Ultrastructural and immunohistochemical study of the influence of fluoride excess on the development of rat incisor tooth buds

Little information is available on the pathogenesis of fluorosis during the fetal and initial postnatal period. In the present study, female rats received 0 (control), 7 or 100 ppm of sodium fluoride in drinking water, one week before breeding and throughout gestation and nursing periods. The hemimandibles of the offspring were collected at 0, 7 and 14 days of postnatal life (n = 5) and processed for morphological analyses by light and electron microscopy, immunohistochemical analysis for amelogenin and morphometric study of enamel matrix and ameloblasts of incisors. The results showed a decrease in matrix production at the secretory phase at all study periods for the 100 ppm group. In this same group, the secretory ameloblasts showed reduction of enamel matrix secretion, disorganization of mitochondrial crests, large vacuoles at the apical portion of the cytoplasm, retention of intracisternal material and dilatation of some cisterns in the rough endoplasmic reticulum. In the groups of animals aged 7 and 14 days, analysis of variance showed significant reduction (

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 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

Absence of pathological changes in dental and periodontal tissues in control group.

<p>Animals were evaluated for dental and periodontal histological changes at 1 (a, b), 3 (c, d), 6 (e, f), 9 (g, h) and 12 (i, j) months after alloxan administration.</p

Reduction of volumetric density of collagen fibers, fibroblasts and blood vessels in diabetic groups.

<p>Histological sections of diabetic rats were investigated by morphometrical analyses for: a) volumetric density of collagen fibers, b) volumetric density of fibroblasts, c) volumetric density of blood vessels.</p

Increases of osteoclasts and inflammatory cells associated with alveolar bone loss in diabetic groups.

<p>Diabetic rats presented significant alveolar bone loss (a) starting at 3 months after alloxan injection when compared to the controls. After histotechnical procedures, sections were investigated by morphometric analyses for: b) volumetric density of osteoclasts, c) volumetric density of inflammatory cells.</p