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Failure of macrophage activation in destructive periodontal disease
Author(s) -
Chapple Cheryl C.,
Srivastava Mukesh,
Hunter Neil
Publication year - 1998
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(1998110)186:3<281::aid-path200>3.0.co;2-7
Subject(s) - macrophage , periodontitis , tartrate resistant acid phosphatase , basic fibroblast growth factor , pathology , immunoperoxidase , immunohistochemistry , monoclonal antibody , acid phosphatase , cd68 , biology , lesion , immunology , m2 macrophage , medicine , antibody , growth factor , biochemistry , in vitro , receptor , enzyme
Macrophage populations in 22 biopsies of untreated advanced periodontitis were compared with those in 26 biopsies of clinically healthy (minimally inflamed) gingival tissue. The immunohistochemical investigation used high specificity monoclonal antibodies, including a pan‐macrophage marker and probes for acute inflammatory, resident histiocytic, and reparative phenotypes. Macrophage expression of the functional activation markers MHC class II, basic fibroblast growth factor (bFGF), acid phosphatase (AP), and tartrate‐resistant acid phosphatase (TRAP) was also examined. The study showed that advanced periodontitis and minimally inflamed tissues displayed similar distribution patterns and numbers for the macrophage phenotypic markers: there were, however, regionally‐specific differences in the populations. In the advanced periodontitis lesion, there was little evidence of macrophage activation for the expression of HLA‐DR, bFGF, and TRAP, although strong expression of HLA‐DR and bFGF was observed in association with blood vessels. Macrophages expressing AP showed a distinct regional distribution; this, however, was not associated with foci of degenerate plasma cells. The apparent failure of recruitment and activation of macrophages may in part be both a cause and a consequence of the pathological features of this disease. Copyright © 1998 John Wiley & Sons, Ltd.