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S3C11VA1-3: In the top portion of this drawing, epidermal residents, other than keratinocytes, are identified, including melanocytes in the basal layer and dendritic histiocytes (including Langerhans cells) above the basal layer. In lichenoid reactions, keratinocytes of the basal, functional unit are adversely affected. In addition, the lytic effects of the lichenoid reaction tend to equally affect melanocytes in the area of the reaction. A cellular process, whereby portions of necrotic keratinocytes are phagocytized and then carried into the dermis, has been promoted as explanation for the presence of colloid bodies in the dermis. On the other hand, the colloid body probably represents a necrotic keratinocyte that has been incorporated in newly formed fibrous tissue in the process of accretive fibrosis (a lytic defect in the basal unit of the epidermis is repaired by an inlay of newly formed fibrous tissue). In this process, necrotic keratinocytes are entrapped in the newly formed fibrous tissue. The colloid body only appears to have moved into the dermis. In reality the dermis has “invaded” a defect in the dermis and, in the process, has entrapped the residual cellular debris of the defect. |
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1. Pattern of perivenular island: lymphocytic infiltrates of the dermis 2. Invasive-destructive pattern: a.) lichen planus; b.) lichen striatus; c.) lichen nitidus; d.) pityriasis lichenoides; e.) erythema multiforme 3. Pattern of vasculo-necrosis: a.) pityriasis lichenoides, including patterns with high component of transformed T lymphocytes; b.) lymphomatoid papulosis
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S3C11VA1-4: The numbered items (all to the left of the colons) might be characterized as variations of patterns encountered in experimental models of cell-mediated immunity. The other items (to the right of the colons) are clinical disorders in which the histologic patterns are somewhat similar to those of the experimental models. |
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S3C11VA1-5: Fibrosing patterns at the dermal-epidermal interface include a pattern in which distinctive fibrous lamellae follow the contours of the rete ridges. This reaction is the common response to external irritation of the skin, as seen in lichen simplex chronicus. An entirely different process, with a product of a different nature, is encountered in cell-rich lichenoid reactions of the lichen planus-like type. The accretive fibrosis at the dermal-epidermal interface of such a process occurs in increments; each step tends to be marked by a deposition of basement membrane material. The duplicated membranous portions are variable in amount and in patterns from area to area. The material in PAS+. |
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Epidermal Interstitial Sclerosis (a pattern of repair in lichen planus-like disorders) 1. broad (confluent), lytic zones in the basal epidermal unit, particularly along the contours of the rete ridges (lysis of broad expanses of basal keratinocytes and keratinocytes of the basal unit). 2. collections of cellular debris, lymphocytes, histiocytes, and coagulated keratinocytes in the defects 3. activation of fibroblasts of the sub-basement membrane zone and migration of fibroblasts into the defects. |
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S3C11VA1-6: Features of the repair process in lichen planus-like disorders are listed. Lytic defects in the epidermal domain are characteristic of lichen planus-like disorders. In the repair of the defects, fibroblasts extend into the defects and new fibrous tissue is inlaid. A new basement membrane forms along the surface of the fibrous inlay. If the process is repeated in steps, locally, the basement membrane material will be reduplicated in variable patterns. |
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Epidermal Interstitial Sclerosis (fibrous inlays in defects related to lichenoid reactions) 1. deposition of newly formed connective tissue in the defects of the epidermal domain (accretive fibrosis), and incorporation of inflammatory cells, and necrotic keratinocytes (colloid bodies)of the defects in the connective tissue. 2. formation of a basement membrane along the surfaces of the newly formed connective tissue (reduplication of basement membranes) 3. in this reaction, a portion of the epidermal domain is lost to the dermis; the contours of the epidermis, and the rete ridges are modified; the basement membrane is reduplicated.
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S3C11VA1-7: The loss of epidermal domain at the dermal-epidermal interface in a lesion of lichen planus is an example of focal epidermal interstitial sclerosis. |
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Epidermal Interstitial Sclerosis 1. the lytic, lichenoid process tends to be cyclic in the basal epidermal unit 2. when fully established, the surviving epidermis acquires the characteristics of a superficial unit (all of the keratinocytes of the affected area show the features of keratinocytes that are committed to terminal differentiation. |
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S3C11VA1-8: In response to a defect in the basal unit of the epidermis (a lichen planus-like feature), the surviving superficial unit undergoes hyperplasia; its cells undergo hypertrophy. In addition, the superficial unit delivers a layer of compactly arranged, keratinized debris to the surface. In a sense, the exaggerations of the process of terminal differentiation, as manifested in a lichen planus-like lesion, are a form of endocytic epithelial sclerosis in which the end-product consists of abnormal amonts of keratinized debris.
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