Type 1 diabetes (T1DM) increases the likelihood of a fracture. Despite serious complications in the healing of fractures among those with diabetes, the underlying causes are not delineated for the effect of diabetes on the fracture resistance of bone. Therefore, in a mouse model of T1DM, we have investigated the possibility that a prolonged state of diabetes perturbs the relationship between bone strength and structure (i.e., affects tissue properties). At 10, 15, and 18 weeks following injection of streptozotocin to induce diabetes, diabetic male mice and age-matched controls were examined for measures of skeletal integrity. We assessed 1) the moment of inertia (I MIN ) of the cortical bone within diaphysis, trabecular bone architecture of the metaphysis, and mineralization density of the tissue (TMD) for each compartment of the femur by microcomputed tomography and 2) biomechanical properties by three point bending test (femur) and nanoindentation (tibia). In the metaphysis, a significant decrease in trabecular bone volume fraction and trabecular TMD was apparent after 10 weeks of diabetes. For cortical bone, type 1 diabetes was associated with decreased cortical TMD, I MIN , rigidity, and peak moment as well as a lack of normal age-related increases in the biomechanical properties. However, there were only modest differences in material properties between diabetic and normal mice at both whole bone and tissue-levels. As the duration of diabetes increased, bone toughness decreased relative to control. If the sole effect of diabetes on bone strength was due to a reduction in bone size, then I MIN would be the only significant variable explaining the variance in the maximum moment. However, general linear modeling found that the relationship between peak moment and I MIN depended on whether the bone was from a diabetic mouse and the duration of diabetes. Thus, these Correspondence: Jeffry S. Nyman, Vanderbilt Orthopaedic Institute, Medical Center East, South Tower, Suite 4200, Nashville, TN 37232, jeffry.s.nyman@vanderbilt.edu, (615) 936-6296. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptBone. Author manuscript; available in PMC 2012 April 1.

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ESIs were noted to cause a significant increase in the blood glucose levels in diabetics. There was no correlation between preinjection diabetic control, represented by hA(1c) levels, and postinjection response. Diabetics who are candidates for ESI should be counseled that a blood glucose increase may be apparent post intervention, but effects should not last longer than approximately 2 days.

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