ArticleScientific reports2018
A WNT protein therapeutic improves the bone-forming capacity of autografts from aged animals.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The Role of Wnt Signaling in Age-Related Alveolar Bone Loss and Regeneration.Journal of periodontal research · 2026Review
- β-catenin mRNA encapsulated in SM-102 lipid nanoparticles enhances bone formation in a murine tibia fracture repair model.Bioactive materials · 2024Article
- Therapeutic approaches to activate the canonical Wnt pathway for bone regeneration.Journal of tissue engineering and regenerative medicine · 2022Review
- The Role of Wnt Signaling in Postnatal Tooth Root Development.Frontiers in dental medicine · 2021Article
- Bioactivating a bone substitute accelerates graft incorporation in a murine model of vertical ridge augmentation.Dental materials : official publication of the Academy of Dental Materials · 2020Article
- Different effects of Wnt/β-catenin activation and PTH activation in adult and aged male mice metaphyseal fracture healing.BMC musculoskeletal disorders · 2020Article
- Effect of Collagen Cross-Link Deficiency on Incorporation of Grafted Bone.Dentistry journal · 2019Article
- A Novel Osteotomy Preparation Technique to Preserve Implant Site Viability and Enhance Osteogenesis.Journal of clinical medicine · 2019Article
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8 authors.
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Abstract
Autografts tend to be unreliable in older patients. Some of these age-related skeletal changes appear to be attributable to a decline in endogenous WNT signaling. We used a functional in vivo transplantation assay to demonstrate that the bone-forming capacity of an autograft can be traced back to a Wnt-responsive cell population associated with the mineralized bone matrix fraction of a bone graft. Micro-CT imaging, flow cytometry and quantitative analyses demonstrate that this mineralized fraction declines with age, along with a waning in endogenous Wnt signaling; together these factors contribute to the age-related deterioration in autograft efficacy. Using a lipid formulation to stabilize the hydrophobic WNT3A protein, we demonstrate that osteogenic capacity can be restored by incubating the bone graft ex vivo with WNT3A. Compared to control bone grafts, WNT-treated bone grafts give rise to three times more bone. These preclinical results establish a pivotal role for WNT signaling in the age-related decline of autologous bone grafting efficacy, and demonstrate a means to restore that efficacy via local, transient amplification of endogenous Wnt signaling.
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