Tongue cancer risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The most potent risk factor in the development of oral cancer is [[alcohol]] intake, [[tobacco use]] and [[human papillomavirus]] transmitted through sexual contact. The other risk factors include history of betel quid intake, male gender, age over 55 year, [[ultraviolet light]], [[Fanconi anemia]], [[dyskeratosis congenita]], [[lichen planus]], [[graft-versus-host disease]] (GVHD), immune system suppression, mouthwash and irritation from dentures. | The most potent risk factor in the development of oral cancer is [[alcohol]] intake, [[tobacco use]] and [[human papillomavirus]] transmitted through sexual contact. The other risk factors include history of betel quid intake, male gender, age over 55 year, [[ultraviolet light]], [[Fanconi anemia]], [[dyskeratosis congenita]], [[lichen planus]], [[graft-versus-host disease]] (GVHD), immune system suppression, mouthwash and irritation from dentures. | ||
==Risk Factors== | ==Risk Factors== | ||
The major risk factors in the development of tongue cancer includes the following:<ref name="radio">Squamous cell carcinoma of the tongue. Radiopedia(2015) http://radiopaedia.org/articles/squamous-cell-carcinoma-of-the-tongue Accessed on November 16, 2015</ref> | The major risk factors in the development of tongue cancer includes the following:<ref name="radio">Squamous cell carcinoma of the tongue. Radiopedia(2015) http://radiopaedia.org/articles/squamous-cell-carcinoma-of-the-tongue Accessed on November 16, 2015</ref> | ||
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=== '''Oral leukoplakia''' === | === '''Oral leukoplakia''' === | ||
* Leukoplaki is a white plaque on surface of tongue. | * [[Leukoplakia|Leukoplaki]] is a white plaque on surface of tongue. | ||
* It often occurs in individuals under the age of 40.<ref name="pmid16580910">{{cite journal| author=Greer RO| title=Pathology of malignant and premalignant oral epithelial lesions. | journal=Otolaryngol Clin North Am | year= 2006 | volume= 39 | issue= 2 | pages= 249-75, v | pmid=16580910 | doi=10.1016/j.otc.2005.11.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16580910 }}</ref> | * It often occurs in individuals under the age of 40.<ref name="pmid16580910">{{cite journal| author=Greer RO| title=Pathology of malignant and premalignant oral epithelial lesions. | journal=Otolaryngol Clin North Am | year= 2006 | volume= 39 | issue= 2 | pages= 249-75, v | pmid=16580910 | doi=10.1016/j.otc.2005.11.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16580910 }}</ref> | ||
* Leukoplakia can be divided into:<ref name="pmid20308005">{{cite journal| author=van der Waal I| title=Potentially malignant disorders of the oral and oropharyngeal mucosa; present concepts of management. | journal=Oral Oncol | year= 2010 | volume= 46 | issue= 6 | pages= 423-5 | pmid=20308005 | doi=10.1016/j.oraloncology.2010.02.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20308005 }}</ref> | * Leukoplakia can be divided into:<ref name="pmid20308005">{{cite journal| author=van der Waal I| title=Potentially malignant disorders of the oral and oropharyngeal mucosa; present concepts of management. | journal=Oral Oncol | year= 2010 | volume= 46 | issue= 6 | pages= 423-5 | pmid=20308005 | doi=10.1016/j.oraloncology.2010.02.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20308005 }}</ref> | ||
* Homogenous lesions: flat, thin, and white<ref name="pmid18674954">{{cite journal| author=van der Waal I| title=Potentially malignant disorders of the oral and oropharyngeal mucosa; terminology, classification and present concepts of management. | journal=Oral Oncol | year= 2009 | volume= 45 | issue= 4-5 | pages= 317-23 | pmid=18674954 | doi=10.1016/j.oraloncology.2008.05.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18674954 }}</ref> | * [[Homogenous]] lesions: flat, thin, and white<ref name="pmid18674954">{{cite journal| author=van der Waal I| title=Potentially malignant disorders of the oral and oropharyngeal mucosa; terminology, classification and present concepts of management. | journal=Oral Oncol | year= 2009 | volume= 45 | issue= 4-5 | pages= 317-23 | pmid=18674954 | doi=10.1016/j.oraloncology.2008.05.016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18674954 }}</ref> | ||
* Nonhomogenous lesions: white and red lesion | * Nonhomogenous lesions: white and red lesion | ||
* Oral leukoplakia should be confirmed by mucosal biopsy | * Oral leukoplakia should be confirmed by mucosal biopsy | ||
* Surgical excision should be recommended in the presence of moderate and severe epithelial dysplasia | * Surgical excision should be recommended in the presence of moderate and severe epithelial [[dysplasia]] | ||
* In case of using topical retinoic acid, | * In case of using [[topical]] [[Retinoic acid|retinoic acid,]] recurrence rates are 50% after withdrawl<ref name="pmid12216093">{{cite journal| author=Gorsky M, Epstein JB| title=The effect of retinoids on premalignant oral lesions: focus on topical therapy. | journal=Cancer | year= 2002 | volume= 95 | issue= 6 | pages= 1258-64 | pmid=12216093 | doi=10.1002/cncr.10874 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12216093 }}</ref> | ||
===== Risk factors of malignant transformation<ref name="pmid20308005" /> ===== | ===== Risk factors of malignant transformation<ref name="pmid20308005" /> ===== | ||
* Female gender | * Female gender | ||
* Long duration of leukoplakia | * Long duration of [[leukoplakia]] | ||
* Leukoplakia in non-smokers | * Leukoplakia in non-smokers | ||
* Location on the tongue and | * Location on the tongue and floor of the mouth | ||
* Size > 200 mm | * Size > 200 mm | ||
* Non-homogenous type | * Non-homogenous type | ||
* Presence of epithelial dysplasia | * Presence of epithelial [[dysplasia]] | ||
=== '''Oral erythroplakia''' === | === '''Oral erythroplakia''' === | ||
* [[Erythroplakia]] is a red patch on the tongue surface.<ref name="pmid15975518">{{cite journal| author=Reichart PA, Philipsen HP| title=Oral erythroplakia--a review. | journal=Oral Oncol | year= 2005 | volume= 41 | issue= 6 | pages= 551-61 | pmid=15975518 | doi=10.1016/j.oraloncology.2004.12.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15975518 }}</ref> | * [[Erythroplakia]] is a red patch on the tongue surface.<ref name="pmid15975518">{{cite journal| author=Reichart PA, Philipsen HP| title=Oral erythroplakia--a review. | journal=Oral Oncol | year= 2005 | volume= 41 | issue= 6 | pages= 551-61 | pmid=15975518 | doi=10.1016/j.oraloncology.2004.12.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15975518 }}</ref> | ||
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=== '''Oral lichen planus''' === | === '''Oral lichen planus''' === | ||
* Lichen planus is | * [[Lichen planus]] is [[chronic inflammatory]] disease which may affect [[oral mucosa]] between other areas of body.<ref name="pmid21093625">{{cite journal| author=Parashar P| title=Oral lichen planus. | journal=Otolaryngol Clin North Am | year= 2011 | volume= 44 | issue= 1 | pages= 89-107, vi | pmid=21093625 | doi=10.1016/j.otc.2010.09.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21093625 }}</ref> | ||
* It mainly occurs in females between third and sixth decade. | * It mainly occurs in females between third and sixth decade. | ||
* It may be multifocal, papular, bullous, erosive, reticular, and atrophic forms. | * It may be multifocal, [[Papule|papular]], [[bullous]], [[Erosion (dental)|erosive]], reticular, and [[Atrophy|atrophic]] forms. | ||
* Atrophic and erosive pattern are associated with a burning sensation and pain. | * [[Atrophy|Atrophic]] and erosive pattern are associated with a burning sensation and pain. | ||
* Increased malignant transformation risk occurs greater in erosive and atrophic types. | * Increased [[malignant transformation]] risk occurs greater in erosive and atrophic types. | ||
* Histologically, lesions show [[liquefactive necrosis]] of the basal cells, infiltrate of [[lymphocytes]] of superficial [[dermis]], sawtooth rete ridges, and [[hyperkeratosis]]. | * Histologically, lesions show [[liquefactive necrosis]] of the basal cells, infiltrate of [[lymphocytes]] of superficial [[dermis]], sawtooth rete ridges, and [[hyperkeratosis]]. | ||
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===== Stem cell transplantation ===== | ===== Stem cell transplantation ===== | ||
* Patients | * Patients after [[stem cell transplantation]] are at a higher risk for oral squamous cell carcinoma. | ||
* Oral cancer in these patients may have more aggressive behavior with poorer prognosis. | |||
* This effect is supposed to be owing to the continuous lifelong [[Immunosuppression|immune suppression]] and chronic oral [[graft-versus-host disease]]. | |||
* The mutations in [[tumor suppressor genes]] has been reported in patients with cancers of the oral cavity. The most abundant carcinogens in tobacco constitute [[nitrosamines]]. Nitrosamines can damage [[DNA]], leading to point [[mutations]]. These point mutations lead to deregulation of [[tumor suppressor genes]] (''[[TP53]]''), which is located on [[chromosome 17]]. | * The mutations in [[tumor suppressor genes]] has been reported in patients with cancers of the oral cavity. | ||
* The most abundant carcinogens in tobacco constitute [[nitrosamines]]. Nitrosamines can damage [[DNA]], leading to point [[mutations]]. | |||
* These point mutations lead to deregulation of [[tumor suppressor genes]] (''[[TP53]]''), which is located on [[chromosome 17]]. | |||
* The other oncogenes associated with oral squamous cell cancers of tongue include ''[[c-myc]]'' and ''erb -b1''. | * The other oncogenes associated with oral squamous cell cancers of tongue include ''[[c-myc]]'' and ''erb -b1''. | ||
Other less potent risk factors includes the following: | Other less potent risk factors includes the following: | ||
| Line 73: | Line 75: | ||
*Genetics | *Genetics | ||
**[[Fanconi anemia]] | **[[Fanconi anemia]] | ||
**Dyskeratosis | **[[Dyskeratosis congenita]] | ||
**[[Family history]] of [[squamous cell carcinoma]] | **[[Family history]] of [[squamous cell carcinoma]] | ||
*General | *General | ||
Revision as of 19:35, 5 December 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Simrat Sarai, M.D. [2]
Overview
The most potent risk factor in the development of oral cancer is alcohol intake, tobacco use and human papillomavirus transmitted through sexual contact. The other risk factors include history of betel quid intake, male gender, age over 55 year, ultraviolet light, Fanconi anemia, dyskeratosis congenita, lichen planus, graft-versus-host disease (GVHD), immune system suppression, mouthwash and irritation from dentures.
Risk Factors
The major risk factors in the development of tongue cancer includes the following:[1]
- Tobacco smoking
- Cancer of the tongue is correlated the closest with the use of tobacco products.
- Approximately 90% of patients with oral cavity cancers use tobacco products and that the relative risk of oral cavity cancers increases with the amount smoked and the duration of the smoking.
- In persons who smoke the incidence of oral cavity cancers is approximately six times that of those who do not smoke.
- Tobacco exposure causes progressive sequential histological changes to the oral mucosa. Prolonged period of exposure eventually leads to neoplastic transformation, in particular changes in the expression of p53 mutations. If the tobacco exposure is discontinued, these changes may be reversible.
- There is compelling evidence supporting the benefit for head and neck cancer patients to cease smoking after treatment for their cancer. Approximately 40% of patients who continued to smoke after definitive treatment for an oral cavity malignancy developed recurrence or developed a second head and neck malignancy. In patients who stopped smoking after treatment, approximately 6% went on to develop a recurrence.
- There has been recent increase in the incidence of oral cavity cancer in young adults in the recent years. The explosive use of smokeless tobacco, or snuff, in certain regions of the United States has lead to increased numbers of mandibular alveolus, buccal mucosa, and tongue cancers.
- Alcohol ingestion
- The correlation between alcohol consumption, particularly hard liquor, and oral cavity cancer is significant, especially in patients taking more than four consumptions per day.
- Approximately 75% of patients who develop oral cavity cancers consume alcohol, and the cancer occurs six times more often in persons who drink than in those who do not drink. The role of alcohol consumption in the development of tongue cancer appears to be independent of smoking.
- The use of alcohol has a synergistic effect on the risk of carcinogenesis rather than cumulative effect. The risk for a person who drinks alcohol and smokes tobacco is fifteen times that of an individual with neither of these habits.
- Human papillomavirus
- The human papillomavirus, is an etiologic agent for carcinogenesis in the tongue cancer. Human papillomavirus (HPV) has been detected in various amounts in persons with leukoplakia, oral dysplasia, and malignancy. In the subset of patients without other risk factors, HPV should be considered as an etiologic factor. Human papillomavirus (HPV), especially HPV type 16.[2]
- Plummer-Vinson syndrome
- Plummer-Vinson syndrome (Fe deficiency anemia; achlorhydria; and mucosal atrophy of the mouth, pharynx, and esophagus) has been associated with an increased risk of cancer of the tongue. Studies have suggested that vitamins A and C, along with the carotenoids, may be protective against epithelial cancers. Iron and riboflavin deficiencies are known to produce dysplastic changes to the oral mucosa.
Precancerous lesions
Oral leukoplakia
- Leukoplaki is a white plaque on surface of tongue.
- It often occurs in individuals under the age of 40.[3]
- Leukoplakia can be divided into:[4]
- Homogenous lesions: flat, thin, and white[5]
- Nonhomogenous lesions: white and red lesion
- Oral leukoplakia should be confirmed by mucosal biopsy
- Surgical excision should be recommended in the presence of moderate and severe epithelial dysplasia
- In case of using topical retinoic acid, recurrence rates are 50% after withdrawl[6]
Risk factors of malignant transformation[4]
- Female gender
- Long duration of leukoplakia
- Leukoplakia in non-smokers
- Location on the tongue and floor of the mouth
- Size > 200 mm
- Non-homogenous type
- Presence of epithelial dysplasia
Oral erythroplakia
- Erythroplakia is a red patch on the tongue surface.[7]
- It occurs in middle aged and elderly patients and affects the soft palate, the floor of the mouth, and the buccal mucosa mainly.[8]
- Tobacco and alcohol consuming are the most common risk factors.
- The lesion is less than 1.5 cm in diameter, but its size may range between one to four cm.
- Early effective treatment is mandatory as malignant transformation rates are very high.
Oral lichen planus
- Lichen planus is chronic inflammatory disease which may affect oral mucosa between other areas of body.[9]
- It mainly occurs in females between third and sixth decade.
- It may be multifocal, papular, bullous, erosive, reticular, and atrophic forms.
- Atrophic and erosive pattern are associated with a burning sensation and pain.
- Increased malignant transformation risk occurs greater in erosive and atrophic types.
- Histologically, lesions show liquefactive necrosis of the basal cells, infiltrate of lymphocytes of superficial dermis, sawtooth rete ridges, and hyperkeratosis.
- Malignant transformation ratio has been reported in 10% of patients.
Other factors
Stem cell transplantation
- Patients after stem cell transplantation are at a higher risk for oral squamous cell carcinoma.
- Oral cancer in these patients may have more aggressive behavior with poorer prognosis.
- This effect is supposed to be owing to the continuous lifelong immune suppression and chronic oral graft-versus-host disease.
- The mutations in tumor suppressor genes has been reported in patients with cancers of the oral cavity.
- The most abundant carcinogens in tobacco constitute nitrosamines. Nitrosamines can damage DNA, leading to point mutations.
- These point mutations lead to deregulation of tumor suppressor genes (TP53), which is located on chromosome 17.
- The other oncogenes associated with oral squamous cell cancers of tongue include c-myc and erb -b1.
Other less potent risk factors includes the following:
- Lifestyle
- Betel quid
- Genetics
- General
- Male gender
- Ultraviolet light
- Age over 55 year
- Graft-versus-host disease(GVHD)
- Immune system suppression
- Lichen planus
- Unproven risk factors
- Mouthwash
- Irritation from dentures
References
- ↑ Squamous cell carcinoma of the tongue. Radiopedia(2015) http://radiopaedia.org/articles/squamous-cell-carcinoma-of-the-tongue Accessed on November 16, 2015
- ↑ Oropharyngeal cancer. National Cancer Institute(2015) http://www.cancer.gov/types/head-and-neck/hp/oropharyngeal-treatment-pdq Accessed on November 16, 2015
- ↑ Greer RO (2006). "Pathology of malignant and premalignant oral epithelial lesions". Otolaryngol Clin North Am. 39 (2): 249–75, v. doi:10.1016/j.otc.2005.11.002. PMID 16580910.
- ↑ 4.0 4.1 van der Waal I (2010). "Potentially malignant disorders of the oral and oropharyngeal mucosa; present concepts of management". Oral Oncol. 46 (6): 423–5. doi:10.1016/j.oraloncology.2010.02.016. PMID 20308005.
- ↑ van der Waal I (2009). "Potentially malignant disorders of the oral and oropharyngeal mucosa; terminology, classification and present concepts of management". Oral Oncol. 45 (4–5): 317–23. doi:10.1016/j.oraloncology.2008.05.016. PMID 18674954.
- ↑ Gorsky M, Epstein JB (2002). "The effect of retinoids on premalignant oral lesions: focus on topical therapy". Cancer. 95 (6): 1258–64. doi:10.1002/cncr.10874. PMID 12216093.
- ↑ Reichart PA, Philipsen HP (2005). "Oral erythroplakia--a review". Oral Oncol. 41 (6): 551–61. doi:10.1016/j.oraloncology.2004.12.003. PMID 15975518.
- ↑ Hashibe M, Mathew B, Kuruvilla B, Thomas G, Sankaranarayanan R, Parkin DM; et al. (2000). "Chewing tobacco, alcohol, and the risk of erythroplakia". Cancer Epidemiol Biomarkers Prev. 9 (7): 639–45. PMID 10919731.
- ↑ Parashar P (2011). "Oral lichen planus". Otolaryngol Clin North Am. 44 (1): 89–107, vi. doi:10.1016/j.otc.2010.09.004. PMID 21093625.