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Lichen Planus-like Reaction Patterns (tier 2)
To characterize a lesion as a lichenoid process is to assign such a lesion to a relatively broad category; there
is relatively little specificity in such a characterization. There are subcategories which carry a great deal more specificity. Some examples of the subcategories include: 1.) lichen planus-like, 2.) erythema
multiforme-like, 3.) pityriasis lichenoides-like, and 4.) lupus erythematosus-like. Graft vs host is another potential category but in practice, the patterns can often be accommodated in either the erythema
multiforme-like category, or the lupus erythematosus-like category.
All these categories share the basic quality of infiltrates of lymphocytes and histiocytes at the
dermal-epidermal interface, but this distribution of cells does not in itself define the respective process as lichenoid. A more significant feature is the migration of lymphoid cells into the epidermis among the
keratinocytes, mostly among cells of the basal unit of the epidermis (S3C12P1-1-5). In the pityriasic variants, the interactions between
lymphoid cells and keratinocytes often has an immunostimulatory quality; the result of this interaction is a hyperplasia of the basal unit of the epidermis. In this type of hyperplasia, the mucinous avenues of the
basal unit of the epidermis are widened. The widened mucoid avenues provide migrating lymphocytes and histiocytes easy access to the keratinocytes of the basal unit (S3C12P1-6).
In the process of repair in the lichen planus-like category, necrotic keratinocytes become entrapped in inlays
of fibrous tissue. Fibrous tissue is inlaid in defects in the basal epidermal unit. A portion of the epidermal domain is lost to an expansion of the fibrous matrix of the dermis. In this reparative process, the
entrapped dead cells become the colloid bodies of the dermis (S3C12P1-1-6). In contrast, in both the erythema multiforme-like and the
pityriasic forms of lichenoid reactions, dead keratinocytes tend to move in concert with keratinocytes into the upper reaches of the epidermis to be discharged at the surface. These different patterns, representing
the manner in which dead cells are disposed of, require some attention. It would seem that at least two processes may be at work in the lichen planus-like lesions. On one hand, the degree and extent of damage to
basement membrane may so modify the nature of the interface that fibroblasts are allowed access to the epidermal domain. An additional consideration might be the possibility that, in the lichen planus-like
disorders, the T lymphocytes may activate fibroblasts of the papillary dermis. The end-result is an ingrowth of fibroblasts, across the damaged basement membrane zone, into the fibrin-rich defects in the basal unit
of the epidermis. In the EM-like and the pityriasis-like disorders, the basal unit of the epidermis often is better preserved than in the LP-like disorders. The basal unit in these categories may be sufficiently
preserved to maintain the transfer of keratinocytes from the basal unit into the superficial unit. In this movement of keratinocytes, the necrotic keratinocytes are passively carried upward out of the basal unit,
through the superficial unit, to the surface of the skin. In addition to these altered epidermal kinetics, the basement membrane in EM-like and pityriasic lesions may not be damaged to the same degree as in the
lichen planus-like lesions. Finally, the composition of the lymphoid infiltrates may be different in the EM-like and the pityriasis-like lichenoid reactions when compared to the composition of the lymphoid
infiltrates in the LP-like category.
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