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Effects of tobacco use on oral health - an overview

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Abstract

Tobacco use is linked with many serious illnesses, such as cancer, cardiopulmonary diseases, as well as with many health problems. Every year, the use of tobacco products causes a heavy toll of deaths and severe human disease worldwide. One of the many health problems linked to tobacco use is its detrimental impact on oral health. Tobacco causes a whole series of oral health problems, ranging from life-threatening (precancerous changes leading to oral cancer) and serious (periodontal disease, teeth decay) to social (bad breath). Tobacco is consumed through the mouth in a variety of forms, varied from smoked tobacco to smokeless tobacco chewing on itself or combined with areca nut. All these forms of tobacco have damaging effects on the oral health. The most significant preventive measure to prevent the oral health problems caused by tobacco use is to stop using tobacco products. The risk of developing oral cancer drops rapidly when a smoker ceases tobacco use. After ten years of not using tobacco, an ex-smoker/user’s risk of oral cancers is about the same as that for someone who has never smoked. To stop using tobacco products is not an easy task. Fortunately, there are a number of therapies available to assist in quitting of tobacco. It is important to remember that, while it will be difficult, ceasing to use tobacco has immediate health benefits, including increased life expectancy and reduced risk of tobacco related diseases and conditions.
EFFECTS OF TOBACCO USE ON ORAL HEALTH – AN OVERVIEW
Review Article
K.H. Awan. Effects of tobacco use on oral health – an
overview. Annal Dent Univ Malaya 2011; 18: 18–23.
K.H. Awan1
1Senior Lecturer
Dental Research & Training Unit,
Research Management Centre,
Faculty of Dentistry, University of Malaya,
50603, Kuala Lumpur, Malaysia.
Tel No (Office): +603 7967 6493
Email: kamranha@um.edu.my
Corresponding author: Dr. Kamran Habib Awan
among young people in North America, and more than
15% of adolescent smokers use these tobacco
products. Pipe smoking is one of the oldest methods
of smoking and was brought to Europe by sailors from
America. Water pipes include special receptacles
through which smoke has to pass, ostensibly to reduce
its harmful effects. Hookah is an Indian water pipe. The
habit of reverse smoking by holding the glowing end
of cigarettes or cigars within the oral cavity is
described in parts of India, South America and the
Philippines. The habit is practiced extensively by older
women living in rural areas.
Smoked tobacco
Many toxins are present in tobacco smoke.
Tobacco smoke is made up of “side-stream smoke”
from the burning tip of the cigarette and “main-stream
smoke” from the filter or mouth end. Tobacco smoke
contains thousands of different chemicals which are
released as particles and gases. The particulate phase
includes nicotine, “tar” (itself composed of many
chemicals), benzene and benzo(a)pyrene. The gas
phase includes carbon monoxide, ammonia,
dimethylnitrosamine, formaldehyde, hydrogen
cyanide and acrolein. Some of these have marked
irritant properties and some 60, including
benzo(a)pyrene and dimethylnitrosamine, have been
shown to cause cancer.
The tar yield of different brands of cigarettes
range from 0.5 mg to 26 mg (averaging 12.5 mg), with
the most popular brands containing 15-17 mg of tar.
In the European Union (EU) cigarettes have to contain
less than 12 mg of tar from 1998 (2). Nicotine yields
range from 0.05 mg to 1.7 mg, with the most popular
brands yielding 1.0 mg of nicotine. In developed
countries over 95% of manufactured cigarettes
consumed are filter-tipped.
About 10% consume tobacco as roll-your-own
cigarettes mostly among lower socioeconomic groups.
ABSTRACT
Tobacco use is linked with many serious illnesses, such
as cancer, cardiopulmonary diseases, as well as with
many health problems. Every year, the use of tobacco
products causes a heavy toll of deaths and severe
human disease worldwide. One of the many health
problems linked to tobacco use is its detrimental
impact on oral health. Tobacco causes a whole series
of oral health problems, ranging from life-threatening
(precancerous changes leading to oral cancer) and
serious (periodontal disease, teeth decay) to social (bad
breath). Tobacco is consumed through the mouth in a
variety of forms, varied from smoked tobacco to
smokeless tobacco chewing on itself or combined with
areca nut. All these forms of tobacco have damaging
effects on the oral health. The most significant
preventive measure to prevent the oral health problems
caused by tobacco use is to stop using tobacco
products. The risk of developing oral cancer drops
rapidly when a smoker ceases tobacco use. After ten
years of not using tobacco, an ex-smoker/user’s risk of
oral cancers is about the same as that for someone who
has never smoked. To stop using tobacco products is
not an easy task. Fortunately, there are a number of
therapies available to assist in quitting of tobacco. It
is important to remember that, while it will be difficult,
ceasing to use tobacco has immediate health benefits,
including increased life expectancy and reduced risk
of tobacco related diseases and conditions.
Key words: Tobacco, smoking, Oral cancer, betel quid,
prevention
INTRODUCTION
Tobacco is the single greatest cause of preventable
death globally (1). Tobacco is consumed in a variety
of different ways, though smoking of manufactured
cigarettes is the most prevalent form of its use. The
emergence of widespread cigar use particularly among
adolescents of both sexes has been reported in the past
decade in the US. Cigars have higher total nicotine
content than cigarettes do and can deliver nicotine
both through smoke and through direct oral contact
with the tobacco wrapper. Cheroots are small cigars
made of heavy bodied tobacco. Bidi smoking is a
popular form of tobacco use in south Asia, accounting
for one-third of the tobacco produced in India for
smoking. Bidis and Kreteks are gaining popularity
Tobacco and oral health 19
Smokeless (chewing) tobacco (ST)
There are two main types of smokeless tobacco -
chewing tobacco and snuff. The most written about is
smokeless tobacco use among Asians taken with betel/
areca quid. Over 90 percent of Indians add tobacco to
the betel quid mixture. Commercially prepared betel
quid products that contain mostly areca nut and flakes
of tobacco are called Gutka. Other ST products which
carry signif icant mutagenicity are Toombak used in the
Sudan, Shamma in the Jizan province in Saudi Arabia,
powdered tobacco and alkali mixtures such as Nass/
Naswar used in northern and central Asia and in
Pakistan, Khaini (a mixture of ST and lime) used in
Bihar state of India and Nepal, and boiled/sweetened
ST called Zarda mostly used by people from
Bangladesh (3). All these forms of tobacco use are
associated with an increased risk of oral cancer.
Second-hand or environmental tobacco smoke (ETS)
ETS is carcinogenic to human beings. Meta-
analyses have shown a significant association between
lung cancer and smoke exposure from a spouse and
also between lung cancer and exposure at work. Risks
for other cancer types are inconclusive. There is at
present insufficient evidence that children exposed to
parental smoke have an altered risk of developing any
cancer.
Epidemiology
Tobacco which annually kills 4.9 million people
worldwide at present is estimated to take 10 million
lives every year by 2020. The more depressing part is
that half of them will die in their middle age. A global
estimate of smoking prevalence by each country is
given in a WHO data base for reference (4). These are
based on adult and youth smoking behaviours
collected from population-based, cross sectional
surveys at a given point of time. China is the largest
producer of tobacco in the world as well as the largest
consumer. A national prevalence survey in 1996
among adults (age 15+) found that 63% of males
smoked. In Malaysia, three National Health and
Morbidity surveys which have been conducted since
1986, the prevalence of smoking among adults age 18
and above were more than 20%; i.e. 21.5% in 1986,
24.8% in 1996 and 22.8% in 2006 (5, 6).
National surveys of persons aged 18 and older
from 1970 onwards report a decline in prevalence in
USA and most western European countries (7, 8). The
rate of decline among women is less than for men, and
the quit index for men is substantially higher than for
women. Both in UK and USA there are now twice as
many former cigarette smokers as current smokers. In
general, the prevalence of smoking in most population
groups is lowest among those with the highest
educational level. By race, smoking among adult
blacks is similar to whites in most countries. Denmark
has the highest rates of smoking in the EU.
Clinical presentation
General effects
Smoking-attributed diseases include cancer of
trachea, lung, bronchus, lip, mouth and pharynx,
ischemic heart disease, stroke, hypertension,
bronchitis, chronic obstructive pulmonary disease,
emphysema and asthma. Due to substantial decrease
in smoking in countries such as the UK, male lung
cancer rates have decreased rapidly in the last decade
(9). On current trends, the annual number of smoking-
attributable deaths among women should exceed that
for men shortly after the year 2000.
Effects of tobacco on teeth and oral health
The damaging and harmful effects of tobacco
usage on oral health are now well recognized, in
particular a higher prevalence and severity of
periodontal diseases among smokers and the
association of tobacco use with candidosis (10, 11),
and with oral malignancies (12, 13). Several recent
documents have reviewed the scientific evidence
relating to the oral disease burden attributable to
tobacco use (14) and have highlighted the role and the
need for the dental profession to get involved with
tobacco intervention (15).
Smoking cause’s discolouration of teeth and some
argue that tobacco in fact might increase dental decay
as it lowers salivary pH and the buffering power.
Smoking is likely to cause halitosis and may affect
smell and taste. Smokers may present with generalised
melanosis of the oral mucosa that often necessitate
investigations to exclude other systemic disorders.
Wound healing is impaired in tobacco smokers
possibly due to local vasoconstriction and poor
neutrophil function. There is fair evidence that tobacco
use is a major factor in the progression of periodontal
disease (16-20). Smokers have an increased prevalence
of periodontitis, and their disease severity is higher
with greater alveolar bone loss resulting in deeper
pockets compared with non-smokers (11). Acute
necrotising ulcerative gingivitis (ANUG) has been
shown to be associated with heavy smoking.
Periodontal therapy often fails among smokers and it
is difficult to halt attachment loss. Possibly for similar
reasons dental implant failure is more common in
smoking subjects compared with non-smokers.
Oral cancer
Over 80 percent of oral cancers are associated with
tobacco use (21). Oral squamous cell carcinoma
presents in a variety of ways such as white and red
patches, non-healing ulcers or exophytic growths.
Most early lesions are asymptomatic. Persistent
ulceration with rolled margins and fixation to
underlying tissues are pathognomonic signs of oral
malignancy. In late stages, disease spreads to adjacent
structures notably involving regional lymph nodes, and
20 Annals of Dentistry, University of Malaya, Vol. 18 2011
can cause mobile teeth and loss of teeth or even
pathological mandibular fractures. These stages may
be associated with pain, numbness or paraesthesia.
The clinical features of oral cancer are described
elsewhere. Currently diagnosing oral cancer relies on
pathological examination by biopsy and use of
imaging techniques to estimate the spread of the
disease. In addition, a number of adjunctive tools are
available which may facilitate the diagnosis of oral
cancer in the early stages (22-24).
Oral leukoplakia
Oral leukoplakia is the most common potentially
malignant lesion defined as a predominantly white
lesion of oral mucosa that cannot be characterised as
any other definable lesion (25). The appearance of
leukoplakia varies from uniformly white homogeneous
lesions to non-homogeneous speckled lesions with
red and/or nodular features. Leukoplakia is often
associated with tobacco use though idiopathic forms
of leukoplakia are recognised. The site of the oral
cavity affected by leukoplakia is often said to be
associated with the type of tobacco habit practiced;
lateral tongue and floor of mouth in cigarette smokers,
palate in pipe smokers and reverse smokers,
commissures in bidi smokers, buccal groves in tobacco
chewers where they park the quid and lower or upper
labial mucosa in snuff dippers. In a recent study in the
Netherlands, 64% of men and 60% of women with oral
leukoplakia were smokers (26). Tobacco use in men
was significantly associated with leukoplakia of
buccal mucosa and with all leukoplakia of floor of
mouth in both sexes. Oral leukoplakia in smokers
needs to be investigated by biopsy to assess any
dysplasia. Moderate to severe oral epithelial dysplasia
when present necessitate surgical intervention.
Intervention studies have demonstrated that
leukoplakia present in smokers might be reversible
when smoking habit was reduced or given up.
Erythroplakia
Erythroplakia is defined as ‘A f iery red patch that
cannot be characterized clinically or pathologically as
any other definable disease’ (27). Tobacco may
underlie some cases of erythroplakia.
Smoker’s palate (Leukokeratosis nicotina palati)
A greyish white discolouration of the palate with
multiple red elevated dots (inflamed minor salivary
gland openings) is often encountered in chronic
smokers. This is considered as a benign lesion as
cancer is not known to arise from this benign keratosis.
Reverse smoker’s keratosis
This is serious potentially malignant lesion
encountered in people who place the glowing end of
the cigar or cigarette inside the mouth. The clinical
appearance is often a mixture of red and white
plaques. Excrescences are found within the lesion
corresponding to inflamed minor salivary glands.
Whereas aforementioned smoker’s palate is not
considered as a precancerous lesion, palatal changes
in reverse smokers are a high risk lesion that is
associated with cancer development (28).
Aetiopathogenesis
Tobacco smoking (i.e., cigarette, pipe or cigar
smoking) particularly when combined with heavy
alcohol consumption has been identified as the
primary risk factor for approximately 80% of oral
malignancies (29). The risk of oral and pharyngeal
cancers is similar for cigarette and cigar smokers, with
an overall risk seven to ten times higher than for never
smokers. This is not surprising as the oral cavity is
exposed to the carcinogens in smoke whether the
smoke is inhaled or not. When the frequency of daily
tobacco use is computed, there is strong dose response
relationship between smoking rates and risk of mouth
cancer. Addition of ST to the areca quid raises the
relative risk of the product by nearly 15 times.
There are 55 carcinogens (Table 1) in cigarette
smoke that have been evaluated by the International
Agency for Research on Cancer (IARC) and for which
there is “sufficient evidence for carcinogenicity” in
either laboratory animals or humans (30). Other
carcinogens not evaluated by the IARC may also be
present.
Table 1. Summary of carcinogens in tobacco*
Type No. of
compounds
Polycyclic aromatic hydrocarbons (PAH) 10
N-Nitrosamines 7
Aza-arenes 3
Aromatic amines 3
Heterocyclic aromatic amines 8
Aldehydes 2
Miscellaneous organic compounds 15
Inorganic compounds 7
*According to the International Agency For Research on Cancer (IARC),
http://www.iarc.fr
Case-control studies from Europe have reported
adjusted odds ratios (ORs) of 11.1 for oral cavity and
12.9 for pharyngeal cancer (31). In particular, smoking
frequency and duration, and age at start have
significant associations. After giving up tobacco for a
decade or so, the risk of oral cancer of a past smoker
drops significantly to levels almost comparable to
never smokers.
Smoking patients show reduction of inflammatory
clinical signs that might be associated with local
vasoconstriction from nicotine, influence on
vasculature and cellular metabolism. This may
suppress symptoms of gingival inflammation.
Pathogenesis of periodontitis in smokers could be
linked to defects in neutrophil function, impaired
Tobacco and oral health 21
serum antibody responses to periodontal pathogens
and potentially diminished gingival fibroblast
function suggesting altered host response and
susceptibility (32). It is claimed that among smokers,
more patients remain culture positive for periodontal
pathogens after therapy. This may contribute to the
often observed unfavourable treatment results among
non-compliant smokers.
Diagnosis
Detection of tobacco consumption is mostly based
on taking a social history. This should include
questions on type of tobacco habit, daily frequency
and duration of use. Age of commencement is also an
important risk factor for many disorders and should be
recorded. Current smokers could be regular or
occasional smokers, regular being daily smokers. Some
have the habit of binge smoking when consuming
alcohol only but are unlikely to be addicted to
tobacco.
Tobacco handling can usually be seen on heavily
smoking patients’ fingers and the tobacco stains on
the oral mucosa and teeth. Dorsal tongue is often
stained in many smokers. A bad breath can also
highlight a smoker.
Validation of smoking can be done using the
carbon monoxide breath test (piCO, Bedfont) or by
measuring salivary, urine or serum cotinine which is a
metabolite of nicotine. Cut off concentration of
salivary cotinine is taken as 14 ng/ml to detect a
regular smoker.
Level of dependence to tobacco can be assessed
using the Fagerström test.
Treatment and interventions
Tobacco dependence shows many features of a
chronic disease. Regular smokers are addicted to the
habit as tobacco use results in true drug dependence.
A minority is able to quit in one attempt but the
majority may need some assistance to cease tobacco
use. Numerous effective treatments are now available,
and the dentists, oral physicians and their team
members should become actively involved in efforts
to reduce smoking.
Smoking cessation advices delivered by dentists
have shown to be effective. Brief advice given by a
clinician lasting about 3 minutes can yield a cessation
rate up to 5% (33, 34). With additional support such
as recommended use of nicotine replacement therapy
the quit rates achieved could be doubled. In treating
a smoker (willing to quit) the 5As (35), designed as a
brief counselling intervention, is helpful (Table 2).
Pharmacotherapy
As with other chronic diseases, the most effective
treatment of smoking requires multiple approaches in
addition to clinician’s advice. Pharmacotherapy is
proven to be effective, and several products are
available; nicotine patches, nicotine gum, nicotine
lozenge, nicotine inhaler and nicotine nasal spray.
Non-nicotine medication approved for smoking
cessation is bupropion (Zyban) therapy starting one
week before the quit date and continued up to 12
weeks after quitting. There are several medical contra-
indications particularly those with a predisposition to
seizures and/or a history of epilepsy. Pregnant and
breast-feeding mothers should not be prescribed this
drug. Bupropion therapy increases the chances of
quitting considerably up to 30%.
Prevention
Prevention of tobacco use is a key element in
public health. As tobacco use and experimentation
starts in early life preventive approaches should be
appropriately targeted to young people. Paedodontists,
orthodontists, school dentists and family practitioners
can take steps to initiate advice to young children
never to start smoking. Banning tobacco smoking in
public places, legislation on tobacco advertising and
taxation are known to effect tobacco sales. Primary
prevention, the helping of people not to use tobacco
in the first place and assisting current smokers to quit,
is an effective way to reduce morbidity and mortality
from oral cancer.
CONCLUSION
The oral health ill-effects of tobacco in whole or in
part are well known, and there is weighty evidence that
tobacco use has considerable influence on oral health.
But tobacco use is a modifiable risk factor for oral
diseases, and an obvious professional interest in
tobacco intervention can make a big difference in the
health of an individual or the outcome of a given
disease. Dentists have probably the greatest access to
‘healthy’ tobacco users in the healthcare system, and
even in the absence of tobacco-related diseases in the
mouth, the dentist will easily recognize these patients.
Therefore, dentists should pursue more formal training
in tobacco cessation counselling, which should be as
much a part of their job as plaque control and dietary
advice.
Table 2. The 5 A’s of tobacco cessation*
1. Ask about tobacco use - every patient/every visit
2. Assess willingness to make a quit attempt
3. Advice (those willing) to quit tobacco use. Those unwilling
will need motivation to return to the topic at a later time
4. Assist in quit attempt – set a quit date, emphasize
total abstinence, prompt support seeking, provide
supplementary material and recommend pharmaco-
therapy (see below)
5. Arrange follow up and refer to a specialist clinic if the
quit attempt has failed
* Fiore MC. US public health service clinical practice guideline: treating
tobacco use and dependence. Respir Care. 2000; 45(10): 1200-62.
22 Annals of Dentistry, University of Malaya, Vol. 18 2011
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... Tobacco usage may be a contributory factor in certain cases of erythroplakia [52] . Some erythroplakias appear to be smooth while others are nodular or granular in appearance. ...
... This lesion appears exclusively in mouth regions where snuff or chewed tobacco has come into close contact, and it is reversible once the user quits [57] . People who put the lighted end of a cigar or cigarette into their mouth get this potentially dangerous malignant lesion [52,58] . Furthermore, when tobacco is consumed, numerous by products such as nitrosamine and nitrosonornicotine are released, which when in close contact with the mucosa enhance penetration of these products into the mucosa and alter cellular morphometry, resulting in significant cellular changes [59] . ...
... • Occasional or regular or daily user [52] ▪ Fagerström test-for smoking dependence check [144] ▪ Modified Fagerström test-for smokeless tobacco dependence check [145] ▪ Questionnaire on Smoking Urges [146] ...
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Chapter
Tobacco's negative effects on oral health, in whole or in part, are well-known, and there is strong evidence that tobacco usage has a significant impact on oral health. As evidenced in the previous studies about the direct effect of tobacco on dental health, by the relationship between oral mucosal changes and tobacco smoking. While other changes show the changes in appearance of the teeth and tissues, such as gingival recession, smoker's melanosis, hairy black tongue and tooth discolouration. Numerous pharmacological and non-pharmacological strategies have been reported to treat tobacco dependence. But what appears to be lacking here is the lack of awareness among tobacco users about the harmful effects of tobacco and if known then knowledge gap about the various cessation strategies as well as their acceptance. It is the professional responsibility of the physician to inform his patients of the dangers and ill effects of tobacco smoking as well as inform the patients adequately and encourage them either to reduce or stop tobacco consumption completely. Dentists may also take an active role in nicotine replacement counselling. Tobacco cessation should be incorporated as an essential teaching element of the dental undergraduate curriculum, especially when it comes to the diagnosis and prevention of tobacco-induced complications. Close collaboration of both dentists and physicians as a team with tobacco cessation programmes is advocated to reduce tobacco use and quitting.
... Despite the continuous innumerable interventions, such programmes failed to apjcc.waocp.com R M Sumudu Himesha B Medawela, et al: Attitudes, Confidence in Practices and Barriers Towards Tobacco Cessation [4]. Among the smokeless tobacco products, the most written about is betel quid mixture with added tobacco [4]. ...
... R M Sumudu Himesha B Medawela, et al: Attitudes, Confidence in Practices and Barriers Towards Tobacco Cessation [4]. Among the smokeless tobacco products, the most written about is betel quid mixture with added tobacco [4]. Besides, commercially prepared smokeless tobacco products such as Gutka, Toombak, Nass, Naswar, Zardaare are popular in use [5]. ...
... The detrimental effects of tobacco smoking on general health are well documented and include cancer of respiratory tract, ischemic heart diseases, stroke, hypertension, chronic obstructive pulmonary diseases, asthma and emphysema [4]. ...
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Introduction: This study aimed to assess attitudes, confidence in practices and perceived barriers toward the promotion of tobacco cessation in the dental setting among clinical dental students in Sri Lanka. Methods: Role of dental schools on moulding future dental professionals with regards to education on tobacco cessation promotion is remarkable. A cross-sectional descriptive study was conducted on all the dental students from clinical years in 2018 using a self-administered structured questionnaire. Ninety-four per cent of the dental students from clinical years of faculty of dental sciences, University of Peradeniya, Sri Lanka completed the questionnaire (65% Females and 35 % Males) with a mean age of 24.65+ 2.24 years.Results: Clinical dental students possessed positive attitudes towards the professional responsibility of dentists in tobacco cessation whilst only 34% strongly agreed counselling offered in the dental setting has an impact on the same. More than half of the students remained neutral or disagreed the fact that nicotine replacement is within the scope of dentistry. Respondents expressed their confidence in tobacco cessation counselling. They identified “patients’ disinterest in receiving advice” as the main barrier to perform tobacco cessation practices in the dental setting. It is prudent to include formal education on tobacco cessation to the undergraduate curriculum of dental students to alleviate misconceptions related to practices of tobacco cessation in dental settings. Conclusion: It is of prime importance to identify training needs related to tobacco cessation promotion among dental undergraduates and compose a separate training module for them.
... Despite the continuous innumerable interventions, such programmes failed to apjcc.waocp.com R M Sumudu Himesha B Medawela, et al: Attitudes, Confidence in Practices and Barriers Towards Tobacco Cessation [4]. Among the smokeless tobacco products, the most written about is betel quid mixture with added tobacco [4]. ...
... R M Sumudu Himesha B Medawela, et al: Attitudes, Confidence in Practices and Barriers Towards Tobacco Cessation [4]. Among the smokeless tobacco products, the most written about is betel quid mixture with added tobacco [4]. Besides, commercially prepared smokeless tobacco products such as Gutka, Toombak, Nass, Naswar, Zardaare are popular in use [5]. ...
... The detrimental effects of tobacco smoking on general health are well documented and include cancer of respiratory tract, ischemic heart diseases, stroke, hypertension, chronic obstructive pulmonary diseases, asthma and emphysema [4]. ...
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Introduction: This study aimed to assess attitudes, confidence in practices and perceived barriers toward the promotion of tobacco cessation in the dental setting among clinical dental students in Sri Lanka. Methods: Role of dental schools on moulding future dental professionals with regards to education on tobacco cessation promotion is remarkable. A cross-sectional descriptive study was conducted on all the dental students from clinical years in 2018 using a self-administered structured questionnaire. Ninety-four per cent of the dental students from clinical years of faculty of dental sciences, University of Peradeniya, Sri Lanka completed the questionnaire (65% Females and 35 % Males) with a mean age of 24.65+ 2.24 years. Results: Clinical dental students possessed positive attitudes towards the professional responsibility of dentists in tobacco cessation whilst only 34% strongly agreed counselling offered in the dental setting has an impact on the same. More than half of the students remained neutral or disagreed the fact that nicotine replacement is within the scope of dentistry. Respondents expressed their confidence in tobacco cessation counselling. They identified “patients’ disinterest in receiving advice” as the main barrier to perform tobacco cessation practices in the dental setting. It is prudent to include formal education on tobacco cessation to the undergraduate curriculum of dental students to alleviate misconceptions related to practices of tobacco cessation in dental settings. Conclusion: It is of prime importance to identify training needs related to tobacco cessation promotion among dental undergraduates and compose a separate training module for them. Keywords: Dental Undergraduates- Sri Lanka- attitudes- confidence in practices and barriers towards- Tobacco cessation
... 92 The risk of developing cancer decreases after the cessation of tobacco use and the risk of developing oral cancer in an exsmoker will be similar to an individual. 93 There is no difference in the risk of oral cancers among smokers/tobacco users who stop smoking within ten years. 93 It is thus important to offer effective treatment to help smokers stop smoking. ...
... 93 There is no difference in the risk of oral cancers among smokers/tobacco users who stop smoking within ten years. 93 It is thus important to offer effective treatment to help smokers stop smoking. 94 ...
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Two hundred and seventy one original published materials related to tobacco use were found in a search through a database dedicated to indexing all original data relevant to Medicine and Health in Malaysia from 1996 - 2015. A total of 147 papers were selected and reviewed on the basis of their relevance and implications for future research. Findings were summarised, categorised and presented according to epidemiology, behaviour, clinical features and management of smoking. Most studies are cross-sectional with small sample sizes. Studies on smoking initiation and prevalence showed mixed findings with many small scale studies within the sub-groups. The majority of the studies were related to factors that contribute to initiation in adolescents. Nonetheless, there are limited studies on intervention strategies to curb smoking among this group. There is a lack of clinical studies to analyse tobacco use and major health problems in Malaysia. In addition, studies on the best treatment modalities on the use of pharmacotherapy and behavioural counselling have also remained unexplored. Reasons why smokers do not seek clinic help to quit smoking need further exploration. A finding on the extent of effort carried out by healthcare providers in assisting smokers to make quit attempts is not known. Studies on economic and government initiatives on policies and tobacco use focus mainly on the effects of cigarette bans, increased cigarettes taxes and the influence of the tobacco industry. Recommendations are given for the government to increase efforts in implementing smoke-free legislation, early and tailored interventions. Clinical studies in this area are lacking, as are opportunities to research on ways to reduce smoking initiation age and the most effective quit smoking strategies.
... The majority of cases of head and neck cancer (notably oral and oropharyngeal cancers and laryngeal cancers) are attributed to the separate and combined use of tobacco, excessive alcohol consumption and human papillomavirus infection. [3][4][5] There is evidence that occupational exposure to various substances is also a risk factor. 6 7 Concerning cancers of the nasopharynx, exposure to Epstein-Barr virus, exposure to formaldehyde and wood dust, salt fish consumption and smoking are all associated risk factors. ...
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Objectives The aim of this study was to analyse, within a French cohort of workers previously occupationally exposed to asbestos, incidence and mortality from various sites of head and neck cancers (larynx excluded) and to examine the potential link of these cancers with pleural plaques. Methods A 10-year follow-up study was conducted in the 13 481 male subjects included in the cohort between October 2003 and December 2005. Asbestos exposure was assessed by industrial hygienist analysis of a standardised questionnaire. The final cumulative exposure index (CEI; in equivalent fibres.years/mL) for each subject was calculated as the sum of each employment period’s four-level CEI. The number of head and neck cancers recorded by the National Health Insurance fund was collected in order to conduct an incidence study. Complementary analysis was restricted to men who had performed at least one chest CT scan (N=4804). A mortality study was also conducted. We used a Cox model with age as the time axis variable adjusted for smoking, time since first exposure, CEI of exposure to asbestos and pleural plaques on CT scans. Results We reported a significant dose–response relationship between CEI of exposure to asbestos and head and neck cancers after exclusion of laryngeal cancers, in the mortality study (HR 1.03, 95% CI (1.01 to 1.06) for an increase of 10 f.years/mL) and a close to significant dose–response relationship in the incidence study (HR 1.02, 95% CI (1.00 to 1.04) for an increase of 10 f.years/mL). No statistically significant association between pleural plaques and head and neck cancer incidence was observed. Conclusions This large-scale study suggests a relationship between asbestos exposure and head and neck cancers, after exclusion of laryngeal cancers, regardless of whether associated pleural plaques were present.
... A systemic review of the three studies among tobacco chewers reported for periodontal inflammation including gingivitis, gingival recession, and periodontal pocketing among tobacco chewers. [4] For most individuals, dental disease is essentially like a dreadful punishment with plaque as the chief executioner. Webster's dictionary defines plaque as "A sticky, usually colorless film on teeth that is formed by and harbors bacteria." ...
... The majority of cases are attributed to the separate and combined use of tobacco (smoked and smokeless), excessive alcohol consumption, betel quid and betel quid substitutes, and human papillomavirus (HPV-16) infection. [2][3][4][5][6][7] Although these risk factors have received the most attention in etiologic research for OPC, and justifiably so, as they are attributed to the vast majority of these tumors, there is evidence to suggest that exposure to occupational substances may also contribute to this disease. 8,9 It is also possible that tobacco and alcohol might interact with occupational carcinogens on the risk of OPCs. ...
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Background Oral and pharyngeal cancers (OPC) represent the seventh most common type of cancer and the seventh leading cause of deaths by cancer worldwide. Few studies have assessed the occupational exposure risks associated with OPC and in many cases the results are conflicting. The aim of this study was to determine, through a systematic review, the association of OPC and exposure to different occupational carcinogenic substances. Methods The addressed focused question was “Is there an association of occupational carcinogenic substances with OPC?” PubMed, MEDLINE, EMBASE, and ISI Web of Science databases were searched between January 1995 up to and including July 2016 using the keywords “oral cancer,” “pharyngeal cancer,” “pharyngeal neoplasms,” “oral neoplasms,” “occupational disease,” “occupational exposure,” and “occupational risk factor” in various combinations. Letters to the Editor, review articles, case reports, and unpublished articles were excluded. Results Fourteen original articles were included. Majority of the studies were conducted in European countries and used a case‐control design. The results showed a significant association between formaldehyde, wood dust, coal dust, asbestos, welding fumes, and risk of developing OPC, while marginal association was observed with metal and leather dust. No associated risk was observed for textile fibers. Conclusion There is some evidence to suggest associations of occupational substances with OPC, particularly in the pharynx. Future well‐designed studies are required to confirm or rule out with confidence the associated exposure risk of these substances.
... Tobacco industry is growing at a faster pace and the number of smokers among women and adolescents is increasing [2]. Any form of tobacco (chewing, smoking, smelling) affects oral cavity and causes life-threatening diseases such as oral cancer and leukoplakia [3]. The most important measure for preventing the oral health pathology caused by tobacco consumption is the termination of use of tobacco products. ...
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Tobacco smoking is associated with the development of many diseases, including oral cancer and leukoplakia. This fact is described in the 2014 annual report of the US Office of the Surgeon General "The results of smoking on health, 50 years of progress". Despite the fact that different forms of tobacco(cigarettes, cigars, pipes, dipping and chewing tobacco or inhaled) are used in order to reduce pulmonary and cardiac complications, tobacco has a negative influence on human health. Tobacco smoking increases the death rate of smokers by 30-80%. Based on the mentioned we can determine the causal relationship between smoking and the development of oral cancer, leukoplakia and chronic impact on oral organs, i.e. lips during constant tobacco use.
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Introduction: Toombak is a form of smokeless tobacco that is not well known in Western Society but is widely used by the Sudanese population and many others in the sub-Sahara region. However, unlike other smokeless tobacco products, information on the carcinogenic potential of toombak is scarce. The present review explored any potential epidemiological association between the use of toombak and oral leukoplakia and oral squamous cell carcinoma (OSCC). Methods: Databases including the Web of Science, SCOPUS, EMBASE, PubMed were searched for literature on the potential association between toombak and oral leukoplakia and OSCC. The search also included grey literature. The search period extended from 1990 to 2018. Following data mining, the study selection was conducted by two reviewers independently. Results: Eight studies that satisfied the inclusion criteria were included. Based on these results there was a 3-to 7-fold increased risk of developing the oral leukoplakia and oral squamous cell carcinoima among toombak users compared to non-users. Conclusion: Based on the results of the systematic review there is strong epidemiological evidence to suggest toombak to be a major risk factor for both oral leukoplakia and OSCC Further studies are necessary to evaluate the molecular pathway of toombak-induced oral carcinogenesis. This article is protected by copyright. All rights reserved.
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 Oral potentially malignant disorders (OPMD) are known to precede the development of oral cancer. Detection of OPMD allows delivery of interventions that may reduce the evolution of these disorders to malignancy. Following oral examinations, the accuracy of detection of OPMD by chemiluminescence was evaluated using a commercially available detection kit - ViziLite. Data derived were compared in relation to conventional oral examination and surgical biopsy. A total of 126 patients, 70 men and 56 women (mean age 58.5 ± 11.9 years) attending Oral Medicine Clinics at King's and Guy's Hospitals, London, with oral white, red, and mixed white and red patches were enrolled. Sixty-one patients were current smokers, 28 were ex-smokers, while 92 were alcohol users. In a detailed investigation, these patients underwent ViziLite examination followed by surgical biopsy.  Based on the clinical diagnosis, 70 patients had oral leukoplakia/erythroplakia, 32 had oral lichen planus, nine had chronic hyperplastic candidiasis, and rest had frictional keratosis (13) or oral submucous fibrosis (2). Of 126 lesions, 95 (75.4%) showed aceto-whitening. Most oral leukoplakias had enhanced visibility and sharpness of the lesion when viewed with the ViziLite system. Following biopsy, 44 had oral epithelial dysplasia (29 mild, eight moderate, and seven severe). The sensitivity (se) and specificity (sp) of chemiluminescence for the detection of a dysplastic lesion were 77.3% and 27.8%, respectively. While ViziLite has the ability to detect OPMD, it does not accurately delineate dysplastic lesions. The device can be used as a general oral mucosal examination system and may in particular improve the visualization of leukoplakias.
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This paper reviews the evidence for cigarette smoking as a risk factor for the development of severe destructive periodontal disease in young adults. A high prevalence of cigarette smoking has been identified among young individuals with aggressive periodontitis and tobacco usage increases the risk of periodontal destruction most significantly in young populations. The effect appears to be dose related and is independent of levels of plaque accumulation. Young smokers have more alveolar bone loss and attachment loss than non smoking equivalents. Prolonged and heavy smoking can reduce gingival bleeding and therefore mask the clinical marker of bleeding on probing often used by dentists to monitor periodontal health. This has implications for potential misdiagnosis and failure to detect periodontitis at an early stage. Nicotine metabolites concentrate in the periodontal tissues and can have local effects as well as the potential to affect the systemic host response. Dentists are well placed to assess the smoking status of their young patients and have a role to play in the delivery of smoking cessation advice especially as it pertains to periodontal health. In this way the dental profession can also make a significant contribution to the general health and well being of our youth and future generations.
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To determine whether postmenopausal bone loss and factors associated with osteoporosis affect tooth retention, we examined vertebral and proximal femoral (postcranial) bone mineral density in relation to tooth loss and attachment loss in a cross-sectional study of 135 postmenopausal women (age range 41–70 yr). Women had at least 10 teeth and no evidence of moderate or severe periodontal disease. Full-mouth attachment loss measurements were made using a pressure-sensitive probe, and bone density was determined by dual-energy X-ray absorptiometry. Attachment loss was correlated with tooth loss (number of remaining teeth, radiologically determined), but not with vertebral or proximal femur bone density. Multivariate analysis showed current smoking (p = 0.01), years since menopause (p = 0.02) and the interaction of age and current smoking (p < 0.01), to be statistically significant predictors of attachment loss in our study population.
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Specific risk indicators associated with either susceptibility or resistance to severe forms of periodontal disease were evaluated in a cross-section of 1,426 subjects, 25 to 74 years of age, mostly metropolitan dwellers, residing in Erie County, New York, and surrounding areas. The study sample exhibited a wide range of periodontal disease experience defined by different levels of attachment loss. Therefore, it was possible to accurately assess associations between the extent of periodontal disease and patient characteristics including age, smoking, systemic diseases, exposure to occupational hazards, and subgingival microbial flora. Age was the factor most strongly associated with attachment loss, with odds ratios for subjects 35 to 44 years old ranging from 1.72 (95% CI: 1.18 to 2.49) to 9.01 (5.86 to 13.89) for subjects 65 to 74 years old. Diabetes mellitus was the only systemic disease positively associated with attachment loss with an odds ratio of 2.32 (95% CI: 1.17-4.60). Smoking had relative risks ranging from 2.05 (95% CI: 1.47-2.87) for light smokers increasing to 4.75 (95% CI: 3.28-6.91) for heavy smokers. The presence of two bacteria, Porphyromonas gingivalis and Bacteroides forsythus, in the subgingival flora represented risks of 1.59 (95% CI: 1.11-2.25) and 2.45 (95% CI: 1.87-3.24), respectively. Our results show that age, smoking, diabetes mellitus, and the presence of subgingival P. gingivalis and B. forsythus are risk indicators for attachment loss. These associations remain valid after controlling for gender, socioeconomic status, income, education, and oral hygiene status expressed in terms of supragingival plaque accumulation and subgingival calculus. Longitudinal, intervention, and etiology-focused studies will establish whether these indicators are true risk factors.
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Refractory periodontal disease is characterized by low plaque scores and low responsiveness to periodontal therapy. The patients often have a history of antibiotic therapy and therefore have a high incidence of resistance in the subgingival microflora. The above features are in contrast to adult chronic periodontal disease and recurrence of disease. The subgingival microflora of refractory disease may be either predominantly gram-positive with elevated levels of Streptococcus intermedius or may be gram negative and contain elevated levels of the classical periodontal pathogens. In some cases serum IgG antibodies against Porphyromonas gingivalis are elevated and seem to decrease after therapy. Smoking may be an important factor in refractory periodontal disease. Treatment with directed antibiotic therapy as an adjunct to scaling and root planing retards the progression of disease for a limited time. Many questions are still not answered and suggestions are made for future directions in research.