This study attempted to evaluate whether oral lichen planus (OLP) has the p
otential to progress to oral squamous cell carcinoma (OSCC) by comparing th
e degree of genetic instability between clinically-curable OLP and lesions
that progressed to OSCC. Fifteen cases of steroid-responsive OLP and two ca
ses of lichenoid dysplasia (LD) that progressed to OSCC were used for this
study. Chromosome in situ hybridization (CISH) was performed for chromosome
s 9 and 17. The fraction of polysomic and monosomic cells for chromosome 9
increased in mucosal epithelium compared to those of lymphocytes in OLP. Th
is difference was statistically significant (P=0.0017, 0.0054, respectively
). Two LD patients showed 15.38% and 22.58% of PI for chromosome 9. In OSCC
that developed from LD, the fraction of monosomic cells for chromosome 9 i
ncreased by more than 70%. We concluded that LD should be treated as a high
-risk premalignant lesion and strongly suggest that the monosomy of chromos
ome 9 may have a critical role in progress to malignancy from LD.