Abstract
Objective: To determine the molar enamel thickness of rat offsprings born to diabetic rat.Material and Methods: This research used sixteen rat offsprings born to 8 diabetic rats who had been injected with STZ dose of 40 mg / kg and 16 rat offsprings born to 8 control rats. Rat offsprings were decapitated on day 5 after birth and taken right mandibular molar tooth germ. Tooth germ then embedded in paraffin block. Haematoxylin eosin staining performed for histological analysis. Enamel thickness measured on the images using ImageJ Software at 5 field of view.Results: The enamel thickness on the Diabetes Mellitus (DM) group (333.02 ± 135.81 µm) were lower than control group (415.39 ± 146.17 µm). Mann Whitney test results showed a significant difference between the DM and control group.Conclusion: It was concluded that enamel thickness decreases in gestational diabetes mellitus rat offspring.
Highlights
The formation of primary teeth or odontogenesis begin at the age of 6-7 weeks intrauterine
Diabetes Mellitus (DM) is a metabolic disorder characterized by hyperglycemia that occurs due to abnormalities of insulin secretion, insulin action, or both.[5]
Pregnancy is normally accompanied by progressive insulin resistance that begins near mid-pregnancy and progresses through the third trimester to levels that approximate the insulin resistance seen in individuals with type 2 diabetes
Summary
The formation of primary teeth or odontogenesis begin at the age of 6-7 weeks intrauterine. Gestational Diabetes Mellitus is reported to cause enamel hypoplasia in children born.[4]. Diabetes Mellitus (DM) is a metabolic disorder characterized by hyperglycemia that occurs due to abnormalities of insulin secretion, insulin action, or both.[5]. Pregnancy is normally accompanied by progressive insulin resistance that begins near mid-pregnancy and progresses through the third trimester to levels that approximate the insulin resistance seen in individuals with type 2 diabetes. Pancreatic β cells normally increase insulin secretion as compensation for insulin resistance during normal pregnancy. Changes in circulating glucose levels over the course of pregnancy are quite small compared with the large changes in insulin sensitivity. Beta cell ability in resolve progressive insulin resistance is the hallmark of normal glucose regulation during pregnancy. Patient with Gestational DM can not provide enough insulin to get normal blood glucose regulation, resulting in elevated blood glucose levels.[7]
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