Abnormal capillary morphology in congenital heart disease

Kontras, Stella B.; Bodenbender, Joann G.

doi:10.1016/s0022-3476(65)81816-9

Cited by 4 publications

(4 citation statements)

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“…For example, Chaney, Eyman & Miller (1979) report that even when severity of mental retardation is held constant, nonambulatory patients are nearly twice as likely to die from pneumonia than ambulatory patients. Furthermore, several investigators (Kontras & Bodenbender, 1966;Chi & Krovetz, 1975) demonstrate morphological abnormalities in the pulmonary vascular bed specific to DS, which predispose to development of pulmonary hypertension and obstructive pulmonary vascular disease. Shaher e/ al.…”

Section: Causes Of Mortalitymentioning

confidence: 99%

Longevity and Mortality in Down's Syndrome

Thase

1982

J intellect Disabil Res

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Section: Causes Of Mortalitymentioning

confidence: 99%

Longevity and Mortality in Down's Syndrome

Thase

1982

J intellect Disabil Res

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“…A faster gingival inflammation may aiso be the result of aberrant morphology of the gingival epithelium (Cohen et al 1961. Kristoffersen et al 1983, The presence in DS of systemic alterations affecting connective tissue and vascularisation, has been suggested (Cohen et al 1961, Claycomb et al 1970, Kontras & Bodenbender 1966. However, the structural composition of the gingiva in children with DS and the early histologic reaction of the tissues towards dental plaque have received little attention.…”

mentioning

confidence: 99%

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

Reuland-Bosma

Liem

Jansen

et al. 1988

J Clinic Periodontology

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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.

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“…Although patients with DS have morphologi cally abnorm al nailbed capillaries [10] and possibly an abnorm al pulmonary vascular bed [11], there is no evi dence for a generalized vascular dysplasia. Since abnor mal collateral channels can appear in individuals pre disposed to cerebral embolism, it is possible that the atrioventricular defect in our patient was a contributing etiology.…”

Section: Discussionmentioning

confidence: 99%