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Functionalized Scaffold and Barrier Membrane with Anti-BMP-2 Monoclonal Antibodies for Alveolar Ridge Preservation in a Canine Model

ABSTRACT: Introduction The aim of this study was to investigate the ability of anti-bone morphogenetic protein 2 monoclonal antibody (anti-BMP-2 mAb) to functionalize scaffolds to mediate bone regeneration in a canine model. Materials and Methods The mandibular right premolar 4 (PM4) was extracted in eight beagle dogs and grafted with anti-BMP-2 mAb+anorganic bovine bone mineral with 10% collagen (ABBM-C) and porcine bilayer native collagen membrane (CM). The ABBM-C and CM were functionalized with either anti-BMP-2 mAb (test group) or an isotype matched control mAb (control group). Animals were euthanized at 12 weeks for radiographic, histologic, and histomorphometric analyses. Outcomes were compared between groups. Results 3D imaging using cone beam computed tomography (CBCT) revealed that sites treated with ABBM-C and CM functionalized with anti-BMP-2 mAb exhibited significantly more remaining bone width near the alveolar crest, as well as buccal bone height, compared with control groups. Histologic and histomorphometric analyses demonstrated that in anti-BMP-2 mAb-treated sites, total tissue volume was significantly higher in the coronal part of the alveolar bone crest compared with control sites. In anti-BMP-2 mAb-treated sites, bone formation was observed under the barrier membrane. Conclusion Functionalization of the ABBM-C scaffold and CM appeared to have led to bone formation within healing alveolar bone sockets.

SUBMITTER: Min S

PROVIDER: S-EPMC7530509 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Project description:Tooth extraction results in alveolar bone resorption and is accompanied by postoperative swelling and pain. Maresin 1 (MaR1) is a proresolving lipid mediator produced by macrophages during the resolution phase of inflammation, bridging healing and tissue regeneration. The aim of this study was to examine the effects of MaR1 on tooth extraction socket wound healing in a preclinical rat model. The maxillary right first molars of Sprague-Dawley rats were extracted, and gelatin scaffolds were placed into the sockets with or without MaR1. Topical application was also given twice a week until complete socket wound closure up to 14 d. Immediate postoperative pain was assessed by 3 scores. Histology and microcomputed tomography were used to assess socket bone fill and alveolar ridge dimensional changes at selected dates. The assessments of coded specimens were performed by masked, calibrated examiners. Local application of MaR1 potently accelerated extraction socket healing. Macroscopic and histologic analysis revealed a reduced soft tissue wound opening and more rapid re-epithelialization with MaR1 delivery versus vehicle on socket healing. Under micro-computed tomography analysis, MaR1 (especially at 0.05 μg/μL) stimulated greater socket bone fill at day 10 as compared with the vehicle-treated animals, resulting in less buccal plate resorption and a wider alveolar ridge by day 21. Interestingly, an increased ratio of CD206+:CD68+ macrophages was identified in the sockets with MaR1 application under immunohistochemistry and immunofluorescence analysis. As compared with the vehicle therapy, local delivery of MaR1 reduced immediate postoperative surrogate pain score panels. In summary, MaR1 accelerated extraction wound healing, promoted socket bone fill, preserved alveolar ridge bone, and reduced postoperative pain in vivo with a rodent preclinical model. Local administration of MaR1 offers clinical potential to accelerate extraction socket wound healing for more predictable dental implant reconstruction.

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Functionalized Scaffold and Barrier Membrane with Anti-BMP-2 Monoclonal Antibodies for Alveolar Ridge Preservation in a Canine Model

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