These results associated with clinical observations suggest that diabetes mellitus can produce alterations in oral epithelial cells, detectable by microscopy and cytomorphometry, which can be used in the diagnosis of this disease.

BackgroundPeriodontal 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 FindingsDiabetes 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/SignificanceThe 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.

The aim of this study was to evaluate the changes caused by chronic diabetes in the rat ventral prostate and to establish a correlation between diabetes and the development of prostatic lesions. Male rats received alloxan (42 mg/kg b.w.) to induce diabetes. Ninety days after diabetes diagnosis, animals were sacrificed and the ventral prostate was removed and prepared for general and immunohistochemical analyses. The total area showing different types of lesions was estimated. Diabetes led to a decrease in the body and prostatic weights, as well as in testosterone levels. The prostate morphology and stereology showed high variation in the diabetic group. Some animals had light changes; the great majority had an intense epithelial atrophy; and other rats showed premalignant and malignant lesions in the prostate. Such epithelial atrophy was, in some samples, combined with chronic inflammation, similar to proliferative inflammatory atrophy (PIA). The diabetic group also presented high incidence of prostatitis, adenocarcinoma and prostatic intra-epithelial neoplasia (PIN). Samples with adenocarcinoma had poorly differentiated acini with high levels of cellular proliferation and nuclear atypia. These lesions exhibited an invasive feature showing Bcl-2-positive cells and interruptions in the basement membrane. An association of PIA, PIN and adenocarcinoma was detected in one sample. Reduced androgen levels have a synergic effect to insulin dysfunction promoting negative effects in the rat prostate. Diabetic individuals had a high incidence of prostatitis, and this inflammation could stimulate the incidence of other forms of prostatic pathology.

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Our aim was to assess the temporal relationship between successful PT and functional changes observed in the sciatic and caudal nerves of untreated alloxan-induced diabetic rats. We hope to elucidate the questions reported herein. Materials and Methods▼ 210 inbred male Lewis rats, approximately 12 weeks old, were randomly assigned to 5 experimental groups: NC -60 age-matched non-diabetic controls; DC -60 untreated diabetic con trols, and PT4, PT12, PT24 -90 diabetic rats divided into 3 groups of 30 rats each that received syngeneic pancreas transplants 4, 12, and 24 weeks, respectively, after alloxan-induced. Rats from NC and DC groups were further divided into 6 subgroups of 10 rats each, which were sacrifi ced after 8, 16, 24, 28, 36, and 48 weeks of follow-up. Rats from PT4, PT12, and PT24 groups were divided into 3 subgroups of 10 rats each, and sacrifi ced after 4, 12, and 24 weeks after pancreas transplantation, corresponding to 3 diff erent periods of follow-up such as: 8, 16, and 28 weeks (PT4), 16, 24, and 36 weeks (PT12), and 28, 36, and 48 weeks (PT24). Animals that died during follow-up were replaced Abstract ▼ This document was downloaded for personal use only. Unauthorized distribution is strictly prohibited.

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