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Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts

  • Authors:
    • Ryuta Sumida
    • Toyonobu Maeda
    • Ichiro Kawahara
    • Junko Yusa
    • Yasumasa Kato
  • View Affiliations / Copyright

    Affiliations: Department of Oral and Maxillofacial Surgery, Ohu University School of Dentistry, Koriyama, Fukushima 963‑8611, Japan, Department of Oral Function and Molecular Biology, Ohu University School of Dentistry, Koriyama, Fukushima 963‑8611, Japan, Department of Oral Medical Sciences, Ohu University School of Dentistry, Koriyama, Fukushima 963‑8611, Japan
    Copyright: © Sumida et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 358-365
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    Published online on: May 8, 2019
       https://doi.org/10.3892/etm.2019.7560
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Abstract

Platelet‑rich fibrin (PRF) is a platelet concentrate derived from complete autologous blood rich in growth factors in the fibrin matrix. Although PRF has been used during oral surgery to optimize wound healing in soft and hard tissue, the precise role of PRF in bone healing remains unclear. The present study assessed the role of PRF in bone remodeling. PRF was prepared from whole blood by low speed centrifugation without any anti‑coagulants. Culture of MC3T3‑E1 cells with PRF induced the expression of osteoprotegerin (OPG), but had no effect on the expression of receptor activator of nuclear factor‑κB ligand (RANKL), increasing the OPG/RANKL ratio. Expression of other osteoblastic differentiation makers, including BMP‑2 and ‑4 and RUNX2, was not affected. PRF filling of a hole defect in the mental foramen bone of rats increased OPG positivity and decreased tartrate‑resistant acid phosphatase positivity compared with unfilled control. In conclusion, PRF increased the OPG/RANKL ratio by inducing OPG expression, suggesting that PRF enhances early stage osteogenesis by optimizing osteoblastic differentiation. The present study provides a scientific basis for clinical findings showing that PRF can enhance bone regeneration such as sinus lift.
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Spandidos Publications style
Sumida R, Maeda T, Kawahara I, Yusa J and Kato Y: Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts. Exp Ther Med 18: 358-365, 2019.
APA
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., & Kato, Y. (2019). Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts. Experimental and Therapeutic Medicine, 18, 358-365. https://doi.org/10.3892/etm.2019.7560
MLA
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., Kato, Y."Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts". Experimental and Therapeutic Medicine 18.1 (2019): 358-365.
Chicago
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., Kato, Y."Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts". Experimental and Therapeutic Medicine 18, no. 1 (2019): 358-365. https://doi.org/10.3892/etm.2019.7560
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Spandidos Publications style
Sumida R, Maeda T, Kawahara I, Yusa J and Kato Y: Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts. Exp Ther Med 18: 358-365, 2019.
APA
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., & Kato, Y. (2019). Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts. Experimental and Therapeutic Medicine, 18, 358-365. https://doi.org/10.3892/etm.2019.7560
MLA
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., Kato, Y."Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts". Experimental and Therapeutic Medicine 18.1 (2019): 358-365.
Chicago
Sumida, R., Maeda, T., Kawahara, I., Yusa, J., Kato, Y."Platelet‑rich fibrin increases the osteoprotegerin/receptor activator of nuclear factor‑κB ligand ratio in osteoblasts". Experimental and Therapeutic Medicine 18, no. 1 (2019): 358-365. https://doi.org/10.3892/etm.2019.7560
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