Oral cancer is an important health issue. The WHO predicts a continuing worldwide increase in the number of patients with oral cancer, extending this trend well into the next several decades. In the US the projected number of new cases of oral and oropharyngeal cancer will exceed 31 000 per year. Mortality due to cancers in this region exceeds the annual death rate is the US caused by either cutaneous melanoma or cervical cancer.
Significant agents involved in the etiology of oral cancer in Western countries include sunlight exposure, smoking and alcohol consumption. Use of the areca or betel nut in many cultures is a major etiological factor outside of the USA. Other etiologic factors associated with oral squamous cell carcinoma, but far less significant statistically, include syphilis and sideropenic dysphagia. Recently, strong evidence for an etiological relationship between human papilloma virus and a subset of head and neck cancers has been noted.
It is generally accepted that most sporadic tumors are the result of a multi-step process of accumulated genetic alterations. These alterations affect epithelial cell behavior by way of loss of chromosomal heterozygosity which in turn leads to a series of events progressing to the ultimate stage of invasive squamous cell carcinoma. The corresponding genetic alterations are reflected in clinical and microscopic pathology from hyperplasia through invasiveness.
A wide range of mucosal alternations fall within the rubric of leukoplakia. Proliferative verrucous leukoplakia represents a relatively new type of leukoplakia that is separate from the more common or less innocuous form of this condition. Erythroplakia is particularly relevant considering its almost certain relationship with dysplasia or invasive carcinoma.
Squamous cell carcinoma will develop from antecedent dysplastic oral mucosal lesions if an early diagnosis has not been made and treatment given. Early diagnosis within stages I and II correspond to a vastly improved 5-year survival rate when compared with more advanced stage III and IV lesions.
Surgical management of this disease remains the mainstay of treatment. Other therapies include radiation and chemotherapy options that may be used adjunctively and palliatively. Following treatment, it is important to understand the significant risks of second primary cancers developing within the upper aerodigestive tract as a result of field cancerization. The most important message is that early detection of the asymptomatic early stage oral cancer translates in general terms to satisfactory clinical outcome and cure in most patients.
Wingo P.E.W., Rawest L.A., Rosenberg A.M., et al. Cancer incidence and mortality, a report card for the U.S. Cancer 1998; 82 (6): 1197–1207PubMedCrossRefGoogle Scholar
Macfarlane G.J., Boyle P., Evstifeeva T.V., et al. Rising trends of oral cancer worldwide: the result of an old public health problem. Cancer Causes Control 1994; 5 (3): 259–265PubMedCrossRefGoogle Scholar
Young Jr J.L., Percy C.L., Ardyce M.S., et al. Cancer incidence and mortality in the United States, 1973–1977. Washington, DC: US Government Printing Office; 1981. NCI Monograph no. 57Google Scholar
Gillison M.L., Koch W.M., Capone R.B., et al. Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. J Natl Cancer Inst 2000; 82 (9): 709–720CrossRefGoogle Scholar
Gillison M.L., Koch W.M., Shah K.V. Human papillomavirus in head and neck squamous cell carcinoma: are some head and neck cancers a sexually transmitted disease? Curr Opin Oncol 1999; 11 (3): 191–199PubMedCrossRefGoogle Scholar
Renan M.J. How many mutations are required for tumor genesis? Implications from human cancer data. Mol Carcinog 1993; 7: 139–146PubMedCrossRefGoogle Scholar
Vogelstein B., Fearon E.R., Hamilton S.E., et al. Genetic alterations during colorectal tumor development. N Engl J Med 1988; 319: 525–532PubMedCrossRefGoogle Scholar
Sidransky D., Mikkelsen T., Schwechheimer K., et al. Clonal expansion of p53 mutant cells is associated with brain tumor progression. Nature 1992; 355: 846–847PubMedCrossRefGoogle Scholar
Simoneau A.R., Jones P.A. Bladder cancer: the molecular progression to invasive disease. World J Urol 1994; 12: 89–95PubMedCrossRefGoogle Scholar
Dalbagui G., Presti J., Reuter V., et al. Genetic alterations in bladder cancer. Lancet 1993; 342: 469–471CrossRefGoogle Scholar
Califano J., van der Reit P., Westra W., et al. Genetic progression model for head and neck cancer: implications for field cancerization. Cancer Res 1996; 56: 2488–2492PubMedGoogle Scholar
Bouquot J.E., Gorlin R.J. Leukoplakia, lichen planus and other oral keratoses in 23,616 white Americans over the age of 35 years. Oral Surg Oral Med Oral Pathol 1986; 61 (4): 373–381PubMedCrossRefGoogle Scholar
Cady B., Caitlin D. Epidermoid carcinoma of the gum: a 20 year survey. Cancer 1969; 22: 551–569CrossRefGoogle Scholar
Guillamondegui O.M., Oliver B., Hayden R. Cancer of the anterior floor of the mouth: selective choice of treatment and analysis of failure. Am J Surg 1980; 140: 560–562PubMedCrossRefGoogle Scholar
White D., Byers R.M. What is the initial preferred method of treatment for squamous cell carcinoma of the tongue? Am J Surg 1980; 140: 553–555PubMedCrossRefGoogle Scholar
Kowalski L.P., Bagietto R., Lara J.R., et al. Prognostic significance of the distribution of neck node metastasis from oral carcinoma. Head Neck 2000; 22 (3): 207–214PubMedCrossRefGoogle Scholar
Johnson J.T., Barnes L., Myers E.N., et al. The extracapsular spread of tumors in cervical lymph nodes metastasis. Arch Otolaryngol 1981; 107: 725–729PubMedCrossRefGoogle Scholar
Khuri F.R., Lippman S.M., Spitz M.R., et al. Molecular epidemiology and retinoid chemoprevention of head and neck cancer. J Natl Cancer Inst 1997; 89 (3): 199–211PubMedCrossRefGoogle Scholar
National Cancer Institute Cancer statistics review, 1973–1990. Bethesda (MD): U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health; 1993. DHHS publication NIH-93-2789Google Scholar
Silverman Jr S. Oral cancer. Hamilton (ON): American Cancer Society, B.C. Decker, 1998Google Scholar
Dimitroulis G., Reade P., Wiesenfield D. Referral patterns of patients with oral squamous cell carcinoma, Australia. Eur J Cancer B Oral Oncol 1992; 288 (Pt B): 23–27CrossRefGoogle Scholar