One‐side gingivitis was induced in 21 individuals by local abolition of tooth cleansing for 15–17 days. Adjoining sections of biopsies from the non‐cleansing side as well as from the control side with good tooth cleansing were stained with toluidine blue (pH 1.0), acridine orange (pH 0.5), astra blue (pH 0.2—0.3), alcian blue‐safranin and the EACNAS‐GBC technique in order to demonstrate mast cells specifically. The clinically normal gingiva was found to be rich in mast cells. In the inflamed tissue, the number was increased, especially in the pocket area of the connective tissue. The difference was due to an increase of both mature and, particularly, of immature mast cells. In those cases, where the inflammatory infiltrates were heavy, however, the number of mast cells was reduced in the area of cellular infiltration. The results indicate that products from the bacterial plaque at the gingival margin may directly or indirectly induce proliferation of mast cells in the adjacent connective tissue. Above a certain degree of stress, however the mast cells may respond by degranulation and release their active substances, which by contributing to the inflammatory reaction may enhance the local resistance.
By way of degranulation, the mast cells release a number of biologically active substances into the connective tissue. The present study is concerned with the relation of the gingival mast cells to the pathogenesis of gingivitis. Following fixation in Newcomer's fluid and non‐aqueous staining at pH 0.5 in acridine orange1, topographically defined zones of sections of normal and inflamed marginal gingiva, histologically classified with regard to degree of inflammation, of 56 different individuals have been studied in the fluorescence microscope. The human gingiva was found to be comparatively rich in mast cells. Three main morphological variants were observed and their topographical distribution within the tissue have been described. Marked differences in stainability between mast cells of different areas of the connective tissue have been recorded, and correlated to the state of inflammation, In spite of individual variations in mast cell density, definite patterns of frequency and distribution were observed. The number of mast cells appeared inversely correlated to the density and distribution of the inflammatory cellular exudate within the pocket area of the connective tissue. Consequently, normal gingivae generally contained more mast cells per tissue unit than the moderately inflamed tissue, which, in turn, contained more than the severely inflamed gingivae. Exceptions were found in some moderately inflamed, fibrous gingiva with evidence of strong fibroblastic activity, where there was an increased number of mast cells. On basis of the distribution, frequency and stainability of the mast cells of the gingiva, it is suggested that the mast cells of the regions adjacent to the tooth are subject to an enzymatic degranulation as elicited by products elaborated by the gingival bacterial plaque or possibly by local antigen‐antibody interactions. Substances released by degranulation may then act as mediators during the course of the inflammatory process as well as contribute to the local resistance against injury.
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