Diagrams 1
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Fig. 3

In this diagram, patterns of epidermal reactions are represented. A common primary patternis characterized by elongation of rete ridges and hyperplasia of the basal unit of the epidermis; the patterns are psoriasiform. Psoriasis is the prototype but such a pattern may also be encountered in early stages of some lichen planus-like reactions. On the other hand, some lesions which are basically lichenoid may evolve in stages and the primary stage oftenhas psoriasiform qualities. Psoriasiform patterns are expressive of immunostimulation with expansion of the domain of the basal unit of the epidermis. In stages. the psoriasiform pattern may give way to immunolytic patterns in which lymphocytes and histiocytes among basal keratinocytes produce death and lysis of neighboring keratinocytes; lytic defects are produced in the basal unit and the superficial unit; then, the superificial unit undergoes compensatory hyperplasia and hypertrophy. The combination of features characterize the lichenoid reaction (particularly, the pattern of the established phase) and are basic to the concept of pathologic apoptosis. The pattern is that of an established lichenoid reaction. For some variants in the stage of resolution, the defect in the epidermal domain is inlaid with firbous tissue and the basement membrane is “duplicated” in the new formed fibrous tissue. The resultant pattern qualifies as a senescent lichenoid reaction. These patterns are commonly encountered in melanocytic neoplasia and tor some examples, the changes may be so extensive that the underlying neoplasm is masked by the reaction. In the diagram, apoptotic cells, lymphocytes and histocytes all are represented in the lytic defect of the established lichenoid reaction and in the fibrous inlay of the senescent lichenoid reaction.

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Fig. 4

In the superficial unit of the epidermis, keratinosomes are released into the interstitial spaces of the epidermis to produce and impervious lipid-rich membrane. Hyperplasia of the superficial unit should be viewed as a contraction of the mucinous avenues of the epidermis. The mucinous avenues allow inflammatory cells and even neoplastic cells access to the epidermial domain.

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Fig. 5

In this diagram, the stages of a lichen planus-like reaction are represented with emphasis on broad domains rather than on cellular events. Normal epidermis is represented on the left. The superifial unit is red and the basal unit is blue. Centrally, there is hyperplasia in psoriasiform patterns, In these patterns, the basal unit is expanded and the superficial unit is thin. The product at the surface is parakeratotic (altered terminal differentiation). The response in the papillary dermis is in part manifested in the vessels of the dermal papillae. In an established lichenoid reaction, the basal unit is compromised and the superficial unit becomes hyperplastic. These reactions, which are so basic in inflammatory disorders, are encountered in melanocytic dysplasias but are seldom afforded significance.

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Fig. 6

Progression are represented in a sequence of diagrams. As the dysplasia progresses, there is an increased prominence of neoplastic cells in the epidermis in both lentiginous and junctional patterns. In addition, the epidermis is stimulated to produce various patterns of hyperplasia (immunostimulation). The curved short lines in stacks are representative of lamellar fibrosis - a marker for host immune response. In progressive phases, the stacks partially outline a rounded nest of atypical cells. With regression of some nests in irregular patterns, the stacks remain behind as a marker for the areas in which nests of cells have undergone regression. With progression, the nests in the papillary dermis increase in number and in size. Patterns in the dermal component determine the difference between a dyaplasia and a thin melanoma with patterns of “vertical growth” as defined in the concept of MDM (as opposed to Clark’s definitions.

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Fig. 7

The blue zones of this diagram might be interpreted as a representation of laterations in the mucinous avenues of the epidermal interstitium in stages of a psoriasiform reaction and then ( as the view shifts from the left to the right) as the patterns that are encountered in a lichen planus-like reaction (including the lytic established phase and at the extreme right the senescent phase in which basement membrane material in laid down in stratified patterns in the fibrous tissue that comes to inlay the lytic defect). They have correspondence with the patterns that are represented in Fig. 3. In psoriasiform hyperplasia, the spaces between individual keratinocytes of the basal unit are expanded and, with the numerical increase in the keratinocytes of the affected unit, are increased in number; they are represented as interconnected blue zones on the left. In the center, the established stage is represented; the lytic defect represents confluence of both the interstitial spaces and a new domain produced by the lysis and coagulaton of basal keratinocytes. In the senescent phase on the right, a portion of the epidermal domain has been replaced by the inlay of fibrous tissue. In the inlay, material of basement membrane-like type is irregularly represented in “duplications.” 

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Fig. 8

This diagram was an attempt to represent sequences in the evolution of a previously undocumented reaction in melanocytic lesions in which the basic patterns were lentiginous and junctional, or compound. For the lesions, the term “sheath cell nevus’ was proposed. The distinctive patterns were interpreted as an adaptation of melanocytic cells to a newly acquired dermal residence. The lesions, so-classified, were subsequently accepted as variations in the category of mild to moderate, premalignant melanocytic dysplasias. The bottome arrow should point in the opposite direction (to the left).

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