Alterations in distribution of tenascin, fibronectin and fibrinogen in vulval lichen sclerosus

Background: The pathophysiology of lichen sclerosus remains uncertain. The clinical features, including increased fragility and scarring, and the hist ology suggest that significant reorganisation of the extracellular matrix i s occurring. Tenascin, fibrinogen and fibronectin are extracellular matrix components that play a significant role in tissue remodelling, for example during wound repair. Aim: To examine the distribution of tenascin, fibrinog en and fibronectin in vulval lichen sclerosus. Materials and Methods: Immun ohistochemical staining was performed to study the distribution of tenascin , fibronectin and fibrinogen in 16 specimens of untreated vulval lichen scl erosus and 1 specimen of extragenital lichen sclerosus. Haematoxylin and eo sin staining of the specimens was also performed to identify the position o f the pale staining homogenous zone/zone of sclerosis and the inflammatory infiltrate below this. The control tissues studied included biopsies taken from the uninvolved thigh of 13 of the lichen sclerosus patients and 6 samp les of normal vulva tissue obtained during gynaecological procedures from w omen of similar age to the lichen sclerosus women. Results: All the lichen sclerosus specimens demonstrated increased immunostaining of tenascin in th e upper dermis and comparing this with the haematoxylin and eosin staining this corresponded to the zone of sclerosis with relatively little tenascin staining associated with the inflammatory band. In 14 out of the 16 vulval lichen sclerosus specimens and the extragenital lichen sclerosus specimen f ibrinogen immunostaining was increased in the upper dermis which correspond ed - in haematoxylin and eosin staining - to the zone of sclerosis. There w as also slightly increased fibrinogen staining in the mid dermis which corr esponded to the inflammatory band. Fibronectin staining was reduced in the upper dermis of 12 of the vulval lichen sclerosus specimens and the extrage nital lichen sclerosus specimen which corresponded to the zone of sclerosis . However, in 14 of the vulval lichen sclerosus specimens and the extrageni tal lichen sclerosus specimen, fibronectin was slightly increased in the mi d and deeper dermis which corresponded to the zone of inflammatory cells an d the area below this. There was also increased fibronectin staining around blood vessel walls both in the mid dermis and within the zone of sclerosis . Conclusion: The distribution of tenascin, fibrinogen and fibronectin is a ltered in lichen sclerosus and the alteration in these extracellular matrix components may be relevant to the initiation of scarring in lichen scleros us and the associated increased skin fragility. Copyright (C) 2000 S. Karge r AG, Basel.