ArticleArthritis research & therapy2020
Ectopic bone formation and systemic bone loss in a transmembrane TNF-driven model of human spondyloarthritis.
Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 21 citations in OpenAlex.
- Differences in lumbar spine bone mineral density measured by quantitative computed tomography and dual-energy X-ray absorptiometry: an age- and sex-specific analysis.Journal of orthopaedic surgery and research · 2026Article
- Recent Advances in the Immunopathology of Axial Spondyloarthritis: with and without HLA-B27.Current rheumatology reports · 2025Review
- Year in Review: Novel Insights in the Pathogenesis of Spondyloarthritis - SPARTAN 2024 Annual Meeting Proceedings.Current rheumatology reports · 2024Review
- Article
- HIF-1α and MIF enhance neutrophil-driven type 3 immunity and chondrogenesis in a murine spondyloarthritis model.Cellular & molecular immunology · 2024Article
- Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023Review
- How Has Molecular Biology Enhanced Our Undertaking of axSpA and Its Management.Current rheumatology reports · 2023Review
- Deep Insight into the Role of MIF in Spondyloarthritis.Current rheumatology reports · 2022Review
- Effects of targeted therapies on bone in rheumatic and musculoskeletal diseases.Nature reviews. Rheumatology · 2022Review
- Quantitative in vivo micro-computed tomography for monitoring disease activity and treatment response in a collagen-induced arthritis mouse model.Scientific reports · 2022Article
- Dual Blockade of TNF and IL-17A Inhibits Inflammation and Structural Damage in a Rat Model of Spondyloarthritis.International journal of molecular sciences · 2022Article
- Lessons on SpA pathogenesis from animal models.Seminars in immunopathology · 2021Review
- Juvenile Spondyloarthritis: What More Do We Know About HLA-B27, Enthesitis, and New Bone Formation?Frontiers in medicine · 2021Review
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14 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe transmembrane-TNF transgenic mouse, TgA86, has been shown to develop spontaneously peripheral arthritis with signs of axial involvement. To assess similarity to human spondyloarthritis, we performed detailed characterization of the axial, peripheral, and comorbid pathologies of this model.
methodsTgA86 bone pathologies were assessed at different ages using CT imaging of the spine, tail vertebrae, and hind limbs and characterized in detail by histopathological and immunohistochemical analysis. Cardiac function was examined by echocardiography and electrocardiography and bone structural parameters by μCT analysis. The response of TgA86 mice to either early or late anti-TNF treatment was evaluated clinically, histopathologically, and by μCT analysis.
resultsTgA86 mice developed with 100% penetrance spontaneous axial and peripheral pathology which progressed with time and manifested as reduced body weight and body length, kyphosis, tail bendings, as well as swollen and distorted hind joints. Whole-body CT analysis at advanced ages revealed bone erosions of sacral and caudal vertebrae as well as of sacroiliac joints and hind limbs and, also, new ectopic bone formation and eventually vertebral fusion. The pathology of these mice highly resembled that of SpA patients, as it evolved through an early inflammatory phase, evident as enthesitis and synovitis in the affected joints, characterized by mesenchymal cell accumulation, and neutrophilic infiltration. Subsequently, regression of inflammation was accompanied by ectopic bone formation, leading to ankylosis. In addition, both systemic bone loss and comorbid heart valve pathology were evident. Importantly, early anti-TNF treatment, similar to clinical treatment protocols, significantly reduced the inflammatory phase of both the axial and peripheral pathology of TgA86 mice.
conclusionsThe TgA86 mice develop a spontaneous peripheral and axial biphasic pathology accompanied by comorbid heart valvular dysfunction and osteoporosis, overall reproducing the progression of pathognomonic features of human spondyloarthritis. Therefore, the TgA86 mouse represents a valuable model for deciphering the role of transmembrane TNF in the pathogenic mechanisms of spondyloarthritis and for assessing the efficacy of human therapeutics targeting different phases of the disease.
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