dermoepidermal junction


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dermoepidermal junction

[¦dər·mō‚ep·ə¦dər·məl ′jəŋk·shən]
(histology)
The area of separation between the stratum basale of the epidermis and the papillary layer of the dermis.
References in periodicals archive ?
Benign melanocytic nevi (Figure 2, A) show a cobblestone pattern of epidermis and ring pattern, with edged papillae at the dermoepidermal junction (Figure 2, B).
Thickness was measured from the surface of stratum corneum upto the dermoepidermal junction. The mean of these three readings was taken as final reading of that sample.
Her immunofluorescence showed linear deposits of C3 and IgG at dermoepidermal junction along with subepidermal bullae containing fibrous exudates.
Histopathological examination revealed marked epidermotropic haloed lymphocytes linearly aligned along the basal layer with blurred dermoepidermal junction and scant spongiosis (figure 2).
Histopathological examination revealed lentiginous hyperplasia, containing some small melanocytic nests at the dermoepidermal junction. Some nests at the tips of rete ridges had a bridging tendency.
The eczema-, psoriasis-, or dermatitis herpetiformis-like lesions on the extensor surfaces of the upper and lower limbs, especially, were confirmed histologically, but immunopathological evaluations revealed pervasive C3 deposits along the dermoepidermal junction in a microgranular /granular pattern (82%).
It is best characterized pathologically by subepidermal bulla (blister) formation, dermal neutrophilic infiltrate and homogeneous linear IgA deposition at the dermoepidermal junction. The diagnosis of linear IgA bullous dermatosis is confirmed by direct immunofluorescence, which reveals the presence of linear deposition of IgA at the basement membrane zone (BMZ) [2-4].
EB has a wide variety of manifestations and complications, the major phenotypes have been described depending on the level of cleavage of the basement membrane at dermoepidermal junction which are; simplex, junctional and dystrophic.1
(4,8,18) Originally extracted from the blister beetle but now synthesized commercially, (19) cantharidin causes vesiculation at the dermoepidermal junction (6) by destroying intercellular connections.
These T-cells are increased in number at the dermoepidermal junction of normal appearing skin; their aberrant activation leads to an inflammatory response, stimulating tissue destruction and formation of the classic fixed-drug lesion.
They are so named because they are cell mediated immune reactions whose targets are basal keratinocytes that reside above the dermoepidermal junction. (1) The lymphocytes infiltrate the basal layer of the epidermis and cause cytotoxic damage to or kill the keratinocytes by induction of apoptosis.
They comprised such characteristic features as lymphohistiocytic bandlike infiltrate occupying the upper dermis and obscuring the dermoepidermal junction, irregular acanthosis resembling the typical saw-toothed appearance, extensive liquefactive degeneration of the basal layer of the epidermis with subepidermal clefts (Max Joseph spaces), pigmentary incontinence, and numerous cytoid bodies forming huge clusters.