In the United States, cancers of the oral cavity and oropharynx represent approximately three percent of all malignancies in men and two percent of all malignancies in women. The American Cancer Society estimates that 28,900 new cases of oral cancer will be diagnosed in 2002, and nearly 7,400 people will die from this disease. Over 90 percent of these tumors are squamous cell carcinomas, which arise from the oral mucosal lining. In spite of the ready accessibility of the oral cavity to direct examination, these malignancies still are often not detected until a late stage, and the survival rate for oral cancer has remained essentially unchanged over the past three decades. The purpose of this article is to review the clinical features of oral cancer and premalignant oral lesions, with an emphasis on early detection.

/pdf/oral-cancer-and-precancerous-lesions-1ae8yh9kz7.pdf

Oral cancer and precancerous lesions.

Objective. Human papillomavirus (HPV) infection is a significant risk factor for uterine cervical carcinoma. However, the role of HPV infection in oral squamous cell carcinoma (OSCC) is less well defined. To determine the significance of the relationship of this virus in the progressive development of oral cancer, we estimated the risk of HPV detection in normal oral mucosa, precancerous oral tissue, and oral carcinoma using meta-analysis. Study design. Case reports and clinical series published in English-language journals were retrieved by searching MEDLINE (January 1980-August 1998). Review articles were also examined to identify additional studies. Studies that used biochemical, immunologic, microscopic, or molecular analyses to detect HPV in tissue or cells derived from normal oral mucosa (n = 25), benign leukoplakia (n = 21), intraepithelial neoplasia (ie, dysplasia and carcinoma in situ; n = 27), and oral cancer (n = 94) were included in the meta-analysis. Information on sample size, age, sex, method of tissue preservation (ie, fresh, frozen, paraffin-embedded), assay, primer amplification region (early, late), high-risk versus low-risk genotype, and use of tobacco or alcohol was abstracted by one author (C.S.M.). Results. Data from 94 reports that analyzed 4680 samples were included in the meta-analysis. Analyses made by means of a random-effects model with and without adjustments for assay sensitivity showed increased probability of HPV detection in tissue with precancerous and cancerous features compared with normal mucosa. The likelihood of detecting HPV in normal oral mucosa (10.0%; 95% confidence interval [CI], 6.1%-14.6%) was significantly less than of detecting benign leukoplakia (22.2%; 95% CI, 15.7%-29.9%), intraepithelial neoplasia (26.2%; 95% CI, 19.6%-33.6%), verrucous carcinoma (29.5%; 95% CI, 23%-36.8%), and OSCC (46.5%; 95% CI, 37.6%-55.5%). Adjustment of findings for differences in assay sensitivity indicated that these estimates may be conservative. Overall, HPV was between 2 and 3 times more likely to be detected in precancerous oral mucosa and 4.7 times more likely to be detected in oral carcinoma than in normal mucosa. The pooled odds ratio for the subset of studies directly comparing the prevalence of HPV in normal mucosa and OSCC was 5.37, confirming the trend observed in the overall sample. The probability of detecting high-risk HPVs in OSCCs was 2.8 times greater than that of low-risk HPVs. Conclusion. This meta-analysis indicates that HPV is detected with increased frequency in oral dysplastic and carcinomatous epithelium in comparison with normal oral mucosa. The findings provide further quantitative evidence that oral infection with HPV, particularly with high-risk genotypes, is a significant independent risk factor for OSCC. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;91:622-35)

Human papillomavirus as a risk factor for oral squamous cell carcinoma: A meta-analysis, 1982-1997

https://www.surgonc.theclinics.com/article/S1055-3207(15)00026-5/pdf

Epidemiology of head and neck cancer.

For both genders, cancer of the mouth and pharynx ranks sixth overall in the world; it is also the third most common site among males in developing countries. In industrialized countries, men are affected two to three times as often as women, largely due to higher use of alcohol and tobacco. Ethnicity strongly influences prevalence due to social and cultural practices, as well as socioeconomic differences. In population terms, survival rates around the world show little improvement. In terms of etiology, the effects of tobacco use, heavy alcohol consumption, and poor diet together explain over 90 percent of cases of head and neck cancer. All forms of tobacco represent risk factors for oral cancer, but on present evidence, snuff habits as they exist in Scandinavia and probably in the United States carry lower risks of serious health hazards, including oral cancer. Alcohol synergizes with tobacco as a risk factor for all upper aerodigestive tract SCC: this is super-multiplicative for the mouth, additive for the larynx, and between additive and multiplicative for the esophagus. The increase in oral cancer in the Western world has been related to rising alcohol use.

/pdf/tobacco-use-and-oral-cancer-a-global-perspective-2jk6arklrc.pdf

Tobacco Use and Oral Cancer: A Global Perspective

The clinical and histologic features alone cannot accurately predict whether potentially malignant disorders of the oral mucosa remain stable, regress or progress to malignancy. Some of them, with or without epithelial dysplasia, may transform to invasive oral squamous cell carcinomas (OSCC). Identification of molecular markers which can predict disease progression is necessary to improve the management of these disorders. Many genes and signaling pathways have been shown to be involved in the development of OSCC. This review summarizes some molecular markers researched in the detection of pre-cancer. We highlight selected markers that are reported to be significantly associated with progression of potentially malignant disorders to OSCC. These include alterations in genes/pathways which control cellular signaling, cell cycle, apoptosis, genomic stability, cytoskeleton, angiogenesis, etc. However, these genetic tumor markers have so far not gained any use in routine diagnosis and their utility in the prediction of risk of malignant transformation remains unknown. It is, however, clear from the large number of studies, some described in this review, that multiple genes/pathways are involved in the progression from normal to metaplastic/dysplastic, and subsequently to cancer. It is therefore necessary to study those significant alterations in multiple genes simultaneously in biopsy samples from large cohorts of subjects.

Molecular markers in oral epithelial dysplasia: review

Oncogenic human papillomaviruses (HPVs) have been detected in oral squamous cell carcinoma (SCC).HPV16 is the most frequently detected HPV type in oral SCC and is present in up to 22% of cases, either alone or in combination with other HPV typeS. HPV18 is present in up to 14% of caseS. HPV16 and HPV18 are present together in approximately 6% of caseS. However, HPV16 and 18 are also detected in normal oral mucosae (10% and 11% of subjects, respectively). These data suggest that high risk HPV infection may be a co-factor in oral carcinogenesis and that latent HPV infection of the oral mucosa is common. A role for HPV infection in oral car-cinogenesis is supported by the ability of high risk HPVs to immortalize oral keratinocytes in vitro. Immortalization may involve (i) deactivation of pre-formed tumor-suppressor proteins by viral oncoproteins, (ii) blocking of tumor-suppressor gene transcription as a result of HPV oncogene insertion or (iii) stimulation of cellular oncog-ene transcription by the upstream insertion of HPV-derived transcription activating sequenceS. Hence, infection of oral keratinocytes with high risk HPV may be involved in the pathogenesis of some oral SCCs although the evidence implicating HPV in oral carcinogenesis is, at present, mainly circumstantial.

The high risk human papillomaviruses and oral cancer: evidence for and against a causal relationship.

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The high risk human papillomaviruses and oral cancer: evidence for and against a causal relationship.