An in vivo study on the cellular, cytokines and chemokines inflammatory response of diabetes to Porphyromonas gingivalis
Date
2003
DOI
Authors
Naguib, Ghada Hussein
Version
OA Version
Citation
Abstract
Diabetes has been identified as an important risk factor for periodontal disease, which results from bacteria-induced inflammation and is a principal cause of adult tooth loss. However, little is known about how diabetes alters the inflammatory response to bacteria in general and to oral pathogens in particular. The objective of this study was to investigate how type I and type II diabetes affects host-bacteria interactions in response to Porphyromonas gingivalis. For type I diabetes we used Stz mice and for type II diabetes db/db (genetically diabetic) mice were used. Diabetic mice and their matched control were injected with P. gingivalis into the scalp. After sacrifice the scalp tissue of the mice was either sectioned for histologic analysis or processed to extract RNA to measure inflammatory cytokine expression. For both type I and type II diabetes, histologic analysis showed that at day 1 there was little difference between the diabetic and control mice; they both exhibited severe inflammation with evidence of cellular necrosis. However, on day 3, there was a significant difference between diabetics and controls. The level of inflammation had subsided in the control group while it had not in the diabetic (p[less than]0.05). Similar results were noted at the molecular level by the persistent expression of TNF a_nd the chemokines MCP-1 and MIP. These results indicate that cytokine dysregulation associated with prolonged TNF expression represents a mechanism through which bacteria may induce a more damaging inflammatory response in diabetic individuals.
The effect of bacteria fimbriae was also tested by using an afimbriated mutant for P.g gingivalis (DPG3). Type I Stz mice were injected with this mutant. Results were similar to those with P.gingivalis 381 indicating no difference in the inflammatory response of the diabetic and control to the mutant bacteria DPG3 (p>0.05). The role of fimbriae was not significant in this study that may be due to the experimental model in which adherence and invasiveness do not play a major role.
Description
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Thesis (D.S.D)--Boston University, Henry M. Goldman School of Dental Medicine, 2003.
Includes bibliography (leaves 205-226).
Thesis (D.S.D)--Boston University, Henry M. Goldman School of Dental Medicine, 2003.
Includes bibliography (leaves 205-226).
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.