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INTERFACE DERMATITIS OF LICHEN PLANUS-LIKE TYPE (tier 2)
Diseases, with infiltrates of lymphoid cells at the dermal-epidermal interface, commonly are characterized as interface dermatitis. This characterization carries little, in the way of
specificity, with it. Conceptually, the sub-epidermal bullous disorders, as well as the lichenoid reactions, are of interface type. To characterize a reaction as lichen planus-like imparts a greater precision. Such
a characterization carries with it implications regarding a relationship in which cytopathic changes (i.e., lysis and coagulation of target cells) affect keratinocytes in the basal unit of the epidermis. Obviously,
the lichenoid disorders form a heterogeneous group; the lichen planus-like category is one among many.
In structuring a lichen planus-like category, we, by definition, give recognition to a stage in the evolution of a rather distinctive response to a destructive lymphoid
infiltrate. The hallmark of the lichen planus-like category is cell-mediated cytopathy; the effects are represented in a piece-meal fashion. The assault on keratinocytes is diffuse at the dermal-epidermal interface
over the space of several rete ridges, but the defects are focal. The defects often are best developed along the perimeter of rete ridges; the lysis and coagulation of keratinocytes is most prominent along the rete
ridges. The rete ridges are progressively eroded; they become thinner and shorter. Seldom are they completely obliterated. The rete ridges are broader at their epidermal attachment than at their dermal extremity;
they have pointed extremities (“saw-toothing”) (S3C19P7-1-7). In addition to the formation of focal lytic defects, lesions of lichen planus-like type
are characterized by a phenotypic transfer of all surviving keratinocytes above the basal layer to the superficial compartment. The keratinocytes above the basal layer enter the pathway of terminal differentiation;
a basal unit, as such, is no longer a feature of the epidermis in the locus of the lesion; this transformation probably seriously impacts on epidermal kinetics. As a result of a slowing in the rate at which
keratinocytes replicate (e.g., the basal layer is the site for replication of cells and, in LP-like disorders, is extensively damaged), fewer cells are available to rapidly fill the lytic defects (S3C18VA2-1, 2 & 4).
Obviously, lichen planus-like lesions have a life history but, if such a process is sampled early on, the patterns are likely to be those of a primary lichenoid reaction; they would
not afford great specificity. Similarly, senescent lesions (senescent patterns characterize atrophic lichen planus) may lose much of what is required for a diagnosis of lichen planus-like dermatitis (S3C19P7-6 & 7, & S3C20P8-1). On the other hand, poorly preserved rete ridges
with pointed extremities, if represented, may provide a clue as to what the patterns might have been at an earlier stage.
Lichen planus-like lesions
are exemplary of the effects of immuno-destructive, cell-mediated immune reactions. Histiocytes as well as lymphocytes are involved as effector cells. In contrast to the spongiotic lesion in which lymphocytes and histiocytes concentrate about a dendritic histiocyte (Langerhans cell) as a nidus, the nidi in lichen planus-like reactions include keratinocytes of the basal layer of the epidermis. The affected keratinocytes undergo lysis and coagulation. Melanocytes perhaps are similarly affected. Dendritic histiocytes are present in the defects among the inflammatory cells and the cellular debris.
Follicles, if involved, show lichenoid changes similar to those at the dermal-epidermal interface (lichen planopilaris) (S3C20P8-2 & 3).
(Sperling LC; Scarring alopecia and the dermatopathologist. J Cutan Pathol 2001;28: 333-42)
Occasional examples of lichen planus are characterized by confluence of the defects at the dermal-epidermal interface; such lesions acquire bullous qualities (S3C20P8-4-7, & S3C21P9-1-3). The bullae show an epidermal roof in
which the features of non-bullous lesions of lichen planus are represented (an almost total commitment to terminal differentiation). In addition, clusters of colloid bodies are common along the floor of the defect.
The diagnosis of bullous lichen planus may also be reinforced by finding the more characteristic changes of lichen planus along the dermal-epidermal interface at the margins of the sub-epidermal defect, if the
attached epidermis is involved by the lichenoid process.
In lichenoid reactions, there is a potential for epidermal hyperplasia with irregular extensions of irregular columns of keratinocytes into the dermis (if the columns extend into the
reticular dermis, the process qualifies as pseudo-epitheliomatous hyperplasia). In the category of hypertrophic variants of lichenoid reactions (which includes occasional examples of lichen planus, as well as
examples of lupus erythematosus), the papillary dermis is expanded. In hypertrophic lichen planus, the widened papillary dermis may show mostly perivascular infiltrates of inflammatory cells; the infiltrates may
contain eosinophils and plasma cells. Focally, at the tips of some of the irregular columns of keratinocytes (the cells manifest
the qualities of a hyperplastic superficial unit, but often with cytoplasmic pallor), the lichenoid patterns will be best developed and, where identified, provide an aid in the characterization of a histologic reaction pattern - an aid that facilitates the interpretation of a pattern that might otherwise present a problem in diagnosis (S3C21P8-4-6).
The erosive effects at the dermal-epidermal interface in a LP-like process are accompanied by attempts at repair. In the interplays, there is accretive growth of the papillary dermis
with inlays of newly formed fibrous tissue within the defects in the basal unit. Basement membrane material may reform in stratified patterns over, and eventually come to lie within, some of these inlays as a repair
is attempted. A well-developed lesion usually will show reduplication of basement membrane (S3C22P10-1-4).
Lichen planus may affect the nails. The histologic patterns basically are similar to those in other sites (S3C23P11-1 & 2). Similarly, lichen planus may affect the mucuous membranes. In such lesions, the granular layer may not be
markedly hyperplastic. In mucous membrane lesions, zones of parakeratosis are more common than over cutaneous lesions. Plasma cells may be found in the dermal infiltrates (S3C22aP10a-1-4). Lesions of “lichen planus” on mucous membranes, in the absence of cutaneous lesions, tend to be chronic and may
evolve into carcinomas. In this sequence, the heterogenecity of the category of lichen planus is revealed.
Lichen Nitidus
Lichen nitidus is a lichenoid reaction characterized by small, papular lesions (S3C23P11-3).
It, like other lichenoid reactions, is variable in its histologic features. The variations relate in part to the stage of the life-history that is represented in the lesion selected for biopsy.
Histologically, focal, small lesions are variably spaced among rete ridges. Some of the lesions are so small that they appear to be localized to a single papilla between neighboring
rete ridges. This appearance, in part, may be misleading; some of the lesions probably replace one or more rete ridges. Early on, the reaction may be pityriasic in character with hyperplasia of both the basal and
superficial units of the epidermis. The lesions tend to be localized to the basal unit of the epidermis, the dermal-epidermal interface, and the adjacent papillary dermis (S3C23P11-4-7). Lymphoid infiltrates, forming each nidus, fill the papillary dermis and are rich in histiocytes. They press upon
the epidermis and migrate into the basal unit. They erode the basal unit. The superficial unit may be minimally altered, or may show hyperplasia with hypertrophy of keratinocytes. The small lesions show
hyperkeratosis, or parakeratosis. Histiocytic giant cells are common in the dermal infiltrates, and often contain melanin pigment granules.
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