Interface dermatitis

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

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 midand upper spinous
layers,

Colloid (Civatte) bodies at dermoepidermal 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 midand deep reticular dermis,
lymphocytic lobular panniculitis
Thickened papillary dermis with sparse
lymphocytic infiltrate and numerous
melanophages. persisting basal cell
vacuolization. Lichen planus pigmentosus

Sclerosis of thickened papillary dermis with

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

Classification of Interface Dermatitis

1. Histologically, classified as:
a) Prominent basal cell
vacuolization (Vacuolarinterface dermatitis):
Basal cell vacuolization is
most prominent
Variable perivascular and
interstitial infiltrates of
lymphocytes.

b) Prominent infiltrate in
papillary dermis aligned in
lichenoid pattern (Lichenoidinterface dermatitis):
Dense band-like infiltrate
in papillary dermis
Basal cell vacuolization

2. Le Boits 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.

Fixed drug eruption. There is obscuration of the dermoepidermal junction with

a mixed inflammatory cell infiltrate composed of lymphocytes
numerous 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 longstanding lichenoid drug eruptions.

Lichen planus. There is compact orthokeratosis with no parakeratosis,

wedgeshaped
hypergranulosis, jagged acanthosis of the epidermis, and a band-like
lymphocytic

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

 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 nitidus. There is a

lymphohistiocytic infiltrate
filling the papillary dermis
with
"claw-like" hyperplasia of
the surrounding epidermis.

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).

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 bluishgrey mucin

between
bundles of
collagen in
reticular

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

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
predominantly
lymphocytic 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

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

Superficial perivascular lymphocytic infiltrate, SUBTLE VACUOLAR

ALTERATIONS,
+/- EXTRAVASTED RBC . Note the thick wafer-like scale containing flat

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