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OTHER LICHENOID DERMATITIDES (tier 2)
Lichen simplex chronicus
is an inflammatory disorder of the skin in which trauma from scratching plays an important pathogenic role but, histologically, the reaction has psoriasiform and mild lichenoid qualities. The response of normal skin to external irritation, such as seen in a scratch papule (picker's nodule), does not include the lichenoid pattern seen in lichen simplex chronicus. This histologic distinction has not been emphasized, but apparently implicates a role for cellular immunity in the histogenesis of lichen simplex chronicus.
The histology of lichen simplex chronicus is, in part, the result of changes induced by external irritation and, in part, the result of lichenoid reactions with features of cell-mediated immunity. The epidermis shows
hyperkeratosis, occasional focal parakeratosis, a prominent granular layer, hyperplasia of the superficial and basal epidermal units, and regular or irregular elongation of rete ridges. The papillary dermis is
widened and fibrotic. In one or more areas, the fibrosing reaction in the papillary dermis produces a pattern of lamellar hyperplasia (32); lamellae of dense
fibrous tissue parallel the contours of the rete ridges. Blood vessels in the upper portion of the dermis are increased in number, tortuous, and surrounded by infiltrates of lymphocytes, histiocytes, and occasional
plasma cells and eosinophils. Focally, the lymphoid cells intermingle among basal keratinocytes of the basal unit. In the inflamed epidermis, individual keratinocytes undergo lysis and coagulation. In focal areas,
the lichenoid reaction may be difficult to distinguish from hypertrophic lichen planus; a distinction may be histologically impossible.
Lichen spinulosus
is characterized by follicular hyperkeratosis with widening of of the lumen of both the infundibulum and the ostium of hair follicles, and atrophy of the outer root sheath, all in the same areas. Lymphoid infiltrates collect in the perifollicular connective tissue sheath at about the level of the infundibulum; in this area, lymphocytes may intermingle with keratinocytes. In the region of the infundibulum, the connective tissue sheath is activated; activated fibrous tissue is loosely cellular. The fibrosing reaction is associated with progressive attrition of the follicular epithelium; the end-result is follicular atrophy. It is debatable whether lichen spinulosis deserves serious attention as a lichenoid and sclerosing perifolliculitis (a follicular occlusive disease), or whether emphasis should be placed primarily on disordered keratinization. The former option seems most likely.
A common variant of a lichenoid keratosis
is seen in association with what is otherwise a typical actinic keratoses. The lichenoid reaction is an expression of a unique, host inflammatory response in an actinically induced keratosis. In such lesions, it often is possible to identify remnants of a keratinocytic dysplasia. The keratosis is usually pigmented in what remains of a basal epidermal unit. In many examples, the patterns adjacent to the area of the lichenoid reaction may resemble those of an atypical senile lentigo (i.e., the pattern of a senile lentigo in combination with keratinocytic dysplasia). Melanophages in the dermis are usually prominent. The pattern of the inflammatory response, all within a single lesion, may vary from a primary, to an established, to a senescent lichenoid process; variations, from one pattern to another, may be represented in a single lesion.
The second clinical variant of lichenoid keratosis known as lichen planus-like, or benign lichenoid keratosis (33) is usually a solitary lesion, most
commonly found on the upper anterior chest of middle aged women, or on the forearms. The changes are lichenoid and may resemble lichenoid actinic keratosis except keratinocytic dysplasia is seldom a prominent
feature. Within the lesion, or at its margin, the epidermis is often hyperplastic; rete ridges are sometimes elongated and hyperpigmented. As in other lichenoid processes, the lesion shows liquefaction degeneration,
colloid bodies, and a dense band of lymphocytes. Some cases have been reported as isolated lichen planus.
OTHER LICHENOID REACTIONS
If the histologic definition of the lichenoid reaction is not restricted to processes in which epidermal migration of lymphocytes play a dominant role, there are at least three additional disorders which qualify on
the basis of liquefaction degeneration at the dermal-epidermal interface, hypertrophy of the cells of the superficial unit, lysis of the basal unit, and pigment incontinence. These processes are lupus erythematosus,
erythema dyschromicum perstans, and lichen sclerosis et atrophicus.
Lupus erythematosus
has the following features of a lichenoid reaction: hyperplasia of superficial unit with compact hyperkeratosis (rare parakeratosis); atrophy of the basal unit (a shift in epidermal kinetics to a phase in which cells above the basal layer are all committed to terminal differentiation); hydropic vacuoles on both sides of a thickened basement membrane; and melanin incontinence. Coagulation of keratinocytes in areas of lysis is not a prominent feature of the established lesion. As a consequence, colloid bodies are infrequent in the dermis and, when identified, seldom are as compactly aggregated as in a lesion of lichen planus. In general, lymphocytes mostly are confined to the perivascular spaces of the reticular dermis. They are relatively sparse in the papillary dermis. They are relatively infrequent on the epidermal side of the basement membrane. Migratory histiocytes often are distributed along the dermal side of the basement membrane.
The lichenoid reaction at the dermal-epidermal interface in established lesions of lupus erythematosus is relatively cell-poor. On the other hand, the follicular changes in lupus erythematosus usually qualify as a
cell-rich lichenoid reaction. Cutaneous mucinosis often is a significant feature of a lesion of lupus erythematosus (34).
In erythema dyschromicum perstans (EDP), the active margin shows the following lichenoid features: focal lysis of keratinocytes in the basal epidermal unit; mild perivascular lymphoid infiltrations with
migration of loosely aggregated lymphocytes into the zones of epidermal lysis; incontinence of melanin with storage of melanin in dermal melanophages; and variable epidermal hyperpigmentation. EDP qualifies as both
a lichenoid reaction and a melanoderma (2). This combination may be shared in other processes such as melanoderma toxica, fixed drug reaction, poikiloderma of Civatte, berloque dermatitis, and lichenoid
melanodermatitis (35).
In extra-genital lichen sclerosis et atrophicus, the epidermis usually shows hyperplasia of the superficial epidermal unit with atrophy and effacement of the basal epidermal unit. Hydropic vacuoles form at the
dermal-epidermal interface. In early lesions, the response at the dermal-epidermal interface is cell-rich. It has features of a primary lichenoid response (36).
A peculiarity of an established lesion of LS&A is the confinement of lymphoid infiltrates to the interface between the widened, edematous and hyalinized dermis (para-epidermis), and the deeper portion of the
reticular dermis that is relatively spared (36).
Mixed Lichenoid Dermatitis: Rarely, a lichenoid reaction has both cell-rich and cell-poor qualities, either in a single lesion, or in multiple disseminated lesions (12). Some of these rare disorders, clinically and histologically, share the features of both lichen planus and lupus erythematosus (overlap syndrome).
They are "mixed" lichenoid disorders and are characterized by chronic, acral lesions which lack small, lichenoid papules. Involvement of the palms and soles, and destruction of nails are variable,
additional features. Occasionally, mucous membranes are involved. Lesions of the face are less common than the acral lesions. The acral lesions tend to be cell-rich with well-developed, lytic clefts and focal
clusters of colloid bodies. Lesions on the face show cell-rich and cell-poor patterns. In the latter areas, the basement membrane is focally thickened and hyalinized. Fibrosis of the papillary dermis and plasma
cells in the infiltrates are additional features. Anti-nuclear antibodies have been identified in a some of these patients. The immunofluorescent changes resemble lichen planus. Occasionally, a thin, linear band of
immunoglobulins and complement is identified at the dermal-epidermal junction. Such lesions qualify as LE-LP overlap syndrome.
Cicatricial pemphigoid, in its chronic phase, is a lichenoid reaction with lytic clefts, or vesicles at the dermal-epidermal junction. The papillary dermis is widened and fibrotic. It contains a band-like
infiltrate of lymphocytes and histiocytes with a variable component of plasma cells and eosinophils. Histologically, there are some similarities between "mixed" lichenoid dermatitis and the lymphocytic
phase of cicatricial pemphigoid.
False, or questionable, “lichens,” which are excluded from this chapter, include lichen myxedematosus, lichen scrofulosorum, lichen urticatus (papular urticaria), and lichen aureus. Lichen and macular amyloidosis
qualify as cell-poor lichenoid reactions. The globular deposits of amyloid may be a counterpart of the fibrous component of “colloid bodies;” they may be a deranged product of keratinocytes (37). In macular amyloidosis, there is, in addition, hypermelanosis, melanocytic hyperplasia, and melanoderma. In some examples, the lichenoid reaction
and pigmentation occur in the absence of demonstrable amyloid (pigmented pruritic patches of Waisman).
The basic insult in a lichenoid reaction produces attrition of the basal epidermal unit. A poorly organized epidermal hyperplasia is an infrequent reaction to the lytic process. In some examples of this reaction,
columns of pale squamous cells invade the reticular dermis. In some examples, the invading epithelium is arranged in the patterns of small, angulated nests (carcinoma-like patterns). These patterns of
pseudoepitheliomatous hyperplasia may involve multiple lesions and are, then, sometimes included in the category of multiple keratoacanthomas. This form of epidermal hyperplasia in a lichenoid reaction may be an
expression of immunostimulation.
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