Cell Biology in Dentistry: Second Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 October 2024 | Viewed by 1350

Special Issue Editors


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Guest Editor
Department of Pediatric Dentistry, Asahi University School of Dentistry, 1851-1, Hozumi, Mizuho, Gifu 501-0296, Japan
Interests: stem cells; cell therapy; pediatric dentistry
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Guest Editor
Department of Molecular Cell Biology and Oral Anatomy, Kyushu University Graduate School of Dental Science, Fukuoka 812-8582, Japan.
Interests: stem cell; induced pluripotent stem cell (iPS cell); induced tissue specific stem cell (iTS cell); cell culture; dental pulp cells; tissue regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The progress of cell biology in dentistry will greatly improve the level of dental care, based on the current state of accumulated knowledge. Cell-based treatments for some dental tissues will become more predictable along with recent advances in tissue engineering and our understanding of progenitor cell biology, overcoming the limitations of present therapeutic techniques. However, most studies are now focused on the characterization of mesenchymal stem cells, bone regeneration and periodontal regeneration. This Special Issue deals with various fields of oral biology, including dental tissue regeneration, dental tissue engineering, the characterization of dental-related stem cells and dental-related cell culture systems as well as developmental biology and neurobiology in the human oral milieu.

Prof. Dr. Issei Saitoh
Prof. Dr. Takayoshi Yamaza
Guest Editors

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Keywords

  • oral biology
  • tissue regeneration
  • dental tissue engineering
  • dental-related stem cells
  • dental-related cell culture system
  • cell biology in the oral milieu
  • dental pulp cells
  • dental progenitor cells

Published Papers (2 papers)

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Research

12 pages, 3320 KiB  
Article
Platelet-Rich Fibrin Increases CXCL8 Expression in Gingival Fibroblasts
by Atefe Imani, Layla Panahipour, Natalia dos Santos Sanches, Lei Wang and Reinhard Gruber
Biomedicines 2024, 12(6), 1326; https://doi.org/10.3390/biomedicines12061326 - 14 Jun 2024
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Abstract
Platelet-rich fibrin (PRF), the coagulated plasma of fractionated blood, is widely used to support tissue regeneration in dentistry, and the underlying cellular and molecular mechanisms are increasingly being understood. Periodontal connective tissues steadily express CXCL8, a chemokine that attracts granulocytes and lymphocytes, supporting [...] Read more.
Platelet-rich fibrin (PRF), the coagulated plasma of fractionated blood, is widely used to support tissue regeneration in dentistry, and the underlying cellular and molecular mechanisms are increasingly being understood. Periodontal connective tissues steadily express CXCL8, a chemokine that attracts granulocytes and lymphocytes, supporting homeostatic immunity. Even though PRF is considered to dampen inflammation, it should not be ruled out that PRF increases the expression of CXCL8 in gingival fibroblasts. To test this hypothesis, we conducted a bioassay where gingival fibroblasts were exposed to PRF lysates and the respective serum. We show here that PRF lysates and, to a lesser extent, PRF serum increased the expression of CXCL8 by the gingival fibroblasts, as confirmed by immunoassay. SB203580, the inhibitor of p38 mitogen-activated protein kinase, reduced CXCL8 expression. Consistently, PRF lysates and, to a weaker range, the PRF serum also caused phosphorylation of p38 in gingival fibroblasts. Assuming that PRF is a rich source of growth factors, the TGF-β receptor type I kinase inhibitor SB431542 decreased the PRF-induced expression and translation of CXCL8. The findings suggest that PRF lysates and the respective serum drive CXCL8 expression by activating TGF-β and p38 signaling in gingival fibroblasts. Full article
(This article belongs to the Special Issue Cell Biology in Dentistry: Second Edition)
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12 pages, 4036 KiB  
Article
L-PRF Secretome from Both Smokers/Nonsmokers Stimulates Angiogenesis and Osteoblast Differentiation In Vitro
by Susana Ríos, Lina Gabriela González, Claudia Gilda Saez, Patricio Cristian Smith, Lina M. Escobar and Constanza Eugenia Martínez
Biomedicines 2024, 12(4), 874; https://doi.org/10.3390/biomedicines12040874 - 16 Apr 2024
Cited by 1 | Viewed by 729
Abstract
Leukocyte and Platelet-Rich Fibrin (L-PRF) is part of the second generation of platelet-concentrates. L-PRF derived from nonsmokers has been used in surgical procedures, with its beneficial effects in wound healing being proven to stimulate biological activities such as cell proliferation, angiogenesis, and differentiation. [...] Read more.
Leukocyte and Platelet-Rich Fibrin (L-PRF) is part of the second generation of platelet-concentrates. L-PRF derived from nonsmokers has been used in surgical procedures, with its beneficial effects in wound healing being proven to stimulate biological activities such as cell proliferation, angiogenesis, and differentiation. Cigarette smoking exerts detrimental effects on tissue healing and is associated with post-surgical complications; however, evidence about the biological effects of L-PRF derived from smokers is limited. This study evaluated the impact of L-PRF secretome (LPRFS) derived from smokers and nonsmokers on angiogenesis and osteoblast differentiation. LPRFS was obtained by submerging L-PRF membranes derived from smokers or nonsmokers in culture media and was used to treat endothelial cells (HUVEC) or SaOs-2 cells. Angiogenesis was evaluated by tubule formation assay, while osteoblast differentiation was observed by alkaline phosphatase and osterix protein levels, as well as in vitro mineralization. LPRFS treatments increased angiogenesis, alkaline phosphatase, and osterix levels. Treatment with 50% of LPRFS derived from smokers and nonsmokers in the presence of osteogenic factors stimulates in vitro mineralization significantly. Nevertheless, differences between LPRFS derived from smokers and nonsmokers were not found. Both LPRFS stimulated angiogenesis and osteoblast differentiation in vitro; however, clinical studies are required to determine the beneficial effect of LPRFS in smokers. Full article
(This article belongs to the Special Issue Cell Biology in Dentistry: Second Edition)
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