Pulpal and periodontal diseases increase triglyceride levels in diabetic rats

Objectives

The aim of this study was to evaluate triglyceride and cholesterol levels in diabetic rats and their relationship with pulpal and periodontal diseases.

Methods

Eighty male rats (Rattus norvegicus albinus, Wistar) were divided into the following eight groups comprising ten animals each: normal rats (G1), rats with pulpal diseases (G2), rats with periodontal diseases (G3), rats with both pulpal and periodontal diseases (G4), diabetic rats (G5), diabetic rats with pulpal diseases (G6), diabetic rats with periodontal diseases (G7), and diabetic rats with both periodontal and pulpal diseases (G8). Diabetes was induced by injecting streptozotocin, periapical lesions were induced by exposing pulpal tissue to the oral environment, and periodontal diseases were induced by periodontal ligature. The animals were killed after 30 days, and lipid profile was enzymatically measured using Trinder’s method. The total assessed values were statistically analyzed by analysis of variance and Tukey test (p?<?0.05).

Results

The triglyceride levels of diabetic rats with periodontal disease and of diabetic rats with both periodontal and pulpal diseases were significantly higher than those of normal rats and nondiabetic group rats, respectively. The differences in the cholesterol levels among the groups were not significant.

Conclusions

We found that the association of pulpal and periodontal diseases with diabetes increased triglyceride levels in rats.

Clinical significance

Changes in lipid profile may be related to the presence of oral infections and diabetes.     

Periodontal disease decreases insulin sensitivity and insulin signaling

Background: The purpose of this study is to investigate whether local inflammatory events, such as periodontal disease, are able to increase tumor necrosis factor‐alpha (TNF‐α) plasmatic concentration and decrease insulin sensitivity and insulin signaling in non‐diabetic rats. Methods: Forty‐eight male Wistar rats (2 months old) were divided into two groups, with either ligature‐induced periodontal disease (LPD) or control conditions (CN). Experiments were performed in both groups 28 days after ligature placement. Plasmatic concentration of glycemia and TNF‐α (n = 10) were analyzed by the glucose oxidase and enzyme‐linked immunosorbent assay method, respectively. Insulin sensitivity (n = 7) was measured using the insulin tolerance test. Insulin signal transduction (n = 7) was measured by pp185 tyrosine phosphorylation status in insulin‐sensitive tissues using the Western blotting method. Results: The LPD group showed decreased insulin sensitivity (P <0.05), although no glycemic alterations were noted (P >0.05). TNF‐α plasmatic concentration was higher in LPD rats compared to CN rats. In addition, a decrease in the pp185 tyrosine phosphorylation status was observed after insulin stimulus in both white adipose and skeletal muscle tissues of the LPD group compared with the CN group. Conclusions: LPD is able to cause alterations to both insulin signaling and insulin sensitivity, probably because of the elevation of TNF‐α plasmatic concentration. Thus, the present results emphasize the importance of the prevention of local inflammatory diseases, such as periodontitis, to prevent diabetes mellitus.     

Measurement and evaluation of the adhesive force between particles by the direct separation method

We developed a new apparatus to measure the adhesive force between particles with a high resolution of approximately 2 nN. The force was measured directly by applying a pulling force to the particles with a contact needle. In addition, the separation process was observed with a 3CCD camera during the measurement. The adhesive force of six kinds of pharmaceutical particles and glass beads was measured, and the effects of moisture, shape, and triboelectrification of the particles on the force were investigated. In the case of moisture-adsorptive particles, the force of adhesion increased rapidly with moisture content under high relative humidity. In the case of moisture-nonadsorptive particles, the force was affected by the particle shape and triboelectrification. The adhesive force of particles having sharp corners was greatly affected by triboelectrification at the corners of the particles.     

Periodontal disease reduces water and sodium intake induced by injection of muscimol into the lateral parabrachial nucleus

ObjectiveGamma-aminobutyric acid A (GABA_A) receptor activation with muscimol in the lateral parabrachial nucleus (LPBN) induces water and 0.3 M NaCl intake. The purpose of this study was to investigate whether a local inflammatory event, such as periodontal disease (PD), is able to alter the effects of muscimol on water and 0.3 M NaCl intake in fluid-replete rats and in rats treated with furosemide (FURO) combined with captopril (CAP) injected subcutaneously.DesignMale Wistar rats were divided into two groups: with PD and those without PD (control condition). Fifteen days after PD, both groups had cannulas implanted bilaterally into the LPBN.ResultsIn fluid-replete rats without PD, injections of muscimol (0.5 nmol/0.2 μl) into the LPBN induced 0.3 M NaCl and water intake and a pressor response. In fluid-replete rats with PD, a decrease was observed in water intake and pressor response but not in 0.3 M NaCl intake. In control rats with FURO + CAP treatment, injections of muscimol into the LPBN increased 0.3 M NaCl and water intake. In PD rats with FURO + CAP treatment, a decrease was observed in 0.3 M NaCl and water intake after muscimol in the LPBN. Alveolar bone loss and interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) plasmatic concentration were higher in PD rats in comparison with controls.ConclusionThese results suggest that PD is able to reduce the pressor response and the dipsogenic and natriorexigenic effects induced by the activation of GABA_A receptors in the LPBN, probably due to the elevation of the plasmatic concentration of pro-inflammatory cytokines IL-6 and TNF-α.     

ULTRASTRUCTURE OF MESODERMAL MIXED TUMOR OF THE UTERUS

A case of mesodermal mixed tumor arising in the uterus of a 57-year-old woman is presented. The tumor was a mixture of adenocarcinoma with occasional squamous metaplasia, stromal sarcoma, myxosarcoma and chondrosarcoma. Light and electron microscopic examinationsof the tumor revealed close transition between stromal sarcomatous component and each of other sarcomatous and carcinomatous component. The histogenesis of mixed mesodermal tumorwas discussed and it was concluded that the tumor might be derived from endometrial stromal cell which possessed the pluripotency to differentiate toward various epithelial and mesenchymal tissues including the heterologous mesenchymal tissue.