Epidemiology of Oral Cancer

Abdullah Marghalani BDS MSD(c) Umm Al-Qura University, faculty of Dentistry

Cancer is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues Cancer cells can spread to other parts of the body through the blood and lymph systems

Oral Cancer has life and death implications Oral cancer has not always received adequate attention from the medical and the dental community Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304.

Oral Cancer is the most common cancer of the head and neck region Oral squamous cell carcinoma comprises the vast majority of all oral cancer cases Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304.

Oral Cancers include: Lip Tongue Buccal mucosa Floor of the mouth Salivary glands Pharynx Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304.

Surveillance, Epidemiology and End Results (SEER) Program, a premier source for cancer statistics in the United States Collected information on incidence, prevalence and survival from specific geographic areas representing 26 percent of the US population and compile reports on all of these plus cancer mortality for the entire country

National Cancer Institute’s (NCI) Survival, Epidemiology and End Results(SEER)

Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304. Incidence 1988 2004 Oral Cancer as a percentage of all cancers 3.1 2.1 Mortality 1988 2004 Oral Cancer as a percentage of all cancers 1.8 1.3

The age-adjusted incidence was 10.4 per 100,000 per year These rates are based on cases diagnosed in 2002-2006 National Cancer Institute’s (NCI) Survival, Epidemiology and End Results(SEER)

SEER incidence and NCHS mortality statistics

SEER incidence and NCHS mortality statistics Race/ Ethnicity Male Female White 15.6 per 100,000 men 6.1 per 100,000 women Black 16.7 per 100,000 men 5.8 per 100,000 women Asian/Pacific Islander 10.8 per 100,000 men 5.4 per 100,000 women American Indian/Alaska Native 9.2 per 100,000 men 5.1 per 100,000 women Hispanic 9.0 per 100,000 men 3.5 per 100,000 women

From 2002-2006, median age at diagnosis for oral cancer was 62 years of age SEER incidence and NCHS mortality statistics

SEER incidence and NCHS mortality statistics Percentage Age 0.6% Under 20 2.4% 20 and 34 6.8% 35 and 44 20.9% 45 and 54 26.2% 55 and 64 21.3% 65 and 74 16.1% 75 and 84 5.8% 85+

The age-adjusted death rate was 2.6 per 100,000 per year These rates are based on patients who died in 2002-2006 SEER incidence and NCHS mortality statistics

SEER incidence and NCHS mortality statistics Race/Ethnicity Male Female White 3.7 per 100,000 men 1.4 per 100,000 women Black 6.5 per 100,000 men 1.6 per 100,000 women Asian/Pacific Islander 3.2 per 100,000 men 1.3 per 100,000 women American Indian/Alaska Native 3.6 per 100,000 men 1.5 per 100,000 women Hispanic 2.5 per 100,000 men 0.8 per 100,000 women

The median age at death for oral cancer was 68 years of age SEER incidence and NCHS mortality statistics

SEER incidence and NCHS mortality statistics Percentage Age 0.2% Under 20 0.8% 20 and 34 3.4% 35 and 44 14.6% 45 and 54 23.6% 55 and 64 23.9% 65 and 74 22.2% 75 and 84 11.2% 85+

Relative survival rate: The percentage of people still alive 5 years after diagnosis, adjusted for those who died for some other reasons over the 5 years It is the likelihood that a person will not die from causes specifically related to cancer over 5 years Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304.

The overall 5-year relative survival rate from 1999-2005 was 61.0% SEER incidence and NCHS mortality statistics

SEER incidence and NCHS mortality statistics 5-year relative survival rate Race/ sex 62.4% White Male 63.8% White Female 38.2% Black Male 53.2% Black Female

Staging provides a measure of disease progression, detailing the degree to which the cancer has advanced. SEER incidence and NCHS mortality statistics Stage Distribution 5 year relative survival rate Local 34% 82.7% Regional 46% 54.3% Distant 14% 31.8% Unknown 7% 53.4%

TNM Staging System Summary Staging System SEER Extent of Disease(EOD) Staging System Collaborative Staging System Collaborative Staging System Manual and Coding Instructions version 01.04.00

Then, staging which range from Stage 0 through Stage IV Collaborative Staging System Manual and Coding Instructions version 01.04.00 T extent of the primary tumor N absence or presence and extent of regional lymph node metastasis M absence or presence of distant metastasis

Has also been called General Staging, California Staging, and SEER Staging It is a single digit system with only 8 categories SEER Summary Staging Manual-2000 Code Definition 0 In situ 1 Localized only 2 Regional by direct extension only 3 Regional lymph nodes involved only 4 Regional by BOTH direct extension AND lymph node involvement 5 Regional, NOS (Not Otherwise Specified) 7 Distant site(s)/node(s) involved 9 Unknown if extension or metastasis (unstaged, unknown, or unspecified)

SEER EOD is a five-field, 10 digit system Collaborative Staging System Manual and Coding Instructions version 01.04.00 Description Digit Tumor size 3 Extension of the primary tumor 2 regional lymph node involvement 1 number of pathologically reviewed regional lymph nodes that are positive 2 number of pathologically examined regional lymph nodes 2

SEER EXTENT OF DISEASE 3 rd EDITION

LYMPH NODES: 0 No lymph node involvement 1 One positive ipsilateral node <=3 cm in greatest diameter 2 One positive ipsilateral node>=3 and <=6 cm in greatest diameter 3 Multiple positive ipsilateral nodes <6 cm 4 Ipsilateral, node size not stated 5 Bilateral and/or contralateral positive nodes <6 cm or size not stated 6 Any positive node(s), at least one >6 cm 7 Other than above 8 Lymph Nodes, NOS 9 UNKNOWN; not stated SEER EXTENT OF DISEASE 3 rd EDITION

Addressed the staging inconsistency Most of the data items have habitually been collected by cancer registries, including tumor size, extension, lymph node status, and metastatic status It was sponsored by: SEER program CDC( National Program of Cancer Registries) American College of Surgeon Commission on Cancer Collaborative Staging System Manual and Coding Instructions version 01.04.00

Tobacco smoke contains as many as 50 known carcinogens Amount and duration of use Whether it is smoked or used smokeless Stopping smoking reduces the risk About 1 out of 3 people who continue to smoke after their cancer seems to be cured will develop a second cancer of the oral cavity, oropharynx, or larynx (voice box), compared with less than 1 in 10 of those who stop smoking www.cda-adc.ca/jcda/vol-74/issue-3/269.html

Amount and duration The risk increases with increased consumption and duration of use. The risk is reduced when the alcohol is stopped www.cda-adc.ca/jcda/vol-74/issue-3/269.html

In a case-control study (1992–1995), the authors examined oral cancer risk in Puerto Rico population Heavy consumers of liquor (≥43 drinks per week) had strongly increased risks of oral cancer (odds ratio = 6.4, 95% confidence interval: 2.4-16.8) Huang WY, Winn DM, Brown LM, et al. Alcohol concentration and risk of oral cancer in Puerto Rico. Am J Epidemiol 2003;157:881–887.

Heavy smokers and drinkers were estimated to have about 50 fold greater risk of OC(OR=50.65; 95%CI, 19.11-134.24) than those who never smoked and never drunk In other studies, they found that, at least 80% of OC cases are attributable to tobacco and alcohol exposure Castellsague X, Quintana MJ, Martinez MC, et al. The role of type of tobacco and type of alcoholic beverage in oral carcinogenesis. Int J Cancer 2004;108:741–749

Long term exposure to strong sunlight (lip cancer) Human Papilloma Virus (HPV) Poor diet Genetics Poorly fitting dentures (lack supportive evidence) Chronic inflammation ( lichen planus) Mouth wash???

HPV is related to sexual behavior, in particular with number of oral sex partners Especially cancer of the tonsils, soft palate and base of the tongue Primarily HPV-16 which accounts for more than 90% of cases of HPV-positive SCC of the head and neck Oral Squamous Cell Carcinomas associated with HPV have been found to have better outcomes, being more responsive to radiotherapy and showing higher survival rates Chocolatewala N, Chaturvedi P, Role of human papilloma virus in the oral canrcinogenesis: An Indian perspective.Cancer Res Ther. 2009;5:71-77

Meta- analysis(2006) of 17 studies found the association of HPV-16 is strongest for tonsillar cancer(OR=15.1; 95%CI: 6.8-33.7) Intermediate for oropharyngeal cancer(OR= 4.3, 95% CI: 2.1–8.9) Weakest for oral cancer (OR=2.0, 95% CI: 1.2–3.4) And laryngeal cancer (OR= 2.0, 95% CI: 1.0–4.2) HobbsC., et al. Human papillomavirus and head and neck cancer: a systematic review and meta-analysis. Clinical Otolaryngology. 31(4): 259-266

Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6) HPV-16 was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio= 19.4; 95% CI: 3.3 to 113.9) and among those without such a history (odds ratio=33.6; 95% CI, 13.3 to 84.8) D’Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakhry C, Koch WM, et al. Case-control study of human papilloma virus and oropharyngeal cancer. N Engl J Med 2007 ;356: 1944-1956

In 2008, a study demonstrated 71% 5-year survival rate in HPV-positive tonsillar cancer subjects Compared to 36% 5-year survival rate in HPV-negative tonsillar cancer subjects(p=0.023) The mechanism of improved survival rate in HPV- associate HNSSC is still unclear Hennessey PT, Westra WH, Califano J.. Human papillomavirus and head and neck squamous cell carcinoma: recent evidence and clinical implications. J Dent Res. 2009 Apr;88(4):300-6

The following points should be considered: Mouth wash use is elevated among drinkers and especially among smokers Underreporting of alcohol consumption by the subjects (overestimation) Not all studies included information about the alcohol content of the used mouth wash(most mouth wash contain ethanol)

In 1979, Waver and colleagues first suggested a link between ACM and OC In a case series of 200 subjects with OC 11 of them did not smoke or drunk 10 of the 11 used mouth wash Case-control study was reported of the 200 cases and 50 controls RR was not provided(NS) But, the results were positive when the case group was restricted to the original 11 subjects Cole P., Rodu B., Mathisen A. Alcohol-containing mouth wash and oropharyngeal cancer A review of the epidemiology. J Am Dent Assoc 2003;134;1079-1087

In 1983, Blot and colleagues conducted a case-control study of OC among women(did not address ACM) Follow up study was designed with 206 cases and352 controls The overall RR was 1.2 for mouth wash use BUT The alcohol content was unknown The results were not adjusted for ACB use No results were shown for non-drinkers Cole P., Rodu B., Mathisen A. Alcohol-containing mouth wash and oropharyngeal cancer A review of the epidemiology. J Am Dent Assoc 2003;134;1079-1087

In 1985, Mashberg and colleauges conducted a case-control study with 95 men cases and 915 men controls in New Jersey Veterans Administration hospital RR was 0.9 after controlling of smoking and ACB use. BUT Generalizability is limited(men and VA hospital) Cole P., Rodu B., Mathisen A. Alcohol-containing mouth wash and oropharyngeal cancer A review of the epidemiology. J Am Dent Assoc 2003;134;1079-1087

Several retrospective analyses of the available literature undertaken in 1995 and 2004 They found no evidence to support an association between the use of daily mouth wash and OC development Elmore JG, Horwitz RI. Oral cancer and mouthwash use: evaluation of the epidemiologic evidence. Otolaryngol Head Neck Surg 1995;113:253–261 Carretero Pelaez MA, Esparza Gomez GC, Figuero RE, Cerero LR. Alcohol-containing mouthwashes and oral cancer. Critical analysis of literature. Med Oral 2004;9:120–123.

Burt B, Ekland S. Dentistry, Dental Practice and the Community. 2005:294-304. www.cda-adc.ca/jcda/vol-74/issue-3/269.html accessed on 11/05/2009 . Chocolatewala N, Chaturvedi P, Role of human papilloma virus in the oral canrcinogenesis: An Indian perspective.Cancer Res Ther. 2009;5:71-77 Guha N, Boffetta P, Wunsch Filho V, et al. Oral health and risk of squamous cell carcinoma of the head and neck and esophagus: results of two multicenteric case-control studies. Am J Epidemiol 2007;166:1159-1173 National Cancer Institute’s (NCI) Survival, Epidemiology and End Results(SEER). Collaborative Staging System Manual and Coding Instructions version 01.04.00 SEER Summary Staging Manual-2000

Bender P. Genetics of Cleft Lip and Palate. Journal of Pediatric Nursing. 2000;15:242-249 Castellsague X, Quintana MJ, Martinez MC, et al. The role of type of tobacco and type of alcoholic beverage in oral carcinogenesis. Int J Cancer 2004;108:741–749 HobbsC., et al. Human papillomavirus and head and neck cancer: a systematic review and meta-analysis. Clinical Otolaryngology. 31(4): 259-266

D’Souza G, Kreimer AR, Viscidi R, Pawlita M, Fakhry C, Koch WM, et al. Case-control study of human papilloma virus and oropharyngeal cancer. N Engl J Med 2007 ;356: 1944-1956 Hennessey PT, Westra WH, Califano J.. Human papillomavirus and head and neck squamous cell carcinoma: recent evidence and clinical implications. J Dent Res. 2009 Apr;88(4):300-6 Cole P., Rodu B., Mathisen A. Alcohol-containing mouth wash and oropharyngeal cancer A review of the epidemiology. J Am Dent Assoc 2003;134;1079-1087 Elmore JG, Horwitz RI. Oral cancer and mouthwash use: evaluation of the epidemiologic evidence. Otolaryngol Head Neck Surg 1995;113:253–261 Carretero Pelaez MA, Esparza Gomez GC, Figuero RE, Cerero LR. Alcohol-containing mouthwashes and oral cancer. Critical analysis of literature. Med Oral 2004;9:120–123. SEER EXTENT OF DISEASE 3 rd EDITION

Epidemiology of Oral Cancer

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