TOBACCO and oral health.ppt

CONTENTS
 Introduction
 Tobacco - Preparations
- Tobacco habits prevailing in India
- Mechanisms of tobacco carcinogenesis.
 Effects of tobacco on oral health
 Oral Cancer
 Studies on smoking and oral cancer
 Smokeless tobacco
 Epidemiology and clinical aspects
 Tobacco associated oral precancerous lesions and conditions
 Leukolplakia
 Erythroplakia
 Palatal changes among reverse smokers
 Oral Submucous Fibrosis
 Oral Lichen Planus

 Tobacco-associated oral mucosal lesions
 Preleukoplakia
 Leukoedema
 Smoker’s Palate
 Palatal Erythema
 Central papillary atrophy of the tongue
 Tobacco-lime user’s lesion
 Pan (betel-quid) stain
 Pan encrustation
 Oral Lichen Planus– like lesion
 Smoker’s Melanosis
 Oral Candidosis

 Effect of tobacco on Periodontal diseases
 Prevalence and severity of periodontal diseases
 Gingivitis
 Periodontitis
 ANUG
 Etiology and pathogenesis of periodontal disease
 Microflora and host response
 Physiology
 Response to periodontal therapy
 Non surgical therapy
 Surgical therapy
 Implants
 maintenance therapy
 Recurrent (refractory) periodontitis

 Effects of tobacco on Saliva and Dental Caries
 Saliva
 Studies on Smoking and Dental caries
 Environmental Tobacco Smoke and Dental Caries in children
 Chewing tobacco and dental caries
 Other Problems related to Tobacco Use
 Aesthetics
 Halitosis
 Smell and taste acuity
 Aphthous ulcers
 Tobacco Intervention – Prevention and Cessation
 Prevention strategies
 Tobacco Free Initiative in India
 Tobacco Intervention and the Dentist
 Conclusion

Introduction
 There is overwhelming evidence that tobacco usage
produces harmful effects in the mouth.
 Oral cancer and periodontal diseases are among the
most serious oral health problems associated with
tobacco use.
 The magnitude of the effect of tobacco on occurrence of
oral disease is high; and he risk declines with increasing
time after smoking cessation.

Introduction
 Controlling tobacco use is one of the most important
steps to make progress in reducing the burden of
tobacco-related oral diseases.
 Dentists are the most frequently in contact with
population, and thus in a favorable position in
connection with tobacco intervention.
 A number of tobacco-related oral health conditions can
be prevented from progressing, and some can even be
reversed with proper knowledge of tobacco and oral
health, as dentists are in a position of early diagnosis of
most of the reversible conditions.

 History
 Mexican Indians used a ‘Y’ shaped piece of cone or pipe called
“tobago” or “tobaca”
 Plant was named as “tobacco”
 “Nicotiana” – from the name of French ambassador Jean Nicot
 Two major varieties – Nicotiana rustica and Nicotiana tobacum
 Tobacco preparations
 Tobacco curing:
 Flue curing – piped warm air
 Fire curing – open slow-burning fire
 Sun-curing – left in the sun for drying
 Tobacco usage:
 Smoked tobacco Smokeless tobacco

Smoked tobacco
 Cigarettes
 Bidis
 Cigars
 Pipes
Smokeless tobacco habits
 Tobacco habits other than smoking are widely prevalent.
 May be taken alone or in combination.
 Predominant use is oral, or may be nasal.

 Smokeless tobacco habits around the globe:
 Europe and USA
 Chewing tobacco
 Firm plug / moist plug
 Loose-leaf tobacco
 Twist or roll tobacco
 Snuff
 Moist snuff
 Dry snuff
 South-East Asia and Africa
 Snuff is widely used
 Other smokeless tobacco habits
 Shammah – Saudi Arabia – used as quid or as snuff
 Nass – Iran and the former Soviet Republics
 Naswar – Afganisthan and Pakistan

Tobacco habits prevailing in India
 Portugese traders introduced tobacco in India – late 16th or
early 17th century.
 Initially tobacco was smoked in India, later used in smokeless
form.
 Prevalence of tobacco use in India
 Among 400 million individuals aged 15 years and over, 47%
use tobacco in some form.
 72% - smoke bidis (most prevalent form tobacco use in India)
 12% - smoke cigarettes
 16% - use smokeless form
 250 million kg tobacco is cleared for domestic use, of this
 86% - for smoking
 14% - smokeless form

Smoking habits in India
 Cigarette
Cigarette smoking is more common in urban areas than rural areas.
 Contains about 1 gm of finely-cut cured tobacco, covered with paper.
 Nicotine content: 1-1.4 mg; Tar content: 19-27 mg.
 Bidi
 Most popular form of tobacco use in India.
 Contains about 0.2 – 0.3 gms of sundried tobacco flakes, handrolled in
a piece of temburni leaf, and tied with a thread.
 Produce smaller volume of smoke than cigarettes.
 Nicotine content: 1.7 – 3 mg; Tar content: 45-50 mg.
 Bidi smoke has higher concentrations of toxic agents such as hydrogen
cyanide, carbon monoxide, ammonia, volatile phenols, and
carcinogenic hydrocarbons than that of locally manufactured cigarettes
as well as U.S cigarettes. Hoffman et al 1974, Pakhale 1990.

 Cigar / Cheroot / Chutta
 Cigars – air-cured fermented tobacco; predominantly urban use.
 Cheroots – small cigars, made of heavy-bodied tobacco.
 Chuttas – coarsely prepared cheroots
- widely used in Tamil Nadu, Andhra Pradesh, Orissa.
 Reverse Chutta smoking
 Habit of smoking with the lighted end inside the mouth.
 Widely practiced in coastal areas of A.P., and parts of Orissa.
 More often by women (62%) than men (38%).
 Dhumti
 This form of smoking is prevalent in Goa.
 “Reverse dhumti smoking” – common among Christian women in Goa.
 Dhumti produces a palatal reaction less severe than that induced by
reverse chutta smoking.

 Hookli
 Is used in Bhavnagar District, Gujarat (Prevalence is 11%)
 Contains about 1-2 gms of sun-dried, flake, or powdered tobacco
moistened with molasses.
 Hookah
 Is an Indian water pipe, the origin of which corresponds with the
introduction of tobacco in India.
 Practiced by 4-18% of villagers in North India
 Cut, shredded tobacco, moistened with molasses is burnt with
charcoal in a bowl, and the smoke is drawn through the water in the
base of the hookah.
 Chillum
 Is a straight, 10-14 cm long conical clay pipe, filled with coarsely cut
tobacco.
 It is practiced in Northern and Eastern parts of India

Smokeless Tobacco
Some common forms of smokeless tobacco use:

Constituents
in tobacco
A list of confirmed constituents in
tobacco smoke (Davidson et al.)

MECHANISMS OF TOBACCO CARCINOGENESIS
 Over 3000 carcinogens have been identified in tobacco.
 Most important are Polycyclic aromatic hydrocarbons and the
tobacco specific nitrosamines (TSNs)
 Polycyclic aromatic Hydrocarbons:
 The carcinogencic agents present in “tars”
 Benzo[a]pyrene is the most powerful carcinogen present in ‘tar’
and found in amounts of 20-40 ng per cigarette
 N- nitrosamines
 Present in the main stream smoke of cigarette
 Generated primarily during pyrolysis.
 Also produced endogenously from smokeless tobacco.

MECHANISM
 The carcinogenic agents present in tobacco produce
DNA adducts
 Interfere with accuracy of DNA replication, leading to
mutations
 Malignant transformation of cell and its clonal
derivatives.
 Damage to all replicating cells, including those of the
immune response.

 Metabolization of carcinogens:
 1. oxygenation p450 enzymes in cytochromes.
 2. conjugation Glutathione-S-Transfrerases (GST)
 Genetic susceptibility may be present related to the
capacity to metabolize these carcinogens, thus leading
to increased risk of tobacco-related cancers in those who
are inherently susceptible.

 According to W.H.O. 1984, 90% of oral cancers
in S.E Asia are attributable to chewing and
smoking tobacco.
 Carcinogenic role of tobacco is related to the
type of product, the way it is used and its use in
combination with other substances.

Smoking
 There is significant association between smoking and oral cancer.
 Types of smoking habits:
 In S.E Asian countries bidi smoking is the most prevalent form of
smoking; several studies have implicated bidi smoking as significantly
associated with oral cancer, and the risk quantified.
 Bidis contain a much higher concentration of toxic agents like tar,
nicotine, a carbon monoxide, hydrogen cyanide, phenols and
benzopyrene as compared to locally manufactured cigarettes, as well
as US cigarettes.
Hoffman et al 1974, Pakhale 1990.
 Bidi smoking is more hazardous than cigarette smoking. Dikshit RP,
Kanhere S 2000.

 The relationship between reverse smoking and palatal
cancer is well established in India, where high frequency of
palatal cancer was seen among reverse chutta smokers.
Reddy et al 1982, Gupta et al 1980.
 Pipe and cigar smokers have also been reported to be at
higher risk for oral cancer as compared to non smokers.
Pipe smokers are particularly at a higher risk of lip cancer.
Keller 1990. Risks for oral cancer are similar for cigar and
cigarette smokers. NCI monograph: USPHS 1998.

Smoking with alcohol consumption
 Tobacco smoking and alcohol drinking combine to account for
approximately three-fourths of all oral and pharyngeal cancers in
the United States.
 Smokers who do not use alcohol have a two-to-four fold risk of
developing oral cancer than non users; the oral cancer risk of
smokers who are heavy drinkers is 6-15 times greater than that of
non smokers / non drinkers, and a dose-response relationship has
also been demonstrated. Blot et al 1988.
 The risk of those who smoke and drink alcohol goes up to 100 fold
depending on the frequency of smoking and amount of alcohol
consumed per day. Blot et al 1988.

 Mc Coy suggested that alcohol may promote the
carcinogenic effect of tobacco by various
mechanisms, including:
 Dehydrating effects of alcohol;
 Increasing mucosal permeability to tobacco smoke;
 Nutritional deficiency;
 Solubilizing tobacco.

Anatomical site of Oral Cancer and Smoking
 Pooling of carcinogens in saliva gives rise to cancers in the ‘gutter’
area – FOM, ventral and lateral tongue.
 Cancers of FOM and retromolar area were significantly more related
to tobacco use than cancers of tongue and cheek. Jovonovich et al
1993.
 Bofetta et al (1993) reported strong association with soft palate
cancers than anterior sites.
 Cancers of the hard and soft palate are strongly associated with
reverse chutta smoking.

 Cessation of cigarette smoking eliminates the increased
risk of oral cancer within 5-10 years after cessation. Blot
et al 1988.
 Attributable risk:
 For the Indian population the proportion attributable to
tobacco use, both smoking and chewing has been
estimated to vary form 61 percent to 70 % (81% for
males and 36% for females) for oral cancer. Notani and
Jayant et al 1977.

Smokeless tobacco
 The use of smokeless tobacco is an important cause of oral cancer,
particularly in India and its evidence is largely derived from case control
studies.
 The reported risks of developing oral cancer in chewers are
2-4 times higher as compared to those with no tobacco habits.
Jussawall and Deshpande 1971, Notani and Jayant 1987,
Sankaranarayanan et al Nandakumar et al 1990.
 Chewing tobacco and snuff increase the risk for oral cancer. Risk
increases with increasing length of exposure, with risk greatest for
anatomic sites where the product is held in contact for the longest time.
Mattson and Winn 1989.

Ecological evidence:
 High frequency of oral cancer in those parts of the world where
areca/tobacco chewing habits are widespread.
Evidence from case-control studies:
 In a meta-analysis of 17 published studies, showed a relative risk
averaging around 10. Thomas and Wilson 1993.
Evidence from prospective studies:
 In a 10-year follow-up of 30,000 individuals in three areas of India, annual
age-adjusted incidence rate of oral cancer among betel quid- tobacco
chewers was 23/100 000, compared with zero in smokers and non
habitues. Gupta et al 1980.
Evidence from intervention studies:
 Cessation of tobacco habits resulted in substantial drop in incidence of
leukoplakia (incidence ratio=0.31) over a 10-year follow up. Gupta et al
1980.
 Significant regression in precancerous lesions seen with intensive health
education programs. Mehta FS 1982.

 The two most common forms of cancer seen in association
with smokeless tobacco use are verrucous carcinoma and
squamous cell carcinoma.
Dose-response relationship:
 Frequency of chewing tobacco showed dose response
relationship with risk for oral cancer. R.R. of 8.4 for 2
quids/day to 17.6 for 6 or more quids/day. Hirayama 1966.

Oral Cancer – Epidemiology and Clinical Aspects
Global epidemiology
 Globally oral cancer is one of the ten most common cancers
and constituting almost 50% of all cancers diagnosed in
males. In highly industrialized countries, it accounts for 3-
5% of all cancers, whereas in developing countries it is up
to 40%.
 Globally almost half a million cancer of the mouth and
pharynx are diagnosed every year, and three fourths of
these are from developing world. In developing world it is 4th
most common cancer of humans.

Oral Cancer in India
 In India, oral cancer forms about 10% of all cancers. India
has one of the highest incidence rates of oral cancer in
the world.
 In India, the annual age standardized incidence rate of
oral cancer is 12.6 per 100 000 population. Peterson PE
2005.
 It ranks number one among men and number three
among women in India, constituting 12% of all cancers in
men and 8% in women. Sankaranarayanan R 1990.

Age and gender distribution
 Generally, oral cancer occurs more commonly among men
than women, proportional to the prevalence of tobacco
habits.
 Peak age of occurrence is in the 6th decade of life, most of
the patients are over 40 years of age.

Clinical Aspects
 Oral cancer has a varied clinical picture, most of the lesions
are described as :
 EXOPHYTIC
 ULCERATIVE
 VERRUCOUS

ORAL CANCER AT DIFFERENT INTRAORAL
LOCATIONS
 The type of tobacco habit contributes to the variation in involvement of
different intraoral sites in different geographical areas.
Lip Cancer:
 Mostly involves lower lip; 95% in males.
 Tobacco and U.V exposure.
 Tobacco- bidi and pipe smokers.
 Generally slow to metastasize – 5-10%.
Labial and Buccal Mucosa:
 Commonest tumor of the oral cavity.
 Lower labial mucosa – khaini users; lymph node involvement is high;
 Labial commissures – bidi smokers.
 Betel-quid chewing – 80% of oral cancers in buccal mucosa.
 Lymph node involvement is high - 65%.

Tongue Cancer:
 2nd most common tumor of the oral cavity, after buccal mucosa.
 Bidi smoking is strongly associated.
 50% of oral cancers in men and 27% in women.
 80% - anterior two-thirds – lateral and ventral surfaces.
 Dorsum and tip of the tongue – common sites in case of OSMF;
 Highest propensity for lymph node metastasis.
Cancer of the Palate:
 Uncommon location for squamous cell carcinoma; except in reverse smokers.
 485 of oral cancers in reverse smokers occur in the hard palate.
 Metastasis occurs in few cases.
Retromolar trigone and alveolar mucosa:
 10% of all oral cancers. Involve the bone in 50% cases.
 Diagnosis is difficult –resemble gingivitis and periodontal disease.
 Lymph node metastasis is high.

Cancer of the Gingiva:
 10% of oral cancers in men and 16% in women.
 More common in maxillary gingiva, and in edentulous areas.
 Invade the underlying structures in most cases – maxillary antrum,
FOM, or laterally into the cheek.
 Metastasis is a common sequelae.
Carcinoma of the Floor of the Mouth (FOM):
 10-15% of oral cavity tumors.
 Not common in India – 3% among men and 2% among women.
 Bidi smoking and alcohol drinking are responsible.

Tobacco-associated Oral Precancerous
Lesions and Conditions

 Precancerous lesion: a morphologically altered tissue in which cancer
is more likely to occur than in its apparently normal counterpart.
 Leukoplakia, Erythroplakia, Palatal changes associated with reverse chutta
smoking.
 Precancerous condition: a generalized state associated with a
significantly increased risk for cancer.
 Oral Submucous Fibrosis, Oral Lichen Planus.
 Precancerous lesions and conditions form a source for over 70% of oral
cancers in India.
 Tobacco users who develop precancer run a risk that is 69 times higher
for development of oral cancer compared to those who do not have
precancer.

LEUKOPLAKIA
 Most common oral precancerous lesion. Prevalence in India varies from
0.2 to 4.9%.
 Men are affected more than women; peak age of occurrence is 35-54
years.
 Tobacco – most important etiological factor.
 Leukoplakia is defined as “a white patch or plaque that cannot be
characterized, clinically or pathologically as any other disease. W.H.O.
1978.
 At the International Seminar at Malmo, 1984: Definition was modified to
include only those lesions that are either idiopathic or associated with
tobacco use.

Tobacco and Oral Leukoplakia
 Development of leukoplakia is related more to the amount of fresh
tobacco that contacts the mucosa than the total number of hours of
contact with tobacco.
 Site-specific relation is observed in the development of leukoplakia
with site of tobacco placement.
 Dose-response relationship:
 Leukoplakia occurs six times more frequently in smokers, than in
non smokers. Baric et al 1982.
 Tobacco cessation:
 Reducing or cessation of tobacco results in regression or even
disappearance of oral leukoplakia. Gupta et al 1995; Roed 1981.

Clinical types of leukoplakia
 Homogenous
 Ulcerative
 Verrucous
 Nodular

Malignant transformation
 3-6% lesions may turn malignant over a period of 10
years.
 Risk of malignant transformation –
nodular > ulcerated > verrucous > homogenous.

Leukoplakia at different intraoral locations
 There is a definite site and tobacco habit relationship.
Labial mucosa:
 Bidi or cigarette is customarily held; who smoke till the
“butt” remains develop leukoplakia at this site.
 Half the lesions in hookli smokers occur at this site.
Labial commissure:
 Most favored location among bidi smokers;
 7-35% of leukoplakias;
 Ulcerated leukoplakias occur almost exclusively in the
commissures.
 Heat produced – pigmented leukoplakia.

‘Mishri’ and ‘khaini’ associated leukoplakia:
 Leukoplakia on the labial mucosa and gingiva;
 In Maharashtra: premolar-canine region of mandibular groove.
 In U.P and Bihar: lower labial groove;
Leukoplakia associated with betel-quid chewing:
 44-64% of leukoplakias;
 Buccal mucosa where the quid is held;
 Almost all are of homogenous or nodular types.
Dorsum of the tongue:
 Less common site for leukoplakia, except in OSMF patients;
 Also seen among reverse chutta smokers;
 Khaini users of Singhbhum district in Bihar – 13% of leukoplakias in
this location.

Floor of the mouth / ventral surface:
 High-risk lesion in Western countries.
 In India, uncommon location – less than 3%.
Palate:
 Uncommon location for leukoplakia, except in reverse chutta
smokers, and even bidi smokers.
Gingiva:
 Accounted for less than 1% of leukoplakias in five regions of
India.
Bhargava et al 1975; Gupta et al 1980; HamnerJE,
Mehta FS, Pindborg JJ, Daftary DK 1971; Mehta et al 1977.

ERYTHROPLAKIA
 A bright red, velvety plaque which cannot be characterized
clinically or pathologically as any other lesion.
 Rare but most severe precancerous lesion.
Tobacco and Erythroplakia:
 Hashibe M and co-workers (2000) in a case-control study
including 100 erythroplakia patients concluded that tobacco
chewing and alcohol drinking are strong risk factors for
erythroplakia in the Indian population.
 In another study, more than 94% of patients having
erythroplakia smoked tobacco and more than 65% used
alcohol. Bouquot JE, Gnepp DR. 2002.

Clinical types:
 Homogenous
 Granular or speckled
Malignant transformation:
 Most severe among the precancerous lesions;
 Microscopically 91% show squamous cell carcinoma.
 Carcinoma and dysplasia occur about 17 times more frequently in
erythroplakic lesions than leukoplakia.
 Malignant transformation has been seen to be associated with reverse
smoking.
HamnerJE, Mehta FS, Pindborg JJ, Daftary DK 1971.

PALATAL CHANGES AMONG REVERSE SMOKERS
 Reverse smoking evokes diverse alterations in the palatal
mucosa.
 Palatal changes occur in up to 46% of reverse smokers;
peak occurrence being in 55-64 year age group. Mehta et al
1977.
Palatal changes in reverse smokers:
 Palatal involvement in reverse chutta smokers was noted in
85% of the 497 leukoplakia cases, and in 57% of the 296
pre-leukoplakias, and in all cases of smoker’s palate.
Daftary et al 1992.

Clinical aspect:
Classification of Palatal changes (Mehta FS et al 1977):
 Keratosis
 Excrescences
 Patches
 Red areas
 Ulcerated areas
 Hyperpigmentation
 Non pigmented areas

Malignant transformation:
 Risk for malignant transformation is strongly associated with the
reverse smoking practice;
 Malignant transformation of palatal changes was responsible for 91%
oral cancers that developed in Srikakulam district of Andhra Pradesh
during a 6-year observation period.
 Red areas showed malignant transformation rate of 118 per 1000,
followed by patches (12 per 1000).
Pindborg JJ& co-workers 1971.

ORAL SUBMUCOUS FIBROSIS (OSMF)
 A high-risk precancerous condition that predominantly
occurs in Indians. First reported in 1953.
Epidemiology:
 Prevalence in random samples in India is up to 0.4%.
 Incidence rate in Ernakulum: 8 for men, and 19 for women
per 100 000.
 There is a general female preponderance;
 Prevalence figures in different states vary due to different
diagnostic criteria.

Definition:
 Submucous fibrosis is a a chronic mucosal condition
affecting any part of the oral mucosa, characterized by
mucosal rigidity of varying intensity due to fibroelastic
transformation of the juxta-epithelial connective tissue
layer.
Etiology:
 Habitual Areca nut chewing has been implicated as a
causative factor.
 Literature reports chillie consumption, autoimmunity, and
genetic predisposition as other potential factors.
 Areca-nut containing preparations are: mawa, paan, and
paan masala.

Clinical aspects and diagnostic criteria:
 Initial symptom – burning sensation, hypersalivation or dryness;
 Initial clinical sign – blanching of the oral mucosa;
 Appearance of blisters, ulcerations or recurrent generalized
inflammation of oral mucosa, and defective gustatory sensation may
occur;
 Palpable fibrous bands – buccal mucosa, retromolar areas and
around the rima oris: diagnostic criterion;
 Tongue involvement – depapillation, impaired mobility;
 Restricted mouth opening – severe cases.

Natural history and malignant transformation:
 Unlike precancerous lesions, it does not regress, either
spontaneously or with cessation of the chewing habit. It
may remain stationary or become severe. Murti et al
1990.
 Oral cancer developed in 7.6% of OSMF cases in a 17-
year follow up study in Ernakulum;
 Relative risk for development of oral cancers in OSMF
patients when compared to individuals who had tobacco
habits, but did not exhibit any lesions.
 Cancer may develop from dorsum or tip of the tongue,
which are otherwise uncommon sites for oral cancer.
(Murti et al 1985).

ORAL LICHEN PLANUS
 Lichen planus is primarily a dermatological disorder, in which oral
mucosa is frequently affected.
 Prevalence in India ranges from 0.1 to 1.5%, highest (3.7%) in those
with mixed oral habits, and lowest (0.3%) in non tobacco users.
Tobacco use and relation with Lichen Planus:
 93% of individuals with oral lichen planus are tobacco users, both
chewing as well as smoking.
 Relative risk for oral lichen planus was highest (13.7) among those
who smoked and chewed tobacco. Bhonsle et al 1977.
 Tobacco use also influences the natural history pf this condition in
the oral mucosa.
 It is categorized as a “probable precancerous condition”.

Clinical aspects:
 Buccal mucosa is commonly affected site -84%;
 Generally asymptomatic, diagnosed on the basis of presence of
Wickham’s striae;
Oral Lichen Planus exists in various morphological forms:
 Reticular form
 Plaque form
 Erosive form
 Malignant transformation is seen in 0.4% of 722 cases over a 10-year
follow-up; Erosive form is more prone to cancer development.
Murti et al 1986.

TOBACCO-ASSOCIATED ORAL
MUCOSAL DISEASES

 Apart from being causally related to oral cancer and precancerous
lesions, tobacco use is also responsible for an array of oral lesions that
are not considered precancerous.
1. PRELEUKOPLAKIA:
 It is a definite entity with specific diagnostic criteria and behavior.
 Preleukoplakia is strongly associated with tobacco smoking and is
considered as a precursor to leukoplakia.
 Clinically it is characterized by low-grade to mild mucosal reaction, grey
or greyish-white, but never completely white, and indistinct borders
blending into adjacent normal mucosa.
 Over a 10 year period, 15% of preleukoplakia progressed to leukoplakia
and 0.4% to oral cancer.

2. LEUKOEDEMA:
 A chronic mucosal condition in which oral mucosa has a grey, opaque
appearance; disappears when the mucosa is stretched and reappears
when relaxed.
 Mostly observed among bidi smokers.
 Prevalence in India – 0.02 to 0.3%.
 Over a 10 year period,36% lesions progressed to cancer.
3. SMOKER’S PALATE (LEUKOKERATOSIS NICOTINA PALATI)
 A common palatal reaction to conventional smoking.
 Prevalence in India: 0.4 to 9.5%.
 Clinically, diffused white palate with numerous excrescences having
central red dots, corresponding to orifices of minor salivary glands.
 52% of the 31 lesions occurred among bidi smokers.
 It shows neither great variability nor malignant transformation, unlike
palatal changes seen in reverse smokers, from which the lesion must be
distinguished.

4. PALATAL ERYTHEMA
 Is associated with bidi smoking .
 Consists of diffused erythematous hard palate, occasionally extending
to soft palate. 87 % occurred among smokers, esp. bidi smokers.
 It may occur independently or seen associated with palatal papillary
hyperplasia, and with central papillary atrophy of the tongue and
bilateral commissural leukoplakias.
 It appears to be a benign lesion, none of the lesions progressed to
cancer.
5. CENTRAL PAPILLARY ATROPHY OF THE TONGUE
 Consists of well defined, oval, pink area in the center of the dorsum of
the tongue, devoid of lingual papillae.
 0.04 - 0.1% prevalent in India. It was present among 2.2% bidi smokers,
1.6% cigarette smokers and 0.3% of non smokers.
 Considered to be due to candidal infection, smoking or both. 87%
regressed lesions was seen in those who stopped their habits. None of
the lesions progressed to cancer.

6. TOBACCO- LIME USER’S LESION
 Tobacco- lime (khaini) produces a well defined, yellowish- white
plaque at the site of placement of the mixture.
 Resembles leukoplakia, but can be scrapped off with a piece of
gauze.
 In Maharashtra, this lesion is more common (2.9%) than
leukoplakia (0.67%).
7. PAN (BETEL- QUID STAIN)
 Pan stain is a red coloration of the oral mucosa in betel squid
chewers.
 The bright red color produced is due to formation of 0- quinone
from the water soluble polyphenols, at the alkaline pH of 8-9 via
secondary reactions.

8. PAN ENCRUSTATION
 In heavily addicted pan chewers, a thick brownish- black encrustation
occurs at the site of placement of the pan.
 It is similar to tobacco-lime user’s lesion.
 It does not seem to progress to leukoplakia.
 Discontinuation of the habit leads to nearly complete clearance of the
encrustation.
9. ORAL LICHEN PLANUS – LIKE LESION
 It almost, exclusively occurs at the site of placement of betel quid
such as mandibular groove and buccal mucosa.
 Some 89% of lesions occur in betel quid chewers, and 11% who
chewed pan and smoked tobacco.
 Consists of white, wavy, parallel, non-elevated fine finger-like
striae, which may radiate from a central fibrin covered area
corresponding to the site of placement of betel quid.
 Occurs predominantly among women (74%) in Ernakulam distt.
Majority of lesions occur in 35-54 years age range.

10. SMOKER’S MELANOSIS
 Melanin pigmentation of the oral mucous membrane is normally
seen in coloured races.
 Heavy cigarette smokers show a pigmentation prevalence of 30%
which is most prevalent on the attached gingiva.
 The change is not premalignant, and the pigmentation is
reversible.
11. ORAL CANDIDOSIS
 Smoking, either alone or in combination with other factors, appears
to be an important predisposing factor for oral candidosis.
 Patients continuing smoking habit after cessation of antimycotic
therapy had relapses of the candidal infection in all cases.
 Furthermore, it is a clinical experience that some candidal
infections disappear following smoking cessation only.

 Role of smoking in periodontal diseases has been
extensively studied for many years.
 Smoking has been identified as a major risk factor for
periodontitis.
 The first reports relating periodontal diseases to smoking
were evident in the 1950s. A major breakthrough was
provided by three separate studies by Bergstrom J,
Feldman RS, and Ismail AL in the year 1983.

 Effects of smoking on periodontal diseases:
1. Prevalence and severity of periodontal diseases
 Gingivitis
 Periodontitis
 ANUG
2. Etiology and pathogenesis of periodontal disease
 Microflora and host response
 Physiology
3. Response to periodontal therapy
 Non surgical therapy
 Surgical therapy
 Implants
 Maintenance therapy
4. Recurrent (refractory) periodontitis

Prevalence and Severity of Periodontal Disease
 GINGIVITIS:
 Controlled studies in human models of experimental gingivitis have
shown that both, gingival inflammation and bleeding on probing in
response to plaque accumulation are reduced in smokers compared
with non smokers. Bergstrom and Preber 1986; Danielsten et al 1990.
 A number of cross-sectional studies have consistently suggested the
same.
 Decreased expression of clinical inflammation. Preber and Bergstrom
1985; Haber and Kent 1993.
 Smoking adversely affected the blood flow to the gingiva, and there was
thus reduced bleeding on probing. Josef G 1990; Clarke and Carey
noted reduced blood flow up to2 to 3 hours after smoking 1 cigarette.

 PERIODONTITIS:
 Multiple cross-sectional and longitudinal studies have demonstrated that
pocket depth, attachment loss and alveolar bone loss are more
prevalent and severe in smokers compared with non smokers.
 In a systematic critical appraisal of the available literature conducted by
Bergstrom J in 2006, in which 129 articles were selected, almost all the
studies showed significant association between smoking and impaired
periodontal health, using probing pocket depth and clinical attachment
loss as the most frequently used end points.
 The NHANES III survey in US on 12,000 patients showed that smokers
were four times as likely to have periodontitis as persons who had never
smoked.

 Former smokers were 1.68 times more likely to have periodontitis
than persons who had never smoked.
 Dose response relationship was observed between cigarettes
smoked per day and the odds of having periodontitis. In subjects
smoking 9 or fewer cigarettes per day, the odds for having
periodontitis were 2.79, as against subjects smoking 31 or more
cigarettes per day, having 6 times more risk.
 The odds ratio for periodontitis in current smokers ranges from 1.5 to
7.3, depending on the observed severity of periodontitis.

Severity of Periodontitis
 Rate of periodontal destruction increased in smokers,
and smoking was significantly associated with higher
prevalence of moderate and severe periodontal disease.
Albander JM and co-workers 2000.
 Over a 10-year period, bone loss was reported to be
twice as rapid in smokers than non smokers and
proceeds more rapidly even in the presence of excellent
plaque control. Bolin et al 1993.

 Older adult smokers are three times more likely to have severe
periodontal disease (Beck et al 1990; Locker D and Leake JL1993); and
number of years of tobacco use is a significant factor in tooth loss,
coronal root caries and periodontal disease. Jette AM, Feldman HA
1993.
 Increased severity of generalized aggressive periodontitis is seen in
younger patients. Those between 19 and 30 years of age who smoke
are 3.8 times more likely to have periodontitis than non smokers.
Schenkein et al 1995.
 Longitudinal studies have shown that young individuals smoking more
than 15 cigarettes per day showed highest risk for tooth loss. Smokers
are more than 6 times as likely as non smokers to demonstrate
continuous attachment loss. Holme G 1994; Ismail et al 1990.

 Effects of cigar and pipe smoking:
 Effects are similar to cigarette smoking.
 Studies have shown that severity of disease is intermediate between the
current cigarette smokers and non-smokers.
Krall and co-workers 1999; Albander et al 2000.
 Smokeless tobacco:
 Localized attachment loss and recession are seen at the site of tobacco
placement. Robertson et al 1990; Amaresena and co-workers 2002.
 Former smokers and cessation of smoking:
 The risk is less than current smokers, but more than non-smokers.
 Risk decreases with increasing number of years since quitting smoking.
Effects on the host are reversible with smoking cessation. Tomar SL, Asma
S 2000.

 Acute Necrotizing Ulcerative Gingivitis:
 Smokers have higher prevalence and severity of ANUG as
compared to non-smokers.
 Etiology and Pathogenesis of periodontal disease:
 Microflora and host resposnse:
 No difference in rate of plaque accumulation;
 Higher subgingival levels of B.Forsythus in smokers than non-smokers;
 Altered host response:
 Downregulation of the immune response to bacterial challenge;
 Functional allterations in chemotaxis,, phagocytosis, and oxidative burst
of neutrophils;
 Decreased IgG2
 Increased tissue destructive enzymes – TNF X, PGE2, MMP-8.

 Physiology:
 Decreased clinical signs of inflammation.
 Alterations in vascular response and inflammatory response.
 Decreased gingival blood flow, oxygen conc., subgingival temp.
 Response to periodontal therapy:
 Poor response to periodontal therapy – non surgical and surgical.
 Decreased levels of clinical attachment gain, and reduction in pocket
depth.
 Negative impacts on the outcome of GTR, and treatment of intrabony
defects with bone allografts.
 Nicotine affects attachment of fibroblast to root surface, and affects
collagen synthesis and protein secretion.

 Implants:
 Detrimental to both the initial and long-term success of dental
implants.
 Most important predisposing factor to implant failure.
 Significantly greater bleeding index, peri-implant pocket depth,
inflammation, and bone loss.
 Smoking cessation definitely improves implant success rates.
 Reccurent (refractory) disease:
 Many smokers become refractory to traditional periodontal
therapy, and tend to show more periodontal breakdown.

Wound Healing
 Tobacco influences wound healing in the mouth.
 Mechanism of impaired healing:
 Nicotine:
 Vasoconstsriction ishaemia;
 Inc. platelet adhesiveness thrombotic microvascular occlusion
tissue ischaemia.
 Reduced proliferation of repairing cells – fibroblasts, macrophages.
 Carbon monoxide:
 Reduces oxygen transport and metabboolism
 Hydrogen Cyanide:
 Inhibits enzyme systems necessary for oxidative metabolism.

 Saliva:
 Decreases salivary flow rate;
 Lower pH in stimulated whole saliva;
 Lowered buffer capacity;
 Shift in bacterial population towards LB and cariogenic streptococci.
 Dental Caries:
 Insufficient evidence of any direct etiological relationship;
 Changes in saliva and poor oral hygiene account for
increased risk of caries in smokers.
 Environmental tobacco smoke (ETS) and caries in children:
 Association between parental smoking behavior and caries
experience in children. Leroy et al 2008; Williams SA 2000.

 Smokeless tobacco and dental caries:
 Increased risk of dental caries is seen in habitual chewers of
smokeless tobacco;
 Risk is higher for root surface caries, and to a lesser extent,
coronal caries.
Tomar SL, Winn DM 1999; Offenbacher and Weathers 1985.
 High levels of fermentable carbohydrates in these products stimulate
growth of cariogenic bacteria;
 Gingival recession – contributory factor;
 Poor oral hygiene – co-factor;
 Increased collegenase activity.

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