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Diabetes Metab Res Rev. 2005 May-Jun;21(3):288-96.

Influence of diabetic metabolic state on fracture healing in spontaneously diabetic rats.

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  • 1Orthopedic Research Laboratories, Department of Orthopedic Surgery, Ernst Moritz Arndt University, Greifswald, Germany.



Type 1 diabetes mellitus (DM) has been shown to alter the properties of bone and impair fracture healing in both humans and animals. The objective of this study was to examine changes in the histomorphometrical, histological and mechanical parameters of bone and remodeling during fracture healing, depending on the diabetic metabolic state in spontaneously diabetic BB/O(ttawa)K(arlsburg) rats, a rat strain that represents a close homology to DM in man.


On the basis of blood glucose values at the time of surgery, postoperative blood glucose course and postoperative insulin requirements, 90 spontaneously diabetic BB/OK rats were divided into groups with well-compensated or poorly compensated metabolic state. Forty-five LEW.1A rats served as the normoglycemic controls. The femurs were fractured in a standardized procedure and then allowed to heal for 2, 4 and 6 weeks.


Our study showed that, in terms of bone histomorphometry, within the first 4 weeks after fracture, severe mineralization disorders occurred exclusively in the rats with poorly compensated diabetic metabolic states with a significant decrease of all fluorochrome-based parameters of mineralization, apposition, formation and timing of mineralization, as well as a delay in cellular differentiation and significantly decreased values of biomechanical properties in comparison to the spontaneously diabetic rats with well-compensated metabolic states and to the control rats.


With a controlled insulin therapy and a resulting well-compensated diabetic metabolic state, mineralization and cellular differentiation disorders, as well as the decreased values of biomechanical properties in the fracture repair in the poorly compensated diabetic metabolic state with very severe hyperglycemia can be avoided.

Copyright 2005 John Wiley & Sons, Ltd.

[PubMed - indexed for MEDLINE]
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