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S2C8VA3-4: The divisions of the epidermis and the functional utility of the divisions are readily apparent in this lichenoid lesion of lichen planus-like type. In this drawing the basal unit is blue and the superficial unit is red. The normal relationships are represented to the far left. In turn, just to the left of the center of the field, the basal unit is hyperplastic in psoriasiform patterns (in a lichenoid process, this pattern of hyperplasia might be characterized as a primary lichenoid reaction). The black dots are representative of lymphoid cells. In psoriasiform processes the avenues are relatively open to the layer of the keratinized cells and inflammatory cells will have access to the avenues. A rapid turn-over of keratinocytes in both the basal and the superficial units will hamper the process of terminal differentiation; cells will be delivered to the surface before they have completed the metabolic processes required for the formation of an impervious barrier at the surface. We speak of the product of this too rapid delivery of keratinocytes to the surface (in the process of terminal differentiation) as parakeratosis. Changes in the caliber of vessels (i.e., ectasia) accompany the hyperplasia of the basal unit. Just to the right of the center of the field, rete ridges are eroded in a characteristic pattern; they are shortened and have pointed extremities. These alterations are indicative of the erosive effects of a lichenoid reaction of lichen planus-like type (a destructive process characterized by cytolysis and by individual cell necrosis [pathologic apoptosis]). The erosive process of a lichen planus-like, lichenoid process will produce defects in the epidermal domain (at the interface between the surviving epidermis and the dermis). The defects contain cellular debris (necrotic keratinocytes - colloid bodies - Civatte bodies), and loosely aggregated histiocytes and T lymphocytes. Much of the basal unit of the epidermis in the area of the lichenoid reaction can be lost to the erosive process. In compensation, the superficial unit undergoes hyperplasia; its cells individually undergo hypertrophy (they enlarge, become more acidophilic and polygonal, and show prominent tonofilaments). The compensatory changes in the superficial unit of the epidermis in a lichenoid reaction are associated with alterations in the nature of the interstitial avenues; the alterations include closure of the interstitial avenues; inflammatory cells are then denied access to the interstitial avenues of the altered superficial unit. All of the changes in the superficial unit, taken together, qualify as an exaggerated defense process. In addition, the delivery of cells to the surface is delayed; keratinization is allowed to proceed at a leisurely pace. The product at the surface is orthokeratotic, multi-layered, and densely aggregated. The overall pattern is that of an established lichenoid reaction. To the far right, rete patterns are effaced; the epithelium has reverted to more normal arrangements in regard to representation of both a basal and a superficial unit. Defects at the dermal-epidermal interface have been inlaid with new fibrous tissue; in the process, necrotic keratinocytes, originally lying free within the defects at the dermal-epidermal interface, have come to lie in the newly formed fibrous tissue. A portion of the original domain of the epidermis has been lost to the dermis (process of accretive fibrosis). The inflammatory infiltrates have regressed; the pattern is that of a senescent lichenoid reaction.
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S2C8VA3-5: Neutrophils migrate into the epidermis in some psoriasiform disorders. In these examples, the interstitial avenues, being relatively open as a result of the more rapid turnover of cells, accommodate the migrations of infiltrating, inflammatory cells. In some examples, the migrating inflammatory cells find ready access to the most superficial layer of the viable superficial unit. As the altered superficial unit finally commits to terminal differentiation, the dead, keratinized cells, as well as the acute inflammatory cells among the dying cells, are delivered to the surface. The neutrophils, in death, are caught up in the process of inspissation; in this manner, a Munro microabscess is formed. If the delivery of neutrophils to the superficial unit is extensive, the inflammatory cells may release enzymes into the interstitium among viable keratinocytes; the keratinocytes in such foci will be injured and will die. The debris with the exception of remnants of keratinized cell walls will be digested. Partially preserved cell walls of the digested keratinocytes will outline irregular spaces in which the immigrating neutrophils collect. This pattern is spoken of a spongioform pustule. It is characteristic, but not diagnostic, of pustular psoriasis. |
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Subcorneal Pustulosis (including spongioform patterns) 1. subcorneal pustular dermatosis 2. pustular psoriasis 3. impetigo herpetiformis 4. acrodermatitis continua 5. bullous impetigo (with pemphigus foliaceus, and SSSS in the differential diagnosis 6. superficial fungus infections |
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S2C8VA3-6: Some disorders characterized by intra-epidermal infiltrates of neutrophils are listed.
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