Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment

Detalhes bibliográficos
Autor(a) principal: Spirlandeli, Adriano L.
Data de Publicação: 2017
Outros Autores: Dick-de-Paula, Ingrid, Zamarioli, Ariane, Jorgetti, Vanda, Ramalho, Leandra N.Z., Nogueira-Barbosa, Marcello H., Volpon, Jose B., Jordão, Alceu A., Cunha, Fernando Q., Fukada, Sandra Y., de Paula, Francisco J.A.
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/132851
Resumo: OBJECTIVES: The present study was designed to evaluate the bone phenotypes and mechanisms involved in bone disorders associated with hepatic osteodystrophy. Hepatocellular disease was induced by carbon tetrachloride (CCl4). In addition, the effects of disodium pamidronate on bone tissue were evaluated. METHODS: The study included 4 groups of 15 mice: a) C = mice subjected to vehicle injections; b) C+P = mice subjected to vehicle and pamidronate injections; c) CCl4+V = mice subjected to CCl4 and vehicle injections; and d) CCl4+P = mice subjected to CCl4 and pamidronate injections. CCl4 or vehicle was administered for 8 weeks, while pamidronate or vehicle was injected at the end of the fourth week. Bone histomorphometry and biomechanical analysis were performed in tibiae, while femora were used for micro-computed tomography and gene expression. RESULTS: CCl4 mice exhibited decreased bone volume/trabecular volume and trabecular numbers, as well as increased trabecular separation, as determined by bone histomorphometry and micro-computed tomography, but these changes were not detected in the group treated with pamidronate. CCl4 mice showed increased numbers of osteoclasts and resorption surface. High serum levels of receptor activator of nuclear factor-κB ligand and the increased expression of tartrate-resistant acid phosphatase in the bones of CCl4 mice supported the enhancement of bone resorption in these mice. CONCLUSION: Taken together, these results suggest that bone resorption is the main mechanism of bone loss in chronic hepatocellular disease in mice.
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spelling Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate TreatmentHepatic OsteodystrophyOsteoporosisMiceBone RemodelingCcirrhosisOBJECTIVES: The present study was designed to evaluate the bone phenotypes and mechanisms involved in bone disorders associated with hepatic osteodystrophy. Hepatocellular disease was induced by carbon tetrachloride (CCl4). In addition, the effects of disodium pamidronate on bone tissue were evaluated. METHODS: The study included 4 groups of 15 mice: a) C = mice subjected to vehicle injections; b) C+P = mice subjected to vehicle and pamidronate injections; c) CCl4+V = mice subjected to CCl4 and vehicle injections; and d) CCl4+P = mice subjected to CCl4 and pamidronate injections. CCl4 or vehicle was administered for 8 weeks, while pamidronate or vehicle was injected at the end of the fourth week. Bone histomorphometry and biomechanical analysis were performed in tibiae, while femora were used for micro-computed tomography and gene expression. RESULTS: CCl4 mice exhibited decreased bone volume/trabecular volume and trabecular numbers, as well as increased trabecular separation, as determined by bone histomorphometry and micro-computed tomography, but these changes were not detected in the group treated with pamidronate. CCl4 mice showed increased numbers of osteoclasts and resorption surface. High serum levels of receptor activator of nuclear factor-κB ligand and the increased expression of tartrate-resistant acid phosphatase in the bones of CCl4 mice supported the enhancement of bone resorption in these mice. CONCLUSION: Taken together, these results suggest that bone resorption is the main mechanism of bone loss in chronic hepatocellular disease in mice.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2017-04-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/13285110.6061/clinics/2017(04)07Clinics; Vol. 72 No. 4 (2017); 231-237Clinics; v. 72 n. 4 (2017); 231-237Clinics; Vol. 72 Núm. 4 (2017); 231-2371980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/132851/128897Copyright (c) 2017 Clinicsinfo:eu-repo/semantics/openAccessSpirlandeli, Adriano L.Dick-de-Paula, IngridZamarioli, ArianeJorgetti, VandaRamalho, Leandra N.Z.Nogueira-Barbosa, Marcello H.Volpon, Jose B.Jordão, Alceu A.Cunha, Fernando Q.Fukada, Sandra Y.de Paula, Francisco J.A.2017-06-02T12:31:57Zoai:revistas.usp.br:article/132851Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2017-06-02T12:31:57Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
title Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
spellingShingle Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
Spirlandeli, Adriano L.
Hepatic Osteodystrophy
Osteoporosis
Mice
Bone Remodeling
Ccirrhosis
title_short Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
title_full Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
title_fullStr Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
title_full_unstemmed Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
title_sort Hepatic Osteodystrophy: The Mechanism of Bone Loss in Hepatocellular Disease and the Effects of Pamidronate Treatment
author Spirlandeli, Adriano L.
author_facet Spirlandeli, Adriano L.
Dick-de-Paula, Ingrid
Zamarioli, Ariane
Jorgetti, Vanda
Ramalho, Leandra N.Z.
Nogueira-Barbosa, Marcello H.
Volpon, Jose B.
Jordão, Alceu A.
Cunha, Fernando Q.
Fukada, Sandra Y.
de Paula, Francisco J.A.
author_role author
author2 Dick-de-Paula, Ingrid
Zamarioli, Ariane
Jorgetti, Vanda
Ramalho, Leandra N.Z.
Nogueira-Barbosa, Marcello H.
Volpon, Jose B.
Jordão, Alceu A.
Cunha, Fernando Q.
Fukada, Sandra Y.
de Paula, Francisco J.A.
author2_role author
author
author
author
author
author
author
author
author
author
dc.contributor.author.fl_str_mv Spirlandeli, Adriano L.
Dick-de-Paula, Ingrid
Zamarioli, Ariane
Jorgetti, Vanda
Ramalho, Leandra N.Z.
Nogueira-Barbosa, Marcello H.
Volpon, Jose B.
Jordão, Alceu A.
Cunha, Fernando Q.
Fukada, Sandra Y.
de Paula, Francisco J.A.
dc.subject.por.fl_str_mv Hepatic Osteodystrophy
Osteoporosis
Mice
Bone Remodeling
Ccirrhosis
topic Hepatic Osteodystrophy
Osteoporosis
Mice
Bone Remodeling
Ccirrhosis
description OBJECTIVES: The present study was designed to evaluate the bone phenotypes and mechanisms involved in bone disorders associated with hepatic osteodystrophy. Hepatocellular disease was induced by carbon tetrachloride (CCl4). In addition, the effects of disodium pamidronate on bone tissue were evaluated. METHODS: The study included 4 groups of 15 mice: a) C = mice subjected to vehicle injections; b) C+P = mice subjected to vehicle and pamidronate injections; c) CCl4+V = mice subjected to CCl4 and vehicle injections; and d) CCl4+P = mice subjected to CCl4 and pamidronate injections. CCl4 or vehicle was administered for 8 weeks, while pamidronate or vehicle was injected at the end of the fourth week. Bone histomorphometry and biomechanical analysis were performed in tibiae, while femora were used for micro-computed tomography and gene expression. RESULTS: CCl4 mice exhibited decreased bone volume/trabecular volume and trabecular numbers, as well as increased trabecular separation, as determined by bone histomorphometry and micro-computed tomography, but these changes were not detected in the group treated with pamidronate. CCl4 mice showed increased numbers of osteoclasts and resorption surface. High serum levels of receptor activator of nuclear factor-κB ligand and the increased expression of tartrate-resistant acid phosphatase in the bones of CCl4 mice supported the enhancement of bone resorption in these mice. CONCLUSION: Taken together, these results suggest that bone resorption is the main mechanism of bone loss in chronic hepatocellular disease in mice.
publishDate 2017
dc.date.none.fl_str_mv 2017-04-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/132851
10.6061/clinics/2017(04)07
url https://www.revistas.usp.br/clinics/article/view/132851
identifier_str_mv 10.6061/clinics/2017(04)07
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/132851/128897
dc.rights.driver.fl_str_mv Copyright (c) 2017 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2017 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 72 No. 4 (2017); 231-237
Clinics; v. 72 n. 4 (2017); 231-237
Clinics; Vol. 72 Núm. 4 (2017); 231-237
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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