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      Human papilloma virus genotypes in dysplasia and epithelial hyperplasia of oral cavity using the luminex xmap technology. A multicenter study

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          Abstract

          Background

          Oral cancer associated with high risk (HPV-HR) human papilloma virus (HPV) has been increasing. HPV-HR has been associated with epithelial dysplasia, however, little information exists on its frequency in epithelial hyperplasia lesions. The aim of this study is to compare HPV genotypes in dysplastic and hyperplastic lesions of oral cavity.

          Material and Methods

          Two hundred and fifty oral lesions: 131 dysplasia and 119 hyperplasia from two regions of Colombia were evaluated. One hundred seventy-four coming from urban area and 104 from a high risk population to oral cancer from a rural area. HPV was identified by qPCR and Twenty-four HPVs genotypes were evaluated by Luminex® technology. Logistic regressions were performed to establish the associations between HPV infections with oral dysplasia.

          Results

          Twenty-eight percent (70/250) of the samples were positives for any HPV and HPV-HRs were more frequently than low risk HPVs. HPV-16 was the most detected genotype (16%) followed by HPV-31, 53, 18 and 45. HPV, HPV-HRs and HPV-16 were only associated with dysplasia in urban area; OR 3.28 (CI 95% 1.49-7.17), OR 7.94 (CI 95% 2.97-21.2) and OR 5.90 (CI 95% 2.05-17). Individuals in rural area showed more HPV and HPV-HRs infection in hyperplasic lesions than urban population. The majority of HPV+ lesions had multi-type of HPV (52/70) and the urban individuals showed more genotypes than rural population.

          Conclusions

          HPV-.HRs are frequently found in hyperplastic and dysplastic epithelial lesions. HPV-HRs and HPV-16 were associated with dysplasia in urban population. Rural high risk population and urban population differ in the frequency and variety of HPV genotypes.

          Key words:Human papilloma virus, epithelial dysplasia, epithelial hyperplasia, HPV-genotypes.

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          Most cited references30

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          Molecular biology of human papillomavirus infection and cervical cancer.

          HPVs (human papillomaviruses) infect epithelial cells and cause a variety of lesions ranging from common warts/verrucas to cervical neoplasia and cancer. Over 100 different HPV types have been identified so far, with a subset of these being classified as high risk. High-risk HPV DNA is found in almost all cervical cancers (>99.7%), with HPV16 being the most prevalent type in both low-grade disease and cervical neoplasia. Productive infection by high-risk HPV types is manifest as cervical flat warts or condyloma that shed infectious virions from their surface. Viral genomes are maintained as episomes in the basal layer, with viral gene expression being tightly controlled as the infected cells move towards the epithelial surface. The pattern of viral gene expression in low-grade cervical lesions resembles that seen in productive warts caused by other HPV types. High-grade neoplasia represents an abortive infection in which viral gene expression becomes deregulated, and the normal life cycle of the virus cannot be completed. Most cervical cancers arise within the cervical transformation zone at the squamous/columnar junction, and it has been suggested that this is a site where productive infection may be inefficiently supported. The high-risk E6 and E7 proteins drive cell proliferation through their association with PDZ domain proteins and Rb (retinoblastoma), and contribute to neoplastic progression, whereas E6-mediated p53 degradation prevents the normal repair of chance mutations in the cellular genome. Cancers usually arise in individuals who fail to resolve their infection and who retain oncogene expression for years or decades. In most individuals, immune regression eventually leads to clearance of the virus, or to its maintenance in a latent or asymptomatic state in the basal cells.
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            Oral sexual behaviors associated with prevalent oral human papillomavirus infection.

            Oral human papillomavirus (HPV) infection is a cause of oropharyngeal cancer. We investigated whether sexual behaviors that elevated the odds of oropharyngeal cancer developing in a case-control study similarly elevated the odds of oral HPV infection developing among control patients. HPV infection was detected in 4.8% of 332 control patients from an outpatient clinic and in 2.9% of 210 college-aged men (age range, 18-23 years). Among control patients, the odds of infection developing independently increased with increases in the lifetime number of oral (P = .007, for trend) or vaginal sex partners (P = .003, for trend). Among college-aged men, the odds of oral HPV infection developing increased with increases in the number of recent oral sex partners (P = .046, for trend) or open-mouthed kissing partners (P = .023, for trend) but not vaginal sex partners. Oral sex and open-mouthed kissing are associated with the development of oral HPV infection.
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              Human papillomaviruses in oral carcinoma and oral potentially malignant disorders: a systematic review.

              Human papillomavirus (HPV) in oral carcinoma (OSCC) and potentially malignant disorders (OPMD) is controversial. The primary aim was to calculate pooled risk estimates for the association of HPV with OSCC and OPMD when compared with healthy oral mucosa as controls. We also examined the effects of sampling techniques on HPV detection rates. Systematic review was performed using PubMed (January 1966-September 2010) and EMBASE (January 1990-September 2010). Eligible studies included randomized controlled, cohort and cross-sectional studies. Pooled data were analysed by calculating odds ratios, using a random effects model. Risk of bias was based on characteristics of study group, appropriateness of the control group and prospective design. Of the 1121 publications identified, 39 cross-sectional studies met the inclusion criteria. Collectively, 1885 cases and 2248 controls of OSCC and 956 cases and 675 controls of OPMD were available for analysis. Significant association was found between pooled HPV-DNA detection and OSCC (OR = 3.98; 95% CI: 2.62-6.02) and even for HPV16 only (OR = 3.86; 95% CI: 2.16-6.86). HPV was also associated with OPMD (OR = 3.87; 95% CI: 2.87-5.21). In a subgroup analysis of OPMD, HPV was also associated with oral leukoplakia (OR = 4.03; 95% CI: 2.34-6.92), oral lichen planus (OR = 5.12; 95% CI: 2.40-10.93), and epithelial dysplasia (OR = 5.10; 95% CI: 2.03-12.80). The results suggest a potentially important causal association between HPV and OSCC and OPMD. © 2011 John Wiley & Sons A/S.
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                Author and article information

                Journal
                Med Oral Patol Oral Cir Bucal
                Med Oral Patol Oral Cir Bucal
                Medicina Oral S.L.
                Medicina Oral, Patología Oral y Cirugía Bucal
                Medicina Oral S.L.
                1698-4447
                1698-6946
                January 2020
                24 December 2019
                : 25
                : 1
                : e61-e70
                Affiliations
                [1 ]Unit of Basic Oral Investigation-UIBO, School of dentistry, Universidad El Bosque, Bogotá-Colombia
                [2 ]Cellular and Molecular Immunology Group-INMUBO, School of Dentistry, Universidad El Bosque, Bogotá-Colombia
                [3 ]Universidad El Bosque, Unit of Oral Epidemiology Investigation-UNIECLO, School of dentistry, Bogotá-Colombia
                [4 ]Biomedical Stomatology Research Group, Universidad de Antioquia U de A, Medellín-Colombia
                [5 ]Public Health Investigation Group-GISPOUC, School of dentistry, Universidad de Cartagena. Cartagena. Colombia
                [6 ]Dentistry Research Group-GIOUMEB, Universidad Metropolitana, Barranquilla-Colombia
                [7 ]Institute of Biotechnology, Universidad Nacional de Colombia. Bogotá-Colombia
                [8 ]Bio-Molecular Laboratory. Bogotá-Colombia
                Author notes
                Universidad El Bosque Av. Carrera 9 No. 131 A – 02 Bogotá-Colombia , E-mail: lafauriegloria@ 123456unbosque.edu.co
                Article
                23188
                10.4317/medoral.23188
                6982976
                31880291
                ec0aa78b-c71b-4b93-9553-06d8a76eaeef
                Copyright: © 2020 Medicina Oral S.L.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 September 2019
                : 3 May 2019
                Categories
                Research
                Oral Medicine and Pathology

                Surgery
                Surgery

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