p53 immunostaining in lichen sclerosus is related to ischaemic stress and is not a marker of differentiated vulvar intraepithelial neoplasia (d-VIN)
Article first published online: 19 JAN 2006
Volume 48, Issue 3, pages 268–274, February 2006
How to Cite
Liegl, B. and Regauer, S. (2006), p53 immunostaining in lichen sclerosus is related to ischaemic stress and is not a marker of differentiated vulvar intraepithelial neoplasia (d-VIN). Histopathology, 48: 268–274. doi: 10.1111/j.1365-2559.2005.02321.x
- Issue published online: 19 JAN 2006
- Article first published online: 19 JAN 2006
- Date of submission 2 May 2005 Accepted for publication 9 May 2005
- hypoxic stress;
- vulvar carcinogenesis;
- vulvar intraepithelial neoplasia
Aim : To analyse p53 immunoreactivity in 207 biopsy specimens of lichen sclerosus (LS) and ‘differentiated vulvar intraepithelial neoplasia’ (d-VIN), a postulated precursor lesion for LS-associated vulvar squamous cell carcinoma (SCC), which is characterized by atypical basal keratinocyte proliferations with p53+ basal/suprabasal keratinocyte nuclei.
Methods and results : Forty early, 78 classic, 30 hypertrophic vulvar LS, 26 paediatric vulvar and penile LS, 33 vulvar LS-associated SCC and 30 vulvar/penile control specimens were examined for p53 expression and the presence of d-VIN. Nuclear p53 staining was observed in 175/207 LS biopsy specimems. Eighty percent of early and 69% of paediatric LS showed discontinuous/continous p53 staining in basal keratinocytes. Classic LS showed no p53 staining in 17%, discontinuous basal keratinocyte staining in 20%, continuous basal keratinocyte staining in 58%, basal/suprabasal staining in 5%. Hypertrophic LS revealed basal keratinocyte staining in 32% and basal/suprabasal staining in 61%. p53 staining was associated with sclerosis of blood vessels and dermis, lymphoid infiltrates, vasculitis and hypertrophic LS. d-VIN was seen in 2% of LS alone and in 24% of LS-associated SCC.
Conclusion : d-VIN in LS is rare, while p53 staining is common and best explained as an ischaemic stress response due to poor oxygenation, vasculitis and inflammation rather than as a marker of a precancerous lesion in LS.