1. Sclerostin antibody enhances implant osseointegration in bone with Col1a1 mutation.
- Author
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Sung HH, Kwon HH, Stephan C, Reynolds SM, Dai Z, Van der Kraan PM, Caird MS, Blaney Davidson EN, and Kozloff KM
- Subjects
- Animals, Mice, X-Ray Microtomography, Bone and Bones diagnostic imaging, Bone and Bones drug effects, Bone and Bones pathology, Intercellular Signaling Peptides and Proteins, Dental Implants, Tibia diagnostic imaging, Tibia pathology, Tibia drug effects, Osseointegration drug effects, Adaptor Proteins, Signal Transducing, Mutation genetics, Collagen Type I genetics, Collagen Type I metabolism, Antibodies pharmacology
- Abstract
We evaluated the potential of sclerostin antibody (SclAb) therapy to enhance osseointegration of dental and orthopaedic implants in a mouse model (Brtl/+) mimicking moderate to severe Osteogenesis Imperfecta (OI). To address the challenges in achieving stable implant integration in compromised bone conditions, our aim was to determine the effectiveness of sclerostin antibody (SclAb) at improving bone-to-implant contact and implant fixation strength. Utilizing a combination of micro-computed tomography, mechanical push-in testing, immunohistochemistry, and Western blot analysis, we observed that SclAb treatment significantly enhances bone volume fraction (BV/TV) and bone-implant contact (BIC) in Brtl/+ mice, suggesting a normalization of bone structure toward WT levels. Despite variations in implant survival rates between the maxilla and tibia, SclAb treatment consistently improved implant stability and resistance to mechanical forces, highlighting its potential to overcome the inherent challenges of OI in dental and orthopaedic implant integration. These results suggest that SclAb could be a valuable therapeutic approach for enhancing implant success in compromised bone conditions., Competing Interests: Declaration of competing interest KMK is a consultant for NextCure, Inc. The remaining authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)
- Published
- 2024
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