Background: Injectable Platelet Rich Fibrin (I-PRF) and Advanced-Platelet Rich Fibrin (A-PRF) are autologous materials derived from patients' blood and employed in periodontal regenerative surgery. Although I-PRF and A-PRF have different characteristics, their biological effects on gingival tissue fibroblasts remain unclear. This research aims to compare the in vitro capacity in inducing gene expression and proliferation of human gingival fibroblasts between A-PRF and I-PRF.
Methods: Human donors undergoing dental implant surgery were sampled for normal human gingival fibroblasts (NHGFCs), followed by preparing A-PRF and I-PRF membranes. Enzyme-linked immunosorbent assay (ELISA) kit was used to assess the release of platelet-derived growth factor-AA (PDGF-AA), transforming growth factor-beta1 (TGF- β1), and insulin growth factor-1 (IGF-1) at different periods. Cell viability and proliferation of A-PRF and I-PRF were compared using CCK-8 assay. The impacts of platelet concentration on human gingival fibroblast cells (HGFCs) were evaluated by quantifying the level or amount of phosphorylated extracellular signal-regulated protein kinase (p-ERK), and Matrix metalloproteinases (MMPs), MMP-1 and MMP-3. The effects of PRF on aged human gingival fibroblast cells were examined retrospectively.
Results: Overall, A-PRF demonstrated a higher release of TGF-B1 and PDGF-AA, while I-PRF reflected higher levels of IGF-1. A significantly higher level of cell proliferation was induced by higher cell proliferation by A-PRF and I-PRF. Additionally, in comparison to I-PRF, the expression of ERK phosphorylation and MMP-1 &MMP-3 in HGFCs was demonstrated by I-PRF and A-PRF. The increase in A-PRF was time-dependent (p < 0.05).
Conclusion: Both I-PRF and A-PRF induced a stimulatory biological impact on the proliferation of human gingiva fibroblasts, with the latter demonstrating better capacity in facilitating the release of different growth factors. A-PRF also induced higher gene expression of p-ERK, MMP-1 &MMP-3, and the proliferation of fibroblasts.
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http://dx.doi.org/10.1007/s13770-023-00586-1 | DOI Listing |
Alzheimers Dement
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Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
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View Article and Find Full Text PDFEur J Dent
December 2024
Department of Oral Biology, Faculty of Dentistry, Mahidol University, Bangkok, Thailand.
Objective: Particulate matter 2.5 (PM2.5), an important air pollution particle, has been previously studied for its effects on various normal and cancer tissues.
View Article and Find Full Text PDFJ Indian Prosthodont Soc
January 2025
Department of Microbiology, Faculty of Medicine and Health Sciences, SGT University, Gurugram, Haryana, India.
Aim: The aim of this study was to investigate and compare the antimicrobial effects of an 810-nanometer diode laser, utilizing or not utilizing toluidine blue as a photosensitizer, in the management of peri-implant mucositis.
Settings And Design: The present study was carried out in 30 implant sites in 15 patients with peri-implant mucositis with a specific inclusion and exclusion criteria. 15 sites were treated utilizing a diode laser (control group) and 15 with photodynamic therapy (test group) in a split-mouth format.
J Orthod
January 2025
Department of Oral Biology, Faculty of Dentistry, Suez Canal University, Ismailia, Egypt.
Aim: To compare microleakage beneath ceramic and metal brackets prepared with either acid etching or laser conditioning.
Design: An in vitro study.
Setting: Department of Orthodontics, Faculty of Dentistry, Suez Canal University, Ismailia, Egypt.
Eur Rev Med Pharmacol Sci
December 2024
Department of Oral Biological and Medical Sciences, Faculty of Dentistry, The University of British Columbia, Vancouver, BC, Canada.
Objective: Monoamine oxidase (MAO) inhibitors reduce inflammation in a number of in vitro and in vivo models. This finding led to the development of a novel MAO-B selective inhibitor (RG0216) designed to reduce blood-brain barrier penetration. To elucidate RG0216's regulatory role in inflammation-relevant signaling pathways, we employed a transcriptome analytic approach to identify genes that are differentially regulated by RG0216 and then globally identified which inflammation-relevant biological signaling pathways were altered by this drug.
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