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Osteoarthritis (OA) animal model

Osteoarthritis (OA) animal model

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Osteoarthritis
Psychiatric & neurological disease models

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Model Introduction

Model Introduction

Platform Service Advantages

Platform Service Advantages

Model Construction

Model Construction

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Osteoarthritis

Introduction to the OA Animal Model

Osteoarthritis (OA) is a common chronic degenerative joint disease among middle-aged and older adults, characterized primarily by articular cartilage degeneration, subchondral bone remodeling, synovial inflammation, and joint dysfunction. Its pathogenesis is complex, and early diagnosis and therapeutic strategies remain in need of further investigation. Rat models of osteoarthritis, by mimicking the processes of articular cartilage injury and degenerative changes, can reproduce hallmark pathological features such as cartilage wear, extracellular matrix degradation, osteophyte formation, and inflammatory responses, thereby effectively reflecting the onset and progression of OA.

Aniphe BioLab’s OA Animal Model Platform Service Advantages

Leveraging a well-established osteoarthritis disease‑model platform and a standardized experimental system, Aniphe BioLab offers high‑quality, one‑stop animal model research services for osteoarthritis (OA).

Comprehensive model coverage

The modeling methods are diverse.

Supports multiple OA modeling approaches, including surgical induction, chemical induction, and combined induction.
Standardization of the modeling process

The model is stable and reliable.

Standardized modeling procedures ensure high consistency in joint pathology and excellent data reproducibility.
Multidimensional Evaluation System

Multidimensional pharmacological evaluation

We offer a range of assays and analyses, including micro-CT, histopathology, behavioral assessments, inflammatory cytokine profiling, and cartilage scoring.
Adaptable to multi-cycle studies

Supports customized research

The modeling cycle, administration route, and observation endpoints can be tailored to meet specific research requirements.
Adaptable to multi-cycle studies

Standardized Quality Management

Comprehensive quality control throughout the entire process ensures that experimental data are authentic, complete, and traceable.
Adaptable to multi-cycle studies

One-stop experimental services

It covers the entire workflow, from animal husbandry and model development to pharmacological intervention, sample analysis, and data interpretation.
Modeling cycle

1–4 weeks

1  Laboratory animals

Mice and rats of SPF grade

1  Positive drug

Commonly used positive‑control drugs include celecoxib, glucosamine, sodium hyaluronate, and diacerein, which can reduce joint inflammation, relieve pain, protect articular cartilage, and slow cartilage degeneration; they are frequently employed in model validation and pharmacological efficacy assessment.

1  Application areas

It is primarily used for research on the pathogenesis of osteoarthritis, screening of anti-inflammatory and analgesic agents as well as chondroprotective drugs, and conducting preclinical in vivo efficacy evaluations and mechanistic studies of biologics, cell therapies, tissue-engineered materials, and regenerative medicine products.

Construction of an OA animal model

Under anesthesia, the knee joint is exposed, the anterior and posterior cruciate ligaments are transected, and the medial meniscus is excised, thereby compromising joint stability and increasing mechanical stress on the articular cartilage. This progressively induces pathological changes, including cartilage degeneration, subchondral bone remodeling, and synovial inflammation, ultimately establishing a stable osteoarthritis model. This approach effectively mimics the onset and progression of post-traumatic OA, with well-defined pathological features and excellent reproducibility, making it widely used in studies of osteoarthritis pathogenesis and in the evaluation of drug efficacy.

Model characteristics: Disruption of joint stability is a commonly used method for inducing osteoarthritis (OA) in animal models; it produces distinct pathological changes and is of great significance for studying chondrocyte apoptosis in OA.

 

Celecoxib treatment data

In the control group, joint architecture was normal, with no abnormal changes observed. In the OA group, as the modeling period progressed, severe joint erythema and edema developed, accompanied by decreased appetite, weight loss, and mild alopecia. Compared with the OA group, the celecoxib‑treated group exhibited a marked attenuation of joint inflammatory responses.

 

 

In the pathological state of osteoarthritis, NF-κB protein expression is upregulated, leading to activation of this inflammatory signaling pathway. The classic positive agent celecoxib can reduce NF-κB protein levels, thereby suppressing downstream inflammatory responses; this constitutes one of the molecular mechanisms underlying celecoxib’s therapeutic effects in osteoarthritis.

 

 

Osteoarthritis can promote NF-κB gene transcription and increase the mRNA expression level of this gene; the positive drug celecoxib can downregulate NF‑κB mRNA levels, thereby inhibiting the activation of the NF‑κB inflammatory pathway at the transcriptional level. This further elucidates the molecular mechanism by which celecoxib alleviates osteoarthritis‑related inflammation, and the trends observed at the transcriptional level are consistent with previous experimental findings on protein expression.

 

 

References: The effect of celecoxib on NF-κB expression in articular cartilage of a rat model of osteoarthritis.