Emergence of micronuclei and apoptosis as potential biomarker of oral carcinogenesis: An updated review

Abstract

More than 95% cancers of oral cavity are squamous cell carcinoma. They contribute major health problems in developing countries like India. The critical etiological factor for oral squamous cell carcinoma (OSCC) is the consumption of tobacco in various forms. OSCC results from alterations in genes that control the cell cycle or that are involved in deoxyribonucleic acid repair and are characterized by the loss of ability of cells to evolve to death when genetic damage occurs. The occurrence of chromosomal damage can be evaluated by counting micronuclei (MNs) and degenerative alterations, indicative of apoptosis such as karyorrhexis, pyknosis, and condensed chromatin. Apoptosis has been associated with the elimination of potentially malignant cells, hyperplasia, and tumor progression. Hence, reduced apoptosis or its resistance plays a vital role in carcinogenesis. MNs are one of such biomarkers that are cytoplasmic chromatin masses with the appearance of small nuclei that arise from lagging chromosomes at anaphase or from acentric chromosome fragments. They are induced in the cells by numerous genotoxic agents that damage the chromosome. Bigger MNs result from exclusion of whole chromosome following damage to the spindle apparatus of the cell (aneugenic effect), whereas smaller MNs result from structural aberrations causing chromosomal fragments (clastogenic effect). Thus, MN count and apoptosis can be a useful biomarker, and it can be used as a screening test for patients with habit of tobacco consumption and patients with manifestations of oral lesion including premalignant and malignant conditions.

Keywords

• apoptosis
• chromosomal damage
• genotoxic damage
• human micronucleus project on exfoliated buccal cells
• micronucleus
• reactive oxygen species production