Context:Significant increase in vascularity occurs during the transition from normal oral mucosa, through differing degrees of dysplasia, to invasive squamous cell carcinoma (SCC).Aims:To evaluate microvessel density (MVD) and vascular endothelial growth factor (VEGF) expression in oral tumorigenesis and correlate it with the clinicopathological characteristics.Settings and Design:VEGF expression and MVD were quantified immunohistochemically using anti-VEGF and anti-CD34 antibody.Materials and Methods:For this study we used a total of 60 archival specimens, including 10 normal oral mucosa (NOM), 7 mild epithelial dysplasia (Mild ED), 8 moderate epithelial dysplasia (Mod ED), 5 severe epithelial dysplasia (SED), 14 well-differentiated SCC, 11 moderately-differentiated SCC, and 5 poorly-differentiated SCC. VEGF expression was assessed in relation to the localization, intensity, and area of the immunohistochemically stained cells. MVD was evaluated using the Image-Pro® Plus software.Statistical Analysis:One-way ANOVA (F test) was carried out for comparing the parameters for multiple groups such as different histopathological grades of dysplasia and carcinoma. Comparison between groups was carried out using the Student's ‘t’ test. Correlations between VEGF score and MVD were estimated using the Karl Pearson coefficient of correlation.Results:VEGF and MVD appeared to increase with disease progression and were statistically higher in oral SCC than in epithelial dysplasia and normal buccal mucosa. There was significant correlation between VEGF expression and MVD.Conclusions:These findings indicate that VEGF expression is upregulated during head and neck tumorigenesis.
Oxygen derived species such as hydrogen peroxide, superoxide anion radical, hydroxyl radical (OH-), and singlet oxygen are well known to be cytotoxic and have been implicated in the etiology of a wide array of human diseases, including cancer. Various carcinogens may also partly exert their effect by generating reactive oxygen species (ROS) during their metabolism. Oxidative damage to cellular DNA can lead to mutations and may, therefore, play an important role in the initiation and progression of multistage carcinogenesis. ROS influences central cellular processes such as proliferation, apoptosis, and senescence which are implicated in the development of cancer. Understanding the role of ROS as key mediators in signaling cascades may provide various opportunities for pharmacological intervention.
Lipid peroxidation induced by reactiveoxygen species (ROS) is involved in the pathogenesis of malignancy. Overall, lipid peroxidation levels are indicated by malondialdehyde (MDA), which is the most frequently used biomarker to detect oxidative changes. Antioxidant defense systems such as glutathione (GSH) limit cell injury induced by ROS. Therefore, MDA and GSH can be used to monitor oxidative stress (OS). Hence, this study aimed to evaluate and compare both salivary and serum levels of MDA and GSH in oral leukoplakia and oral squamous cell carcinoma (OSCC) patients, and healthy controls. The study included 100 subjects comprising 30 apparently healthy controls, 30 patients with oral leukoplakia and 40 clinically and histologically diagnosed patients with OSCC. Saliva and blood samples were obtained and evaluated for MDA and GSH. The study revealed enhanced MDA levels in saliva and serum in oral leukoplakia and OSCC patients as compared to controls. On the other hand, significant decreases were seen in serum and salivary GSH levels in oral leukoplakia and OSCC patients as compared to controls. Augmentation of OS in blood and saliva is reflected by increase in MDA and decrease in GSH levels, indicating that tumor processes cause an imbalance of oxidant-antioxidant status in cell structures.(J Oral Sci 56, 135-142, 2014)
Oral cancer is one of the most common cancers and it constitutes a major health problem particularly in developing countries. Oral squamous cell carcinoma (OSCC) represents the most frequent of all oral neoplasms. Several risk factors have been well characterized to be associated with OSCC with substantial evidences. The etiology of OSCC is complex and involves many factors. The most clearly defined potential factors are smoking and alcohol, which substantially increase the risk of OSCC. However, despite this clear association, a substantial proportion of patients develop OSCC without exposure to them, emphasizing the role of other risk factors such as genetic susceptibility and oncogenic viruses. Some viruses are strongly associated with OSCC while the association of others is less frequent and may depend on cofactors for their carcinogenic effects. Therefore, the exact role of viruses must be evaluated with care in order to improve the diagnosis and treatment of OSCC. Although a viral association within a subset of OSCC has been shown, the molecular and histopathological characteristics of these tumors have yet to be clearly defined.
Extranodal NK/T-cell lymphoma, nasal type (ENKL) is a rare lymphoid neoplasm, which in the past has been grouped with a variety of granulomatous diseases. It is an aggressive non-Hodgkin’s type characterized clinically by aggressive, nonrelenting destruction of the midline structures of the palate and nasal fossa. Despite the malignant clinical course, histological diagnosis can be difficult because of extensive tissue necrosis and multiple biopsies that are often required and has an ominous prognosis, as the average survival rate is between 6 and 25 months as reported with a large number of Asian studies. Several American and European studies have shown similar results. This is the case report of a 60-year-old male patient who presented with nasal obstruction and foul smelling, ulcerative lesion over the palate of 6 months duration, which had been treated with antibiotics and anti-inflammatories without success. After performing a number of diagnostic tests, it was found histologically and confirmed by immunohistochemical analysis that the patient had an ENKL, nasal type (also known as angiocentric T-cell lymphoma).
These findings are suggestive of role of MFs with the creation of a permissive environment for tumor invasion in OSCC. Hence the presence of MF is a prognostic marker and evaluation of the frequency in the stroma can be used as therapeutic targets.
Oral cancer appears to be increasing in incidence, and mortality has hardly improved over the past 25 years. Better understanding of the etiopathogenesis should lead to more accurate and earlier diagnosis and more effective treatments with fewer adverse effects. Despite increasing interest in the possible relationships between bacteria and the different stages of cancer development, the association of bacteria with cancer of the oral cavity has yet to be adequately examined. Different bacteria have been proposed to induce carcinogenesis, either through induction of chronic inflammation or by interference, either directly or indirectly, with eukaryotic cell cycle and signaling pathways or by metabolism of potentially carcinogenic substances like acetaldehyde, causing mutagenesis. This review presents the possible carcinogenesis pathway involved in bacterial carcinogenesis, commonly implicated bacteria in oral carcinogenesis and their role in cancer therapeutics as well.
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