Alterations of cartilage and collagen expression during fracture healing in experimental diabetes.

We investigated alterations in the expression of mRNA for type II and type X collagen in fracture callus of experimentally induced diabetic animals compared with controls and performed radiographic, histological, immunocytochemical and biomechanical studies. Experimentally induced diabetic rats exhibited an alteration in the temporal expression of type II and type X collagen mRNA and a decrease in type X mRNA expression as compared to controls. Radiographs showed a more intense periosteal reaction and a more rapid reconstitution of cortices in control versus diabetic animals. Histologically there was a delay in chondrocyte maturation and hypertrophy seen in diabetics. Immunolocalization of type X collagen demonstrated a delay in type X collagen expression around the hypertrophic chondrocytes. Biomechanical analysis showed a decrease in the strength of healing fractures in diabetic animals. Fracture healing in diabetic patients is compromised and may lead to delays in bone union. Though the exact mechanisms are unknown, we present evidence of decreased mechanical strength of the fracture and suggest that associated changes in collagen expression and chondrocyte maturation are mechanisms leading to delayed healing in untreated and poorly controlled diabetes.

Biomechanical evaluation of early fracture healing in normal and diabetic rats.

Diabetes mellitus 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 document changes in the structural and material properties of intact bone and bone with healed fractures in diabetic rats compared with nondiabetic controls after 3 and 4 weeks of healing. Rods were inserted in the right femurs of control rats and rats with streptozotocin-induced diabetes, and the femurs were fractured in a standardized procedure and then allowed to heal for 3 and 4 weeks. After death, all femurs were mechanically tested to failure in torsion. The degree of healing was quantified for each animal by normalizing mechanical parameters for the femur with a healed fracture with those for the intact contralateral femur. At both time points of healing, diabetic rats exhibited inferior healing compared with that of control animals in terms of failure torque, failure stress, structural stiffness, and material stiffness of the femur with the healed fracture relative to the intact contralateral femur (p < 0.05). Our results demonstrate that the recovery of structural and material strength in femurs with healed fractures in diabetic rats is delayed by at least 1 week compared with that in controls.