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Cellular aspects of and effects on the gingiva in children with Down's syndrome during experimental gingivitis
Author(s) -
ReulandBosma Wimke,
Liem Robert S. B.,
Jansen Henk W. B.,
Dijk L. Johan,
Weele Leo Th.
Publication year - 1988
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1988.tb01588.x
Subject(s) - gingivitis , connective tissue , medicine , inflammation , phagocytosis , oral hygiene , dentistry , physiology , immunology , pathology
In a previous experimental gingivitis study, it was shown that in children with Down's syndrome (DS), gingival inflammation started earlier, was more extensive and developed faster, than in normal healthy control children. In both groups, the start of the process was accompanied by an acute inflammatory response and an increase of the infiltrated connective tissue area (ICT). The purpose of the present study was to investigate how these facts were reflected at a cytological level. The study was carried out in 8 DS and 8 matched control children. Their ages ranged from 5–10 years. A “normal” healthy gingiva was attained after strict oral hygiene procedures. During a period of 21 days in which oral hygiene was abolished, gingival biopsies were taken on days 0, 7, 14, and 21. In both groups, junctional epithelium (JE) and ICT contained low numbers of polymorphonuclear leucocytes (PMNs). The start of the inflammation (day 7 for the DS and day 14 for the control children) was marked by a significant positive correlation between the numbers of PMNs in the JE and the ICT, and a significant increase of the numbers of PMNs in ICT. In ICT, a concomitant decrease in collagen fibre density was observed. In the control group, the decrease correlated with the numbers of PMNs in ICT, which suggests that this collagen breakdown is caused by PMN products. After the initial decrease, the collagen fibre density remained fairly constant in this group throughout the study. In the DS group, there was a tendency to a further decrease in the ICT3 area, correlated with the numbers of PMNs in ICT, Whereas the PMN response reflected the start of the clinically assessed inflammation, the lymphocytes did not follow this pattern. The DS children showed an impaired lymphocyte migration; in the control children, the numbers of lymphocytes increased significantly. On days 7 and 21. the numbers of lymphocytes found in the DS were significantly lower than in the control children. The early PMN response and the impaired lymphocyte migration may be the result of impaired lymphocyte and/or PMN function in DS children. These factors constitute the more likely explanation for the specific character of the gingival inflammation in DS children.