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{{Tongue cancer}}
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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.<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 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:<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>
==Tongue cancer risk factors==
*[[Tobacco]] smoking
The major risk factors in the development of tongue cancer include the following:<ref name="risk">{{cite book | last = Doherty | first = Gerard | title = Current diagnosis & treatment : surgery | publisher = Lange Medical Books/McGraw-Hill | location = New York | year = 2010 | isbn = 0071635157 }}</ref> <ref name="risk1">{{cite book | last = Som | first = Peter | title = Head and neck imaging | publisher = Mosby | location = St. Louis, Mo | year = 2003 | isbn = 0323009425 }}</ref> <ref name="risk2">{{cite book | last = Harrison | first = Louis | title = Head and neck cancer : a multidisciplinary approach | publisher = Lipppincott Williams & Wilkins | location = Philadelphia | year = 2009 | isbn = 0781771366 }}</ref>
**Cancer of the tongue is correlated the closest with the use of tobacco products.
*'''[[Tobacco]] smoking'''
**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.
**Cancer of the tongue is correlated the closest with the use of [[tobacco]] products.
**In persons who smoke the incidence of oral cavity cancers is approximately six times that of those who do not smoke.  
**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.
**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.
**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]]. A prolonged period of exposure eventually leads to [[Neoplastic|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 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.
**There has been a 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
*'''[[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.  
**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]].  
**Approximately 75% of patients who develop oral cavity cancers consume alcohol, and 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.
**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]]
*[[Human papillomavirus|'''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.<ref name="NIH">Oropharyngeal cancer. National Cancer Institute(2015) http://www.cancer.gov/types/head-and-neck/hp/oropharyngeal-treatment-pdq Accessed on November 16, 2015</ref>
**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.<ref name="NIH">Oropharyngeal cancer. National Cancer Institute(2015) http://www.cancer.gov/types/head-and-neck/hp/oropharyngeal-treatment-pdq Accessed on November 16, 2015</ref>
*[[Plummer-Vinson syndrome]]
*[[Plummer-Vinson syndrome|'''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]].  
**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 ==
== Precancerous lesions ==


=== '''Oral leukoplakia''' ===
=== '''Oral leukoplakia''' ===
* Leukoplaki is A white plaque it often occurs in individuals under the age of 40[12].  
* [[Leukoplakia]] is a white plaque on surface of tongue
* Leukoplakia is seen six times more among smokers than among non-smokers[1].
* 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 two subtypes including homogeneous and non-homogeneous types[1].  
* [[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 are characterized by uniformly flat, thin, uniformly white in colour and shows shallow cracks of the surface keratin[1,13].  
**[[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 have been defined as a white and red lesion (known as ''erythroleukoplakia'') that may be either irregularly flat (speckled) or nodular (Figure 1).
**Nonhomogenous lesions: white and red lesion  
* Verrucous leukoplakia is yet another type of non-homogenous leukoplakia[ 14].
* Oral [[leukoplakia]] should be confirmed by biopsy
* Histopathologically, two distinct appearances may be seen as dysplastic or non-dysplastic leukoplakia.  
* Surgical excision should be recommended in the presence of moderate and severe epithelial [[dysplasia]]  
 
* In case of using [[topical]] [[Retinoic acid|retinoic acid,]] recurrence rates are 50% after withdrawal<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 =====
'''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/or floor of the mouth
* Location on the tongue and floor of the mouth
* Size > 200 mm2
* Size > 200 mm
* Non-homogenous type
* Non-homogenous type
* Presence of epithelial dysplasia
* Presence of epithelial [[dysplasia]]
The diseases should be considered in the differential diagnosis including aspirin burn, chemical injury, oral pseudomembranous and hyperplastic candidiasis,
 
frictional lesions, oral hairy leukoplakia, leukoedema, linea alba, lupus erythematosus, morsicatio buccarum, papilloma and allied lesions, mucous patches in secondary syphilis, tobacco-induced lesions, smoker’s palate (nicotinic stomatitis), stuff-induced lesion, white sponge nevus, oral lichen planus (OLP), and lichenoid reaction[1,13].
 
Oral leukoplakia should be confirmed by mucosal biopsy.
 
Surgical excision should be recommended in the presence of moderate and severe epithelial dysplasia.
 
Recurrence of leukoplakia was reported as approximately 50% after withdrawing the topical retinoic acid[21].
 
=== '''Oral erythroplakia''' ===
=== '''Oral erythroplakia''' ===
* Erythroplakia is a red patch that cannot be characterized clinically or pathologically as any other definable disease.  
* [[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>
* It mainly occurs in the middle aged and the elderly.
* It occurs in middle aged and elderly patients and affects the [[soft palate]], the floor of the mouth, and the buccal mucosa mainly<ref name="pmid10919731">{{cite journal| author=Hashibe M, Mathew B, Kuruvilla B, Thomas G, Sankaranarayanan R, Parkin DM et al.| title=Chewing tobacco, alcohol, and the risk of erythroplakia. | journal=Cancer Epidemiol Biomarkers Prev | year= 2000 | volume= 9 | issue= 7 | pages= 639-45 | pmid=10919731 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10919731  }}</ref>
* Most commonly affected areas were reported as the soft palate, the floor of the mouth, and the buccal mucosa[14,22].
* Tobacco and alcohol consuming are the most common risk factors  
* Chewing tobacco and alcohol use are the possible etiologic factors for the development erythroplakia.[23]
* Lesion is usually less than 1.5 cm in diameter, but its size may range between 1-4 cm
* Typical lesion of oral erythroplakia is less than 1.5 cm in diameter, but it also be less than 1 cm and larger than 4 cm[22].
* Early effective treatment is mandatory as [[malignant]] transformation rates are very high
* Histopathologically, moderate or severe dysplasia was usually seen in lesion with erythroplakia.
* Malignant transformation rates is very high (vary from 14% to 50%), so it needs to be treated expeditiously.[14,22].
* Early effective treatment is mandatory.[22]
* Surgery is the recommended therapy.[1]


=== '''Oral lichen planus''' ===
=== '''Oral lichen planus''' ===
* The disease is a chronic, autoimmune, inflammatory disease which may affect skin, oral mucosa, genital mucosa, scalp, and nails[26].  
* [[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 among female gender and the age of onset is usually between third and sixth decade[25,27] [28].
* It mainly occurs in females between third and sixth decade
* OLP may be seen as six types including papular, reticular, plaque-like, atrophic, erosive, and bullous type[25].
* It may be multifocal, [[Papule|papular]], [[bullous]], [[Erosion (dental)|erosive]], reticular, and [[Atrophy|atrophic]] forms 
 
* [[Atrophy|Atrophic]] and erosive pattern are associated with a burning sensation and pain  
* lesions present symmetrically and bilaterally, and usually asymptomatic.  Atrophic pattern presents as a red lesion. Erosive pattern is usually seen as irregular erosion or ulceration covered with a fibrinous plaque or pseudomembrane. atrophic and erosive pattern are generally associated with a burning sensation and pain that exacerbated by trauma and hot, spicy or acidic foods.
* Increased [[malignant transformation]] risk occurs greater in erosive and atrophic types 
 
* Multifocal plaque type lesions may be seen.
* This subtype is more common among tobacco smokers.
* The papular pattern, which is rarely seen, is characterized by small, white, raised papules with fine white striation at the periphery of the lesion.
* Bullous pattern is the least common type of OLP that characterized by bullae formation range from a few millimeters to several centimeters in diameter[26].


* histologic features include liquefactive degeneration of the basal cells, colloid bodies (known as ''Civatte'' bodies), homogenous infiltrate of lymphocytes in a dense, band-like pattern along the epithelium-connective tissue interface in the superficial dermis, cytologically normal maturation of the epithelium, sawtooth rete ridges, and hyperkeratosis. In erosive lichen planus, ulceration may be seen in the surface epithelium[31].
* Histologically, lesions show [[liquefactive necrosis]] of the basal cells, infiltrative [[lymphocytes]] of superficial [[dermis]], sawtooth rete ridges, and [[hyperkeratosis]]


* Malignant transformation ratio has been reported in 0% to 10% of patients, according to the sample’s characteristics and study design, after mean follow-up of 1.5 to 10 years[25].
* [[Malignant transformation]] ratio has been reported in 10% of patients


* Increased malignant transformation risk occurs greater in erosive and atrophic forms and in cases of lesions of lateral border of the tongue[27].
=== Other factors ===


*Other factors
===== Stem cell transplantation =====
**A number of other factors have been associated with an increased incidence of tongue cancer such as the use of the product of the areca catechu tree, the betel nuts or quid as well as the use of slaked lime. This mixture is highly irritating to the oral mucosa, and as well as carcinogenic.
* After [[stem cell transplantation]], the risk for oral squamous cell carcinoma significantly increase.
**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''.
* Oral cancer in these patients may have more aggressive behavior with poorer prognosis.
Other less potent risk factors includes the following:
* This effect is due to the continuous lifelong [[Immunosuppression|immune suppression]] and chronic oral [[graft-versus-host disease]].
*Lifestyle
* 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 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
**Betel quid
*Genetics
*'''Genetics'''
**[[Fanconi anemia]]
**[[Fanconi anemia]]
**Dyskeratosis congenital
**[[Dyskeratosis congenita]]
**[[Family history]] of [[squamous cell carcinoma]]
**[[Family history]] of [[squamous cell carcinoma]]
*General
*'''General'''
**Male gender
**Male gender
**[[Ultraviolet light]]
**[[Ultraviolet light]]
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**Immune system suppression
**Immune system suppression
**[[Lichen planus]]
**[[Lichen planus]]
*Unproven risk factors
*'''Unproven risk factors'''
**Mouthwash
**Mouthwash
**Irritation from dentures
**Irritation from dentures
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==References==
==References==
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[[Category:Types of cancer]]
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Latest revision as of 18:17, 6 December 2018

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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] Mohammed Abdelwahed M.D[3] Roukoz A. Karam, M.D.[4]

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.

Tongue cancer risk factors

The major risk factors in the development of tongue cancer include the following:[1] [2] [3]

  • 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. A 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 a 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 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.[4]
  • 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

  • Leukoplakia is a white plaque on surface of tongue
  • It often occurs in individuals under the age of 40[5]
  • Leukoplakia can be divided into:[6]
    • Homogenous lesions: flat, thin, and white[7]
    • Nonhomogenous lesions: white and red lesion
  • Oral leukoplakia should be confirmed by 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 withdrawal[8]

Risk factors of malignant transformation[6]

  • 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[9]
  • It occurs in middle aged and elderly patients and affects the soft palate, the floor of the mouth, and the buccal mucosa mainly[10]
  • Tobacco and alcohol consuming are the most common risk factors
  • Lesion is usually less than 1.5 cm in diameter, but its size may range between 1-4 cm
  • Early effective treatment is mandatory as malignant transformation rates are very high

Oral lichen planus

Other factors

Stem cell transplantation

Other less potent risk factors includes the following:

References

  1. ↑ Doherty, Gerard (2010). Current diagnosis & treatment : surgery. New York: Lange Medical Books/McGraw-Hill. ISBN 0071635157.
  2. ↑ Som, Peter (2003). Head and neck imaging. St. Louis, Mo: Mosby. ISBN 0323009425.
  3. ↑ Harrison, Louis (2009). Head and neck cancer : a multidisciplinary approach. Philadelphia: Lipppincott Williams & Wilkins. ISBN 0781771366.
  4. ↑ Oropharyngeal cancer. National Cancer Institute(2015) http://www.cancer.gov/types/head-and-neck/hp/oropharyngeal-treatment-pdq Accessed on November 16, 2015
  5. ↑ 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.
  6. ↑ 6.0 6.1 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.
  7. ↑ 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.
  8. ↑ 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.
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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.

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