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The effect of levamisole on experimental gingivitis in juvenile periodontitis
Author(s) -
BudtzJörgensen E.,
Ellegaard B.,
Ellegaard J.,
Jörgensen F.,
Kelstrup J.
Publication year - 1978
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1978.tb00199.x
Subject(s) - gingivitis , levamisole , oral hygiene , medicine , periodontitis , dental plaque , lymphocyte , antibody , immunology , concomitant , dentistry
In four patients with juvenile periodontitis (group A), five adults with advanced periodontitis (group B), and in four controls (group C) the concentration of serum immunoglobulins, serum complement (C 3 C 4 , and C 5 ) T and B lymphocyte ratio, leukocyte migration inhibition and lymphocyte transformation responses to dental plaque bacteria ( A. viscosus, B. melaninogenicus, F. nucleatum, and V. parvula ) and PPD or PHA, and lymphocyte ATP‐ase activity were assessed before and during development of experimental gingivitis. All the patients in group A and B Had completed extensive periodontal treatment, and at the time of the experiment the periodontal conditions were excellent. Plaque accumulation and gingival inflammation were assessed and blood samples were drawn: at day 0; after plaque accumulation for 14 d (no oral hygiene) (period I); after 14 d with optimal oral hygiene (period II); after plaque accumulation for 14 d (no oral hygiene) and concomitant immunostimulatory treatment with levamisole (period III); after 14 d with optimal oral hygiene. After period I, gingival inflammation and increased gingival fluid flow developed in all groups; however, in group C some of the clinical and immunological responses were slightly enhanced as compared wiht group A and group B. On the other hand, after period III (plaque accumulation + levamisole) more pronounced clinical and immunological changes were recorded in group A and B than in group C, including a significant rise in gingival fluid flow, LIF production, and lymphocyte ATP‐ase activity. The present study has supported the asumption that a state of immunodeficiency can be an underlying, predisposing factor for juvenile periodontitis. The results, however, give only vague information on the nature of this deficiency

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