Histological clonal change - A feature for dysplasia diagnosis

Abstract

Aims: Histological diagnostic criteria are used for the assessment of the degree of dysplasia and hence the risk of cancer progression for premalignant lesions. Clonal changes in the form of hyperorthokeratosis and hyperchromasia that are sharply demarcated from adjacent areas are not currently part of the criterion for dysplasia diagnosis. The objective of this study was to determine whether such clonal change should be regarded as a diagnostic feature for dysplasia. The following histological conditions were used to defi ne such change: (1) hyperorthokeratosis; (2) hyperchromatism but no other features of dysplasia; (3) sharp margin demarcation from adjacent area by both the hyperorthokeratosis and hyperchromasia (clonal change), and (4) no prominent rete ridges, marked acanthosis or heavy infl ammation. Lesions fi tting these criteria were termed orthokeratotic lesions with no dysplasia. Methods: Patients from a population-based longitudinal study with more than 10 years of follow up were analyzed. Of the 214 patients with primary oral premalignant lesions, 194 had mild or moderate dysplasia (dysplasia group) and 20 fi t the criteria for orthokeratotic lesions without dysplasia (orthokeratotic with no dysplasia group). The two groups were compared for their cancer risks using clinical (site and toluidine blue), histological (nuclear phenotype score), and molecular criteria (loss of heterozygosity) and by outcome (progression). Results and conclusions: The lesions from orthokeratotic with no dysplasia group showed a similar cancer risk (clinical, histological and molecular risk) and time to progression as the dysplastic lesions. We recommend that the clonal change should be included as a criterion for dysplasia diagnosis. Research Article Histological clonal change A feature for dysplasia diagnosis Lewei Zhang1-3*, Tarinee Lubpairee1,3, Denise M Laronde1,3,4, Martial Guillaud3,4, Calum E MacAulay3,4 and Miriam P Rosin3-5 1Department of Oral Biological and Medical Sciences, Faculty of Dentistry, the University of British Columbia (BC), Vancouver, Canada 2BC Oral Biopsy Service, Vancouver General Hospital, Vancouver, Canada 3BC Oral Cancer Prevention Program, BC Cancer Agency, Vancouver, Canada 4BC Cancer Research Centre, Vancouver, Canada 5School of Biomedical Physiology and Kinesiology, Simon Fraser University, Burnaby, Canada *Address for Correspondence: Lewei Zhang, Department of Oral Biological and Medical Sciences, Faculty of Dentistry, University of British Columbia, BC Oral Biopsy Service, Vancouver General Hospital, BC Oral Cancer Prevention Program, BC Cancer Agency, 2199 Wesbrook Mall, Vancouver BC, Canada, V6T 1Z3, Tel: +1-604-875-4318 / 778-387-3885; Email: leweizhang888@gmail.com Submitted: 23 September 2017 Approved: 27 August 2018 Published: 28 August 2018 Copyright: © 2018 Zhang L, et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited