Epidermal mast cells

Green, R.

doi:10.1001/archderm.113.2.166

Cited by 14 publications

(9 citation statements)

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“…The presence of intraepithelial mast cells was observed in periodontal disease19 and in certain oral diseases in which gingiva were involved, such as lichen planus and benign mucous pemphigoid.20'21 Mast cells were present in mucous membranes in which a rapid cellular turnover associated with hyperplasia and intense cell division was observed. 22 Indeed, in the gingival epithelium of patients following prolonged CsA treatment which we described earlier, we showed formation of several basal cell layers indicating rapid cellular turnover.2 Thus, the present study further supports the earlier conclusions that the observed gingival enlargement in human patients suffering from Behcet's disease and following prolonged CsA administration is due primarily to the epithelial response rather than to that of the connective tissue stroma.…”

Section: Discussionsupporting

confidence: 91%

Prolonged Systemic Administration of Cyclosporin A Affects Gingival Epithelium

Pisanty¹,

Rahamim²,

BenEzra³

et al. 1990

Journal of Periodontology

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Gingival biopsies were obtained from 12 patients suffering from Behcet's disease who were treated with Cyclosporin A (CsA) for up to 20 months. Preparations were made for examination with both light and scanning electron microscopy (SEM). Along with known changes in the gingival epithelial structure observed following CsA treatment, we also found unusual clusters of needle-like crystallites embedded in the epithelium, mostly at the base of the acanthotic projections. Toluidin blue staining revealed increased numbers of both intact and degranulated mast cells in the attached epithelium. It is concluded that CsA affects the gingival epithelium and that the clinically observed enlargement of gingival tissue following prolonged treatment with CsA is due primarily to CsA-epithelial interaction.

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Section: Discussionsupporting

confidence: 91%

Prolonged Systemic Administration of Cyclosporin A Affects Gingival Epithelium

Pisanty¹,

Rahamim²,

BenEzra³

et al. 1990

Journal of Periodontology

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“…Disregarding the enigma of causation, we are presenting a reproducible experimental entity of accelerated cell proliferation, hyperplasia and hypertrophy of the epithelium, now known also to be associated with greatly increased numbers of subepithelial mast cells. Other known instances of increase in the number of mast cells which invite comparison with these responses to zinc deficiency are a number of naturally occurring cutaneous and oral mucous membrane lesions (Green et al 1977), psoriasis and experimentally induced hypervitaminosis A.…”

Section: Discussionmentioning

confidence: 99%

Increased numbers of mast cells in the hyperplastic buccal mucosa of the zinc‐deficient rat

Kravich

Meyer

Waterhouse

1981

J Oral Pathology Medicine

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Six weanling male Sprague Dawley rats were fed a diet eontaining 0.4 ppm Zn and seven were fed an identieal diet exeept for 40 ppm Zn. After 4 weeks, speeimens of bueeal mueosa in the region faeing the molar teeth were removed. Paraffin seetions, eut at 6 ^m, were stained with toluidine blue, and traeings made of five seetions per animal, spaeed no less than 60 pim apart. Counts of mast eells over a measured length of seetion were made in a superfieial zone of the lamina propria of 50 ^m width and a deeper zone of 250 pim width.The average number of mast eells per mm in the subepithelial zone of the experimental animals was 15.4, the range 9.2-33.1. The eontrol average was 4.0; the range was 2.9-5.3. No inerease was found in the deeper zone.The epithehum was parakeratotie and its thiekness was inereased two-fold. In the peripheral portion of the seetion, eellular and keratin layers were evenly inereased in thiekness, but in the eentral portion a disproportionate, nearly four-fold inerease oeeurred in the keratin layer and a lesser inerease in the eellular layer.

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“…Mast cells are normal constituents of human skin where they are mostly confined to the upper dermis and can only on rare occasions be found in the epidermis. However, epidermal mast cells are found in conditions characterized by chronic skin inflammation and epidermal cell proliferation (1). In psoriatic lesions, tryptase and chymase containing mast cells are increased in number in the upper dermis, and are frequently in apparent contact with the basal keratinocyte layer (2, 3).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of keratinocyte growth in cell culture and whole skin culture by mast cell mediators

Huttunen

Hyttinen²,

Nilsson

et al. 2001

Experimental Dermatology

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Mast cells are suggested to participate in regenerative processes, but their influence on epithelialization and wound healing has not been well studied. Since mast cells can be found in contact with epidermis in chronic inflammatory skin diseases and venous ulcers, the effect of mast cells on keratinocyte growth was studied. Keratinocytes were cultured in serum-free conditions with (complete medium) or without (basal medium) epidermal growth factor (EGF) and bovine pituitary extract (BPE) to reach subconfluence in a 24-well plate, and the cells were treated with different mast cell mediators histamine, heparin and tryptase, or lysate from HMC-1 cells, a human leukemic mast cell line. Whole skin cultures were used as a model for in vitro wounds to study the effect of mast cells on epithelial outgrowth from skin specimens. Histamine inhibited 3H-thymidine incorporation of keratinocytes dose-dependently by 29% at 1 mM, and 89% at 5 mM histamine. In whole skin culture, histamine inhibited epithelial outgrowth dose-dependently by 64% already at 0.1 mM histamine and maximally (91%) at 1 mM histamine. Heparin inhibited 3H-thymidine incorporation dose-dependently by up to 33% at 2 microg/ml in the absence, but not in the presence, of EGF/BPE. In contrast, in whole skin culture, heparin first inhibited the epithelial outgrowth by up to 27% at 2 microg/ml, but then reversed the inhibition to 30% stimulation at 200 microg/ml. Skin tryptase (0.0285 to 2.85 microg/ml) with or without heparin (0.5 to 20 microg/ml) did not affect thymidine incorporation in keratinocytes. Lysate from HMC-1 cells, but not that from control, neuroblastoma cells, inhibited 3H-thymidine incorporation in keratinocytes dose-dependently, and maximal (47%) inhibition was reached with 16,700 lysed HMC-1 cells/ml. In whole skin culture, HMC-1 lysate inhibited the epithelial outgrowth by up to 36% at 67,000 lysed cells/ml. The results show that mast cells and their mediators are inhibitory to keratinocyte 3H-thymidine incorporation and epithelial outgrowth in vitro, although, the inhibitory effect of histamine was seen at high concentrations suggesting a requirement for close morphologic vicinity of mast cells to keratinocytes. Thus, mast cells are assumed to control epidermal regeneration and to impair epithelialization of chronic ulcers.

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Epidermal mast cells

Cited by 14 publications

References 0 publications

Prolonged Systemic Administration of Cyclosporin A Affects Gingival Epithelium

Prolonged Systemic Administration of Cyclosporin A Affects Gingival Epithelium

Increased numbers of mast cells in the hyperplastic buccal mucosa of the zinc‐deficient rat

Inhibition of keratinocyte growth in cell culture and whole skin culture by mast cell mediators

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