ArticleArthritis research & therapy2022
Senescence-accelerated mice prone 8 (SAMP8) in male as a spontaneous osteoarthritis model.
Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Hysterectomy accelerates sarcopenia risk in US women and mouse models.Frontiers in endocrinology · 2026Article
- Echinacoside Improves Memory Function and Bone Mineral Density in the Aged SAMP8 Mouse Model.Molecular neurobiology · 2025Article
- Osteoarthritis as an evolutionary legacy: Biological ageing and chondrocyte hypertrophy.Osteoarthritis and cartilage open · 2025Review
- Advancing Osteoarthritis Research: Insights from Rodent Models and Emerging Trends.Journal of orthopaedics and sports medicine · 2025Article
- Article
- Feasibility of administration of calcitonin gene-related peptide receptor antagonist on attenuation of pain and progression in osteoarthritis.Scientific reports · 2023Article
- Effects of low-intensity exercise on spontaneously developed knee osteoarthritis in male senescence-accelerated mouse prone 8.Arthritis research & therapy · 2023Article
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16 authors.
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Abstract
backgroundAnimal models of spontaneous osteoarthritis (OA) are sparse and not well characterized. The purpose of the present study is to examine OA-related changes and mechanisms in senescence-accelerated mouse prone 8 (SAMP8) that displays a phenotype of accelerated aging.
methodsKnees of male SAMP8 and SAM-resistant 1 (SAMR1) mice as control from 6 to 33 weeks of age were evaluated by histological grading systems for joint tissues (cartilage, meniscus, synovium, and subchondral bone), and µCT analysis. Gene expression patterns in articular cartilage were analyzed by real-time PCR. Immunohistochemistry was performed for OA-related factors, senescence markers, and apoptosis.
resultsStarting at 14 weeks of age, SAMP8 exhibited mild OA-like changes such as proteoglycan loss and cartilage fibrillation. From 18 to 33 weeks of age, SAMP8 progressed to partial or full-thickness defects with exposure of subchondral bone on the medial tibia and exhibited synovitis. Histological scoring indicated significantly more severe OA in SAMP8 compared with SAMR1 from 14 weeks [median (interquartile range): SAMR1: 0.89 (0.56-1.81) vs SAMP8: 1.78 (1.35-4.62)] to 33 weeks of age [SAMR1: 1.67 (1.61-1.04) vs SAMP8: 13.03 (12.26-13.57)]. Subchondral bone sclerosis in the medial tibia, bone mineral density (BMD) loss of femoral metaphysis, and meniscus degeneration occurred much earlier than the onset of cartilage degeneration in SAMP8 at 14 weeks of age.
conclusionsSAMP8 are a spontaneous OA model that is useful for investigating the pathogenesis of primary OA and evaluating therapeutic interventions.
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