Transcutaneous CO(2) application accelerates fracture repair in streptozotocin-induced type I diabetic rats

INTRODUCTION: Diabetes mellitus (DM) negatively affects fracture repair by inhibiting endochondral ossification, chondrogenesis, callus formation, and angiogenesis. We previously reported that transcutaneous CO(2) application accelerates fracture repair by promoting endochondral ossification and angiogenesis. The present study aimed to determine whether CO(2) treatment would promote fracture repair in cases with type I DM. RESEARCH DESIGN AND METHODS: A closed femoral shaft fracture was induced in female rats with streptozotocin-induced type I DM. CO(2) treatment was performed five times a week for the CO(2) group. Sham treatment, where CO(2) was replaced with air, was performed for the control group. Radiographic, histologic, genetic, and biomechanical measurements were taken at several time points. RESULTS: Radiographic assessment demonstrated that fracture repair was induced in the CO(2) group. Histologically, accelerated endochondral ossification and capillary formation were observed in the CO(2) group. Immunohistochemical assessment indicated that early postfracture proliferation of chondrocytes in callus was enhanced in the CO(2) group. Genetic assessment results suggested that cartilage and bone formation, angiogenesis, and vasodilation were upregulated in the CO(2) group. Biomechanical assessment revealed enhanced mechanical strength in the CO(2) group. CONCLUSIONS: Our findings suggest that CO(2) treatment accelerates fracture repair in type I DM rats. CO(2) treatment could be an effective strategy for delayed fracture repair due to DM.