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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Nuclear and Particle Science 38 (1988), S. 659-703 
    ISSN: 0163-8998
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of oral pathology & medicine 27 (1998), S. 0 
    ISSN: 1600-0714
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Progression factors for periodontal diseases have been suggested by in vitro study of peripheral blood and gingival cells; however, those factors are not established in vivo. This investigation assessed biopsies of three groups of gingival tissues: those adjacent to a 1) 〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:09042512:JOP101:les" location="les.gif"/〉3 mm (normal), 2) 4-6 mm, and 3) 〈6 mm gingival sulcus, to determine changes in the gingival microenvironment coincident to the progression of periodontal disease. Superoxide dismutase (SOD) and catalase activity, and IL-12 and bc1-2 levels, were decreased at 〉6 mm; total protein and IL-6 concentrations were increased adjacent to 〉6 mm, as compared to 〈3 and 4-6 mm, sites. Apoptotic cells were evident only within gingiva adjacent to 〉6 mm sites. These data suggest that IL-12 is an important factor in the shift from a TH1 to TH2 cell profile and that a favorable gingival microenvironment for hyper-inflammation may develop coincident to progression of periodontal diseases due to decreased bcl-2 and increased IL-6 concentrations within gingiva. These changes in the gingival microenvironment could impair apoptosis and promote enhanced release of reactive oxygen species (ROS) by phagocytes; decreased catalase and SOD activity could promote accumulation of ROS and result in additional tissue destruction.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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