Causes of lichenoid interface dermatitis

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.