Here, we report a model to study ␤-cell proliferation in living rats by administering three different doses of dexamethasone (0.1, 0.5, and 1.0 mg/kg ip, DEX 0.1, DEX 0.5, and DEX 1.0, respectively) for 5 days. Insulin sensitivity, insulin secretion, and histomorphometric data were investigated. Western blotting was used to analyze the levels of proteins related to the control of ␤-cell growth. DEX 1.0 rats, which present moderate hyperglycemia and marked hyperinsulinemia, exhibited a 5.1-fold increase in ␤-cell proliferation and an increase (17%) in ␤-cell size, with significant increase in ␤-cell mass, compared with control rats. The hyperinsulinemic but euglycemic DEX 0.5 rats also showed a significant 3.6-fold increase in ␤-cell proliferation. However, DEX 0.1 rats, which exhibited the lowest degree of insulin resistance, compensate for insulin demand by improving only islet function. Activation of the insulin receptor substrate 2/phosphatidylinositol 3-kinase/serine-threonine kinase/ribosomal protein S6 kinase pathway, as well as protein retinoblastoma in islets from DEX 1.0 and DEX 0.5, but not in DEX 0.1, rats was also observed. Therefore, increasing doses of dexamethasone induce three different degrees of insulin requirement in living rats, serving as a model to investigate compensatory ␤-cell alterations. Augmented ␤-cell mass involves ␤-cell hyperplasia and, to a lower extent, ␤-cell hypertrophy. We suggest that alterations in circulating insulin and, to a lesser extent, glucose levels could be the major stimuli for ␤-cell proliferation in the dexamethasone-induced insulin resistance.␤-cell growth; glucocorticoid; hyperglycemia; hyperinsulinemia; insulin resistance PANCREATIC ␤-CELLS ARE the only significant source of insulin, which is required for maintaining appropriate metabolic homeostasis and particularly to maintain glucose levels within a narrow range. However, failure of the ␤-cell capacity (␤-cell dysfunction and/or insufficient ␤-cell mass) contributes to the pathogenesis of both type 1 (T1DM) and type 2 diabetes mellitus (T2DM) (10, 18). Physiological or pathological states such as aging, pregnancy, insulin resistance, and obesity demand an increase in circulating insulin. Several ␤-cell adaptations are observed in these conditions, including increased insulin synthesis and secretion, hyperplasia, and hypertrophy (23,28,30). ␤-Cell mass plays an essential role in limiting the amount of insulin that is secreted in these systemic conditions of increased insulin demand. Patients with T2DM show reduced ␤-cell mass as a result of impaired ␤-cell proliferation and/or increased ␤-cell apoptosis, suggesting that adequate ␤-cell mass is required for prevention of diabetes (10, 18). Although remarkable improvements in the management of diabetic patients have occurred over recent years, new therapies are still needed to further improve metabolic control of this pathology (36).Amelioration of ␤-cell function and increase in ␤-cell number are important goals in diabetes research. Pancreatic ␤-cell mass r...

Autogenous bone grafts are used to repair bone defects, and the stabilization is needed for bone regeneration. Laser photobiomodulation is a modality of treatment in clinical practice for tissue regeneration, and it has therapeutic effects as an anti-inflammatory, analgesic and modulating cellular activity. The aim of the present study was to evaluate the effects of low-level laser therapy (LLLT) on an autogenous bone graft integration process stabilized with a new heterologous fibrin sealant. Forty rats were divided into two groups: Autogenous Fibrin Graft (AFG, n=20), in which a 5mm dome osteotomy was conducted in the right parietal bone and the graft was adhered to the left side using fibrin sealant; and Autogenous Fibrin Graft Laser (AFGL, n=20), which was subjected to the same procedures as AFG with the addition of LLLT. The treatment was performed immediately following surgery and then three times a week until euthanasia, using an 830nm laser (30mW, 6J/cm(2), 0.116cm(2), 258.6mW/cm(2), 2.9J). Five animals from each group were euthanized at 10, 20, 30 and 40days postoperative, and the samples were submitted to histomorphological and histomorphometric analysis. Partial bone regeneration occurred, with new bone tissue integrating the graft to the recipient bed and small areas of connective tissue. Comparative analysis of the groups at the same intervals revealed minor interfaces in group AFGL, with statistically significant differences (p<0.05) at all of the analyzed intervals (10days p=0.0087, 20days p=0.0012, 30days p<0.0001, 40days p=0.0142). In conclusion, low-level laser therapy stimulated bone regeneration and accelerated the process of integration of autogenous bone grafts.

The sBDAB block can be used to promote repair of CSDs and bone augmentation in the craniomaxillofacial region, due to its good osteoconductive and slow resorptive properties.

The present data suggest an important role for VEGF in the progression of periodontal disease. Systemic therapy with meloxicam can modify the progression of experimentally induced periodontitis in rats by reducing VEGF expression and alveolar bone loss.

Fluoride (F) is a potent anti-cariogenic element, but when ingestion is excessive, systemic toxicity may be observed. This can occur as acute or chronic responses, depending on both the amount of F and the time of exposure. The present study identified the profile of protein expression possibly associated with F-induced chronic hepatotoxicity. Weanling male Wistar rats (three-weeks old) were divided into three groups and treated with drinking water containing 0, 5 or 50 mg/L F for 60 days (n=6/group). At this time point, serum and livers were collected for F analysis, which was done using the ion-sensitive electrode, after hexamethyldisiloxane-facilitated diffusion. Livers were also submitted to histological and proteomic analyses (2D-PAGE followed by LC-MS/MS). Western blotting was done for confirmation of the proteomic data A dose-response was observed in serum F levels. In the livers, F levels were significantly increased in the 50 mg/L F group compared to groups treated with 0 and 5 mg/L F. Liver morphometric analysis did not reveal alterations in the cellular structures and lipid droplets were present in all groups. Proteomic quantitative intensity analysis detected 33, 44, and 29 spots differentially expressed in the comparisons between control vs. 5 mg/L F, control vs. 50 mg/L F, and 5 mg/L vs. 50 mg/L F, respectively. From these, 92 proteins were successfully identified. In addition, 18, 1, and 5 protein spots were shown to be exclusive in control, 5, and 50 mg/L F, respectively. Most of proteins were related to metabolic process and pronounced alterations were seen for the high-F level group. In F-treated rats, changes in the apolipoprotein E (ApoE) and GRP-78 expression may account for the F-induced toxicity in the liver. This can contribute to understanding the molecular mechanisms underlying hepatoxicity induced by F, by indicating key-proteins that should be better addressed in future studies.