Resumo

SOUZA, Rodrigo Tadeu de Puy e et al. Histomorphometry, apoptosis and cell proliferation in cervical intraepithelial neoplasia. J. Bras. Patol. Med. Lab. [online]. 2011, vol.47, n.6, pp. 625-634. ISSN 1676-2444.  http://dx.doi.org/10.1590/S1676-24442011000600009.

INTRODUCTION: Cervical dysplasias are precursor to squamous cell carcinoma of the uterine cervix. Carcinogen induced mutations correlate with proliferative alterations. Accumulation of such mutations and unbalance of genomic homeostasis induce changes in certain genes as well as affect cell proliferation and apoptosis. Immunohistochemical markers of cellular proliferation, apoptosis and cell survival in cervical intraepithelial lesions still require morphometric studies in order to define their role in the development of dysplasias caused by invasive carcinoma. OBJECTIVES: In order to better understand the processes of cellular proliferation, apoptosis and epithelial turn over in such precursory lesions, histomorphometric evaluation for mitosis and apoptosis as well as immunohistochemical reactions for Bax, Bcl-2 and Ki-67 proteins (reactivity, localization and intensity) were carried out in cervical biopsies. METHODS: Samples were split into four groups: 1. cervicitis (n = 20); 2. light dysplasia (n = 20); 3. moderate dysplasia (n = 20); 4. severe dysplasia (n = 20). RESULTS: Intense proliferation and apoptosis were observed in lesions with high, extensive, intense, and diffuse Ki-67 and Bax immunolabeling. Proliferation and apoptosis were mild or null in groups 1 and 2. Bcl-2 immunolabeling was more intense in high degree lesions and mild in the other groups. Extensive Ki-67 and Bax immunolabeling suggests an increased cellular turn over, which was also corroborated by histomorphometry. The more severe the dysplasia is the higher Bcl-2 expression. CONCLUSION: These data indicate that the pre-neoplastic process is dynamic and is concomitant with apoptosis and mitosis.

Palavras-chave : Cervical pathology; Cervical intraepithelial neoplasia; Cell proliferation; Apoptosis; Ki-67; Bcl-2; Bax.