ABSTRACT
Odontogenic myxomas (OMs) represent asymptomatic, slowly expanding gnathic lesions with aggressive biological behaviour. Though the spectrum of OMs remains classical with multilocular radiolucency and presentation of stellate-shaped cells embedded in a mucoid stroma, they may mimic many other lesions radiographically or histopathologically. We hereby discuss a case of OM in a 28-year-old woman with special emphasis on pathogenesis and differential diagnosis.
ABSTRACT
BACKGROUND: Mitochondrial genome (mtDNA) exhibits greater vulnerability to mutations and/or copy number variations than nuclear counterpart (nDNA) in both normal and cancer cells due to oxidative stress generated by inflammation, viral infections, physical, mechanical, and chemical load. The study was designed to evaluate the mtDNA content in oral potentially malignant disorders (OPMDs) and oral squamous cell carcinoma (OSCC). Various parameters were analyzed including its variation with human papillomavirus (HPV) during oral carcinogenesis. METHODS: The present cross-sectional study comprised of two hundred patients (100 OPMDs and 100 OSCCs) and 100 healthy controls. PCR amplifications were done for mtDNA content and HPV in OPMDs and OSCC using real-time and conventional PCR respectively. RESULTS: The relative mtDNA content was assessed quantitatively and it was observed that mtDNA was greater in OSCC (7.60±0.94) followed by OPMDs (5.93±0.92) and controls (5.37±0.95). It showed a positive linear correlation with habits and increasing histopathological grades. Total HPV-positive study groups showed higher mtDNA content (7.06±1.64) than HPV-negative counterparts (6.21±1.29). CONCLUSIONS: An elevated mutant mtDNA may be attributed to increased free radicals and selective cell clonal proliferation in test groups. Moreover, sustained HPV infection enhances tumorigenesis through mitochondria mediated apoptosis. Since, mtDNA content is directly linked to oxidative DNA damage, these quantifications might serve as a surrogate measure for invasiveness in dysplastic lesions and typify their malignant potential.
ABSTRACT
Oral ulcers constitute one of the most common chief complaints of patients attending any dental practice. The cause of oral mucosal ulceration is generally attributed to acute or chronic trauma from local factors. However, oral lesions may be the initial manifestation of many systemic conditions. Moreover, a group of oral ulcerative lesions have been reported to exhibit vast numbers of eosinophils and known as Traumatic Ulcerative Granuloma with Stromal Eosinophilia (TUGSE). We present two cases of oral ulcers which on microscopic examination exhibited numerous eosinophils from ulcerated epithelium to deep into the submucosa and an exuberant lymphoid proliferation. CD15 immunohistochemical marker was used in these cases to ease the identification of the eosinophils. We also highlight the differential diagnosis of TUGSE that may manifest as oral lesions, as an important diagnostic guide for clinicians in contemporary practice.
Subject(s)
Eosinophilia , Oral Ulcer , Connective Tissue , Eosinophils , Granuloma , HumansABSTRACT
BACKGROUND: Free radicals (FRs) are active chemical substances having unpaired electron(s) which participate in the causation of precancerous lesions or cancer in tobacco habituates. Alterations in the antioxidant levels are reflected throughout the antioxidant enzyme activities in blood, wherein erythrocytes are considered highly sensitive to those enzymes. Our study was therefore aimed to assess the effects of tobacco consumption on erythrocyte antioxidant enzyme- Superoxide dismutase (E-SOD) and evaluate its defensive action. METHODS: E-SOD was estimated in 32 participants categorized in 2 groups (tobacco users and controls). 3 mL venous blood was withdrawn and antioxidant levels were assessed using RANSOD kit (Randox, Catalogue No.-125) as per the manufacturer's instructions. The E-SOD activity was then determined using spectrophotometry and the data was statistically evaluated. RESULTS: The Two-tailed Paired t-test was applied in smokers-SOD intergroup (mean=-124.45, P<0.0001) and chewers-SOD intergroup (mean=-66.70, P=0.1017). The mean SOD values (139.72±36.94) in cases were found to be significantly lower as compared to controls (212.75±37.04). The lowest SOD level was seen with chewers compared to other groups. CONCLUSIONS: E-SOD was found to be lowest among tobacco chewers probably due to the fact of excessive enzyme activity against prolonged release of carcinogens. The variability in the enzyme activity envisaged its potential as a biomarker in establishing the oral potentially malignant disorders (OPMDs) much before the lesions arises or detect the progression of existing lesion to malignancy.
