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Diabetes-enhanced Inflammation and Apoptosis—Impact on Periodontal Pathology
D.T. Graves1,*,
R. Liu2,
M. Alikhani1,
H. Al-Mashat1 and
P.C. Trackman1
1 Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, W-202 D, 700 Albany Street, Boston, MA 02118, USA; and
2 Department of Periodontology, Faculty of Stomatology, Capital University of Medical Science, Beijing, China
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Figure 1. A more pronounced inflammatory infiltrate was present in diabetic compared with normoglycemic mice three days after inoculation of P. gingivalis. P. gingivalis was inoculated subcutaneously into the scalp. On day 1, there was a pronounced inflammatory infiltrate in both the type 2 diabetic (db/db) mice and the normoglycemic (db/+) mice (data not shown). (A) On day 3, there was still a pronounced infiltrate in the diabetic mice and considerably less in the control group. (B) Effect of TNF inhibition on persistent inflammation in diabetic mice. Diabetic db/db mice were inoculated with P. gingivalis and treated with etanercept (TNF-inh) or vehicle alone (PBS). RNA was extracted 3 days following inoculation and compared with the zero time point (0). The expression of MIP-2 and MCP-1 was measured by the RNase protection assay, and the density of each band was quantified and normalized by GAPDH in the same lane. * MCP-1 and MIP-2 expression was significantly reduced in TNF inhibitor compared with the PBS-treated group (p < 0.05). Adapted from Naguib et al.(2004).
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Figure 3. This diagram represents a summary of several pathways that may be altered by diabetes to enhance apoptosis. (NB: Not all possible connections are shown, for greater legibility.)
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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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Journal of Dental Research, Vol. 85, No. 1,
15-21 (2006)
DOI: 10.1177/154405910608500103
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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 He et al.(2004). Panel C adapted from Al-Mashat et al.(2006).