Incidence Rates Of Oral Cancer Research Articles

Trends in oral cancer rates in the United States, 1973-1996.

To explore changes in demographic distribution, incidence and survival rates of oral cancer in the United States from 1973 through 1996. From the Surveillance, Epidemiology, and End Results (SEER) data, we computed the proportion of oral cancer by demographic characteristics, site, and stage at diagnosis for 1973-84 and 1985-96. We estimated incidence and 5-year relative survival rates of oral cancer by age, gender, and race/ethnicity, and compared survival rates between the two periods. The estimated annual percent change (EAPC) was used to explore trends in incidence rate from 1973 through 1996. Most of the tongue and floor of mouth cancers (>54%) reported during 1973-84 and 1985-96 had spread to a distant site at time of diagnosis. The age-adjusted annual incidence rates of oral cancer decreased among white men from 1973 through 1996, but increased among black men aged 65-69 years, and among young white men (aged 30-34 years) and women (aged 25-29 years). These changes in trend were all statistically significant (testing EAPC=0 at the 0.05 level). Overall, there was no improvement in the 5-year relative survival rate of either whites or blacks with oral cancer. There was little change in early detection of oral cancer or in 5-year relative survival rates between 1973-84 and 1985-96 in nine SEER regions. This suggests a deficiency in professional and public education regarding early diagnosis of oral cancer. Furthermore, the increasing trend of oral cancer among older black men and among younger whites merits further investigation.

Trends in the incidence of lip, oral, and pharyngeal cancer: Connecticut, 1935-94.

Using Connecticut Tumor Registry data we explored trends in age-adjusted (AARs) and age-specific (ASRs) incidence rates for lip, oral, and pharyngeal cancer over the 60-year period 1935-94. Particular attention was given to findings from the most recent series of 5-year periods that have not been previously analyzed. There was a long-term decline in lip cancer AARs by period, and ASRs generally fell over time and with successive birth cohorts. This notable decrease in rates continued through 1990-94 and with the more recent cohorts, particularly among males. Oral cancer AARs for males peaked in the early 1960s and the late 1970s while rates for pharyngeal cancer increased into the late 1970s. For each of these sites, rates began to decline in 1980-84 and have continued to fall into the first half of the 1990s. Among females AARs for oral and pharyngeal cancer increased more than threefold between 1935-39 and 1980-84; however, encouragingly, and in sharp contrast to the earlier trend, rates fell during the most recent 10-year period. ASRs for oral and pharyngeal cancer were increasing by the birth cohort of 1900 and tended to increase through the cohort of 1920 for males and the cohorts of 1920-30 for females. ASRs for subsequent cohorts have remained relatively unchanged or decreased modestly. It is doubtful that the observed trends in lip, oral and pharyngeal cancer incidence are primarily artifactual, but more likely represent secular changes in exposure to environmental risk factors.

Oral cancer in a tobacco-chewing US population—no apparent increased incidence or mortality

Objective. Smokeless tobacco use is an accepted risk factor for oral cancer in the United States, but the major proof of this is based largely on a single epidemiologic (case-control) comparison of women, whereas the chewing of tobacco is predominantly a habit of men. The present investigation sought to compare gender-specific oral cancer mortality and incidence rates in West Virginia, the state with the highest per capita consumption of smokeless tobacco, with rates from other states and with the US average rates. It was hypothesized that the cancer rates for West Virginia males would be significantly greater than the US average and greater than the rates for states with less smokeless tobacco consumption. Study design. Data from the West Virginia Cancer Registry for the years 1993 through 1995 were compared with data from contemporary Surveillance and Epidemiology End Results for the US (with respect to incidence) and from the Center for Disease Control and Prevention's National Center for Health Statistics (with respect to mortality). Results. The average annual incidence rates (per 100,000 population) for oral/pharyngeal cancer in West Virginia males and females were 13.4 and 5.1, respectively; these compared with rates of 15.4 and 5.7 for the US. The average annual mortality rates (per 100,000 population) for the disease in West Virginia males and females were 4.2 and 1.6, respectively; these compared with 4.4 and 1.5 for the US. West Virginia oral/pharyngeal mortality rates for both genders were statistically significantly lower than US rates throughout the years 1950 through 1980. Among other potential oral cancer etiologic factors, the very low prevalence of alcohol abuse in West Virginia seemed to be relevant. Conclusions. The hypothesis was not confirmed by data analysis. West Virginia is the state with the highest per capita consumption of smokeless tobacco, yet it has less oral/pharyngeal cancer than the US average. The authors strongly urge additional and improved epidemiologic evaluation of the oral cancer risk of smokeless tobacco use in US males.

Oral cancer in the UK: to screen or not to screen.

Although oral squamous cell carcinoma accounts for only a small proportion of malignant neoplasms in the UK, oral cancer incidence and mortality rates have been rising in recent years. The natural history of oral cancer is not adequately understood at present and there is very little information about the epidemiology of precancerous lesions in the UK. There are also insufficient data to provide firm evidence that the percentage of cases arising de novo is greater in the UK and the Western world as compared to the Indian subcontinent. Screening for oral cancer by visual examination is simple, inexpensive and causes little discomfort; however, there is no evidence for the effectiveness of screening for oral cancer either in reducing mortality from the disease or in reducing the incidence of invasive disease by detection and treatment of precancerous lesions. There is currently insufficient evidence to recommend population screening for oral cancer in the UK. Measures aimed at primary prevention of the disease may be a more feasible method of disease control at present.

Squamous cell carcinomas of the head and neck in Norway, 1953-92: an epidemiologic study of a low-risk population.

Trends in incidence, five-year relative survival, and mortality among patients in Norway with squamous cell carcinoma of the oral sites, oro-/hypopharynx, and larynx were studied for the period 1953-92. Throughout the first part of the study period, age-adjusted incidence rates (AAIR) of oral cancer remained stable in both genders. Since the end of the 1960s, AAIRs increased by 13 percent per five-year period in males and 12 percent in females. The figures suggest increased male incidence rates of oral cancer in younger age groups. During the same period, AAIRs of cancers of the oro-/hypopharynx in males increased by 19 percent per five-year period. The AAIRs of laryngeal cancer increased steadily from 1953-92 among both males and females by 17 percent and 21 percent per five-year period, respectively. For all sites, changes in AAIRs for males were greater in rural than in urban areas. No improvement in detection of disease at a localized stage was observed for either gender. There are indications of improvements in the five-year relative survival rates for oral and pharyngeal cancer in both genders. For all sites, relative survival was better in younger than in older patients. Only in the case of pharyngeal cancer in males was an increase in disease-specific mortality rates positive for a time trend.

Bionutrition and oral cancer in humans.

Tobacco (smoking and smokeless) use and excessive consumption of alcohol are considered the main risk factors for oral cancer (ICD9 140-149). Conspicuous national and international variations in oral cancer incidence and mortality rates, as well as observations in migrant populations, raise the possibility that diet and nutritional status could be an important etiologic factor in oral carcinogenesis. As shown in this report, abuse of alcohol and tobacco has serious nutritional implications for the host, and generates increased production of reactive free radicals as well as eliciting immunosuppression. Maintenance of optimal competence of the immune system is critical for cancer surveillance. Active oxygen species and other reactive free radicals mediate phenotypic and genotypic alterations that lead from mutation to neoplasia. Consequently, the most widely used chemopreventive agents against oral cancer (e.g., vitamins A, E, C, and beta-carotene) are anti-oxidants/free radical scavengers. These anti-oxidants, both natural and synthetic, neutralize metabolic products (including reactive oxygen species), interfere with activation of procarcinogens, prevent binding of carcinogens to DNA, inhibit chromosome aberrations, restrain replication of the transformed cell, suppress actions of cancer promoters, and may even induce regression of precancerous oral lesions such as leukoplakia and erythroplakia. Malnutrition is characterized by marked tissue depletion of anti-oxidant nutrients, including GSH (gamma-glutamyl-cysteinyl-glycine), a key cellular anti-oxidant as well as a modulator of T-cell activation. GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB(NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia. Alcohol-, tobacco-, and/or malnutrition-induced immunosuppression promotes impaired salivary gland function and oral mucosal immunity, a prominent reduction in the number of helper CD4 cells with less marked changes in number of suppressor T-cells, and depressed NK cell activity, among others. These suggest a breakdown in capacity or the malnourished to mount effective tumor surveillance. This review article underscores the compounding but important roles of nutritional/dietary factors in the long-established causal link between abuse of alcohol and tobacco (smoking and smokeless) and oral cancer.

Oral and pharyngeal cancer incidence in Slovakia 1968-1989.

Slovakia currently has one of the highest incidence rates of oral cancer in Europe. Incidence data from the Slovakian Cancer Registry relating to oropharyngeal cancer are analyzed for the period 1968-1989 to examine trends in the incidence of these malignancies, representing the first such reported time-series from Central Europe. Over this period, rates in males have increased from 4.5 per 100,000 in 1968-1970 to 17.9 per 100,000 in 1987-1989, with more marked increases noted amongst middle-aged males (35 to 64 years), among whom rates have increased from 6.8 to 47.9 per 100,000 over the same period. Rates in women have been relatively low and stable. Changes in rates in men follow a period during the 1950s and 1960s when there was a marked increase in alcohol and tobacco consumption. The magnitude of the increases have resulted in oropharyngeal cancer becoming an important public health problem in Slovakia and emphasizes the importance of measures to prevent further increases in the consumption of tobacco and alcohol.

Changing trends in oral cancer in the United States, 1935 to 1985: A Connecticut study

An extensive epidemiologic study was undertaken in an attempt to analyze patterns of oral cancer distribution and demography in Connecticut between 1935 and 1985. Sources of data for the investigation included both the Connecticut Tumor Registry (CTR) and the University of Connecticut Oral Pathology Biopsy Service. During the 51-year study period, 9,708 cases of primary oral cancer were reported to the CTR. Male age-adjusted incidence rates for overall oral cancer remained stable between 1935 and 1964 (14.5 to 14.8 per 100,000), with a gradual decline to 10.9 per 100,000 in the early 1980s. In contrast, age-adjusted rates for females advanced approximately threefold, from 1.4 per 100,000 in the 1930s to 4.1 per 100,000 in the early 1980s. There was a decrease in age-specific rates of oral cancer in males aged 70 and older; in contrast, age-specific incidence rates in females increased steadily over the same period. It was also found that female birth cohorts born in 1900 and later exhibited higher oral cancer incidence rates than those of previous cohorts. Between the 1960s and the present, male patients 30 to 39 years of age exhibited a nearly fourfold increase in oral cancer incidence; this was not observed among similarly aged females. Connecticut counties with highest oral cancer incidence rates in both sexes were the more densely populated Hartford and New Haven counties. In general, the picture of oral cancer, as revealed through analysis of cases accessioned by the University biopsy service between 1975 and 1986, exhibited similar trends to those disclosed by analysis of CTR data. The increase in female oral cancer incidence combined with the reduced incidence in males appears to account for the dramatic decline in male-to-female ratio for oral cancer in Connecticut between 1935 and 1985. If this trend continues, the incidence of oral cancer in Connecticut women will equal that of men by the mid-1990s.

Oral Cancer Screening in the Elderly

Oral cancers represent approximately 3% of all cancers diagnosed in the United States. Oral cancer is one-fifth as common as cancer of the breast, colon, and lung but more than twice as common as cervical cancer. Incidence rates for oral cancer are highest among older men. Epidemiologic data identify alcohol and tobacco as major risk factors associated with the disease. Screening for oral cancer is a simple, non-invasive procedure which can be easily incorporated into the comprehensive assessment of older patients. Oral cancer screening can detect early, localized lesions which are associated with an improved prognosis. Five-year survival rates are more than four times greater in individuals with localized lesions than those with distant metastases. Since older Americans visit their physician more often than their dentist, the physician's medical examination provides an excellent opportunity to screen for oral cancers.

Leukoplakia and incidence of oral cancer.

Reports from India showing comparatively lower prevalence rates of oral leukoplakia and lower malignant transformation rates than in western countries appear paradoxical because of high incidence rates of oral cancer in India. On a closer examination of available data however, it becomes clear that there is no inconsistency.

Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow-up study of Indian villagers.

Incidence rates of oral cancer and natural history of oral precancerous lesions in a 10-year follow-up study of Indian villagers.

Incidence of oral cancer among 30,000 villagers in india in a 7-year follow-up study of oral precancerous lesions.

In three districts of India where an oral precancer registry comprising 30,000 individuals was established in 1967, regular follow-up surveys have been conducted. This paper discusses the results of a 7-year follow-up study. In Bhavnagar district only one case or oral cancer was reported in this study. In the districts of Ernakulam and Srikakulam, age-adjusted annual incidence rates for oral cancer were found to be 33 and 22 per 100,000 respectively. The significance of tobacco habits and oral submucous fibrosis as etiologic factors is discussed.

Oral squamous cell carcinoma patients which human papilloma virus infection: a case control study in Muwardi Hospital Surakarta, Central Java, Indonesia

Abstract. Prayitno A, Aznar E, Poernomo, Putra ST. 2011. Oral squamous cell carcinoma patients which human papillomavirus infection: a case-control study in Muwardi Hospital Surakarta, Central Java, Indonesia. Nusantara Bioscience 3: 64-67. Annual incidence rates for oral and pharyngeal cancer are estimated at 25 cases per 100,000 in developing countries. Human papillomavirus (HPV) was implicated in pathogenesis of Oral Squamous Cell Carcinoma (OSCC). Aims of this research were to know the incidence of OSSC patient which realized HPV infection. Women OSCC (15) and Benign Oral Squamous Cells (BOSC) (40) tissue biopsy frozen sections were from Departement of Oral and Dental, Muwardi Hospital in Surakarta from January to December 2007. Tissue was cut into two parts. To ascertain the type of neoplasm was subsequently stains with HE. To amplify the L1-HPV gene for 450bp long. Chi-Square Test analyzed the collected data. The result of this experiment showed nine patients from 40 patients BOSC identified have HPV infections (9/40 = 23%). Eleven patient from 15 patient OSCC identified have HPV infections (11/15 = 73%). From Chi-Square analysis have significant differences between BOSC and OSCC. HPV is a factor for OSCC pathogenesis.