Apoptosis, including the programmed cell death, is important event in normal cell turnover and maintenance of adult tissues. Apoptosis exerts a homeostatic function in relation to tissues dynamics, as the steady state of continuously renewing tissues achieved by a balance between cell replication and cell death. This study was undertaken to investigate the association between apoptosis and development of the cervical neoplasia. Archival cervical samples from normal epithelium (n 10), low-grade squamous intraepithelial lesions (LSIL, n = 10), high-grade squamous intraepithelial lesions (HSIL, n 10), microinvasive squamous cell carcinomas (n 10), and invasive squamous cell carcinomas (n = 10) were evaluated for apoptosis. We used in situ end-labeling of DNA strand breaks by terminal deoxynucleotidyltransferase incorporation of biotinylated deoxyuridine to 3-OH ends of DNA, identified by nickel-avidine-peroxidase. The apoptotic index (sum of apoptotic bodies divided by the total nuclei times 100) significantly decreased (P<0.05) as the degree of neoplasia increased: 3.1 + 0.9 % in normal epithelium, 5.5 +/- 1.4 % in LSIL, 1.6 +/- 0.4 % in HSIL, 1.9 +/- 0.5 % in microinvasive carcinomas, and 0.6 +/- 0.3 % in invasive carcinomas. Compared to normal epithelium, the total cell number per 200x field increased significantly (P<0,05): 379 +/- 47 in normal epithelium, 462 +/- 228 in LSIL, 670+/-293 in HSIL, 1035 +/- 254 in microinvasive carcinomas, and 1389 +/- 247 in invasive carcinomas. Consequently, these results suggest that progession of cervical carcinogenesis is associated with a decrease in apoptotic index and an increase in the number of the total cell.