Evaluation of premalignant potential in oral lichen planus using interphase cytogenetics

Abstract

This study attempted to evaluate whether oral lichen planus (OLP) has the potential to progress to oral squamous cell carcinoma (OSCC) by comparing the degree of genetic instability between clinically-curable OLP and lesions that progressed to OSCC. Fifteen cases of steroid-responsive OLP and two cases of lichenoid dysplasia (LD) that progressed to OSCC were used for this study. Chromosome in situ hybridization (CISH) was performed for chromosomes 9 and 17. The fraction of polysomic and monosomic cells for chromosome 9 increased in mucosal epithelium compared to those of lymphocytes in OLP. This 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 increased by more than 70%. We concluded that LD should be treated as a high-risk premalignant lesion and strongly suggest that the monosomy of chromosome 9 may have a critical role in progress to malignancy from LD.

Chromosomal Numerical Aberrations in Oral Lichen Planus

“…To uncover some of the molecular genetic aberrations associated with OLP, investigators have used molecular and genetic methods such as loss of heterozygosity (LOH) (Zhang et al, 2000), chromosome in situ hybridization (Kim et al, 2001), p53 and c-erbB2 expression (Girod et al, 1994(Girod et al, , 1995Kilpi et al, 1996;Ogmundsdottir et al, 2002), and telomerase activity (O'Flatharta et al, 2002). However, none of these methods appears to provide definitive predictive information with regard to the malignant potential of a lesion diagnosed as OLP.…”

“…In head and neck cancer, and particularly in OSCC, the incidence of aneuploidy is high (up to 80% of cases) (Stell, 1991;Milroy et al, 1997;Wennerberg et al, 1998;Bockmühl and Petersen, 2002) and has been found to be an early event in humans as well as in animal models (Remmerbach et al, 2001;Maraki et al, 2004;Raimondi et al, 2005;Pektas et al, 2006). Kim et al (2001), using chromosomal in situ hybridization, found a certain extent of genetic instability for chromosome 9 in OLP. Nevertheless, the study used biopsy-based material and is therefore not suitable for clinical follow-up, where a non-invasive approach is required.…”

High proliferative activity and chromosomal instability in oral lichen planus

“…In 1997, ZHANG et al 25 showed that a loss of heterozygosity (LOH) on chromosomes arms 3p, 9p and 17p is found in 6% of OLP patients. In addition, chromosome 9 monosomy was demonstrated to play a critical role in progress to malignancy in two cases of lichenoid dysplasia 14 . More recently, FEMIANO et al 7 found 5% DNA aneuploidy in patients with OLP.…”

“…Two investigated specific chromosome alterations, and another aimed to detect gross genomic damage 7,14,25 . In 1997, ZHANG et al 25 showed that a loss of heterozygosity (LOH) on chromosomes arms 3p, 9p and 17p is found in 6% of OLP patients.…”

Líquen plano bucal: considerações clínicas e histopatológicas

“…The possibility of malignant transformation is a reflection of many intrinsic molecular alterations within cells, all of which are found in lichenoid dysplasia. 43 Kim et al 44 (2001) assessed the malignant potential of oral lichen planus by comparing the degree of genetic instability in clinically cured cases and in those that had undergone malignant transformation. These authors concluded that lichenoid dysplasia should be seen as a high-risk premalignant lesion, and that chromosome nine monossomia may have an important role in the malignant transformation of this lesion.…”