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Spongiotic Dermatitis
Spongiosis is a morphologic correlate of an alteration in the physiologic properties of the inter-cellular matrix of squamous epithelium. The inter-cellular matrix, under certain conditions, can absorb water; in the
process, the added fluid expands the inter-cellular spaces. The inter-cellular matrix is rich in acid mucopolysaccharides (glycosaminoglycans); it is mucinous, hydrophilic, and provides an avenue for the metabolic
support of keratinocytes.
The common dermatitides generally are expressed in patterns that have a spongiotic quality. Initially, the increase in fluid components merely expands the inter-cellular spaces. In more extreme reactions, the
progressive expansion of the inter-cellular space will eventually disrupt the cohesive junctions among keratinocytes; the liberated cells are pushed aside; a fluid-rich space is the result; all things being equal,
the defect is likely to be symmetrically rounded. Such a defect is a spongiotic vesicle.
Spongiosis is a focal process. It is often most pronounced at the tip of a dermal papilla in the inter-rete expanse of the epidermis. In addition, it is a peculiar attribute of the basal unit of the epidermis. The
superficial unit is relatively resistant; the resistance of this unit is related to the process of terminal differentiation - a fatal destiny of cells of the superficial unit. In the process of terminal
differentiation, cellular cohesion is reinforced and the inter-cellular spaces are obliterated by a lipid-rich membrane. In most spongiotic disorders, the edema generally is spotty in distribution; not all
inter-rete expansions in the affected site will be uniformly involved. In contrast, a lichenoid reaction tends to be diffuse along the plane of several adjoining rete ridges and the respective inter-rete expanses.
The distribution of sites of spongiosis is not capricious; it is correlated with the distribution of Langerhans cells of the epidermis. The Langerhans cells are important mediators of immune reactions; T-cell
responses are initiated at the level of antigens that are fixed upon the surface of dendritic histiocytes. These distinctive dendritic histiocytes, in part, reside among keratinocytes of the epidermis; they fix
antigens to their surface and present the antigens. The reaction attracts lymphocytes and migratory histiocytes. In the company of lymphocytes and histiocytes, the events lead to various alterations in the epidemis
in the immediate vicinity of the reactions and the reacting cells; the changes alter the hydophilia of the intercellular matrix. Depending on the nature of the reactive lymphoid cells, the process may be associated
with both a proliferation of cells of the basal unit of the epidermis and an alteration in the contour of the interface between the epidermis and the dermis (i.e., an immunostimulatory reaction). In such a reaction,
keratinocytes are delivered in greater number, and more rapidly, to the superficial unit of the epidermis. In the altered kinetics, the terminal differentiation of cells of the superficial unit may be affected. They
may be delivered to the skin surface before all the phenomena of normal terminal differentiation have been accomplished. The result is manifested histologically in zones of parakeratosis (with a parakeratotic zone
representing a defective barrier at the surface of the skin). The effects of a disease, affecting the basal unit of the epidermis in an immunostimulatory manner, eventually will be manifested in the quality of the
keratin layer. In the process of terminal differentiation, the rate of delivery of keratinocytes, first to the superficial unit and then to the surface, may be accelerated; the freshly delivered cells may not have
an opportunity to fully differentiate terminally as the cells move upward. The alterations in cellular kinetics find expression in the formation of a defective product along the surface. The product clinically is
moist; histologically, the keratinized lamellae are less contracted. In addition, the lamellae retain a small, pyknotic nucleus (i.e., parakeratosis).
The identification of inflammatory cells in the epidermis provides evidence that the basement membrane has been violated. At the dermal-epidermal interface, the focal changes may include vacuolar alterations. If too
much emphasis is placed on the changes at the dermal-epidermal interface, an observer may have problems in making distinctions between a spongiotic and a lichenoid reaction. Generally, lichenoid reactions are more
diffuse at the dermal-epidermal interface; they lack the irregular focality of a spongiotic reaction. In addition, lichenoid reactions are more likely to be associated with both markers for the death of
keratinocytes (i.e., colloid (Civatte) bodies, or apoptotic debris) and the formation of irregular, lytic defects (not the rounded defects of spongiotic vesiculation).
Spongiotic and psoriasiform disorders are closely related; they commonly are combined in a single lesion.
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