bone microarchitecture, perfectly simulating glucocorticoid-induced secondary osteoporosis in humans.

Q3: What evaluation indicators are applied?

A3: We monitor body weight, detect serum ALP levels, and perform X-ray imaging and H&E staining to assess bone structure and pathological changes.

Q4: What is the modeling operation?

A4: Dexamethasone is administrated twice per week starting from Day 0. All detections and observations are carried out after the model is fully established.

Q5: What are the advantages and applications?

A5: This model features stable bone loss phenotypes and high reproducibility. It is widely used for efficacy screening and mechanism research of anti-osteoporosis and bone-protective drugs.