Journal of Pharmacy And Bioallied Sciences

: 2017  |  Volume : 9  |  Issue : 5  |  Page : 55--67

Prevalence of oral mucosal lesions among dental patients with mixed habits in Salem district - A study

R Karthik, N Mohan 
 Department of Oral Medicine, Vinayaka Missions Sankarachariyar Dental College, Salem, Tamil Nadu, India

Correspondence Address:
R Karthik
Door No. 65/10, Third Cross Street, Mayor Nagar, Peramanur, Salem - 636 007, Tamil Nadu


Background: The practice of betel nut chewing with or without tobacco is still practiced in south india, salem inspite of its harmful effects. Methodology: 200 Patients visiting the outpatient department, Oral medicine and radiology from Aug 2015 to Aug 2016. Result and Conclusion: In our study, 3 women were exclusively churut smokers. Thirty-eight percent of the dental patients were beedi smoker, 32% were tobacco chewers, 12% were both betel nut and tobacco chewers, 8% were exclusively betel nut chewers, 1% of the dental population were exclusively churut smokers. Mean age group of the study population is 50.2 (14.4). There are 28 females and 172 males in the study group. Chi-square test revealed a statistically significant difference (P = 0.001) between males and females based on soft-tissue findings and no statistically significant difference (P = 0.572) between males and females based on distribution of hard-tissue findings.

How to cite this article:
Karthik R, Mohan N. Prevalence of oral mucosal lesions among dental patients with mixed habits in Salem district - A study.J Pharm Bioall Sci 2017;9:55-67

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Karthik R, Mohan N. Prevalence of oral mucosal lesions among dental patients with mixed habits in Salem district - A study. J Pharm Bioall Sci [serial online] 2017 [cited 2022 Aug 15 ];9:55-67
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Betel nut is derived from the tropical palm tree Arecha catechu, is the fourth commonly abused substance and is used with or without tobacco. The pattern of oral mucosal lesions vary in which the tobacco is smoked or pouched.


The aim of this study was to find out the prevalence of pattern of distribution of oral mucosal lesions among dental patients with mixed habits in Salem district.

Inclusion criteria

Patients aged ≥25 years, who currently are smoking, chewing tobacco, betel nut, or betel quid (BQ) or both or has a combination of these habits for a minimum of 12 months were included in the study.

Exclusion criteria

(1) People aged <25 years; (2) people who did not have any deleterious oral habits such as smoking or tobacco chewing and betel nut or quid chewing; (3) patients who could not open their mouths adequately for intraoral clinical examination, for example, pericoronitis, pericoronal abscess, masseteric space infections associated with severe trismus with mouth opening <1 cm; (4) patients who were unconscious or sedated or bed ridden; (5) patients who had a recent history of maxillofacial trauma by road traffic accidents or any other means; (6) patient who gives history of chronic debilitating diseases such as tuberculosis, anemia, and jaundice are excluded from the study; (7) patient who had treatment for jaw fractures; (8) postsurgical cases, for example, after surgical treatment of oral carcinoma; (9) patients who are undergoing radiotherapy for head and neck cancer; (10) patient who are revisiting the outpatient department of oral medicine, diagnosis and radiology for follow-up and evaluation for any of the above treatments during this period; and (11) patients with recurrent cases such as recurrent aphthous ulcer, autoimmune disorders such as lichen planus, pemphigus, and systemic lupus erythematosus are not included in this study.

 Materials and Methods

A descriptive analytical study comprising 200 patients is conducted in Vinayaka Missions Sankarachariyar Dental College, who attended the Outpatient Department of Oral Medicine and Radiology, from August 2015 to August 2016. Informed consent is obtained from all the patients. Diagnosis was exclusively based on the history, clinical findings, and the characteristic location of the lesions. The lesions were recorded as proposed by the WHO international nomenclature and classification of oral potentially malignant disorders as proposed by Warnakulasuriya et al under proper Halogen light illumination in a dental chair.[1]

Statistical analysis used

Chi-square test is used to find the significance of study parameters on categorical scale between the groups using IBM, S. P. S. S software analytical Tool version 11.0.


The male gender (86%) had mixed habits compared to female gender (14%). Among the smoking forms of tobacco, Beedi smoking is the most common habit among South Asian population in Salem district. In our study, 3 women were exclusively churut smokers. Thirty-eight percent of the dental patients were beedi smoker, 32% were tobacco chewers, 12% were both betel nut and tobacco chewers, 8% were exclusively betel nut chewers, 1% of the dental population were exclusively churut smokers.

Mean age group of the study population is 50.2 (14.4). There are 28 females and 172 males in the study group [Table 1]. All 28 females and 172 males have habits. Of the 28 females, 17 females have hard-tissue findings and 26 females have soft-tissue findings [Table 2]. Among the 172 males, 96 have hard-tissue findings and 169 have soft-tissue findings [Figure 1]. The most common hard-tissue findings were extrinsic stains which is found to be more among the beedi and churut smokers due to the unfiltered nature of such tobacco products enhancing the formation of more tobacco smoke containing coal tar stains to be deposited on the external surfaces of the teeth. Attrition of teeth is more commonly seen among people who use either only chewing form of betel nut and tobacco or both than people who use only smoking forms of tobacco. Among females, 3 were exclusively churut smokers, 11 are betel nut chewers, 7 are BQ chewers, 6 are hans chewers, and 1 is a pan chewer. Betel nut chewing happens to be the predominant habit among females [Figure 2]. Among males, 81 are beedi smokers, 39 are hans chewers, 24 are cigarette smokers, and 18 are betel nut chewers. Beedi smoking happens to be the predominant habit among males [Figure 3]. There is statistically significant difference (P = 0.000) between males and females based on the type of habit. Among females, 10 have extrinsic stains due to smoking form of tobacco, 6 have extrinsic stains due to smokeless form of tobacco, and one has extrinsic stain due to betel nut [Figure 4]. Among men, 59 have extrinsic stains due to smoking form of tobacco, 16 have extrinsic stains due to smokeless form of tobacco, 11 have extrinsic stains due to betel nut, 4 have extrinsic stains due to BQ and attrition, vertical crown fracture, and extrinsic stains due to ghutka are found in 2 men, respectively [Figure 5]. Chi-square test revealed no statistically significant difference (P = 0.572) between males and females based on distribution of hard-tissue findings.{Table 1}{Table 2}{Figure 1}{Figure 2}{Figure 3}{Figure 4}{Figure 5}

 Distribution of Study Participants Based on Soft Tissue Findings

Among females, 4 have smoker's melanosis due to smoking form of tobacco and 4 have lichenoid reaction due to chewing form of tobacco. Among males, 37 had smoker's melanosis due to smoking form of tobacco, 20 had tobacco pouch keratosis due to chewing form of tobacco, 20 had leukoplakia due to smoking form of tobacco, 18 had smokers palate, 11 had betel nut lichenoid reaction on the oral mucosa, and 10 had betel nut encrustations [Table 3]. Chi-square test revealed a statistically significant difference (P = 0.001) between males and females based on soft-tissue distribution. Among females, 10 were betel nut chewers, 4 use smoking form of tobacco and smokeless form of tobacco, and 7 use betel nut and quid in each, respectively. Among males, 105 were users of smoking form of tobacco, 44 were smokeless form of tobacco, 18 were betel nut chewers, 4 were betel nut and quid, 1 is an alcoholic [Figure 6]. Chi-square test reveals statistically significant difference between males and females based on form of habit (P = 0.000).{Table 3}{Figure 6}

Distribution of soft tissue findings based on habit

Among beedi smokers

Smoker's melanosis present among 25.15 had smokers palate, 2 had hairy tongue, 21 had leukoplakia, 2 had median rhomboid glossitis, 1 had carcinoma in the floor of the mouth, 2 had carcinoma in the alveolar mucosa, 1 had carcinoma in buccal mucosa, 1 had carcinoma in the vermilion border of lip, 1 had carcinoma on the soft palate, 1 had palatal petechiae, and 2 had leukedema [Figure 7].{Figure 7}

Among cigarette smokers

Smoker's melanosis present among 13 individuals, 4 had smokers palate, 1 had leukoplakia, 1 had linea alba buccalis, 2 had frictional keratosis, and 1 had carcinoma in the buccal mucosa [Figure 8].{Figure 8}

Among churut smokers

One had smokers palate and 1 had carcinoma in floor of mouth.

Among betel nut chewers

Betel nut-induced lichenoid reaction present in 12, 8 had oral submucous fibrosis (OSMF), 1 had chronic periodontal abscess, 2 had tobacco pouch keratosis, 1 had carcinoma of buccal mucosa, 1 had frictional keratosis, and 1 had betel nut encrustations [Figure 9].{Figure 9}

Among betel quid chewers

8 had Betel nut encrustations and is the predominant oral finding, 3 had Betel induced lichenoid reactions [Figure 10].{Figure 10}

Among hans chewers

Tobacco pouch keratosis is the predominant oral lesion seen among hans' chewer and seen among total of 18 individuals, 2 had chronic periodontal abscess, 6 had tobacco-induced lichenoid reaction, 7 had chemical burn, carcinoma of the oral cavity is seen among 5 cases of hans chewers [Figure 11].{Figure 11}


Tobacco is obtained from the chief commercial crop Nicotiana tabacum, one among seventy species of tobacco. Bidi is the most common form of smoking tobacco used among South asian population among Salem district. Bidi is a leaf-rolled cigarette made of coarse, uncured tobacco, tied with a string at one end. The word bidi is derived from “beeda” (a word in Marwari – a dialect of Hindi predominantly spoken by the trader caste from Marwar of Gujarat and Rajasthan).[2] Bidi is obtained from tendu leaves of Asian ebony tree called diospyros melanoxylon. The dried tendu leaves are selected for making Bidis as they are pliable and can be rolled and burnt without altering the taste of tobacco flavor. In India, bidis account for about 60% of smoking forms of tobacco and cigarettes account for 20% (IIPS, 2010).[3] Bidis may have higher amounts of chemicals such as phenol (250 vs. 150 μg), hydrogen cyanide (903 vs. 445 μg), benzopyrenes, carbon monoxide (7.7 vs. 3.5 vol%), and ammonia (284 vs. 180 μg).

Areca nut, the seed of the fruit of Arecha catechu palm tree, is the fourth commonly abused substance worldwide next to nicotine, ethanol, and caffeine.[4] Gutkha is the processed and packaged areca nut with added tobacco. The term “quid” denotes a substance or a mixture of substances that is placed and retained in the mouth, and often spitted out. Paan is a quid consisting of piper betel leaf that contains areca nut, lime, condiment, sweeteners, and sometimes tobacco.[4] Sanskrit writing describes 12 desirable qualities of betel nut chewing as symbol of esteem and display of respect and reverence, pungency, bitter, sweet, spicy, salty, astringent, it expels and kills worms, removes phlegm, eradicates odors, purifies all organs of the body, and even induces passion.[4]

The main reasons for chewing tobacco among South Asians is to keep them awake or to relieve stress. They create a sense of well-being (euphoria) and heightened alertness, sweating, salivation, a hot sensation in the body, and increased capacity to work.[5],[6] International Agency for Research on Cancer has shown that chewing arecanut or BQ with or without tobacco is considered carcinogenic.[5] The oral lesions associated with mixed habits can be classified as hard-tissue (effects on teeth) and soft-tissue findings.(effects on the oral mucosa). The most common hard-tissue findings among smokers and betel nut chewers are extrinsic stains.

Extrinsic stains

The color of the extrinsic stains on the teeth varies depending on the use of smoking or chewing betel nut. Most of the Beedi smokers had black extrinsic stains on their tooth due to the deposition of coal tar on the enamel surface biofilm of the teeth [Figure 12]. The betel associated stains teeth brownish-red has been reported to be caused by polymers of orthoquinones released from betel chewing that produces sticky copious red saliva that gets deposited on the tooth surface among BQ chewers [Figure 13]. With regular BQ chewing, this stain becomes embedded in the teeth, gingiva, and oral mucosa.[6]{Figure 12}{Figure 13}


Attrition of teeth is seen common among betel nut or BQ chewers due to the physiological contact of the opposing tooth during betel nut chewing. Betel nut chewers, however, do not had sensitivity in their attrited teeth. This may be due to the fact that sclerotic dentin formed as a response to chronic attrition in betel nut chewers. The physiological attrition of betel nut chewers alters the normal pit and fissure morphology of occlusal surface of the teeth to flat, shiny areas which eliminates the harboring of dental caries causing streptococcus mutans organisms in the teeth of betel nut chewers [Figure 14]. The tannic acid in betel nut chewers further acts as a bacteriostatic agent, preventing the formation of dental caries.[6]{Figure 14}

Vertical crown fracture

Vertical crown fracture is seen exclusively among betel nut chewers due to the sudden masticatory force exerted on the teeth by the hard nature of the betel nut [Figure 15]. In our study, 3 out of 50 cases are reported with vertical crown fracture only who use betel nut chewers with or without tobacco.{Figure 15}

Soft tissue findings

Betel induced lichenoid reaction

The alkaloids present in the betel nut mainly arecoline and free radicals that are released on chewing the betel nut are cytotoxic to epithelial cells of the oral mucosa and can induce lichenoid reaction. These lichenoid reactions are a form of delayed mediated hypersensitivity reactions which develop at the contact areas of the betel nut or quid or chewing tobacco (usually hans, pan, or gutkha) where it is kept inside the oral cavity which recognizes it as haptens. Oral lichenoid reactions so termed because these lesions resemble lichen planus. Avon described Betel induced lichenoid reactions are characterized by the presence of fine discrete grayish wavy striations or discrete areas of pigmentations at regular intervals or fine reticular (net-like) patterns on the areas which are in contact with the oral mucosa.[7] In our study, three different patterns of oral lichenoid reactions that are induced by betel nut is recognized [Figure 16]a,[Figure 16]b,[Figure 16]c. Lichenoid reactions occurring on the dorsum of the tongue are characterized by discrete areas of greyish pigmentation. In our case, most of the betel-induced lichenoid reactions are seen on the buccal mucosa followed by dorsum of the tongue characterized by the occurrence of discrete areas of grayish pigmentation when the patient ingest the betel nut juices.[4]{Figure 16}

Angular cheilitis: (Rhagades, perleche, commissural cheilitis, angular cheilosis)

Angular cheilitis refers to inflammation of one or both of the corners of the mouth [Figure 17]. Most commonly, it represents an infectious etiology, as an opportunistic fungal (candidiasis) or bacterial pathogen (Staphylococcus aureus or beta-hemolytic streptococcus species) and leads to a spectrum of varying severities.[8] Devani et al mentioned that excess use of alcohol containing mouthrinses and aggressive use of dental floss may contribute to the development of Angular cheilitis.[9] Angular cheilitis are usually caused by anemia secondary to oral submucous fibrosis which has developed due to the chronic chewing of betel nut.[10]{Figure 17}

Acute necrotizing ulcerative gingivitis

Acute-necrotizing ulcerative gingivitis (ANUG) (Trench mouth) so called because of the occurrence of ANUG in soldiers who were in trenches during the World War I.[11] ANUG is caused by specific bacteria, namely, Bacteroides, Fusobacterium fusiform bacillus, and Spirochetes is introduced by Plaut and Vincent.[12],[13] The palatal surface behind the maxillary incisors and the labial surface of the mandibular incisors are the frequent sites of ANUG. Patients with ANUG usually have fetid odor due to necrosis of interdental papilla [Figure 18]. Nicotine present in the tobacco causes release of local and systemic catecholamines leading to constriction of finer capillaries leading to decreased gingival papillary flow, resulting in papillary necrosis. Nicotine further alters the matrix metalloproteinases and tissue inhibitor of matrix metalloproteinase ratio, thereby causing increased destruction of collagen in the periodontal ligament leading to loss of attachment and gingival recession.[12] Pindborg reported that 98% of his patients with ANUG were smokers and that the frequency of this disease increases with the increasing exposure to tobacco smoke. In our study, one such case reported in the labial aspect of marginal gingiva in relation to mandibular anterior teeth.[13]{Figure 18}

Betel nut encrustations

Fine betel nut particles seen attached to the abraded mucosa is referred to as betel nut encrustations are seen in betel nut or BQ chewers [Figure 19]. They are characterized by discrete orange brownish discolorations of the abraded oral mucosa.[11],[14] In our study, 5% of dental patients had such betel nut encrustations and are most commonly seen on the buccal mucosa.[14]{Figure 19}

Chemical burn

Chemical burn is usually seen among hans chewers. They are characterized by whitish peeling of the epithelium leaving a raw erythematous area [Figure 20]. Such chemical burns were seen exclusively among betel chewers caused by the harmful chemicals leached from betel nut.{Figure 20}

Frictional keratosis

A localized whitish area due to keratinization that is caused by chronic friction from sharp attrited teeth seen among chronic betel nut chewers [Figure 21]. Smokers exhibited a decrease in several pro-inflammatory cytokines (tumor necrosis factor-α, IL-6) and chemokines and certain regulators of T-cells and NK-cells and augments Porphyromonas gingivalis and Streptococcus gordonii biofilm formation causes periodontal ligament destruction, which aggravates periodontitis resulting in tooth loss.[15] Loss of mandibular molar tooth occurs more common as these teeth are more commonly subjected to heavy, occlusal forces due to periodontal disease due to smoking which leads to early loss of mandibular permanent molar tooth and causing the pathological migration of opposing maxillary teeth cusp to frequently impinge on the edentulous alveolar ridge mucosa.{Figure 21}


Leukedema is a benign condition of the oral mucosa that clinically presents with whitish translucent hue usually on the buccal mucosa and which disappears on stretching the buccal mucosa [Figure 22]. It was first described by Sandstead and Lowe in 1953 occurring around lesions of leukoplakia.[16] Leukedema is present among 2 dental patients in our study who were chronic smokers.{Figure 22}

Linea alba buccalis

Frictional keratosis due to buccal cheek bite is referred to as linea alba buccalis. Such lesions are identified by the presence of a whitish line seen along the occlusal plane on the buccal mucosa [Figure 23]. They are nonscrapable, nontender on palpation.{Figure 23}


The term leukoplakia as defined by Warnakulasuriya et al. should be restricted only to recognizable white plaques of questionable risk occurring on the oral mucosa having excluded other known diseases or disorders that carry no increased risk for cancer [Figure 24]. The term “Leukoplakia” was proposed by Schwimmer to describe a white plaque on the tongue in 1877. Pindborg pointed out that the habit of bidi smoking was associated with a far higher percentage of leukoplakia than any other smoking or chewing habits. The rate of malignant transformation of leukoplakia as suggested by various authors was EinhornWersall (4%), Silvermann (6%), Pindborg (4.4%), Kramer (4.8%), Roed Peterson (3.6%), Banockzy (6%), Silverman (17.5%), Lind (8.9%), and Bouquot and Gorlin (10.3%).[17]{Figure 24}

Hairy tongue (nigrites-hyperkeratosis linguae, lingua villa nigrosa)

The term black hairy tongue was first coined by Amatus Lusitanus in the year 1557. It is a reactive hypertrophy and defective desquamation of filiform papilla causing hair-like projections on the dorsum of the tongue. In our study, 2 of the beedi smokers had black hairy tongue [Figure 25]. Gurvis et al. reported that casual smoking poses a slightly increased risk of having black hairy tongue compared to nonsmokers (15% to 10% in men, 5.5% to 5.2% in women).[10] Our study is in accordance with the study by Henry corsi who reported 2 cases of black hairy tongue in 1931 and Waggoner and Volpe in 1967 who reported a prevalence rate of 0.4%.[18],[19] In 1901 Lucet identified it as yeast cells and named it as cryptococcus linguae pilosae. Buxton in 1925 reported this peculiar lesion on a 64 year old male during routine examination of the tongue as a thin, hair-like processes, about one-third of an inch long, cover the center of the dorsum over an area infront of circumvallate papilla which is blackish in color, feels soft, and there is no induration. Ralph found a symbiosis of a Cryptococcus with a nocardia growing in very fine filaments of stained hypertrophied filiform papilla in 1931. Barnard believes it as a disease of old age due to normal rubbing of hard food. An acid reaction of the mouth seems to be the essential underlying factor, whether produced by excess of fermentable food, gastritis, or paucity of saliva in the aged. The acid reaction favors the growth of yeasts and filiform acidophilous bacilli, and adhesion of the epithelial scales to each other. Dr. Barber identified three different species of monilia from hairy tongue as monilia meta-tropicalis, monilia krueei, and monilia pinoyi.[18] Dr. Price reported a case of black hairy tongue during autopsy on a 71-year-old man who died from generalized arteriosclerosis. Whittle in 1946 described black hairy tongue in a 32 aged postoffice worker who smoke thirteen cigarettes per day. In 1999, Manabe et al. using antikeratin probes on black hairy tongue epithelium, found that the “hairs” are highly elongated cornified spines that result from delayed desquamation of the cells in the central column of filiform papillae and marked retention of secondary papillary cells that expressed hair-type keratins.[20] In 2016, Andreas Korber reported a case of black hairy tongue in 85 year-old male cigar smoker. This shows that there exists a definite correlation of the occurrence of black hairy tongue in smokers.[21]{Figure 25}

Smoking or chewing tobacco, poor oral hygiene, xerostomia, substance abuse like cocaine, using peroxide containing mouth washes and drugs like steroids, bismuth, methyldopa, Linezolid, tetracycline are the predisposing factors of Black hairy tongue.[22]

Oral submucous fibrosis (distrophica idiopathica mucosa oris)

Oral submucous fibrosis was first reported in India in 1953 by Joshi. This disease is called as Vidari by sushruta in Ancient Medicine. OSF was initially described in 1966 by Pindborg and Sirsat as an insidious, precancerous, chronic disease that may affect the entire oral cavity and that sometimes extends to the pharynx.[14],[23] Although it is occasionally preceded by the formation of vesicles, OSF is always associated with a subepithelial inflammatory reaction followed by fibroelastic changes of the lamina propria, accompanied by epithelial atrophy. This process leads to stiffness of the oral mucosa, which results in trismus and inability to eat In 1953, Lal reported cases of oral submucous fibrosis in patients who had history of Betel nut chewing.[24] The malignant transformation rate of OSMF is reported as 7.6% over a 10 year period.[14],[25] This disease is characterized by loss of normal resiliency of oral mucosa with pale blanched appearance of the mucosa [Figure 26] with the formation of vertical fibrotic bands resulting in progressive inability to open the mouth. In later stage, the disease affects the tubal and paratubal muscles leading to degeneration of eustachian tube and pharynx leading to difficulty in deglutition of foods.[14.25]In vitro studies with cultured fibroblasts have shown that areca nut alkaloids such as arecoline and its hydrolyzed product arecaidine stimulate proliferation and collagen synthesis in a dose-dependent manner, higher concentrations being cytotoxic.[26]{Figure 26}

Smokers melanosis

The nicotine and heat associated with tobacco smoke found to stimulate the melanocytes in the basal epithelial cells of the oral epithelium leading to formation of melanin resulting in diffuse grayish pigmentation of the hard palate mucosa [Figure 27] with varying amounts of melanin incontinence[27] (Hedin et al. 1986). Such pigmentations are commonly encountered on the hard palate mucosa, buccal mucosa, and labial aspect of mandibular anterior attached gingiva in relation to mandibular anterior teeth. In our study, 34% of the Beedi smokers had smokers melanosis.[28]{Figure 27}

Smokers palate (stomatitis nicotina palati)

Thoma first described smokers palate in 1947. Papular elevations up to 2–3 mm in height with central umbilications with red spots or without pigmentation of the surrounding mucosa seen on the hard palate mucosa in smokers are referred to as smoker's palate [Figure 28]. The red spots represent the inflamed orifices of the minorsalivary gland ducts. The high temperature and chemical constituents of tobacco smoke play a synergistic effect in the etiology. In 1977, Mehta et al. stated that the hypertrophied ductal openings of minor salivary glands act as portal of entry for the toxins of tobacco smoke and the pseudostratified columnar epithelial linings of ducts is found to undergo squamous metaplasia. In our study, 15 beedi smokers and 4 cigarette smokers had smokers palate among the total 105 males who use smoking forms of tobacco.[27]{Figure 28}

Tobacco pouch keratosis

Tobacco pouch keratosis is seen among tobacco in the form of hans which is chewed and pouched frequently in the mandibular buccal vestibule or maxillary labial vestibule. Such lesions are characterized by the presence of whitish-wrinkled appearance of the oral mucosa characteristically seen extending along the buccal vestibule or labial vestibule and part of the attached gingiva which is in contact with the chewing tobacco [Figure 29]. Chewing tobacco consists of sweetened, coarsely ground tobacco leaves that can be loose leaf or in the form of plugs or twists. It is used in the form of a “chew” or “quid” that is chewed or held in the cheek. According to Axéll et al., tobacco pouch keratosis may occur due to chronically stretched tissues in the area of tobacco placement and the lesion is confined to areas in direct contact with spit tobacco.[29] Our study results were in accordance Naveen-Kumar et al. conducted with an observational cross-sectional study conducted by Naveen-Kumar et al. in Vishnu dental college, Bhimavaram, on total of 450 patients out of which 23 had tobacco pouch keratosis.[29]{Figure 29}

Palatal petechiae

Palatal Petechiae are pinpoint hemorrhages <1 mm in diameter that are confined near the junction of the hard and soft palate. Such palatal petechiae were seen among 1% of beedi smokers due to chronic cough secondary to chronic bronchitis.

Median rhomboid glossitis associated with a kissing lesion on the hard palate

Goregen et al. in his study mentioned that there was a significant association between median rhomboid glossitis and Candida.[30] The underlying risk factors being smoking and chronic denture wearing. They isolated Candida albicans, Candida kefyr, Candida tropicalis, Candida krusei, and Candida glabrata from 18, 3, 2, 2, and 2 patients with median rhomboid glossitis, respectively. Farman suggested that an impaired blood supply to the middorsal surface of the tongue might predispose it to the development of candidiasis and resulting consequent loss of filiform papillae.[31] Whitaker and Singh suggested that since the tongue maintains close contact with the palatal mucosa during swallowing and at rest, the area of the tongue contacting the particular portion of hard palate develops candida infection. When median rhomboid glossitis on the dorsum of the tongue is found in association with hard palate, it is called kissing lesion; [Figure 30] immunosuppression should be suspected and it has been considered a marker of AIDS.[32]{Figure 30}


The word carcinoma is derived from the Greek word “Karkinos” meaning crab. Carcinoma is an abnormal mass of tissue, the growth of which exceeds that of the adjacent tissue and it persists in the same excessive manner, even after the cessation of the stimuli, which evoked the change. In Indian subcontinent, 92%–95% of the oral carcinomas are squamous cell carcinomas. Chronic smoking or chewing tobacco or use of betel or quid with or without tobacco is associated with the etiology of carcinoma of the oral cavity. Such lesions are characterized clinically by the presence of painless nonhealing ulcer or growth or as an ulceroproliferative growth in the oral cavity. The first study of tobacco and oral cancer in Tamil Nadu was conducted by Shanta and Krishnamurthi in 1959. They concluded that the habit of prolonged combined tobacco, betel and nut chewing over a long period (15-20 Years) together with the oral sepsis is the most important single factor in the causation of oral squamous cell carcinomas. Our study correlated with the prevalence rate of 1.09% in lip. Smokeless tobacco is derived from species Nicotina rustica. Which contains higher amount of nitrosoamines, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N9-nitrosonornicotine and are consistently carcinogenic.[33] Sundqvist et al. and Li et al. concluded that areca nut induced cytotoxicity and genotoxicity in normal oral epithelium leading to greater susceptibility for tumor formation. Prolonged incubation of areca nut ingredients provides substantial oncogenic inputs resulting in cellular transformation of normal oral epithelium into malignant cells, mainly by the activation of various intrinsic tumorigenic signals, including extracellular receptor kinase, Akt (a serine-threonine protein kinase that plays a role in cellular apoptosis) and NF-kappa-beta pathways.[34],[35]

The carcinogenicity of BQ was first evaluated in 1984 (IARC, 1985), the relationship between BQ chewing and cancer of the oral cavity had been investigated in the meta-analytical studies in India by Orr (1933), Sanghvi (1955), Sarma (1958), Khanolkar (1959), Chandra (1962), Shanta and Krishnamurti (1963), Wahi (1965), Hirayama (1966), Wahi (1968), Jussawalla and Deshpande (1971), Khanna (1975), Notani and Sanghvi (1976), Jaffrey and Zaidi (1977), Gupta (1980), Sankaranarayanan (1989), Nandakumar (1990), Rao et al.(1994), Rao and Desai et al.(1998), Wasnik et al.(1998), Merchant et al. (2000), Dikshit and kanhere (2000), Balaram et al.(2002), Znoar et al.(2003), Subapriya et al. (2007), Muwonge et al.(2008), Fernando et al.(2009), Jeyalakshmi et al.(2009), Gajalakshmi et al., Madani et al. (2012).[36]

Several researchers have conducted the study in India and associated the risk of betel chewing with or without tobacco in India Davis (1915), Mendelson and Ellis (1924), Eisen (1946), Paymaster (1956), Padmavathy and Reddy (1960), Paymaster (1962), Farago (1963), Chang, Agarwal and Arora and Sidiq et al.(1964), Balendra (1965) Singh and Von Essen and Wahi et al. (1966), Srivastava and Sharma (1968), Gandagule and Agarwal and Samuel et al.(1969).[36]

The following case–control studies of cancer of the oral cavity stated an increased risk of oral cancer from BQ chewing without tobacco (Nandakumar et al., 1990; Ko et al., 1995; Lu et al., 1996; Wasnik et al., 1998; Dikshit and Kanhere, 2000; Merchant et al., 2000; Balaram et al., 2002; Chen et al., 2002; Znaor et al., 2003; Subapriya et al., 2007; Thomas et al., 2007; Muwonge et al., 2008; Znaor et al. 2003).[36]

Acetaldehyde, the metabolic product of alcohol, is a known carcinogenic. Smoking increases the acetaldehyde burden following alcohol consumption, and alcohol-drinking enhances the activation of procarcinogens present in tobacco due to increased metabolic activation, by an induced cytochrome P450-2E1-dependent microsomal biotransformation system in the mucosa and the liver.[37]

The consumption of alcohol in addition to the use of smoking or chewing tobacco increases the risk for oral cancer. The various mechanisms by which alcohol acts as a risk factor for oral cancer are as follows. Alcohol increases the mucosal permeability to other toxins and carcinogens, alters the mucosal morphology with a reduction in thickness of oral epithelium, disrupts the normal salivary gland function enhancing the dryness of oral mucosa, and reduces the clearance of locally acting carcinogens, thereby potentiate the carcinogenic effects of other agents. The International Head and Neck Cancer Epidemiology consortium concluded that the joint effect of tobacco and alcohol is responsible for large number of head and neck cancers.[37],[38] Further acetaldehyde (the first metabolite of ethanol) is a mutagenic and carcinogenic substance which causes cellular damage to the oral epithelial cells (Reidy et al. 2011).[39] The International classification of Diseases affecting oral cavity diagnosis code C06.9 classifies the malignant neoplasms of the mouth. In our study, 45% of oral carcinomas occurred in the alveolar mucosa [Figure 31], 22% in buccal mucosa, 11% of carcinoma was seen in the floor of the mouth [Figure 32], 1 among the 100 dental patients had carcinoma in the palatine tonsil. Among 47% of Beedi smoker among males, 1 had Carcinoma in the base of the tongue [Figure 33].{Figure 31}{Figure 32}{Figure 33}


There exists a definite association of smoking or chewing forms of tobacco and betel nut chewing with the potential of transforming normal oral mucosa to oral cancer. The risk of oral cancer increases with the duration and frequency of chewing or smoking form of tobacco. Consumption of alcohol increases the dryness of oral mucosa and increases the susceptibility of leaching the harmful chemical constituents of tobacco or betel nut in contact with the oral mucosa making it more potential for oral mucosa to progress into oral cancer. Betel nut is cytotoxic and genotoxic to buccal epithelial cells. Betel nut has a definitive correlation with association of oral submucous fibrosis which in turn can lead to oral cancer. The risk increases with the duration, type, and frequency of habits. Smoking or chewing tobacco or the use of betel nut alone or in the form of quid must be strictly banned to ensure oral health.[40]

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