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Platelet‐rich fibrin suppresses in vitro osteoclastogenesis

BACKGROUND: Platelet‐rich fibrin (PRF) membranes can preserve alveolar ridge dimension after tooth extraction. Thus, it can be presumed that PRF suppresses the catabolic events that are caused by osteoclastic bone resorption. METHODS: To address this possibility, we investigated the impact of solubl...

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Autores principales: Kargarpour, Zahra, Nasirzade, Jila, Strauss, Franz Josef, Di Summa, Francesca, Hasannia, Sadegh, Müller, Heinz‐Dieter, Gruber, Reinhard
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7155126/
https://www.ncbi.nlm.nih.gov/pubmed/31381154
http://dx.doi.org/10.1002/JPER.19-0109
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author Kargarpour, Zahra
Nasirzade, Jila
Strauss, Franz Josef
Di Summa, Francesca
Hasannia, Sadegh
Müller, Heinz‐Dieter
Gruber, Reinhard
author_facet Kargarpour, Zahra
Nasirzade, Jila
Strauss, Franz Josef
Di Summa, Francesca
Hasannia, Sadegh
Müller, Heinz‐Dieter
Gruber, Reinhard
author_sort Kargarpour, Zahra
collection PubMed
description BACKGROUND: Platelet‐rich fibrin (PRF) membranes can preserve alveolar ridge dimension after tooth extraction. Thus, it can be presumed that PRF suppresses the catabolic events that are caused by osteoclastic bone resorption. METHODS: To address this possibility, we investigated the impact of soluble extracts of PRF membranes on in vitro osteoclastogenesis in murine bone marrow cultures. Osteoclastogenesis was induced by exposing murine bone marrow cultures to receptor activator of nuclear factor kappa B ligand (RANKL), macrophage colony‐stimulating factor (M‐CSF) and transforming growth factor‐beta 1 (TGF‐β1) in the presence or absence of PRF. Osteoclastogenesis was evaluated based on histochemical, gene expression, and resorption analysis. Viability was confirmed by formation of formazan crystals, live‐dead staining and caspase‐3 activity assay. RESULTS: We report here that in vitro osteoclastogenesis is greatly suppressed by soluble extracts of PRF membranes as indicated by tartrate‐resistant acid phosphatase (TRAP) staining and pit formation. In support of the histochemical observations, soluble extracts of PRF membranes decreased expression levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell‐specific transmembrane protein (DCSTAMP), nuclear factor of activated T‐cells (NFATc1), and osteoclast‐associated receptor (OSCAR). PRF membranes, however, cannot reverse the process once osteoclastogenesis has evolved. CONCLUSION: These in vitro findings indicate that PRF membranes can inhibit the formation of osteoclasts from hematopoietic progenitors in bone marrow cultures. Overall, our results imply that the favorable effects of PRF membranes in alveolar ridge preservation may be attributed, at least in part, by the inhibition of osteoclastogenesis.
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spelling pubmed-71551262020-04-15 Platelet‐rich fibrin suppresses in vitro osteoclastogenesis Kargarpour, Zahra Nasirzade, Jila Strauss, Franz Josef Di Summa, Francesca Hasannia, Sadegh Müller, Heinz‐Dieter Gruber, Reinhard J Periodontol Translational Periodontology BACKGROUND: Platelet‐rich fibrin (PRF) membranes can preserve alveolar ridge dimension after tooth extraction. Thus, it can be presumed that PRF suppresses the catabolic events that are caused by osteoclastic bone resorption. METHODS: To address this possibility, we investigated the impact of soluble extracts of PRF membranes on in vitro osteoclastogenesis in murine bone marrow cultures. Osteoclastogenesis was induced by exposing murine bone marrow cultures to receptor activator of nuclear factor kappa B ligand (RANKL), macrophage colony‐stimulating factor (M‐CSF) and transforming growth factor‐beta 1 (TGF‐β1) in the presence or absence of PRF. Osteoclastogenesis was evaluated based on histochemical, gene expression, and resorption analysis. Viability was confirmed by formation of formazan crystals, live‐dead staining and caspase‐3 activity assay. RESULTS: We report here that in vitro osteoclastogenesis is greatly suppressed by soluble extracts of PRF membranes as indicated by tartrate‐resistant acid phosphatase (TRAP) staining and pit formation. In support of the histochemical observations, soluble extracts of PRF membranes decreased expression levels of the osteoclast marker genes TRAP, Cathepsin K, dendritic cell‐specific transmembrane protein (DCSTAMP), nuclear factor of activated T‐cells (NFATc1), and osteoclast‐associated receptor (OSCAR). PRF membranes, however, cannot reverse the process once osteoclastogenesis has evolved. CONCLUSION: These in vitro findings indicate that PRF membranes can inhibit the formation of osteoclasts from hematopoietic progenitors in bone marrow cultures. Overall, our results imply that the favorable effects of PRF membranes in alveolar ridge preservation may be attributed, at least in part, by the inhibition of osteoclastogenesis. John Wiley and Sons Inc. 2019-09-17 2020-03 /pmc/articles/PMC7155126/ /pubmed/31381154 http://dx.doi.org/10.1002/JPER.19-0109 Text en © 2019 The Authors. Journal of Periodontology published by Wiley Periodicals, Inc. on behalf of American Academy of Periodontology This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Translational Periodontology
Kargarpour, Zahra
Nasirzade, Jila
Strauss, Franz Josef
Di Summa, Francesca
Hasannia, Sadegh
Müller, Heinz‐Dieter
Gruber, Reinhard
Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title_full Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title_fullStr Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title_full_unstemmed Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title_short Platelet‐rich fibrin suppresses in vitro osteoclastogenesis
title_sort platelet‐rich fibrin suppresses in vitro osteoclastogenesis
topic Translational Periodontology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7155126/
https://www.ncbi.nlm.nih.gov/pubmed/31381154
http://dx.doi.org/10.1002/JPER.19-0109
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