engleski

Expressin of Tissue Antigen c-erbB-2 in Patients with Oral Lichen Ruber (OLR) in Corelation with Clinical Status

INTRODUCTION In recent years the results of various studies point to premalignant potential of oral lichen lesions which may cause potential inception of oral planocellular carcinoma (OPCC). The frequency of malignant transformation i.e. frequency of oral lichen lesions transformation in OPCC varies, ranging from 0, 3% -10% . In some clinical forms like atrophic, erosive and ulcerous lesions, more frequent inception and development of OPCC has been observed (1). Proto-oncogene c-erbB-2 located on chromosome 17 at band q21 encodes the synthesis of phosphoglycoprotein receptor p185erbB2 (p185HER-2/neu) which has tyrosine kinase activity. c-erbB-2 receptor can be found in many tissue cells (2). Excessive expression of c-erbB-2 oncogene is present in many premalignant and malignant lesions and tumors i.e. tumors of lung, ovaries and breast (3, 4, 5). The aim of this examination was to datected modified tissue expression of c-erbB-2 antigen in ORL lesions, as important indicator of the prognosis and course of the disease in relation with specific clinical forms of oral lichen ruber, clinical intensity of the inflammation of oral mucosal membrane and clinical intensity of hyperkeratosis of oral mucosal membrane. MATERIALS AND METHODS Subjects. This study included 30 patients with oral lichen ruber, 15 with clinical manifestations of lichen ruber planus (LRP) and 15 with clinical manifestations of erosive lichen ruber (LRE). Control group included 15 patients diagnosed with homogenous oral leukoplakia (OL). Clinical status of OLR and OL was evaluated through the clinical parameters of the disease, inflammation, hyperkeratosis, lesion volume (erosions, bullae) and graded 0, 1, 2 and 3. The clinical diagnosis of OLR and OL determined on a basis of described clinical oral tests and parameters was confirmed in all patients through the pathohistologic diagnosis. Biopsy samples. Biopsy samples were collected from the pathologically changed oral mucosal membrane, from the border between healthy and diseased tissue, after the administration of 1 ml of local anesthetic solution (3% Mepivastein, ESPE, Germany). Immunohistochemical analysis of biopsy samples. Tissue samples were fixated in purified 4% paraformaldehyde for 24 h, embedded in paraffin and sectioned with cryo-microtome to 4 nm thick slices. After deparaffination and rehydration, tissue slices were processed and stained with haematoxylin-eosin and mounted on a slide with Canada balsam. For the purpose of immunohistochemical analysis antigen demasking was performed by heating tissues sections in a microwave oven (MOULINEX) 3x5' at 800 W and processed with APAAP (DAKO) and LSAB (DAKO) method. The final product of the reaction was either blue (APAAP) or brown (LSAB) precipitate in cellular membrane depending on method used. The intensity of immunohistochemical reaction of tissue antigen c-erbB-2 expression was evaluated semiquantitatively and marked as a reaction of negative intensity (-), low positive intensity (+), moderate positive intensity (++) and high positive intensity (+++). CONCLUSION This study showed changed expression of tissue antigen c-erbB-2 in OLR lesions, manifested as a membranous-type reaction whose polymorphy varied according to the intensity and topology. Described low expression reaction of tissue antigen c-erbB-2 in basal and parabasal epithelium layer of OLR lesions combined with strong intensity reaction in tonofibrils of spinous layer can be the early sign of tissue transformation. Weakened or negative immunohistochemical reaction in oral lichen lesions, opposite to the stronger reaction in OL lesions, reveals the existence of some internal provoking signal which can induce the malignant transformation of OLR lesions. It can be concluded that such altered expression of c-erbB-2 antigen in OLR lesions points to altered nature of these lesions with the potential to undrgo malignant transformation.

oral lichen ruber; tissue antigenes; c-erbB-2

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