Interface dermatitis

By: Dr. Daulat Ram Dhaked

Introduction• Primary pathology involves the "interface,“• Pattern of inflammation in which lymphocytes aggregate around the

dermal-epidermal junction, obscuring the junction at scanning magnification.

• T-cell-mediated cytokine damage is most likely mechanism • -> cytotoxic damage, or apoptosis of keratinocytes • -> become detached from their neighbors, • -> become round, • -> undergo a sequence of events,

– degradation of nuclear DNA,– lysis of nuclei – coagulation of proteins in cytoplasm, without spilling enzymes

• Termed as dyskeratotic cells, • When they find their way into papillary dermis, termed as colloid,

cytoid or Civatte bodies

Morphological changes

1.Primary changes A) Basal cell vacuolization

(Vacuolar alteration):• Most prominent feature• Partial or complete destruction of

basal cells and other structures due to expansion of cytoplasm produces tiny vacuoles along dermoepidermal junction,

• Total absence of basal cell with spinous keratinocytes abutting papillary dermis results in squamatization of basal layer.

• Confluent basal cell damage results in formation of clefts and subepidermal vesicles.

Vacuolar changes of basal cells with sparse perivascular lymphocytic infiltrate. Morbilliform drug eruption (H and E, ×100)

B) Apoptotic keratinocytes (Colloid or Civatte bodies) : • Seen as small, rounded,

eosinophilic, hyaline, anucleate structures,

• Are slightly smaller than basal keratinocyte.

• May be seen in basal layer, in upper papillary dermis, individually or in clumps, or in mid- and upper spinous layers, Colloid (Civatte) bodies at dermo-

epidermal junction with basal cell vacuolization with melanophages in the upper papillary dermis. Lupus erythematosus (H and E, ×400)

C) Obscuring of dermo-epidermal junction by inflammatory cells :

• Lymphocytes are M/c• Eosinophils,

neutrophils, mast cells, and histiocytes may be seen.

• Obliterates clear distinction between epidermis and papillary dermis

• Density of inflammatory infiltrate is variable

Several lymphocytes in basal cell layer obscuring dermo-epidermal junction with basal cell vacuolization and few apoptotic keratinocytes in lower spinous zone. Erythema multiforme (H and E, ×400)

2. Secondary changes A) Epidermal changes: • Depend on disease, time of biopsy in course of

evolution or devolution of disease, and site of biopsy.

• Acanthosis, hypergranulosis • Thick compact orthokeratotic stratum corneum • Thin and atrophic epidermis, • Irregular epidermal hyperplasia

B) Papillary dermal changes: • Secondary to basal cell damage. • Papillary dermis undergoes expansion

to accommodate inflammatory infiltrate,

• Fibrosis or sclerosis, • "Incontinence" of melanin into

papillary dermis• Melanophages in papillary dermis C) Other changes• Mucin deposits in reticular dermis• Perivascular and periadnexal infiltrates

of lymphocytes in mid- and deep reticular dermis,

• lymphocytic lobular panniculitis

Sclerosis of thickened papillary dermis with smudging of dermo-epidermal junction. Note bluish-grey mucin in upper reticular dermis. LE

Thickened papillary dermis with sparse lymphocytic infiltrate and numerous melanophages. persisting basal cell vacuolization. Lichen planus pigmentosus

Classification of Interface Dermatitis

b) Prominent infiltrate in papillary dermis aligned in lichenoid pattern (Lichenoid-interface dermatitis): • Dense band-like infiltrate in

papillary dermis • Basal cell vacuolization may be

inconspicuous or absent.

1. Histologically, classified as:a) Prominent basal cell vacuolization (Vacuolar-interface dermatitis): • Basal cell vacuolization is most

prominent• Variable perivascular and interstitial

infiltrates of lymphocytes.

2. Le Boit’s classification depending on epidermal changes

a) Acute cytotoxic type: • Characterized by basal cell vacuolization with lymphocytes

infiltrating lower epidermis • Scattered necrotic keratinocytes at various levels in epidermis. • Entire process is rapid, Does not interfere with epidermal

keratinization, • Horny layer is unaffected and maintains its normal basket weave

arrangement. • EM is prototype. • Few necrotic keratinocytes: Early EM, morbilliform drug and viral

eruptions, • Numerous necrotic keratinocytes: Fully developed EM, acute LE,

TEN, radiation and chemotherapy-induced skin damage, FDE (eosinophils, neutrophils, and melanophages), pityriasis lichenoides (parakeratosis).

Numerous necrotic keratinocytes scattered in lower spinous zone with lymphocytes obscuring dermo-epidermal junction. Note normal basket weave stratum corneum. EM

E M . There is obscuration of the dermoepidermal junction with vacuolar alteration of the basal keratinocytes (A and B). Necrotic keratinocytes may be individual or confluent (B). The process may progress to frank subepidermal vesiculation (C). Toxic epidermal necrosis with confluent, fullthickness epidermal necrosis (D). Note the preservation of the basket-weave horn. Density of dermal inflammatory infiltrate is inversely proportionate to epidermal damage. Fairly dense in EM, Very sparse or even absent in TEN. Eosinophils are not seen as a rule

Fixed drug eruption. There is obscuration of the dermoepidermal junction with a mixed inflammatory cell infiltrate composed of lymphocytesnumerous eosinophils and neutrophils (A and B). Necrotic keratinocytes can be identified throughout all levels of the epidermis (A)and may tend toward confluence. A mixed perivascular infiltrate can be present in the deep dermis (C).

b) Premature terminal differentiation: • Refers to an early development of a thick granular layer and

compact stratum corneum• A/w dense lichenoid infiltrates of lymphocytes. • LP is prototype• Dense lymphocytic infiltrates: LP, lichenoid keratosis, lichenoid

drug reaction especially photolichenoid, acute GVHD, DLE, lichen striatus.

• Few lymphocytes: Dermatomyositis, lichenoid GVHD. • Mixed infiltrates: Lichenoid drug reaction (eosinophils),

keratosis lichenoides chronica (plasma cells).

c) Irregular epidermal hyperplasia: variant of above • Show marked irregular epidermal hyperplasia • Seen in hypertrophic LP, verrucous DLE, and some long-

standing lichenoid drug eruptions.

Lichen planus. There is compact orthokeratosis with no parakeratosis, wedgeshapedhypergranulosis, jagged acanthosis of the epidermis, and a band-like lymphocyticinfiltrate obscures the dermoepidermal junction (A–C). Necrotic keratinocytes are in thelower one-third of the epidermis with colloid bodies in the superficial papillary dermis (D)

Lichenoid dermatitis involving contiguous follicular infundibula. Hypertrophic lichen planus

Wedge shaped hypergranulosis, lichenoid lymphocytic infiltrate at base of infundibulum, few colloid bodies at dermo-epidermal junction

Clumps of numerous colloid bodies in upper papillary dermis with numerous melanophages. Lichen planus pigmentosus

• Lichenoid drug eruption. The histologic presentation can be identical to lichen planus (A). Differentiating features may include focal pararkeratosis, necrotic keratinocytes in all layers of the epidermis, and eosinophils within the infiltrate (B and C).

• Lichenoid pigmented purpura. There is a band-like lymphocytic infiltrate that does not obscure the dermoepidermal junction (A).

• Extravasated erythrocytes and/or hemosiderin-laden macrophages are a prominent feature (B and C).

• Lichen striatus. There is a superficial and deep perivascular and periadnexal lymphohistiocytic infiltrate with a band-like component that obscures the dermoepidermal junction (A). Shows psoriasiform hyperplasia of epidermis Foci of mild to moderate spongiosis and may show exocytosis of lymphocytes (B).

Lichen nitidus. There is a lymphohistiocytic infiltrate filling the papillary dermis with"claw-like" hyperplasia of the surrounding epidermis.

Acute graft versus host reaction (GvHR). There is a sparse lymphocytic infiltrate obscuring the dermoepidermal junction (A).Lymphocytes are present in the epidermis (exocytosis) with adjacent individually necrotic keratinocytes (satellite cell necrosis) (B). Chronic GvHR. There is acanthosis of the epidermis with hypergranulosis and a patchy band-like lymphocytic infiltrate. The dermis is fibrotic (C).

Superficial and deep perivascular and periadnexal lymphocytic infiltrates. Note thin epidermis, basal cell vacuolization with

subepidermal clefts that involve follicular infundibular epithelium, follicular plugging at one end of the sections. LE

Pools of bluish-grey mucin between bundles of collagen in reticular dermis. LE

Systemic lupus erythematosus. There is obscuration of the dermoepidermal junction with vacuolar alteration of the basal keratinocytes with a sparse lymphocytic infiltrate (A and B). Dermatomyositis. This may appear identical to systemic lupus erythematosus. There is a sparse lymphocytic infiltrate with vacuolar alteration of the basal keratinocytes (C). Abundant mucin interposed between the dermal collagen bundles (D

Discoid lupus erythematosus. There is a superficial and deep perivascular and periadnexal lymphocytic infiltrate with vacuolar alteration of the basal keratinocytes (A and B). A dense lymphocytic infiltrate surrounds the follicular adnexae with obscuration of the epithelial-stromal junction(C). Note the marked thickening of the basement membrane (D)

d) Interface dermatitis with psoriasiform hyperplasia: • Show interface changes as a secondary pathological feature • Not classified as primary interface dermatitis. • Lymphocytes and siderophages: Lichenoid purpura. • Eosinophils predominant: Urticarial pemphigoid, some drug eruptions. • Lymphocytes mostly: Mycosis fungoides, lichen striatus, pityriasis

lichenoides, lichen sclerosus, center of porokeratosis. • Plasma cells: Secondary syphilis, early acrodermatitis chronica

atrophicans.

e) Interface dermatitis with epidermal atrophy: • Represents late atrophic phase of several dermatoses • Plasma cells: Late stage of acrodermatitis chronica atrophicans. • Band of melanophages: Regressing malignant melanoma, late

pigmented patches of FDE. • Lymphocytic infiltrate: Atrophic LP, long-standing lesions of LE,

dermatomyositis, poikiloderma, atrophic lesions of lichen sclerosus, center of porokeratosis.

Lichen sclerosus et atrophicus (LS et A), atrophy, follicular plugging, papillary dermal edema, and sclerosis with a patchy, band-like predominantlylymphocytic infiltrate interposed between the altered collagen of the upper dermis and normal collagen of lower dermis (A and B). Fully developed LS et A. There is effacement of rete ridge pattern of epidermis with vacuolar alteration of basal keratinocytes and sclerosis of dermis (C)

Pityriasis lichenoides et varioliformis acuta (PLEVA). There is a superficial and deep perivascular lymphocytic infiltrate that obscures dermoepidermal junction (A). Neutrophils are in stratum corneum admixed with degenerated necrotic keratinocytes and parakeratotic corneocytes (B). Necrotic keratinocytes are scattered throughout epidermis and erythrocytes are interposed between keratinocytes (C).

Superficial perivascular lymphocytic infiltrate, SUBTLE VACUOLAR ALTERATIONS, +/- EXTRAVASTED RBC . Note the thick wafer-like scale containing flat parakeratosis and flecks of melanin. Pityriasis lichenoides chronica

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