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Collagen Fibers and Inflammatory Cells in Healthy and Diseased Human Gingival Tissues: A Comparative and Quantitative Study by Immunohistochemistry and Automated Image Analysis
Author(s) -
Séguier Sylvie,
Godeau Gaston,
Brousse Nicole
Publication year - 2000
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2000.71.7.1079
Subject(s) - cd68 , cd8 , pathology , connective tissue , gingivitis , immunohistochemistry , cd11c , sirius red , medicine , periodontitis , cd20 , cd3 , extracellular matrix , immune system , chemistry , immunology , dentistry , phenotype , gene , biochemistry
Background: Periodontal disease is histologically characterized by the degradation of extracellular matrix components associated with a gingival infiltration of inflammatory cell populations. The purpose of this in situ study was to quantify inflammatory cell subsets and the area fraction (AA%) occupied by collagen fibers in healthy and diseased upper gingival connective tissue in order to investigate the association, if any, between collagen loss and inflammatory cell infiltrate. Methods: Paraffin gingival tissue sections from 10 healthy controls (C), 9 patients with gingivitis (G), and 10 patients with severe chronic periodontitis (P) were immunohistochemically stained by antibodies against CD45, CD3, CD8, CD20, CD68, TIA‐1, and GrB molecules, and the collagen fibers were stained using sirius red F3Ba. The quantitative evaluations of inflammatory cell numbers and the AA% occupied by collagen fibers were performed by morphometric and automated image analysis. Results: In group P, CD45+, CD20+, CD68+, TIA‐1+, and GrB+ cell numbers were significantly increased ( P <0.05) when compared to both C and G groups. The present study revealed significant differences ( P <0.01) between means of AA% observed in group C (63%), group G (46%), and group P (26%), and AA% of group G and group P was inversely correlated with the numbers of TIA‐1+ cells ( P <0.01) and GrB+ cells ( P <0.01 and P <0.05, respectively). Conclusions: This study showed great differences in the number of the distinct inflammatory cell subsets according to the severity of the periodontal disease and suggested that activated cytotoxic cells could play a pivotal role in the loss of collagen fibers observed during these pathological states. During periodontitis, collagen loss was significantly correlated with all inflammatory cell subset numbers. Finally, the quantitative evaluation of the area fraction occupied by gingival collagen fibers may reflect the clinical severity of the periodontal disease. J Periodontol 2000;71:1079‐1085.