Smokeless tobacco (SLT) has been smoked, chewed, and inhaled in various forms for hundreds of years. The primary oral, mucosal, and hard tissue changes associated with SLT use include SLT keratosis (STK); gingival inflammation, periodontal inflammation, and alveolar bone damage; and dental caries, tooth abrasion, and dysplasia and oral squamous cell carcinoma (SCC). Some high-risk STKs are human papillomavirus associated, and the highest level of transition of STK to dysplasia or oral SCC appears to be in those lesions that have a diffuse velvety or papillary texture clinically. There is minimal risk for oral cancer associated with SLT use.
For hundreds of years, tobacco has been smoked, chewed, and inhaled in various forms. The use of smokeless tobacco (SLT) in North America seems to have originated with American Indians, and before 1900, the dominant form of tobacco used in North America was in fact SLT rather than cigarettes. With the advent of cigarettes, SLT use declined, until the 1970s when there was resurgence in its use. Some investigators have suggested that there was a 10% increase in the use of SLT from the early 1970s until 1986, when the US Surgeon General’s first report on SLT usage was published. There was a brief decline in sales in the United States after the issuance of this report, but there has been a steady growth in usage since then. Until this resurgence, there was a paucity of information concerning longitudinal cross-sectional evaluation of SLT-induced oral lesions of any kind in juveniles, adults, or geriatric patients. Since then research into the use and health consequences of all forms of SLT occurred, related with certainty to not only an upsurge in usage but also the lack of standardized clinical and histopathologic criteria detailing the oral manifestations of SLT use.
SLT is a broad encompassing term that includes both chewing tobacco and snuff. Three types of SLT are commonly manufactured: loose-leaf chewing tobacco, moist snuff, and dry snuff. Loose-leaf chewing tobacco is processed and manufactured in the United States largely from tobacco plants grown in the Midwest. The product consists of shredded flakelike aggregates of air-cured leaf tobacco that is flavored with sweetening agents. Loose-leaf tobacco usage, long been favored by men, has declined during the past 2 decades.
In contrast, moist snuff usage has dramatically gained popularity in the United States over the past 2 decades, with sales increasing as much as 77% over the 15-year period, from 1985 to 2000. Known as snus in Sweden, moist snuff is composed of finely ground tobacco that can be placed discreetly in the oral cavity, most often between the buccal vestibular mucosa and gingiva. The product can be extracted from a small round tin or carton and delivered to the mouth via what is known colloquially as a tobacco “pinch.”
Moist snuff produces minimal juices when used and requires very little expectoration. Moist snuff products in the United States undergo fermentation, whereas moist snuff products from Sweden, which undergo high-heat treatment, do not. Fermentation tends to give moist snuff its unique flavor, but the fermentation process also enhances cancer-inducing bacterial associated by-products, such as tobacco-specific N’ nitrosamines and certain nitrites.
Dry snuff, also fermented and fire cured, was first inhaled nasally by users and later used in oral form, primarily by women in the Southern states of the United States. The product was in common usage in the late nineteenth and early twentieth centuries. However, since the mid-20th century dry snuff usage has declined dramatically.
Oral use of snuff is colloquially referred to as “snuff dipping.” In 1984, it was estimated that the number of moist snuff sales in the United States was approximately 37.5 million pounds. Albert and colleagues, in 2008, reported that moist snuff sales had increased to the point that the sales accounted for 71% of the SLT market. Dry snuff sales are generally considered to be less than 10 million pounds annually and on the decline.
Epidemiology
The number of Americans who currently use SLT in any of its forms can only be estimated. Estimates have ranged from 6 million to 22 million. The American Cancer Society has placed the usage figure at closer to 7 million, whereas the American Council for Drug Education places the figure at a largely unsubstantiated 47 million.
In addition to the United States and Sweden, SLT is also widely used in India. In the largest single study of SLT usage in India, which included the assessment of 255,194 individuals from 9 geographic areas, the usage was reported to range from 11% to 49%.
Some Swedish studies have reported that 35% of men in the age group of 16- to 24-years were regular or occasional users of snuff. However, the frequency of snuff use seems to decline with the increasing age of subjects in each of the countries referenced.
Investigators in the United States have long attempted to determine the prevalence and specific usage patterns of SLT. In 1985, a national representative geographic study revealed that 60% of men in the United States between the ages of 12 and 17 years had used some form of SLT within the previous year. Of those who had used SLT, approximately one-third used the product one or more times per week. Grady and colleagues reviewed 8 surveys of adolescent and adult SLT users in the United States and Canada published between 1981 and 1983 and found that between 8% and 10% of the young men were regular users of SLT.
Oral manifestations of SLT use
The principle changes seen in the oral cavity related to SLT use include oral mucosal lesions (MLs) typically defined as (1) SLT-induced keratoses (STKs); (2) gingival inflammation, periodontal inflammation, and alveolar bone damage; (3) dental caries, tooth abrasion, and staining of tooth structure; and (4) dysplasia and oral cancer.
STK
Most studies related to SLT usage and the production of STKs have limitations. Most fail to control for confounding determinants such as cigarette smoking and alcohol usage. Negative confounding in some studies is also a possibility, especially in those in which smoking rates are lower in SLT users than in nonusers. It would necessarily appear that the relative risk (RR) for oral cancer would turn out to be remarkably low for SLT users in such studies. Nonetheless, most of the studies that have been reported over a period of approximately 47 years, primarily in the United States and Scandinavia, show a consistent clinical pattern as it relates to changes in the oral mucosa when SLT is used. The earliest study, by Pindborg and Renstrup in 1963, described the effect of snuff on oral epithelium. Since that time, approximately 50 studies, including a study in 1986 concerning the noncancerous effects of SLT by the US Surgeon General, have been reported.
Table 1 summarizes 16 of the most significant studies in the United States and Europe, which have detailed the oral manifestations of SLT usage with an end point of STK. The studies have been broken down into the following categories: prospective, experimental, and cross-sectional.
| Primary Author | Study Duration | Sex | Age | Population | Unique Details of Study Design | Ending Determinant |
|---|---|---|---|---|---|---|
| Experimental studies | ||||||
| Grasser & Childers, 1977 | 10 d | M, F | 18–47 y | 214 soldiers | 4 SLT users with oral leukoplakia told to stop SLT use | STK |
| Payne et al, 1998 | 7 d | M | Mean 25 y | 16 snuff users with oral lesions at habitual sites | Site of snuff placement altered | STK |
| Martin et al, 1999 | 6 wk | M | 17–34 y | 3051 air force trainees | 119 SLT users with oral leukoplakia ordered to stop SLT use | STK |
| Cross-sectional studies of populations unselected by SLT use | ||||||
| Greer & Poulson, 1983 | 2 y | M, F | 14–19 y | 1119 high school students | — | STK |
| Poulson et al, 1984 | 18 mo | M, F | 14 to 19 y, mean 16.7 y | 445 high school students | — | STK |
| Offenbacher & Weathers, 1985 | Not stated | M | 10–17 y, mean 13.8 y | 565 grammar and high school students | — | STK |
| Wolfe & Carlos, 1987 | Not stated | M, F | 14–19 y, mean 16 y | 226 Native American children at boarding school | — | STK |
| Cummings et al, 1989 | 1985 | M | 22–44 y, mean 29 y | 25 baseball players and coaches | — | STK |
| Creath et al, 1988 | Not stated | M | 11–18 y | 995 adolescent football players | — | STK |
| Stewart et al, 1989 | Not stated | M | 10–18 | 114 middle and high school students | 5588 men and women interviewed, 182 examined orally, no results for 68 women | STK |
| Ernster et al, 1990 | 1988 | M, F | 20–29 y | 1109 professional baseball players | — | STK |
| Tomar et al, 1997 | 1986–1987 | M, F | 12–17 | 17,027 school students | NIDCR National Survey on Oral Health | STK |
| Sinusas et al, 2006 | 1991–2000 | M | Mean 26 y | 190–259 baseball players and coaches examined each year | Men attending spring training. Multiple occasion attendance | STK |
| Cross-sectional studies of populations selected by SLT use and/or presence of oral lesions | ||||||
| Smith, et al 1970 | Not stated | M, F | Mean 55 y | 15,000 long-term snuff users | — | STK |
| Little et al, 1992 | Not stated | M | 15–77 y | 245 SLT users in a Kaiser Permanente Dental Care Program | 223 age-matched non-SLT users included in study | STK |
| Greer et al, 1986 | Not stated | M, F | 15–75 y | 45 SLT users | Patients segregated into 3 age groups | STK |
The placement of SLT, regardless of the type, in direct contact with the oral mucosa produces a thickened layer of keratin on the oral epithelial surface that occurs directly in the anatomic site where the SLT is placed. STKs occur at the site of SLT placement in 60% of SLT users within 6 months to 3 years of initiation of use. The studies by Greer and Poulson suggest that moist snuff, which is alkaline, tends to produce lesions that are more prominent and more readily identifiable than those that occur in relation to the use of dry snuff or loose-leaf tobacco. However, regardless of the form of the SLT used, lesions nearly always appear directly in the anatomic site where the product is placed.
A central problem in the experimental design of many studies that have accessed the oral mucosa changes associated with SLT use is that the end point, that is STK, often does not exclude the possibility that the same type of keratotic lesion being evaluated may also be present in non-SLT users. Greer and colleagues have only recently helped to clear up this confounding issue by defining the specific histology of SLT lesions compared with benign alveolar ridge hyperkeratoses (ARK) control tissue samples, thereby defining a specific type of hyperkeratotic histologic appearance that is benign and unique to STKs.
Axéll and colleagues were the first to develop standardized clinical guidelines for grading STKs in adult snuff dippers. Their studies were followed by that of Hirsch and colleagues who reviewed the clinical, histomorphologic, and histochemical features of snuff-induced lesions in 50 habitual adult snuff dippers. Hirsch and colleagues graded STKs according to an original 4-point clinical scale devised by Axéll and colleagues. Hirsch and colleagues further reported that all the lesions they accessed were hyperkeratotic to some degree, all lesions had color variations ranging from white to brown to yellow, and the surface texture of all lesions evaluated showed a variation in the mucosal surface pattern that ranged from wrinkled to leathery to deeply furrowed. Twelve significant additional Scandinavia clinical studies of STK have complemented the investigations of Axéll and colleagues and Hirsch and colleagues. Kallischnigg and colleagues summarized the findings of 50 studies documenting the oral changes associated with SLT use in both Europe and the United States in a review article in 2008.
In studies conducted in the United States during 1980 to 1982, Greer and Poulson developed a standardized method for grading STKs that represented a modification of the Axéll classification, ultimately dividing STKs into 3 categories: degree I, degree II, and degree III lesions. Degree I lesions were defined by these investigators as those STKs that were superficially keratotic with slight opaqueness and color similar to that of the surrounding mucosa and with only slight wrinkling and no obvious mucosal thickening. Degree II lesions were classified as those lesions that were also superficial keratoses, typically white with occasional reddish areas and with moderate wrinkling and no obvious or dramatic thickening. Grade III lesions were white lesions that showed intervening furrows of normal mucosal color, obvious mucosal thickening, and dramatic wrinkling. Examples of the 3 grades of STK are shown in Figs. 1–3 . In addition to evaluating the clinical appearance of STKs associated with SLT use, Greer and Pulson classified all lesions according to their texture, contour, and color. The vast majority of the 117 lesions that were ultimately evaluated and classified from a total of 1119 teenagers screened were white, corrugated, and raised.
The prevalence of STK has been found to increase with the increased frequency of SLT use or with the amount of SLT used. One study of note reported a resolution of STKs. This study involved US Air Force trainees with STKs who were evaluated after 6 weeks of mandated discontinuance of SLT.
Although the initial investigations of Greer and Poulson assessed oral tissue alterations associated with SLT use in teenagers, Greene and colleagues completed a 3-year study of STKs in major and minor league baseball players and found that in a somewhat older population, in which the subjects were between the ages of 20 and 29 years, 4 different types of leukoplakic lesions could be identified: (1) STKs that had no or only very slight color change, with some obvious change in mucosal texture; (2) STKs that had a color and texture change with no mucosal thickening; (3) STKs that had a color and texture change, with mild or moderate mucosal thickening; and (4) STKs that had no semblance of normal mucosal color, severe texture change, and heavy mucosal thickening. However, this classification that offered slight modifications to those of Axéll and colleagues and Greer and Poulson is rarely used. Greene and colleagues also found no focally erythroplakic component to the lesions in their study, as did Greer and Poulson.
In a study of SLT use in India, Murti and colleagues identified STKs in patients who chewed tobacco. However, the tobacco that was used was typically used in association with betel quid, a mixture of betel leaves, areca nut, slaked lime, and catechu. These investigators did not classify the lesions identified into any clinical grade.
Greer and colleagues completed a follow-up study to their original study in 1983 of STK in teenagers with an assessment that involved an evaluation of STK in juvenile, adult, and geriatric patients. These investigators found that the 3 clinical classifications of SLT lesions that they had originally developed for teenagers, including alterations in the color, texture, and contour of the mucosal lining of the mouth, were equally applicable to adults and geriatric patients. The lesions the investigators identified in the adult population were site specific, just as in teenagers. However, there were associated confounding variables in both studies. Some subjects in each of the studies also used alcohol, and as high as 18% had smoked cigarettes in addition to using SLT. Although these factors likely played no role in the initiation of site-specific STK, their possible causative role cannot be ignored.
In addition to the 16 studies of STK in the United States outlined in Table 1 , Kallischnigg has reported on 21 similar European studies. The European studies report findings similar to those from the United States, although the Kallischnigg review defined SLT-associated lesions documented by investigators in both the United States and Europe as simply MLs and suggested that the lesions were not necessarily SLT specific.
Histopathology of STK
STK occurs directly in the area of tobacco quid placement, and most lesions occur in the mandibular mucobuccal folds where the tobacco quid is held between the alveolus and the buccal or labial mucosal surface. Other anatomic sites, most often the maxillary alveolar mucosa and buccal mucosa, can be affected. Although as many as 33 scientific articles published between 1963 and 2007 have described the clinical appearance of STK, only a few studies describe the histopathology of such lesions. The largest studies describing such histopathologic changes have included evaluations of 45, 27, 77, 81, 92, and 142 tissue samples. These studies include a study by Greer and colleagues in which 45 tissue samples were examined, the study by Greer and Eversole in which 27 tissue samples were examined, the investigation by Greer and colleagues in which 77 tissue samples were examined, the 81 STK samples studied by Greer and colleagues, the studies of Grady and colleagues in which 92 biopsy samples were examined, and the investigations of Daniels and colleagues in which 142 samples were examined.
A remarkably consistent pattern has been documented by these investigators in cataloging the microscopic features associated with STK. The lesions evaluated in the aforementioned 6 studies were principally classified as degree I, degree II, or degree III lesions, using the clinical grading criteria established by Greer and Poulson. Each category of lesion showed a distinct pattern of mild, moderate, or severe hyperkeratosis or parakeratosis along the epithelial surface. These histologic patterns can be seen in Figs. 4–6 . The pattern of keratinization often demonstrates streaks of parakeratosis that extends above the epithelial surface, giving the lesion a focal wavy, “chevron,” or church spire appearance (see Fig. 5 ). The chevron streaks often show parakeratinized streams of cells arranged in a latticelike pattern, resembling a pine tree. Between chevrons, the epithelial cells typically demonstrate vacuolated cytoplasm, and keratohyalin granules tend to be prominent. Chevron keratinization can be judged as either mild, moderate, or severe, and although the chevron pattern is not unique to STK because it has also occasionally been documented in lesions from pipe smokers and cigarette smokers, Greer and colleagues found this specific form of church spire–like keratinization to be present in 93% of the samples they examined in 4 different studies. Matched control samples from cigar and cigarette smokers demonstrated chevron keratinization in only 30% of cases, and chevron keratinization was absent in 30 cases of matched control alveolar keratoses in the study by Greer and colleagues.
The epithelium in most STKs does not demonstrate cytologic atypia, although basal layer hyperplasia, a form of altered cellular maturation, can be quite prominent.
Another histologic feature commonly associated with STK is the presence of dark cell keratinocytes. This special form of keratinocyte is characterized by its strong affinity for basic dyes and by the electron density of the cell’s cytoplasm and nucleus. Dark cell keratinocytes are not unique to SLT lesions and have been reported in other keratoses as well as normal epithelium. The presence or absence of dark cell keratinocytes cannot be correlated with a specific grade of STK, and these keratinocytes do not appear to represent any form of premalignant alteration. On electron microscopic evaluation, dark cell keratinocytes appear almost exclusively in a basal or parabasal position in the epithelium. When compared with cheek biting controls or hyperkeratoses caused by denture trauma, the dark cell keratinocytes in STK can be identified 15 times more frequently.
Subepithelial Collagen Eosinophilia
Pindborg and Renstrup in Sweden and Archard and Tarpley in the United States reported finding a band of homogeneous eosinophilic material in the connective tissue of mucosal sites chronically exposed to SLT. Initially, these changes were thought to be related to the use of a particular brand snuff, and neither investigative team was able to characterize this material as amyloid. Greer and colleagues were able to find the eosinophilic band in only 2 of the 45 cases they studied, and the impression of these investigators was that the band represented a form of collagen sclerosis and that it was of extracellular origin. Further investigations of this special form of collagen eosinophilia have not been undertaken.
In addition to the band of homogenous eosinophilic material described by Pindborg and Renstrup, the connective tissue in STKs can demonstrate salivary gland fibrosis and chronic sialadenitis (see Fig. 6 ). Dilated excretory ducts have been identified in STK and seem to be most common in grade III lesions. Tables 2–4 delineate the histopathologic features of STK originally identified by Greer and colleagues in their studies of juvenile, young adult, and adult SLT users.
| Case | Age (y) | Salivary Gland Fibrosis | Dark Cell Keratinocytes | Eosinophilic Band | Chevron Keratinization | Basal Layer Hyperplasia | Koilocytosis |
|---|---|---|---|---|---|---|---|
| 1 | 16 | NE | + | — | + | — | — |
| 2 | 16 | NE | — | — | — | — | — |
| 3 | 20 | — | + | — | + | + | + |
| 4 | 15 | NE | + | + | +++ | ++ | + |
| 5 | 17 | NE | NE | — | ++ | ++ | + |
| 6 | 17 | NE | — | — | + | — | + |
| 7 | 13 | NE | — | — | + | — | + |
| 8 | 20 | NE | — | — | +++ | + | + |
| 9 | 21 | +++ | + | — | +++ | — | + |
| 10 | 22 | — | NE | — | ++ | + | — |
| 11 | 21 | — | — | — | ++ | + | — |
| 12 | 17 | NE | — | — | ++ | + | + |
| 13 | 22 | — | — | — | ++ | + | — |
| 14 | 18 | NE | + | — | + | ++ | + |
| 15 | 25 | ++ | + | — | ++ | + | + |
| Case | Age (y) | Salivary Gland Fibrosis | Dark Cell Keratinocytes | Eosinophilic Banc | Chevron Keratinization | Basal Layer Hyperplasia | Koilocytosis |
|---|---|---|---|---|---|---|---|
| 16 | 46 | NE | + | — | +++ | +++ | + |
| 17 | 42 | NE | — | — | +++ | — | + |
| 18 | 29 | NE | + | — | ++ | — | + |
| 19 | 50 | + | — | — | +++ | ++ | + |
| 20 | 47 | NE | — | — | +++ | ++ | + |
| 21 | 27 | NE | + | — | ++ | — | — |
| 22 | 28 | — | — | — | + | — | — |
| 23 | 51 | NE | — | — | ++ | + | — |
| 24 | 29 | NE | + | — | ++ | + | — |
| 25 | 30 | NE | — | — | +++ | + | — |
| 26 | 54 | NE | + | — | +++ | ++ | — |
| 27 | 41 | — | — | — | ++ | + | + |
| 28 | 38 | NE | + | — | ++ | — | + |
| 29 | 25 | — | — | — | ++ | ++ | + |
| 30 | 54 | — | — | — | ++ | — | + |
| Case | Age (y) | Salivary Gland Fibrosis | Dark Cell Keratinocytes | Eosinophilic Band | Chevron Keratinization | Basal Layer Hyperplasia | Koilocytosis |
|---|---|---|---|---|---|---|---|
| 31 | 62G | NE | — | — | +++ | +++ | + |
| 32 | 66G | NE | — | — | + | + | + |
| 33 | 66G | NE | — | + | — | + | — |
| 34 | 63G | — | — | — | +++ | — | + |
| 35 | 67G | NE | — | — | +++ | — | + |
| 36 | 69G | NE | + | — | +++ | — | — |
| 37 | 66G | ++ | — | — | — | + | — |
| 38 | 63G | NE | + | — | +++ | ++ | — |
| 39 | 73G | — | + | — | ++ | ++ | + |
| 40 | 74G | — | + | — | ++ | + | — |
| 41 | 64G | — | + | — | ++ | + | + |
| 42 | 72G | — | + | — | ++ | + | — |
| 43 | 66G | — | — | — | + | — | — |
| 44 | 55G | — | — | — | + | — | — |
| 45 | 56G | — | — | — | ++ | — | + |
Koilocytosis
An additional histologic feature common to the epithelium of biopsy samples from SLT users is koilocytotic change within epithelial cells ( Fig. 7 ). Koilocytes represent the inclusion of intranuclear viruslike particles from human papillomavirus (HPV) in the epithelium. Koilocytes have been identified in uterine cervical carcinoma as well as in oral squamous cell carcinoma (SCC). Greer and colleagues found koilocytes to be present in 26 of 45 STK biopsy specimens they examined in a study of STK in 1986. When these tissue samples were immunohistochemically stained for the presence of HPV capsid antigen, 6 of the 26 cases were positive for the antigen. These studies, along with others by the same research group, were the first to suggest a possible link between HPV infection, STK, and oral SCC.
Gingival and Periodontal Inflammation and Alveolar Bone Damage
A second significant clinical effect that has been reported in association with SLT use is gingival and periodontal inflammation and alveolar bone damage. However, there is a considerable divergence in findings reported in the United States and the Scandinavian literature concerning the subject. From 21 Swedish studies that Kallischnigg and colleagues evaluated, only 1 study showed a relationship between gingivitis and snuff use and no studies demonstrated a statistically significant relationship between the presence of calculus, plaque, pocket depth attachment loss, or alveolar bone loss and snuff use.
Studies in the United States, however, report high rates of gingival recession and loss of periodontal ligament attachment in SLT users. In all, a total of 8 studies from the United States strongly support that SLT use results in attachment loss, particularly gingival recession, ( Fig. 8 ) and ultimately periodontal disease and bone loss. It seems that the association between SLT and periodontal or gingival recession is related to the quantity of SLT used In the United States, initial gingivitis in the area of SLT placement seems to promote the ensuing and damaging SLT effect. Bastiaan found routine gingivitis in the area of SLT contact in 31% to 92% of young adult SLT users. Greer and Poulson, in their study of oral tissue alterations associated with SLT use by teenagers, also documented tobacco-associated periodontal deterioration or advanced periodontal disease.
Periodontal pathology is most likely related to long-term use of SLT and is more typical in adult population than in teenagers, as several investigations have reported.
Although gingival and periodontal inflammation and bone damage can clearly be seen in association with SLT use, there have been no relevant studies completed that totally eliminate confounding variables, such as the use of other forms of tobacco; periodontal damaging systemic diseases, such as diabetes; or simply preexisting periodontal disease that may already exist in concert with SLT use. Therefore, although SLT can clearly cause damage to the periodontium, most commonly seen in the form of gingival migration and attachment loss, graded forms of that damage similar to the clinical grading schemes that have been devised for STK have not been established.
Dental Caries, Tooth Abrasion, and Staining of Teeth
Dental caries in association with SLT use has been investigated extensively in 7 studies in the United States and 3 important studies from Sweden. These 7 studies in the United States showed minimal relationship between dental caries and SLT use. However, the use of loose-leaf chewing tobacco was specifically found to be associated with decayed teeth, decay in filled permanent teeth, and caries of root surfaces in several studies. The amount of dental caries increased with the number of packs of chewing tobacco used on a weekly basis and also with the number of years of use in a comprehensive study done by Tomar and Winn. Two Swedish investigations showed no relationship between SLT use and dental caries, whereas a third study reported a slight increase in caries among snuff users. The overall evidence from both the studies in Sweden and the United States suggests that there is a relationship between the use of SLT and dental caries and that the risk increases significantly with the use of loose-leaf chewing tobacco.
It has been speculated that the relative lack of dental caries in heavy users of SLT may be because of the accelerated salivary flow that the tobacco stimulates, thus washing the bacteria necessary to induce caries away from tooth structure and in effect causing a physical cleanings action and a mild buffering action that inhibits the accumulation of plaque and carcinogenic material on the teeth. It has also been reported by Christen that certain SLT products contain fluoride, which may be instrumental in the suppression of dental caries in SLT users as well.
Both tooth abrasion and severe staining of teeth (see Fig. 8 ) can be seen in association with SLT use. However, Greer and Poulson reported only a single case of abrasion in their study of 117 teenage SLT users, which at the time of the study was thought to be chemical erosion of tooth structure. Whether or not abrasion is related to the presence of some agent other than tobacco in SLT or, in fact, is related merely to a constant placement of the SLT in the same anatomic site has not been established.
Rare instances of SLT-associated melanosis and prosthetic appliance stains associated with SLT use as well as delayed alveolar wound healing in association with SLT use after tooth extractions have been reported. These changes appear to be as dependent on the amount of available plaque and calculus in the patient’s mouth as they are to the amount of SLT used.
Oral Cancer and Dysplasia
The most significant issue to be debated in relation to the oral manifestations of SLT use is whether or not SLT plays a role in causing oral epithelial dysplasia, as seen in the clinical and biopsy histopathologic photographs of an SLT user in Figs. 9 and 10 , or oral SCC, as seen in the clinical and biopsy histopathologic photographs of an SLT user in Figs. 11 and 12 . In a study in 1986 of 45 STK biopsy specimens from juveniles, adults, and geriatric patients, with 15 patients assigned to each category, Greer and colleagues found 1 instance of mild dysplasia in a 44-year-old man. The subject was also a smoker but did not use alcohol. Thus, it was not possible to determine if SLT alone accounted for the dysplastic epithelial change, even though the lesion biopsied was site specific for SLT placement. No assays for HPV, another important potential participant in the oral SCC cascade, were completed on the dysplastic tissue sample.
