Oral Effects of Tobacco Abuse
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A papillary squamous cell carcinoma (oral cancer) of the lower gums in a tobacco smoker.
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Note: This information was first published in the Journal of the American Dental Institute for Continuing Education, 1992; 43:3-17. Authors: Drs. Jerry Bouquot & Kathy Schroeder, Department of Oral Pathology, West Virginia University, Morgantown, West Virginia. It is updated periodically.
Tobacco has been variously hailed as a gift from the gods, a miraculous cure-all for life's physical ills, a solace to the lonely soldier or sailor, a filthy habit, a corrupting addiction, and the greatest disease-producing product known to man. This diversity of opinion has continued unchanged for centuries and has appeared until very recently to be little affected by research results from more than 900,000 papers thus far published on the topic. It is common knowledge that cigarette smoking is the single major cause of cancer and cardiovascular disease in the United States, contributing to hundreds of thousands of premature deaths each year, yet one-fourth to one-third of American adults continue to smoke.
The dental profession has been repeatedly warned against the use of tobacco, perhaps accounting for the very low proportion of dentists (6-8%) currently considered to be regular users. More than 130 years ago Brodie was telling dental surgeons that "the use of tobacco in any ordinary way, by the dentist, is a practice which we consider reprehensible in point of propriety and etiquette. It is in all cases offensive and disgusting." He emphasized that patients should not be forced to tolerate a dentist's "smoker's breath" or spitting. "How a dentist of any refinement can persist in such an infliction upon his patients is more than we can comprehend." Today, of course, we are more concerned about the health effects and addiction potential of tobacco use by out patients, but our concern is no less ardent.
It is especially important to understand that harmful effects of tobacco products are dose-dependent, that they depend more on abuse than on simple use. In this light its addicting aspects acquire ominous overtones. The nicotine found in substantial amounts in tobacco products is widely considered to be a powerfully addicting drug, so much so that its addictive processes and potential have been equated with heroine, morphine and cocaine. It's rapid absorption through the lungs of cigarette smokers is widely accepted, but its equally ready absorption through the oral mucosa under the alkaline conditions normally found in cigar, pipe and smokeless tobacco use is less publicized. Once in the blood stream, of course, nicotine acts on the central nervous and cardiovascular systems in identical fashion regardless of the method of absorption.
These systemic effects have been extensively explored and reported, but
the local oral effects of various tobacco habits have received little attention
outside of the potential for cancer. The purpose of the present article is
to summarize current concepts of such local effects, especially the nonmalignant
changes in the mouth.
The smoking and chewing of tobacco leaves was a part of the Native American culture long before Europeans discovered and conquered the Americas, and to this day North American Indian males have one of the highest smoked and smokeless tobacco usage rates in the Western world. But the white populations of Europe and the U.S. so readily adopted these habits that within a few decades after Columbus' historic voyages its cultivation, production and sale had become a major industry on both sides of the Atlantic, and tobacco had become a standard form of payment (i.e. "money") in the U.S. Snuff production was one of the major industries of the Mid-Atlantic states throughout the seventeenth and eighteenth centuries, and tobacco chewing was so common that by the early nineteenth century tobacco spitting was perceived by foreigners as our "national characteristic".
This all changed, however, with the advent of the germ theory of disease and the discovery of the dreaded tuberculosis bacillus in expectorated tobacco juices. By the end of the nineteenth century it was no longer socially acceptable to chew and spit tobacco products, and by 1920 cigarette sales surpassed smokeless tobacco sales for the first time. Ironically, cigarettes were seen as a safe alternative to chewing tobacco.
By the Second World War cigarettes were used by at least 75% of U.S. men, and women were beginning to smoke as well. This trend would probably have continued were it not for the strong antismoking campaign generated by the 1964 U.S. Surgeon General's report linking smoking to several lung and cardiovascular diseases. Today only 25-33% of adult males and females smoke cigarettes, and these numbers are expected to diminish to 15-20% over the next three decades. Unfortunately, remaining smokers appear to be the heavier smokers and so the effects on the mouth may be even greater than the typical effects noted in the past.
Before examining the negative health effects of tobacco use, we would remind
the reader that a popular emphasis on negative aspects is a rather new
phenomenon. Since the Middle Ages tobacco leaves have been used as medicinal
herbs in ointments, poultices, mouth rinses and smoke. Oral ulcers, caries
and "toothache" were all treated with this wonder drug. A product is
still readily available today, called "Dental Snuff" (Figure
1) which was advertised
more than a century ago as a cure for toothache, gingivitis, facial neuralgia,
caries, and scurvy. Given this positive image throughout most of its
history it's universal popularity is not surprising. It is surprising, rather,
that some persons have always been moved to speak out against it,
even to the extent of proclaiming its use a capital offense in some European
and Asian countries as early as the sixteenth century.
A wide variety of mucosal changes have been noted in habitual users of smoked and smokeless tobacco. These changes most likely result from the many irritants, toxins, and carcinogens found naturally in cured or burned tobacco leaves, but may also arise from the mucosal drying effects, the high intraoral temperatures, intraoral pH changes, local alteration of membrane barriers and immune responses, or altered resistance to fungal and viral infections. The following are significant mucosal changes noted in tobacco users:
ORAL CANCER. Squamous cell carcinoma is quit naturally the most worrisome mucosal change encountered in smokers, but it is not intended here to dwell on this aspect of tobacco's effect. Certain premalignant lesions are mentioned below, but suffice it to say that tobacco's role in producing squamous carcinomas of the oral, pharyngeal and laryngeal mucosae is well established. At least 80% of oral cancer patients are smokers; oral cancer patients who continue smoking after treatment are much more likely to develop a new head and neck cancer; animal studies have produced oral cancers in a variety of animals via forced cigarette smoking; and case-control studies in humans have determined that a smoker is as much as 7 times more likely than a nonsmoker to develop oral malignancy.
It is important to remember that oral cancers develop by way of cocarcinogenesis, multiple factors are usually involved. Excessive alcohol intake by itself has little impact on the prevalence of oral carcinoma, but alcohol is a powerful "promoter" capable of altering mucosal cells to make them much more susceptible to malignant transformation by tobacco carcinogens. Even the alcohol in concentrated mouthwashes is thought to play a role in this process.
Tobacco chewers also develop oral carcinomas. The oral cancer risk for these users is about 4 times greater than nonusers, although the data proving this is very sparse. A very unique low-grade oral malignancy, verrucous carcinoma, is so seldom diagnosed in nonchewers that it is aptly called the "snuff dipper's cancer" (Figure 2). This carcinoma typically develops in the exact site of chronic tobacco placement. It differs from the usual oral cancer in that it enlarges very slowly, is essentially nonmetastasizing, and consists of very mature epithelial cells, i.e. has little dysplasia. The mortality rate for verrucous carcinoma is among the lowest for any cancer of the human body, so low that it would be a blessing were it the usual type of oral cancer diagnosed in smokeless tobacco users. Unfortunately, this is not the case. Verrucous carcinoma is extremely rare (1/1,000,000 persons annually), hence, the typical smokeless tobacco cancer is the same as the typical smoker's oral cancer, i.e. invasive squamous cell carcinoma.
LEUKOPLAKIA. While the exact etiology of oral leukoplakia still eludes us, tobacco smoking is by far the most broadly accepted factor. Approximately 80% of leukoplakia patients are smokers and when large groups of adults are examined we find that smokers are much more likely to have leukoplakia than nonsmokers (23% vs. 4%). Pipe smokers and heavy cigarette smokers have greater numbers of lesions and larger lesions than other smokers, especially after many years of tobacco abuse. Sixty percent of smoke-induced leukoplakias, furthermore, disappear 6-12 months after affected patients stop smoking.
Leukoplakia in smokers is usually seen as a well-defined white plaque of the oral mucosa (Figure 3). The average patient is 50-60 years of age and male, while the average lesion is 1.4 cm. in diameter and has been present for 2-4 years at the time of diagnosis. The overall cancer transformation potential of leukoplakias is approximately 4%, but certain clinical forms of leukoplakia are much more prone to cancer than others. Speckled leukoplakia (erythroleukoplakia), for example has a cancer potential of at least 25%, in some studies as high as 41%. Do leukoplakias in smokers become malignant more frequently than those in nonsmokers? We presently lack the data to say with confidence, but it appears that leukoplakias in nonsmokers, or those remaining after smoking cessation, are more likely to transform than those in smokers. Hence, smokers have much more leukoplakia but their lesions seem to be less aggressive.
NICOTINE PALATINUS (STOMATITIS). Once a common mucosal change of the hard palate, nicotine palatinus (Figure 4) has become something of a rarity as cigar and pipe smoking have lost popularity. Even before it became an uncommon lesion, however, it's status as a precancerous condition had been lost. While this lesion is most certainly produced by heavy and frequent contact with tobacco smoke and is just as certainly a white keratotic change, it does not transform into malignancy and is a response to the heat of tobacco smoke rather than the chemicals in the smoke. It is completely reversible within a few months of quitting the smoking habit, even when present for many decades before the habit is stopped. Today we primarily see this entity in heavy cigarette smokers (more than two packs per day) and its intensity is typically much less than lesions of a few decades ago.
SMOKELESS TOBACCO KERATOSIS. Snuff pouch or smokeless tobacco keratosis (Figure 5) is, like nicotine palatinus, no longer considered to be a true leukoplakia. It is a white keratotic plaque, as is leukoplakia, but there the similarity ends. It typically has a semitranslucent appearance rather than a flat whiteness, and it has a microscopic appearance different from the simple excessive keratin by which leukoplakia is characterized. It also is located only in areas of direct contact with snuff or chewing tobacco and is almost always completely reversible when the affected patient quits his or her habit. While there can be no doubt that it is a precancerous entity, its malignant potential is less than true leukoplakia by a magnitude of ten (4% vs. O.4% estimated lifetime risk for leukoplakia and smokeless tobacco keratosis, respectively). More wrinkled and more intensely white smokeless tobacco keratoses are considered to be "higher grade" lesions, but these clinical grades seem to have little correlation with the eventual development of cancer. Today the only smokeless tobacco keratosis feature known to have an increased risk of cancer transformation is continued presence after tobacco cessation. Those lesions remaining after two months without smokeless tobacco should be considered to be true leukoplakias, possibly developed from or hidden by the previous smokeless tobacco keratosis.
SMOKER'S MELANOSIS. Smoking is capable of stimulating oral mucosal melanocytes to produce excessive melanin, thereby creating patches of brown pigmentation on gingival or buccal mucosae in 5-22% of heavy smokers (Figure 6). The number and intensity of these smoker's melanoses are dose-dependent and smoking cessation seems to reverse the process completely. In vitro testing has demonstrated that it is the nicotine itself which activates one of the steps in melanin production. To date no case has transformed into a carcinoma or melanoma and no case has been reported in nonsmoking users of smokeless tobacco, but an occasional lesion may have leukoplakia superimposed on it. In the latter event, we use the term "melanoleukoplakia" (or "leukomelanosis") and presume that at least the keratotic aspect of the plaque will behave as any other leukoplakia without melanosis.
SUBMUCOUS FIBROSIS. Oral submucous fibrosis is a precancerous condition characterized by a progressive stiffening of the oral mucosa to the point wherein affected persons have difficulty opening their mouths. A 10-year malignant transformation rate of 8% has been determined in India, where tobacco chewers routinely mix betel leaf, areca nuts, and/or slaked (shell) lime with their tobacco. This entity, which frequently has leukoplakia superimposed on it, is seldom seen in the U.S. but is found in the mouths of 0.4% of India's villagers.
LEUKOEDEMA. A poorly demarcated, grayish-white, opalescent change of the buccal mucosa, bilaterally, is frequently seen in persons with darkly pigmented skin (Figure 7). Always a benign lesion and usually considered a simple variation of normal, it is nevertheless capable of an increased whiteness and size in smokers. Axell and Henricsson found leukoedema in 60% of Swedish adult smokers but in only 36% of nonsmokers.
HAIRY TONGUE. The condition of elongated filiform papillae
mimicking hair on the dorsum of the tongue is frequently seen in heavy smokers
(Figure 8). Theoretically tobacco smoke prevents the epithelial cells from
sloughing in a normal fashion and they accumulate into a very thickened and
white (unless stained brown, black, etc.) surface which extends as long "hairs"
at the tips of the papillae. We have no clinical research definitively linking
hairy tongue with smoking but it frequently decreases or disappears when
the habit is stopped. Smokeless tobacco use is also thought to contribute
to this condition, but there is no scientific evidence to prove the association.
GINGIVITIS. Frequent studies have concluded that tobacco smokers are more likely to demonstrate gingival redness, hemorrhage and inflammatory enlargement (edema) than nonsmokers with similar oral hygiene habits. Others, however, have found no increased gingival bleeding in smokers, possibly because of the vasoconstriction produced by nicotine. Smokeless tobacco users likewise have no more gingivitis than nonusers, but this habit is well known to produce a characteristic painless loss of gingival tissues in the area of tobacco contact. This gingival "recession" frequently includes bony destruction but is seldom associated with the inflammatory changes noted clinically in routine gingivitis (Figure 9). It may result from a combination of factors, including abrasion and the local tobacco-induced release of collagenase and other protein-destroying enzymes.
Logic would seem to indicate that tobacco use must have some effect on the gingival and periodontal structures. Tobacco contains, after all, several cytotoxic substances which have been shown to be secreted in salivary and gingival crevicular fluids. Smokers also have markedly more calculus than nonsmokers, and heavy smokers have more calculus than light smokers. Nicotine's well-known vasoconstriction effects have been shown to be strong in periodontal tissues, even in the face of elevated blood pressures, and gingival circulation has been shown to decrease by as much as 70% during the smoking of a cigarette. Tobacco smoking, furthermore, also suppresses human immune responses, including responses to oral microbial toxins. Oral leukocytes, especially neutrophils, have a diminished ability to move, to phagocytize, or to secrete enzymes in smokers.
PERIODONTITIS. While research has been equivocal relative to the production of gingivitis, overwhelming evidence from a large number of investigations has made it obvious that smokers have considerably more severe periodontitis than nonsmokers. After controlling for different oral hygiene habits, patient age, gender, and socioeconomic levels, smokers still have deeper pockets, more alveolar bone loss, more tooth mobility, and greater tooth loss than nonsmokers. Solomon et al have gone so far as to state that the periodontal status of smokers is at least 15 years more advanced than the status of nonsmokers of the same chronological age. Even in persons under 40 years of age, smokers are known to have twice the periodontitis and tooth loss that nonsmokers have.
As previously mentioned, smokeless tobacco users are also prone to a localized periodontal destruction or recession resulting from the combination of nicotine's chemical effects and the effects of physical abrasion on local gingival tissues. This association between smokeless tobacco use and gingival/periodontal recession in the site of chronic tobacco placement is a rather strong one, and recession correlates well with both the quantity of daily use and the duration of the smokeless tobacco habit. It should be emphasized, however, that routine gingivitis in the area of tobacco contact appears necessary to either initiate or promote this change, a change identified in 31-92% of young adult smokeless tobacco users.
ACUTE NECROTIZING ULCERATIVE GINGIVITIS (ANUG). ANUG is strongly correlated with tobacco use. Ninety-eight percent of ANUG patients are smokers, and persons who smoke more than 10 cigarettes per day have a tenfold increase in ANUG prevalence compared to nonsmokers. The exact cause of ANUG is, of course, unknown, but it occurs most frequently in teenagers and young adults and may result from defective neutrophil function allowing bacterial and possibly viral (cytomegalovirus) invasion of gingival tissues. The vasoconstrictive action of nicotine and other tobacco components is thought to contribute strongly to the painful tissue necrosis and ulceration seen in this disease, but emotional stress and poor oral hygiene appear to play roles almost as important.
Smoking seems to contribute as much to unsuccessful periodontal therapy as to the promotion of periodontitis. In fact, Miller has very recently concluded that no postoperative factor contributes more to the failure of periodontal soft tissue grafting than does this habit, a feature which also holds true for skin grafts outside the mouth. Apparently active smoking is required. Patients who stop smoking before periodontal surgery and refrain from smoking for several weeks thereafter have a graft success rate similar to that of nonsmokers.
DELAYED ALVEOLAR WOUND HEALING. Delayed wound healing in
smokers is noted in other situations as well. Routine periodontal surgery
and tooth extraction are also adversely affected, possibly because of the
direct contact of smoke constituents on open wounds, or reduced blood flow,
or impaired leukocyte function, or diminished fibrinolytic activity, or the
drying effect of mouth-breathing, or the clot-disrupting effect of the negative
intraoral pressure produced during tobacco smoking. Regardless of the
cause, smokers have significantly less blood filling of extraction sockets
and develop five times more dry sockets than do nonsmokers.
CARIES (Tooth decay). Nineteenth century dental surgeons presumed that tobacco smoking protected against caries and as late as 1968 Schmidt felt able to state that caries reduction was the only advantage of smoking. Most recent investigators, however, have concluded that cigarette smoking is most certainly associated with an increased caries rate but that a cause-and-effect relationship is still not proven. Smokers have a significantly greater number of carious or repaired tooth surfaces than nonsmokers, and heavy smokers are more affected than light smokers. Smokers also have higher plaque rates than nonsmokers. It has been suggested that smokers as a group have poorer oral hygiene habits and skills, make fewer visits to dentists, and have lesser overall health standards than nonsmokers. As this has not been adequately controlled for in past investigations it may be the real reason for the increased caries rate.
More than one-fifth of the content of some brands of smokeless tobacco is sugar and a few brands are even capable of serving as growth media for several bacteria implicated in the production of caries. Smokeless tobacco users, moreover, have significantly greater numbers of caries-associated bacteria at the site of quid placement when compared to nonusers. The caries that results from smokeless tobacco use is frequently cervical or root caries, but regardless of the caries type carious destruction is seen far more frequently in smokeless tobacco users who also have gingivitis. While the evidence would appear to conclusively associate smokeless tobacco use with dental caries, a cause-and-effect relationship is not conclusively established and several well-designed contemporary investigations have found little or no correlation.
ABRASION. Tooth abrasion resulting in a notching of incisal edges and cusp tips is a well-established consequence of holding a pipe in the same location while smoking. But long-term smokeless tobacco users also demonstrate excessive and frequently generalized wear of occlusal and incisal surfaces, especially in persons employed in dusty environments, such as coal mines and textile mills (Figure 10). This abrasion, produced by sand and other gritty materials remaining in processed tobacco, usually takes many years to develop, but the present authors have seen severe abrasion after only four years of smokeless tobacco use.
EROSION. The chemical dissolution of enamel has occasionally
been reported in tobacco smokers and chewers, but only as a secondary consequence
of using breath mints or as idiopathic cases. Erosion does not seem to be
a serious problem and, in fact, chewers may be somewhat protected by the
natural alkalinity of smokeless tobacco.
DIMINISHED BLOOD FLOW. Several physiological oral alterations produced by tobacco use have already been mentioned. The average smoker experiences a 60-70% reduction in oral mucosal blood flow while smoking, and laser Doppler evaluation of gingival blood flow has determined that smokeless tobacco users have, on the average, a 45% decrease compared to nonusers. Decreased flow lasts for 2-3 hours after smoking a single cigarette and is the most likely explanation for the known lack of gingival hemorrhage in smokers with otherwise obvious signs of poor oral hygiene and/or advanced periodontitis.
POOR PERIODONTAL ATTACHMENT. The cytotoxic substances absorbed from tobacco, especially nicotine and cotinine (its major metabolite), are found in secreted saliva and crevicular fluids. Lab studies suggest that the attachment of fibroblasts to cementum is altered by nicotine and new investigations are underway to further evaluate the local effects of tobacco cytotoxins.
INCREASED SALIVARY FLOW. While cigarette smoking typically causes a noticeable short-term increase in salivary flow rates, the long-term influence of tobacco use is unclear. Certainly, intense smokeless tobacco use has been shown to result in degenerative changes of more than 40% of minor salivary glands located in the site of chronic tobacco placement, and immunoglobulin A (IgA) levels are depressed in smokers, but the clinical impact of these changes appears minimal.
BACTERIA. Smoking reduces the overall concentration of bacteria in the mouth, but the mix of oral microflora does not appreciably alter, nor is the rate of plaque formation enhanced, at least not when differing oral hygiene levels are controlled for. Smokeless tobacco usage does, however, appear to enhance the presence of several periodontal pathogens, namely Veillonella, Bacteroides, and Fusobacterium.
CANDIDIASIS AND MEDIAN RHOMBOID GLOSSITIS. The great majority (83%) of oral candidiasis patients are moderate to heavy cigarette smokers. Candida, a normal component of approximately 50% of the mouths of healthy, normal individuals (without dentures), can be variably affected by smoking, becoming either more or less intense in different individuals. Heavy smokers who also abuse alcohol are more likely to lack oral Candida than any other group. Median rhomboid glossitis, a candida-induced tongue change, is most frequently (85%) seen in smokers and is markedly improved upon smoking cessation.
SINUSITIS. Tobacco smokers are much more prone to maxillary sinusitis than nonusers and this condition typically resolves or is significantly reduced when the smoking habit is discontinued. This effect is probably secondary to a tobacco-induced edema of the sinus membranes and by diminished ciliary activity of respiratory epithelial cells. The edema tends to narrow sinus openings or orifices while the weakened ciliary movement prevents mucous and bacterial transport out of the sinuses.
ALTERED TASTE. We all have predetermined thresholds for the sensations of taste and smell. Tobacco smoking is well known to greatly increase these thresholds, thereby diminishing our ability to detect various tastes and smells. Relative to taste, a dose-related association is known for bitter sensations, and to a lesser extent for salty tastes, but there appears to be little change in the ability to detect sweet or sour substances. The diminished taste acuity becomes progressively worse with each additional year of tobacco use. Smokeless tobacco use seems to have no or little effect on taste acuity. Interestingly, persons who are able to quit smoking express a very strong preference for sweet foods, a feature which probably helps to explain the weight gain so commonly noted after smoking cessation.
APHTHOUS ULCERS AND FEVER BLISTERS. Recurring aphthous ulcers, or canker sores, are exquisitely painful and very common, affecting 10-20% of the general population and as much as 50% of health professionals. Rather than producing or inducing this ulcerative disorder, tobacco smoking seems to prevent its occurrence or diminish its effects. Aphthae frequently begin to appear or reappear in persons who stop smoking, and almost all (96%) affected individuals are nonsmokers. Canker sores are likewise less prevalent in smokeless tobacco users than in nonusers. The reasons for this "protection" are unclear, but may be related to an increased mucosal keratinization or a reduced immune attack against the bacterial antigens thought to trigger ulcer formation.
Swango and Kleinman are the only investigators to study the relationship
between tobacco users and secondary herpes simplex or fever blisters. They
found a slightly higher prevalence in smokeless tobacco users when compared
to nonusers (1.3% vs. 0.8%).
HALITOSIS. Both smoked and smokeless tobacco usage produce unpleasant breath odors or "bad breath". With smoking the halitosis is produced predominantly by the retention and subsequent exhalation of inhaled smoke in the lungs. Regardless of the method of absorption, however, numerous noxious elements characteristically escape from the lungs via the blood/air interchange. Pipe and cigar tobacco contains more sulfur than cigarettes, hence users tend to have a more offensive halitosis than cigarette smokers.
TOOTH AND PROSTHETIC STAINS. Tobacco stain, a brown/black
extrinsic stain, is typically found on the enamel surfaces of smokers and
tobacco chewers. It is especially pronounced in cervical areas and the lingual
aspects of the mandibular incisors. Its intensity is more dependent on the
amount of available plaque and calculus than on the amount of tobacco used,
but as a general rule smokers have almost twice as much tooth staining as
nonsmokers and heavy smokeless tobacco users have nine times as much as light
users. Smoked tobacco staining of dentures is a special problem
because it is often too heavy and too deeply embedded to be removed by denture
cleansers. This is especially true for persons with poor oral hygiene, possibly
because of the softening of plastics secondary to plaque-produced acids. Smoking is also known
to contribute to or accentuate the staining properties
of chlorhexidine solutions and gels.
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Preber H, Kant T, Bergstrum J. Cigarette smoking, oral hygiene and periodontal health in Swedish army conscripts. J Clin Perio 1980; 7:106-113.
Kowolik MJ, Nisbet T. Smoking and acute ulcerative gingivitis: a study of 100 patients. Brit Dent J 1983; 154:241-242.
Lie T, Enersen M. Effects of chlorhexidine gel in a group of maintenance care patients with poor oral hygiene. J Perio 1986; 57:364-369.
Bergstrom J, Senkel H. Influence of smoking on gingival bleeding in periodontal patients. J Dent Res 1988; 67:687.
Palmer RM. Tobacco smoking and oral health: review. Brit Dent J 1988; 164: 258-260.
Raulin LA, McPherson JC, McQuade MJ, Hanson BS. The effect of nicotine on the attachment of human fibroblasts to glass and human root surfaces in-vitro. J Perio 1988; 18:23-30.
Ahlqwist M, Bengtsson C, Hollender L, et al. Smoking habits and tooth loss in Swedish women. Comm Dent Oral Epidemiol 1989; 17:144-147.
Clark NG, Carey SE. Etiology of chronic periodontal disease: an alternative perspective. 1989
Schroeder KL, Bailey JH, Sauvinsky JA. Laser Doppler evaluation of smokeless tobacco users' gingival blood flow. J Dent Res 1989; 68:291.
Miller PD. Using periodontal plastic surgery techniques. JADA 1990; 121: 485-488.
Asmussen E, Hansen EK. Surface discoloration of restorative resins in relation to surface softening and oral hygiene. Scan J Dent Res 1986; 94: 174-177.
Schroeder KL, Rosen S, Ramamurthy NS, Strayer M. Root caries, associated microflora and collagenase from smokeless tobacco users. J Dent Res 1989; 68:390.
Microbiology & Immunology Effects
Arendorf TM, Walker DM. The prevalence and intraoral distribution of candida albicans in man. Arch Oral Biol 1980; 25:1-10.
Arendorf TM, Walker DM. Tobacco smoking and denture wearing as local aetiological factors in median rhomboid glossitis. Intnl J Oral Surg 1984; 13:411-415.
Falker WA, Zimmerman ML, Martin SA, Hall ER. The effect of smokeless tobacco extracts on the growth of oral bacteria of the genus streptococcus. Arch Oral Biol 1987; 32:221-223.
Bennet KR, Reade PC. Salivary immunoglobulin A levels in normal subjects, tobacco smokers, and patients with minor aphthous ulceration. Oral Surg Oral Med Oral Path 1982; 53:461-465.
Axéll T, Henricsson V. Association between recurrent aphthous ulcers and tobacco habits. Scan J Dent Res 1985; 93:239-242.
Henricsson V, Axéll T. Treatment of recurrent aphthous ulcers with aureomycin mouth rinse or zendium dentifrice. Acta Odont Scan 1985; 43: 47-52.
Taste Alteration, Halitosis & Weight Change
Nilsson B. Taste acuity of the human palate. III. Studies with taste solutions on subjects in different age groups. Acta Odont Scan 1979; 37: 235-252.
Rodin J. Weight change following smoking cessation: the role of food intake and exercise. Addictive Behav 1987; 12:303-317.
Mela, 1989. No taste changes in ST users.
Sinus & Throat Diseases
Slavin RG. Sinusitis in adults. J Allergy Clin Immunology 1988; 81: 1028-1032.
Swango PA, Kleinman DV. The effect of tobacco use on oral mucosal
pathologies. Abst #47, Amer Assoc Pub Health Dent Ann Meeting, Boston, Mass,
October 12, 1990.
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|Figure 1: Dental Snuff is still available today, 125 years after it first became available. It was once sold as a health product.|
|Figure 2: Example of verrucous carcinoma, i.e. "snuff dipper's cancer."|
Figure 3: Leukoplakia.
|Return to Text||Figure 4: Nicotine palatinus.|
|Return to Text||Figure 5: Smokeless tobacco keratosis.|
Figure 6: Smoker's melanosis is a combination of a relatively well-demarcated brown patch or macule and a superimposed white or gray keratosis (leukoplakia).
|Figure 7: Leukoedema.|
|Figure 8: Hairy tongue.|
|Figure 9: Enamel abrasion in tobacco user.|
|Figure 10: Enamel abrasion in tobacco user.|