ORIGINAL PAPER Odontogenic Epithelium: Immunolabeling of Ki-67, EGFR and Survivin in Pericoronal Follicles, Dentigerous Cysts and Keratocystic Odontogenic Tumors Ma ´rcia Gaiger de Oliveira • Isabel da Silva Lauxen • Anna Cecı ´lia Moraes Chaves • Pantelis Varvaki Rados • Manoel Sant’Ana Filho Received: 10 January 2008 / Accepted: 13 October 2010 / Published online: 30 October 2010 Ó Humana 2010 Abstract The aim of this study was to evaluate the bio- logical profile of odontogenic epithelium by immunola- beling of epidermal growth factor receptor (EGFR), Ki-67 and survivin in keratocystic odontogenic tumors (KOT), dentigerous cysts (DC), and pericoronal follicles (PF). Immunohistochemical analysis was performed in 13 KOTs, 14 DCs and 9 PFs. Immunolabeling was analyzed in the basal and suprabasal layers of KOTs and DCs, and in the islands of odontogenic epithelium and/or reduced enamel epithelium of PFs. KOTs showed the highest proliferation rate among the three groups, mainly in suprabasal layers. EGFR immunolabeling was observed mainly in the cyto- plasm in basal and suprabasal layers of KOTs and in the suprabasal layer of DCs. Immunolabeling in both membrane and cytoplasm was greater in PFs. In PFs, membrane-only staining was observed. Survivin immu- nolabeling showed a greater percentage of positive cells (scoring ???) in the suprabasal layer of KOTs. In DCs, both layers showed similar percentages of cells scoring ???; PFs showed the highest percentage of these cells. In KOTs, epithelial cells showed stimulus-independent neo- plastic proliferative characteristics, suggesting the presence of a suprabasal proliferative compartment, maintained by inhibition of apoptosis. In DCs, the basal layer seemed to proliferate in response to stimulus. Although PFs showed low proliferative activity, the expression of EGFR indicates that some cells have a high capacity to respond to stimuli, which could probably explain the origin of odontogenic lesions. Keywords Survivin Á Ki-67 Á EGFR Á Odontogenic cysts Á Odontogenic tumors Á Odontogenic lesions Á Epithelium Á Immunohistochemistry Á Pericoronal follicles Á Dentigerous cyst Á Keratocyst odontogenic tumor Introduction The epithelium involved in odontogenesis and/or its rem- nants are the origin of different odontogenic lesions, with distinct clinical behavior. Several studies have reported differences in the proliferative potential of odontogenic epithelial cells, with significant impacts on the formation of odontogenic cysts and tumors [1–5]. Tissue homeostasis is maintained by a regulated balance between cell prolifera- tion and cell death, and changes in the regulation of these mechanisms are implicated in the pathogenesis of several lesions. Baumgart et al. [3] assessed pericoronal follicles and normal oral mucosa and found that 7% of the islands of odontogenic epithelium presented immunolabeling of epi- dermal growth factor receptor (EGFR) compatible with neoplasia (oral squamous cell carcinoma) in the membrane only. Reduced enamel epithelium showed EGFR immu- nolabeling in 63.3% of the cells, a result that is similar to findings of normal oral mucosa, in both the membrane and the cytoplasm (membrane-only staining did not occur in these cells). On the other hand, in the study conducted by Payeras et al. [5], the behavior of odontogenic epithelium in ameloblastomas suggested differences in the prolifera- tive potential of islands depending on their size. Membrane EGFR expression was usually observed in smaller islands, M. G. de Oliveira (&) Á I. da Silva Lauxen Á A. C. M. Chaves Á P. V. Rados Á M. Sant’Ana Filho Graduate Program in Dentistry, Oral Pathology, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2492, sala 503, Porto Alegre, RS CEP 90035-003, Brazil e-mail: marciago@gmail.com 123 Head and Neck Pathol (2011) 5:1–7 DOI 10.1007/s12105-010-0216-0