Increased inflammation in response to Porphyromonas gingivalis in diabetic mice
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Abstract
Diabetic individuals are more susceptible to infection than normal individuals.
Infections of diabetics tend to be more severe and are more likely to have serious
systemic complications. Porphyromonas gingivalis , an anaerobic Gram-negative
bacterium, is associated with adult periodontitis and lesions of endodontic origin.
Infections by P. gingivalis result in necrosis of soft tissues and the activation of
inflammatory responses that lead to induction of osteoclastogenesis. Polymorphonuclear
cells (PMNs), components of the innate immune response, act as the primary leukocyte
that counteracts bacterial infection.
The objective of this study was to test the hypothesis that diabetes alters the
inflammatory response to P. gingivalis. The host response to P. gingivalis in diabetic and
matched control mice following injection with live P. gingivalis or P. gingivalis
lipopolysaccharide (LPS) into the scalp was evaluated and the recruitment of PMNs and
the necrosis of P. gingivalis infected tissue was assessed.
Mice were sacrificed 1 day and 3 days after injection. On day 1, P. gingivalis
induced areas of necrosis that were similar in normal and diabetic mice (p>0.05 ,
Student 's T test). On day 3, there were 3.35 PMN/field in the diabetic mice, which was
55% greater than control mice, (2.17 PMN/field) , and was statistically significant
(p<0.05). Similar results were obtained with P. gingivalis LPS. These results indicate
that the initial responses to P. gingivalis are similar in normal and diabetic mice, but that there are prolonged inflammatory responses in diabetic mice.
Description
Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2002 (Endodontics).
Includes bibliographical references (leaves 56-75).
Includes bibliographical references (leaves 56-75).
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This work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.