Document 0256
 DOCN  M9460256
 TI    Host responses in patients with generalized refractory periodontitis.
 DT    9404
 AU    Hernichel-Gorbach E; Kornman KS; Holt SC; Nichols F; Meador H; Kung JT;
       Thomas CA; Department of Periodontics, University of Texas Health
       Science; Center at San Antonio.
 SO    J Periodontol. 1994 Jan;65(1):8-16. Unique Identifier : AIDSLINE
       MED/94180279
 AB    Although patients with refractory periodontitis have been widely
       reported, no clear biologic profile of these patients has been noted.
       The purpose of the present study was to evaluate host responsiveness of
       a well-defined group of refractory periodontitis patients by determining
       the effect of a lipopolysaccharide (LPS) challenge on monocyte surface
       receptor density and on the release of inflammatory mediators. Venous
       blood was obtained from 7 refractory periodontitis, 8 stable periodontal
       maintenance, and 8 gingivitis patients with no evidence of
       periodontitis. Mononuclear cells were cultured in either control media
       or media treated with Actinobacillus actinomycetemcomitans (Aa),
       Porphyromonas gingivalis (Pg), or Salmonella typhimurium (S. typh) LPS.
       At 0 and 24 hours supernatants were assayed for prostaglandin-E2 (PGE2)
       and interleukin-1 beta (Il-1 beta) release by ELISA. Using flow
       cytometry the density of specific monocyte surface receptors were
       assayed with Mo3e and LeuM3 monoclonal antibodies (mAb); T-cell CD4/CD8
       ratios were assayed with OKT-3, OKT-4, and OKT-8 mAb. After 24 hours
       incubation with Pg or S. typh LPS, the upregulation of the Mo3e receptor
       was significantly decreased for refractory periodontitis patients (P <
       0.05) when compared to gingivitis and to stable maintenance patients. In
       refractory periodontitis patients the T-cell CD4/CD8 ratio was
       decreased. Upon stimulation with Pg or S. typh LPS, monocytes from
       stable maintenance and refractory periodontitis patients released more
       Il-1 beta (P < 0.05) and PGE2 (P = 0.13 and 0.15) than monocytes from
       gingivitis subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
 DE    Adult  Aged  Analysis of Variance  Chi-Square Distribution  Chronic
       Disease  CD4-CD8 Ratio  Dinoprostone/SECRETION  Female  Flow Cytometry
       Fluorescent Antibody Technique  Human  Interleukin-1/SECRETION
       Lipopolysaccharides/IMMUNOLOGY  Male  Middle Age
       Monocytes/IMMUNOLOGY/SECRETION  Periodontitis/*IMMUNOLOGY  Receptors,
       Cell Surface/IMMUNOLOGY  Support, U.S. Gov't, P.H.S.  Up-Regulation
       (Physiology)  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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