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J Bone Joint Surg Am. 1989 Jun;71(5):722-33.

Defects of early fracture-healing in experimental diabetes.

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Orthopaedic Research Unit, National Institute of Arthritis and Musculoskeletal Diseases, Bethesda, Maryland 20892.


Diabetes has been implicated as a cause of impaired fracture-healing. To test this hypothesis, we tested the tensile strength of femora from normal rats and from untreated and insulin-treated diabetic rats two weeks after the production of a closed fracture. One week before the fracture, diabetes was induced by administration of streptozotocin (sixty-five milligrams per kilogram of body weight). The concentration of serum glucose increased from 6.1 +/- 0.3 millimoles per liter (110 +/- 5 milligrams per deciliter) in the control animals to 31.1 +/- 0.8 millimoles per liter (560 +/- 15 milligrams per deciliter) in the untreated diabetic animals. After two weeks of healing, fracture callus from the untreated diabetic animals had a 29 per cent decrease in tensile strength and a 50 per cent decrease in stiffness compared with the controls. Treatment of the diabetic animals with insulin resulted in a mean concentration of serum glucose of 14.4 +/- 0.6 millimoles per liter (260 +/- 10 milligrams per deciliter) and restored the tensile strength and stiffness of the callus to a value that was not statistically different from that of the controls. Between the fourth and eleventh days of healing, there was a 50 to 55 per cent decrease in the collagen content of the callus of the untreated diabetic animals compared with the controls. In addition, on the fourth day of healing, DNA content, an indicator of cellularity of the callus, was decreased 40 per cent in the untreated diabetic group. Between the fourth and eleventh days of healing, the collagen-to-DNA ratio, which was determined as an indicator of net collagen synthesis per cell, was decreased 15 to 50 per cent in callus from the untreated diabetic animals.

[Indexed for MEDLINE]

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