Background: Diabetes mellitus is a metabolic disorder caused by insufficient insulin production due to pancreatic β cell destruction, whereas in gestational diabetics an increase of hormone estrogen induces insulin resistance. Oral candidiasis constitutes an opportunistic fungal infection due to a compromised immune system that is a medical condition reported by diabetics, including those suffering from gestational diabetes. Purpose: To determine the severity of oral candidiasis in female Wistar rats with type 1 and gestational diabetes mellitus. Methods: This research constituted a laboratory experiment incorporating a post test-only group control design whose subjects were female Wistar rats divided along the following lines: group 1 consisted of diabetic non-pregnant rats, group 2 contained diabetic pregnant rats induced by streptozotocin and the control group members constituted normal female rats. Diabetes induction was performed by means of 40 mg/kgBW streptozotocin administrated intraperitoneally. Diabetes mellitus was confirmed when the blood glucose level ≥ 120 mg/dL. All groups were exposed to 0.2 ml Candida albicans suspension (5x108 CFU/ml) in the oral buccal vestibule between the distal incisors and mesial maxillary first molar for three days. A swab was performed on the third day after final exposure before the samples were observed under a light microscope. Candida albicans cultivation and calculation of the resulting colonies was carried out on Sabouraud Dextrose Agar after they had been identified by means of a germ tube test. Results: The result confirmed the absence of hyphae in the control group, while in group 1 all samples contained hyphae. Moreover, group 2 featured a dense hyphae population. A chi-square test indicated a statistical significance (p<0.05) between all groups. Conclusion: Oral candidiasis in gestational diabetes is more severe than that occurring during type 1 diabetes mellitus.
Background and aims. Hyperglycemia in pregnancy was caused by reduced insulin production that led to tooth germ growth disorder. Thymoquinone could increase insulin production through pancreatic β-cells regeneration. The purpose of this study was to determine the effect of thymoquinone to prevent tooth disorder in rat offspring born from hyperglycemia pregnant rat. Material and method. Wistar rat offspring used in this research taken from pregnant rat induced hyperglycemia with streptozotocin 40 mg/kgBW divided into four groups. Rat offspring observation had been done on 3rd, 5th, and 7th day postnatal. The histological image of first maxillary molar tooth germ stained with Haematoxilin Eosin and Mallory’s Trichrome. The parameters of rat offspring were body weight, blood glucose levels, tooth growth stages, tooth dimension width, and tooth germ enamel matrix. Results. Thymoquinone group had the widest tooth germ dimension compare to other groups. All rat offspring tooth germs were at the appositioncalcification stage in matrix enamel (pre-enamel). The analysis showed that no statistical differences between thymoquinone group and metformin group (p>0.05). Conclusions. Thymoquinone has same function with metformin to prevent tooth disorder in rat offspring born from pregnant rat induced hyperglycemia.
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