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

在兔模型中,利用富含白细胞和血小板的纤维蛋白和骨髓来源的单核细胞加强骨软骨缺损的修复

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Abstract

BACKGROUND: The 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. METHODS: A 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(3) of PRF in group B, 6000k of BM-MNCs in group C or a combination of 0.8 cm(3) of PRF and BM-MNCs in group D. RESULTS: Gross 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. CONCLUSIONS: The 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.

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