Effects of ethanol on human periodontal ligament fibroblasts subjected to static compressive force

Consumption of toxic substances such as alcohol is widespread in the general population and thus also in patients receiving orthodontic treatment. Since human periodontal ligament (hPDL) fibroblasts play a key role in orthodontic tooth movement (OTM) by expressing cytokines and chemokines, we wanted...

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Veröffentlicht in:Alcohol (Fayetteville, N.Y.) N.Y.), 2019-06, Vol.77, p.59-70
Hauptverfasser: Schröder, Agnes, Küchler, Erika Calvano, Omori, Marjorie, Spanier, Gerrit, Proff, Peter, Kirschneck, Christian
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container_start_page 59
container_title Alcohol (Fayetteville, N.Y.)
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creator Schröder, Agnes
Küchler, Erika Calvano
Omori, Marjorie
Spanier, Gerrit
Proff, Peter
Kirschneck, Christian
description Consumption of toxic substances such as alcohol is widespread in the general population and thus also in patients receiving orthodontic treatment. Since human periodontal ligament (hPDL) fibroblasts play a key role in orthodontic tooth movement (OTM) by expressing cytokines and chemokines, we wanted to clarify whether ethanol modulates the physiological activity and expression pattern of hPDL fibroblasts during static compressive force application. We pre-incubated hPDL fibroblasts for 24 h with different ethanol concentrations, corresponding to casual (0.041% blood alcohol concentration [BAC], % by volume) and excessive (0.179%) alcohol consumption. At each ethanol concentration, we incubated the cells for another 48 h with and without an additional physiological compressive force of 2 g/cm2 occurring during orthodontic tooth movement in compression areas of the periodontal ligament. Thereafter, we analyzed expression and secretion of genes and proteins involved in OTM regulation by RT-qPCR and ELISA. We also performed co-culture experiments to observe hPDL-fibroblast-mediated osteoclastogenesis. We observed no effects of ethanol on cytotoxicity or cell viability of hPDL fibroblasts in the applied concentrations. Ethanol showed an enhancing effect on angiogenesis and activity of alkaline phosphatase. Simultaneously, ethanol reduced the induction of IL-6 and increased prostaglandin E2 synthesis as well as hPDL-fibroblast-mediated osteoclastogenesis without affecting the RANK-L/OPG-system. hPDL fibroblasts thus seem to be a cell type quite resistant to ethanol, as no cytotoxic effects or influence on cell viability were detected. High ethanol concentrations, however, seem to promote bone formation and angiogenesis. Ethanol at 0.179% also enhanced hPDL-induced osteoclastogenesis, indicating increased bone resorption and thus tooth movement velocity to be expected during orthodontic therapy. •hPDL fibroblasts play a key mediating role in orthodontic tooth movement.•0.041% and 0.179% of ethanol did not affect hPDL fibroblast viability or vitality.•Ethanol may increase alveolar angiogenesis, bone formation, and collagen synthesis.•Ethanol increased hPDL-fibroblast-mediated osteoclastogenesis.•Ethanol may increase tooth movement and bone loss during orthodontic treatment.
doi_str_mv 10.1016/j.alcohol.2018.10.004
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Since human periodontal ligament (hPDL) fibroblasts play a key role in orthodontic tooth movement (OTM) by expressing cytokines and chemokines, we wanted to clarify whether ethanol modulates the physiological activity and expression pattern of hPDL fibroblasts during static compressive force application. We pre-incubated hPDL fibroblasts for 24 h with different ethanol concentrations, corresponding to casual (0.041% blood alcohol concentration [BAC], % by volume) and excessive (0.179%) alcohol consumption. At each ethanol concentration, we incubated the cells for another 48 h with and without an additional physiological compressive force of 2 g/cm2 occurring during orthodontic tooth movement in compression areas of the periodontal ligament. Thereafter, we analyzed expression and secretion of genes and proteins involved in OTM regulation by RT-qPCR and ELISA. We also performed co-culture experiments to observe hPDL-fibroblast-mediated osteoclastogenesis. We observed no effects of ethanol on cytotoxicity or cell viability of hPDL fibroblasts in the applied concentrations. Ethanol showed an enhancing effect on angiogenesis and activity of alkaline phosphatase. Simultaneously, ethanol reduced the induction of IL-6 and increased prostaglandin E2 synthesis as well as hPDL-fibroblast-mediated osteoclastogenesis without affecting the RANK-L/OPG-system. hPDL fibroblasts thus seem to be a cell type quite resistant to ethanol, as no cytotoxic effects or influence on cell viability were detected. High ethanol concentrations, however, seem to promote bone formation and angiogenesis. 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Since human periodontal ligament (hPDL) fibroblasts play a key role in orthodontic tooth movement (OTM) by expressing cytokines and chemokines, we wanted to clarify whether ethanol modulates the physiological activity and expression pattern of hPDL fibroblasts during static compressive force application. We pre-incubated hPDL fibroblasts for 24 h with different ethanol concentrations, corresponding to casual (0.041% blood alcohol concentration [BAC], % by volume) and excessive (0.179%) alcohol consumption. At each ethanol concentration, we incubated the cells for another 48 h with and without an additional physiological compressive force of 2 g/cm2 occurring during orthodontic tooth movement in compression areas of the periodontal ligament. Thereafter, we analyzed expression and secretion of genes and proteins involved in OTM regulation by RT-qPCR and ELISA. We also performed co-culture experiments to observe hPDL-fibroblast-mediated osteoclastogenesis. We observed no effects of ethanol on cytotoxicity or cell viability of hPDL fibroblasts in the applied concentrations. Ethanol showed an enhancing effect on angiogenesis and activity of alkaline phosphatase. Simultaneously, ethanol reduced the induction of IL-6 and increased prostaglandin E2 synthesis as well as hPDL-fibroblast-mediated osteoclastogenesis without affecting the RANK-L/OPG-system. hPDL fibroblasts thus seem to be a cell type quite resistant to ethanol, as no cytotoxic effects or influence on cell viability were detected. High ethanol concentrations, however, seem to promote bone formation and angiogenesis. Ethanol at 0.179% also enhanced hPDL-induced osteoclastogenesis, indicating increased bone resorption and thus tooth movement velocity to be expected during orthodontic therapy. •hPDL fibroblasts play a key mediating role in orthodontic tooth movement.•0.041% and 0.179% of ethanol did not affect hPDL fibroblast viability or vitality.•Ethanol may increase alveolar angiogenesis, bone formation, and collagen synthesis.•Ethanol increased hPDL-fibroblast-mediated osteoclastogenesis.•Ethanol may increase tooth movement and bone loss during orthodontic treatment.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>30336201</pmid><doi>10.1016/j.alcohol.2018.10.004</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-9473-8724</orcidid></addata></record>
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source Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE; ProQuest Central UK/Ireland
subjects Adolescent
Adult
Alcohol
Alcohol use
Alcoholic beverages
Alkaline phosphatase
Angiogenesis
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Blood levels
Bone growth
Bone resorption
Cell culture
Cell viability
Cells, Cultured
Chemokines
Compression
Compressive force
Compressive Strength - drug effects
Compressive Strength - physiology
Cytokines
Cytotoxicity
Enzyme-linked immunosorbent assay
Ethanol
Ethanol - administration & dosage
Ethics
Female
Fibroblasts
Fibroblasts - drug effects
Fibroblasts - physiology
Genes
Humans
Interleukin 6
Ligaments
Male
Orthodontics
Osteoclastogenesis
Osteogenesis
Osteoprotegerin
PDL
Periodontal ligament
Periodontal Ligament - cytology
Periodontal Ligament - drug effects
Periodontal Ligament - physiology
Periodontal ligament fibroblast
Physiology
Prostaglandin E2
Teeth
Toxic substances
TRANCE protein
Tumor necrosis factor-TNF
Young Adult
title Effects of ethanol on human periodontal ligament fibroblasts subjected to static compressive force
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