Interface dermatitis

Interface dermatitis

Lichenoid interface dermatitis

• Basal layer is destroyed

• Civatte bodies

• Sawtooth rete pattern

Causes of lichenoid interface dermatitis

• Lichen planus

• Benign lichenoid keratosis (BLK, lichen planus-like keratosis)

• Lichenoid drug eruption

• Lichenoid graft-versus-host disease (GvHD)

• Hypertrophic lupus erythematosus

• Lichenoid regression of a melanocytic lesion (usually lentigo maligna)

The biopsy in each of these conditions demonstrates a sawtooth rete ridge pattern with destruction of the basal layer, a band-like lymphoid infiltrate, and presence of Civatte bodies. Compact hyperkeratosis and beaded hypergranulosis are typically present. The cells of the stratum spinosum are enlarged and more eosinophilic than the normal epidermis. Vacuoles may be present in the lowest cells of stratum spinosum, but the basal layer is gone. An underlying band-like lymphoid infiltrate is common.

If neither parakeratosis nor eosinophils are noted, the changes are consistent with lichen planus. Lichenoid interface dermatitis with neither eosinophils nor parakeratosis may also be seen in BLK (lichen planus-like keratosis), lichenoid drug eruption, lichenoid GvHD, hypertrophic lupus erythematosus, and lichenoid regression of lentigo maligna. Clinical correlation is essential. Direct immunofluorescence (DIF) will distinguish hypertrophic lupus erythematosus (continuous granular band of immunoglobulins and complement plus cytoid bodies) from lichen planus (shaggy fibrin, cytoid bodies).

When parakeratosis is present, lichen planus is very unlikely. The differential diagnosis still includes BLK, lichenoid drug eruption, lichenoid GvHD, and lichenoid regression of a melanocytic lesion. Hypertrophic lupus erythematosus rarely demonstrates parakeratosis.

The presence of eosinophils strongly favors a diagnosis of lichenoid drug eruption. The presence of eosinophils weighs strongly against a diagnosis of lichen planus. They are rarely seen in hypertrophic lupus erythematosus, BLK, lichenoid GvHD, or lichenoid regression of a melanocytic lesion.

Fig 7-1 Interface versus spongiotic dermatitis (eos, eosinophils; PLEVA, pityriasis lichenoides et varioformis acuta; PLC, pleomorphic lobular carcinoma)

An analogy that those with teenagers may appreciate:

• Lichen planus is like a strict parent: “You will not hang around with eosinophils or parakeratosis”

• Lichenoid drug eruption and the remaining lichenoid processes are more permissive: “You don’t have to have eosinophils or parakeratosis, but if you want to, it’s OK”

Fig 7-2 Lichenoid interface dermatitis

Late-phase (burnt-out) lichenoid dermatitis

• Effacement of the rete pattern

• Melanin pigment incontinence (melanoderma)

• Civatte bodies

Fig 7-3 Vacuolar interface dermatitis for comparison

Fig 7-4 Late-stage lichenoid dermatitis

Lichen planus

• Lichenoid interface dermatitis

• No parakeratosis or eosinophils

• Sawtooth rete ridges

Fig 7-5 Lichen planus

Lichenoid drug eruption

• Lichenoid interface dermatitis

• Typically has eosinophils

• Often has parakeratosis

Fig 7-6 Lichenoid drug eruption

Benign lichenoid keratosis

• Lichenoid interface dermatitis

• May have parakeratosis

• Rarely has eosinophils

• Solar lentigo commonly present at the margin

BLK usually presents as a solitary pearly pink macule on the trunk or an extremity. The biopsy is usually performed to rule out basal cell carcinoma. Most lesions represent lichenoid regression of benign solar lentigines. The earliest stage of evolution may show vacuolar interface dermatitis with a lymphocyte in every vacuole.

Fig 7-7 Benign lichenoid keratosis

Lichenoid graft-versus-host disease

• Lichenoid interface dermatitis

• May have parakeratosis

• Rarely has eosinophils

Fig 7-8 Lichenoid GvHD

Hypertrophic lupus erythematosus

• Lichenoid interface dermatitis

• Rarely has parakeratosis

• Rarely has eosinophils

• DIF: continuous granular band of immunoglobulin (Ig) G/A/M and C3 (full house) at the basement membrane zone (BMZ)

• Superficial and deep infiltrate

• Follicular plugging

• Many CD123+ plasmacytoid dendritic cells adjacent to epithelium (helps differentiate from squamous cell carcinoma in situ)

Hypertrophic lupus erythematosus is lichenoid histologically. It is distinguished from lichen planus by the DIF pattern, occasional presence of basement membrane zone thickening or dermal mucin, and by clinical history and serologic findings. This is the form of chronic cutaneous lupus erythematosus that is most likely to give rise to invasive squamous cell carcinoma.

Fig 7-9 Hypertrophic lupus erythematosus

Lichenoid regression of lentigo maligna

• Lichenoid interface dermatitis

• Heavily sun-damaged skin

• Adjacent rete pattern may be effaced

• May have parakeratosis

• Rarely has eosinophils

Fig 7-10 Lichenoid regression within a lentigo maligna

Porokeratosis

• Cornoid lamella (column of parakeratosis at 45° angle, dyskeratotic cells below)

• Zone between cornoid lamellae may appear lichenoid or psoriasiform

Vacuolar interface dermatitis

Tags: Dermatopathology

Apr 26, 2016 | Posted by admin in Dermatology | Comments Off

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