Journal
JOURNAL OF ENDODONTICS
Volume 43, Issue 3, Pages 433-438Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2016.11.002
Keywords
Human dental pulp cells; lipopolysaccharide; odonto-blastic; differentiation; platelet-rich fibrin
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Funding
- Chonnam National Hospital Research Institute of Clinical Medicine [CRI 13004-1]
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [2011-0030121, 2015R1A2A2A01006595]
- National Research Foundation of Korea [2015R1A2A2A01006595] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Introduction: Platelet-rich fibrin (PRF), as an autologous fibrin matrix, is known to contain platelets, leukocytes, and growth factors to control inflammation and to facilitate the healing process. The purpose of this study was to investigate the effects of PRF on odontoblastic differentiation in human dental pulp cells (HDPCs) treated with lipopolysaccharide (LPS). Methods: Gene expression of inflammatory cytokines and adhesion molecules on the HDPCs cultured with or without LPS and PRF extract (PRFe) were evaluated by reverse transcription polymerase chain reaction and Western blot analysis. In addition, odontoblastic differentiation was determined by measuring alkaline phosphatase (ALP) activity using ALP staining, the expression of odontogenesis-related genes, and the extent of mineralization using alizarin red S staining. Results: Treatment with PRFe significantly attenuated the LPS-stimulated expression of interleukin (IL)-1 beta, IL-6, and IL-8 in HDPCs. In addition, PRFe inhibited the up-regulation of vascular cell adhesion molecule 1 and the production of intracellular adhesion molecule 1 in HDPCs exposed to LPS. Expression of dentin sialophosphoprotein and dentin matrix acidic phosphoprotein 1, ALP activity, and mineralization were enhanced by PRFe in LPS-treated HDPCs. Conclusions: These results suggest that PRF has effects associated not only with inhibition of inflammation in HDPCs exposed to LPS but also stimulation of odontoblastic differentiation.
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