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A large group of skin diseases is characterized by histologic changes categorized as interface dermatitis (Fig. 3-1). At a minimum, a variable combination of leukocyte infiltration of the dermis, vacuolar change of the basilar epidermis, accumulation of melanophages in the upper dermis, and necrosis of keratinocytes must be observed. The term “interface dermatitis” is therefore apt because these findings occur at the interface between the epidermis and dermis. This common thread binds otherwise disparate entities together. Other terms applied to this group of disorders include vacuolar dermatitis, vacuolar interface dermatitis, and lichenoid tissue reaction. Before considering specific diseases, a definition and illustration of the common histologic findings are in order.


Interface dermatitis: diagnostic algorithm.


The term “leukocyte infiltration of the dermis” is cumbersome but more generally accurate than inflammation because, in the case of mycosis fungoides, some portion of the infiltrating lymphocytes is neoplastic and not inflammatory in nature. In all other disorders considered here, lymphoid infiltration represents inflammation. Some degree of upper dermal perivascular accumulation of leukocytes is observed in interface dermatitides. Extension of cells into surrounding collagen may impart a bandlike appearance (or lichenoid appearance, given the similarity to lichen planus) to the infiltrate. Density, pattern, and composition of the infiltrate are variable elements of interface dermatitis that aid in establishing more specific diagnosis.


Vacuolar alteration of the basilar epidermis is also termed “basal vacuolization.” At the junction between the epidermis and dermis, small, often contiguous, discrete vacuoles are observed. This should be distinguished from edema of the basal cells, associated with papillary dermal edema. The vacuolization imparts a ragged appearance to the base of the epidermis, with flattening of the basal cells. When there is sufficient vacuolar destructive interface change, subepidermal clefts form, best exemplified by lesions of bullous lichen planus and grade 3 or 4 lesions of graft-versus-host disease.

Melanin generally resides mostly in keratinocytes and to a lesser degree in melanocytes. Damage to basilar keratinocytes, as part of an interface dermatitis, results in deposition of melanin granules in the upper dermis. The pigment is phagocytosed by macrophages, which become progressively more melanin-laden and are termed “melanophages.” Recognition of melanophages correlates with the stage in evolution of the interface dermatitis and constitutive degree of pigmentation. The presence of many melanophages suggests that the process is well established. In fact, the presence of pigment incontinence should trigger a search for evidence of interface changes, which may be subtle in some cases of interface dermatitis.

Extension of leukocytes into the epidermis is also termed “exocytosis.” The definition of exocytosis also encompasses extension of erythrocytes into the epidermis. The small, round nuclei of lymphocytes are seen to intercalate between keratinocytes, admixed with variable but ...

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