Background:Anomalies in primary dentition are often found to be associated with anomalies in permanent dentition.Aims:This study was performed to evaluate the prevalence of supernumerary teeth, hypodontia, double teeth, and talon cusp in the primary dentition, and their effect on succedaneous permanent teeth.Materials and Methods:In this prospective cross-sectional study, we clinically investigated 2757 Bengali speaking nursery children (1474 girls and 1283 boys), of age four to six years, at their respective schools, and the presence of supernumerary teeth, hypodontia, double teeth, and talon cusp in the primary dentition were recorded. Children with anomalous primary teeth were further subjected to periapical and panoramic radiographic examination, to determine the status of the underlying permanent teeth.Results:The total prevalence of all anomalies in this study was 1.8%. A total of 38 children (21 girls and 17 boys) had anomalies. The prevalence of anomalies was as follows: Supernumerary teeth (0.4%), hypodontia (0.5%), double teeth (0.4%), and talon cusp (0.07%), in both sexes combined. Radiographic examination showed 50% of the patients (19 children) had anomalies in the permanent dentition.Conclusions:Anomalies in primary dentition exhibited a correlation with anomalies in permanent dentition.
Reactive oxygen species, if produced in excess by oxidative phosphorylation, contributes to mitochondrial DNA damage and progressive respiratory chain dysfunction, leading to various diseases including carcinogenesis. Mitochondria are susceptible to oxidative stress (OS) owing to lack of introns, protective histones, and DNA repair enzymes. However, mitochondria are protected from OS by numerous antioxidants such as superoxide dismutase 2 (SOD2), catalase, glutaredoxin 2 (GLRX2), reduced glutathione (GSH), glutathione peroxidase (GPX), and thioredoxin 2 (TXN2). To obtain insights regarding expression of these mitochondrial antioxidants in oral squamous cell carcinoma (OSCC), we performed qualitative and quantitative estimations of key molecular players of mitochondrial antioxidants during various stages of OSCC by immunoblotting with specific antibodies against antioxidant enzymes and/or biochemical assays. Different mitochondrial antioxidants varied in their expression levels as OSCC progressed. The levels of GPX1, GPX4, and catalase reduced with progression of OSCC. However, GLRX2, PXR3, TXN2, and reduced GSH gradually increased. Expression of SOD2 decreased initially in Stages II and III of OSCC but increased in Stage IV. In conclusion, our findings indicate a complex interplay of various mitochondrial antioxidants in different stages of OSCC, and further insights regarding these molecular players can help us better understand the pathogenesis of OSCC in context of mitochondrial redox status.
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