Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture

Detalhes bibliográficos
Autor(a) principal: Diniz, Sandoval Felicíssimo
Data de Publicação: 2008
Outros Autores: Amorim, Fernanda Penna Lima Guedes de, Cavalcante Neto, F. F., Bocca, Anamélia Lorenzetti, Batista, A. C., Simm, G.E.P.M, Silva, Tarcília Aparecida da
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UCB
Texto Completo: http://hdl.handle.net/123456789/190
https://repositorio.ucb.br:9443/jspui/handle/123456789/7464
Resumo: A closed fracture was performed on the left tibia of 3-month-old Wistar rats weighing 250 to 350 g that were either healthy (N = 24) or made diabetic with alloxan (N = 24) to investigate the effect of alloxan-induced diabetes on the course of bone fracture healing. Histomorphometric analysis of the fracture site was performed at 7, 14, 25, and 35 days. After 7 days, diabetic rats had significantly less cartilage (P = 0.045) and greater fibrous connective (P = 0.006) tissue formation at the fracture site compared to controls. In contrast, marked callus formation was seen in diabetic rats with significant osteogenesis (P = 0.011, P = 0.010, P = 0.010, respectively, for 14, 25, and 35 days) and chondrogenesis (P = 0.028, P = 0.033, P = 0.019) compared to controls. Radiographic analysis revealed a displaced fracture with poor bone fragment alignment and delayed consolidation at these times in the diabetic group. The levels of alkaline phosphatase were significantly higher in diabetic rats at 25 days (P = 0.009). These results suggest that the initial excessive formation of fibrous connective tissue associated with delay in chondrogenesis and osteogenesis may not provide suitable stability of the fractured site, contributing to the inappropriate alignment of fragments and an increase in the volume of callus in later stages of repair. The resulting displaced fracture in diabetic rats requires long periods for remodeling and complete bone consolidation
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spelling Diniz, Sandoval FelicíssimoAmorim, Fernanda Penna Lima Guedes deCavalcante Neto, F. F.Bocca, Anamélia LorenzettiBatista, A. C.Simm, G.E.P.MSilva, Tarcília Aparecida da2016-10-10T03:51:34Z2016-10-10T03:51:34Z2008DINIZ, Sandoval Felicíssimo et al. Alloxan-induced diabetes delays repair in a rat model of closed tibia fracture. Brazilian Journal of Medical and Biological Research, v.41, p.373-379, 2008.0100-879Xhttp://hdl.handle.net/123456789/190https://repositorio.ucb.br:9443/jspui/handle/123456789/7464A closed fracture was performed on the left tibia of 3-month-old Wistar rats weighing 250 to 350 g that were either healthy (N = 24) or made diabetic with alloxan (N = 24) to investigate the effect of alloxan-induced diabetes on the course of bone fracture healing. Histomorphometric analysis of the fracture site was performed at 7, 14, 25, and 35 days. After 7 days, diabetic rats had significantly less cartilage (P = 0.045) and greater fibrous connective (P = 0.006) tissue formation at the fracture site compared to controls. In contrast, marked callus formation was seen in diabetic rats with significant osteogenesis (P = 0.011, P = 0.010, P = 0.010, respectively, for 14, 25, and 35 days) and chondrogenesis (P = 0.028, P = 0.033, P = 0.019) compared to controls. Radiographic analysis revealed a displaced fracture with poor bone fragment alignment and delayed consolidation at these times in the diabetic group. The levels of alkaline phosphatase were significantly higher in diabetic rats at 25 days (P = 0.009). These results suggest that the initial excessive formation of fibrous connective tissue associated with delay in chondrogenesis and osteogenesis may not provide suitable stability of the fractured site, contributing to the inappropriate alignment of fragments and an increase in the volume of callus in later stages of repair. 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dc.title.pt_BR.fl_str_mv Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
title Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
spellingShingle Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
Diniz, Sandoval Felicíssimo
Alloxan
Diabetes
Fracture repair
Closed fracture
title_short Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
title_full Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
title_fullStr Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
title_full_unstemmed Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
title_sort Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture
author Diniz, Sandoval Felicíssimo
author_facet Diniz, Sandoval Felicíssimo
Amorim, Fernanda Penna Lima Guedes de
Cavalcante Neto, F. F.
Bocca, Anamélia Lorenzetti
Batista, A. C.
Simm, G.E.P.M
Silva, Tarcília Aparecida da
author_role author
author2 Amorim, Fernanda Penna Lima Guedes de
Cavalcante Neto, F. F.
Bocca, Anamélia Lorenzetti
Batista, A. C.
Simm, G.E.P.M
Silva, Tarcília Aparecida da
author2_role author
author
author
author
author
author
dc.contributor.author.fl_str_mv Diniz, Sandoval Felicíssimo
Amorim, Fernanda Penna Lima Guedes de
Cavalcante Neto, F. F.
Bocca, Anamélia Lorenzetti
Batista, A. C.
Simm, G.E.P.M
Silva, Tarcília Aparecida da
dc.subject.por.fl_str_mv Alloxan
Diabetes
Fracture repair
Closed fracture
topic Alloxan
Diabetes
Fracture repair
Closed fracture
dc.description.abstract.por.fl_txt_mv A closed fracture was performed on the left tibia of 3-month-old Wistar rats weighing 250 to 350 g that were either healthy (N = 24) or made diabetic with alloxan (N = 24) to investigate the effect of alloxan-induced diabetes on the course of bone fracture healing. Histomorphometric analysis of the fracture site was performed at 7, 14, 25, and 35 days. After 7 days, diabetic rats had significantly less cartilage (P = 0.045) and greater fibrous connective (P = 0.006) tissue formation at the fracture site compared to controls. In contrast, marked callus formation was seen in diabetic rats with significant osteogenesis (P = 0.011, P = 0.010, P = 0.010, respectively, for 14, 25, and 35 days) and chondrogenesis (P = 0.028, P = 0.033, P = 0.019) compared to controls. Radiographic analysis revealed a displaced fracture with poor bone fragment alignment and delayed consolidation at these times in the diabetic group. The levels of alkaline phosphatase were significantly higher in diabetic rats at 25 days (P = 0.009). These results suggest that the initial excessive formation of fibrous connective tissue associated with delay in chondrogenesis and osteogenesis may not provide suitable stability of the fractured site, contributing to the inappropriate alignment of fragments and an increase in the volume of callus in later stages of repair. The resulting displaced fracture in diabetic rats requires long periods for remodeling and complete bone consolidation
dc.description.version.pt_BR.fl_txt_mv Sim
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description A closed fracture was performed on the left tibia of 3-month-old Wistar rats weighing 250 to 350 g that were either healthy (N = 24) or made diabetic with alloxan (N = 24) to investigate the effect of alloxan-induced diabetes on the course of bone fracture healing. Histomorphometric analysis of the fracture site was performed at 7, 14, 25, and 35 days. After 7 days, diabetic rats had significantly less cartilage (P = 0.045) and greater fibrous connective (P = 0.006) tissue formation at the fracture site compared to controls. In contrast, marked callus formation was seen in diabetic rats with significant osteogenesis (P = 0.011, P = 0.010, P = 0.010, respectively, for 14, 25, and 35 days) and chondrogenesis (P = 0.028, P = 0.033, P = 0.019) compared to controls. Radiographic analysis revealed a displaced fracture with poor bone fragment alignment and delayed consolidation at these times in the diabetic group. The levels of alkaline phosphatase were significantly higher in diabetic rats at 25 days (P = 0.009). These results suggest that the initial excessive formation of fibrous connective tissue associated with delay in chondrogenesis and osteogenesis may not provide suitable stability of the fractured site, contributing to the inappropriate alignment of fragments and an increase in the volume of callus in later stages of repair. The resulting displaced fracture in diabetic rats requires long periods for remodeling and complete bone consolidation
publishDate 2008
dc.date.issued.fl_str_mv 2008
dc.date.accessioned.fl_str_mv 2016-10-10T03:51:34Z
dc.date.available.fl_str_mv 2016-10-10T03:51:34Z
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dc.identifier.citation.fl_str_mv DINIZ, Sandoval Felicíssimo et al. Alloxan-induced diabetes delays repair in a rat model of closed tibia fracture. Brazilian Journal of Medical and Biological Research, v.41, p.373-379, 2008.
dc.identifier.uri.fl_str_mv http://hdl.handle.net/123456789/190
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dc.identifier.issn.none.fl_str_mv 0100-879X
identifier_str_mv DINIZ, Sandoval Felicíssimo et al. Alloxan-induced diabetes delays repair in a rat model of closed tibia fracture. Brazilian Journal of Medical and Biological Research, v.41, p.373-379, 2008.
0100-879X
url http://hdl.handle.net/123456789/190
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