Vorpommern-Greifswald, Alemania
To date, no detailed knowledge from animal experiments is available on the kind and extent of osseous and mineral metabolic disorders in genetically determined, insulin-dependent Type I diabetes. The purpose of this study was to examine the influence of the diabetic metabolic state in spontaneously diabetic BB/O(ttawa)K(arlsburg) rats on bone defect healing. Eighty spontaneously-diabetic BB/OK rats with a blood-glucose value of 391±106 mg% (mean ± SD) at the time of manifestation were used in the study. Based on blood-glucose values at the time of surgery (mg%), postoperative blood-glucose course (mg%) and postoperative insulin requirements (IU/kg), the animals were divided into groups with well-compensated (n=40, 170±101 mg%; 221±120 mg%; 2.1±1 IU/kg) or poorly compensated (n=40; 371±158 mg%; 357±83 mg%; 5.2±1.4 IU/kg) metabolic state. Forty LEW.1A rats served as the normoglycemic controls (95±18 mg%). Using a 1-mm-diameter Kirschner wire, a hole of femoral bone ca. 1 cm proximal to the knee joint space was centrally drilled. Ten animals from each group were killed on postoperative days 7, 14, 24, and 42, and specimens were taken for analysis. Using SEM to measure regions of new bone semiautomatically and quantitatively, also determining the number, area, and circumference of regions not yet filled with new bone. Up to postoperative day 14, very significant differences (p<0.0001) for all investigated characteristics were found between the spontaneously-diabetic BB/OK rats and the control animals – in favor of the controls – and up to postoperative day 24 within the group of spontaneously-diabetic BB/OK rats, where the wellcompensated animals had significantly better results in terms of number and area of regions of bone not yet filled with new bone formations. Forty-two days postoperatively, SEM observations showed no differences between examination groups. The process of bone defect healing in spontaneously-diabetic rats was disturbed only in the early phase and exhibited retardation in its progression. After 42 days, bone defect healing was complete, regardless of the diabetic metabolic state; no differences were detected with the SEM between examination groups at this time point.
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