Author: Dr Ben Tallon, Dermatologist/Dermatopathologist, Tauranga, New Zealand, 2011.
Histology of lichen sclerosus
Scanning power of lichen sclerosus reveals a lichenoidinflammatory pattern in early stage lesions or a superficial sclerosing process in late stage lesions (Figure 1 and 2). The epidermis shows hyperkeratosis, significant thinning with loss of the normal rete ridge pattern and plugging of follicular infundibulae (Figure 3). An atrophicepidermis is not a requirement as some cases particularly in the vulva can show significant epidermalhyperplasia. Vacuolar degeneration of the basal layer can be seen though typically mild especially in late stage lesions. Clefting can be evident between the epidermis and dermis as a result of this basal layer degeneration and the underlying dermal changes. The dominant feature is of broad condensation of the dermalcollagen. These changes are typically superficial, while in early lesions may show marked overlying papillary dermaloedema. When extending into the deep dermis discrimination from scleroderma may become difficult. The inflammatoryinfiltrate evolves from a dense lichenoidlymphocyticinfiltrate to a sparse superficial interstitialinfiltrate in late stage disease. Scattered plasma cells, histiocytes and mast cells can be seen (Figure 4).
Differential diagnosis of lichen sclerosus pathology
Scleroderma: In this condition the overlying epidermis and superficial dermis is spared. The inflammatoryinfiltrate is typically sparse and around deep adnexal and vascular structures. Overlap can occur where superficial and deep changes co-exist.
Lichen planus: The presence of a well formed granular layer and numerous cytoid bodies, and a lack of basement membrance thickening or epidermalatrophy favour lichen planus over lichen sclerosus.
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