Alloxan-Induced Diabetes Triggers the Development of Periodontal Disease in Rats
Contribuinte(s) |
Universidade Estadual Paulista (UNESP) |
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Data(s) |
20/05/2014
20/05/2014
19/12/2007
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Resumo |
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. |
Formato |
6 |
Identificador |
http://dx.doi.org/10.1371/journal.pone.0001320 Plos One. San Francisco: Public Library Science, v. 2, n. 12, 6 p., 2007. 1932-6203 http://hdl.handle.net/11449/36111 10.1371/journal.pone.0001320 WOS:000207459600008 WOS000207459600008.pdf |
Idioma(s) |
eng |
Publicador |
Public Library Science |
Relação |
PLOS ONE |
Direitos |
openAccess |
Tipo |
info:eu-repo/semantics/article |