Kinin B 1 Receptor Deletion Affects Bone Healing in Type 1 Diabetic Mice

The effects of kinin B 1 receptor (B 1 R) deletion were examined on femur bone regeneration in streptozotocin (STZ)‐type 1 diabetes. Diabetes induction in wild‐type C57/BL6 (WTC57BL6) mice led to decrease in body weight and hyperglycemia, compared to the non‐diabetic group of the same strain. The lack of B 1 R did not affect STZ‐elicited body weight loss, but partially prevented hyperglycemia. Diabetic mice had a clear delay in bone regeneration, and displayed large areas of loose connective tissue within the defects, with a reduced expression of the mineralization‐related protein osteonectin, when compared to the non‐diabetic WTC57/BL6. The non‐diabetic and diabetic B 1 R knockout (B 1 RKO) mice had bone regeneration levels and osteonectin expression comparable to that seen in control WTC57/BL6 mice. WTC57/BL6 STZ‐diabetic mice also showed a marked reduction of collagen contents, with increased immunolabeling for the apoptosis marker caspase‐3, whereas diabetic B 1 RKO had collagen levels and caspase‐3 activity comparable to those observed in non‐diabetic WTC57/BL6 or B 1 RKO mice. No significant difference was detected in the number of tartrate‐resistant acid phosphatase (TRAP)‐stained cells, or in RANK/RANKL/OPG system immunolabeling throughout the experimental groups. Data bring novel evidence on the relevance of kinin B 1 R under type 1 diabetes with regards to its role in bone regeneration. J. Cell. Physiol. 230: 3019–3028, 2015. © 2015 Wiley Periodicals, Inc.