Histopathological evaluation of topical Lipoxin treatment on porphyromonas gingivalis-induced periodontitis in rabbits
Date
2003
DOI
Authors
Behbehani, Balsam
Version
OA Version
Citation
Abstract
Multi-cellular host responses to infection or inflammatory stimuli lead to the formation of a broad spectrum of chemical mediators by the host. Recent data in the literature indicate that endogenous lipid mediators that suppress pro-inflammatory gene expression and dampen leukocyte trafficking control successful resolution of inflammation. Many molecules play a counter-regulatory role in this resolution stage of the inflammatory response. These counter-regulatory systems have evolved to control the magnitude and duration of the inflammatory response. Lipoxins are lipid mediators derived from the eicosanoid cascade, that can be formed during cell-cell interactions in human tissues to self limit key responses in host defense and promote the resolution of inflammation. This branch of the eicosanoid cascade generates specific tetraene containing products such as lipoxins, which serve as stop signals, that regulate leukocyte trafficking and prevent leukocyte mediated tissue injury.
Synthetic stable lipoxin analogs represent a class of novel lipid mediators that are shown to prevent neutrophil mediated tissue injury. Previously, we have found that experimental periodontal disease in rabbits can be interrupted by local application of LXA [4] analogs. The purpose of this study was to quantitatively analyze the histopathological changes associated with experimental periodontitis in rabbits in response to topically applied stable lipoxin analogs (LXA [4]).
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Description
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Thesis(M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2003 (Oral Biology).
Includes bibliographical references (leaves 67-83).
Thesis(M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2003 (Oral Biology).
Includes bibliographical references (leaves 67-83).
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.