S2C9P3PsoriasicMisc

S2C9P3-1: (seborrheic dermatitis): The common association between spongiotic and psoriasiform disorders is illustrated in this field. Focally, the spongiotic changes qualify as early spongiotic vesiculation. This degree of edema would be unacceptable in uncomplicated psoriasis.

In the category of psoriasiform disorders, psoriasis is prototypic. A lesion of psoriasis, in full expression, embodies all the qualities of the category, but remains something in the nature of a perverse tissue response. It is not a defined antigen-antibody response and is deficient in some of the defining features of cell mediated immunity.

S2C9P3-2 a, b, & c (psoriasis): This is classic psoriasis with a parakeratotic cap, inspissated, intracorneal abscesses (Munro micro-abscesses), thin suprapapillary plates, regularly elongated rete ridges, minimal inter-cellular edema (expansion of the mucinous interstitium), and edematous, club-shaped dermal papillae.

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	In S2C9P3-2 a, b, & c, the basic reaction pattern is that of relatively pure basal unit hyperplasia. The basal unit is the replicating unit and, commonly, in its hyperplasias, cells are delivered more rapidly to the surface of the skin. As a consequence, there is an interference with the sequences which provide a normally keratinized product at the skin surface. A rush of cells to the surface is manifested by a moist product in which defunct nuclei (parakeratotic debris) are preserved. In addition, the rush to the surface compromises the closure of the inter-cellular avenues of the superficial unit, interfering with the formation of an impervious lipid membrane (a product derived in part from keratinosomes). In all these distortions, neutrophils are attracted to the poorly defended superficial unit. They, like the neighboring keratinocytes of the superficial unit (i.e., cells caught in the process of terminal differentiation), are carried to the surface. The neutrophils persist among the dead keratinocytes of the keratin layer in the pattern of an inspissated pustule. The Munro microabscess is a marker for the presence of a defective immunological and physical barrier at the surface of the skin. More striking is the relative absence of lymphocytes in the vicinity of activated dendritic histiocytes (Langerhans cells) in the hyperplastic basal unit. This deficiency contrasts strongly with the prominence of lymphocytes in the epidermis in the common immune-mediated psoriasiform disorders (See P3-2c above in which the apparently naked nuclei of histiocytes are obvious among keratinocytes of the basal unit, but are not associated with lymphocytes. Perhaps, the naked nuclei are merely migratory histiocytes and should not be compared with the true (fixed) dendritic histiocyte [Langerhans’ cell]).

S2C9P3-3 & 4 (psoriasis): On the left, the suprapapillary plate is thin. The extremity of the dermal papilla is edematous and somwhat club-shaped. Inflammation is minimal. A dilated, tortuous capillary extends close to the dermal-epidermal interface. There is mild intra-cellular edema (as manifested by the perinucear halos) in the overlying epidermis. In P3-4 (right), inflammatory cells extend in continuity from the edematous papillary dermis into the epidermis in an area of mild spongiosis (pattern of squirting papilla). The cells of the epidermal infiltrates are mostly neutrophils and histiocytes. A few of these cells are present in defects among keratinocytes in the region of the granular layer. An abscess, on its way to inspissation, has arrived at the surface, in concert with the keratinized lamellae of a zone of parakeratosis. The lesion in the parakeratotic cap is a Munro microabscess.

S2C9P3-5 & 6 (psoriasis): In P3-5 (left), a well-developed Munro abscess is represented. Neutrophils are also evident in the superficial unit of the epidermis among viable keratinocytes. In the vicinity of the fuschia arrows, the patterns have a spongioform quality. At the tip of the blue arrow, a neutrophil is captured among viable keratinocytes of the superficial unit. Lipid membranes, to allow for this pattern of migration, must be deficient. Perhaps psoriasis is a disease of defective formation of keratinosomes. Below the blue arrow and just to the left, there is a sinuous defect among the keratinocytes. This is an open interstitial avenue, but may be the tract of the dendritic process of a Langerhans cell. Note the paucity of mature lymphocytes in the epidermal domain. On the right (P3-6), a late stage in the evolution of the interplay between basal and superficial units of the epidermis in psoriasis is represented. There is minimal inter-cellular edema of the basal unit of the epidermis over the bulbous extremity of a club-shaped dermal papilla. A parakeratotic cap contains an inspissated microabscess. The neutrophils in company with terminally differentiating keratinocytes have been moved to the surface layer of the epidermis and, there, the neutrophils have died.

S2C9P3-7 (pustular psoriasis): The migrating neutrophils are more numerous; they have produced lytic defects that are outlined by the keratinized cell membranes of dead keratinocytes. The keratinocytes mostly have been lysed by the effects of the enzymes that neutrophils have released. The remnants of the cell walls of dead keratinocytes form a lattice; neutrophils have collected in the defects. The cell-rich patterns qualify as a spongioform pustule.

The richness of the exudate in the superficial unit of the epidermis in psoriasiform disorders and in psoriasis reflects the perviousness of what in its normal state is an impervious barrier at the surface of the skin. The barrier consists of layers which comprise the superficial functional unit of the epidermis. In part, it includes the keratin and granular layers. From another perspective, it includes the component epidermal cells whose long axes are parallel to the surface of the skin. These also are the cells which are either committed to terminal differentiation, or have accomplished terminal differentiation. It seems reasonable that neutrophils usually do not actively infiltrate the epidermis beyond the reaches of the population of viable keratinocytes. Neutrophils, among the necrotic keratinocytes of the keratin layer, probably have moved into the site passively in company with the continuous movement of cells to the surface, as keratinization and cell death (terminal differentiation) are completed. Their presence in viable epidermis is evidence of open, watery, inter-cellular, mucinous avenues.

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