Evidence map›Paper›PMID 40713617›Full record

ArticleBMC musculoskeletal disorders2025

Reinforcement of osteochondoral defects repair with leukocyte platelet-rich fibrin and bone marrow-derived mononuclear cells in a rabbit model.

Mohamed Salem, Awad Rizk, Esam Mosbah, Adel Zaghloul, Gamal Karrouf

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Article in BMC musculoskeletal disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Mohamed SalemDepartment of Surgery, Anesthesiology, and Radiology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt.
Awad RizkDepartment of Surgery, Anesthesiology, and Radiology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt.
Esam MosbahDepartment of Surgery, Anesthesiology, and Radiology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt.
Adel ZaghloulDepartment of Surgery, Anesthesiology, and Radiology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt.
Gamal KarroufDepartment of Surgery, Anesthesiology, and Radiology, Faculty of Veterinary Medicine, Mansoura University, Mansoura, 35516, Egypt. gamalkarrouf@mans.edu.eg.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe spontaneous healing of the osteochondral defects leads to the formation of fibrous or fibrocartilage tissue that lack normal cartilage characteristics. Therefore, there are different methods were approved for the functional treatment of osteochondral defects including, microfracture osteochondral mosaicoplasty, autologous chondrocyte implantation, platelets-rich plasma (PRP), bone marrow-derived mononuclear cells (BM-MNCs), Mesenchymal stem cells (MSCs) and platelets-rich fibrin (PRF). The present study evaluate the regeneration of osteochondoral defects in rabbits using PRF and BM-MNCs through immunohistochemical (IHC) and gene expression of collagen type II and aggrecan in the regenerated tissue at 3, 6 and 12 weeks postoperative.

methodsA total of 48 adult male New Zealand white rabbits, aged 5-6 months and weighed 3.5 to 4.0 kg, were used in this study and divided into four experimental groups, where all animals received an osteochondral defect of a 4 mm diameter and 5 mm depth was made in the trochlear groove of the left stifle joints. The defects were left for spontaneous repair in group A. They were filled either with 1 cm

resultsGross observation of the defect, based on the degree of defect repair, the integration to border zone and the appearance of the defect area, was significantly higher in group D than other experimental groups (P ≤ 0.05). Microscopical evaluation including surface architecture, tissue morphology, cell distribution and safranin O staining of the matrix was significantly higher in group D than other groups (P ≤ 0.05). IHC staining showed a high concentration of collagen type II in groups B and D respectively; a moderate to high amount in groups and a moderate amount in group A (2.0 ± 0.5). The relative gene expression showed a significant increase of collagen type II and aggrecan in group D compared to other groups at all-time points.

conclusionsThe current study's findings show that when PRF and BMNCs are combined, osteochondral lesions mend more quickly, and the regenerated tissue has stronger collagen type II and proteoglycan deposition than when either substance is utilized alone. To gather proof of the positive benefits of the combination of PRF and BMNCs, more research on clinically afflicted cases is required. Also, Autologous PRF is capable of stimulating BMSC growth and has good biocompatibility and can aid in the restoration of cartilage and subchondral bone.

Indexed as

Bone Marrow TransplantationCartilage, ArticularLeukocytes, MononuclearMesenchymal Stem Cell TransplantationPlatelet-Rich FibrinWound HealingAggrecansAnimalsCollagen Type IIDisease Models, AnimalMaleRabbitsAggrecansCollagen Type IIBM-MNCsImmunohistochemical studyOsteochondral defectPRFRabbitsRelative gene expression

Identifiers

PMID40713617
PMCPMC12297477

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