Activated lymphocytes do not play a protective role in lesions of endodontic origin
Date
1998
DOI
Authors
Mejia, Armando R.
Version
OA Version
Citation
Abstract
Lesions of endodontic origin develop due to noxious materials leaching out of the root canal system through different portals of exit. Bacteria and their by-products, as well as host derived products, can cause tissue damage. Both the immune and nonimmune host response are intimately associated with and play a significant role and impact on the pathogenesis and formation of lesions of endodontic origin. Thirty five normal female BALB / c mice were used. The dental pulp of mandibular right and left first molars was exposed, inoculated with a combination of 4 anaerobic bacteria and left open for 7, 14, 21 days. A highly specific pharmacologic reagent, DAB389-IL2, was injected intra-arterially to the experimental group to delete activated lymphocytes and cells expressing the IL2-R. Paraffin sections were prepared from the specimens and stained with H & E for microscopic examination. Using a computer assisted image analysis system to examine periapical area of the distal root, width and height of lesion was measured. Pulp necrosis progression within the root canal system was assessed as well. Development of lesion size was compared between the experimental groups and control groups overtime. The results indicate that there was little difference between results in the experimental and control groups, suggesting that activated lymphocytes do not contribute to the pathogenesis of lesions of endodontic origin.
Description
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Thesis (M.Sc.D.)--Boston University, Henry M. Goldman School of Graduate Dentistry. Dept. of Endodontics, 1998.
Includes bibliography: leaves 37-44.
Thesis (M.Sc.D.)--Boston University, Henry M. Goldman School of Graduate Dentistry. Dept. of Endodontics, 1998.
Includes bibliography: leaves 37-44.
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.