Oxidative stress' is employed to describe the relation between free radicals and disease and can be defined as the state at which oxidation of the cell exceeds the antioxidant repair systems in the body (Rai et al., 2014; Katakwar et al., 2016). Reactive Oxygen Species (free radicals) formed due to oxidative stress play a vital role in the etiology and evolution of major degenerative disorders including oral cancer and precancerous conditions (Bahar et al., 2007). The highly reactive and unstable ROS produce oxidative harm which ultimately leads to deoxyribonucleic acid (DNA) base modifications and single as well as double-strand breakages (Gupta et al., 2014). ROS and

Adenomatoid odontogenic tumor (AOT) is a relatively rare benign, epithelial tumor of odontogenic origin. There is varying class of thoughts contemplating this lesion to be a hamartoma or neoplastic growth of odontogenic epithelium. Controversy regarding the histogenesis of the lesion is plentiful in earlier literature. The recent advent of immunohistochemical and ultrastructural studies has aided in throwing light on the tissue of origin of this tumor. This review aims at understanding the evolving concepts of histogenesis of AOT to better understand the biological behavior of the lesion. The review of AOT was carried out using PubMed and Google Scholar databases and 39 articles from the year 2001 to 2016 which contributed to the histogenesis of AOT were included for review. Since the origin of the cystic lining is similar to a reduced enamel epithelium and not the dental lamina, we propose the former to be the progenitor of AOT. Furthermore, we consider extra-follicular, as well as peripheral AOTs, originate from the remnants of Hertwig’s epithelial root sheath (epithelial rests of Malassez), which complies with the common histology for all these variants.

Method:A narrative review of all the articles known to the authors was conducted.Results: Tobacco and diet are the two major sources of exogenous AGE and the foremost characteristic of the glycotoxins, formed from tobacco curing reaction, is their high reactivity and innate ability to cross the cell membrane and bind with serum proteins and formation of adducts with amino acids of nucleic acids. Binding of AGEs to their receptor for AGE activates mechanisms which favor production of reactive oxidative species and proinflammatory cytokines. AGEs are also implicated as key players in cell survival, proliferation, invasion, and metastasis of tumor cells and also significantly contribute to genotoxicity. Salivary estimation of AGEs is a promising exposition to monitor the prognosis of oral pre-cancers and cancer. Conclusion:This review aims in eliciting the role of AGEs in pathogenesis of oral cancer and its possible development as a biomarker to monitor the initiation and progression of cancer.