Morphological aspects of the gingiva in children with Down's syndrome during experimental gingivitis

Abstract

In a previous investigation, children with Down's syndrome (DS) showed an earlier, more rapid and more extensive gingival inflammation than normal healthy control children. These differences in gingival inflammation may be the result of aberrant morphology of the gingiva related to the genetic disorder in DS children. The aims of the present study were (i) to describe the structural composition of "normal" gingiva in DS compared to control children, (ii) to analyse the histological changes in the gingiva during plaque development and (iii) to investigate whether the clinical findings could be supported by morphological observations. The study was carried out in 8 DS and 8 matched control children. Their ages ranged from 5-10 years. Gingival normality was guaranteed by strict oral hygiene procedures. During a period of 21 days in which oral hygiene was abolished, gingival biopsies were taken from buccal sites of deciduous teeth following a predetermined schedule on days 0, 7, 14 and 21. Results on day 0 showed no morphological differences between the DS and control children regarding oral epithelium, junctional epithelium or connective tissue. During the experimental phase of the study, the amount of plaque accumulation in the DS children gave rise to a more extensive gingival inflammation than in the control children. The gingival inflammation in the DS group started earlier and included: (1) an acute inflammatory response, (2) an increase of the junctional epithelium area, (3) an increase of the infiltrated connective tissue area (ICT) and (4) a decrease in collagen fibre density of about 35-40% compared to day 0. The same phenomena were not seen until 7 days later in the control group. Conversely, the development of a perivascular lymphocyte infiltrate (LI) in the DS children was delayed compared to the control group. This may be caused by the impaired delayed-type hypersensitivity response in DS children. The development of 2 separate infiltrates (ICT and LI) in this age group and the different temporal development of ICT (day 7 for the DS and day 14 for the control group) and LI (day 14 for the DS and day 7 for the control group) does suggest different immunological mechanisms for both areas and both groups.

Immunohistological study of neuronal markers in inflamed gingiva obtained from children with Down's syndrome

“…In addition, hyperplasia of both the sulcus and the buccal epithelium was found in the biopsies from the DS children, even in those DS subjects where no clinical signs of infiammation were seen. The observed epithelial hyperplasia is in agreement with findings from studies on the gingival morphology under clinically normal conditions (Cohen et al 1961) as well as after experimentally induced gingivitis (Reuland-Bosma et al 1988a). Thus, DS patients appear to have profound infiammatory involvement of the gingiva.…”

Prostaglandin E2Level in Gingival Crevicular Fluid from Patients with Down Syndrome

“…T h e greater volume of gingival exudate collected in noninflamed sites among the Down syndrome patients as compared with controls is compatible with previous fmdings of a more pronounced outflow of PMN cells in the tissue during a period of experimental gingivitis in Down syndrome patients than in the controls (25,26). In addition, children with Down syndrome also had more gingival inflammation than controls, although the plaque accumulation was similar in the two groups (10).…”

Periodontal diseases: current and future indications for local antimicrobial therapy

“…The evidence provided by studies on trisomy 21 (Down's syndrome) subjects also supports this possible link between susceptibility to periodontitis and susceptibility to gingivitis. Down's syndrome patients exhibit severe periodontal disease early on (Reuland‐Bosma et al , 1986; Modeer et al , 1990) and also manifest greater gingival inflammation much sooner than age‐ and sex‐matched controls, despite similar plaque accumulation (Reuland‐Bosma et al , 1986; Reuland‐Bosma et al , 1988).…”