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Background The clinical features of lichen sclerosus, which include atrophy, scarring, fragility and tendency to form ecchymoses with only slight trauma, suggest that there is an alteration in the extracellular matrix fibres that are responsible for the tensile strength of the dermis. However, the precise nature of these changes is poorly understood. Methods Biopsies from 16 patients with untreated, histologically confirmed, vulval lichen sclerosus were examined immunohistochemically using polyclonal antibodies to collagens I and III and a monoclonal antibody to elastin. Twelve of the lichen sclerosus specimens were also stained with a monoclonal antibody to fibrillin. Normal vulva tissue and patients’ uninvolved thigh were used as controls. Results In the lichen sclerosus specimens, collagens I and III stained with a more homogeneous pattern than in the control tissues. Reduced numbers of elastin fibres were seen in the zone of sclerosus in 15 of the 16 lichen sclerosus specimens. In the control tissue fibrillin fibres were seen as a fine network of fibres in the upper dermis arranged at right angles to and inserting into the basement membrane and forming a fine network throughout the dermis. In the lichen sclerosus specimens, although fibrillin microfibrils were still seen inserting at right angles into the basement membrane, below this the fibrillin staining was reduced in the upper dermis in 11 of the 12 lichen sclerosus specimens. The zone of reduced fibrillin staining was greatest in those specimens where the band of inflammation was deep in the dermis. Conclusions The distribution of collagens I and III, elastin and fibrillin are altered in lichen sclerosus and this is likely to contribute to the fragility, scarring and atrophy seen clinically in lichen sclerosus.

Although there is evidence to support an autoimmune basis for lichen sclerosus, there have also been some studies which suggest an infective aetiology. These include reports of the presence of spirochaetal forms with Steiner silver stains and purplish coccoid forms with Fite stains. We have repeated these studies on vulval biopsies obtained from 16 patients with vulval lichen sclerosus. Using the Steiner silver method we found no evidence of spirochaetal forms in any of the specimens. With the Fite stain we observed purple-staining coccoid forms within the dermis of 13 of the 16 lichen sclerosus specimens. However, these coccoid forms also stained strongly positive with toluidine blue, suggesting they were mast cell granules rather than micro-organisms. We were therefore unable to demonstrate evidence for an infective aetiology in vulval lichen sclerosus, although this cannot yet be excluded. Further work is also needed to understand the significance of mast cells in lichen sclerosus.

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