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Melanocytic Dysplasia
with Lichenoid Reaction
A host immune response is an integral part of the reaction to a population of dysplastic (premalignant and neoplastic) melanocytes (Here, I encounter images of Wally Clark but, in
introducing the concept of dysplasia, images of a resistant Bernie Ackerman also compete). In evaluating degree of dysplasia (with cytologic and pattern atypia, exclusive of vertical growth, as parameters of
neoplasia, and with degrees of atypia as the measure of stages of non-invasive neoplasia), there usually is a direct relationship of the degree of atypia with the intensity of the cellular immune response. There are
exceptions with occasional examples of marked dysplasia showing only mild host immune response. There are two components to the host immune response; they include lymphoid infiltrates and fibrosis (often in
laminated patterns). The lymphoid infiltrates usually are perivascular with variable interstitial components. They cluster about nests of atypical melanocytes in the papillary dermis and also invade junctional nests
of melanocytes at the dermal-epidermal interface. The patterns at the dermal-epidermal interface may provide a lichenoid quality. The fibrosing component tends to be, in part, a compensation for the effects of the
lymphoid infiltrates but, on the other hand, it serves to isolate nests of melanocytes in a pattern of sclerosing entrapment (i.e., concentric, fibrous lamellae about individual nests of neoplastic cells). The
immune response is double-edged; it eradicates some, or all, of the neoplastic cells in the papillary dermis; it sequesters the nests in a fibrous shell and, in the process, protects the nests of neoplastic cells
from the injurious effects of the lymphoid cells. Finally, it entraps the nests in a fibrous matrix, restricting opportunities for local growth. If, from cells in such a stage, vertical growth patterns emerge (with
a measure of condescension to those who are unable to recognize vertical growth components), they often initially are manifested in patterns of variant vertical growth (patterns that also would qualify as arrested).
In variant vertical growth, nests of neoplastic cells are widely but regularly spaced in a widened papillary dermis; a minimal representation of neoplastic nests would be 5 or 6 nests in at least strata with cells
showing at least moderate atypia. If the nests of a variant vertical growth component are each isolated by concentric fibrous lamellae, the pattern qualifies as arrested. Patterns of arrested variant vertical
growth may be a favorable prognostic feature, if represented as the sole manifestation of vertical growth.
For some examples, the lymphoid response is diffuse (throughout the lesion, or in a local area). Lymphoid cells in these diffuse infiltrates migrate freely into nests of neoplastic
cells, both in the papillary dermis and at the dermal-epidermal interface; they involve both the lentiginous component and the junctional components. This type of cell-rich response is of halo nevus-like type. This
type of lymphoid response may mask the markers for the underlying melanocytic dysplasia.
Sclerosis in the dermal component of a halo nevus-like reaction usually is of a different order than that at the dermal-epidermal interface in common melanocytic dysplasias. Thin
shells of hyalin outline dermal nests of melanocytes in the dermal component of a regressing halo nevus. In the process, they may partition the nests to isolate individual cells.
In melanocytic lesions of halo nevus-like type (including examples in the category of progressive neoplasia), the melanocytic component may be obscured by the lymphoid infiltrates. Such lesions might be misdiagnosed
as an inflammatory process.
There are occasional lichenoid processes which are associated with epidermal hyperplasia and hyperpigmentation. Melanophages tend to be a feature of the reaction in the underlying
dermis. Some of these reactions are associated with a melanocytic hyperplasia in which the melanocytes are not only enlarged, but also increased in number. The melanocytes of such lesions have prominent pigmented
dendrites and plump, round nuclei. Such lesions may be misdiagnosed as a common premalignant melanocytic dysplasia.
Halo Nevus-like Lesion with Focal Regression
Atypical halo nevi with areas of regression and with prominent lymphoid infiltrates pose a problem in differential diagnosis. Halo nevi of both the common and the atypical type (i.e., lesions with atypical
lentiginous and junctional components that spread in the epidermis away from any dermal components and are associated with the patterns of a melanocytic dysplasia), if they show patterns of regression, pose a
problem in differential diagnosis. Cytologic atypia, often with distinctive cytologic patterns, is a common feature of the dermal component of halo nevi and halo nevus-like lesions; the unwary may be influenced by
the atypia (since it is not a commonly emphasized feature) in a manner that would favor a diagnosis of melanoma. The patterns of regression would then take on added significance. Atypical lesions of halo nevus-like
type, with regression, qualify as atypical halo nevus-like lesions of indeterminate malignant potential. Such lesions should be completely excised and the patient followed.
Xerodermia Pigmentosa
with Melanocytic Dysplasia
Xeroderma pigmentosa is a disease related to defective repair of damaged DNA. The process, from an early onset, progresses with an increased likelihood for the development of skin
tumors, including keratinocytic, melanocytic, and vascular tumors.
Plotnick H, Lupulescu A: Ultrastructural studies of xeroderma pigmentosa. J Am Acad Dermatol 1983;9: 876-82.
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