ArticleCalcified tissue international2021
Deletion of Coagulation Factor IX Compromises Bone Mass and Strength: Murine Model of Hemophilia B (Christmas Disease).
Article in Calcified tissue international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Bone mineral density, bone remodeling biomarkers, and hemostatic correlates in hemophilia and von Willebrand disease.Blood advances · 2026Article
- Early Biological Orchestration in Fracture Healing: Decoding the Crosstalk between Inflammation, Coagulation, and Metabolism.Stem cell reviews and reports · 2026Review
- Effects ofThe British journal of nutrition · 2025Article
- The influence of severity of hemophilia on bone mineral density and fracture risk.Research and practice in thrombosis and haemostasis · 2024Article
- Assessment of jaw bone mineral density, resorption rates, and oral health in patients with severe hemophilia: a case-control study.Acta odontologica Scandinavica · 2024Article
- Managing Relevant Clinical Conditions of Hemophilia A/B Patients.Hematology reports · 2023Article
- Pathogenesis and treatment of osteoporosis in patients with hemophilia.Archives of osteoporosis · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopenia and osteoporosis have increasingly become a recognized morbidity in those persons with hemophilia (PwH) receiving inadequate prophylactic clotting factor replacement. Animal models can control or eliminate genetic and environmental factors and allow for invasive testing not clinically permissible. Here, we describe the skeletal phenotype of juvenile and adult male mice with a genetically engineered deficiency in coagulation factor IX (FIX KO). Although the somatic growth of FIX KO mice matched that of their wild-type (WT) littermates at 10 and 20 weeks of age, the FIX KO mice displayed reduced bone mineral density (BMD), reduced cortical and cancellous bone mass, and diminished whole bone fracture resistance. These findings coupled with parallel observations in a murine model of hemophilia A (FVIII deficiency) point to an effector downstream of the coagulation cascade that is necessary for normal skeletal development. Further study of potential mechanisms underlying the bone disease observed in rare clotting factor deficiency syndromes may lead to new diagnostic and therapeutic insights for metabolic bone diseases in general.
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Registered trials
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