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Journal of Dental Research
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Inflammation is More Persistent in Type 1 Diabetic Mice

D.T. Graves*, G. Naguib, H. Lu, C. Leone, H. Hsue and E. Krall

Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Suite W-202D, 700 Albany Street, Boston, MA 02118, USA;


Figure 1
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Figure 1. P. gingivalis stimulates formation of a more persistent inflammatory infiltrate in diabetic mice. Diabetes was induced by multiple low-dose streptozotocin treatment, while control mice were treated with citrate buffer alone. (A) P. gingivalis (5 x 108) or (B) P. gingivalis (1 x 108) was inoculated s.c. into the scalp. The degree of PMN infiltration was measured in H&E-stained sections at the center of the infiltrate. A scale was used ranging from no inflammation to severe inflammation with necrosis (0–9). Results are shown as mean ± SEM of 6 mice per group. *A significant difference (P < 0.05) between the control and diabetic groups.

 

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Figure 2. Diabetes causes prolonged expression of MIP-2 in response to P. gingivalis. Diabetes was induced and P. gingivalis was inoculated into the scalp as described in Fig. 1Go. RNA was extracted from the soft tissue and analyzed by RPA. The density of each band was quantified and normalized according to the level of GAPDH expression in the same lane. Each value represents the mean of 3 different RPAs ± standard deviation. (A) P. gingivalis (5 x 108); (B) P. gingivalis (1 x 108). *A significant difference (P < 0.05) between the control and diabetic groups.

 

Figure 3
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Figure 3. Diabetes causes prolonged expression of MCP-1 in response to P. gingivalis. Diabetes was induced and P. gingivalis was inoculated into the scalp as described in Fig. 1Go. RNA was extracted from the soft tissue and analyzed by RPA. The density of each band was quantified and normalized according to the level of GAPDH expression in the same lane. Each value represents the mean of 3 different RPAs ± standard deviation. (A) P. gingivalis (5 x 108); (B) P. gingivalis (1 x 108). *A significant difference (P < 0.05) between the control and diabetic groups.

 

Journal of Dental Research, Vol. 84, No. 4, 324-328 (2005)
DOI: 10.1177/154405910508400406


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