RESEARCH ARTICLE Predictive value of p63, ki-67, and survivin expression in oral leukoplakia: A tissue microarray study Kelly Bienk Dias | Anacl  audia Pereira Costa Flores | M  arcia Gaiger Oliveira | Pantelis Varvaki Rados | Manoel Sant’ana Filho Oral Pathology, School of Dentistry, Universidade Federal do Rio Grande do Sul, Brazil Correspondence M arcia Gaiger Oliveira, Rua Ramiro Barcelos, 2492 sala 503, CEP 90035-003, Porto Alegre, RS, Brazil. Email: marciago@gmail.com Review Editor: Prof. George Perry Abstract The aim of this study was to analyze the immunohistochemical expression of survivin, ki-67, and p63 in oral leukoplakic lesions, histopathologically differentiated into dysplastic and nondysplastic. A tissue microarray containing 57 samples of biopsies from clinically classified lesions, such as leu- koplakia, was immunolabeled for survivin, ki-67, and p63. Samples were scored for percentage of positively stained. Scores were designated as follows: low 5 less than 25% of positive cells; and high 5 more than 25% of positive cells. On performing histopathological diagnosis, 20 dysplastic lesions and 37 nondysplastic lesions were seen, in which female patients (56.1%) were predomi- nant with an average age of 58.27 years. The study showed a high expression of 37.5% for survivin, 43.7% for ki-67, and 88.2% for p63 in dysplastic lesions. However, there was a high expression of 16.7% for survivin, 16.7% for ki-67, and 92% for p63 in nondysplastic lesions. There is a positive correlation of expression among the three antibodies. In the association of immunore- activity, in both dysplastic and nondysplastic lesions, increased expression of survivin reflects on the increased expression of ki-67, and there is an overexpression of p63. In leukoplakia, the expression of survivin associated with that of ki-67 reinforces the assumption that all these lesions are potentially malignant, regardless of histopathology; and the overexpression of p63 may indi- cate carcinogenic potential. These findings may help in the treatment of patients with this type of lesion. KEYWORDS Immunohistochemistry, leukoplakia, oral, tissue microarray 1 | INTRODUCTION Oral leukoplakia is the most common potentially malignant lesion in the oral cavity (van der Waal, 2009). It is characterized by a pre- dominantly white plaque or stain that cannot be classified clinically or pathologically as any other disease (Zyada & Fikry, 2010). This condition may present a number of epithelial histopathological alterations that include hyperplasia, hyperkeratosis, acanthosis, and dysplasia. Squamous cell carcinoma (SCC) may be preceded by leu- koplakia and the presence of epithelial dysplasia is an important predictor of the development of this type of neoplasm (Reibel, 2003). In the world, among which are premalignant lesions, 1 to 5% affect the oral cavity. Among these lesions, leukoplakia is the most common having an overall prevalence of 2.6%. The index of malignant transfor- mation of oral leukoplakia may vary from 0.13% to 17.5%, in follow-up periods between 1 and 30 years (Abe, Hamada, Yamaguchi, Amagasa, & Miura, 2011). Clinical studies suggest that 10 6 20% of leukoplakic lesions that present dysplasia progress to SCC, and 20 6 30% of them increase the severity of the dysplastic condition in 10 years (Speight & Morgan, 1993). The histopathological diagnosis of dysplasia can vary greatly depending on the examiner, making it often subjective (Abbey et al., 1995). Thus, there is a need for markers that can predict the malignant potential of leukoplakia effectively as well as guide the appropriate clinical intervention of these lesions (Montebugnoli et al., 2008). The recognized evolutionary ability of carcinogenic cells is due to changes in cell cycle regulation (Matsumoto et al., 2001). Therefore, Microsc Res Tech. 2017;1–7. wileyonlinelibrary.com/journal/jemt V C 2017 Wiley Periodicals, Inc. | 1 Received: 24 December 2016 | Revised: 13 March 2017 | Accepted: 14 March 2017 DOI: 10.1002/jemt.22872