METHODS: Dentists were recruited through two main dental associations in Malaysia and attended a 1-day training session on recognizing abnormalities within the oral cavity. Following the training, the dentists conducted screening and provided risk habits cessation advice at their respective clinics for 6 months. The impact of the program was evaluated by determining the number of patients who were screened and/or provided with risk habits cessation advice.
RESULTS: Twenty-six dentists took part in the program and conducted opportunistic screening on a total of 2603 individuals. On average, they screened about 23.0% of their patients and 5.1% were given risk habits cessation advice. Notably, dentists who had lower patient load were more likely to conduct opportunistic screening.
CONCLUSIONS: While the participating private dentists state that they have a role in performing opportunistic screening and providing risk habits cessation advice, these activities are still not a priority area in the private clinics, strongly suggesting that strategies to motivate dentists in this setting are urgently needed.
DESIGN: This was a population-based, cross-sectional study whereby subjects were adults aged 18 years old and above. A workshop on the identification of OML was held to train and calibrate dental officers prior to data collection in the field. Sociodemographic and risk habits data were collected via face-to-face interview, whilst presence of OML and clinical details of lesions such as type and site were collected following clinical oral examination by the examiners. Data analysis was carried out using the Statistical Package for Social Science (SPSS) version 12.0. The association between risk habits and risk of OPMD was explored using logistic regression analysis.
RESULTS: A total of 1634 subjects were recruited. Prevalence of OML for this population was 54.1%. Linea alba was the most common lesion seen (28.7%). This study showed an overall OPMD prevalence of 5.6%. The most common type of OPMD was leukoplakia (64.8%), followed by lichen planus (30.8%). Subjects who only smoked were found to have an increased risk for OPMD of almost four-fold (RR 3.74, 95%CI 1.89-7.41). The highest risk was found for betel quid chewers, where the increased risk observed was more than six times (RR 6.75, 95%CI 3.32-13.72). Alcohol consumption on its own did not seem to confer an increased risk for OPMD, however when practiced concurrently with smoking, a significant risk of more than five times was noted (RR 5.69 95%CI 3.14-10.29).
CONCLUSION: The prevalence of OML was 54.1%, with linea alba being the most commonly occurring lesion. Smoking, alcohol consumption and betel quid chewing were found to be associated with the prevalence of OPMD, which was 5.6%.
MATERIALS AND METHODS: Wistar rats were divided into three groups: T4 group (4-week cigarette smoke exposure), T8 group (8-week cigarette smoke exposure), and control group, which was not exposed to cigarette smoke. The oropharyngeal tissue of the rats from each group was examined histopathologically to count the number of apoptotic cells, and then the blood serum was made to measure the MDA level.
STATISTICAL ANALYSIS: Bonferroni test was performed to see the differences in each group for MDA level. While the data from tissue apoptosis were analyzed using Mann-Whitney U test for the significance. All data were considered significant if p < 0.05.
RESULTS: The MDA level and TA count increased as the duration of cigarette smoke exposure increased. In the T8 group, the MDA level and TA count were significantly higher compared with the T4 and control groups with a p-value
MATERIALS AND METHODS: Thirty Rattus norvegicus will be exposed to two kinds of cigarette smoke by a smoking pump for 4 and 8 weeks. The tongues were collected to analyze the number of macrophages, lymphocytes, and plasma cells with hematoxylin-eosin. The MMP-9 expression was similarly analyzed with immunohistochemical staining and then compared with the control group.
RESULTS: The number of macrophages, lymphocytes, and MMP-9 expression was higher in the 8-week cigarette smoke exposure compared to the 4-week cigarette smoke exposure and the control group (p < 0.000). The number of plasma cell did not differ in the 8-week cigarette smoke exposure from that of the control group (p > 0.05). The number of plasma cells in the tongue tissue during the 4-week cigarette smoke exposure was not determined.
CONCLUSION: Cigarette smoke exposure induces the risk of oral cancer development as a result of an increase in the number of macrophages, lymphocytes, and MMP-9 expression in the tongue epithelial.
METHODS: Seven oral squamous cell carcinoma (OSCC)-related publications, corresponding to 312 samples, were identified for this meta-analysis. The data were analyzed in a 4-step process that included the genome assembly coordination of multiple platforms, assignment of chromosomal position anchors, calling gains and losses, and functional annotation analysis.
RESULTS: Gains were more frequent than losses in the entire dataset. High-frequency gains were identified in chromosomes 5p, 14q, 11q, 7p, 17q, 20q, 8q, and 3q, whereas high-frequency losses were identified in chromosomes 3p, 8p, 6p, 18q, and 4q. Ingenuity pathway analysis showed that the top biological function was associated with immortalization of the epithelial cells (p = 1.93E-04).
CONCLUSION: This study has identified multiple recurrent CNAs that are involved in various biological annotations associated with oral carcinogenesis. © 2015 Wiley Periodicals, Inc. Head Neck 38: E783-E797, 2016.
METHODS: Array comparative genomic hybridization (aCGH) was used to profile unique deletions and amplifications that are involved with tongue and cheek SCC, respectively. This was followed by pathway analysis relating to CNA genes from both sites.
RESULTS: The most frequently amplified regions in tongue SCC were 4p16.3, 11q13.4, and 13q34; whereas the most frequently deleted region was 19p12. For cheek SCC, the most frequently amplified region was identified on chromosome 9p24.1-9p23; whereas the most common deleted region was located on chromosome 8p23.1. Further analysis revealed that the most significant unique pathway related to tongue and cheek SCCs was the cytoskeleton remodeling and immune response effect on the macrophage differentiation pathway.
CONCLUSION: This study has showed the different genetic profiles and biological pathways between tongue and cheek SCCs. © 2013 Wiley Periodicals, Inc. Head Neck 36: 1268-1278, 2014.
METHOD: An electronic search to collate all the information on studies on homeobox gene expression in odontogenic lesions was carried out in four databases (PubMed, EBSCO host, Web of Science and Cochrane Library) with selected keywords. All papers which reported expression of homeobox genes in odontogenic lesions were considered.
RESULTS: A total of eleven (11) papers describing expression of homeobox genes in odontogenic lesions were identified. Methods of studies included next generation sequencing, microarray analysis, RT-PCR, Western blotting, in situ hybridization, and immunohistochemistry. The homeobox reported in odontogenic lesions includes LHX8 and DLX3 in odontoma; PITX2, MSX1, MSX2, DLX, DLX2, DLX3, DLX4, DLX5, DLX6, ISL1, OCT4 and HOX C in ameloblastoma; OCT4 in adenomatoid odontogenic tumour; PITX2 and MSX2 in primordial odontogenic tumour; PAX9 and BARX1 in odontogenic keratocyst; PITX2, ZEB1 and MEIS2 in ameloblastic carcinoma while there is absence of DLX2, DLX3 and MSX2 in clear cell odontogenic carcinoma.
CONCLUSIONS: This paper summarized and reviews the possible link between homeobox gene expression in odontogenic lesions. Based on the current available data, there are insufficient evidence to support any definite role of homeobox gene in odontogenic lesions.