A wrinked yellow-white area on the gingibal mucosa flexure and mandibular
buccal or labial mucosa is indicative of intraoral use of unburned tobacco. Smokeless tobacco may take various forms (snuff, dip, plug, or quid), leaving its characteristic mark at the preferential site of tobacoo placement. Posterior sites are commonly utilized for dip, plig, or quid, whereas anterior sites are preferential for snuff. Individuals who vary intraoral sites have multiple, less prominent lesions. Male teenagers are most frquently affected, largely because of intensive marketing efforts by tobacco companies. Early snuff dippers patches are pale pink in color, with the surface appearing corrugated and wrinkled. A progression to white, yellow-white, and ye;ow-brown may ensue as hyperkeratosis and exogenous staining occur. Chronic smokeless tobacco use is associated with periodontal alterations, caries, epidermal dysplastic changes, and verrucous carcinoma. To achieve resolution, cessation of use is recommended,. If normal appearance does not return 14 days after cessation, biopsy is necessary
There arc marked geographic and gender differences
in tobacco use. In the United Slates there is a relatively high prevalence of smokeless tobacco users in the southern and western states. Usage by men in New York and Rhode Island is less than 1 % of the population, but in West Virginia it exceeds 20%. Among teenagers, whites are the predominant users of smokeless tobacco, with males making up nearly all of this group. Smokeless tobacco is also used in Sweden, and in regions such as the Indian subcontinent and Southeast Asia, usage is even more common and the materials more destructive in Southeast Asia. The tobacco preparations are generally of a higher (alkaline) pH and are often mixed with other ingredients, including shredded areca (betel) nut, and also containing lime, camphor, and spices. The general increase in smokeless tobacco consumption
has been related to both peer pressure and
increased media advertising, which often glamorizes the use of smokeless tobacco, or snuff dipping. In addition, individuals who have been intense smokers or those who wish to avoid smoking may gravitate to this alternative. The clinical results of long-term exposure to smokeless tobacco include the development of oral mucosal white patches with a slightly increased malignant potential, dependence, alterations of taste, acceleration of periodontal disease, and significant amounts of dental abrasion. Etiology. A causal relationship has been documented between smokeless tobacco and white tissue changes. Although all forms of smokeless tobacco may potentially cause alterations in the oral mucosa, snuff (paniculate, finely divided, or shredded tobacco) appears to be much more likely to cause oral lesions than chewing tobacco. Oral mucosa responds to the topically induced effects of tobacco with inflammation and keratosis. Dysplastic changes may follow, with a low-potential risk of malignant change. Smokeless tobacco-induced alterations in tissues are thought to be a response to tobacco constituents and perhaps other agents that are added for flavoring or moisture retention. Carcinogens, such as nitrosonornicotine, an organic component of chewing tobacco and snuff, have been identified in smokeless tobacco. The pH of snuff, which ranges between 8.2 and 9.3, may be another factor that contributes to the alteration of mucosa. Duration of exposure to smokeless tobacco that is necessary to produce mucosal damage is measured in terms of years. It has been demonstrated that leuko plakia can be predicted with the use of three tins of tobacco per week or duration of the habit for more than 2 years. Clinical Features. White lesions associated with smokeless tobacco develop in the immediate area where the tobacco is habitually placed (Figures 3-9 and 3-10). The most common area of involvement is the mucobuccal fold of the mandible in either the incisor or the molar region. The mucosa develops a granular to wrinkled appearance. In advanced cases a heavy, folded character may be seen. Less often, an erythroplakic or red component may be admixed with the white keratotic component. The lesions are generally painless and asymptomatic, and] their discovery is often incidental to routine oral examination.
Chewing tobacco is an important established risk factor for the
development of oral carcinoma in the United States.52 Habitually chewing tobacco leaves or dipping snuff results in the development of a well-recognized white mucosal lesion in the area of tobacco contact, called smokeless tobacco keratosis, snuff dippers keratosis, or tobacco pouch keratosis.53 90 Diagnosis and Management of Oral and Salivary Gland Diseases
While these lesions are accepted as precancerous, they are significantly
different from true leukoplakia and have a much lower risk of malignant transformation.54 This habit was once almost universal in the United States and is very common among certain other populations, most notably in Sweden, India, and Southeast Asia.52,5560 Smokeless tobacco use among white males in the United States has shown a recent resurgence.6062 The estimated proportion of adult men in the United States who regularly use spit tobacco ranges from 6 to 20%.58,63 This range is attributed to significant geographic, cultural, and gender variations in chewing habits.54 The cumulative incidence for smokeless tobacco use was highest for non-Hispanic white males.54 Unfortunately, the habit starts relatively early in life, usually between the ages of 9 and 15 years, and is rarely begun after 20 years of age. Recent epidemiologic data indicate that over five million Americans use smokeless tobacco and that more than 750,000 of these users are adolescents. It is estimated that each year in the United States, approximately 800,000 young people between the ages of 11 and 19 years experiment with smokeless tobacco and that about 300,000 become regular users.5559,63 Smokeless tobacco contains several known carcinogens, including N-nitrosonornicotine (NNN), and these have been proven to cause mucosal alterations.64 In addition to its established role as a carcinogen, chewing tobacco may be a risk factor in the development of root surface caries and, to a lesser extent, coronal caries. This may be due to its high sugar content and its association with increased amounts of gingival recession.58 The duration of exposure is very important in the production of mucosal damage. Leukoplakia has been reported to develop with the habitual use of as little as three cans of snuff per week for longer than 3 years.53 Although all forms of smokeless tobacco may result in mucosal alterations, snuff (a finely powdered tobacco) appears to be much more likely to cause such changes than is chewing tobacco.53,59 Smokeless tobacco is not consistently associated with increased rates of oral cancer.54Approximately 20% of all adult Swedish males use moist snuff, yet it has not been possible to detect any significant increase in the incidence of cancer of the oral cavity or pharynx in Sweden. By international standards,
the prevalence of oral cancer is low in Sweden.52 This has been
attributed to variations in the composition of snuff, in particular, the amount of fermented or cured tobacco in the mixture. The carcinogen NNN is present in much lower concentrations in Swedish snuff, probably because of a lack of fermentation of the tobacco. Also, the high level of snuff use might decrease the amount of cigarette smoking and therefore lead to a lesser prevalence of oral cancer.52,54 TYPICAL FEATURES
Numerous alterations are found in habitual users of smokeless
tobacco. Most changes associated with the use of smokeless tobacco are seen in the area contacting the tobacco. The most common area of involvement is the anterior mandibular vestibule, followed by the posterior vestibule.53 The surface of the mucosa. appears white and is granular or wrinkled (Figure 5-9); in some cases, a folded character may be seen (tobacco pouch keratosis). Commonly noted is a characteristic area of gingival recession with periodontal-tissue destruction in the immediate area of contact (Figure 5-10). This recession involves the facial aspect of the tooth or teeth and is related to the amount and duration of tobacco use. The mucosa appears gray or gray-white and almost translucent. Since the tobacco is not in the mouth during examination, the usually stretched mucosa appears fissured or rippled, and a pouch is usually present. This white tobacco pouch may become leathery or nodular in long-term heavy users (Figure 511). Rarely, an erythroplakic component may be seen.The lesion is usually asymptomatic and is discovered on routine examination. Microscopically, the epithelium is hyperkeratotic and thickened. A characteristic vacuolization or edema may be seen in the keratin layer and in the superficial epithelium. Frank dysplasia is uncommon in tobacco pouch keratosis.62 TREATMENT AND PROGNOSIS
Cessation of use almost always leads to a normal mucosal
appearance within 1 to 2 weeks.54,64,65 Biopsy specimens should be obtained from lesions that remain after 1 month. Biopsy is particularly indicated for those lesions that appear clinically atypical and that include such features as surface ulceration, erythroplakia, intense whiteness, or a verrucoid or papillary surface.53, 62, 64 The risk of malignant transformation is increased fourfold for chronic smokeless tobacco users.66