AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , , , , , , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Repositório Institucional da UNESP |
Texto Completo: | http://dx.doi.org/10.1002/JPER.19-0064 http://hdl.handle.net/11449/201122 |
Resumo: | Background: The initiation and progression of periodontitis might involve a local renin-angiotensin system in periodontal tissue. This study hypothesized that Losartan treatment could promote protection to rats submitted to experimental periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cytokines, better reactive oxidant species regulation and maintenance of the balance between bone formation and resorption factors. Methods: One hundred and thirty rats were submitted to EP with a silk suture thread (4.0) placed around the lower right first molar for 1, 3, 7, and 14 consecutive days. The study comprised four groups: G1—control without EP; G2—animals with EP treated with water; G3—Losartan-treated animals (treatment started at the same day of EP induction), and G4—animals previously treated with Losartan for 30 days followed by induction of EP and continuity of treatment. Results: G2 rats had greater bone loss volume, increased number, and thickness and decreased separation of trabeculae. On the other hand, G4 animals showed significant improvements in these parameters. Histological analysis revealed that EP favors inflammatory cell infiltration and junctional epithelium, cementum with alveolar bone crest destruction, but animals pretreated with Losartan (G4) did not show these features. Although the G3 animals did not demonstrate the improvements detected in G4, mRNA expression results were similar. In mandibular tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as decreases for antioxidant enzymes. However, Losartan treatments attenuated these responses in addition to promoting an increase in bone formation markers and transcription factors. Conclusion: AT1 receptor modulates EP progression. |
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AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markersanti-inflammatory agentsantioxidant(s)bone biologyconnective tissue biologycytokine(s)experimental periodontitisgene expressionBackground: The initiation and progression of periodontitis might involve a local renin-angiotensin system in periodontal tissue. This study hypothesized that Losartan treatment could promote protection to rats submitted to experimental periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cytokines, better reactive oxidant species regulation and maintenance of the balance between bone formation and resorption factors. Methods: One hundred and thirty rats were submitted to EP with a silk suture thread (4.0) placed around the lower right first molar for 1, 3, 7, and 14 consecutive days. The study comprised four groups: G1—control without EP; G2—animals with EP treated with water; G3—Losartan-treated animals (treatment started at the same day of EP induction), and G4—animals previously treated with Losartan for 30 days followed by induction of EP and continuity of treatment. Results: G2 rats had greater bone loss volume, increased number, and thickness and decreased separation of trabeculae. On the other hand, G4 animals showed significant improvements in these parameters. Histological analysis revealed that EP favors inflammatory cell infiltration and junctional epithelium, cementum with alveolar bone crest destruction, but animals pretreated with Losartan (G4) did not show these features. Although the G3 animals did not demonstrate the improvements detected in G4, mRNA expression results were similar. In mandibular tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as decreases for antioxidant enzymes. However, Losartan treatments attenuated these responses in addition to promoting an increase in bone formation markers and transcription factors. Conclusion: AT1 receptor modulates EP progression.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Department of Biological Sciences Bauru School of Dentistry University of São PauloDepartment of Basic Sciences School of Dentistry São Paulo State University-UNESPDepartment of Biomedical Engineering Medical College of WisconsinDepartment of Basic Sciences School of Dentistry São Paulo State University-UNESPFAPESP: 2015/03965-2Universidade de São Paulo (USP)Universidade Estadual Paulista (Unesp)Medical College of WisconsinDionísio, Thiago J.Souza, Gabriela P.Colombini-Ishikiriama, Bella L.Garbieri, Thais F.Parisi, Viviane A.Oliveira, Gabriela M.Cano, Isadora P.Rodini, Camila O.Oliveira, Sandra H. P. [UNESP]Greene, Andrew S.Santos, Carlos F.2020-12-12T02:24:36Z2020-12-12T02:24:36Z2020-04-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/article533-544http://dx.doi.org/10.1002/JPER.19-0064Journal of Periodontology, v. 91, n. 4, p. 533-544, 2020.0022-3492http://hdl.handle.net/11449/20112210.1002/JPER.19-00642-s2.0-85084167889Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengJournal of Periodontologyinfo:eu-repo/semantics/openAccess2024-04-23T15:23:40Zoai:repositorio.unesp.br:11449/201122Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestopendoar:29462024-08-05T20:17:52.207630Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
title |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
spellingShingle |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers Dionísio, Thiago J. anti-inflammatory agents antioxidant(s) bone biology connective tissue biology cytokine(s) experimental periodontitis gene expression |
title_short |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
title_full |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
title_fullStr |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
title_full_unstemmed |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
title_sort |
AT1 receptor antagonism promotes bone loss attenuation in experimental periodontitis, blocks inflammatory mediators, and upregulates antioxidant enzymes and bone formation markers |
author |
Dionísio, Thiago J. |
author_facet |
Dionísio, Thiago J. Souza, Gabriela P. Colombini-Ishikiriama, Bella L. Garbieri, Thais F. Parisi, Viviane A. Oliveira, Gabriela M. Cano, Isadora P. Rodini, Camila O. Oliveira, Sandra H. P. [UNESP] Greene, Andrew S. Santos, Carlos F. |
author_role |
author |
author2 |
Souza, Gabriela P. Colombini-Ishikiriama, Bella L. Garbieri, Thais F. Parisi, Viviane A. Oliveira, Gabriela M. Cano, Isadora P. Rodini, Camila O. Oliveira, Sandra H. P. [UNESP] Greene, Andrew S. Santos, Carlos F. |
author2_role |
author author author author author author author author author author |
dc.contributor.none.fl_str_mv |
Universidade de São Paulo (USP) Universidade Estadual Paulista (Unesp) Medical College of Wisconsin |
dc.contributor.author.fl_str_mv |
Dionísio, Thiago J. Souza, Gabriela P. Colombini-Ishikiriama, Bella L. Garbieri, Thais F. Parisi, Viviane A. Oliveira, Gabriela M. Cano, Isadora P. Rodini, Camila O. Oliveira, Sandra H. P. [UNESP] Greene, Andrew S. Santos, Carlos F. |
dc.subject.por.fl_str_mv |
anti-inflammatory agents antioxidant(s) bone biology connective tissue biology cytokine(s) experimental periodontitis gene expression |
topic |
anti-inflammatory agents antioxidant(s) bone biology connective tissue biology cytokine(s) experimental periodontitis gene expression |
description |
Background: The initiation and progression of periodontitis might involve a local renin-angiotensin system in periodontal tissue. This study hypothesized that Losartan treatment could promote protection to rats submitted to experimental periodontitis (EP) by attenuating alveolar bone loss due to reduction in inflammatory cytokines, better reactive oxidant species regulation and maintenance of the balance between bone formation and resorption factors. Methods: One hundred and thirty rats were submitted to EP with a silk suture thread (4.0) placed around the lower right first molar for 1, 3, 7, and 14 consecutive days. The study comprised four groups: G1—control without EP; G2—animals with EP treated with water; G3—Losartan-treated animals (treatment started at the same day of EP induction), and G4—animals previously treated with Losartan for 30 days followed by induction of EP and continuity of treatment. Results: G2 rats had greater bone loss volume, increased number, and thickness and decreased separation of trabeculae. On the other hand, G4 animals showed significant improvements in these parameters. Histological analysis revealed that EP favors inflammatory cell infiltration and junctional epithelium, cementum with alveolar bone crest destruction, but animals pretreated with Losartan (G4) did not show these features. Although the G3 animals did not demonstrate the improvements detected in G4, mRNA expression results were similar. In mandibular tissue, EP promoted mRNA increases for ACE, AT1 receptor, and inflammatory mediators as well as decreases for antioxidant enzymes. However, Losartan treatments attenuated these responses in addition to promoting an increase in bone formation markers and transcription factors. Conclusion: AT1 receptor modulates EP progression. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-12-12T02:24:36Z 2020-12-12T02:24:36Z 2020-04-01 |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://dx.doi.org/10.1002/JPER.19-0064 Journal of Periodontology, v. 91, n. 4, p. 533-544, 2020. 0022-3492 http://hdl.handle.net/11449/201122 10.1002/JPER.19-0064 2-s2.0-85084167889 |
url |
http://dx.doi.org/10.1002/JPER.19-0064 http://hdl.handle.net/11449/201122 |
identifier_str_mv |
Journal of Periodontology, v. 91, n. 4, p. 533-544, 2020. 0022-3492 10.1002/JPER.19-0064 2-s2.0-85084167889 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
Journal of Periodontology |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
533-544 |
dc.source.none.fl_str_mv |
Scopus reponame:Repositório Institucional da UNESP instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
Repositório Institucional da UNESP |
collection |
Repositório Institucional da UNESP |
repository.name.fl_str_mv |
Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
|
_version_ |
1808129184577355776 |