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Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats

BACKGROUND: Periodontal disease in diabetic patients presents higher severity and prevalence; and increased severity of ligature-induced periodontal disease has been verified in diabetic rats. However, in absence of aggressive stimuli such as ligatures, the influence of diabetes on rat periodontal t...

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Autores principales: Claudino, Marcela, Ceolin, Danielle Santi, Alberti, Sandra, Cestari, Tania Mary, Spadella, César Tadeu, Rubira-Bullen, Izabel Regina Fischer, Garlet, Gustavo Pompermaier, de Assis, Gerson Francisco
Formato: Texto
Lenguaje:English
Publicado: Public Library of Science 2007
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2121129/
https://www.ncbi.nlm.nih.gov/pubmed/18091993
http://dx.doi.org/10.1371/journal.pone.0001320
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author Claudino, Marcela
Ceolin, Danielle Santi
Alberti, Sandra
Cestari, Tania Mary
Spadella, César Tadeu
Rubira-Bullen, Izabel Regina Fischer
Garlet, Gustavo Pompermaier
de Assis, Gerson Francisco
author_facet Claudino, Marcela
Ceolin, Danielle Santi
Alberti, Sandra
Cestari, Tania Mary
Spadella, César Tadeu
Rubira-Bullen, Izabel Regina Fischer
Garlet, Gustavo Pompermaier
de Assis, Gerson Francisco
author_sort Claudino, Marcela
collection PubMed
description BACKGROUND: Periodontal disease in diabetic patients presents higher severity and prevalence; and increased severity of ligature-induced periodontal disease has been verified in diabetic rats. However, in absence of aggressive stimuli such as ligatures, the influence of diabetes on rat periodontal tissues is incompletely explored. The aim of this study was to evaluate the establishment and progression of periodontal diseases in rats only with diabetes induction. METHODOLOGY/PRINCIPAL FINDINGS: Diabetes was induced in Wistar rats (n = 25) by intravenous administration of alloxan (42 mg/kg) and were analyzed at 1, 3, 6, 9 and 12 months after diabetes induction. The hemimandibles were removed and submitted to radiographical and histopathological procedures. A significant reduction was observed in height of bone crest in diabetic animals at 3, 6, 9 and 12 months, which was associated with increased numbers of osteoclasts and inflammatory cells. The histopathological analyses of diabetic rats also showed a reduction in density of collagen fibers, fibroblasts and blood vessels. Severe caries were also detected in the diabetic group. CONCLUSIONS/SIGNIFICANCE: The results demonstrate that diabetes induction triggers, or even co-induces the onset of alterations which are typical of periodontal diseases even in the absence of aggressive factors such as ligatures. Therefore, diabetes induction renders a previously resistant host into a susceptible phenotype, and hence diabetes can be considered a very important risk factor to the development of periodontal disease.
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spelling pubmed-21211292007-12-19 Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats Claudino, Marcela Ceolin, Danielle Santi Alberti, Sandra Cestari, Tania Mary Spadella, César Tadeu Rubira-Bullen, Izabel Regina Fischer Garlet, Gustavo Pompermaier de Assis, Gerson Francisco PLoS One Research Article BACKGROUND: Periodontal disease in diabetic patients presents higher severity and prevalence; and increased severity of ligature-induced periodontal disease has been verified in diabetic rats. However, in absence of aggressive stimuli such as ligatures, the influence of diabetes on rat periodontal tissues is incompletely explored. The aim of this study was to evaluate the establishment and progression of periodontal diseases in rats only with diabetes induction. METHODOLOGY/PRINCIPAL FINDINGS: Diabetes was induced in Wistar rats (n = 25) by intravenous administration of alloxan (42 mg/kg) and were analyzed at 1, 3, 6, 9 and 12 months after diabetes induction. The hemimandibles were removed and submitted to radiographical and histopathological procedures. A significant reduction was observed in height of bone crest in diabetic animals at 3, 6, 9 and 12 months, which was associated with increased numbers of osteoclasts and inflammatory cells. The histopathological analyses of diabetic rats also showed a reduction in density of collagen fibers, fibroblasts and blood vessels. Severe caries were also detected in the diabetic group. CONCLUSIONS/SIGNIFICANCE: The results demonstrate that diabetes induction triggers, or even co-induces the onset of alterations which are typical of periodontal diseases even in the absence of aggressive factors such as ligatures. Therefore, diabetes induction renders a previously resistant host into a susceptible phenotype, and hence diabetes can be considered a very important risk factor to the development of periodontal disease. Public Library of Science 2007-12-19 /pmc/articles/PMC2121129/ /pubmed/18091993 http://dx.doi.org/10.1371/journal.pone.0001320 Text en Claudino et al. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Claudino, Marcela
Ceolin, Danielle Santi
Alberti, Sandra
Cestari, Tania Mary
Spadella, César Tadeu
Rubira-Bullen, Izabel Regina Fischer
Garlet, Gustavo Pompermaier
de Assis, Gerson Francisco
Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title_full Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title_fullStr Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title_full_unstemmed Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title_short Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
title_sort alloxan-induced diabetes triggers the development of periodontal disease in rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2121129/
https://www.ncbi.nlm.nih.gov/pubmed/18091993
http://dx.doi.org/10.1371/journal.pone.0001320
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