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{{Oral cancer}}
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==Overview==
==Overview==
Common causes of oral cancers include [[premalignant]] lesions, [[tobacco]], [[alcohol]], [[human papillomavirus]], and [[hematopoietic]] [[stem cell]] transplantation. [[Tobacco]] use is the cause of 75% oral cancer cases . It causes an irritation of [[mucous membrane]] in the [[mouth]]. [[Human papillomavirus|HPV]] type 16 is the most common sub-type of [[Human papillomavirus|human papilloma virus]] associated with oral cancer.
==Causes==
==Causes==
*Premalignant lesion
Common causes of oral cancer include:
A premalignant (or precancerous) lesion is defined as "a benign, morphologically altered tissue that has a greater than normal risk of malignant transformation." There are several different types of premalignant lesion that occur in the mouth. Some oral cancers begin as white patches (leukoplakia), red patches (erythroplakia) or mixed red and white patches (erythroleukoplakia or "speckled leukoplakia"). Other common premalignant lesions include oral lichen planus (particularly the erosive type), oral submucous fibrosis and actinic cheilitis. In the Indian subcontinent oral submucous fibrosis is very common. This condition is characterized by limited opening of mouth and burning sensation on eating of spicy food. This is a progressive lesion in which the opening of the mouth becomes progressively limited, and later on even normal eating becomes difficult. It occurs almost exclusively in India and Indian communities living abroad. The overall prevalence of oral potentially malignant disorders in the Middle East was 2.8%. Lichen planus/lichenoid lesions were the most common lesions (1.8%) followed by leukoplakias (0.48%), chronic hyperplastic candidiosis (0.38%), and erythroplakia (0.096%).
* Pre-[[malignant]] lesion<ref name="pmid4266835">{{cite journal |vauthors=Colvin RB, Pinn VW, Simpson BA, Dvorak HF |title=Cutaneous basophil hypersensitivity. IV. The "late reaction": sequel to Jones-Mote type hypersensitivity. Comparison with rabbit Arthus reaction. Effect of passive antibody on induction and expression of Jones-Mote hypersensitivity |journal=J. Immunol. |volume=110 |issue=5 |pages=1279–89 |year=1973 |pmid=4266835 |doi= |url=}}</ref>
*Tobacco
** [[Benign]] and morphologically-altered [[Tissue (biology)|tissue]]
In a study of Europeans, smoking and other tobacco use was associated with about 75 percent of oral cancer cases, caused by irritation of the mucous membranes of the mouth from smoke and heat of cigarettes, cigars, and pipes. Tobacco contains over 60 known carcinogens, and the combustion of it, and by-products from this process, is the primary mode of involvement. Use of chewing tobacco or snuff causes irritation from direct contact with the mucous membranes. Tobacco use in any form by itself, and even more so in combination with heavy alcohol consumption, continues to be an important risk factor for oral cancer. However, due to the current trends in the spread of HPV16, as of early 2011 the virus is now considered the primary causative factor in 63% of newly diagnosed patients.
** Pre-malignant lesions are of various types:
*Alcohol
*** [[Leukoplakia]] - benign white patches  
Alcohol consumption is a major risk factor for certain head and neck cancers, particularly cancers of the oral cavity (excluding the lips), pharynx (throat), and larynx (voice box). People who consume 50 or more grams of alcohol per day (approximately 3.5 or more drinks per day) have at least a two to three times greater risk of developing these cancers than nondrinkers. Moreover, the risks of these cancers are substantially higher among persons who consume this amount of alcohol and also use tobacco
*** [[Erythroplakia]] -  red patches  
*Human Papilloma Virus
*** Erythroleukoplakia - mixed red and white patches
Infection with human papillomavirus (HPV), particularly type 16 (there are over 180 types), is a known risk factor and independent causative factor for oral cancer. (Gillison et al. Johns Hopkins) A fast-growing segment of those diagnosed does not present with the historic stereotypical demographics. Historically that has been people over 50, blacks over whites 2 to 1, males over females 3 to 1, and 75% of the time people who have used tobacco products or are heavy users of alcohol. This new and rapidly growing sub population between 30 and 50 years old,[17] is predominantly nonsmoking, white, and males slightly outnumber females. Recent research from multiple peer-reviewed journal articles indicates that HPV16 is the primary risk factor in this new population of oral cancer victims. HPV16 (along with HPV18) is the same virus responsible for the vast majority of all cervical cancers and is the most common sexually transmitted infection in the US. Oral cancer in this group tends to favor the tonsil and tonsillar pillars, base of the tongue, and the oropharynx. Recent data suggest that individuals that come to the disease from this particular etiology have a significant survival advantage, as the disease responds better to radiation treatments than tobacco etiology disease.
*** [[lichen planus|Lichen planus]]
*Hematopoietic Stem Cell Transplantation
*** [[Oral]] sub-[[mucous]] [[fibrosis]] - very common in Indian sub-continents
Patients after hematopoietic stem cell transplantation (HSCT) are at a higher risk for oral squamous cell carcinoma. Post-HSCT oral cancer may have more aggressive behavior with poorer prognosis, when compared to oral cancer in non-HSCT patients.[18] This effect is supposed to be owing to the continuous lifelong immune suppression and chronic oral graft-versus-host disease.
*** [[actinic cheilitis]]
 
* [[Tobacco]]
** 75% cases of oral cancers occur due to [[tobacco]] use.  
** Use of it causes irritation of the [[mucous membrane]] in the [[mouth]].  
** Both [[smoking]] and [[chewing tobacco]] can lead to irritation of [[mucous membrane]] of the mouth.  
** 60 types of [[carcinogens]] are known to be present in [[tobacco smoke]].  
** If any form of [[tobacco]] use is combined with heavy [[alcohol]] intake, the [[carcinogenic]] potential increases.
 
* [[Alcohol]]<ref name="pmid29342885">{{cite journal |vauthors=Stornetta A, Guidolin V, Balbo S |title=Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity |journal=Cancers (Basel) |volume=10 |issue=1 |pages= |year=2018 |pmid=29342885 |doi=10.3390/cancers10010020 |url=}}</ref>
** Heavy alcohol intake can lead to cancer of [[pharynx]] and [[larynx]].  
** [[Carcinogenic]] potential increases when combined with [[tobacco use]].
 
* [[Human papillomavirus|Human Papilloma Virus]]( [[Human papillomavirus|HPV]])
** [[HPV]] type 16 is the most common sub-type associated with oral cancer.
** Unprotected oral sexual behaviors with a patient suffering from [[HPV]] can transmit this [[virus]].<ref name="pmid28778951">{{cite journal |vauthors=Shah A, Malik A, Garg A, Mair M, Nair S, Chaturvedi P |title=Oral sex and human papilloma virus-related head and neck squamous cell cancer: a review of the literature |journal=Postgrad Med J |volume=93 |issue=1105 |pages=704–709 |year=2017 |pmid=28778951 |doi=10.1136/postgradmedj-2016-134603 |url=}}</ref> 
** It most commonly involves the [[tonsils]], which are at the base of the [[tongue]] and the [[oropharynx]].  
 
* [[Hematopoietic stem cell transplantation]]
** This causes an increased risk for [[squamous cell carcinoma]].
 
==References==
==References==
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{{Reflist|2}}
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sargun Singh Walia M.B.B.S.[2], Simrat Sarai, M.D. [3]; Grammar Reviewer: Natalie Harpenau, B.S.[4]

Overview

Common causes of oral cancers include premalignant lesions, tobacco, alcohol, human papillomavirus, and hematopoietic stem cell transplantation. Tobacco use is the cause of 75% oral cancer cases . It causes an irritation of mucous membrane in the mouth. HPV type 16 is the most common sub-type of human papilloma virus associated with oral cancer.

Causes

Common causes of oral cancer include:

References

  1. ↑ Colvin RB, Pinn VW, Simpson BA, Dvorak HF (1973). "Cutaneous basophil hypersensitivity. IV. The "late reaction": sequel to Jones-Mote type hypersensitivity. Comparison with rabbit Arthus reaction. Effect of passive antibody on induction and expression of Jones-Mote hypersensitivity". J. Immunol. 110 (5): 1279–89. PMID 4266835.
  2. ↑ Stornetta A, Guidolin V, Balbo S (2018). "Alcohol-Derived Acetaldehyde Exposure in the Oral Cavity". Cancers (Basel). 10 (1). doi:10.3390/cancers10010020. PMID 29342885.
  3. ↑ Shah A, Malik A, Garg A, Mair M, Nair S, Chaturvedi P (2017). "Oral sex and human papilloma virus-related head and neck squamous cell cancer: a review of the literature". Postgrad Med J. 93 (1105): 704–709. doi:10.1136/postgradmedj-2016-134603. PMID 28778951.


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