INTERFACE DERMATITIS

Rajendra Singh, MD
DEJ is the key zone of pathologic changes for many
skin diseases
 PATHOPHYSIOLOGY
Damage to basal keratinocytes at the DEJ leads
to::

 intercellular edema
 Blebbing and separation of basal keratinocytes from
lamina densa
 Lichenoid infiltrate
 Necrotic keratinocytes
 Basement membrane alterations
 PATHOPHYSIOLOGY
Prolonged injury leads to:
 Atrophy of epidermis
 Poor wound healing
 Pigmentary alteration
 Decreased resistance to infections
 Increased susceptibility to cancers
All these findings are histologically summed up as

INTERFACE DERMATITIS
What causes the damage to the basal
keratinocytes?
Immune mechanisms Non-immune mechanisms

 Cytotoxic antibodies  Activation of photoreactive

 Immune complexes substances
 Hypersensitivity reactions  Defective DNA repair
mechanisms
HISTOLOGICAL CLASSIFICATION

VACUOLAR DERMATITIS LICHENOID DERMATITIS

 Lichenoid Dermatitis
Lichen Planus
Lichen planus like keratosis
Lichenoid drug eruption
Lichen Nitidus
Lichen Striatus
 LICHEN PLANUS
Pruritic, polygonal, erythematous to violaceous
flat-topped papules
Extremities and genitalia
Wickham’s striae, visible white lines in a lacy
pattern
Flexural surfaces
Nail dystrophy
Mucosal lesions
 LICHEN PLANUS
Hyper or orthokeratosis
Foci of wedge-shaped hypergranulosis
Irregular epidermal hyperplasia with "saw-tooth" rete
ridges
Dense band-like lymphohistiocytic infiltrate
obscuring the dermo-epidermal junction
Vacuolization of the basal cell layer
clefts called "Max Joseph spaces"
 LICHEN PLANUS
Eosinophilic squamatization of the basal layer
Eosinophilic, dyskeratotic cell remnants in the
epidermis and papillary dermis
Civatte bodies, Colloid bodies
Hypertrophic lichen planus
Hyper- and parakeratosis
More marked epidermal hyperplasia with rounded,
instead of saw-toothed, rete ridges
Thickened papillary dermis
Patchy lichenoid inflammatory infiltrate and
melanophages
Atrophic lichen planus
Resolving/late lesions of
Lichen Planus
Lichen Planopilaris
Females > Males 4:1
Tufts of normal hair
appear in cicatricial
areas of alopecia
Perifollicular
erythema and
keratotic spiny
papules
LICHENOID DRUG ERUPTION
Hyperkeratosis
Focal parakeratosis
Squamatization of the basal layer and Civatte bodies
Eosinophils and plasma cells
Perivascular infiltrate of lymphocytes and eosinophils
may be prominent superficially and may be deep
Lichen planus-like keratosis
Benign solitary lesion
Keratotic violaceous brown papule
May be annular
Upper chest but may occur anywhere
Clinicopathologic correlation is always necessary
May be inflammatory/regressing stage of solar lentigo or
reticulated seborrheic keratosis.
LICHEN PLANUS-LIKE
KERATOSIS
Focal parakeratosis
Variable granular layer
Dense band-like lymphohistiocytic infiltrate
Vacuolization of the basal layer, may form clefts called "Max
Joseph" spaces
Occasional plasma cells and eosinophils in the dermal infiltrate
Usually numerous Civatte bodies
LICHEN NITIDUS
Asymptomatic
Multiple flesh-colored
1 to 3 mm papules may be grouped
Abdomen, arms and genitalia
Children and young adults
LICHEN NITIDUS
Focal parakeratosis
Rete ridges surround dermal dense lichenoid infiltrate in a "ball
and claw" configuration
Histiocytes and lymphocytes filling and expanding dermal
papillae
Ill-formed granulomas including occasional multinucleate giant
cells may be present
As in lichen planus, plasma cells may sometimes predominate
in the infiltrate
 Lichen Striatus
Common, Linear, erythematous or hypopigmented
papules, scaly, asymptomatic, follow Blaschko’s lines,
nails may be involved
Children age 3, females > males
Active lesions last for months, then resolve
Histology varies, lichenoid or spongiotic, possibly
even granulomatous. Dense eccrine infiltrate helps
differentiate from LP
Lichen Striatus
Lichen Sclerosis et Atrophicus
Females > Males, Itching may be severe
Anogenital “hourglass” or “figure eight” with
dyspareunia
Glans penis (balanitis xerotica obliterans)
Chest, breasts, back, oral mucosa, tongue
Histology may have features of morphea
Genital SCC risk higher than general population, but
lifetime risk is < 5%
Lichen Sclerosis et Atrophicus
Erythema Dyschromicum Perstans
Onset before age 40.
Chronic generalized, symmetrical
Various sizes & shapes, ashy-gray macules, sometimes
with a palpable non-scaling border. Feels “like a small
cord”
Histology: lichenoid infiltrate with pigment laden
macrophages in the dermis
Keratosis Lichenoides Chronica
Rare, acral & buttocks, onset childhood
Violaceous papulonodular, hyperkeratotic lesions
covered with gray scales; discrete or may coalesce to
form reticulate or linear arrays, keratotic plugs and
prominent telangiectasias
Associated facial “seb derm” pattern
Nail thickening, longitudinal ridging, onycholysis,
warty periungual lesions
Painful oral apthae, keratoconjunctivitis
Vacuolar Interface Dermatitis
Vacuolar Interface Dermatitis
Interface Dermatitis of Collagen vascular disease
Erythema multiforme
Fixed drug eruption
Viral and drug morbilliform reactions
Graft versus host disease
Main Connective Tissue Disease
Syndromes associated with interface
dermatitis
Lupus Erythematosus
 SLE
 Discoid LE

 SCLE

Dermatomyositis
Mixed connective tissue disease
Systemic LupusErythematosus
Criteria for a diagnosis of SLE:
Acombination of cutaneous, renal, neurologic, hematologic and
musculoskeletal features along with select antibodies
Malar Rash Serositis
Discoid rash Glomerulonephritis
Photosensitivity Neurologic disorder
Oral Ulcers Cytopenia
Arthritis Select antibodies
Systemic Lupus Erythematosus
Cutaneous Manifestations:
Malar erythema
Hand erythema
Diffuse nonscarring alopecia
Ulcers
Palpable purpura
Perniosis
Raynaud’s phenomonen
Systemic
Lupus
Erythematosus
HISTOLOGY
Superficial and deep perivascular and periadnexal
lymphocytic inflammation
Interface with vacuolar alteration
Pigment incontinence
Pilosebaceous and epidermal atrophy
Hyperkeratosis with follicular plugging
Basement membrane thickening
Increased dermal mucin
 Systemic Lupus Erythematosus

Morphologic Changes may be subtle:

Comprising a cell poor interface dermatitis
Sparse lymphocytic infiltrate, dermal mucin
deposition
Positive Lupus Band Test
The Lupus Band Test
The lupus band test is usually conducted on lesional
skin
When the lupus band test is performed on
nonlesional skin, a positive result indicates systemic
lupus erythematosus
In general a positive lupus band test on nonlesional
skin does not occur in the setting of DLE or SCLE.
 Subacute cutaneous lupus erythematosus:
Histopathology

Lichenoid interface dermatitis with suprabasilar exocytosis of

lymphocytes to necrotic keratinocytes
Profound epidermal atrophy with hyperkeratosis
Absent deep extension
Subacute Cutaneous Lupus Erythematosus
 IgG within epidermal
Subacute Cutaneous Lupus Keratinocytes reflecting
Erythematosus Antibodies to Ro

I
g
G
Discoid Lupus Erythematosus
Dermatomyositis
Clinical Features
Histopathology
Direct Immunofluorescent findings
The Classic
Heliotrope
Of
Dermatomyositis
Dermatomyositis is essentially a C5b-9 mediated
Ischemic dermopathy syndrome
Characteristically there is vascular drop out with
Residual vessels showing endothelial cell necrosis/degeneration
Erythema Multiforme
Self limited cytotoxic (type IV) immune reaction directed at the
epidermis that occurs in response to certain exogenous antigens
Commonest Antigenic triggers:
1.Microbial agents: Herpes simplex, mycoplasma
2. Drugs: sulfonamides, penicillin, barbiturates
Erythema Multiforme induced by recurrent
herpes labialis
Erythema
Variants:
Multiforme
Stevens Johnson Syndrome (SJS)
Extensive and febrile form of erythema multiforme that is
more common in children.
It is typified by involvement of the mucosa, in addition to
skin, especially of the oral mucosa.
Toxic Epidermal Necrolysis
This variant of EM results in diffuse necrosis and sloughing
of the cutaneous and mucosal surfaces
Toxic Epidermal Necrolysis and SJS
Erythema Multiforme
Basilar keratinocyte degeneration with lymphocyte
satellitosis around keratinocytes
No epidermal changes of chronicity
Perivascular lymphocytic infiltrate
Eosinophils and greater keratinocyte necrosis
suggest drug based etiology
Less epidermal injury, a more pronounced
perivascular lymphocytic infiltrate suggest viral
trigger
Erythema Multiforme
Cytotoxic
lymphocytes

Necrotic
keratinocyte
 TOXIC EPIDERMAL NECROLYSIS

Necrotic epidermis

Blister cavity

Dermis

Full thickness epidermal necrosis consistent

toxic epidermal necrolysis
Fixed Drug Eruption
a unique cellular cytotoxic epidermal response
triggered by drug developing at the same site
(unilesional) or sites (generalized) when the agent is
ingested
most common sites are the head and neck, especially
the face, the lips, the buttocks, and the genitalia
(Snowden et al 1990)
Acute Graft Versus Host
Disease
Develops after bone marrow, allogeneic stem cell and
nonirradiated red blood cell and or platelet transfusion
Can appear as early as day 20
Liver and GI involvement is characteristic
A predictor of chronic GVHD is one of multiple episodes of
acute GVHD
Interface dermatitis typically very focal with accentuation in
follicles and the eccrine apparatus
Secondary Syphilis
Often combined psoriasiform and
lichenoid pattern
Plasma cells
When in doubt, silver stains for
spirochetes; serology
TAKE HOME MESSAGE
DEJ is the key zone of pathologic changes for many
skin diseases
Main DDx for a lichenoid dermatitis include LP,
LPLK and Lichenoid drug eruption
Main DDx for a vacuolar dermatitis include CTD, EM,
FDR and AGVD