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Figure 4. Mechanisms through which diabetes may affect wound healing. Diabetes-induced production of ROS, TNF, or AGEs can have direct effects on repair that include the inhibition of collagen production by osteoblasts or fibroblasts derived from the gingiva or skin. However, they could also have profound indirect effects by promoting inflammation or, potentially, through enhanced apoptosis. Taken together, direct and indirect effects of AGEs could contribute to impaired healing in diabetics.
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) and normal littermate control (
) mice was undertaken. (A) New bone formation was measured by image analysis of van Gieson-stained sections and is expressed as the area of new bone per bone length (mm2/mm). (B) Apoptosis of bone-lining cells was measured by the TUNEL assay and is expressed as the number per bone length. For each assay, the mean ± standard error are shown based on 6 specimens per data point. (C) Bacteria were inoculated into the scalps of db/db mice. One group was treated with the pancaspase inhibitor, Z-VAD-FMK, to block apoptosis, and mice were killed 8 days later. The area of newly formed bone matrix was identified in Van Gieson-stained sections. Each value represents the mean area divided by the length of bone ± SEM. * indicates statistical significance in the control compared with diabetic mice, p < 0.05. It should be noted that the period when apoptosis of bone-lining cells was higher in the diabetic group corresponded to the period of peak bone formation. Panels A and B adapted from 