European Journal Of Oral Sciences · 1989 · 14 citations · 24 references
MedicineBiochemistryEndocrinologyBone MetabolismDiabetologyRenal PathophysiologyBone Metabolism DisordersDiabetes MellitusDiabetes Mellitus BiochemistryInsulin ResistanceMetabolic Bone DiseaseMetabolic DisordersAlveolar Bone MorphologyBone Matrix BiochemistryDiabetes Mellitus MetabolismHydroxyproline ContentNew Bone FormationPancreatic Beta-cell FunctionPancreatic Beta-cell SecretionSerum Calcium Measurement
Adult male and female rats were used as test animals. The experimental diabetes mellitus was provoked with one dose of i.v. injection of streptozotocin (65 mg/kg body weight), which interferes with the insulin release mechanism in pancreatic beta cells. After a follow-up period of 10 wk an average loss of 10% of body weight and an increase of 25% in the amount of blood obtained by decapitation was recorded in the test animals. The biochemical assays performed on the serum of the diabetic rats showed, for both sexes, a fourfold rise in the plasma glucose level, a threefold rise in plasma alkaline phosphatase activity and plasma alanine transferase activity as well as a 1.5-fold rise in plasma creatine value. The two latter values indicated systematic disorders reflected in the liver and the kidneys. An increase in serum total calcium and hydroxyproline values was also detected. The clinical studies of the gingiva showed diminished tissue resistance in diabetic rats. The histologic studies of alveolar bone revealed retarded formation of bone matrix and new bone in diabetic animals. However, the stimulated metabolism in alveolar bone, due to the artificially induced stress, increased marginal bone cell activity in both the diabetic and the control group, resulting in increased crestal resorption in the former group. The differences in tissue response observed among the diabetic animals affected and unaffected by stress originated from the disturbed recovering mechanism typically found in diabetic animals.
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