Differential Diagnosis
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Discussion
Atrophic lichen planus and atrophic discoid lupus erythematosus pose problems in differential diagnosis histopathologic because they have several findings in common, among them compact orthokeratosis, focal hypergranulosis, epidermis thinned and associated with flat rete ridges and dermal papillae, vacuolar alteration along the dermoepidermal junction, individual necrotic keratocytes, infiltrates of lymphocytes of variable density, melanophages, and altered collagen in the upper part of the dermis. Despite the many attributes shared by the two very different diseases whose lesions longstanding end in atrophy, they can be differentiated histopathologically by an exceedingly thin epidermis often in discoid lupus erythematosus, overtly wedge-shaped hypergranulosis in repeatable manner in lichen planus, a thickened epidermal basement membrane in discoid lupus erythematosus, peri-infundibular fibrosis in lichen planus, and melanophages situated beneath a thickened basement membrane in discoid lupus erythematosus, but scattered throughout a fibrotic papillary dermis in lichen planus.
Atrophic discoid lupus erythematosus tends to occur not only at sites exposed to sunlight, e.g., malar eminences, nose, and cheeks, but also on covered places such as the hairy scalp, in the ears, and, sometimes, on mucous membranes. In contrast, lesions of lichen planus have no predilection for sites exposed to sunlight and favor flexor surfaces of the forearms, glans penis, and oral mucosa. When lesions of discoid lupus erythematosus pass through all of the stages in their sequence chronologic, they come to atrophy, that being the terminus that follows on macules and patches of erythema, scaly papules and plaques, including plugs of horny material in widened infundibula, and hyper- and hypopigmentation. In contrast, lichen planus does not eventuate often in atrophy, but resolves usually with hyperpigmentation only. When lesions of lichen planus proceed to atrophy they appear as hyperpigmented macules that are depressed slightly below the surface of the skin. Those atrophic lesions represent regression of typical violaceous polygonal papules that represent lesions of lichen planus developed fully.
It also must be noted that the epidermis in an early lesion of discoid lupus erythematosus may be thinned, but not as dramatically as in a late one. Furthermore, in an early lesion, there is no fibrosis in the upper part of the dermis and no signs clinically of atrophy clinically.
Atrophy in lichen planus and in discoid lupus erythematosus is of the superficial type characterized clinically by a slight depression below the skin surface, shininess, wrinkled appearance, pigmentary alteration, telangiectases, and absence of hairs. Superficial atrophy results largely from obliteration of dermal papillae by fibrosis and also from loss of rete ridges secondary to the fibroplasia. The loss of volume of dermal papillae accounts for most of the atrophy seen clinically. A second type of atrophy, not at play in either discoid lupus erythematosus or lichen planus, is typified by loss mostly of elastic fibers, but also of collagen, from the reticular dermis. The manifestation clinical of this deeper type of atrophy is anetoderma, including so-called macular atrophy that, paradoxically, actually is papular. A third, and last, type of atrophy involves the subcutaneous fat where pronounced loss of adipocytes results in an appearance clinical of one or more gullies. Stereotypical examples are lipodystrophy, the end stage of the panniculitis of discoid lupus erythematosus, known also as lupus profundus, and pancreatic panniculitis.
In sum, atrophic lichen planus and atrophic discoid lupus erythematosus sometimes may be difficult to distinguish from one another, clinically and histopathologically. If attention is paid to the contrasting criteria listed in the columns at the outset of this chapter, differentiation histopathologic can be accomplished with facility in most instances.
Atrophic lichen planus and atrophic discoid lupus erythematosus pose problems in differential diagnosis histopathologic because they have several findings in common, among them compact orthokeratosis, focal hypergranulosis, epidermis thinned and associated with flat rete ridges and dermal papillae, vacuolar alteration along the dermoepidermal junction, individual necrotic keratocytes, infiltrates of lymphocytes of variable density, melanophages, and altered collagen in the upper part of the dermis. Despite the many attributes shared by the two very different diseases whose lesions longstanding end in atrophy, they can be differentiated histopathologically by an exceedingly thin epidermis often in discoid lupus erythematosus, overtly wedge-shaped hypergranulosis in repeatable manner in lichen planus, a thickened epidermal basement membrane in discoid lupus erythematosus, peri-infundibular fibrosis in lichen planus, and melanophages situated beneath a thickened basement membrane in discoid lupus erythematosus, but scattered throughout a fibrotic papillary dermis in lichen planus.
Atrophic discoid lupus erythematosus tends to occur not only at sites exposed to sunlight, e.g., malar eminences, nose, and cheeks, but also on covered places such as the hairy scalp, in the ears, and, sometimes, on mucous membranes. In contrast, lesions of lichen planus have no predilection for sites exposed to sunlight and favor flexor surfaces of the forearms, glans penis, and oral mucosa. When lesions of discoid lupus erythematosus pass through all of the stages in their sequence chronologic, they come to atrophy, that being the terminus that follows on macules and patches of erythema, scaly papules and plaques, including plugs of horny material in widened infundibula, and hyper- and hypopigmentation. In contrast, lichen planus does not eventuate often in atrophy, but resolves usually with hyperpigmentation only. When lesions of lichen planus proceed to atrophy they appear as hyperpigmented macules that are depressed slightly below the surface of the skin. Those atrophic lesions represent regression of typical violaceous polygonal papules that represent lesions of lichen planus developed fully.
It also must be noted that the epidermis in an early lesion of discoid lupus erythematosus may be thinned, but not as dramatically as in a late one. Furthermore, in an early lesion, there is no fibrosis in the upper part of the dermis and no signs clinically of atrophy clinically.
Atrophy in lichen planus and in discoid lupus erythematosus is of the superficial type characterized clinically by a slight depression below the skin surface, shininess, wrinkled appearance, pigmentary alteration, telangiectases, and absence of hairs. Superficial atrophy results largely from obliteration of dermal papillae by fibrosis and also from loss of rete ridges secondary to the fibroplasia. The loss of volume of dermal papillae accounts for most of the atrophy seen clinically. A second type of atrophy, not at play in either discoid lupus erythematosus or lichen planus, is typified by loss mostly of elastic fibers, but also of collagen, from the reticular dermis. The manifestation clinical of this deeper type of atrophy is anetoderma, including so-called macular atrophy that, paradoxically, actually is papular. A third, and last, type of atrophy involves the subcutaneous fat where pronounced loss of adipocytes results in an appearance clinical of one or more gullies. Stereotypical examples are lipodystrophy, the end stage of the panniculitis of discoid lupus erythematosus, known also as lupus profundus, and pancreatic panniculitis.
In sum, atrophic lichen planus and atrophic discoid lupus erythematosus sometimes may be difficult to distinguish from one another, clinically and histopathologically. If attention is paid to the contrasting criteria listed in the columns at the outset of this chapter, differentiation histopathologic can be accomplished with facility in most instances.
Ref:
Differential Diagnosis In Dermatopathology I, Ii, Iii, Iv.chm
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