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 »  Abstract
 » Introduction
 »  Tobacco Induced ...
 »  Tobacco Induced ...
 »  Tobacco Induced ...
 »  Tobacco Induced ...
 » Conclusion
 »  References

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Year : 2014  |  Volume : 51  |  Issue : 1  |  Page : 80-85

Epidemiology, control and prevention of tobacco induced oral mucosal lesions in India

Department of Oral Pathology and Microbiology, YMT Dental College and Hospital, Institutional Area, Sector 4, Kharghar, Navi Mumbai, Maharashtra, India

Date of Web Publication18-Jun-2014

Correspondence Address:
G Sridharan
Department of Oral Pathology and Microbiology, YMT Dental College and Hospital, Institutional Area, Sector 4, Kharghar, Navi Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-509X.134651

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 » Abstract 

Oral cancer is one of the leading causes of human morbidity and mortality especially in developing countries like India. Tobacco consumption in smokeless and smoking form along with alcohol is considered as the primary risk factors. Tobacco is a major health challenge with various tobacco products available for use which are known to have deleterious effects on the oral mucosa. The oral lesions caused by tobacco are inclusive of those that are less likely to progress to cancer; lesions with increased tendency to develop into cancer and cancerous lesions. Prevention and control of tobacco induced oral mucosal lesions is the prime requisite currently and mainly involves measures undertaken at primary, secondary and tertiary levels. Primary prevention plays a pivotal role in tobacco induced lesions and steps can be taken at policy level, community as well as individual level. This review paper focuses on the epidemiological data of tobacco induced oral mucosal lesions in India available in the literature with an overview on various strategies for their prevention and control.

Keywords: Epidemiology, oral squamous cell carcinoma, potentially malignant disorders, prevention and control, tobacco induced oral mucosal lesions

How to cite this article:
Sridharan G. Epidemiology, control and prevention of tobacco induced oral mucosal lesions in India. Indian J Cancer 2014;51:80-5

How to cite this URL:
Sridharan G. Epidemiology, control and prevention of tobacco induced oral mucosal lesions in India. Indian J Cancer [serial online] 2014 [cited 2022 Aug 19];51:80-5. Available from:

 » Introduction Top

Oral cavity is prone for a myriad of changes with advancing age as well as a result of the environmental and life style related factors. Oral mucosal lesions can occur as a result of infections, local trauma or irritation, systemic diseases and excessive consumption of tobacco, betel quid and alcohol. [1] The prevalence and incidence rates of oral mucosal lesions are available from various countries, but the information thereby obtained may not always be applicable to Indian population due to the existence of cultural, ethnic and demographic differences. Despite the efforts made by the different groups, establishment of prevalence data related to oral mucosal lesions is meager in Indian literature. [2]

Chewing and smoking of tobacco along with consumption of alcohol beverages have become common social habits in India. [3] Tobacco was introduced in India by the Portuguese nearly 400 years ago and since then it rapidly became a part of socio-cultural milieu in various communities. [4] India is the second largest producer and consumer of tobacco next only to China. [4],[5] The prevalence of tobacco use among Indian adults is 35%. [6] Introduced initially in India as a product to be smoked, tobacco gradually began to be used in several other forms such as paan (betel quid) chewing and leaf tobacco. [7] In India, beedi smoking is the most popular form of tobacco smoking and paan with tobacco is a major chewing form. Dry tobacco-areca nut preparations such as paan masala, gutkha and mawa are also popular and highly addictive. It has been estimated that the number of tobacco users in India among those 10 years of age and above is around 250 million. [7]

Alcohol use often co-exists with tobacco consumption. In India, 4.5% of the population use alcohol regularly. [8] The various types of alcoholic beverages used in India are wine, beer, toddy, whisky, gin, rum, brandy, arrack and liqueurs. [9] Epidemiological studies have shown that alcohol consumption in association with tobacco is a significant risk factor for oral pre-cancer and cancer. [10],[11] The metabolized product of alcohol, acetaldehyde, is known for its carcinogenic activity. Alcohol also causes an increased rate of penetration of substances from the oral environment across the mucosa due to alteration of mucosal permeability that may play a role in carcinogenesis. [12]

Smoking, drinking and tobacco chewing have been positively associated with oral lesions such as leukoplakia, oral submucous fibrosis and oral lichen planus which have the potential for malignant transformation. [3] Tobacco consumption also remains the most important avoidable risk factor for oral cancer. Tobacco related cancers account for nearly 50% of all cancers in men and 25% in women. [13] Oral squamous cell carcinoma may occur either de novo or from the precursor lesions. As a result, prompt intervention at appropriate levels may aid in prevention and better control of tobacco induced lesions. Keeping in view the major risk factors for oral mucosal lesions and its associated effects, a range of preventive measures could be implemented at primary, secondary or tertiary levels.

Though oral pre-cancer and cancer is widespread in India, epidemiological data from various geographical areas is scarce. The present article attempts to compile the prevalence and incidence rates of tobacco induced oral mucosal lesions in India that is documented in the literature with a note on the different preventive measures that could be implemented at various levels.

 » Tobacco Induced Oral Mucosal Lesions Top

Long term contact of tobacco with the oral mucosa induces variety of changes which could be due to the carcinogen itself or as a protective mechanism of the oral cavity. These changes could be categorized as tobacco induced oral mucosal lesions which are less likely to cause cancer, lesions that are potentially malignant and tobacco induced malignancies.

 » Tobacco Induced Non-Neoplastic Oral Mucosal Lesions Top

The tobacco induced mucosal lesions which are less likely to cause cancer are betel chewer's mucosa, leukedema, smoker's palate, lichenoid reaction, smoker's melanosis, tobacco pouch keratosis, palatal erythema andpalatal erythema with hyperplasia.

Betel chewer's mucosa was first described by Mehta et al, and is characterized as brownish discoloration of oral mucosa. [14],[15] The lesion might occur at the site of quid placement because of either the direct action of quid or traumatic effect of chewing or both with a tendency for the oral mucosa to desquamate or peel. The underlying areas assume a psuedomembranous or wrinkled appearance. [16] The bright red color produced by betel chewing is due to the formation of O-quinone from the water soluble polyphenols notably leucocynidins at alkaline pH of 8 to 9 via secondary reactions. [14] Several epidemiological studies have shown a prevalence rate of 0.2% to 60.8% in different South-East Asian populations. [15] Indian studies have shown prevalence rates of 0.25%, [3] 0.84%, [17] and 0.13%. [2] Refraining from habit or repeated washing clears the stain and discontinuance of the betel quid chewing habits leads to nearly complete clearance of the encrustation. [14]

Leukedema is a chronic white mucosal condition in which the oral mucosa has a grey opaque appearance. When the mucosa is stretched, the lesions disappear and reappear on releasing the mucosa. It develops due to piling of spongy cells and its prevalence in India varies from 0.02 to 0.3 %. [14] Other results of epidemiological survey showed prevalence rates of 3.7%, [17] 0.25%, [3] and 2.6%. [2]

Smoker's palate is also known as leukokeratosisnicotina palate and is a common reaction of palatal mucosa to smoking. Clinically the lesion appear as diffuse white patch with numerous excrescences having central red dots corresponding to minor salivary gland ducts. The prevalence in India varies from 0.4% to 9.5%. [14] Results obtained from other studies showed prevalence rates of 1.18%, [2] 0.89%, [3] and 4.4%. [17] These lesions are more prevalent in men due to increased usage of tobacco smoke among them.

Lichenoid lesions grossly resemble oral lichen planus but have certain specific differences. The lesion is characterized by the presence of fine, white, wavy parallel lines that do not overlap or criss-cross, is not elevated and in some instances radiate from a central erythematous area. The lesion generally occurs at the site of quid placement. [16] Some 89% of the lesions occur among betel quid chewers and 11% among those who chewed pan and smoked tobacco. Most of these lesions remain stationary or sometimes regress on discontinuance of the habit thereby requiring no further treatment. [1] Sufficient epidemiological data is unavailable regarding this lesion.

Oral pigmentation secondary to smoking may occur at any site with increased tendency to affect facial gingiva. The frequency of the lesions increases with heavy usage of cigarette smoke. Literature review have shown prevalence rates of 3.5%, [2] 1.14%, [3] 2.3% [1] and 4.17%. [18] Most of the studies have reported smokers' melanosis as the most frequently encountered oral mucosal lesion. Since the condition is harmless, no treatment is required. It has been suggested that melanin production in the oral mucosa of smokers serves as a protective response against some of the harmful substances in tobacco smoke. [19]

 » Tobacco Induced Pre-Malignancies Top


Leukoplakia is defined as a predominantly white lesion or plaque affecting the oral mucosa that cannot be characterized clinically or histopathologically as any other disease and is not associated with any other physical or chemical agents except tobacco. [20] Leukoplakia is the term used to recognize white plaques of questionable risk having excluded other known diseases or disorders that carry no increased risk of cancer. [21] A biopsy is mandatory. A definitive diagnosis is made when any etiological cause other than tobacco/areca nut use has been excluded and histopathology has not confirmed any other specific disorder.

Leukoplakia is considered as a potentially malignant disorder with a malignancy conversion rate ranging from 0.1% to 17.5%. [22] In India, the prevalence of leukoplakia varies from 0.2% to 5.2% and malignant transformation ranges between 0.13% and 10% according to various studies. [7] Among the recent studies, leukoplakia was evident in 1.59% of the study sample, [17] 0.59%, [3] 7.4% [9] and 2.04%. [2]


Erythroplakia is an uncommon but severe form of pre-cancerous lesion defined by WHO as "any lesion of the oral mucosa that presents as bright red velvety plaques which cannot be characterized clinically or histopathologically as any other recognizable condition". [23] There are few documented reports related to the prevalence of erythroplakia owing to its rarity and also the similarities with speckled leukoplakia. Only 9 cases (0.02%) among 51000 villagers were reported in a study from five states of India. [14] Another study showed a prevalence rate of 0.6%, [9] while a study in USA reported a rate of 0.09%. [23]

Palatal changes among reverse smokers

Palatal changes secondary to reverse chutta smoking can be categorized as palatal keratosis, excrescences, patches, red areas, ulceration and pigmentation changes. These changes are seen in upto 46% of reverse smokers and carry increased tendency for malignant transformation. No concrete epidemiological data exist regarding the prevalence of these changes.

Oral submucous fibrosis

OSMF as a potentially malignant disease was first described in 1950's with increased tendency to affect people of Asian descent. [24] It is a chronic disorder characterized by fibrosis of the lining mucosa of the upper digestive tract involving the oral cavity, oro- and hypopharynx and the upper third of oesophagus. [25] The fibrosis involves the lamina propria and the submucosa and may extend into the underlying musculature resulting in the deposition of dense fibrous bands, resulting in limited mouth opening. [26]

Areca nut has been proved to be the single most important etiological factor responsible for OSMF. [26] The pre-cancerous nature was first described by Paymaster in 1956 that was later confirmed by various studies. [24] A malignant transformation rate was shown to be in the range of 7 to 13% and a transformation rate of 7.6% was reported in cohort study. [24],[27] Previous data indicated that the prevalence of OSMF was in the range of 0.03% to 3.2%. [28],[29] The incidence is progressively increasing owing to the excessive usage of areca nut among various groups of population. Recent epidemiological studies have shown OSMF in 0.55% of study group, [3] 8%, [9] 2.01%, [17] 0.7% [2] and 9.7%. [1]

Lichen planus

Lichen planus is a mucocutaneous disorder affecting the skin and mucous membrane with increased potential for malignant transformation. The condition most commonly affects individuals in the 5 th to 6 th decade although younger individuals are also affected and is twice more common in women than in men. [30] The malignant potential of lichen planus has been a subject of intense research with studies showing malignant transformation in the range of 0 to 12.5%. [31] Other reports put the overall prevalence rate at 0.5 to 2.2%. [32],[33] In India, the prevalence was reported to be in the range of 0.1 to 1.5%. [14] Several findings showed prevalence of 0.1 to 1.5%, [34] 0.15%, [3] 1.20%, [17] 0.46% [2] and 2.7%. [1]

 » Tobacco Induced Malignancies Top

Oral squamous cell carcinoma

Oral squamous cell carcinoma (OSCC) is a multifactorial disease with tobacco and alcohol being the major risk factors. Oral and pharyngeal cancer grouped together is the sixth common cancer in the world. [35] Despite the recent advances in early diagnosis and treatment of oral cancer, the burden of oral cancer is increasing worldwide especially in developing countries. An estimated incidence is around 2,75,000 with two- thirds of the cases occurring in developing countries. [36]

OSCC affects men more than women which would be attributed to heavier indulgence of risk factors by men. However, the ratio of males to females has declined over the years with cases being increasingly reported in women. Tongue seems to be the predominant site affected in Western countries, but in India, alveolo-buccal complex is mainly affected due to tobacco chewing habit. [35]

In India, population based cancer registry (PBCR) is the source of data in estimating the incidence and mortality as it records all cancer cases occurring in defined region. There are 13 PBCRs located at various centres in India since its inception in Mumbai in 1963. [13] The age standardized incidence rate of oral cancer is reported at 12.6/100000 population. [37] Data obtained from the different cancer registries in India showed that in males an age adjusted incidence (AAR) rates of mouth cancer per 100,000 population to be in the range of 3.3 to 10.7 with the highest incidence seen in Bhopal. The range for tongue cancer is between 2.3 and 10 with highest being in Ahmedabad. In females, the AAR of mouth cancer is between 2.2 and 8.9 with highest occurrence being reported in Bangalore while in tongue cancer it is in the range of 1.5 to 2.7. [13] The data obtained from other studies reported in the literature have shown OSCC in 0.93%, [1] 0.16% [2] and 1.76% of the study samples. [17]

Prevention and control

Oral cancer is the one of the most important cause of morbidity and the current magnitude of the problem is extensive. The Government of India developed the first statement on cancer control as early as 1971. The National cancer control programme for India was formulated in 1984 with four major goals that included: [38]

  • Primary prevention of tobacco related cancers
  • Early detection of cancers of easily accessible sites
  • Augmentation of treatment facilities
  • Establishment of equitable, pain control and palliative care network throughout the country.

The preventive strategies are broadly categorized into primary, secondary and tertiary. Primary prevention refers to avoiding cancer causing substances in the environment or dietary elements associated with increased risk. Secondary prevention aims at early detection and removal of benign tumors. Tertiary intervention involves management through surgery, radiotherapy and chemotherapy followed by post treatment palliative care. Considering that oral cavity cancer is mainly caused by tobacco usage, implementation of primary preventive measures would be highly beneficial. The Indian government has put forth various tobacco control policies which when applied along with steps taken at community level would prove highly successful in preventing oral cancers.

Primary prevention

The main strategy for control of tobacco related diseases would be through primary prevention.Primary prevention mainly aims at eliminating or minimizing exposure to causative agent and includes reducing individual susceptibility to the effect of such causes. [38] The measures involving tobacco control as primary mode of cancer prevention needs interventions at policy level, community level and at the level of an individual. [39]

Policy level interventions would include levy of taxes to raise prices of tobacco products and act as disincentive for purchase; regulation of tobacco products aimed to progressively reduce the levels of harmful chemicals and alter their physical characteristics and measures to reduce supply. [39] Recognizing the health hazards of tobacco, the Government of India promulgated the Cigarette (regulation of production, supply and distribution) act in 1975 and modified it in due to course of time. Under the act, it is mandatory to include strong and rotatory warnings in regional languages on tobacco products; ban on advertisements on tobacco products; prohibition of tobacco smoking in public places; initiation of measures for awareness on tobacco through health infrastructure, educational institutions and mass media and initiation of efforts for persuasion of farmers to switch over to alternative crops. [40] Another aspect of policy intervention would be to protect vulnerable groups such as the poor, the young and women from becoming victims of tobacco related hazards. [39]

Community interventions mainly focus on protecting youth from tobacco, maintaining smoke free public places and promoting health literacy on tobacco related matters. Educating the community with an aim to increase the knowledge and awareness about the harmful effects of tobacco use among the public is one of the ways to reduce tobacco use. Health education leads to a long lasting reduction in tobacco use, when it is imparted through the mass media and continued with a school and community based education program. Protecting the youth from tobacco is an important aspect of community level prevention as the most susceptible time for initiation of tobacco use is during adolescence and early adulthood. Measures should be undertaken to educate the school growing kids about the harmful effects on tobacco and alcohol. This can be done by the implementing methods like conducting drawing and essay competitions for school growing children; debates, discussions and seminars for university students; participatory workshops and training sessions and structured training and field activities. [38] In addition appropriate legislative measures needs to be undertaken for prohibitory sales of tobacco to youngsters. [41]

At individual level the interventions would focus on behavioral change especially aimed at tobacco cessation. This requires the availability of services ranging from counseling to de-addiction therapies and affordable supply of pharmacological agents for those who need it. [39]

Health professionals are a critical source for advancing the agenda of tobacco control as they form the medium through which information on the health consequences of tobacco is communicated to people. They can provide direct services for tobacco cessation through counseling and other forms of therapy.

The role of dentists/dental surgeons in tobacco health programs needs to be given importance as they form a major part of the health professional who come in direct contact with the patients involved with tobacco use. It is preferable that dentists be involved in various areas of tobacco intervention such as tobacco cessation activities, prevention and public policy development. [42] The main barriers to providing tobacco cessation counseling include lack of reimbursement, lack of confidence in the effectiveness of advice from the dental professional and lack of knowledge and material to hand out to patients. [43]

In order to facilitate effective participation of dental professionals, concrete steps are needed to be implemented at various levels. These could be effective training at various educational levels on the different aspects of tobacco usage and their effects on oral and general health. Conduct continuing dental health education and workshops on tobacco control for the benefit of the practicing dentists. Training dentists for identifying tobacco induced oral lesions at an early stage and provide appropriate therapy if possible. Encouraging dentists to participate in community level programs aimed at educating the public on harmful effects of tobacco. Encourage dentists to identify individual patients who are tobacco users and provide them with necessary help regarding cessation of such habits. Involve dental professionals in policy control programs for framing tobacco control guidelines. provide incentives to dentists participating in tobacco control programs.

Secondary prevention

Secondary prevention mainly aims at the early diagnosis of cancer/pre-cancer and initiate treatment at an early stage to prevent further progression. Currently no standardized methods or practices exist for early detection of oral cancer although several diagnostics aids are being constantly evaluated. Simple oral visual examination with adequate light is followed on a regular basis and is considered as a fairly good screening method for early detection of oral mucosal lesions.

Performing oral screening to detect suspicious lesions could be done as a part of routine oral examination during regular practice or at various screening camps. However, several drawbacks such as lack of adequate staff as well as under-trained staff who are unable to adequately perform oral screening exist. Training camps aimed at training health professionals to perform oral screening could be implemented. In India, under the district cancer control programme, the paramedical staffs of primary health centre have been trained to conduct oral examination for early detection and for providing health education. [44]

Screening and early detection in population at risks are mandatory to decrease morbidity and mortality associated with oral cancer. Visual oral examination, although considered as an effective screening method, is problematic in many aspects with varying sensitivity and specificity rates. This could be due to the fact that initial presentations of oral cancer and pre-cancer are often subtle and rarely demonstrate the clinical characteristics observed in advanced cases. [45] Besides their clinical subtlety, pre-malignant lesions are highly heterogeneous in their presentation and may mimic a variety of common benign or reactive conditions. Furthermore, there is a growing realization that some pre-malignant and early cancerous lesions are not readily detectable to the naked eye. [46] As a result, additional screening aids are needed which can be employed along with oral visual examination. Research is underway in this aspect but till date no technique has provided definite evidence to suggest that it improves the sensitivity or specificity of oral screening beyond conventional oral examination alone. [47] These diagnostic tests include toluidine blue staining, brush cytology, tissue reflectance (Vizilite plus, Microlux DL), narrow emission tissue fluorescence which are light based detection systems and use of tumor markers for early diagnosis.

Each of these methods have their own advantages in aiding conventional oral examination for screening of high risk lesions though none of them are confirmed for routine use. Hence, efforts should be made to identify various diagnostic aids to help in identifying lesions that are not noticed by conventional examination techniques thereby helping at-risk individuals become long term survivors of this disease. Attempts should be made to validate the efficacy of diagnostic tests by including long term screening studies (including patients who are symptom free for whom these tests would be useful), comparing the findings with gold standard and appropriate inclusion of the patient population. Also, efforts should be directed towards identifying the presence of various biomarkers in body samples which could be useful in identifying high risk individuals with increased potential for malignant transformation.

Intervention at tertiary level

Tertiary care of OSCC mainly aims in surgically removing the tumor mass along with chemotherapy and radiotherapy followed by palliative care and post-operative follow-up to reduce morbidity. Surgical management involves the removal of tumor mass and neck dissection in case of cervical metastasis. [48] Recent studies have explored targeted molecular treatment with trials underway for epidermal growth factor, insulin like growth factor receptor, C-Met and inducers of apoptotic markers. [49]

Inspite of advances in the treatment modalities of OSCC, the 5-year survival rate is low. One of the possibilities could be due to the deficiency in quality of life and palliative care after surgical management. The health related quality of life of patients is a critical aspect in treatment planning process of OSCC and is evaluated based on the assessment of the impact of the disease and its influence on physical, psychological and social aspects. [50]

Quality of life remains an individually based consideration that can be achieved by shared decision making that acknowledges the values and preferences of the patient and the family. [51] The issue that must be addressed includes physical symptoms linked to diet and feeding, communication disorders, pain and their general state of health; psychological symptoms including depression, loss of self esteem and social dysfunction. [52] Another important aspect of palliative care is the nutrition management as it is observed that nutritional compromise may arise due to factors such as loss of appetite, inability to eat secondary to treatment. [53] Nutritional management mainly concentrates on providing sufficient nutrients in the form of vitamins, iron and other minerals. Antioxidant supplementation in the form of commercial preparation or through diet might be beneficial in patients who have undergone treatment for OSCC or undergoing chemotherapy and radiotherapy.

 » Conclusion Top

Tobacco smoking and chewing is one of the prime factors responsible for oral pre-cancer and cancer. The incidence and prevalence of such lesions in South Asian countries like India is high owing to the increased production and consumption of tobacco. Also relative lack of awareness regarding the harmful effects of tobacco is a major reason for the same. In order to determine the overall incidence and prevalence rates, attempts should be made to accumulate epidemiological data over a wide geographical area that may help in formulating appropriate prevention and control measures. Preventive measures should begin at grass root levels aimed at individuals who are at high risk for tobacco usage along with intervention at community level and policy level interventions by the concerned policy makers. Health professionals including dentists should also play an active role in prevention and control of tobacco induced lesions due to the direct contact with patients who are at increased risk.

 » References Top

1.Patel P, Patel V. Oral mucosal lesions among residents of a town in North Gujarat. National J Med Res 2011;1:3-6.  Back to cited text no. 1
2.Sudhakar S, Praveen Kumar B, Prabhat MP. Prevalence of oral mucosal changes in Eluru, Andhra Pradesh (India) - An institutional study. J Oral Health Comm Dent 2011;5:42-6.  Back to cited text no. 2
3.Saraswati TR, Ranganathan K, Shanmugam S, SowmyaRamesh, Narasimhan PD, Gunaseelan R. Prevalence of oral lesions in relation to habits: Cross sectional study in south India. Indian J Dent Res 2006;17:121-5.  Back to cited text no. 3
4.Kaur J, Jain DC. Tobacco control policies in India: Implementation and challenges. Indian J Public Health 2011;55:220-7.  Back to cited text no. 4
[PUBMED]  Medknow Journal  
5.World Health Organization (WHO). Fresh and alive: MPOWER, WHO report on the global tobacco epidemic, Geneva, Switzerland: WHO; 2008.  Back to cited text no. 5
6.Government of India, Ministry of health and family welfare, Global adult tobacco survey, India 2010.  Back to cited text no. 6
7.Reddy KS, Gupta PC. Economic History of tobacco production: From colonial origins to contemporary trends. In: Report on tobacco control in India. Joint report supported by Ministry of Health and family welfare, Government of India, Centre of disease control and prevention, USA: World Health Organization;p. 19-32.  Back to cited text no. 7
8.Neufeld KJ, Peters DH, Rani M, Bom S, Brooner RK. Regular use of alcohol and tobacco in India and its association with age, gender and poverty. Drug Alcohol Depend 2005;77:283-91.  Back to cited text no. 8
9.Rooban T, Rao A, Joshua E, Ranganathan K. The prevalence of oral mucosal lesions in alcohol misusers in Chennai, South India. Indian J Dent Res 2009;20:41-6.  Back to cited text no. 9
[PUBMED]  Medknow Journal  
10.Harris CK, Warnakulasuriya KA, Cooper DJ, Peters TJ, Gelbur S. Prevalence of oral mucosal lesions in alcohol misusers in south London. J Oral Pathol Med 2004;33:253-9.  Back to cited text no. 10
11.Zain RB. Cultural and dietary risk factors factors of oral cancer and pre-cancer. A brief overview. Oral Oncol 2001;37:205-16.  Back to cited text no. 11
12.Hindle I, Downer MC, Moles DR, Speight PM. Is alcohol responsible for more intra-oral cancer? Oral Oncol 2000;36:328-33.  Back to cited text no. 12
13.Murthy NS, Mathew A. Cancer epidemiology, prevention and control. Curr Sci 2004;86:518-27.  Back to cited text no. 13
14.Mehta FS, Hamner JE. Tobacco related oral mucosal lesions and conditions in India. A guide for dental students, dentists and physicians. Mumbai: Published by basic dental research unit, Tata institute of fundamental research;1993.  Back to cited text no. 14
15.Trivedy CR, Craig G, Warnakulasuriya S. The oral health consequence of chewing areca nut. Addict Biol 2002;7:115-25.  Back to cited text no. 15
16.Avon SL. Oral mucosal lesions associated with the use of quid. J Can Dent Assoc 2004;70:244-8.  Back to cited text no. 16
17.Mathew AL, Pai KM, Sholapurkar AA, Vengal M. The prevalence of oral mucosal lesions in patients visiting a dental school in Southern India. Indian J Dent Res 2008;19:99-103.  Back to cited text no. 17
[PUBMED]  Medknow Journal  
18.Mehrotra R, Thomas S, Nair P, Pandya S, Singh M, Nigan NS, et al. Prevalence of oral soft tissue lesions in Vidisha. BMC Res Notes 2010;3:23-8.  Back to cited text no. 18
19.Neville B, Damm DD, Allen CM, Bouquot J. Oral and maxillofacial pathology. 2 nd ed. St. Louis, Missouri: Elsevier publishers; 2001.  Back to cited text no. 19
20.Axell T, Holmstrup P, Karmer IR, Pindborg JJ, Shear M. International seminar on oral leukoplakia and associated lesions related to tobacco habits. Comm Dent Oral Epidemiol 1984;12:145-54.  Back to cited text no. 20
21.Warnakulasuriya S, Johnson NW, Vander Waal I. Nomenclature and classification of potentially malignant disorders of the oral mucosa. J Oral Pathol Med 2007;36:575-80.  Back to cited text no. 21
22.Vander Waal I, Schepman KP, Vander Meij EH, Smeele LE. Oral leukoplakia: A clinicopathological review. Oral Oncol 1997;33:291- 301.  Back to cited text no. 22
23.Hashihe M, Marhew B, Kuruvilla B,Thomas G, Shankarnarayan R, Partin DM, et al. Chewing tobacco, alcohol and the risk of erythroplakia. Cancer Epidemiol Biomarkers Prev 2000;9:639-45.  Back to cited text no. 23
24.Tilakaratne WM, Klinikowski MF, Saku T, Peter TJ, Warnakulasuriya S. Oral submucous fibrosis: Review on aetiology and pathogenesis. Oral Oncol 2006;42:561-8.  Back to cited text no. 24
25.Johnson NW, Maher R, Trivedy C, Warnakulasuriya S. The clinical condition and pathology of oral submucous fibrosis. Oral Dis 1997;3:278-9.  Back to cited text no. 25
26.Rajendran R, Shivapathasundaram B. Shafer′s Textbook of oral pathology. 6 th ed. India: Elsevier Publishers; 2009.  Back to cited text no. 26
27.Murty PR, Bhonsle RB, Pindborg JJ, Daftary DK, Gupta PC, Mehta FS. Malignant transformation rate in oral submucous fibrosis over a 17 year period. Community Dent Oral Epidemiol 1985;13:340-1.  Back to cited text no. 27
28.Pindborg JJ, Mehta FC, Gupta PC, Daftary DK. Prevalence of oral submucous fibrosis among 50,915 Indian villagers. Br J Cancer 1968;22:646-54.  Back to cited text no. 28
29.Wahi PN, Vittal VP, Lahiri B, Luthera UK, Seth RK, Arora GD. Epidemiological studies of precancerous lesions of the oral cavity: A preliminary report. Indian J Med Res 1970;50:1361-91.  Back to cited text no. 29
30.Eisen D, Carrazzo M, Sebastian JV, Thongprasom K. Oral lichen planus: Clnicalfeatures and management. Oral Dis 2005;11:338-49.  Back to cited text no. 30
31.Gonzalez-Moles MA, Scully C, Gil-Montoya JA. Oral lichen planus: Controversies surrounding malignant transformation. Oral Dis 2008;14:229-43.  Back to cited text no. 31
32.Al-Hashimi I, Schifter M, Lockhart PB, Brennan M, Bruce AJ, Epstein JB, et al. Oral lichen planus and oral lichenoid lesions: Diagnostic and therapeutic considerations. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;103:S25. e1-12.  Back to cited text no. 32
33.vander Meij EH, Schepman KP, Smele LE, van der Waal JE, Bezemer PD, Vander Waal I. A review of the recent literature regarding malignant transformation of oral lichen planus. Oral Surg Oral Med Oral Pathol Oral RadiolEndod 1999;88:307-10.  Back to cited text no. 33
34.Pindborg JJ, Mehta FS, Daftary DK, Gupta PC, Bhonsle RB. Prevalence of oral lichen planus among 7639 Indian villagers in Kerala, South India. Acta Derm Venereol 1972;52:216-20.  Back to cited text no. 34
35.Warnakulasuriya S. Global epidemiology of oral and oro-pharyngeal cancer. Oral Oncol 2009;45:309-16.  Back to cited text no. 35
36.Ferlay J, Pisani P, Parkin DM. Globocon. Cancer incidence, mortality and prevalence worldwide. IARC cancer base (2002 estimates). Lyon: IARC press; 2004.  Back to cited text no. 36
37.Peterson PE. The world oral health report 2003, continuous improvement of oral health in the 21 st century-the approach of the WHO global oral health programme. Community Dent Oral Epidemiol 2003;31:3-24.  Back to cited text no. 37
38.Dinshaw KA, Shastri SS, Patil SS. Cancer control programme in India: Challenges for the new millenium. Health administrator 2004;XVII:10-3.  Back to cited text no. 38
39.Reddy KS, Gupta PC. Report on tobacco control in India. Executive summary. Joint report supported by Ministry of Health and family welfare, Government of India, Centre of disease control and prevention, USA: World Health Organization; 2004.  Back to cited text no. 39
40.LokSabhasecrateriat. Committee on subordinate legislation (10 th Loksabha) rules/regulation framed under the cigarrette (Regulation and production, supply and distribution) Act 1975. LokSabha of India; 1995.  Back to cited text no. 40
41.Chaudhary K. Tobacco control in India. In 50 years of cancer control in India, Director General of Health services. New Delhi: Government of India; 2001. p. 196-211.  Back to cited text no. 41
42.Reibel J. Tobacco and oral diseases. Update on the evidence with recommendation. Med PrincPract 2003;12:22-32.  Back to cited text no. 42
43.Warnakulasuriya KA, Johnson NW. Dentists and oral cancer prevention in United Kingdom: Opinions, attitudes and practices to screening for mucosal lesions and to counseling patients on tobacco and alcohol use: Baseline data from 1991. Oral Dis 1995;5:10-4.  Back to cited text no. 43
44.Mathew B, Shankarnarayanan R, Sunilkumar KB, Kuruvila B, Pisani P, Nair MK. Reproducibility and validity of oral visual inspection by trained health workers in the detection of oral pre-cancer and cancer. Br J Cancer 1997;76:390-4.  Back to cited text no. 44
45.Mashberg A, Feldman LJ. Clinical criteria for identifying early oral and oropharyngeal carcinoma: Erythroplakiarevisited. Am J Surg 1988;156:273-5.  Back to cited text no. 45
46.Thomson PJ. Field change and oral cancer: New evidence for widespread carcinogenesis? Int J Oral MaxillofacSurg 2002;31:262- 6.  Back to cited text no. 46
47.Lingen MW, Kalmar JR, Karrison T, Speight PM. Critical evaluation of diagnostic aids for the detection of oral cancer. Oral Oncol 2008;44:10-22.  Back to cited text no. 47
48.Scully S, Bagan J. Oral squamous cell carcinoma overview. Oral Oncol 2009;45:301-8.  Back to cited text no. 48
49.Lorch JH, Posner MR, Wirth LJ, Hasdad RI. Seeking alternative biological therapies: The future of targeted molecular treatment. Oral Oncol 2009;45:447-53.  Back to cited text no. 49
50.Rogers NS. Quality of life for head and neck cancer patients- has treatment planning altered? Oral Oncol 2009;45:435-9.  Back to cited text no. 50
51.Steinhauser KE, Christakis A, Clipp EC, McNeilly M, McIntyre L, Tulsky JA. Factors considered important at the end of life by patients, family, physicians and other care providers. J Am Med Assoc 2000;284:2476-82.  Back to cited text no. 51
52.Babin E, Sigston E, Hitier M, Dehesdin D, Marie JP, Choussy O. Quality of life in head and neck cancer patients: Predictive factors, functional and psychosocial outcome. Eur Arch Otorhinolaryngol 2008;265:265-70.  Back to cited text no. 52
53.Sciubba JJ. End of life considerations in the head and neck cancer patient. Oral Oncol 2009;45:431-4.  Back to cited text no. 53

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