ABSTRACT
Oral malignant melanoma (OMM) is a very rare disease entity accounting <1% of all other melanomas. Till date, no comprehensive meta-analysis has been conducted regarding the prevalence of malignant melanoma in the oral cavity. Therefore, the present meta-analysis was conducted to update on the prevalence of malignant melanoma in anatomical sites of the oral cavity. Literature search was performed to congregate reports of last 10 years using databases, such as PubMed and ScienceDirect. The search strings used were "palate," "buccal," "gingiva," "gum," "maxillary," "mandibular," "lip," "tongue," "melanoma," "oral melanoma," "malignant melanoma," "prognosis," "risk factors," "noncutaneous" and "diagnosis" of OMM by combining terms using the Boolean operators. MedCalc 16.4.3 software was used for the analysis. "Random effects model" was used in the analysis due to significant heterogeneity in the studies. Proportion method was used to analyze the prevalence. Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed to report the analysis. Out of 130 studies screened, 19 were included in the meta-analysis and a total of 1323 patients were included. The median age of the patients was found to be 61.87 ± 7.78 years (confidence interval 53.8-67 years). All the screened studies showed significant heterogeneity in gender as well as tumor sites (P < 0.0001). Palate (34.29%) was the most commonly affected site in OMM patients. Overall, the results of the meta-analysis suggest that palate is the most prevalent site in OMM. Furthermore, OMM is high in patients between the fifth and sixth decade of life with a male predominance.
ABSTRACT
BACKGROUND: FHIT (Fragile histidine triad) a member of tumor suppressor family, has been extensively studied in many solid tumors including head and neck squamous cell carcinoma. Among all head and neck cyst and tumors odontogenic lesions account approximately 3%-9%. The molecular pathogenesis of these lesions is less explored. Defects in cell cycle regulators and tumor suppressor genes could result in the development of odontogenic cyst and tumors. Hence, we aimed to determine the significant role of a tumor suppressor gene FHIT in most commonly occurring odontogenic lesions mainly ameloblastoma, odontogenic keratocyst and dentigerous cyst. SUBJECTS AND METHODS: Immunohistochemical analysis of FHIT was done in ameloblastoma, odontogenic keratocyst, dentigerous cyst and dental follicle. Interpretation of the stained slides were done using standard scoring criteria by two pathologist. The results were subjected for statistical analysis. RESULTS: Expression of FHIT varied among the groups, with highest negative expression in ameloblastoma 44.4% followed by odontogenic keratocyst 14% and 100%positive expression was seen in dentigerous cyst. The expression levels between the groups were statistically insignificant. CONCLUSION: The varied expression or negative expression of FHIT could be considered as an indicator for aggressive behavior and transformation of preneoplastic/cystic epithelium.
Subject(s)
Acid Anhydride Hydrolases/genetics , Ameloblastoma/genetics , Dentigerous Cyst/genetics , Gene Expression , Neoplasm Proteins/genetics , Odontogenic Cysts/genetics , Humans , Immunohistochemistry , Odontogenic TumorsABSTRACT
BACKGROUND: Oral cancer accounts for 6% of all cancers. The most prevalent form of oral cancer is oral squamous cell carcinoma (OSCC), which accounts for 90% of the oral cancer cases. The major risk factor for development of OSCC is the use of tobacco in various forms. NO has been studied widely over the years due to its role in various physiological and pathophysiological processes, including its complex role in carcinogenesis. MATERIALS AND METHODS: A total of 20 cases of OSCC in tobacco habituers and tobacco non-habituers were retrieved respectively from the archival biopsy specimens. Immunohistochemistry was done to assess the inducible nitric oxide synthase (iNOS) protein. RESULTS: This study was performed to assess the correlation between tobacco and nitric oxide in OSCC in order to know the association of these two in the process of carcinogenesis. The results showed the enhanced expression of iNOS in tobacco habituers in comparison with tobacco non-habituers. Though the increased expression of iNOS is found, significant difference is not obtained with scores, but significant difference was found with intensity of staining. CONCLUSIONS: The results of the present study indicate the enhanced expression in OSCC of tobacco habituers when compared to OSCC of tobacco non-habituers indicating the effect of tobacco on nitric oxide. Carcinogenic chemical compounds in Tobacco induce nitric oxide production by iNOS, by its tumor-promoting effects which may enhance the process of carcinogenesis.
