Information on the skin biopsy

The timing of the biopsy

Inflammatory dermatoses

When biopsies should be performed on inflammatory dermatoses is more hard to say, as in these cases account must also be taken of the stage of development seen in the efflorescences. If the biopsy is performed at the early or later stages, a definite histopathological classification is frequently not possible. In, for example, early Lichen planus a most uncharacteristic picture appears, with peri-vascular infiltrate, indications of vacuolar changes at the dermo-epidermal junction, slight epidermis hyperplasia and focal thickening of the horny cell layer. At a slightly later stage of Lichen planus, this finding is diagnostic: one sees an irregular epithelium hyperplasia with hypergranulosa and compact orthokeratosis, a thick tape-shaped lymphocyte infiltrate at the upper dermis, vacuolar changes at the the dermo-epidermal junction and individual necrotic keratinocytes. In due course, the progress of the inflammation slows down; the epidermis becomes atrophic, and at the final stages of the Lichen planus, one sees only residues remaining – a mild superficial fibrosis with some melanophages –, such as also arise in the later stages of other diseases.(4) In such cases, the histopathologist is able only to confirm post-inflammatory hyper-pigmentation: the findings do not permit any more precise diagnosis.

Even more important is choosing the correct moment for a biopsy of ephemeral or easily-destroyed lesions, as in urticaria or bullous and pustulent dermatoses. In cases of bullous dermatoses, the clinical picture may be completely dominated by erosions or urticarial changes, whereas blisters, on the other hand, are completely absent. Biopsies from erosions only rarely produce usable findings due to the lack of any bulla coating and secondary indications of an inflammation. At their urticarial stage, bullous dermatoses certainly do show characteristic, though non-specific, changes. For example, in both Pemphigus vulgaris as well as bullous pemphigoid, a spongiform with eosinophile granulocytes is found in epidermis and upper corium. When these findings are present, there may certainly be a suspicion of bullous dermatosis; however, a specific histopathological diagnosis is possible only with the start of blister formation: when there is Pemphigus, this takes place through acantholysis within the epidermis; for bullous Pemphigoid, it takes place subepidermally. Microscopically, the tiniest fission formations are often in evidence at urticarial foci. However, targeted biopsies of clinically barely-detectable blisters that are not yet eroded and do not yet show any re-epithelialisation of the blister floor are ideal for diagnosing bullous dermatoses, with the result that the blister-forming mechanism is clearly in evidence. If there is a clinical suspicion of a bullous dermatosis but without any blisters being present, it may make sense to ask the patient to come back for a biopsy at a later date, or to ask him/her to present once more in the event of a small, intact blister appearing.

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