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Hemophilia A and B mice, but not VWF−/−mice, display bone defects in congenital development and remodeling after injury
Open accessAbstract
While joint damage is the primary co-morbidity of hemophilia, osteoporosis and osteopenia are also observed. Coagulation factor VIII deficient (FVIII−/−) mice develop an osteoporotic phenotype in the absence of induced hemarthrosis that is exacerbated two weeks after an induced joint injury. Here we have compared comprehensively the bone health of clotting factor VIII, factor IX, and Von Willebrand Factor knockout (FVIII−/−, FIX−/−, and VWF−/− respectively) mice both in the absence of joint hemorrhage and following induced joint injury. We found FVIII−/− and FIX−/− mice, but not VWF−/− mice, developmentally have an osteoporotic phenotype. Unilateral induced hemarthrosis causes further bone damage in both FVIII−/− and FIX−/− mice, but has little effect on VWF−/− bone health, indicating that the FVIII.VWF complex is not required for normal bone remodeling in vivo. To further investigate the bone healing following hemarthrosis in hemophilia we examined a two week time course using microCT, serum chemistry, and histological analysis. Elevated ratio of osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B ligand (RANKL), increased osterix+ osteoblastic cells, and decreased smoothness of the cortical bone surface were evident within several days of injury, indicative of acute heterotopic mineralization along the cortical surface. This was closely followed by increased interleukin-6 (IL-6) levels, increased osteoclast numbers, and significant trabecular bone loss. Uncoupled and disorganized bone formation and resorption continued for the duration of the study resulting in significant deterioration of the joint. Further elucidation of the shared mechanisms underlying abnormal bone homeostasis in the absence of FVIII or FIX is needed to guide evidence-based approaches to the screening and treatment of the prevalent bone defects in hemophilia A and B.
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Mice and patients with hemophilia due to lack of clotting factor VIII or IX are osteoporotic and osteopenic.
“It is also known that mice (and patients) with hemophilia due to lack of clotting factor VIII or IX are osteoporotic and osteopenic (36, 38).”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [36]
Mice lacking VWF have been reported to have normal bone density.
“Although mice lacking VWF have been reported to have normal bone density (36), transgenic mice expressing a mutant form of the protein corresponding to that seen in patients with platelet-type von Willebrand disease exhibit a high bone mass phenotype (37).”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [36]
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Metadata
- Authors
- Taves, S., Sun, J., Livingston, E. W., Chen, X., Amiaud, J., Brion, R., Hannah, W. B., Bateman, T. A., Heymann, D., & Monahan, P. E.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Inserm (FR)
- Corresponding author
- Heymann, Dominique
- Monahan, Paul E.
- ORCID
- Venue
- Scientific Reports
- Published
- 2019-10-08
- Volume
- 9
- Issue
- 1
- Pages
- 14428-14428
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6783554
- OpenAlex
- W2980314399
- Cited by
- 26
- References
- 52
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 7 · 2020: 7
- FWCI
- 3.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- HAL (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Novo Nordisk
- During the conduct of these studies Sarah Taves was an employee of Novo Nordisk via the STAR Fellowship mechanism.
- Topics
- Health Sciences › Medicine › Hematology › Hemophilia Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Hematology › Platelet Disorders and Treatments
- Keywords
- hemophilia A, hemophilia B, von Willebrand factor, factor VIII, factor IX, hemarthrosis, osteoporosis, bone remodeling, bone defects, osteoclasts, osteoblasts, RANKL/OPG ratio, interleukin-6, trabecular bone loss, bone homeostasis, knockout mice
- MeSH terms
- Sp7 Transcription Factor, Animals, Blood Coagulation Tests, Bone and Bones, Hemophilia B, Factor IX, Factor VIII, Hemophilia A, Humans, Male, Osteoclasts, Osteoporosis, Phenotype, von Willebrand Factor, Interleukin-6, Mice, Knockout, Mice, RANK Ligand
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