Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction
Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate wh...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Nokhbehsaim, Marjan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2010 |
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| Anmerkung: |
© Urban & Vogel, Muenchen 2010 |
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| Übergeordnetes Werk: |
Enthalten in: Journal of orofacial orthopedics - München : Urban & Vogel, 1931, 71(2010), 6 vom: Nov., Seite 390-402 |
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| Übergeordnetes Werk: |
volume:71 ; year:2010 ; number:6 ; month:11 ; pages:390-402 |
| Links: |
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| DOI / URN: |
10.1007/s00056-010-1031-7 |
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SPR000445207 |
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| 100 | 1 | |a Nokhbehsaim, Marjan |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction |
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| 520 | |a Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. | ||
| 700 | 1 | |a Deschner, Birgit |4 aut | |
| 700 | 1 | |a Winter, Jochen |4 aut | |
| 700 | 1 | |a Reimann, Susanne |4 aut | |
| 700 | 1 | |a Bourauel, Christoph |4 aut | |
| 700 | 1 | |a Jepsen, Søren |4 aut | |
| 700 | 1 | |a Jäger, Andreas |4 aut | |
| 700 | 1 | |a Deschner, James |4 aut | |
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10.1007/s00056-010-1031-7 doi (DE-627)SPR000445207 (SPR)s00056-010-1031-7-e DE-627 ger DE-627 rakwb eng Nokhbehsaim, Marjan verfasserin aut Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Urban & Vogel, Muenchen 2010 Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. Deschner, Birgit aut Winter, Jochen aut Reimann, Susanne aut Bourauel, Christoph aut Jepsen, Søren aut Jäger, Andreas aut Deschner, James aut Enthalten in Journal of orofacial orthopedics München : Urban & Vogel, 1931 71(2010), 6 vom: Nov., Seite 390-402 (DE-627)320627837 (DE-600)2023540-9 1615-6714 nnns volume:71 year:2010 number:6 month:11 pages:390-402 https://dx.doi.org/10.1007/s00056-010-1031-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2010 6 11 390-402 |
| spelling |
10.1007/s00056-010-1031-7 doi (DE-627)SPR000445207 (SPR)s00056-010-1031-7-e DE-627 ger DE-627 rakwb eng Nokhbehsaim, Marjan verfasserin aut Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Urban & Vogel, Muenchen 2010 Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. Deschner, Birgit aut Winter, Jochen aut Reimann, Susanne aut Bourauel, Christoph aut Jepsen, Søren aut Jäger, Andreas aut Deschner, James aut Enthalten in Journal of orofacial orthopedics München : Urban & Vogel, 1931 71(2010), 6 vom: Nov., Seite 390-402 (DE-627)320627837 (DE-600)2023540-9 1615-6714 nnns volume:71 year:2010 number:6 month:11 pages:390-402 https://dx.doi.org/10.1007/s00056-010-1031-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2010 6 11 390-402 |
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10.1007/s00056-010-1031-7 doi (DE-627)SPR000445207 (SPR)s00056-010-1031-7-e DE-627 ger DE-627 rakwb eng Nokhbehsaim, Marjan verfasserin aut Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Urban & Vogel, Muenchen 2010 Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. Deschner, Birgit aut Winter, Jochen aut Reimann, Susanne aut Bourauel, Christoph aut Jepsen, Søren aut Jäger, Andreas aut Deschner, James aut Enthalten in Journal of orofacial orthopedics München : Urban & Vogel, 1931 71(2010), 6 vom: Nov., Seite 390-402 (DE-627)320627837 (DE-600)2023540-9 1615-6714 nnns volume:71 year:2010 number:6 month:11 pages:390-402 https://dx.doi.org/10.1007/s00056-010-1031-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2010 6 11 390-402 |
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10.1007/s00056-010-1031-7 doi (DE-627)SPR000445207 (SPR)s00056-010-1031-7-e DE-627 ger DE-627 rakwb eng Nokhbehsaim, Marjan verfasserin aut Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Urban & Vogel, Muenchen 2010 Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. Deschner, Birgit aut Winter, Jochen aut Reimann, Susanne aut Bourauel, Christoph aut Jepsen, Søren aut Jäger, Andreas aut Deschner, James aut Enthalten in Journal of orofacial orthopedics München : Urban & Vogel, 1931 71(2010), 6 vom: Nov., Seite 390-402 (DE-627)320627837 (DE-600)2023540-9 1615-6714 nnns volume:71 year:2010 number:6 month:11 pages:390-402 https://dx.doi.org/10.1007/s00056-010-1031-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2010 6 11 390-402 |
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10.1007/s00056-010-1031-7 doi (DE-627)SPR000445207 (SPR)s00056-010-1031-7-e DE-627 ger DE-627 rakwb eng Nokhbehsaim, Marjan verfasserin aut Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Urban & Vogel, Muenchen 2010 Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. Deschner, Birgit aut Winter, Jochen aut Reimann, Susanne aut Bourauel, Christoph aut Jepsen, Søren aut Jäger, Andreas aut Deschner, James aut Enthalten in Journal of orofacial orthopedics München : Urban & Vogel, 1931 71(2010), 6 vom: Nov., Seite 390-402 (DE-627)320627837 (DE-600)2023540-9 1615-6714 nnns volume:71 year:2010 number:6 month:11 pages:390-402 https://dx.doi.org/10.1007/s00056-010-1031-7 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4277 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 71 2010 6 11 390-402 |
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Nokhbehsaim, Marjan @@aut@@ Deschner, Birgit @@aut@@ Winter, Jochen @@aut@@ Reimann, Susanne @@aut@@ Bourauel, Christoph @@aut@@ Jepsen, Søren @@aut@@ Jäger, Andreas @@aut@@ Deschner, James @@aut@@ |
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This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. 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Nokhbehsaim, Marjan |
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Nokhbehsaim, Marjan Deschner, Birgit Winter, Jochen Reimann, Susanne Bourauel, Christoph Jepsen, Søren Jäger, Andreas Deschner, James |
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contribution of orthodontic load to inflammationmediated periodontal destruction |
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Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction |
| abstract |
Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. © Urban & Vogel, Muenchen 2010 |
| abstractGer |
Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. © Urban & Vogel, Muenchen 2010 |
| abstract_unstemmed |
Aim: Orthodontic malpractice as well as hyperocclusal forces can aggravate periodontitis-induced destruction of tooth-supporting tissues, but the underlying mechanisms for the co-destructive effect of biomechanical loading are yet to be elucidated. This in-vitro study was performed to investigate whether biomechanical forces modulate the response of periodontal ligament (PDL) cells to inflammation. Materials and Methods: PDL cells (from six donors) grown on $ BioFlex^{®} $ plates were treated with interleukin (IL) 1, which is increased at inflamed periodontal sites, and/or subjected to cyclic tensile strain (CTS) of low (3%) and high (20%) magnitudes for 1β and 6 d. The synthesis of proinflammatory mediators (IL1β, IL8, COX2), growth factors (IGF1, VEGF, TGFβ1), collagen type 1 (COL1) and osteogenic proteins (ALP, RUNX2) was analyzed by real-time PCR and ELISA. The wound fill rate was examined in an in-vitro wound healing assay. For statistical analyses, Student’s t-test and ANOVA were applied (p<0.05). Results: In general, the IL1β-induced expression of proinflammatory mediators was significantly enhanced by CTS on day 1 and significantly downregulated on day 6. CTS of high magnitude significantly inhibited the IGF1 synthesis but significantly upregulated VEGF under normal and inflammatory conditions. In general, CTS also downregulated the IL1β-induced COL1, ALP, and RUNX2 expression. From day 5 on, the lowest wound fill rate was observed in cells which were simultaneously exposed to inflammatory and biomechanical signals. Conclusion: These findings suggest that orthodontic and occlusal loading may contribute to periodontal destruction in periodontally-diseased patients through downregulation of matrix and osteogenic proteins but not via augmentation of periodontal inflammation. © Urban & Vogel, Muenchen 2010 |
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Contribution of Orthodontic Load to Inflammationmediated Periodontal Destruction |
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Deschner, Birgit Winter, Jochen Reimann, Susanne Bourauel, Christoph Jepsen, Søren Jäger, Andreas Deschner, James |
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Deschner, Birgit Winter, Jochen Reimann, Susanne Bourauel, Christoph Jepsen, Søren Jäger, Andreas Deschner, James |
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10.1007/s00056-010-1031-7 |
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| score |
7.3984175 |